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minibabyqq 2007-1-3 22:45

[color=Magenta][size=5][b]食道藥物效力[/b][/size][/color]

Efficacy of Gastrointestinal Drugs: What Works in the Dog   


I. 胃反分泌藥物
擴散障礙
Sucralfate 是一種cytoprotective 藥物組成由被硫化的蔗糖和polyaluminum 氫氧化。在胃的酸性環境裡, sucralfate 廣泛地十字架被聚合形成束縛對壞死的組織蛋白質在潰瘍的一個黏膠凝體。除作為擴散障礙之外, sucralfate 也許有另外的有利作用(即, 前列腺素生產的膽汁鹽的刺激, 吸附, 和鈍化作用胃蛋白酵素) 。Sucralfate 是一種有效的藥物在對待的胃erosion/ulcer 在人, 但它的效力在伴侶動物嚴謹地未被展示。雖然沒有回顧展或預期研究, 對藥物的用途會似乎有道理根據人和實驗性動物研究。組合療法(sucralfate + 氨基酸H2 反對者, 或sucralfate + H+, K+ - ATPase 抗化劑) 頻繁地被使用, 但仍然有沒有好證據, 組合療法比組分療法好在伴侶動物醫學。終於, 如果組合療法將被考慮, sucralfate 活化作用和氨基酸H 2 感受器官反對者吸收的 體外研究建議, 二種藥物應該獨立地被執行。它不是確切是否這是重要 活體內。 Sucralfate 證明了效力在esophagitis 的治療在狗和貓。的確, sucralfate 大概是最重要的藥物考慮在esophagitis 的治療。
氨基酸H2 感受器官反對者
氨基酸H2 感受器官反對者(即, 腸潰藥、ranitidine 、famotidine, nizatidine) 禁止胃酸分泌物由對抗氨基酸H2 感受器官在胃頭頂骨細胞。這些代理證明了效力在對待的胃潰瘍疾病在伴侶動物。沒有令人相信的證據, 然而, 一種藥物比另有效的在同樣分類。Famotidine 和nizatidine 比ranitidine 有力, 並且ranitidine 比腸潰藥有力, 但藥物有力大概不是那重要在動物中(即, 狗和貓) 以低基礎酸分泌物。在藥物的這個分類, ranitidine 和nizatidine 有另外的好處(或不利) 刺激胃倒空和大腸能動性。Ranitidine, 例如, 是有用的在恢復正常胃倒空的樣式在實驗性似犬胃潰瘍。
Acetylcholine M1 感受器官反對者
糞膽鹼反對者禁止酸分泌物由對抗muscarinic 糞膽鹼感受器官在胃頭頂骨細胞。大多現在可以得到的反對者無選擇性, 然而, 和不應該被使用作為胃反分泌代理。Pirenzepine 和telenzepine, 有選擇性M1 糞膽鹼反對者, 禁止cholinergically 斡旋的胃酸分泌物沒有對斡旋GI 、導氣管, 和泌尿膀胱光滑的肌肉收縮的其它muscarinic 感受器官的重大作用(M 2, M 3) 。因而, pirenzepine 和telenzepine 能被推薦在胃潰瘍疾病療法在伴侶動物。Telenzepine 比pirenzepine 有力在狗; 藥物不是可利用的在美國(加拿大和歐洲, 只) 。
H+, K+ - ATPase 抗化劑
被替代的benzimidazoles (即, omeprazole, lansoprazole) 禁止胃酸分泌物由不可逆地束縛氫核運輸的酵素在頭頂骨細胞的luminal 表面。Omeprazole, 例如, 禁止胃酸分泌物在狗至少24 小時在唯一口頭藥量以後(0.7 mg/kg) 。Omeprazole 像腸潰藥是一樣有效的在癒合機械導致的潰瘍, 但omeprazole 比腸潰藥有效的在癒合阿斯匹靈導致的胃炎。另外的研究將是需要的確定這些藥物比較效力在對待其它胃炎和胃潰瘍的形式。有當前較少臨床經驗以lansoprazole, 但藥物是沒有被報告的副作用在貓和狗。Lansoprazole 不看上去有藥物行動的有力和期間相似與omeprazole, 和有明顯的另外的好處。
前列腺素E1 類似物
內在被生產的前列腺素促進胃黏膜防禦機制由禁止頭頂骨細胞酸分泌物和由刺激黏膜血流、重碳酸鹽分泌物、黏液分泌物, 和上皮細胞更新。Nonsteroidal 抗發炎藥物禁止這內在前列腺素生產和安置動物在增加的風險為胃炎、胃侵蝕, 和胃潰瘍。前列腺素E 1 (即, misoprostol) 綜合性類似物減少病理學由阿斯匹靈和其它NSAIDs 導致。預防反對胃黏膜傷害由NSAIDs 導致因而是主要徵兆為misoprostol 。這個小組藥物明顯地沒有分明好處在氨基酸H2 感受器官反對者在對待潰瘍沒與相關NSAIDs 。
II 。食道Prokinetic Agents.Dopaminergic 藥物(即, Metoclopramide)
降低食管括約肌混亂
Metoclopramide 增加壓力在gastroesophageal 括約肌和刺激胃倒空。被延遲的胃倒空促進gastroesophageal 倒回由增加胃容量和壓力梯度。因而, metoclopramide 也許被推薦在gastroesophageal 倒回療法。
胃倒空的混亂
Metoclopramide 是選擇藥物為治療延遲胃倒空混亂在cisapride 的可及性之前。除它的中央anti-emetic 作用之外, metoclopramide 增加antral 收縮高度和頻率, 禁止fundic 易接收的放鬆, 和協調胃, 幽門, 和十二指腸的能動性, 導致加速的胃倒空。它被使用在0.2 到0.5 mg/kg 體重劑量每八個小時, 口頭或腸外地被執行。連續的靜脈內注入可能被執行在0.01 到0.02 mg/kg/hour 或1.2 mg/kg/day 劑量。metoclopramide 的作用在胃倒空在狗看來是重要為液體比對於固體。
小腸能動性混亂
Metoclopramide 是最有效的當被延遲的胃倒空歸結於粗劣的antropyloroduodenal 協調。Metoclopramide 是較不有效的在末端小腸和冒號。
中央斡旋的嘔吐
metoclopramide 的antiemetic 作用歸結於多巴胺D2 感受器官對抗性在化學受體觸發器區域。Metoclopramide 禁止次要地嘔吐通過對能動性的作用。
III 。食道Prokinetic Agents.Serotonergic 藥物(即, Cisapride 、Prucalopride, Tegaserod)
食管混亂
Cisapride 會看來是一種合理的藥物在gastroesophageal 倒回疾病的治療因為它刺激胃倒空並且增加gastroesophageal (GE) 括約肌壓力。GE 倒回的發生和流行在狗和貓是未知的, 雖然最近報告建議倒回esophagitis 也許是共同的個體。機制為GE 括約肌和GE 倒回的瞬變放鬆存在在這個種類, 正他們做在人。比較研究表示, cisapride 比metoclopramide 有力在刺激胃倒空的和增長的GE 括約肌壓力。Cisapride 並且刺激末端食管蠕動在那些動物種類(即, 貓, 人) 末端食管muscularis 由光滑的肌肉組成。明顯的例外是狗, 整個食管身體由條紋的肌肉組成的種類。Cisapride 不應該被推薦為似犬megaesophagus 的治療。
胃倒空的混亂
被延遲的胃倒空現在被認可是上部胃腸道標誌, 即, 厭食和嘔吐的重要起因, 在狗和貓。被延遲的胃倒空被報告了在動物中恢復從胃膨脹和volvulus, 在感染和激動胃疾病, 和在實驗性胃潰瘍。cisapride 劑量在0.05.0.2 mg/kg 的範圍提高胃倒空在狗以正常胃倒空。但是, 劑量在0.5.1.0 mg/kg 的範圍是需要的提高胃倒空在狗以被延遲的胃倒空被α 導致;2- 腎上腺素能的苦悶者、多巴胺、disopyramide, 或antral tachygastria 。Cisapride 加速胃倒空在狗由刺激幽門和十二指腸的馬達活動, 由提高antropyloroduodenal 協調, 和由增加卑鄙傳播距離十二指腸的收縮。Cisapride 看來是優越在metoclopramide 和domperidone 在刺激胃倒空。
小腸能動性混亂
Cisapride 刺激jejunal 釘破裂遷移、jejunal 推進能動性, 和antropyloroduodenal 協調從事小腸油脂注入在狗。因而, cisapride 會看上去有一個合理的地方在手術後腸塞痛和小腸冒充阻礙的治療。
Colonic 能動性混亂
許多的作用食道prokinetic 代理(即, metoclopramide 、domperidone, 和紅黴素) 對接近胃腸道被限制。不同於這些代理, cisapride 並且刺激大腸能動性。Cisapride 會看上去有一個合理的地方在先天便秘的治療。正常大腸能動性的中斷仿造了結果在便秘在家養的貓。Cisapride 改進大腸能動性在溫和地或適度地影響以先天便秘的貓; 貓以耐久hypomotility 和擴張通常較不敏感。
同邊白金導致的嘔吐
Cisapride 對抗5-HT3 感受器官和禁止嘔吐與相關同邊白金化療。有力cisapride 的5-HT3 anti-emetic 作用(ED50 = 0.6 mg/kg IV; ED100 = 2.6 mg/kg IV) 是決不它的5-HT4 prokinetic 作用。因而, cisapride 能被推薦作為一個antiemetic 代理為癌症化療患者只如果其它5-HT3 反對者(即, ondansetron) 立刻不是可利用的。
新藥物
二種新5-HT4 苦悶者藥物, prucalopride 和tegaserod, 被提名為行銷2001 年或2002 年。這些藥物也許為cisapride 從市場被去除了的國家提供適當的選擇。
IV 。食道Prokinetic Agents.Motilin 像藥物(即, 紅黴素)
降低食管括約肌混亂
Erythromycin 增加gastroesophageal 括約肌的壓力, 和應該是有用的在gastroesophageal 倒回和倒回esophagitis 的治療。
胃倒空的混亂
紅黴素加速胃倒空由導致antral 收縮相似與階段III interdigestive 狀態。收縮聯繫了階段III 通常發生只在齋戒的狀態期間, 並且他們清除胃難消化固體。與紅黴素, 加速的胃倒空固體發生犧牲胃篩在被哺養的狀態期間。不充分地被磨碎的食物(> 0.5 毫米) 倒空入十二指腸。如果被延遲的胃倒空對臨床標誌貢獻, 然後倒空被保留的固體的胃也許是有利的。口頭紅黴素被推薦的抗菌劑量在狗和貓是10.20 mg/kg 每八個小時。prokinetic 劑量是低在0.5.1.0 mg/kg 每八個小時。
小腸能動性混亂
紅黴素導致發起於胃竇和移居對十二指腸、空腸, 和終端迴腸的收縮。紅黴素也許是有用的在手術後腸塞痛的治療。
V. 食道Prokinetic Agents.Acetylcholinesterase 抗化劑
(即, Nizatidine 和Ranitidine)
Nizatidine Antisecretory 活動
Nizatidine 是氨基酸H 2 的一個競爭, 反演性反對者- 感受器官, 特別那些在頭頂骨細胞裡。競爭對抗性氨基酸H2- 感受器官與nizatidine 有效地減少胃酸分泌物。H2- 感受器官反對者臨床被使用在胃潰瘍的治療。Nizatidine 是更新的H2- 感受器官反對者以有力相似與那ranitidine 。nizatidine 當前的被推薦的口頭劑量(2.5-5.0 mg/kg/day) 從胃酸分泌物的研究被獲得在Heidenhain 囊狗。
Nizatidine Prokinetic 活動
Nizatidine 刺激胃倒空和大腸收縮在胃antisecretory 劑量主要通過它的膽鹼酯抑制劑(疼痛) 活動。Nizatidine 極大增加胃倒空並且大腸能動性, 但是其它H2- 感受器官反對者(即, 腸潰藥, famotidine) 沒有這樣的作用。
Ranitidine Antisecretory 活動
H2- 感受器官反對者, 包括ranitidine, 競爭地禁止氨基酸導致的胃酸分泌物由頭頂骨細胞。ranitidine 被推薦的反分泌劑量為狗和貓口頭是1.2 mg/kg 每八個到十二個小時。
Ranitidine Prokinetic 活動
Ranitidine 刺激食道能動性主要通過它的膽鹼酯抑制劑(疼痛) 活動。胃潰瘍被認為瑕疵胃推進力的起因在狗。治療與ranitidine 會是有利的不僅由禁止胃酸分泌物而且由加速胃倒空。所以, ranitidine 像nizatidine, 有效力沒被發現以一些另一H2- 感受器官反對者在食道能動性的刺激。


I. Gastric Anti-Secretory Drugs
Diffusion Barriers
Sucralfate is a cytoprotective drug composed of sulfated sucrose and polyaluminum hydroxide. In the acidic environment of the stomach, sucralfate is extensively cross-polymerized to form a viscous gel that binds to the necrotic tissue proteins in an ulcer. In addition to acting as a diffusion barrier, sucralfate may have additional beneficial effects (e.g., stimulation of prostaglandin production, adsorption of bile salts, and inactivation of gastric pepsins). Sucralfate is an effective drug in treating gastric erosion/ulcer in human beings, but its efficacy in companion animals has never been rigorously demonstrated. Although there are no retrospective or prospective studies, use of the drug would seem to make sense based on human and experimental animal studies. Combination therapy (sucralfate + histamine H2 antagonist, or sucralfate + H+, K+ - ATPase inhibitor) is frequently employed, but there is still no good evidence that combination therapy is better than component therapy in companion animal medicine. Finally, if combination therapy is to be considered, in vitro studies of sucralfate activation and histamine H2 receptor antagonist absorption suggest that the two drugs should be administered independently. It is not clear whether this is important in vivo. Sucralfate has proven efficacy in the treatment of esophagitis in dogs and cats. Indeed, sucralfate is probably the most important drug consideration in the treatment of esophagitis.
Histamine H2 Receptor Antagonists
Histamine H2 receptor antagonists (e.g., cimetidine, ranitidine, famotidine, nizatidine) inhibit gastric acid secretion by antagonizing the histamine H2 receptor on gastric parietal cells. These agents have proven efficacy in treating gastric ulcer disease in companion animals. There is no convincing evidence, however, that one drug is more efficacious than another in the same classification. Famotidine and nizatidine are more potent than ranitidine, and ranitidine is more potent than cimetidine, but pharmacologic potency is probably not that important in animals (e.g., dogs and cats) with low basal acid secretion. In this classification of drugs, ranitidine and nizatidine have the additional advantage (or disadvantage) of stimulating gastric emptying and colonic motility. Ranitidine, for example, is useful in restoring normal gastric emptying patterns in an experimental canine gastric ulcer.
Acetylcholine M1 Receptor Antagonists
Cholinergic antagonists inhibit acid secretion by antagonizing the muscarinic cholinergic receptor on gastric parietal cells. Most of the currently available antagonists are nonselective, however, and should not be used as gastric anti-secretory agents. Pirenzepine and telenzepine, selective M1 cholinergic antagonists, inhibit cholinergically mediated gastric acid secretion without significant effects on other muscarinic receptors (M2, M3) that mediate GI, airway, and urinary bladder smooth muscle contraction. Thus, pirenzepine and telenzepine could be recommended in the therapy of gastric ulcer disease in companion animals. Telenzepine is more potent than pirenzepine in the dog; neither drug is available in the United States (Canada and Europe, only).
H+, K+ - ATPase Inhibitors
The substituted benzimidazoles (e.g., omeprazole, lansoprazole) inhibit gastric acid secretion by irreversibly binding the proton-transporting enzyme at the luminal surface of the parietal cell. Omeprazole, for example, inhibits gastric acid secretion in dogs for at least 24 hours after a single oral dose (0.7 mg/kg). Omeprazole is as effective as cimetidine in healing mechanically-induced ulcers, but omeprazole is more effective than cimetidine in healing aspirin-induced gastritis. Additional studies will be needed to determine the comparative efficacy of these drugs in treating other forms of gastritis and gastric ulcer. There is less clinical experience with lansoprazole at the present time, but the drug is without reported side effects in both cats and dogs. Lansoprazole appears to have pharmacologic potency and duration of action similar to omeprazole, and has no apparent additional advantages.
Prostaglandin E1 Analogues
Endogenously produced prostaglandins promote gastric mucosal defense mechanisms by inhibiting parietal cell acid secretion and by stimulating mucosal blood flow, bicarbonate secretion, mucus secretion, and epithelial cell renewal. Nonsteroidal anti-inflammatory drugs inhibit this endogenous prostaglandin production and place animals at increased risk for gastritis, gastric erosion, and gastric ulcer. Synthetic analogues of prostaglandin E1 (e.g., misoprostol) diminish the pathology produced by aspirin and other NSAIDs. Prophylaxis against gastric mucosal injury induced by NSAIDs thus is the primary indication for misoprostol. This group of drugs apparently does not have distinct advantages over histamine H2 receptor antagonists in treating ulcer not associated with NSAIDs.
II. Gastrointestinal Prokinetic Agents𤒈opaminergic Drugs (e.g., Metoclopramide)
Lower Esophageal Sphincter Disorders
Metoclopramide increases pressure in the gastroesophageal sphincter and stimulates gastric emptying. Delayed gastric emptying promotes gastroesophageal reflux by increasing the gastric volume and pressure gradient. Thus, metoclopramide may be recommended in the therapy of gastroesophageal reflux.
Gastric Emptying Disorders
Metoclopramide was the drug of choice for treatment of delayed gastric-emptying disorders prior to the availability of cisapride. In addition to its central anti-emetic effect, metoclopramide increases the amplitude and frequency of antral contractions, inhibits fundic receptive relaxation, and coordinates gastric, pyloric, and duodenal motility, all of which result in accelerated gastric emptying. It is used at a dosage of 0.2 to 0.5 mg/kg body weight every eight hours, administered orally or parenterally. Continuous intravenous infusions can be administered at dosages of 0.01 to 0.02 mg/kg/hour or 1? mg/kg/day. The effects of metoclopramide on gastric emptying in the dog appear to be more important for liquids than for solids.
Small Bowel Motility Disorders
Metoclopramide is most effective when delayed gastric emptying is due to poor antropyloroduodenal coordination. Metoclopramide is less effective in the distal small intestine and colon.
Centrally-Mediated Emesis
The antiemetic effect of metoclopramide is due to dopamine D2 receptor antagonism at the chemoreceptor trigger zone. Metoclopramide inhibits vomiting secondarily through effects on motility.
III. Gastrointestinal Prokinetic Agents𣶷erotonergic Drugs (e.g., Cisapride, Prucalopride, Tegaserod)
Esophageal Disorders
Cisapride would appear to be a rational drug in the treatment of gastroesophageal reflux disease because it stimulates gastric emptying and increases gastroesophageal (GE) sphincter pressure. The incidence and prevalence of GE reflux in the dog and cat are unknown, although recent reports suggest that reflux esophagitis may be a common entity. The mechanisms for transient relaxation of the GE sphincter and GE reflux exist in these species, just as they do in human beings. Comparative studies have shown that cisapride is more potent than metoclopramide in stimulating gastric emptying and increasing GE sphincter pressure. Cisapride also stimulates distal esophageal peristalsis in those animal species (e.g., cat, human) in which the distal esophageal muscularis is composed of smooth muscle. The obvious exception is the dog, a species in which the entire esophageal body is composed of striated muscle. Cisapride should not be recommended for the treatment of canine megaesophagus.
Gastric Emptying Disorders
Delayed gastric emptying is now recognized to be an important cause of upper gastrointestinal tract signs, e.g., anorexia and vomiting, in dogs and cats. Delayed gastric emptying has been reported in animals recovering from gastric dilatation and volvulus, in infectious and inflammatory gastric diseases, and in experimental gastric ulcer. Dosages of cisapride in the range of 0.05?.2 mg/kg enhance gastric emptying in dogs with normal gastric emptying. However, dosages in the range of 0.5?.0 mg/kg are needed to enhance gastric emptying in dogs with delayed gastric emptying induced by α2-adrenergic agonists, dopamine, disopyramide, or antral tachygastria. Cisapride accelerates gastric emptying in dogs by stimulating pyloric and duodenal motor activity, by enhancing antropyloroduodenal coordination, and by increasing the mean propagation distance of duodenal contractions. Cisapride appears to be superior to metoclopramide and domperidone in stimulating gastric emptying.
Small Bowel Motility Disorders
Cisapride stimulates jejunal spike burst migration, jejunal propulsive motility, and antropyloroduodenal coordination following intestinal lipid infusion in the dog. Thus, cisapride would appear to have a rational place in the treatment of post-operative ileus and intestinal pseudo-obstruction.
蟖olonic Motility Disorders
The effects of many of the gastrointestinal prokinetic agents (e.g., metoclopramide, domperidone, and erythromycin) are limited to the proximal gastrointestinal tract. Unlike these agents, cisapride also stimulates colonic motility. Cisapride would appear to have a rational place in the treatment of idiopathic constipation. Disruption of the normal colonic motility patterns results in constipation in domestic cats. Cisapride improves colonic motility in cats that are mildly or moderately affected with idiopathic constipation; cats with long-standing hypomotility and dilation are usually less responsive.
Cis-platinum-Induced Emesis
Cisapride antagonizes 5-HT3 receptors and inhibits vomiting associated with cis-platinum chemotherapy. The potency of cisapride's 5-HT3 anti-emetic effect (ED50 = 0.6 mg/kg IV; ED100 = 2.6 mg/kg IV) is less than its 5-HT4 prokinetic effect. Thus, cisapride could be recommended as an antiemetic agent for the cancer chemotherapy patient only if other 5-HT3 antagonists (e.g., ondansetron) are not immediately available.
New Drugs
Two new 5-HT4 agonist drugs, prucalopride and tegaserod, are slated for marketing in 2001 or 2002. These drugs may provide suitable alternatives for countries in which cisapride has been removed from the marketplace.
IV. Gastrointestinal Prokinetic Agents𦳀otilin-Like Drugs (e.g., Erythromycin)
Lower Esophageal Sphincter Disorders
𪊲rythromycin increases the pressure of the gastroesophageal sphincter, and should be useful in the treatment of gastroesophageal reflux and reflux esophagitis.

minibabyqq 2007-1-3 22:47

[color=Magenta][size=5][b]Hypercalcemia 在狗: 對診斷和治療的方法  [/b][/size][/color]

[size=12px]介紹
當清液樣品遞交給實驗室, 總清液鈣含量典型地是什麼被報告。總鈣包括被電離的鈣、complexed 鈣, 和protein-bound 鈣。在多數實驗室, hypercalcemia 被提供當清液總鈣含量是> 12.0 mg/dL 在狗。確切值當hypercalcemia 存在必須是堅定的為各個實驗室。清液總鈣和清液被電離的鈣價值是低在貓比在狗。在我們的實驗室, hypercalcemia 在狗被定義當總清液鈣是大於11.6 mg/dL 並且被電離的鈣含量是大於6.0 mg/dL 。
在臨床正常動物, 清液被電離的鈣與清液共計鈣的水平是典型地比例(被電離的鈣通常是50.60% 總鈣) 。但是, 在害病的動物, 清液被電離的鈣與總清液鈣不是比例, 和無法被預言從總清液鈣。被電離的鈣比被預言經常低在有腎衰竭病人, 不管他們的清液共計鈣水平(低, 正常, 或高) 。有hypoalbuminemia 和corrected. 清液共計鈣價值病人也許仍然減少了被電離的鈣的水平。患者與適度對嚴厲新陳代謝的酸中毒進行在他們的被電離的鈣分數的增量由於轉移鈣從鈣protein-bound 商店。為這些原因, 清液被電離的鈣含量的測量被推薦在所有患者與腎衰竭或hypercalcemia 。因為被電離的清液鈣含量由對氧氣和酸鹼度的暴露影響, 清液樣品應該絕氧被收集和被處理在分析之前。清液被電離的鈣含量不改變在樣品被存放72 個小時在室溫, 或在4.C 當樣品絕氧被收集和被存放。當延遲在清液樣品的測量是必要的(和在寄發樣品到外部實驗室), 絕氧收藏以冷藏72 個小時導致對清液被電離的鈣的最準確的評估。
HYPERCALCEMIA 的臨床標誌
在被電離的清液鈣含量的小增量在法線之上可能有有害生理學後果, 但是情況增加總清液鈣沒有增量在被電離的鈣裡不陳列有害作用。因而, 被電離的清液鈣含量的測量是最大重要。程度互作用與清液磷和那些與共計清液鈣時間磷含量產品大於70 很可能有嚴厲組織變動與相關成礦重要, 。Hypercalcemia 可能是毒性的對所有身體組織, 但主要有害作用是在腎臟、神經系統, 和心血管系統。多數動物與總清液鈣大於15.0 mg/dL 將顯示系統標誌, 並且那些以清液鈣含量大於18.0 mg/dL 是嚴厲地不適。煩渴、polyuria, 和厭食是最共同的臨床標誌歸因於hypercalcemia, 雖則消沉, 弱點, 嘔吐, 並且便秘可能並且發生。不凡地, 心率失常, 奪取, 和肌肉抽動被觀察。迅速地顯現了出的嚴厲hypercalcemia (維他命過多症D) 可能導致死亡。
HYPERCALCEMIA 有差別的診斷
疾病導致hypercalcemia 由導致鈣、被減少的腎臟排泄鈣, 增加的GI 吸收鈣, 增加的清液捆綁鈣對proteins/complexes, 或這些過程的組合的增加的骨頭吸回。hypercalcemia 的起因被注意在提及醫院不能反射診斷同樣頻率遇到在主要關心設施。觀察從一個主要關心生化實驗室表明, 腎衰竭是最共同地伴生的與hypercalcemia 在狗。
Hypercalcemia 可能是瞬變和無關緊要(共同), 堅持和無關緊要(偶爾地), 或堅持和病理性的。有差別的診斷為堅持病理性hypercalcemia 沉重被偏心往敵意。Nonpathologic 情況聯繫了hypercalcemia 包括非齋戒(最小的增量), 幼小動物生理學成長, 實驗室錯誤, 和假由於lipemia 或sample/tube 的洗滌劑汙穢。Transient/inconsequential 起因聯繫了hypercalcemia 包括hemoconcentration 、hyperproteinemia 、hypoadrenocorticism, 和嚴厲環境低體溫症。疾病導致病理性, 堅持hypercalcemia 由導致增加的骨頭吸回, 鈣的被減少的腎臟排泄, 鈣的增加的GI 吸收, 鈣增加的清液這些過程的捆綁對proteins/complexes, 或組合。HARDIONS 是eponym 技術使用提醒也許導致hypercalcemia 的我們疾病幾個類別: H = Hyperparathyroidism (主要和三重), HHM (敵意體液hypercalcemia); A = Addison.s 疾病; R = 腎臟病; D = 維生素D toxicosis (包括granulomatous 疾病); I = 先天(主要貓); O = Osteolytic (骨髓炎, 鉗製), N = 瘤形成(HHM 和地方osteolytic hypercalcemia); S = 假。
敵意典型地聯繫了hypercalcemia 包括淋巴瘤、肛門sac 肺、胰腺、皮膚、鼻洞、甲狀腺、乳房封墊, 和腎上腺骨髓的apocrine 封墊腺癌、thymoma, 和癌。其它血液學敵意聯繫了hypercalcemia 包括多個骨髓瘤、淋巴瘤、myeloproliferative 疾病, 和白血病。Granulomatous 疾病造成hypercalcemia 包括芽苞黴菌病和其它黴菌疾病、皮炎、panniculitis, 和射入站點肉芽腫。維生素D toxicosis 可能起因於植物的oversupplementation 與維生素D3, 攝取包含calcitriol glycosides, cholecalciferol 殺鼠劑曝光, 和calcipotriol (Dovonex anti-psoriatic 奶油) 。Nonmalignant 骨骼損害包括骨髓炎(bacterial/mycotic), 肥大性骨營養不良(煤斗), 和不用osteoporosis (鉗製) 。其它hypercalcemia 的起因也許包括對小腸磷酸鹽黏合劑、過份鈣補充(碳酸鈣), 維他命過多症A, 牛奶鹼綜合症狀、thiazide 利尿藥、肢端肥大症、thyrotoxicosis 、postrenal 移植, 和鋁曝光的過份用途。
在hypercalcemic 狗, 瘤形成是最共同的部下的診斷, 被hypoadrenocorticism 跟隨, 主要hyperparathyroidism, 和慢性腎衰竭。大約70% hypercalcemic 狗是還azotemic, 與azotemia 不凡只在狗與hyperparathyroidism 。
疾病頻率聯繫了Hypercalcemia [table][tr][td=1,1,249][/td][td=1,1,173][align=center][b]發生43 狗
(Kruger 1996)[/b][/align][/td][td=1,1,158][align=center][b]發生40 狗[/b][/align][align=center][b](Elliott 1991)[/b][/align][/td][td=1,1,173][align=center][b]總鈣(mg/dL) (Kruger)[/b][/align][/td][td=1,1,167][align=center][b]被電離的鈣(mmol/L) (Kruger)[/b][/align][/td][/tr][tr][td=1,1,249][b]瘤形成[/b]
[/td][td=1,1,173][align=center]32.5%[/align][/td][td=1,1,158][align=center]57.5%[/align][/td][td=1,1,173][align=center]15.8 (12.0.20.9)[/align][/td][td=1,1,167][align=center]1.8 (1.6.2.2)[/align][/td][/tr][tr][td=1,1,249][b]Hypoadrenocorticism[/b]
[/td][td=1,1,173][align=center]28%[/align][/td][td=1,1,158][align=center]27.5%[/align][/td][td=1,1,173][align=center]13.1 (12.1.15.0)[/align][/td][td=1,1,167][align=center]ND[/align][/td][/tr][tr][td=1,1,249][b]主要Hyperparathyroidism[/b]
[/td][td=1,1,173][align=center]21%[/align][/td][td=1,1,158][align=center]2.5%[/align][/td][td=1,1,173][align=center]13.4 (12.2.16.8)[/align][/td][td=1,1,167][align=center]1.76 (1.60.2.21)[/align][/td][/tr][tr][td=1,1,249][b]慢性腎衰竭[/b]
[/td][td=1,1,173][align=center]16%[/align][/td][td=1,1,158][align=center]7.5%[/align][/td][td=1,1,173][align=center]12.8 (12.1.13.6)[/align][/td][td=1,1,167][align=center]1.20 (1.0.1.37)[/align][/td][/tr][tr][td=1,1,249][b]維他命過多症D[/b]
[/td][td=1,1,173][align=center]2.3%[/align][/td][td=1,1,158][/td][td=1,1,173][align=center]13.8[/align][/td][td=1,1,167][align=center]ND[/align][/td][/tr][tr][td=1,1,249][b]慢性Panniculitis[/b]
[/td][td=1,1,173][/td][td=1,1,158][align=center]2.5%[/align][/td][td=1,1,173][/td][td=1,1,167][/td][/tr][tr][td=1,1,249][b]Undiagnosed[/b]
[/td][td=1,1,173][/td][td=1,1,158][align=center]2.5%[/align][/td][td=1,1,173][/td][td=1,1,167][/td][/tr][/table]HYPERCALCEMIA 的治療
緊急設立進取的治療直接地反對hypercalcemia 主要取決於臨床標誌嚴肅, 不管hypercalcemia 的具體水平。趨向在巨大hypercalcemia 充當在這個決定的一個角色, 因為迅速地上升的hypercalcemia 辯解更加進取的干預。不幸地, 沒有可能使用作為指南為決定進取地對待的absolute 清液鈣含量。
根本原因的撤除是明確的治療為hypercalcemia, 但這總不是立刻可能的。許多動物與病理性hypercalcemia 將有迅速被診斷的一份伴生的敵意, 但不欣然對待。被隔絕的瘤完全切除將廢除hypercalcemia, 並且在動物中以傳播的轉移, multicentric 瘤形成、或nonresectable 主要敵意、腫瘤負擔和hypercalcemia 也許由適當的化療、放射治療, 和免疫療法減少。支援療法經常是必要減少清液鈣含量對較不毒性水平。不幸地, 沒有治療協議一致地有效為所有hypercalcemia 的起因, 並且養生之道必須因而被剪裁為各名患者。
腸外流體、furosemide 、小蘇打、這些治療的glucocorticosteroids, 或組合有效地將減少清液鈣含量在多數動物與hypercalcemia 。可變的療法的第一目標是改正失水, 因為hemoconcentration 對增加的清液被電離的鈣含量貢獻。生理學鹽(0.9% NaCl) 是選擇的解答為血管內的容量缺乏的更正, 和為進一步溫和的容量擴展。鉀補充經常是必要維護正常清液鉀在可變的治療的延長的期間。
Furosemide (Lasix。) 跟隨再水化和流體容量擴展在重要性為堅持hypercalcemia 的治療。Furosemide (5 mg/kg IV 最初的一小團藥量被5 mg/kg/hr 注入跟隨) 可能是有用的在深刻地越來越少的清液鈣含量由大約3 mg/dL 最大值。較不furosemide 管理進取的養生之道也許是有效的與其它治療的組合, 或為hypercalcemia 的慢性管理。
Glucocorticosteroids 可能極大貢獻在減少巨大堅持hypercalcemia 在有lymphosarcoma (細胞溶解), 多個骨髓瘤、hypoadrenocorticism 、維他命過多症D, 或granulomatous 疾病病人, 但他們有少許作用在其它hypercalcemia 的起因。類固醇施加他們的作用主要由減少骨頭吸回, 越來越少的小腸鈣吸收, 和增加腎臟鈣排泄。類固醇應該被扣壓如果一個明確的診斷未建立。
最近, 副甲狀腺的封墊的化工燒蝕被報告了作為減少清液鈣含量有效的手段在狗與主要hyperparathyroidism 。由超聲波引導, 對氨基苯甲酸二被注射入副甲狀腺的大量。共計和電離了鈣含量恢復正常在24 小時之內在多數狗。瞬變hypocalcemia 也許顯現出, 和也許要求治療。
療法的幾種形式經常伴隨地是必要的。Diphosphonates 是協助降低清液鈣的osteoclast poisons. 。Etidronate (Didronel.EHDP) 是不是好的口頭被吸收的第一代化合物, 但可能仍然是有用的。Pamidronate 和risedronate 是更好被吸收的新世代bisphosphonates, 但不廣泛被應用在獸醫方面。Calcitonin 是一種解毒劑為cholecalciferol 鼠毒物, 但也許是有用的在骨頭吸回是hypercalcemia 的主要起因的其它案件。Calcitonin 治療是昂貴的, 作用也許是短命的(幾小時), 並且巨大它的作用是變化莫測的。未對其它治療起反應小蘇打的注入也許被給在hypercalcemic 危機(心率失常、嚴厲消沉, 急性腎衰竭期間) 。Mithramycin 並且被顯示了對減退清液鈣水平幾天, 雖然極端必須當心適當地灌輸低藥量在幾個小時減少腎臟和肝毒力。低鈣飲食是只有用的在極大地降低清液鈣在hypercalcemia 由剩餘維生素D 代謝產物的行動造成。
Hypercalcemia 的治療 [table=98%][tr][td=1,1,204][b]治療[/b]
[/td][td=1,1,233][b]藥量[/b]
[/td][td=1,1,188][b]徵兆[/b]
[/td][td=1,1,255][b]評論[/b]
[/td][/tr][tr][td=4,1,879][b]容量擴展[/b]
[/td][/tr][tr][td=1,1,204]平方鹽(0.9%)
[/td][td=1,1,233]75-100 mL/kg/day
[/td][td=1,1,188]溫和的hypercalcemia
[/td][td=1,1,255]Contraindicated 如果周邊腫鼓是存在
[/td][/tr][tr][td=1,1,204]IV 鹽(0.9%)
[/td][td=1,1,233]100-125 mL/kg/day
[/td][td=1,1,188]減輕對嚴厲hypercalcemia
[/td][td=1,1,255]Contraindicated 在充血的心力衰竭和高血壓
[/td][/tr][tr][td=4,1,879][b]利尿藥[/b]
[/td][/tr][tr][td=1,1,204]Furosemide
[/td][td=1,1,233]2-4 mg/kg q12h 對q8h, IV, 平方, PO
[/td][td=1,1,188]減輕對嚴厲hypercalcemia
[/td][td=1,1,255]容量擴展是必要的在對這種藥物的用途之前
[/td][/tr][tr][td=4,1,879][b]Alkalinizing 代理[/b]
[/td][/tr][tr][td=1,1,204]小蘇打
[/td][td=1,1,233]1 mEq/kg IV 慢一小團; 可以繼續在0.3 X 基本的缺乏x 公斤每天
[/td][td=1,1,188]嚴厲hypercalcemia
[/td][td=1,1,255]要求接近的監視
[/td][/tr][tr][td=4,1,879][b]Glucocorticoids[/b]
[/td][/tr][tr][td=1,1,204]強體松
[/td][td=1,1,233]1-2.2 mg/kd q12h, PO, 平方, IV
[/td][td=1,1,188]減輕對嚴厲hypercalcemia
[/td][td=1,1,255]對這些藥物的用途在原因論的證明之前也許使明確的診斷困難
[/td][/tr][tr][td=1,1,204]Dexamethasone
[/td][td=1,1,233]0.1-0.22 mg/kg q12h, IV, 平方
[/td][td=1,1,188][/td][td=1,1,255][/td][/tr][tr][td=4,1,879][b]骨頭吸回的禁止[/b]
[/td][/tr][tr][td=1,1,204]Calcitonin
[/td][td=1,1,233]4-6 IU/kg 平方q12h 對q8h
[/td][td=1,1,188]維他命過多症D 毒力
[/td][td=1,1,255]反應也許是短命的。嘔吐也許發生。
[/td][/tr][tr][td=4,1,879][b].[/b][b]Bisphosphonates[/b]
[/td][/tr][tr][td=1,1,204]EHDP-Didronel 。
[/td][td=1,1,233]5-15 mg/kg q12.24h
[/td][td=1,1,188]減輕對嚴厲hypercalcemia
[/td][td=1,1,255]昂貴, 使用在狗被限制
[/td][/tr][tr][td=1,1,204]Clodronate
[/td][td=1,1,233]20-25 mg/kg 在4 個小時IV 注入
[/td][td=1,1,188][/td][td=1,1,255]批准用於人在歐洲; 可及性在美國被限制
[/td][/tr][tr][td=1,1,204]Pamidronate- Aredia 。
[/td][td=1,1,233]1.3 mg/kg 在150 機器語言0.9% 鹽在2 個小時IV 注入; 能重覆在一個到三個星期
[/td][td=1,1,188][/td][td=1,1,255]非常昂貴
[/td][/tr][tr][td=1,1,204]Mithramycin
[/td][td=1,1,233]25 ug/kg IV 在D5W 2-4 小時每q2-4 幾星期
[/td][td=1,1,188]嚴厲hypercalcemia, 加工困難的敵意伴生的hypercalcemia
[/td][td=1,1,255]有限的用途在狗和貓。Nephrotoxicity, hepatotoxicity
[/td][/tr][tr][td=4,1,879][b]混雜[/b]
[/td][/tr][tr][td=1,1,204]鈉EDTA
[/td][td=1,1,233]25-75 mg/kg/hr
[/td][td=1,1,188]嚴厲hypercalcemia
[/td][td=1,1,255]毒害腎臟
[/td][/tr][tr][td=1,1,204]腹膜透析
[/td][td=1,1,233]低鈣dialysate
[/td][td=1,1,188]嚴厲hypercalcemia
[/td][td=1,1,255]反應的短期。用途在hypercalcemia 沒被報告。
[/td][/tr][/table]INTRODUCTION
When a serum sample is submitted to the laboratory, typically the total serum calcium concentration is what is reported. Total calcium includes ionized calcium, complexed calcium, and protein-bound calcium. In most laboratories, hypercalcemia is documented when serum total calcium concentration is > 12.0 mg/dL in dogs. The exact value when hypercalcemia exists must be determined for each laboratory. Serum total calcium and serum ionized calcium values are lower in cats than in dogs. In our laboratory, hypercalcemia in dogs is defined when the total serum calcium is greater than 11.6 mg/dL and the ionized calcium concentration is greater than 6.0 mg/dL.
In clinically normal animals, serum ionized calcium is typically proportional to the level of serum total calcium (ionized calcium is usually 50?0% of total calcium). However, in diseased animals, serum ionized calcium is NOT proportional to total serum calcium, and cannot be predicted from total serum calcium. Ionized calcium is often much lower than predicted in patients with renal failure, regardless of their serum total calcium level (low, normal, or high). Patients with hypoalbuminemia and 𡤧orrected?serum total calcium values may still have decreased levels of ionized calcium. Patients with moderate to severe metabolic acidosis undergo increases in their ionized calcium fraction due to shifting of calcium from protein-bound stores of calcium. For these reasons, measurement of serum ionized calcium concentration is recommended in all patients with renal failure or hypercalcemia. Since ionized serum calcium concentration is affected by exposure to oxygen and pH, serum samples should be collected and handled anaerobically before analysis. Serum ionized calcium concentration does not change in samples stored up to 72 hours at room temperature, or at 4蚓 when samples are collected and stored anaerobically. When delay in measurement of serum samples is necessary (as in sending samples to an outside laboratory), anaerobic collection with cold storage up to 72 hours will result in the most accurate assessment of serum ionized calcium.
CLINICAL SIGNS OF HYPERCALCEMIA [table][tr][td=1,1,249][/td][td=1,1,173][align=center][b]Incidence 43 dogs
(Kruger 1996)[/b][/align][/td][td=1,1,158][align=center][b]Incidence 40 dogs[/b][/align][align=center][b](Elliott 1991)[/b][/align][/td][td=1,1,173][align=center][b]Total Calcium (mg/dL) (Kruger)[/b][/align][/td][td=1,1,167][align=center][b]Ionized Calcium (mmol/L) (Kruger)[/b][/align][/td][/tr][tr][td=1,1,249][b]Neoplasia[/b]
[/td][td=1,1,173][align=center]32.5%[/align][/td][td=1,1,158][align=center]57.5%[/align][/td][td=1,1,173][align=center]15.8 (12.0?0.9)[/align][/td][td=1,1,167][align=center]1.8 (1.6?.2)[/align][/td][/tr][tr][td=1,1,249][b]Hypoadrenocorticism[/b]
[/td][td=1,1,173][align=center]28%[/align][/td][td=1,1,158][align=center]27.5%[/align][/td][td=1,1,173][align=center]13.1 (12.1?5.0)[/align][/td][td=1,1,167][align=center]ND[/align][/td][/tr][tr][td=1,1,249][b]Primary Hyperparathyroidism[/b]
[/td][td=1,1,173][align=center]21%[/align][/td][td=1,1,158][align=center]2.5%[/align][/td][td=1,1,173][align=center]13.4 (12.2?6.8)[/align][/td][td=1,1,167][align=center]1.76 (1.60?.21)[/align][/td][/tr][tr][td=1,1,249][b]Chronic Renal Failure[/b]
[/td][td=1,1,173][align=center]16%[/align][/td][td=1,1,158][align=center]7.5%[/align][/td][td=1,1,173][align=center]12.8 (12.1?3.6)[/align][/td][td=1,1,167][align=center]1.20 (1.0?.37)[/align][/td][/tr][tr][td=1,1,249][b]Hypervitaminosis D[/b]
[/td][td=1,1,173][align=center]2.3%[/align][/td][td=1,1,158][/td][td=1,1,173][align=center]13.8[/align][/td][td=1,1,167][align=center]ND[/align][/td][/tr][tr][td=1,1,249][b]Chronic Panniculitis[/b]
[/td][td=1,1,173][/td][td=1,1,158][align=center]2.5%[/align][/td][td=1,1,173][/td][td=1,1,167][/td][/tr][tr][td=1,1,249][b]Undiagnosed[/b]
[/td][td=1,1,173][/td][td=1,1,158][align=center]2.5%[/align][/td][td=1,1,173][/td][td=1,1,167][/td][/tr][/table][table=98%][tr][td=1,1,204][b]Treatment[/b]
[/td][td=1,1,233][b]Dose[/b]
[/td][td=1,1,188][b]Indications[/b]
[/td][td=1,1,255][b]Comments[/b]
[/td][/tr][tr][td=4,1,879][b]Volume Expansion[/b]
[/td][/tr][tr][td=1,1,204]SQ Saline (0.9%)
[/td][td=1,1,233]75-100 mL/kg/day
[/td][td=1,1,188]Mild hypercalcemia
[/td][td=1,1,255]Contraindicated if peripheral edema is present
[/td][/tr][tr][td=1,1,204]IV Saline (0.9%)
[/td][td=1,1,233]100-125 mL/kg/day
[/td][td=1,1,188]Moderate to severe hypercalcemia
[/td][td=1,1,255]Contraindicated in congestive heart failure and hypertension
[/td][/tr][tr][td=4,1,879][b]Diuretics[/b]
[/td][/tr][tr][td=1,1,204]Furosemide
[/td][td=1,1,233]2-4 mg/kg q12h to q8h, IV, SQ, PO
[/td][td=1,1,188]Moderate to severe hypercalcemia
[/td][td=1,1,255]Volume expansion is necessary prior to use of this drug
[/td][/tr][tr][td=4,1,879][b]Alkalinizing Agent[/b]
[/td][/tr][tr][td=1,1,204]Sodium Bicarbonate
[/td][td=1,1,233]1 mEq/kg IV slow bolus; may continue at 0.3 X base deficit X kg per day
[/td][td=1,1,188]Severe hypercalcemia
[/td][td=1,1,255]Requires close monitoring
[/td][/tr][tr][td=4,1,879][b]Glucocorticoids[/b]
[/td][/tr][tr][td=1,1,204]Prednisone
[/td][td=1,1,233]1-2.2 mg/kd q12h, PO, SQ, IV
[/td][td=1,1,188]Moderate to severe hypercalcemia
[/td][td=1,1,255]Use of these drugs prior to identification of etiology may make definitive diagnosis difficult
[/td][/tr][tr][td=1,1,204]Dexamethasone
[/td][td=1,1,233]0.1-0.22 mg/kg q12h, IV, SQ
[/td][td=1,1,188][/td][td=1,1,255][/td][/tr][tr][td=4,1,879][b]Inhibition of Bone Resorption[/b]
[/td][/tr][tr][td=1,1,204]Calcitonin
[/td][td=1,1,233]4-6 IU/kg SQ q12h to q8h
[/td][td=1,1,188]Hypervitaminosis D toxicity
[/td][td=1,1,255]Response may be short-lived. Vomiting may occur.
[/td][/tr][tr][td=4,1,879][b]?/b>[b]Bisphosphonates[/b]
[/b][/td][/tr][tr][td=1,1,204]EHDP-Didronel?/p>
[/td][td=1,1,233]5-15 mg/kg q12?4h
[/td][td=1,1,188]Moderate to severe hypercalcemia
[/td][td=1,1,255]Expensive, use in dogs limited
[/td][/tr][tr][td=1,1,204]Clodronate
[/td][td=1,1,233]20-25 mg/kg in a 4 hr IV infusion
[/td][td=1,1,188][/td][td=1,1,255]Approved for use in humans in Europe; availability in USA limited
[/td][/tr][tr][td=1,1,204]Pamidronate- Aredia ?/p>
[/td][td=1,1,233]1.3 mg/kg in 150 mL 0.9% saline in a 2 hr IV infusion; can repeat in one to three weeks
[/td][td=1,1,188][/td][td=1,1,255]Very expensive
[/td][/tr][tr][td=1,1,204]Mithramycin
[/td][td=1,1,233]25 ug/kg IV in D5W over 2-4 hr every q2-4 weeks
[/td][td=1,1,188]Severe hypercalcemia, refractory malignancy associated hypercalcemia
[/td][td=1,1,255]Limited use in dogs and cats. Nephrotoxicity, hepatotoxicity
[/td][/tr][tr][td=4,1,879][b]Miscellaneous[/b]
[/td][/tr][tr][td=1,1,204]Sodium EDTA
[/td][td=1,1,233]25-75 mg/kg/hr
[/td][td=1,1,188]Severe hypercalcemia
[/td][td=1,1,255]Nephrotoxic
[/td][/tr][tr][td=1,1,204]Peritoneal Dialysis
[/td][td=1,1,233]Low calcium dialysate
[/td][td=1,1,188]Severe hypercalcemia
[/td][td=1,1,255]Short duration of response. Use in hypercalcemia not reported.
[/td][/tr][/table][/size]

minibabyqq 2007-1-4 22:47

[color=Magenta][b][size=5]治療複雜的糖尿病 [/size][/b][/color]

Treating the Complicated Diabetic Patient   


什麼是區別在二名明顯相似的糖尿病患者之間, 其中之一是雄偉地被穩定的一次每日胰島素, 和其他從未似乎有一天充分控制不管胰島素政權被實施? 有也許對所謂的brittle. 糖尿病貢獻然而它值得記住的許多因素那, 當前, 許多保留未經說明並且它是由出席的獸醫決定, 經常與專家一道, 構想將最大化控制和, 特別是, 使臨床重大低血糖症減到最小風險的管理策略。
什麼做他們複雜化了?
有可能的起因一張廣泛的名單使一隻糖尿病狗或貓難穩定或保留好受控。或許一致可能否則隱密, hyperadrenocorticism 必須被認為和總排除。
一致傳染、孕激素療法、dysmenorrhea 、肢端肥大症、甲狀腺官能不良和一般未指明的一致瘤形成必須所有被考慮和被評估因為他們不能導致否則明顯的臨床標誌只是有深刻作用在糖尿病控制。結果在重大腎臟或肝官能不良可能做處理糖尿病患者一個特別難題的任何過程。
有重大胰臟炎症病人能提出一個診斷和治療挑戰。特殊稍尖的胰腺炎可能生產重覆了復發在動物的一般健康與修改過的胰島素要求一起。這提出少許問題對深刻臨床工作者當動物展示胰腺炎的classical. 標誌, 然而有smouldering. 胰臟炎症許多糖尿病病人也許簡單地提出unwell. 沒有生物化學的證據建議活躍或持續的胰臟破壞。這是特別真實的在情況由不太可靠的協會覆蓋進一步在hyperamylasemia/hyperlipasemia 和活躍胰臟炎症之間的貓。
在某種胰腺炎的形式被懷疑的任何患者當一個可能的使複雜化的因素在糖尿病管理, 專家胃腸ultrasonography 應該被考慮作為這個過程可能澄清的一個更多機制。
但是, 總記住有一定數量的糖尿病患者, 是idiopathically 易碎的狗和貓。這些患者表面上沒有部下的疾病仍然能證明卓越地難穩定。通常這些患者難穩定從外邊。在很好被控制了得有一段時間了和突然退出控制的那些患者, 原因通常是某一一致疾病的發展。
什麼可能做?
通常, 每當可能, 改正根本原因是明顯的解答雖然這頻繁地難達到。每當可能, 使用與飯食相符迅速地行動的胰島素的更小的藥量, 並且是改進控制優秀手段, 然而使這是可行的這實踐必須是與家庭的正常活動兼容。
處理SICK 。糖尿病
通常是不適, 或者由於在過程中發生的疾病或由於內在毒血症起因於明顯的ketosis 的一名糖尿病患者, 將是inappetent, 使標準皮膚下胰島素療法困難。在這些情況下, 連續的靜脈內胰島素可能是非常短期管理有效的手段。此外, 只要有一個容量泵浦可利用, 連續的靜脈內胰島素注入是最簡單和最少勞動密集型的手段為這些患者的治療。
腸外可變的療法
這些患者通常需要總腸外水合作用, 和由於他們惡劣受控糖尿病, 有相對地高可變的維護要求。結果, 流動的靜脈內流體在150 ml/kg/24hr 前後一般將提供一些替換和充分維護。最宜的可變的構成是0.45% NaCl 與KCl 30.40 mmol/l 增加。它經常是慎密增加鉀因為相等的數量鉀氯化物和鉀磷酸鹽。這不僅使hypokalemia 風險, 而且hypophosphatemia 減到最小。當一個目標將重新水化患者, 其他必須是提供糖尿病控制某一措施或至少禁止持續的周邊分解和因此開始減少在ketoacidosis 的潛力。
胰島素療法
當胰島素療法被認為臨床對待重大ketoacidosis, 選擇是連續的靜脈內胰島素療法或反覆肌肉內胰島素射入。在兩個情況, 胰島素應該是在可溶物, 相對地迅速地行動的形式。雖然靜脈注射胰島素注入聽起來嚇人它, 一定是治療糖尿病患者最簡單和最少勞動密集型的手段以GIT 標誌充足地嚴厲擔保一nil 每os. 推薦。在這個情況, 我們嘗試對充分葡萄糖homeostasis 在患者是腸外藥物並且營養素交付是唯一的可利用的路線為管理。
一個容易的方法為設定靜脈內胰島素可變的線將增加可溶解胰島素25 個單位來一個500 機器語言袋子流體, 導致50 mU/ml 的胰島素集中。因為標準胰島素注入率是40.60 mU/kg/hr, 方便妥協將流動這種解答1 ml/kg/hr 。明顯地, 大約1 ml/kg/hr 的流速是不充分為維護。結果, 靜脈內胰島素必須被執行通過第二條注入線, 通常附有維護可變的線的Y. 片斷。
胰島素被灌輸以1 ml/kg/hr 的率直到血漿葡萄糖含量落對10.12 mmol/l 。此時流速應該被對分(0.5 ml/kg/hr) 並且一致葡萄糖注入被介紹通過維護可變的線。達到平衡你個簡單和有效的手段在胰島素和葡萄糖之間被灌輸將改變維護流體從0.45% NaCl 和30 mmol/l K 到0.45% NaCl 和 2.5% 葡萄糖與30 mmol/l KCl 當繼續跑這個組合在150 ml/kg/hr 。這將介紹應該平衡胰島素被灌輸在0.5 ml/kg/hr 大約150 mg/kg/hr 的葡萄糖注入率。
在這時間期間, 患者的血液葡萄糖和血漿鉀通常被檢查。在48.72 小時中, 血液葡萄糖應該保留相對地平穩, 酮血症, 當禮物, 應該消失, 並且一般, 患者回到一個正常水和營養素進水閘。一旦這個正常性的水平建立, 它是可能的, 至少近期, 患者能被穩定在一個規則哺養的政權和一個規則胰島素藥量政權。
為各種各樣的原因, 它總不會是可能執行靜脈內胰島素注入對需要相對地迫切胰島素療法的一名anorectic 糖尿病患者。在一些場合, 臨床工作者也許嘗試和使用一種每日兩次皮膚下地被執行的lente 準備的更低的藥量。雖然這實踐也許是有效和相對地安全的如果藥量被保留在0.25.U/kg/12hr 前後, 有總給一少許太多的可能性。任一藥劑過量在這個情況是可能的對為時至少12 個小時。
結果, 在沒有一個可靠的注入泵浦時, 一個更加有吸引力的選擇對連續的靜脈內胰島素注入是可溶解胰島素的重覆的肌肉注射。
狗和貓應該接受可溶解胰島素在0.2 U/kg 裝貨藥量被0.1 U/kg 每小時跟隨爾後。所有射入應該肌肉內被執行。血液葡萄糖水平通常被監測(每2.3 小時) 直到他們下落了對12 -15 mmol/l 。這時, 它通常是令人滿意變成皮膚下可溶解胰島素每六個小時(0.2.0.4 U/kg) 。由於酮血症和因此inappetence 可能的堅持, 它是重要維護充分血液葡萄糖含量由介紹葡萄糖入靜脈內流體。通常, 2.5% 葡萄糖解答跑以兩次正常維護率是令人滿意的, 雖然血液葡萄糖水平應該被檢查每四個到六個小時。

What is the difference between two apparently similar diabetic patients, one of which is superbly stabilised on once daily insulin, and the other which never seems to have a single day of adequate control no matter what insulin regime is implemented? There are many factors which may contribute to so called 弎rittle?diabetes however it is worth remembering that, at present, many remain unexplained and it is up to the attending veterinarian, often in conjunction with a specialist, to devise a management strategy which will maximise control and, in particular, minimise the risk of clinically significant hypoglycemia.
WHAT MAKES THEM COMPLICATED?
There is an extensive list of possible causes for a diabetic dog or cat to be difficult to stabilise or to keep well controlled. Perhaps concurrent possibly otherwise occult, hyperadrenocorticism must always be considered and ruled out.
Concurrent infections, progestin therapy, dysmenorrhea, acromegaly, thyroid dysfunction and general non-specific concurrent neoplasia must all be considered and evaluated as they may not produce otherwise obvious clinical signs but have profound effects on diabetic control. Any process that results in significant renal or hepatic dysfunction can make managing a diabetic a particularly difficult task.
Patients with significant pancreatic inflammation can present both a diagnostic and therapeutic challenge. Particularly sub-acute pancreatitis can produce repeated relapses in the general health of the animal along with altered insulin requirements. This presents little problem to the acute clinician when the animal demonstrates the 𡤧lassical?signs of pancreatitis, however many diabetic patients with 𦽳mouldering?pancreatic inflammation may simply present 𠀾nwell?with no biochemical evidence to suggest active or ongoing pancreatic destruction. This is particularly true in cats where the situation is further clouded by the even less reliable association between hyperamylasemia/hyperlipasemia and active pancreatic inflammation.
In any patient in whom some form of pancreatitis is suspected as a possible complicating factor in diabetic management, specialist abdominal ultrasonography should be considered as one more mechanism by which this process can be clarified.
However, always remember there are a number of diabetic patients, both dogs and cats that are 𧗽diopathically brittle? These patients have seemingly no underlying disease and yet can prove remarkably difficult to stabilise. Usually these patients are difficult to stabilise from the outset. In those patients who have been well controlled for some time and suddenly drop out of control, the reason is usually the development of some concurrent disease.
WHAT CAN BE DONE?
Generally, whenever possible, correcting the underlying cause is the obvious solution although this is frequently difficult to achieve. Whenever possible, using smaller doses of rapidly acting insulin that coincide with meals, is also an excellent means of improving control, however for this to be feasible this practice has to be compatible with the household's normal activities.
MANAGING THE 廍ICK?DIABETIC
Usually a diabetic patient that is unwell, either because of intercurrent disease or due to the endogenous toxemia that results from marked ketosis, will be inappetent, making standard subcutaneous insulin therapy difficult. In these cases, continuous intravenous insulin can be a very effective means of short-term management. Furthermore, as long as there is a volumetric pump available, a continuous intravenous insulin infusion is the simplest and least labor-intensive means for treatment of these patients.
PARENTERAL FLUID THERAPY
These patients usually require total parenteral hydration, and by virtue of their poorly controlled diabetes, have relatively high fluid maintenance requirements. Consequently, flowing intravenous fluids at around 150 ml/kg/24hr generally will provide some replacement and adequate maintenance. The optimum fluid composition is 0.45% NaCl with 30?0 mmol/l of KCl added. It is often prudent to add the potassium as equal amounts of potassium chloride and potassium phosphate. This not only minimizes the risk of hypokalemia, but also of hypophosphatemia. While one aim is to rehydrate the patient, the other must be to provide some measure of diabetic control or at least inhibit ongoing peripheral lipolysis and hence to start to reduce the potential for ketoacidosis.
INSULIN THERAPY
When insulin therapy is being considered to treat clinically significant ketoacidosis, the choice is continuous intravenous insulin therapy or repetitive intramuscular insulin injections. In both situations, the insulin should be in a soluble, relatively rapidly acting form. Although an intravenous insulin infusion sounds daunting it, is certainly the simplest and least labor intensive means of treating diabetic patients with GIT signs sufficiently severe to warrant a 忛il per os?recommendation. In this situation, we are trying to adequate glucose homeostasis in a patient were parenteral drug and nutrient delivery is the only available route for administration.
One easy method for setting up the intravenous insulin fluid line is to add 25 units of soluble insulin to a 500 ml bag of fluids, producing an insulin concentration of 50 mU/ml. Since the standard insulin infusion rate is 40?0 mU/kg/hr, a convenient compromise is to flow 1 ml/kg/hr of this solution. Obviously, a flow rate of approximately 1 ml/kg/hr is inadequate for maintenance. Consequently, intravenous insulin has to be administered through a second infusion line, usually attached to the 㛝?piece of the maintenance fluid line.
The insulin is infused at a rate of 1 ml/kg/hr until plasma glucose concentrations fall to 10?2 mmol/l. At this time the flow rate should be halved (0.5 ml/kg/hr) and a concurrent dextrose infusion introduced through the maintenance fluid line. One simple and effective means of achieving a balance between the insulin and glucose infused is to change the maintenance fluids from 0.45% NaCl and 30 mmol/l K to 0.45% NaCl and 2.5% dextrose with 30 mmol/l KCl while continuing to run this combination at 150 ml/kg/hr. This will introduce a glucose infusion rate of around 150 mg/kg/hr that should balance the insulin being infused at 0.5 ml/kg/hr.
During this time, the patient's blood glucose and plasma potassium are checked regularly. Over a period of 48?2 hours, the blood glucose should remain relatively steady, ketonemia, when present, should disappear, and generally, the patients return to a normal water and nutrient intake. Once this level of normality is established, it is likely that, at least in the short term, the patient will be able to be stabilised on a regular feeding regime and a regular insulin dose regime.
For a variety of reasons, it will not always be possible to administer an intravenous insulin infusion to an anorectic diabetic patient who requires relatively urgent insulin therapy. On some occasions, the clinician may try and use lower doses of a subcutaneously administered lente preparation twice daily. Although this practice may be effective and relatively safe if the dose is kept at around 0.25U/kg/12hr, there is always the possibility of giving a little too much. Any overdose in this situation is likely to last at least 12 hours.
Consequently, in the absence of a reliable infusion pump, a more attractive alternative to a continuous intravenous insulin infusion is repeated intramuscular injections of soluble insulin.
Dogs and cats should receive soluble insulin at a loading dose of 0.2 U/kg followed by 0.1 U/kg hourly thereafter. All injections should be administered intramuscularly. Blood glucose levels are monitored regularly (every 2? hours) until they have fallen to 12 -15 mmol/l. At this point, it is usually satisfactory to change to subcutaneous soluble insulin every six hours (0.2?.4 U/kg). Because of the likely persistence of ketonemia and hence inappetence, it is important to maintain adequate blood glucose concentrations by introducing dextrose into the intravenous fluids. Generally, a 2.5% dextrose solution run at twice normal maintenance rates is satisfactory, although blood glucose levels should be checked every four to six hours.?

minibabyqq 2007-1-4 22:49

[color=Magenta][b][size=5]犬甲狀腺機能不足[/size][/b][/color]

Canine Hypothyroidism   


在過去幾年, 我們非常得知似犬甲狀腺機能不足發病原理和診斷。這是適當在大部份對在診斷測試的改善可利用對臨床工作者。自動免疫的甲狀腺炎是甲狀腺機能不足的同道會。一項最近研究看自身抗體的價值測試在狗。清液樣品從狗以各種各樣的內分泌反常性和從30 名肥胖成年女性有Tyroglobulin 自身抗體(TgAA) 集中被確定利用ELISA 。六個實驗完成: 1) 正面結果的定義為TgAA 使用樣品從法線和T3 自身抗體(T3.AA) 正面狗; 2) 正面結果的流行的創立在91 條臨床正常狗; 3) 正面結果的評估為清液從狗以nonthyroidal 病症; 4) 測試樣品從狗以主要甲狀腺機能不足但缺乏T4.AA 或T3.AA, 或兩個; 5) 假消極結果的流行的決心在是T4.AA 並且/或者T3.AA 正面, 是的狗(18 條狗) 或(22 條狗) 沒有接受L 甲狀腺素替換療法; 並且6) 甲狀腺切片檢查法標本的考試從18 條狗(8 TgAA 正面和10 TgAA 陰性) 。
正面結果作為至少(200%) 消極控制樣品的光學密度兩次被定義了。假正面結果被獲得了為只3.4% 146 條狗以nonthyroidal 病症。狗的百分之三十七以主要甲狀腺機能不足, 但T4.AA 或T3.AA 的證據, 或兩個, 不是TgAA 正面。假消極結果被發現了在22 和二中18 條T3.AA 正面狗的當中一個以和沒有甲狀腺替換療法, 各自地。甲狀腺切片檢查法標本從八條TgAA 正面狗有lymphocytic 甲狀腺炎的證據, 但是那些從10 條TgAA 消極狗沒有。分析用試樣是敏感和具體為lymphocytic 自動免疫的甲狀腺炎的證明在狗, 和有在可能援助甲狀腺炎早期的診斷在狗和辨認狗的潛力使甲狀腺機能不足永存在助長節目。
一定數量的療程和非thyroidal 病症可能干涉各種各樣的甲狀腺功能考驗。幾張紙審查了anti-convulsant 療法的作用在腦下垂體甲狀腺軸。multicentric 預期研究進行監測苯巴比妥在清液共計甲狀腺素(T4) 並且甲狀腺刺激的激素(TSH) 集中的作用在癲癇的狗。清液T4 集中是堅定的為22 條癲癇的狗在苯巴比妥療法(時間0 的) _蒙之前並且在三個星期、六個月, 和12 個月在苯巴比妥以後開始。中間T4 集中是顯著低在三個星期並且六個月與時間0 比較了。
狗的百分之三十二有T4 集中在參考範圍之下在六個和12 個月。十九22 條狗有清液TSH 集中被確定在所有採樣次。重大上升趨勢在中間TSH 集中被發現了。協會未被發現在T4 苯巴比妥集中、藥量, 和清液苯巴比妥含量之間。公開甲狀腺機能不足的標誌不是顯然的在狗與低T4, 有一例外。TSH 刺激測試執行了在六七條狗以低T4 集中在12 個月, 並且所有除了一個有正常反應。
總而言之, 苯巴比妥療法減少了清液T4 集中但沒出現導致甲狀腺機能不足的臨床標誌。清液TSH 集中和TSH 刺激測試建議, 下丘腦腦下垂體甲狀腺軸適當地起作用。第二項研究評估了變化在清液共計T4 (TT4), 自由T4 上(FT4), 甲狀腺刺激激素(TSH), 膽固醇和白蛋白含量, 和活動在胺基代丙酸aminotransferase (ALT), 鹼性磷酸鹽(阿爾卑斯), 和伽瑪glutamyl transferase 清液(GGT) 在長期苯巴比妥管理的中止以後在正常狗。十二條正常狗是被執行的苯巴比妥在大約4.4-6.6 mg/kg q12h PO 劑量27 個星期。血液被收集了為分析在27 個星期苯巴比妥管理前後和然後每週10 個星期在藥物的中止以後。狗臨床是法線在研究期間過程中。清液ALT 和阿爾卑斯活動和TSH 和膽固醇含量比基礎線顯著高級在星期27 。清液T4 和FT4 是顯著更低。清液白蛋白和GGT 未被改變從基礎線在星期27 。變化在甲狀腺上的估計起作用(TT4 、FT4, TSH) 堅持一個到四個星期在苯巴比妥的中止以後, 但是變化在肝□活性(ALT, 阿爾卑斯上) 並且膽固醇含量被解決在三個到五個星期。
避免假的正面結果, 它建議, 甲狀腺測試進行至少四個星期在苯巴比妥管理的中止以後。肝酵素的被舉起的清液活動六個到八個星期在苯巴比妥的中止以後也許表明肝疾病。苯巴比妥的作用再被估計了在甲狀腺並且在腎上腺作用。苯巴比妥的作用在甲狀腺軸、腎上腺軸, 和腎上腺功能考驗預期地被調查了在12 條法線, 成人狗。苯巴比妥被執行了在5 毫克每公斤體重(範圍, 4.8-6.6 mg/kg q12h PO 29 個星期, 造成治療清液集中(20-40 microg/mL) 。清液總甲狀腺素(TT4), 自由甲狀腺素(FT4) 由平衡透析, 總triiodothyronine (TT3), thyrotropin (TSH), 和膽固醇是堅定的在和在苯巴比妥治療期間之前。LDDST, 促腎上腺皮質激素刺激測試, 和腎上腺封墊的ultrasonographic 評估執行了在和在治療期間之前。TT4 和FT4 顯著被減少(P < 或= 05), TT3 有最小的波動, TSH 有唯一被延遲的賠償增量, 和膽固醇被增加在苯巴比妥治療期間。
The 在TSH 的被延遲的增量, 儘管堅持hypothyroxinemia, 建議, 加速的肝甲狀腺素排除不能是苯巴比妥的唯一的作用在甲狀腺軸。沒有苯巴比妥的重大作用在或者腎上腺功能考驗。一項更大的研究審查了78 條癲癇的狗接受苯巴比妥(小組1) 和48 條未經治療的癲癇的狗(小組2) 。清液生物化學的分析, 包括T4 和TSH 集中, 執行了為所有狗。另外的 體外 分析執行在清液從健康狗確定是否苯巴比妥在清液干涉T4 分析用試樣或修改自由T4 (fT4) 集中。卑鄙清液T4 集中顯著更高是顯著更低, 和手段清液TSH 集中, 在狗在小組1, 比較那些在小組2 。三十一條(40%) 狗在小組1 有清液T4 集中比參考範圍, 比較4 (8%) 狗在小組2 。所有狗在小組2 以低清液T4 集中最近有奪取活動。五(7%) 狗在小組1, 但無狗在小組2, 有清液TSH 集中大於參考範圍。協會未被查出在清液T4 集中和TSH 集中、年齡、苯巴比妥治療的劑量、期間之間, 清液苯巴比妥含量, 或程度奪取控制。公開甲狀腺機能不足的標誌不是顯然的在狗以低T4 集中。苯巴比妥的加法 對 清液在試管內沒有影響T4 集中和唯一最小地影響的fT4 集中的決心。作者認為, 臨床工作者應該意識到在phenobarbita 治療的潛力減少清液T4 和增加TSH 集中, 應該當心當解釋甲狀腺的結果測試在狗接受苯巴比妥。
最後, 其它研究確定是否苯巴比妥、鉀溴化物, 或兩種藥物的管理一致地同反常性聯繫在一起在基礎線清液共計甲狀腺素(T4), triiodothyronine (T3), 自由T4, 或thyrotropin (甲狀腺刺激的激素; TSH) 集中在癲癇的狗。
沒有接受任何療程的七十八條狗以沒有任何甲狀腺混亂的證據的奪取混亂(55 對待了與苯巴比妥單獨, 15 被對待與苯巴比妥和溴化物, 和八被對待與溴化物單獨) 並且150 條正常狗臨床被評估了。清液總T4, 總T3, 自由T4, 和TSH 集中, 並且anticonvulsant 藥物的清液集中, 被測量了在78 條狗以奪取混亂。參考範圍為激素集中建立了臨床根據了結果從150 條正常狗。總和自由T4 集中是顯著低在狗接受苯巴比妥(單獨或與溴化物), 比較集中在臨床正常狗。溴化物的管理單獨未同低總或自由T4 聯繫在一起集中。總T3 和TSH 集中沒有不同在小組狗之中。這些結果表明, 清液總和自由T4 集中也許是降低(即, 在範圍典型為狗以甲狀腺機能不足) 在狗被對待與苯巴比妥。清液總T3 和TSH 集中顯著未被改變與苯巴比妥管理有關係。溴化物治療未同任何重大的變化聯繫在一起在這些清液甲狀腺激素集中上。
被確認的分析用試樣出現為TSH 和fT4.ED 很大地改進了我們的能力區別在甲狀腺機能不足和病的euthyroidism 之間。在第一紙在TSH 測試, 甲狀腺機能不足導致了在狗被鈉碘化物I 131 的IV 管理 解答。隨後, L 甲狀腺素口頭被執行得正常化清液甲狀腺素含量。TSH 分析用試樣看來是具體的和是充足地敏感的查出TSH 在這些狗清液在甲狀腺機能不足的歸納之前。有35 摺疊在卑鄙清液TSH 集中的增量跟隨甲狀腺機能不足的歸納, 並且在甲狀腺替換療法的_蒙以後, 卑鄙清液TSH 集中35 天不是顯著大於卑鄙基值。作者認為, 清液分析用試樣TSH 可能證明有用在主要, 次要, 和三重甲狀腺機能不足有差別的診斷在狗, 並且在對甲狀腺激素替換治療的監視反應。
同樣小組工作者然後看62 條健康狗和49 條狗以臨床標誌一致與甲狀腺機能不足(16 甲狀腺機能不足並且33 是euthyroid 以一致疾病) 。樣品從健康狗被使用建立參考範圍為清液TSH 集中。49 條狗被分類了作為甲狀腺機能不足或euthyroid 以一致疾病根據臨床標誌, 另外的診斷和甲狀腺刺激的激素(TSH) 反應對levothyroxine 鈉的管理的測試, 和反應的結果。甲狀腺的作用被認為了正常當清液總甲狀腺素(T4) 含量六個小時在TSH 管理以後是> 2.5 micrograms/dl 。甲狀腺機能不足被診斷了當清液T4 集中在TSH 管理以後是< 或= 1.5 microgram/dl 。結果: 清液TSH 集中極大不同在所有三個小組之中。四33 條(12%) euthyroid 狗有大於參考範圍的TSH 集中, 但是六16 條(38%) 甲狀腺機能不足的狗有TSH 集中在參考範圍之內。特異性為清液TSH 集中是0.88 並且敏感性是0.63 。當解釋與清液T4 集中的組合, 特異性增加到1.0 。作者建議TSH 分析用試樣有好特異性至於使用在甲狀腺機能不足診斷在狗。由於這個分析用試樣有低敏感性, 甲狀腺機能不足診斷不能被排除根據了是在參考範圍之內的清液TSH 集中。
其它研究並且看TSH 和fT4.ED 。五十四條狗以甲狀腺機能不足, 54 條euthyroid 狗以nonthyroidal 疾病最初地被懷疑有甲狀腺機能不足, 和150 條正常狗臨床被學習了。在54 條狗以甲狀腺機能不足, 診斷建立了根據了臨床定期實驗室和TSH 刺激測試的標誌、一致nonthyroidal 疾病結果, 排除, 和對治療的一個好臨床反應與L 甲狀腺素。血樣從所有狗被收集了和被測試了為甲狀腺激素和TSH 集中。參考範圍為激素集中建立了臨床根據了結果為150 條正常狗。54 條甲狀腺機能不足的狗, 48 (89%) 有低共計T4 集中, 三有低正常集中, 並且三有高濃度由於T4 自身抗體。相反, 只10 條(18%) euthyroid 狗有低共計T4 集中。只三31 條(10%) 甲狀腺機能不足的狗有低T3 集中; 23 有集中在參考範圍之內, 並且五有高濃度由於T3 自身抗體。只三38 條euthyroid 狗有低T3 集中。甲狀腺機能不足的狗, 53 (98%) 有低自由T4 集中和你有低正常集中。只四(7%) euthyroid 狗有低自由T4 集中。甲狀腺機能不足的狗, 41 (76%) 有高TSH 集中, 和13 有TSH 集中在參考範圍之內。euthyroid 狗, 只四(8%) 有高TSH 集中。所有唯一激素測量被評估, 自由T4 的測量集中有最高的敏感性(0.98), 特異性(0.93), 和準確性(0.95) 作為一個測試為甲狀腺機能不足; 總T4 的測量集中有一種更低的敏感性(0.89), 特異性(0.82), 和準確性(0.85) 。比較總或自由T4 的測量集中, TSH 集中的測量有更低的敏感性(0.76) 並且準確性(0.84) 僅特異性(0.93) 均等對那為自由T4 的測量集中。當T4 (總或釋放) 並且TSH 集中一起被評估了, 特異性高級比當T4 或TSH 集中單獨被評估了。只一條euthyroid 狗有低T4 (總和釋放) 並且高TSH 集中。這些結果表明, 清液自由T4 的測量和TSH 集中是有用的為甲狀腺機能不足診斷在狗。有趣的是, 狗四分之一以被證實的甲狀腺機能不足有清液TSH 集中在參考極限內。這被調查了在一項分開的研究中。
確定是否這歸結於波動在TSH 發行, TSH 血漿外形被分析在七條小獵犬母狗被收集血樣每10 分鐘六個小時, 兩個在主要甲狀腺機能不足的歸納前後。在主要甲狀腺機能不足的歸納以後, 37 摺疊在卑鄙基礎血漿TSH 集中的增量並且34 摺疊在卑鄙區域的增量在曲線之下為TSH 被發現了。分析由脈衝星節目展示了TSH 的脈搏分泌物在甲狀腺機能不足的狀態, 為相對地低高度脈衝(手段[ +/-SEM ]) 高度41 +/- 3% 基礎血漿TSH 水平) 描繪和一個卑鄙脈衝頻率2.0 +/- 0.5 pulses/6 小時。在euthyroid 狀態, 重大TSH 脈衝被辨認了在只二條狗。卑鄙基礎血漿TSH 水平正面地關聯了(r = 0.84) 以TSH 脈衝的卑鄙高度, 和消極地關聯了(r = -0.88) 以TSH 脈衝頻率。這項研究的結果展示TSH 的脈搏分泌物在狗在甲狀腺機能不足和唯一小波動期間在血漿TSH 集中在euthyroidism 期間。研究結果並且建議, 低值TSH 偶爾地發現了在狗以自發主要甲狀腺機能不足, 可以在某些情況下, 是一部分ultradian 波動的結果。
誘惑測試由一些仍然認為黃金本位制特別是當基礎甲狀腺功能考驗(TT4 、fT4.ED, TSH) 是模稜兩可或不和的。一張最近紙估計了人的再組合TSH 的作用在甲狀腺作用在正常狗。六條健康小獵犬狗被使用了在每個三個階段這項研究。階段I: 甲狀腺刺激的激素反應測試由使用執行了25 微克、50 微克, 和100 微克總藥量rhTSH, 靜脈內被執行。階段II 和III: 甲狀腺刺激的激素反應測試由使用執行了50 微克rhTSH 由肌肉內和皮膚下路線執行, 各自地。在□階段和跟隨rhTSH 所有規定的藥量, 在清液TT4 集中的增量是著名, 雖然它總不是重大的。為階段I, 有在清液TT4 集中的重大增量。根據這項研究, 50 微克被判斷了rhTSH 優選的靜脈內藥量。階段II 和III, 那裡是在清液的沒有重大增量TT4 在這項研究的rhTSH. 結果的管理建議之後rhTSH 能是遲鈍的TSH 的一個好替補, 當由靜脈內路線使用, 為TSH 刺激測試在狗。進一步研究必需證實它的臨床有用性。

Over the past few years, we have learned a great deal about the pathogenesis and diagnosis of canine hypo-thyroidism. This has been due in large part to improvements in the diagnostic tests available to the clinician. Autoimmune thyroiditis is the most common cause of hypothyroidism. A recent study looked at the value of autoantibody testing in dogs. Serum samples from dogs with various endocrine abnormalities and from 30 obese adult females had Tyroglobulin Autoantibodies (TgAA) concentrations determined by use of the ELISA. Six experiments were done: 1) definition of positive results for TgAA using samples from normal and T3 autoantibody (T3AA) positive dogs; 2) establishment of prevalence of positive results in 91 clinically normal dogs; 3) evaluation of positive results for sera from dogs with nonthyroidal illnesses; 4) testing of samples from dogs with primary hypo-thyroidism but absence of T4AA or T3AA, or both; 5) determination of prevalence of false-negative results in dogs that are T4AA and/or T3AA positive, which were (18 dogs) or were not (22 dogs) receiving L-thyroxine replacement therapy; and 6) examination of thyroid biopsy specimens from 18 dogs (8 TgAA positive and 10 TgAA negative).
Positive results were defined as at least twice (200%) the optical density of the negative-control sample. False-positive results were obtained for only 3.4% of 146 dogs with nonthyroidal illness. Thirty-seven percent of dogs with primary hypothyroidism, but no evidence of T4AA or T3AA, or both, were TgAA positive. False-negative results were found in one of 22 and two of 18 T3AA-positive dogs with and without thyroid replacement therapy, respectively. Thyroid biopsy specimens from eight TgAA-positive dogs had evidence of lymphocytic thyroiditis, whereas those from 10 TgAA-negative dogs did not. The assay was sensitive and specific for identification of lymphocytic autoimmune thyroiditis in dogs, and has potential for aiding early diagnosis of thyroiditis in dogs and identifying dogs likely to perpetuate hypothyroidism in breeding programs.
A number of medications and non-thyroidal illness can interfere with the various thyroid function tests. Several papers examined the effects of anti-convulsant therapy on the pituitary-thyroid axis. A multicentric prospective study was conducted to monitor the effect of phenobarbital on serum total thyroxine (T4) and thyroid-stimulating hormone (TSH) concentrations in epileptic dogs. Serum T4 concentrations were determined for 22 epileptic dogs prior to initiation of phenobarbital therapy (time 0) and at three weeks, six months, and 12 months after the start of phenobarbital. Median T4 concentration was significantly lower at three weeks and six months compared to time 0.
Thirty-two percent of dogs had T4 concentrations below the reference range at six and 12 months. Nineteen of the 22 dogs had serum TSH concentrations determined at all sampling times. A significant upward trend in median TSH concentration was found. No associations were found between T4 concentration, dose of phenobarbital, and serum phenobarbital concentration. No signs of overt hypothyroidism were evident in dogs with low T4, with one exception. TSH stimulation tests were performed on six of seven dogs with low T4 concentrations at 12 months, and all but one had normal responses.
In conclusion, phenobarbital therapy decreased serum T4 concentration but did not appear to cause clinical signs of hypothyroidism. Serum TSH concentrations and TSH stimulation tests suggest that the hypothalamic-pituitary-thyroid axis is functioning appropriately. A second study evaluated the changes in serum total T4 (TT4), free T4 (FT4), thyroid-stimulating hormone (TSH), cholesterol and albumin concentrations, and activities in serum of alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT) after discontinuation of long-term phenobarbital administration in normal dogs. Twelve normal dogs were administered phenobarbital at a dosage of approximately 4.4-6.6 mg/kg q12h PO for 27 weeks. Blood was collected for analysis before and after 27 weeks of phenobarbital administration and then weekly for 10 weeks after discontinuation of the drug. The dogs were clinically normal throughout the study period. Serum ALT and ALP activity and TSH and cholesterol concentrations were significantly higher than baseline at week 27. Serum T4 and FT4 were significantly lower. Serum albumin and GGT were not changed from baseline at week 27. Changes in estimate of thyroid function (TT4, FT4, TSH) persisted for one to four weeks after discontinuation of phenobarbital, whereas changes in hepatic enzyme activity (ALT, ALP) and cholesterol concentration resolved in three to five weeks.
To avoid false positive results, it is recommended that thyroid testing be performed at least four weeks after discontinuation of phenobarbital administration. Elevated serum activity of hepatic enzymes six to eight weeks after discontinuation of phenobarbital may indicate hepatic disease. The effects of phenobarbital were again assessed on thyroid as well as on adrenal function. The effects of phenobarbital on the thyroid axis, the adrenal axis, and adrenal function tests were prospectively investigated in 12 normal, adult dogs. Phenobarbital was administered at 5 mg per kilogram of body weight (range, 4.8-6.6 mg/kg q12h PO for 29 weeks, resulting in therapeutic serum concentrations (20-40 microg/mL). Serum total thyroxine (TT4), free thyroxine (FT4) by equilibrium dialysis, total triiodothyronine (TT3), thyrotropin (TSH), and cholesterol were determined before and during phenobarbital treatment. LDDST, ACTH stimulation tests, and ultrasonographic evaluation of the adrenal glands were performed before and during treatment. TT4 and FT4 decreased significantly (P < or = .05), TT3 had minimal fluctuation, TSH had only a delayed compensatory increase, and cholesterol increased during phenobarbital treatment.
�he delayed increase in TSH, despite persistent hypothyroxinemia, suggests that accelerated hepatic thyroxine elimination may not be the only effect of phenobarbital on the thyroid axis. There was no significant effect of phenobarbital on either of the adrenal function tests. A larger study examined 78 epileptic dogs receiving phenobarbital (group 1) and 48 untreated epileptic dogs (group 2). Serum biochemical analyses, including T4 and TSH concentrations, were performed for all dogs. Additional in vitro analyses were performed on serum from healthy dogs to determine whether phenobarbital in serum interferes with T4 assays or alters free T4 (fT4) concentrations. Mean serum T4 concentration was significantly lower, and mean serum TSH concentration significantly higher, in dogs in group 1, compared with those in group 2. Thirty-one (40%) dogs in group 1 had serum T4 concentrations less than the reference range, compared with 4 (8%) dogs in group 2. All dogs in group 2 with low serum T4 concentrations had recently had seizure activity. Five (7%) dogs in group 1, but none of the dogs in group 2, had serum TSH concentrations greater than the reference range. Associations were not detected between serum T4 concentration and TSH concentration, age, phenobarbital dosage, duration of treatment, serum phenobarbital concentration, or degree of seizure control. Signs of overt hypothyroidism were not evident in dogs with low T4 concentrations. Addition of phenobarbital in vitro to serum did not affect determination of T4 concentration and only minimally affected fT4 concentration. The authors concluded that clinicians should be aware of the potential for phenobarbita treatment to decrease serum T4 and increase TSH concentrations and should use caution when interpreting results of thyroid tests in dogs receiving phenobarbital.
Lastly, another study determined whether administration of phenobarbital, potassium bromide, or both drugs concurrently was associated with abnormalities in baseline serum total thyroxine (T4), triiodothyronine (T3), free T4, or thyrotropin (thyroid-stimulating hormone; TSH) concentrations in epileptic dogs.
Seventy-eight dogs with seizure disorders that did not have any evidence of a thyroid disorder (55 treated with phenobarbital alone, 15 treated with phenobarbital and bromide, and eight treated with bromide alone) and 150 clinically normal dogs that were not receiving any medication were evaluated. Serum total T4, total T3, free T4, and TSH concentrations, as well as serum concentrations of anticonvulsant drugs, were measured in the 78 dogs with seizure disorders. Reference ranges for hormone concentrations were established based on results from the 150 clinically normal dogs. Total and free T4 concentrations were significantly lower in dogs receiving phenobarbital (alone or with bromide), compared with concentrations in clinically normal dogs. Administration of bromide alone was not associated with low total or free T4 concentration. Total T3 and TSH concentrations did not differ among groups of dogs. These results indicate that serum total and free T4 concentrations may be low (i.e., in the range typical for dogs with hypothyroidism) in dogs treated with phenobarbital. Serum total T3 and TSH concentrations were not changed significantly in association with phenobarbital administration. Bromide treatment was not associated with any significant change in these serum thyroid hormone concentrations.

minibabyqq 2007-1-4 22:51

[color=Magenta][size=5][b]臨床Hemopoiesis Clinical Hemopoiesis   [/b][/size][/color]


在哺乳動物的胎兒, hematopoiesis 最初地發生在卵黃質sac 並且以後在肝臟和hematopoiesis spleen.(1) 海島顯現出在這些組織和然後斷開線雖然骨髓變得主要站點為血細胞forma.tion 在第七個月胎兒development.(2) 以前除嚴重的損傷譬如那發生以myelofibro.sis 或輻射傷害, 骨髓保留站點為血細胞形成在剩餘生活過程中。在哺乳動物的成長期間有活躍hematopoiesis 在中央軸向骨骼(即, 肋骨、椎骨, 和骨盆) 並且肢的骨髓空間延伸到腕、tarsus, 和calvarium 。以正常成長, hematopoiesis 從周圍逐漸讓步。這變動是反演性的, 然而; 末端骨髓引伸可能發生以密集的刺激, 和發生與嚴厲溶血貧血症、hematopoietic 成長因素的長期管理, 和血液學malignan.cies 。期限髓心hematopoiesis 提到血細胞的pro.duction 在骨髓; extramedullary hematopoiesis 表明血細胞生產在骨髓之外在脾臟、肝臟, 和其它地點譬如淋巴腺組織(特別是在貓) 。
HEMATOPOIETIC 組織的組織
hematopoietic 細胞顯現出的髓心空間包含, 通常, 許多adipocytes 和富有的血管供應。血管內皮細胞的細胞、骨髓成纖維細胞, 和stromal 細胞是重要來源為提供結構對骨髓空間並且為hematopoietic 成長因素生產刺激細胞proliferation.(3) 血管內皮細胞的細胞並且形成一個重要障礙保留發育未全的細胞在骨髓和許可證成熟hematopoietic 元素進入血液的矩陣蛋白質。adipocytes 也許影響hematopoiesis 通過他們的對雄激素和女性荷爾蒙新陳代謝的作用。骨髓巨噬細胞用於去除筋疲力盡或apoptotic 細胞, 並且清除血液雜質當它進入骨髓。Osteoblasts 和osteoclasts 維護和改造周圍的can.cellous 骨頭和鈣化的格子, 交叉往來骨髓space.(3)
胸腺、淋巴結、mucosa 伴生的淋巴組織(麥芽), 和脾臟有多個hematopoietic 作用。及早在開發中, 他們是主要站點為hematopoiesis 。在成年, 他們主要地是站點為淋巴細胞發展, 處理抗原, 動作器T 細胞的develop.ment, 和抗體生產。在myeloproliferative 混亂, 這些組織大小和多孔的建築學是de.ranged, 導致許多這些混亂的臨床顯示。
Hematopoietic 乾細胞。 hematopoietic 系統的所有細胞從共同的前體細胞, hematopoietic 詞根cells.(4) 被獲得這些細胞將難辨認, 一部分因為他們通常代表只大約骨髓cells.(5) 的百分之0.05 通過自新, 這人口被維護沒有取盡儘管提升大約1010 個 紅血球並且109 粒 白血球每小時為終身individual.(6) 運用認可具體細胞表面分子有選擇性地被表達在開發hematopoietic 細胞和其它專業技術的monoclonal 抗體, 乾細胞可能現在被分離從其它骨髓細胞。以這些方法, 人的hematopoietic 乾細胞被發現正面的為CD34 、c 成套工具、和thy-1 和陰性為HLA-DR, CD15, 和CD77.(6) 為臨床目的, CD34+ 祖先包含乾細胞和有些成熟細胞的細胞人口, (7), 經常被使用為hematopoiet.ic 乾細胞移植。
乾細胞 提升女兒細胞, 接受不可逆的承諾對分化沿各種各樣的hematopoietic 細胞後裔。許多最早期的步的方面在這個分化過程中不是好的被瞭解。以後裔承諾, 然而, 分化、細胞成熟性, 和發行對血液受到明確定義的hematopoietic 成長因素控制。這些成長因素有重疊的活動為早期的階段differentiation.(8) 以後在develop.ment, 一些成長因素是後裔具體, 意味, 他們治理唯一後裔的成熟性和部署。Erythropoietin (EPO), thrombopoietin (TPO), 和granulocyte 殖民地刺激的因素(G-CSF) 是佳被描繪的後裔具體因素。
Hematopoietic 成長因素。 hematopoietic 成長因素, 並且指hematopoietic cytokines, 是糖蛋白家庭pro.duced 在骨髓由內皮細胞的細胞, stromal 細胞, 成纖維細胞, 巨噬細胞, 並且淋巴細胞和並且生產在他們被運輸對骨髓通過blood.(9) 命名 這些因素的遙遠的站點是有些纏擾不清的。Erythropoietin 和thrombopoietin 從希臘詞poiesis 獲得一部分的他們的 名字, 意味做。殖民地刺激的因素第一次被認可了由於他們的容量刺激早期hematopoietic 細胞增長入群並且大殖民地在組織文化systems.(10) Interleukin 是規定使用描述由白血球導致並且影響其它白血球的因素。這是因素主要地治理的lymphocytopoiesis 一個大家庭, 但許多成員並且有寬廣的作用在其它後裔。在新成長因素和缺乏的生物後果的這些因素發現上或剩餘繼續迅速地演變。
Hematopoietic 細胞有成長因素感受器官表示的特別樣式, 並且樣式演變當細胞differentiate.(11) 每個成長因素困境只對它具體receptor.(12) 它現在知道為一些成長因素, 那裡是分享感受器官(即, interleukin-3 的組分[ IL-3 ], IL-5, 和granulocyte 巨噬細胞殖民地刺激的因素[ GM-CSF ] 份額他們的感受器官一個共同的ss 鏈子), 僅特異性來自其它獨特或receptor.(13) 束縛的私有組分ligand 對感受器官導致conformational 細胞內kinases 的變動, 活化作用, 和, 最後, 觸發細胞proliferation.(14) 為一些成長因素, 這些路很好被定義; 為其他人, 路是不明的
Hematopoietic 成長因素不僅刺激細胞擴散而且延長細胞生存; 那是他們有antiapoptotic effects.(15) 為一些後裔, 譬如嗜中性和monocytes, 那裡是成長因素感受器官在充分地成熟細胞, 並且這些細胞暴露對因素奘填細胞為改進的快速響應對細菌或他們新陳代謝的活動其它刺激品。因而, 為嗜中性後裔的細胞, 成長因素G-CSF 和GM-CSF 可能刺激早期的hematopoietic 細胞擴散, 增加細胞的數量導致由骨髓, 延長這些細胞壽命, 和增添細胞functions.(16)
Erythropoietin 。 peritubular 細胞間的細胞位於腎臟的內在外皮和外面骨髓是主要站點為erythropoietin production.(17) 以回應低氧症, erythropoietin 基因的副本在這些細胞增量, 造成erythropoietin 的增加的分泌物。蛋白質然後被運輸通過血液對骨髓刺激紅血球生成。以腎衰竭, erythropoietin 生產嚴厲地被削弱。在傳染和許多慢性激動情況, erythropoietin 反應blunted 並且erythropoietin 水平是低。
Erythropoietin 是調整紅血球生成由影響幾步在紅細胞development.(18) 裡最原始的可識別的erythroid 細胞的葡基化的蛋白質, 破裂形成單位erythroid (BFU-E), 是相對地厚臉皮的對erythropoietin 。更加成熟的細胞, colony-forming 單位erythroid (CFU-E), 是非常敏感的。Erythropoietin 治療延長erythroid 前體生存, 變短時間在細胞分裂之間, 和增加細胞的數量由個體導致precursors.(17)
Erythropoietin 可能靜脈內被執行或為貧血症的治療由erythropoietin.(19) 治療的不充分的內在生產造成皮膚下地是最大地有效的當骨髓有鋼和其它營養素慷慨的供應, 譬如維生素B12 和葉酸。增加的內在或外生erythropoietin 的最容易地被監測的直接作用是在血液reticulocyte 計數的增量。通常, 作為紅細胞前體成熟, 細胞擠壓他們的中堅力量在正常疾風階段。收效的reticulocytes, 由他們殘餘的核糖體supravital 汙點辨認, 堅持在大約三天在骨髓和一天在血液。Erythropoietin 變短運輸時間通過骨髓, 導致在血液reticulocytes 的數量和比例的增量在幾days.(17) 之內
在一些情況, 特殊慢性激動疾病, erythropoietin 的有效率可能被預言從清液erythropoietin 集中的測量由immunoassay.(20) 它也許是有效的測量集中在創始治療之前在有貧血症病人可歸屬對被壓制的erythropoietin 生產, 譬如有傳染、癌症、腎臟病和其它慢性激動疾病病人。特定種類的erythropoietin 也許是essential.(21-24)
Thrombopoietin 。 megakaryocytes 的發展從hematopoietic 乾細胞和小片的水平在血液由thrombopoietin.(25) Thrombopoietin 治理(TPO) 主要由肝臟生產和有結構相似性對erythropoietin.(26) 血漿thrombopoietin 水平相反地與thrombopoietin 起因thrombocytopenia 有關血液小片count.(27) 缺乏, 並且剩餘導致thrombocytosis 。再組合人的thrombopoietin 是在調查之中為thrombocytopenia 的不同的起因的治療; 但, 在人的醫學不是批准至於臨床使用。
Granulocyte 殖民地刺激的因素 是一葡基化的蛋白質由monocytes, 巨噬細胞, 成纖維細胞, stromal 細胞生產, 並且內皮細胞的細胞在過程中body.(28) 它刺激嗜中性的成長和分化兩個 在試管內 和 in-vivo 。 G-CSF 水平通常是非常低或探測不到的但增量以細菌傳染或在細菌endotoxin.(16) G-CSF (以後被綜合的形式知道作為filgrastim 或lenograstim) 管理的管理導致在血液嗜中性的dose-dependent 增量計數在法線persons(29); 動物短少在G-CSF 上比法線有neutropenia.(30) 像erythropoietin, G-CSF 管理從骨髓加速嗜中性的發展在骨髓, 轉移他們在早期到血液。
在人的醫學G-CSF 是批准為嗜中性白細胞減少症的治療在癌症化療以後, 為嗜中性補救的加速度在骨髓移植以後, 為hematopoietic 祖先細胞的動員從骨髓對血液為hematopoietic 移植, 並且為治療嚴厲慢性neutropenia.(28) 它廣泛被應用對待其它neutropenic 情況。副作用是主要musculoskeletal 痛苦和頭疼在迅速骨髓擴展的期間在療法被創始之後。對方作用是不凡的。在獸醫種類具體G-CSF 和rHG-CSF 如上所述被使用了, 和在parvoviral 腸炎和遲鈍的乳腺炎的治療。
Granulocyte 巨噬細胞殖民地刺激的因素 是一葡基化的蛋白質由許多類型細胞生產, 包括T cells.(13) GM-CSF 刺激嗜中性、monocytes, 和eosinophils 的形成, 也許並且提高早期細胞成長其它lineages.(10) 與G-CSF 對比, GM-CSF 集中一般不增加以傳染或深刻激動情況, (31) 和嗜中性白細胞減少症不起因於GM CSF.(32) 缺乏G-CSF 的骨髓作用並且GM-CSF 相似, 但GM-CSF 是較不有力在舉起血液嗜中性計數。GM-CSF (被綜合的形式知道作為sargramostim 或molgramostim) 被批准在人的醫學在美國為骨髓補救的加速度在骨髓移植以後和廣泛被應用從骨髓加速補救在化療以後和為祖先細胞的動員。它的副作用包括骨頭和musculoskeletal 痛苦和射入站點反應。
其它成長因素。 幾個其它hematopoietic 成長因素是在發展中。IL-3 行動在一個早期的階段在hematopoiesis 刺激細胞擴散但有較少作用在周邊計數。IL-3 分子被結合對其它成長因素, 包括GM-CSF, G-CSF, 和TPO, 生產是在調查之中的雜種分子。IL-11 是舉起血液platelets.(33) 乾細胞因素的一個及早行動的因素(SCF)(34) 並且fms 像酚基乙氨酸kinase 3 (FLT-3) lig- and(35) 是其它及早行動的因素在調查之中。巨噬細胞殖民地刺激的因素(M-CSF) 是一個有選擇性的因素為monocytes 和巨噬細胞形成, (36) 和IL-5 是一個相似的有選擇性的因素為世代的eosinophils.(37)
它被假定, 通常, hematopoietic 細胞形成由因素的組合治理, 被發布在小瀑布, 協調嚴密這些細胞的發展。細節怎樣這個過程發生, 然而, 不是清楚的。有還眾多的實驗室和因素的組合的臨床研究, 但使用多個成長因素的公共事業治療地不被證明。
HEMATOPOIESIS 動力學
最佳的估計是, 需要10 到14 天為事件影響血細胞形成早期被反射在周邊血液count.(38) 這時間間隔帳戶為許多臨床觀察, 譬如延遲在乾細胞的注入的時間和上升之間在血液嗜中性、小片, 和紅血球以hematopoietic 移植。
在骨髓, 血液元素顯現出在二個階段, proliferative 和maturational 階段。在細胞擴散期間, 血細胞前體進行細胞分裂; 通常, mitoses 發生在發展最新階段在大約18- 對24 小時間隔時間。在maturational 階段, 細胞分裂停止, 但最後的特點增加在細胞進入血液之前。例如, 在這個階段期間, 紅血球丟失所有他們的核材料, 獲取他們兩面凹的形狀, 和通常開發酵素他們最後的內容必要為維護兩面凹的形狀和抵抗破壞由氧化stress.(17) 在proliferative 階段期間, 嗜中性獲取大多他們的粒子-- 以是必要的為他們microbiocidal activities.(38) 在成熟性期間, 他們的核chromatin 凝聚的主要, 次要, 和三重粒子著名--, 細胞質的糖朊內容增加, 並且表面物產治理循環、緊持, 和遷移對組織增加。Monocytes 和eosinophils 仿效相似的發展形式。晚了在成熟性, 骨髓嗜中性是足夠成熟的是欣然被發布和工作; 在這個狀況下, 他們被認為是在骨髓嗜中性儲備。定量地, 這個嗜中性水池比總流通的供應是極大地大的-- 大概五到10 次更大-- neutrophils.(38)
小片形成從megakaryocytes 細胞質, 從hematopoietic 詞根cells.(39) Megakaryocytes 並且被獲得接受他們的核chromatin 加倍沒有細胞分裂, 導致極端大細胞的生產。小片形成從分開充分地成熟megakaryocytes 的細胞質或從filopodia 。當骨髓損傷發生從化學療法的代理和在hematopoietic 移植以後, megakaryocytes 經常是最緩慢的細胞恢復並且thrombocytopenia 經常是最後cytopenia 解決。
有還在紅血球、小片, 和白血球動力學或動能學上的重要區別在血液。例如, 嗜中性迅速地移交在血液, 以六個到八個小時血液半衰期, 並且嗜中性的新血液人口根本上被形成每24 hours.(38)
紅血球持續顯然最長: 正常生活間距是大約100 位天在狗和人的, 大約150 天在馬, 牛, 和綿羊, 並且大約80 天在cats.(l7) 這些區別部份地解釋為什麼嗜中性和紅細胞和他們的前體是主要骨髓細胞, 但是紅血球數量上超過嗜中性在血液。同樣, 嗜中性的短的半衰期和高轉交率解釋為什麼嗜中性白細胞減少症是最頻繁的血液學後果當骨髓被藥物或輻射損壞。終於, 紅血球滲流和小片是可行的由於他們的相對地長壽間距, 但是嗜中性短的壽命很大地妨礙了努力開發嗜中性滲流療法。

In the mammalian fetus, hematopoiesis takes place initially in the yolk sac and later in the liver and the spleen.(1) Islands of hematopoiesis develop in these tissues and then involute as the marrow becomes the primary site for blood cell forma負ion by the seventh month of fetal development.(2) Barring serious damage such as that which occurs with myelofibro貞is or radiation injury, the bone marrow remains the site for blood cell formation throughout the rest of life. During mammalian growth there is active hematopoiesis in the marrow spaces of the central axial skeleton (i.e., ribs, vertebrae, and pelvis) and the extremities extending to the carpus, tarsus, and the calvarium. With normal growth and development, hematopoiesis gradually withdraws from the periphery. This change is reversible, however; distal marrow extension can occur with intensive stimulation, as occurs with severe hemolytic anemias, long-term administration of hematopoietic growth factors, and hematologic malignan苞ies. The term medullary hematopoiesis refers to the pro苓uction of blood cells in the bone marrow; extramedullary hematopoiesis indicates blood cell production outside the marrow in the spleen, liver, and other locations such as the lymphoid tissue (especially in cats).
ORGANIZATION OF HEMATOPOIETIC TISSUES
The medullary space in which hematopoietic cells develop contains, normally, many adipocytes and a rich vascular supply. Vascular endothelial cells, marrow fibroblasts, and stromal cells are important sources for the matrix proteins that provide structure to the marrow space and for production of the hematopoietic growth factors that stimulate cell proliferation.(3) The vascular endothelial cells also form an important barrier that keeps immature cells in the marrow and permits mature hematopoietic elements to enter the blood. The adipocytes may influence hematopoiesis through their effects on the metabolism of androgens and estrogens. Marrow macrophages serve to remove effete or apoptotic cells, as well as to clear the blood of foreign materials when it enters the marrow. Osteoblasts and osteoclasts maintain and remodel the surrounding can苞ellous bone and the calcified lattice, which crisscrosses the marrow space.(3)
The thymus, lymph nodes, mucosa-associated lymphatic tissues (MALT), and the spleen have multiple hematopoietic functions. Early in development, they are major sites for hematopoiesis. In adulthood, they are principally sites for lymphocyte development, processing of antigens, develop衫ent of effector T cells, and antibody production. In the myeloproliferative disorders, the size and cellular architecture of these tissues are de訃anged, leading to many of the clinical manifestations of these disorders.
Hematopoietic Stem Cells. All cells of the hematopoietic system are derived from common precursor cells, the hematopoietic stem cells.(4) These cells are difficult to identify, in part because they normally represent only about 0.05 percent of marrow cells.(5) Through self-renewal, this population is maintained without depletion despite giving rise to approximately 1010 erythrocytes and 109 leukocytes an hour for the lifetime of an individual.(6) Utilizing monoclonal antibodies that recognize specific cell surface molecules expressed selectively on developing hematopoietic cells and other specialized techniques, the stem cells can now be separated from other marrow cells. With these methods, the human hematopoietic stem cell has been found to be positive for CD34, c-kit, and thy-1 and negative for HLA-DR, CD15, and CD77.(6) For clinical purposes, CD34+ progenitor cell populations,(7) which contain stem cells and some more mature cells, are often used for hematopoiet虹c stem cell transplantation.
Stem cells give rise to daughter cells, which undergo irreversible commitment to differentiation along various hematopoietic cell lineages. Many aspects of the earliest steps in this differentiation process are not well understood. With lineage commitment, however, differentiation, maturation, and release of cells to the blood come under the control of well-defined hematopoietic growth factors. These growth factors have overlapping activities for the early phases of differentiation.(8) Later in develop衫ent, some growth factors are lineage specific, meaning that they govern the maturation and deployment of single lineages. Erythropoietin (EPO), thrombopoietin (TPO), and granulocyte colony-stimulating factor (G-CSF) are the best-characterized lineage-specific factors.
Hematopoietic Growth Factors. The hematopoietic growth factors, also referred to as hematopoietic cytokines, are a family of glycoproteins pro苓uced in the bone marrow by endothelial cells, stromal cells, fibroblasts, macrophages, and lymphocytes and also produced at distant sites from which they are transported to the marrow through the blood.(9) The naming of these factors is somewhat confusing. Erythropoietin and thrombopoietin derive part of their names from the Greek word poiesis, meaning to make. The colony-stimulating factors were first recognized because of their capacity to stimulate early hematopoietic cells to grow into clusters and large colonies in tissue culture systems.(10) Interleukin is a term used to describe factors that are produced by leukocytes and that affect other leukocytes. This is a large family of factors predominantly governing lymphocytopoiesis, but many members also have broad effects on other lineages. The discovery of new growth factors and the biologic consequences of deficiencies or excesses of these factors continues to evolve rapidly.
Hematopoietic cells have distinctive patterns of expression of growth factor receptors, and the patterns evolve as the cells differentiate.(11) Each growth factor binds only to its specific receptor.(12) It is now known that for some growth factors, there is sharing of components of the receptor (e.g., interleukin-3 [IL-3], IL-5, and granulocyte-macrophage colony-stimulating factor [GM-CSF] share a common ß chain of their receptor), but specificity comes from other unique or private components of the receptor.(13) Binding of the ligand to the receptor leads to a conformational change, activation of intracellular kinases, and, ultimately, the triggering of cell proliferation.(14) For some growth factors, these pathways are well defined; for others, the pathways are still unclear
Hematopoietic growth factors not only stimulate cell proliferation but also prolong cell survival; that is, they have antiapoptotic effects.(15) For some lineages, such as neutrophils and monocytes, there are growth factor receptors on fully mature cells, and exposure of these cells to the factors primes the cells for an enhanced responsiveness to bacteria or other stimulators of their metabolic activity. Thus, for cells of the neutrophil lineage, the growth factors G-CSF and GM-CSF can stimulate early hematopoietic cell proliferation, increase the number of cells produced by the marrow, prolong the life span of these cells, and augment cell functions.(16)
Erythropoietin. The peritubular interstitial cells located in the inner cortex and outer medulla of the kidney are the primary site for erythropoietin production.(17) In response to hypoxia, transcription of the erythropoietin gene in these cells increases, resulting in increased secretion of erythropoietin. The protein is then transported through the blood to the marrow to stimulate erythropoiesis. With renal failure, erythropoietin production is severely impaired. In infections and many chronic inflammatory conditions, the erythropoietin response is blunted and erythropoietin levels are low.
Erythropoietin is a glycosylated protein that modulates erythropoiesis by affecting several steps in red cell development.(18) The most primitive identifiable erythroid cells, the burst-forming unit-erythroid (BFU-E), are relatively insensitive to erythropoietin. More mature cells, the colony-forming unit-erythroid (CFU-E), are very sensitive. Erythropoietin treatment prolongs survival of erythroid precursors, shortens the time between cell divisions, and increases the number of cells produced from individual precursors.(17)
Erythropoietin can be administered intravenously or subcutaneously for the treatment of anemia caused by inadequate endogenous production of erythropoietin.(19) Treatment is maximally effective when the marrow has a generous supply of iron and other nutrients, such as cobalamin and folic acid. The most easily monitored immediate effect of increased endogenous or exogenous erythropoietin is an increase in the blood reticulocyte count. Normally, as red cell precursors mature, the cells extrude their nucleus at the normal blast stage. The resulting reticulocytes, identified by the supravital stain of their residual ribosomes, persist for about three days in the marrow and one day in the blood. Erythropoietin shortens the transit time through the marrow, leading to an increase in the number and proportion of blood reticulocytes within a few days.(17)

minibabyqq 2007-1-4 22:53

[color=Magenta][size=5][b]臨床分析儀 Errors and Pitfalls Associated with Clinical Analyzers   [/b][/size][/color]


介紹
最後十年看見機構內部的(在診所) 化學和血液學分析儀的增加的運用並且在POC 的增量(點關心) 鍵入分析儀被使用在緊急醫學。以這增加的運用來另外的責任。它是由實習者決定提供這項實驗室服務保證, 服務有益於患者。實習者有質量管理的單一責任。這是特別重要在章程不存在治理儀器製造商為獸醫實驗室試驗的北美洲(或實驗室試驗動物標本的) 。
重要認為
題目今天圍繞主要定期化學分析儀。化學分析儀沒有在血液學分析儀是固有的fail 安全機制。實習者罐頭(和應該) 總評估血液影片; 並且這將提供一張迅速和準確支票在機器引起的血液學結果有效性。你們大家通曉突然的outbreak 。thrombocytopenia 那顯現了出當在診所血液學分析儀被使用了沒有血液影片的評估。這個特殊問題反射困難在測量的小片而不是有任一臺分析儀的具體問題。實習者責任將評估影片和確信, 血液影片匹配結果。
除折射計之外測量血漿蛋白質因為機器的可靠性的支票引起了總蛋白含量, 沒有quick. 簡單的方式訪問化學結果的可靠性。反而實習者必須遵循標準quality 保證指導方針。不幸地, 沒有投入觀眾更快的方法睡覺比開始談論質量管理。所以, 為這次討論我們將提到這個主題當critical 認為的目的。作為科學界一部分, 我們所有被教了對是方法我希望使用在評估的儀器工作的problems.and 的scientific 方法方法。這要求我們是懷疑的和評估機器當我們會患者。我們必須首先建立什麼我們想要達到(目標) 。什麼是test(s) 的目的? 我們評估好的動物(前外科屏幕)? 我們訪問對治療的反應在病的動物嗎? 我們使用這個機器做診斷嗎?
我們決定了在目的Once 我們然後需要考慮儀器工作和測試。
什麼標本必需? 樣品怎麼被處理?
機器怎麼提供標本對反應分庭?
這是什麼test.is 的依據電子procedure/photometric 等?
什麼是機器可能測量的範圍?
溫度怎麼被控制?
什麼機器的零件需要替換? 什麼技術支持是可利用的?
什麼是維護必需保證, 機器運轉在最宜?
什麼可能導致errors.both 分析和physiologic.in 測試結果?
什麼是必要保證那1 + 1 = 2? 有是檢查固有在機器之內如果那樣, 怎麼我知道他們執行並且什麼是他們?
我們怎麼解釋引起的結果?
影響機器的因素
自動化的化學機器包括提供試劑和樣品交付, 船在裡反應發生, 混合二個項目, 一個受控溫度、時間設備和然後反應的實際測量的儀器。許多乾燥化學機器根據反射率光度學當電解質被測量與電極。
可能影響反應的因素有:
液體階段的遷移的速度通過或沿幻燈片, 即, 黏度。
多數反應是enzymatic 和因而高度溫度受撫養者。
被分與的容量樣品和試劑的準確性。
反應的時間。
個體執行測試
它非常重要有視覺上估計這些因素方式或或作為一般機器維護的部份以便我們能證實表現。
PREANALYTICAL 可變物
樣品怎麼被收集?
止血帶的應用導致多血脈性的stasis 和允許血液彙集可能導致重大的變化在有的analytes 上:
增加的總蛋白含量, AST/CK (一樣高像10%) 。
被減少的鉀(一樣高像8%) 。
增加的磷和被電離的鈣。
增加的膽紅素(沒有可看見的hemolysis) 。
麻醉被使用為彙集。
減少在總蛋白含量裡, pmns/wbcs 。
可變性在PCV 。
增加的肌肉酵素, 葡萄糖, 減少了鈣。
修改過的電解質。
凹道管的汙穢。
總填裝首先沒有抗凝劑的管。
什麼變動發生與Na F/oxalate 管?
什麼變動發生與EDTA?
什麼變動發生以鍛煉?
(一些貓特別接受吃力鍛煉在血液彙集期間)
增加的CK 、AST 、肌氨酸酐和磷。
被減少的鋼、白蛋白和鉀。
個體的熟練執行測試。
所有個體使用測試從事相同規程(有是一個一致的做法指南) 嗎? 二個人可以做同樣曲奇餅嗎?
是時間考慮醫療決定水平嗎?
一個醫療決定水平是重要value.this 價值可能只建立如果您知道:
reference 範圍, 。怎麼是這建立, 它真實地代表normal. 個體在您的實踐區域嗎? 年齡、性, 和養殖重要嗎?
需要知道多麼精確您的儀器是為各analyte 。鈣是2.4 實際上2.35 到2.45 或它是2.41 嗎? 如果它是2.45, 什麼那個手段如果您的參考範圍上限是2.43? 精確度真正地是增殖率測試: 如果您測量10 次做價值變動的一analyte 並且由多少?
準確性是一個另外概念, 不能是測試的要求如果它是可再生的, 並且可能區別在normal 之間和反常。
分析可變物
什麼是各種各樣的藥物的作用在方法學由機器使用?
頭孢菌素, 胺基移轉; Metronidazole 減少胺基移轉。
血紅蛋白替補將減少阿爾卑斯胺基移轉, 為多久?
其它因素將影響什麼方法學?
樣品的存貯將影響結果嗎? 這重要如果您想要預先的樣品與樣品比較三天以後被需要。如果結果不同, 結果多少是差距的怎樣樣品被存放了?
樣品的顏色干涉嗎? 任何可能完成關於樣品顏色嗎?
改變在蛋白質裡當前在樣品將影響結果嗎?
何時使用整體血液, 血流比容計影響結果或反常WBC 計數可能影響結果嗎?
POST-ANALYTICAL 可變物
必須演講的主要崗位分析可變物是怎麼您解釋結果。解釋要求:
1 。 交互作用以歷史和體格檢查。
2 。 對分析用試樣的極限的理解。
3 。 對疾病和治療的作用的理解在各種各樣的參量; 任何特殊疾病的可能性的感覺創造一套修改過的參量。
4 。 記住各個單獨動物的獨特, 而不是統計。
例子: Glucometer
Glucometers 定期地使用估計對胰島素的反應在糖尿病動物和確定定期血液葡萄糖曲線作為對糖尿病控制的評估:
美國糖尿病協會公眾輿論聲明推薦, 總錯誤(分析+ 用戶) 10% 是少於葡萄糖含量在30 和400 mg/dL (SI 單位之間。1.7. 22.2 mol/L), 100% 時間。另外, 測量應該是在15% 參考葡萄糖價值之內。在11 不同米的研究中; 19.48% 分析沒有達到結果在15% 之內, 並且錯誤率為準確性(10%) 是36.68% 。
在獸醫方面, 最近紙分析了各種各樣的glucometers 表現。基礎技術是或者電子的或測光和統計評估是令人滿意的。在範圍由ADA 建議, 米沒有執行對規格。這牌子區別嗎? 如果米讀在一個單獨唯一hyperglycemic 樣品或4.0 mol/L 在或在參考範圍之下之上, 那重要嗎? 如果然而, 您跑曲線, 能是或在或在實際價值之下之上, 並且如果在您的患者裝入價值是所有在一個方向, 您會有對胰島素的一個平的curve.no 反應和hyperglycemic animal.would 產生變化對您的治療?

INTRODUCTION
The last decade has seen an increased utilization of in-house (in-clinic) chemistry and hematology analyzers as well as an increase in the POC (point-of-care) type analyzers used in emergency medicine. With this increased utilization comes additional responsibility. It is up to the practitioner providing this laboratory service to assure that the service is going to benefit the patient. The practitioner has the sole responsibility of quality assurance. This is especially important in North America where no regulations exist to govern the manufacturer of instruments for veterinary laboratory testing (or laboratories testing animal specimens).
CRITICAL THINKING
The topic today revolves primarily around routine chemistry analyzers. Chemistry analyzers do not have 𡜻ail safe?mechanisms that are inherent in the hematology analyzers. A practitioner can (and should) always evaluate a blood film; and this will provide a rapid and accurate check on the validity of machine generated hematology results. Many of you are familiar with the sudden 㺸utbreak ?of thrombocytopenia that developed when in-clinic hematology analyzers were used without evaluation of the blood film. This particular problem reflects the difficulty in measuring platelets rather than specific problems with any analyzer. The practitioners?responsibility is to evaluate the film and make sure that the blood film matches the results.
Other than a refractometer to measure plasma protein as a check of the reliability of a machine generated total protein, there are no 𢖾uick?simple ways to access the reliability of chemistry results. Instead the practitioner must follow standard 𢖾uality assurance?guidelines. Unfortunately, there is no quicker method of putting an audience to sleep than to begin to discuss Quality Control. Therefore, for the purpose of this discussion we will refer to this subject as 𡤧ritical thinking.?As part of the scientific community, we have all been taught the 𦽳cientific method?approach to problems㻡nd that is the method I wish to employ in evaluating instrumentation. This requires us to be skeptical and to evaluate the machine as we would the patient. We must first establish what we want to achieve (goal). What is the purpose of the test(s)? Are we going to be evaluating well animals (pre-surgical screen)? Are we going to be accessing response to treatment in sick animals? Are we going to use this machine to make a diagnosis?
𤪻nce we have decided on the purpose then we need to consider the instrumentation and the test.
What specimen is required? How is the sample handled?
How does the machine deliver the specimen to the reaction chamber?
What is the basis of the test𡟙s this an electrical procedure/photometric etc?
What is the range that the machine can measure?
How is temperature controlled?
What parts of the machine need replacing? What technical support is available?
What is the maintenance required to assure that the machine is working at optimum?
What can induce errors𤪳oth analytical and physiologic𡟙n the test results?
What is necessary to assure that 1 + 1 = 2? Are there checks inherent within the machine and if so, how do I know they are performed and what are they?
How do we interpret the results that are generated?
FACTORS THAT INFLUENCE THE MACHINE ITSELF
The automated chemistry machine consists of an instrument that provides both reagent and sample delivery, a vessel in which the reaction occurs, a mixing of the two items, a controlled temperature, a timing device and then the actual measurement of the reaction. Many dry chemistry machines are based on reflectance photometry while electrolytes are measured with electrodes.
Factors that can influence the reactions include:
Speed of migration of the liquid phase through or along the slide, i.e., viscosity.
Most reactions are enzymatic and thus highly temperature dependent.
The accuracy of the dispensed volume both sample and reagent.
The timing of the reaction.
The individual performing the test
It is very important to have a way of assessing these factors either visually or as a part of the general machine maintenance so that we can confirm performance.
PREANALYTICAL VARIABLES
How is the sample collected?
Application of a tourniquet to induce venous stasis and allow blood collection can cause significant changes in analytes that include:
Increased Total Protein, AST/CK ( as high as 10%).
Decreased Potassium (as high as 8%).
Increased phosphorus and ionized calcium.
Increased bilirubin (even without visible hemolysis).
Anesthesia used for collection.
Decrease in total protein, pmns/wbcs.
Variability in PCV.
Increased muscle enzymes, glucose, decreased calcium.
Altered electrolytes.
Contamination of draw tubes.
Always fill tubes that have no anticoagulant first.
What changes occur with Na F/oxalate tubes?
What changes occur with EDTA?
What Changes Occur With Exercise?
(Some cats particularly undergo strenuous exercise during blood collection)
Increased CK, AST, creatinine and phosphorus.
Decreased iron, albumin and potassium.
The proficiency of the individual performing the test.
Are all individuals using the test following identical procedures (is there a uniform procedure manual)? Can two people make the same cookies?
Is it Time to Consider Medical Decision Levels?
A medical decision level is a critical value鍟his value can only be established if you know:
The 𩂈eference range,?how was this established, does it truly represent 忛ormal?individuals in your practice area? Is age, sex, and breed important?
Need to know how precise your instrument is for each analyte. Is a calcium of 2.4 actually 2.35 to 2.45 or is it 2.41? If it is 2.45, what does that mean if your reference range upper limit is 2.43? Precision is really a test of reproducibility: if you measure an analyte 10 times does the value change and by how much?
Accuracy is a different concept and may not be a requirement of a test if it is reproducible, and can distinguish between 忛ormal and abnormal.?/p> ANALYTICAL VARIABLES
What is the effect of various drugs on the methodology used by the machine?
Cephalosporin, transaminases; Metronidazole decreases transaminases.
Hemoglobin substitutes will decrease ALP transaminases, for how long?
What other factors will influence the methodology?
Will storage of the sample affect the result? This is important if you want to compare prior samples with a sample taken three days later. If the results are disparate, how much of the disparity is the result of how the sample was stored?
Does the color of the sample interfere? Can anything be done about the sample color?
Will an alteration in protein present in the sample affect the result?
When using whole blood, does the hematocrit influence the result or can an abnormal WBC count influence the result?
POST-ANALYTICAL VARIABLES
The major post analytical variable that must be addressed is how you are going to interpret the results. The interpretation requires:
1. Correlation with the history and physical examination.
2. Understanding of the limits of the assay.
3. Understanding of the effects of disease and treatment on the various parameters; a sense of the probabilities of any particular disease creating a set of altered parameters.
4. Remembering the uniqueness of each individual animal, rather than the statistics.
Example: Glucometer
Glucometers are routinely used to assess the response to insulin in diabetic animals and to determine routine blood glucose curves as an assessment of diabetic control:
The American Diabetes Association consensus statement recommends that the total error (analytical + user) be less than 10% of the glucose concentrations between 30 and 400 mg/dL (SI units ?1.7?22.2 mol/L), 100% of the time. In addition, the measurements should be within 15% of the reference glucose value. In a study of 11 different meters; 19?8% of the analyses failed to achieve results within 15%, and the failure rate for accuracy (10%) was 36?8%.
In veterinary medicine, recent papers have analyzed the performance of various glucometers. The basic technology is either electrical or photometric and the statistical evaluations have been satisfactory. Over the range suggested by the ADA, the meters did not perform to specifications. Does this make a difference? If the meter reads on an individual single hyperglycemic sample either 4.0 mol/L above or below the reference range, is that important? If however, you are running a curve and can be either above or below the actual value, and if in your patients case the values were all in one direction, you would have a flat curve瑈o response to insulin and a hyperglycemic animal𨫎ould that make a difference to your treatment?

minibabyqq 2007-1-4 22:54

[color=Magenta][size=5][b]血液學分析儀 [/b][/size][/color]

The Diagnostic Power of Graphical Reports   


A 圖片值得一千個詞。所有太經常, 獸醫不接受細胞圖形顯示由血液學儀器的新一代引起。這決定, 由提及實驗室的主任做出, 是因為他們不相信獸醫能解釋cytograms 和直方圖。這位unfortunate, 共同性, 決定很大地減少報告的診斷公共事業作遞交的獸醫。
儀器
大多評論和例子被使用在這個介紹提到貝爾H-1 和Advia 120 個系統因為作者最工作了以這些系統。其它例子是普遍的在型和提到導致非常相似的類型圖表多數獸醫將看見實踐上的阻抗系統。貝爾系統使用雷射技術測量紅血球和小片的數量、大小, 和內部複雜。阻抗基於的系統使用多數血液學分析儀最共同的計數的方法。阻抗技術並且稱犁刀原則。犁刀血液學儀器使用了它幾年來以便命名Coulter 櫃臺是同義字的與hematology 分析儀。阻抗測量細胞的大小和數量。Abbott 細胞達因使用阻抗技術測量小片和紅血球的大小和數字和使用阻抗和雷射技術計數白血球的數量。許多更小的血液學分析儀使用阻抗技術計數所有三種細胞類型。
ERYTHROCYTE-PLATELET 容量直方圖
紅血球小片容量直方圖是最共同的圖表由獸醫看見。它是從阻抗類型細胞櫃臺。它應該顯示二個分明峰頂根據有些容量(Y軸) 並且細胞容量(X軸的) 細胞的數字。小峰頂到左邊代表小片(更小的大小和小數字細胞) 並且一個更大的峰頂在右邊代表紅血球。那裡應該是分明谷在峰頂之間表示, 儀器是能區分二種細胞類型。二個峰頂的一個共同的原因對合併是鋼缺乏貧血症。在鋼缺乏貧血症, 紅血球是小(microcytic) 並且那裡經常是thrombocytosis 與大小片因此二種細胞類型合併在大小, 也許重疊。這導致小紅血球算作是小片和大小片算作是紅血球。由於小片比紅血球是較少數量上, 小片錯誤通常是更加引人注目的。這個變化在圖表(直方圖上) 是診斷和顯露實驗室錯誤。注意, 這張圖表有二個好處(技術和診斷) 。
如果儀器圖解不顯示紅血球和小片並且如果唯一數字被報告, 錯誤結果然後不被查出並且診斷也許是被錯過或誤譯。鋼缺乏貧血症是或許在哪裡儀器圖表改進診斷的最佳的例子。Weiser 顯露, 70% 五隻week 老小貓有鋼缺乏貧血症但必要的改善的儀器工作顯示什麼紅血球的百分比比法線小。多數獸醫得到在他們的血液學報告唯一手段corpuscular 容量(MCV) 並且意味corpuscular 血紅蛋白含量(MCHC) 。這些卑鄙(平均) 價值太厚臉皮的以至於不能顯露鋼缺乏在小貓並且鋼缺乏貧血症早期在狗。經常有很少microcytic 紅血球拉扯平均值(MCV 並且/或者MCHC) 在參考價值之下。小片紅血球直方圖也許顯示變動及早。貝爾RBC cytograms 和直方圖是非常敏感的在查出鋼缺乏貧血症。
貝爾系統圖表
貝爾系統測量容量並且內部複雜(光學密度) 的紅血球, reticulocytes 和小片, 不同於阻抗抵抗那唯一這些細胞的措施容量。所以, 貝爾cytograms 和直方圖是最佳為形象化的疾病變化在這些細胞上。這並且是最佳的系統為計數小片因為它可能區分小片從紅血球既使小片比紅血球大的。
鋼缺乏貧血症由貝爾系統查出及早因為少量microcytic hypochromic RBCs 非常必要在patient.s 血液被看見在RBC cytogram 。貝爾RBC cytogram 顯示每RBC 在樣品, 因此它採取相對地少數被看見在正常區域之外。這並且是唯一的儀器有血紅蛋白含量直方圖。由於每RBC 的大小和血紅蛋白含量被測量, 小子集的百分比和absolute 數量非典型RBCs 可能被報告。貝爾・Advia 120 確定細胞容量和是有用的在鋼缺乏貧血症診斷在人血各自的紅血球和reticulocytes 的細胞血紅蛋白, 也許是有用的以似犬鋼缺乏貧血症評估。
再生貧血症最好被診斷以貝爾系統。它容易直接地確定macrocytic hypochromic RBCs 的百分比從RBC 容量和血紅蛋白集中直方圖和百分比可得到從儀器。我相信macrocytic hypochromic RBCs 的數字比reticulocyte 數字更好說明骨髓的再生作用特別是在最新階段(10.15 天) 對貧血症的反應在狗和早期(4.7 天) 在貓。似犬reticulocyte 數字減少在峰頂以後看4.7 天在貧血症的起始以後。因而, reticulocytes 的數量在10.15 天也許不足地似乎敏感為貧血症的嚴肅。在這個狀況下, macrocytic hypochromic 細胞的數量保留高更好反射活躍骨髓。聚集reticulocytes 在貓是型及早看(4.7 天) 在一個再生反應但可能是(5%) 與一個強烈的似犬reticulocyte 反應(25.33%) 相對地低比較。因而, 有經常很少聚集reticulocytes 影響MCV 和MCHC, 導致引入歧途的結論(normocytic normochromic 或macrocytic hypochromic) 貧血症。貝爾RBC cytogram 清楚地顯示macrocytic hypochromic RBCs 出現在這些貓雖然MCV 和MCHC 經常不顯露過程。
小片CYTOGRAM 和直方圖
貝爾小片cytogram 是獨特的在顯示小片由大小和光學密度。能力計數小片由60 fl 決定是系統的清楚的好處但增加風險, 大微粒不同於小片可能進入計數的區域。小片cytogram 可能顯露其它微粒譬如紅血球鬼魂細胞。鬼魂細胞可能是一個樣品問題在小片計數在被存放的馬血液或lipemic 似犬血液。我們發現是一到二天年紀的馬血樣能有的鬼魂細胞的重大數字能是miscounted 作為小片。審查小片cytogram 容易地展示了鬼魂細胞的分明人口。貝爾有軟體調整為這個鬼魂細胞問題在馬血液。油脂小滴也許算作是小片在有非常低大小門限為計數小片的系統。這些小顆粒由貝爾H-1 系統的小片容量直方圖並且展示了。圖表的一項主要公共事業將視覺上顯示什麼計數並且展示是未被發現由更加早期的系統的實驗室錯誤。
白血球CYTOGRAMS 和直方圖
白血球圖表通常顯露是否自動化的有差別的白血球計數可能是準確的。血液學系統不提供一致地準確白血球有差別的計數, 或是足夠敏感的查出多數左移或含毒物改變在嗜中性。系統不查出似犬或似貓的basophils 很好或根本。Monocyte 計數通常是與手工monocyte 計數不同。一些獸醫系統做執行有差別的白血球計數一個充分工作在正常馬、狗和甚而貓但經常有增長的錯誤在有差別的白血球計數在不適的動物。因而你應該至少掃描血液汙跡為左移、毒性變動、異常的細胞類型、RBC 形態學和小片叢在動物血液, 特別是不適的動物。
在之前的例外是毒性左移在馬依照由貝爾白血球cytograms 查出。我相信, 貝爾系統的basophil cytogram 說明毒性左移在馬更好比看馬血液汙跡的多數人民。一部分的這歸結於馬嗜中性非常通常看上去成熟比嗜中性在其它種類。因而, 溫和的變化在中堅力量上依照由laser 系統看見經常是未被發現的由肉眼但由中堅力量的被減少的光學密度查出。肉眼是好, 然而, 在查出左移和毒性變化在似犬和似貓的嗜中性上比自動化的系統。
自動化的有差別的白血球計數對那些是有用的做手工有差別的白血球計數但手工有差別的計數是敏感的在診斷。這特別真實系統那授予只二個或三個細胞有差別的計數。
白血病診斷由圖表援助。疾風細胞很好被展示在貝爾basophil 和peroxidase cytogram 。有許多易反應的淋巴細胞和lymphoblasts 偶爾的病人把一些細胞被展示在圖形顯示。類型具體診斷白血病要求血液汙跡評估。
總結
血液學分析儀圖形顯示形象化變化在血細胞上很好。這些圖片比數字或更舊的圖表顯露變動由於疾病和實驗室錯誤更好。圖表應該供給遞交血液或臨床病理學家在實驗室裡需要讀圖表和解釋診斷特點為遞交的獸醫的獸醫。實驗室人員需要查出實驗室錯誤由這些圖形顯示顯露。


picture is worth a thousand words.?All too often, veterinarians do not receive the graphic displays of cells generated by the newer generation of hematology instruments. This decision, made by directors of referral laboratories, is because they do not believe veterinarians can interpret the cytograms and histograms. This unfortunate, yet common, decision reduces greatly the diagnostic utility of the report given to the submitting veterinarian.
INSTRUMENTS
Most of the comments and examples used in this presentation refer to the Bayer H-1 and Advia 120 systems because the author has worked most with these systems. Other examples are more universal in type and refer to impedance systems that produce very similar types of graphics that most veterinarians will see in practice. The Bayer systems use laser technology to measure the number, size, and internal complexity of erythrocytes and platelets. Impedance based systems use the most common counting method of most hematology analyzers. Impedance technology is also called the Coulter principle. Coulter hematology instruments used it for years so that the name 鏠oulter counters?was synonymous with 蘔ematology analyzers.?Impedance measures the size and number of cells. The Abbott Cell Dyne uses impedance technology to measure size and number of platelets and erythrocytes and uses impedance and laser technology to count the number of leukocytes. Many smaller hematology analyzers use impedance technology to count all three cell types.
ERYTHROCYTE-PLATELET VOLUME HISTOGRAM
The erythrocyte-platelet volume histogram is the most common graphic seen by veterinarians. It is from impedance type cell counters. It should display two distinct peaks based on number of cells of a certain volume (y-axis) and cell volume (x-axis). The small peak to the left represents the platelets (smaller size and smaller number of cells) and a larger peak to the right represents erythrocytes. There should be distinct valley between the peaks to show that the instrument was capable of differentiating the two cell types. A common reason for the two peaks to merge is iron deficiency anemia. In iron deficiency anemia, the erythrocytes are smaller (microcytic) and there is often thrombocytosis with large platelets so the two cell types merge in size and may overlap. This results in small erythrocytes being counted as platelets and large platelets being counted as erythrocytes. Because platelets are fewer in number than erythrocytes, the platelet error is usually more noticeable. This change in the graphic (histogram) is both diagnostic and reveals a laboratory error. Notice that this graphic has two benefits (technical and diagnostic).
If an instrument does not display the erythrocytes and platelets graphically and if only numbers are reported, then erroneous results are not detected and the diagnosis may be missed or misinterpreted. Iron deficiency anemia is perhaps the best example of where instrument graphics improve diagnosis. Weiser revealed that 70% of five 馼eek-old kittens had iron deficiency anemia but needed improved instrumentation to show what percentage of erythrocytes were smaller than normal. Most veterinarians get in their hematology reports only mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC). These mean (average) values are too insensitive to reveal iron deficiency in kittens as well as the early stages of iron deficiency anemia in dogs. Often there are too few microcytic erythrocytes to pull the mean values (MCV and/or MCHC) below the reference values. The platelet-erythrocyte histogram may show the change earlier. Bayer RBC cytograms and histograms are very sensitive in detecting iron deficiency anemia.
BAYER SYSTEMS GRAPHICS
The Bayer system measures both the volume and internal complexity (optical density) of erythrocytes, reticulocytes and platelets, unlike impedance counters that only measure volume of these cells. Therefore, the Bayer cytograms and histograms are the best for visualizing disease changes in these cells. It also is the best system for counting platelets because it can differentiate platelets from erythrocytes even if platelets are larger than erythrocytes.
Iron deficiency anemia is detected earliest by the Bayer system because very few microcytic hypochromic RBCs are needed in the patient𠏋 blood to be seen on the RBC cytogram. The Bayer RBC cytogram displays every RBC in a sample, so it takes relatively few to be seen outside the normal area. It also is the only instrument to have a hemoglobin concentration histogram. Because the size and hemoglobin concentration of every RBC is measured, the percentage and absolute number of small subsets of atypical RBCs can be reported. Bayer Advia 120 can determine cell volume and cell hemoglobin of individual erythrocytes and reticulocytes which is helpful in the diagnosis of iron deficiency anemia in human blood and may be helpful with canine iron deficiency anemia evaluation.
Regenerative anemias are best diagnosed with Bayer systems. It is easy to determine the percentage of macrocytic hypochromic RBCs from the RBC volume and hemoglobin concentration histograms and the percentages directly available from the instrument. I believe the number of macrocytic hypochromic RBCs better illustrates the regenerative function of the bone marrow than reticulocyte numbers especially in later stages (10?5 days) of response to anemia in dogs and early stages (4? days) in cats. Canine reticulocyte numbers decrease after the peak seen 4? days after onset of an anemia. Thus, the number of reticulocytes at 10?5 days may seem insufficiently responsive for the severity of the anemia. At this stage, the number of macrocytic hypochromic cells remains high to better reflect an active bone marrow. Aggregate reticulocytes in the cat are the type seen early (4? days) in a regenerative response but can be relatively low (5%) compared to a strong canine reticulocyte response (25?3%). Thus, there are often too few aggregate reticulocytes to affect the MCV and MCHC, leading to misleading conclusions (normocytic normochromic or macrocytic hypochromic) anemias. The Bayer RBC cytogram clearly shows the presence of macrocytic hypochromic RBCs in these cats though the MCV and MCHC often do not reveal the process.
PLATELET CYTOGRAM AND HISTOGRAM
The Bayer platelet cytogram is unique in displaying platelets by both size and optical density. The ability to count platelets up to 60 fl is a clear advantage of the system but does increase the risk that large particles other than platelets can enter the counting area. The platelet cytogram can reveal other particles such as erythrocyte ghost cells. Ghost cells can be a sample problem in platelet counting in stored equine blood or lipemic canine blood. We found that equine blood samples that were one to two days old could have significant numbers of ghost cells that could be miscounted as platelets. Examining the platelet cytogram easily demonstrated the distinct population of ghost cells. Bayer has a software adjustment for this ghost cell problem in equine blood. Lipid droplets may be counted as platelets in systems that have a very low size threshold for counting platelets. These small particles were also demonstrated by the platelet volume histogram of the Bayer H-1 system. A major utility of graphics is to display visually what is being counted and to demonstrate laboratory errors that went undetected by earlier systems.
LEUKOCYTE CYTOGRAMS AND HISTOGRAMS
Leukocyte graphics usually reveal whether the automated differential leukocyte count was likely accurate. No hematology system provides a consistently accurate leukocyte differential count, or is sensitive enough to detect most left shifts or toxic changes in neutrophils. No system detects canine or feline basophils well or at all. Monocyte counts are usually different from manual monocyte counts. Some veterinary systems do an adequate job of performing a differential leukocyte count on normal horses, dogs and even cats but often have increasing error in differential leukocyte counts in ill animals. Thus one should at least scan blood smears for left shifts, toxic change, unusual cell types, RBC morphology and platelet clumps on animal blood, especially ill animals.
An exception to the preceding is toxic left shifts in horses as detected by the Bayer leukocyte cytograms. I believe that the basophil cytogram of the Bayer system illustrates toxic left shifts in horses better than most people that look at equine blood smears. Part of this is due to the equine neutrophil normally appearing so much more mature than neutrophils in other species. Thus, mild changes in the nucleus is often undetected by the human eye but detected by decreased optical density of the nucleus as seen by the laser system. The human eye is better, however, in detecting left shifts and toxic change in canine and feline neutrophils than the automated systems.
The automated differential leukocyte counts are helpful to those doing a manual differential leukocyte count but the manual differential count is more sensitive in diagnosis. This especially true of systems that give only a two or three cell differential count.
The diagnosis of leukemia is aided by graphics. Blast cells are well demonstrated on the Bayer basophil and peroxidase cytogram. Even occasional patients with many reactive lymphocytes and lymphoblasts will have some cells demonstrated on graphic displays. Specific diagnosis of types of leukemia requires blood smear evaluation.
SUMMARY
Graphic displays of hematology analyzers visualize changes in blood cells well. These pictures reveal changes due to disease and laboratory error better than numbers or older graphics do. The graphics should be available to veterinarians who submit the blood or clinical pathologists in the laboratories need to read the graphics and interpret the diagnostic features for the submitting veterinarian. Laboratory personnel need to detect laboratory errors revealed by these graphic displays.

minibabyqq 2007-1-26 01:56

[color=Magenta][size=5][b]緊急呼吸評估 Emergency Respiratory Assessment  [/b][/size][/color]


動物的成功的緊急管理以困難呼吸的要求, 臨床工作者保留深刻地明白dyspneic 患者的脆弱。在一個重要地dyspneic 動物, 甚而一個簡要的主要身體系統評估可能證明致命, 特別是在貓。結果, 任一操作風險必須仔細地斟酌反對潛在的好處。威脅生命的疾病重音被結合與運輸和一個喧鬧的緊急診所的不熟悉的周圍應該從未被低估。Dyspneic 動物經常是當他們最易碎在介紹和柔和的克制後可能證明生活威脅。除最嚴厲的上部航線堵塞之外, 多數動物將受益於一個期間100% 氧氣在氧氣籠子在一個完全主要身體系統評估之前。一旦動物遭受了呼吸拘捕, 可能性巨大地被堆積反對you.prevention 比治療無節制地好!
呼吸評估
呼吸系統的最初的評估包括呼吸率、努力和呼吸聽診。一個正常動物應該有15.30 呼吸的呼吸率每分鐘並且, 因為休息的_發的多數歸結於diaphragmatic 收縮, 那裡應該是很少明顯的胸口運動。在正常_發期間, diaphragmatic 收縮尾部偏移胃腸內臟並且胃腸牆壁行動在被動地之外(即, 胸口和腹部一起行動) 。它應該因此是直覺的, 腹肌(胃腸努力的) 收縮可能只協助失效。這不應該與似是而非的胃腸運動被混淆, 是嚴厲呼吸困難的顯示。資訊可能被搜集從簡單地觀察患者的呼吸的樣式當100% 氧氣。你應該尋找呼吸困難的姿勢顯示譬如一張延長的脖子、被拐騙的手肘、開放嘴呼吸, 一個急切面部表示、增加的胃腸運動, 和似是而非的胃腸運動。調直脖子和開放嘴呼吸發生在狗並且貓, 然而, 更加嚴厲的呼吸困難的其它姿勢顯示變化在種類之間。狗喜歡站立與被拐騙的手肘, 當貓傾向於坐在sternal recumbency 。經常改變的身體位置在貓比它做在狗暗示更壞的程度呼吸困難。側向recumbency 由於呼吸困難是嚴肅的簽到狗; 但是, 它經常意味緊急呼吸拘捕在貓。其它旗子拔出氣管內管是貓將開發立刻在呼吸拘捕之前的明顯的mydriasis 。記得, 決定活躍地接管經常只要求非常鎮靜劑小藥量在嚴厲地dyspneic 貓) 的導氣管(在管材是浩大地優越他們跟隨呼吸拘捕。
似是而非的胃腸運動發生當增加的肋間的收縮畫膜片並且胃腸內臟cranially 在_發和胃腸牆壁行動(即, 胸口和腹部行動相反方向) 。這可能發生由於被減少的肺服從、上部航線堵塞、diaphragmatic 破裂或痲痺, 和偶爾地, 在貓以嚴厲胸膜流出。射線照相到左邊是從一隻貓與散開細胞間的轉移和極端non-compliant 肺。除似是而非的胃腸運動之外, 肋間的肌肉實際上被吮在_發。
呼吸系統可能被劃分成五分裂: 上部導氣管、小導氣管、肺柔膜組織、胸膜空間和胸口牆壁, 和膜片。在一個dyspneic 動物, 呼吸樣式可能有時幫助地方化呼吸道的水平影響。動態上部航線堵塞通常同長時期的_發聯繫在一起與吸入的stridor 或stertor, 被短的失效跟隨。吸入的呼吸困難沒有stridor 在貓可能偶爾地發生以嚴厲, 慢性胸膜流出。小導氣管疾病, 譬如似貓的哮喘, 古典地提出以混雜的吸入和呼氣呼吸困難但以更長的呼氣階段和增加的胃腸努力。多數呼吸困難的其它起因同混雜的呼吸樣式聯繫在一起。雖然它被建議胸膜空間疾病同短的淺呼吸作用聯繫在一起, 這個樣式在不具體為胸膜空間疾病, 亦不所有動物以胸膜空間疾病當前以短的淺呼吸作用。經常同這個呼吸樣式聯繫在一起的一個臨床情節是pneumothorax, 和在狗與自發, 而不是traumatically 導致pneumothorax, 程度胸口運動可能是驚奇溫和的為pneumothorax 的容量。
肺聽診
肺聽診在dyspneic 患者是獸醫的當中一個真實的藝術。它要求好聽診器和努力實踐。基本上, 您必須做嚴肅的努力; 無精打采的聽診是同等對無用。以致力, 許多呼吸反常性可能被區分在體格檢查中單獨, 特別是在貓。最容易的方式保證完全聽診將劃分胸口成tic TAC 腳趾板, 然後auscult 各個正方形。這使能頭蓋骨, 中間, 和尾部肺領域的背部, 中間, 和腹方面比較。在一名更加穩定的患者, 各個單獨聽診器領域可能是ausculted 。肺聲音應該被比較用不同的區域在胸口的一邊和在同樣區域在反面。肺聲音通常是輕微地大聲和粗糙的在cranioventral 肺領域與dorsocaudal 領域比較。的確, 在一些大養殖狗和在動物中採取非常淺呼吸, 它可能難聽見肺聲音在caudodorsal 胸口。肺聲音是對稱的當同樣區域被比較在胸口的雙方除了心臟病鈍澀區域在左腹胸口的頭蓋骨部份。這意味著, 不管是否你可能確定哪些是更加大聲或更加安靜的邊, 任一非對稱是反常的。
反常肺聲音作為爆裂聲或苛刻的肺聲音可能被分類(即, 大聲和粗糙比法線) 。期限wheeze 。是相當隱晦的和經常用於混淆而不是澄清。在人的醫學, 細分類喘息(鼾音) 有診斷相關性但在獸醫患者, 鼾音的subclassification 有用可疑的。偶爾地, 氣喘貓和動物以使舉辦的導氣管狹窄引起真實喘息的其它過程, 僅許多陳列唯一苛刻的肺聲音。在決定是否肺聲音比法線苛刻的, 你必須考慮到呼吸率和努力和所有被提到的上部導氣管聲音。是tachypneic 隨後而來的鍛煉的一條正常狗將有苛刻的肺聲音。所以, 你必須確定是否肺聲音比被期望苛刻的為程度呼吸迫促。這是特別重要在狗跟隨機動車精神創傷。許多是tachypneic 從恐懼或痛苦和在肺聲音的增量從呼吸迫促 必須 就其本身而言被區分從那肺挫傷。苛刻的肺聲音可能歸結於parenchymal 或導氣管疾病。有些驚奇, 許多狗以肺炎或肺挫傷展覽苛刻的肺聲音但不是爆裂聲。肺爆裂聲可能是或美好或粗糙的。罰款爆裂聲通常聽見在_發最後和由倒塌的小導氣管開頭大概引起。這些是那□您聽見在十六年的長捲毛狗沒有parenchymal 疾病! 粗糙的爆裂聲同parenchymal 疾病聯繫在一起但通常可能偶爾地歸結於導氣管疾病。在author.s 經驗, 最嚴厲的導氣管爆裂聲發生以嗜伊紅的支氣管炎在狗。
反常肺聲音的發行是非常有用的在區分呼吸疾病。例如, 多數狗以志向肺炎經常有苛刻的肺聲音或爆裂聲在cranioventral 肺領域。苛刻的肺的dorsocaudal 發行聽起來或爆裂聲可能有時被讚賞在小狗與神經原的腫鼓。溫和減輕心臟性的腫鼓大聲經常同苛刻的肺聲音或爆裂聲聯繫在一起在心臟基地。
胸膜流出允許肺漂浮在胸口洞的背部方面那麼那裡是缺乏腹肺聲音並且背部聲音經常是苛刻的。Don.t 由心音唬弄在貓以胸膜流出: 他們比法線不被裹住和通常無法偶爾地放熱在胸口的一個更大的區域。與胸膜流出對比, pneumothorax 導致裹住肺聲音在背部胸膜空間當空氣積累在這個區域。多數人民比pneumothorax 發現胸膜流出容易查出由聽診因為肺聲音的發行是法線對面(安靜腹上和苛刻背部地) 。許多狗以pneumothorax 在乘汽車以後被擊中並且有可能使聽診複雜化的肺挫傷。pneumothorax 挫傷肺聲音但是肺挫傷使他們更加大聲和更加粗糙。這可能有時導致absolute 容量緊挨法線。以實踐, 你可能讚賞, 肺聲音是苛刻的並且裹住, 然而, 嚴厲呼吸困難在有正常容量肺聲音這樣一名病人應該指嚮往一致肺挫傷和pneumothorax 。
彙集它全部
能力建立一個運作的診斷根據歷史和體格檢查沒有另外的診斷, 譬如胸口射線照相, 可能意味區別在生與死之間在一些dyspneic 動物。巨大資訊量可能由簡單地觀看獲得動物呼吸在氧氣籠子並且由估計動物身體條件, 與歷史和程度困厄一道動物體驗相對程度胸口運動。例如, 一隻幼小貓在好身體情況以咳嗽的歷史和混雜的呼吸困難以增加的胃腸努力在失效是可能有似貓的哮喘。雖然胸口射線照相會是必要的當然, 苛刻的肺聽起來在所有領域並且缺乏心臟私語或疾馳, 會關於緊抱診斷在多數情況。
當經驗主義的治療必須被設立在一個明確的診斷之前, 好臨床推理和維護的透視至於可能的差別同等。提出為呼吸困難的大多數貓有胸膜流出、心臟病, 或哮喘。臨床研究結果在每個這些情況經常分明。一隻嚴厲地dyspneic 貓以心臟私語或疾馳節奏和散開雙邊爆裂聲幾乎總通常將安排心肌病或endomyocarditis 和靜脈內或肌肉內furosemide 的好處勝過潛力風險。作為早先被提及的, 胸膜流出導致安靜的腹肺聲音和苛刻的背部聲音, 但是多數氣喘貓有是苛刻的在所有領域的肺聲音(和有希望地不是一句偶然發生的心臟私語!) 並且咳嗽的一致歷史。維護透視其它例子是在小狗以呼吸困難。多數二對提出對我們的緊急情況服務的六月的小狗有神經原的腫鼓、殺鼠劑醉、或偶爾地, 肺炎隨後而來的狗窩咳嗽或慍怒病毒傳染。
雖然沒有替換為從事problem-oriented 方法以一張完全問題名單和所有診斷差別, 緊急臨床必需總維護透視至於什麼是很可能可能的診斷。呼吸困厄是最富挑戰性的情況的當中一個面對緊急臨床工作者。成功地處理這些箱子要求優秀體格檢查技能、聲音臨床推理和能力平衡dyspneic 病人的脆弱有慎密地獲得診斷資訊。

Successful emergency management of the animal with difficulty breathing demands that the clinician remain acutely aware of the fragility of the dyspneic patient. In a critically dyspneic animal, even a brief major body system evaluation can prove fatal, especially in cats. Consequently, the risks of any manipulation must be carefully weighed against the potential benefits. The stress of life-threatening disease coupled with transport and the unfamiliar surroundings of a noisy emergency clinic should never be underestimated. Dyspneic animals are often as their most fragile immediately following presentation and gentle restraint can prove life threatening. Apart from the most severe upper airway obstructions, most animals will benefit from a period in 100% oxygen in an oxygen cage prior to a complete major body system evaluation. Once an animal has suffered a respiratory arrest, the odds are hugely stacked against you炥revention is inordinately better than cure!
Respiratory assessment
Initial evaluation of the respiratory system comprises respiratory rate, effort and respiratory auscultation. A normal animal should have a respiratory rate of 15?0 breaths per minute and, because the majority of a resting inspiration is due to diaphragmatic contraction, there should be very little apparent chest movement. During normal inspiration, diaphragmatic contraction displaces abdominal viscera caudally and the abdominal wall moves out passively (i.e., the chest and abdomen move out together). It should therefore be intuitive that contraction of the abdominal muscles (abdominal effort) can only assist with expiration. This should not be confused with paradoxical abdominal movement, which is a manifestation of severe dyspnea. Much information can be gleaned from simply observing the breathing pattern of the patient while in 100% oxygen. One should look for the postural manifestations of dyspnea such as an extended neck, abducted elbows, open mouth breathing, an anxious facial expression, increased abdominal movement, and paradoxical abdominal movement. Straightening of the neck and open mouth breathing occur in both dogs and cats, however, some other postural manifestations of more severe dyspnea vary between species. Dogs prefer to stand with abducted elbows, while cats tend to sit in sternal recumbency. Constantly changing body position in cats implies a much worse degree of dyspnea than it does in dogs. Lateral recumbency due to dyspnea is a serious sign in a dog; however, it often means impending respiratory arrest in a cat. Another flag to pull out the endotracheal tubes is the marked mydriasis that cats will develop immediately prior to respiratory arrest. Remember that deciding to actively take control of the airway (which often only requires very small doses of sedative in severely dyspneic cats) is vastly superior to tubing them following a respiratory arrest.
Paradoxical abdominal movement occurs when increased intercostal contraction draws the diaphragm and abdominal viscera cranially on inspiration and the abdominal wall moves in (i.e., the chest and abdomen move in opposite directions). This can occur due to decreased lung compliance, upper airway obstruction, diaphragmatic rupture or paralysis, and occasionally, in cats with severe pleural effusion. The radiograph to the left is from a cat with diffuse interstitial metastasis and extremely non-compliant lungs. In addition to paradoxical abdominal movement, the intercostal muscles were actually being sucked in on inspiration.
The respiratory system can be divided into five divisions: the upper airway, small airways, pulmonary parenchyma, pleural space and the chest wall, and diaphragm. In a dyspneic animal, the respiratory pattern can sometimes help localize the level of the respiratory tract affected. Dynamic upper airway obstruction is usually associated with prolonged inspiration with inspiratory stridor or stertor, followed by a short expiration. An inspiratory dyspnea without stridor in a cat can occasionally occur with severe, chronic pleural effusion. Small airway disease, such as feline asthma, classically presents with a mixed inspiratory and expiratory dyspnea but with a longer expiratory phase and increased abdominal effort. Most other causes of dyspnea are associated with mixed respiratory patterns. Although it has been suggested that pleural space disease is associated with short shallow respirations, this pattern in not specific for pleural space disease, nor do all animals with pleural space disease present with short shallow respirations. One clinical scenario that is often associated with this respiratory pattern is pneumothorax, and in dogs with spontaneous, rather than traumatically induced pneumothorax, the degree of chest movement can be surprisingly mild for the volume of pneumothorax.
Pulmonary Auscultation
Pulmonary auscultation in the dyspneic patient is one of the true arts of veterinary medicine. It requires a good stethoscope and diligent practice. Basically, you have to make a serious effort; lackadaisical auscultations are tantamount to useless. With dedication, many respiratory abnormalities can be differentiated on physical examination alone, especially in cats. The easiest way to ensure a complete auscultation is to divide the chest into a tic-tac-toe board, then auscult each square. This enables comparison of dorsal, middle, and ventral aspects of the cranial, middle, and caudal lung fields. In a more stable patient, each individual stethoscope field can be ausculted. Lung sounds should be compared in different areas on one side of the chest and in the same area on opposite sides. Lung sounds are normally slightly louder and coarser in the cranioventral lung fields compared to the dorsocaudal fields. Indeed, in some large breed dogs and in animals taking very shallow breaths, it can be difficult to hear lung sounds in the caudodorsal chest. Lung sounds are symmetrical when the same area is compared on both sides of the chest except for the area of cardiac dullness in the cranial portion of the left ventral chest. This means that, regardless of whether one can determine which is the louder or quieter side, any asymmetry is abnormal.
Abnormal lung sounds can be classified as crackles or harsh lung sounds (i.e., louder and coarser than normal). The term 𢘛heeze?is rather vague and often serves to confuse rather than clarify. In human medicine, subclassifying wheezes (rhonchi) has diagnostic relevance but in veterinary patients, subclassification of rhonchi is of questionable use. Occasionally, asthmatic cats and animals with other processes that narrow the conducting airways generate true wheezes, but many exhibit only harsh lung sounds. In deciding whether lung sounds are harsher than normal, one has to take into account the respiratory rate and effort and any referred upper airway sounds. A normal dog that is tachypneic following exercise will have harsh lung sounds. Therefore, one must determine whether the lung sounds are harsher than expected for the degree of tachypnea. This is especially important in dogs following motor vehicle trauma. Many are tachypneic from fear or pain and the increase in lung sounds from the tachypnea per se must be differentiated from that of pulmonary contusions. Harsh lung sounds can be due to parenchymal or airway disease. Somewhat surprisingly, many dogs with pneumonia or pulmonary contusions exhibit harsh lung sounds but not crackles. Pulmonary crackles can be either fine or coarse. Fine crackles are usually heard at the very end of inspiration and are probably generated by the opening of collapsed small airways. These are the ones you hear in sixteen-year-old Poodles with no parenchymal disease! Coarse crackles are usually associated with parenchymal disease but occasionally can be due to airway disease. In the author𠏋 experience, the most severe airway crackles occur with eosinophilic bronchitis in dogs.
The distribution of abnormal lung sounds is very useful in differentiating respiratory disease. For example, most dogs with aspiration pneumonia often have harsh lung sounds or crackles in the cranioventral lung fields. The dorsocaudal distribution of harsh lung sounds or crackles can sometimes be appreciated in puppies with neurogenic edema. Mild to moderate cardiogenic edema is often associated with harsh lung sounds or crackles loudest over the heart base.
Pleural effusion allows the lungs to float in the dorsal aspect of the chest cavity so there is an absence of ventral lung sounds and the dorsal sounds are often harsh. Don㦙 be fooled by the heart sounds in cats with pleural effusion: they are not usually muffled and occasionally can radiate over a larger area of the chest than normal. In contrast to pleural effusion, pneumothorax results in muffling of the lung sounds in the dorsal pleural space as air accumulates in this area. Most people find pleural effusion easier to detect by auscultation than pneumothorax because the distribution of lung sounds is the opposite of normal (quiet ventrally and harsh dorsally). Many dogs with pneumothorax after being hit by a car also have pulmonary contusions that can complicate auscultation. The pneumothorax dampens lung sounds whereas the pulmonary contusion makes them louder and coarser. This can sometimes result in an absolute volume close to normal. With practice, one can appreciate that the lung sounds are both harsh and muffled, however, the severe dyspnea in such a patient with normal volume lung sounds should point towards concurrent pulmonary contusions and pneumothorax.
Putting it all together
The ability to establish a working diagnosis based on history and physical examination without additional diagnostics, such as chest radiographs, can mean the difference between life and death in some dyspneic animals. An immense amount of information can be obtained by simply watching the animal breathe in the oxygen cage and by assessing the animals body condition, in conjunction with the history and the degree of distress the animal is experiencing relative to the degree of chest movement. For example, a young cat in good body condition with a history of coughing and a mixed dyspnea with increased abdominal effort on expiration is more likely to have feline asthma. Although chest radiographs would be necessary to be sure, harsh lung sounds in all fields and the absence of a heart murmur or gallop, would just about clinch the diagnosis in most situations.
When empirical treatment must be instituted prior to a definitive diagnosis, good clinical reasoning and maintaining perspective as to the likely differentials is tantamount. The vast majority of cats that present for dyspnea have pleural effusion, heart disease, or asthma. The clinical findings in each of these conditions are often distinct. A severely dyspneic cat with a heart murmur or gallop rhythm and diffuse bilateral crackles will usually have cardiomyopathy or endomyocarditis and the benefits of intravenous or intramuscular furosemide almost always outweigh the potential risks. As previously mentioned, pleural effusion results in quiet ventral lung sounds and harsh dorsal sounds, whereas most asthmatic cats have lung sounds that are harsh in all fields (and hopefully not an incidental heart murmur!) and a concurrent history of coughing. Another example of maintaining perspective is in the puppy with dyspnea. The majority of two- to six-month-old puppies that present to our emergency service have neurogenic edema, rodenticide intoxication, or occasionally, pneumonia following kennel cough or distemper virus infection.
Although there is no replacement for following the problem-oriented approach with a complete problem list and all diagnostic differentials, the emergency clinical must always maintain perspective as to what are the most likely probable diagnoses. Respiratory distress is one of the most challenging situations facing the emergency clinician. Successfully managing these cases requires excellent physical examination skills, sound clinical reasoning and the ability to balance the fragility of the dyspneic patient with prudently obtaining diagnostic information.

minibabyqq 2007-1-26 01:58

[color=Magenta][b][size=5]通風筒導致的傷害IPPV: Minimizing Ventilator Induced Injury  [/size][/b][/color]


正面壓力透氣(PPV) 規程也許同一定數量的問題聯繫在一起。不適當的通風筒設置和通風筒故障; 呼吸的電路和氣管管問題; 患者通風筒asynchrony; 導氣管、嘴、眼睛、bladder/urine, 和colon/fecal 問題; 並且麻醉的與代理相關的複雜化被認可了。
胸部血流損傷
正面壓力透氣削弱intrathoracic 血流由增加胸膜壓力, 妨礙多血脈性的回歸到心臟的正確和左邊。在某種程度上多血脈性的回歸被減少, 舒張心室裝填、行程排量、心輸出量, 和動脈血壓並且被減少。程度intrathoracic 血流的損傷與增量的巨大直接地是比例在胸膜壓力的, 壓力是應用的每呼吸的時間(吸入的時間) 並且每分鐘(週期率), 並且間接地比例與基礎線中央多血脈性的壓力(血液容量) 。循環損傷的巨大可能由觀察估計各_發的作用在脈衝質量或動脈血壓。如果它被確定過份循環損傷是存在, 吸入的壓力和吸入的時間或呼吸的率能被減少, 或血液容量能被增加。害病的肺惡劣服從, 並且當它也許要求更高的導氣管壓力通風這些肺, 無足輕重壓力被傳達給胸膜空間並且有較少傾向削弱循環。
齒齦音氏族的破裂
對高的導氣管的用途pressures/volumes 在正常和反常肺裡也許同齒齦音氏族的破裂、pneumomediastinum 、pneumothorax 、肺出血, 和空氣栓塞聯繫在一起。齒齦音氏族的破裂被報告發生以率的在3 和40% (Streiter 之間; Amato; Weg; Stewart; 國王) 。有在感受性上被標記的單獨變化對這個問題。Weg, 等, 報告了: there 是之上患者總沒有發展齒齦音氏族的破裂和導氣管壓力在之下它從未發生的沒有導氣管壓力在。已存在parenchymal bullae 或最近parenchymal 破裂, 降低門限對通風筒導致的齒齦音氏族的破裂。導氣管壓力和潮汐容量設置像最小地必要達到可接受的透氣和oxygenation 應該只是一樣高的。在散開肺parenchymal 疾病, 功能肺單位的總數被減少。正常潮汐容量的介紹導致殘餘的功能肺單位的在膨脹。肺防護戰略運用更小比正常潮汐容量幫助防止這volutrauma 。
監視為一pneumothorax 的發展在正面壓力透氣期間必須是持續的努力。它應該是第一規則出口的當中一個為患者通風筒asynchrony 。如果pneumothorax 顯現出, 胸口流失必須被插入並且連續的胸口排水設備被提供。
自動窺視
當吸入是當前進展由通風筒譜寫音樂, 發散作用是一個被動過程取決於肺和胸口牆壁倒電容。如果發散作用不是完全的在下呼吸的_蒙之前, 下潮汐容量將被相當數量空氣增加餘留在肺從在先的呼吸。這air 誘捕。或breath 堆積。或auto 窺視可能導致肺單位(volutrauma) 在擴展。空氣誘捕是可能發生如果發散作用被延遲由變窄的更低的導氣管(慢性導氣管疾病, bronchospasm) 並且以更高的通風筒週期率。如果被測量的結束呼氣壓力超出那個集合在通風筒, 自動窺視發生□。
自動窺視不一定是壞除非它過份。窺視(是否它故意地來自自通風筒或有意無意地患者通風筒互作用) 改進肺氧化的效率。它重要知道自動窺視是存在並且決定可能然後被做出是否保留它或做它走開。
血絲內皮細胞的損傷
導氣管和小窩由膠原和有彈性纖維子線一起束縛。當導氣管被擴展, 正切和縱向牽引被安置在毗鄰內皮細胞層數。這加寬細胞間的連接點和增加血絲滲透性和流體漲潮入肺interstitium 。
導氣管和齒齦音上皮損傷
在肺病, 增量在導氣管流體裡增加表面張力和增加傾向為小導氣管並且小窩崩潰(當transpulmonary 壓力和功能殘餘的容量是在重要關閉的點之下) 。這些單位Re-opening 在下呼吸期間要求打破表面張力封印在二個毗鄰上皮細胞之間。這些正切力量最終損壞細胞膜。
毗鄰肺單位, 為各種各樣的原因, 有不同的時間常數, 同時不擴展或率。這造成剪傷害對齒齦音皮膜在形成共同的牆壁在二毗鄰小窩之間的各稀薄的氏族的膜的邊。
激動斡旋人發行
肺單位的正面壓力透氣和, 特殊, 在膨脹, 被認為導致leuco 活化作用造成激動斡旋人(Ranieri) 發行。這些至少提高血絲滲透性和至多, 起因內皮細胞和上皮細胞損傷和死亡。
這些內皮細胞和上皮損傷的過程惡化是難區分的從部下的散開infiltrative 疾病動物接受通風筒療法散開parenchymal 疾病的巨大有些。窺視, 充足防止airway/alveolar 關閉使表面緊張導致的和異步肺單位減到最小擴展導致的上皮損傷。窺視應該被設置在關閉的壓力之上。
肺炎
肺炎是長期正面壓力透氣規程的共同的後果: 1) 位置stasis 預先處理對atelectasis 和被減少的分泌物清除從更低的肺地區; 2) 嘴和咽的細菌人口激增和成為由gram-negative 有機體拓殖; 3) 這些微生物不變地移居在氣管下(通過膨脹的袖口) 並且入更低的導氣管; 4) 蔓延性規程譬如氣管插管法和氣管suctioning 預先處理對細菌的介紹入更低的導氣管; 5) 如果抗生素被運用, 患者是事先安排好的對殖民化由抵抗微生物; 並且6) 如果氨基酸2 預鍛模被運用, 患者是事先安排好的對細菌殖民化在胃(這樣流體不變地發現那裡方式食道和入導氣管) 。正面壓力透氣做法, 就其本身而言, 不被認為一個徵兆為預防疾病的抗藥性療法。在一個未出版的實驗性系列(Haskins), 所有狗被安置了在抗生素在一個星期底之前。規則改變位置, 無菌導氣管規程, 和規則嘴和咽關心幫助使肺炎的發展減到最小。被通風的患者應該被監測為傳染的徵兆並且安置在適當的抗生素if/when 需要出現。
打開肺techniques/lung 防護通風筒戰略
一個 開放肺技術 是概念而不是一個具體技術。想法是吸收許多個齒齦音單位因為可能(打開他們) 並且然後防止他們再崩潰(保持他們開放) 。這將優選血液oxygenation 和使通風筒導致的傷害減到最小。正面壓力透氣可能導致肺傷範圍從齒齦音氏族的破裂和pneumothorax 對是難區分的從疾病PPV 被實施的散開infiltrative 呼吸困厄綜合症狀。這傷害從各自的肺單位(volutrauma 的) over-inflation 的各種各樣的有害方面獲得。 肺防護透氣戰略 尋找宗旨和開放肺透氣技術一樣: 1) 吸收許多個齒齦音單位儘可能; 2) 防止他們re 倒塌; 並且3) 使齒齦音在膨脹減到最小。這些戰略介入高最初的高峰壓力(40 到60 cm H2O) 為齒齦音補充, 易變的時期(一呼吸的期間, 由一分鐘決定) 並且演變成激烈的窺視(10.20 cm H2O) 保留小窩打開, 和然後減輕(通常少於40 cm H2O) 高峰壓力(Amato; Stewart; Brochard; Brower; ARDS 網路; Kloot; Medoff) 。高窺視壓力和適度高峰壓力的不可避免的後果是小(與法線比較) 潮汐容量。一個正常肺可能容易地處理正常潮汐容量, 然而, 一個肺以被減少的重要容量不能(沒有volutrauma); 潮汐容量需要是適當的為患者。不幸地, 疾病導致的減少的巨大對重要容量的無法事先被預言。它需要被估計在各名患者和必須頻繁地然後被再評價因為服從和重要容量可能改變在幾個小時中。潮汐容量是由導氣管壓力和胸部服從確定的一個因變量。防護肺戰略也許並且減少促進血絲內皮細胞和導氣管上皮損傷激動斡旋人的發行(Ranieri) 。
我們提出在這兒我們認為會是可適用的對獸醫患者的方法。這個做法應該嚮動物只被運用以散開肺parenchymal 疾病; 它沒有目的在動物中與相對地正常肺被通風為神經學原因。您將需要能測量導氣管壓力和潮汐容量, 和有能力設置窺視。開始與大約+5 cm H2O 窺視, 設置高峰壓力到10 cm H2O 以久吸入的時光的大約一秒, 和記錄潮汐容量。增加高峰壓力到15 cm H2O 和記錄新潮汐容量。計算變化在潮汐容量上由變化引起在高峰壓力(即, 新早先潮汐容量上) 。重覆過程, 增加高峰壓力5 cm H2O 每次或者直到在潮汐容量的增加增量開始減少, 或直到高峰壓力60 cm H2O 被獲得。無論如何, 總肺容量被認為被到達了。高峰壓力設置聯繫了在潮汐容量的最巨大的增加增量現在被選擇。高峰壓力與相關在潮汐容量的第一大增量現在被選擇作為窺視設置。供選擇地, 如果您的通風筒有能力顯示pressure-volume 曲線, 偷看被選擇以代表對高峰容量的50% 減少使用曲線的塌陷部份的導氣管壓力。如果這些通風筒設置導致潮汐容量超出10 ml/kg, 高峰壓力應該進一步被減少直到潮汐容量是10 ml/kg 。通風筒週期率應該然後被調整保留PaCO2 在60 毫米百克以下。通風筒週期率現在被選擇。當有必要開始於25 呼吸每分鐘和調整獲得可接受的PaCO2。

Positive pressure ventilation (PPV) procedures may be associated with a number of problems. Inappropriate ventilator settings and ventilator malfunction; breathing circuit and tracheal tube problems; patient-ventilator asynchrony; airway, mouth, eye, bladder/urine, and colon/fecal problems; and anesthetic agent-related complications have been recognized.
Thoracic blood flow impairment
Positive pressure ventilation impairs intrathoracic blood flow by increasing pleural pressure, which impedes venous return to both the right and the left side of the heart. To the extent that venous return is diminished, diastolic ventricular filling, stroke volume, cardiac output, and arterial blood pressure are also diminished. The degree of impairment of intrathoracic blood flow is directly proportional to the magnitude of the increase in pleural pressure, the length of time that the pressure is applied per breath (the inspiratory time) and per minute (the cycle rate), and indirectly proportional to the baseline central venous pressure (the blood volume). The magnitude of the circulatory impairment can be assessed by observing the effect of each inspiration on pulse quality or arterial blood pressure. If it is determined that excessive circulatory impairment is present, the inspiratory pressure and the inspiratory time or the breathing rate could be decreased, or the blood volume could be increased. Diseased lungs are poorly compliant, and while it may require higher airway pressures to ventilate these lungs, less of the pressure is transmitted to the pleural space and there is less tendency to impair circulation.
Alveolar septal rupture
The use of high airway pressures/volumes in normal and abnormal lungs may be associated with alveolar septal rupture, pneumomediastinum, pneumothorax, pulmonary hemorrhage, and air embolism. Alveolar septal rupture is reported to occur at a rate of between 3 and 40% (Streiter; Amato; Weg; Stewart; King). There is marked individual variation in susceptibility to this problem. Weg, et al., reported: 懀here was no airway pressure above which patients always developed alveolar septal rupture and no airway pressure below which it never occurred.?Pre-existing parenchymal bullae or recent parenchymal rupture, lower the threshold to ventilator-induced alveolar septal rupture. Airway pressure and tidal volume settings should only be as high as is minimally necessary to achieve acceptable ventilation and oxygenation. In diffuse pulmonary parenchymal disease, the total number of functional lung units is reduced. The introduction of normal tidal volumes causes over-distention of the remaining functional lung units. Lung protective strategies utilize smaller than normal tidal volumes to help prevent this volutrauma.
Monitoring for the development of a pneumothorax during positive pressure ventilation must be an ongoing endeavor. It should be one of the first rule-outs for patient-ventilator asynchrony. If a pneumothorax develops, a chest drain must be inserted and continuous chest drainage provided.
Auto-PEEP
While inhalation is an active process orchestrated by the ventilator, exhalation is a passive process depending upon lung and chest wall elastance. If exhalation is not complete prior to initiation of the next breath, the next tidal volume will be increased by the amount of air remaining in the lung from the preceding breath. This 弌ir trapping?or 弎reath stacking?or 弌uto-PEEP?can result in over-expansion of lung units (volutrauma). Air trapping is more likely to occur if exhalation is delayed by narrowed lower airways (chronic airway disease, bronchospasm) and with higher ventilator cycle rates. If the measured end-expiratory pressure exceeds that set on the ventilator, auto-PEEP is occurring.
Auto-PEEP is not necessarily bad unless it is excessive. PEEP (whether it comes intentionally from the ventilator or unintentionally from the patient-ventilator interaction) improves lung-oxygenating efficiency. It is important to know when auto-PEEP is present and then a decision can be made whether to keep it or to make it go away.
Capillary endothelial damage
Airways and alveoli are tethered together by strands of collagenous and elastic fibers. When the airways are expanded, tangential and longitudinal traction is placed upon on the adjacent endothelium cell layer. This widens intercellular junctions and increases capillary permeability and the flux of fluids into the pulmonary interstitium.
Airway and alveolar epithelial damage
In pulmonary disease, an increase in airway fluids increases surface tension and increases the tendency for small airway and alveoli collapse (when the transpulmonary pressure and functional residual capacity are below the critical closing point). Re-opening of these units during the next breath requires breaking the surface tension seal between two adjacent epithelial cells. These tangential forces eventually damage the cell membranes.
Adjacent lung units, for a variety of reasons, have different time constants and do not expand at the same time or rate. This causes a shear injury to the alveolar epithelium on each side of the thin septal membranes that form the common wall between the two adjacent alveoli.
Release of inflammatory mediators
Positive pressure ventilation and, particularly, over-distention of lung units, is thought to cause leuco-activation resulting in the release of inflammatory mediators (Ranieri). These at least enhance capillary permeability and at most, cause endothelial and epithelial cell damage and death.
These processes of endothelial and epithelial damage worsen the magnitude of the diffuse parenchymal disease in a manner that is indistinguishable from the underlying diffuse infiltrative disease for which the animal is receiving ventilator therapy. PEEP, sufficient to prevent airway/alveolar closure will minimize surface tension-induced and asynchronous lung unit expansion-induced epithelial damage. PEEP should be set above closing pressure.
Pneumonia
Pneumonia is a common consequence of long-term positive pressure ventilation procedures: 1) positional stasis predisposes to atelectasis and decreased secretion clearance from the lower lung regions; 2) the bacterial population of the mouth and pharynx proliferate and become colonized by gram negative organisms; 3) these micro-organism invariably migrate down the trachea (past the inflated cuff) and into the lower airways; 4) invasive procedures such as tracheal intubation and tracheal suctioning predispose to the introduction of bacteria into the lower airways; 5) if antibiotics are utilized, the patient is predisposed to colonization by resistance micro-organisms; and 6) if histamine-2 blockers are utilized, the patient is predisposed to bacterial colonization in the stomach (such fluids invariably find there way up the esophagus and into the airways). The procedure of positive pressure ventilation, per se, is not considered an indication for prophylactic antibiotic therapy. In an unpublished experimental series (Haskins), all dogs were placed on antibiotics by the end of one week. Regular repositioning, aseptic airway procedures, and regular mouth and pharynx care help minimize the development of pneumonia. Ventilated patients should be monitored for indications of infection and placed on appropriate antibiotics if/when the need arises.
Open lung techniques/lung protective ventilator strategies
An open lung technique is a concept rather than a specific technique. The idea is to recruit as many alveolar units as possible (open them up) and then prevent them from collapsing again (keep them open). This will optimize blood oxygenation and minimize ventilator-induced injury. Positive pressure ventilation can induce lung injury ranging from alveolar septal rupture and pneumothorax to a diffuse infiltrative respiratory distress syndrome that is indistinguishable from the disease for which PPV was implemented. This injury derives from various deleterious aspects of over-inflation of individual lung units (volutrauma). Lung protective ventilation strategies seek the same objectives as the open lung ventilation techniques: 1) to recruit as many alveolar units as possible; 2) to prevent their re-collapse; and 3) to minimize alveolar over-distention. These strategies involve high initial peak pressures (40 to 60 cm H2O) for alveolar recruitment, for variable periods of time (the duration of one breath, up to a minute) and moderate to high PEEP (10?0 cm H2O) to keep alveoli open, and then moderate (usually less than 40 cm H2O) peak pressures (Amato; Stewart; Brochard; Brower; ARDS Network; Kloot; Medoff). The inevitable consequence of high PEEP pressures and moderate peak pressures is a small (compared to normal) tidal volume. A normal lung can easily handle a normal tidal volume, however, a lung with reduced vital capacity cannot (without volutrauma); the tidal volume needs to be appropriate for the patient. Unfortunately, the magnitude of the disease-induced reduction in vital capacity cannot be predicted in advance. It needs to be assessed in each patient and then must be re-assessed frequently since compliance and vital capacity can change over the course of a few hours. Tidal volume is a dependent variable that is determined by airway pressures and thoracic compliance. Protective lung strategies may also diminish the release of inflammatory mediators that promote capillary endothelial and airway epithelial damage (Ranieri).
We propose here a method that we think would be applicable to veterinary patients. This procedure should only be applied to animals with diffuse pulmonary parenchymal disease; it has no purpose in animals with relatively normal lungs being ventilated for neurologic reasons. You will need to be able to measure airway pressures and tidal volumes, and have the capability to set PEEP. Start with about +5 cm H2O of PEEP, set the peak pressure to 10 cm H2O with a long inspiratory time of about one second, and record the tidal volume. Increase the peak pressure to 15 cm H2O and record the new tidal volume. Calculate the change in tidal volume generated by the change in peak pressure (i.e., new-previous tidal volume). Repeat the process, increasing the peak pressure by 5 cm H2O each time either until the incremental increase in tidal volume starts to decrease, or until a peak pressure of 60 cm H2O is attained. In either case, total lung capacity is considered to have been reached. The peak pressure setting associated with the greatest incremental increase in tidal volume is now selected. The peak pressure associated with the first large increase in tidal volume is now selected as the PEEP setting. Alternately, if your ventilator has the ability to display a pressure-volume curve, PEEP is selected at the airway pressure that represents a 50% reduction in peak volume using the deflation portion of the curve. If these ventilator settings result in a tidal volume exceeding 10 ml/kg, the peak pressure should be further decreased until the tidal volume is 10 ml/kg. The ventilator cycle rate should then be adjusted to keep the PaCO2 below 60 mm Hg. The ventilator cycle rate is now selected. Start at 25 breaths per minute and adjust as necessary to obtain an acceptable PaCO2.

minibabyqq 2007-1-26 01:59

[color=Magenta][size=5][b]斷絕從通風的支持 Slippery Slope of Weaning from Ventilatory Support  [/b][/size][/color]


斷絕一個動物通風的支持要求特別留意因為它也許是慢的開發能力維護它自己的透氣和oxygenation 要求。嚴厲散開肺parenchymal 疾病慢慢地癒合; 逐漸撤退支持需要反映在氧化的效率的進步改善。通風的肌肉接受不用萎縮並且通風的支持必須慢慢地被撤出以便動物有時間再開發肌肉力量。
實際上, 斷絕過程開始動物被設定和槽櫪在通風筒的片刻。就是說, 那一個頻繁地測試動物在透氣做法的路線期間由嘗試輕微地較不進取的通風筒設置和然後估計animal.s 反應。如果沒有惡化在肺表現, 通風筒設置被減少更, 等等。如果有不能接受的惡化在肺表現, 設置返回到他們的早先水平因為它是明顯的動物沒準備好被斷絕。在之後有人可能期待可測量的改善的時期(但不長期比24 小時), 過程被重覆。
能力安全地中斷通風的支持總是一個回顧展評估。weanability. 的預期預報因子不非常可靠, 必須演講動物最初地被安置在通風筒的原因(即, don.t 神色在oxygenation 參量如果動物被通風由於tetraplegia) 。
1 。 呼吸中心斡旋的hypoventilation/apnea 通常同其它顱內的疾病聯繫在一起的標誌譬如昏迷。這些動物不需要沉著被維護在通風筒。當這些患者收復充足的知覺以便他們不再容忍透氣做法和氣管內插管法, 他們大概將收復他們的呼吸中心的充足的作用維護充分透氣。通風筒設置進步地被減少看如果患者能維護自己。
2 。 患者與脊髓或周邊neuromuscular 疾病斡旋的hypoventilation 應該被通風通過氣管造口術管以便他們不必須是sedated/anesthetized 。肌肉作用和力量回歸可能更加容易地然後被估計。撤退反射的力量; 對配件彎曲的抵抗; 自發呼吸的努力的力量; 能力引起低於大氣層的壓力大於5 到15 cm H20 (貓對大狗, 各自地) 當_發反對一支閉合的導氣管; 並且能力坐直或立場是所有可能的weanability 的標誌。
3 。 有肺parenchymal 疾病病人最難估計。他們也許準備好斷絕機械透氣當他們要求唯一最小的通風筒設置引起可接受的動脈oxygenation; oxygenation 參量不需要是正常, 公正可接受的, 以被_發的氧濃度少於40% 。能力維護PaCO2 少於45 mmHg 以正常範圍tidal/minute 容量和高峰壓力並且建議, 患者也許是weanable 。能力維護PaO2 大於80 mmHg 以窺視< 4 cm H2O 和被_發的氧氣< 40% 並且令人鼓舞。
一系列的掩護問題估計潛在的weanability 被建議。對任何問題的一個no. 答復建議, 患者不能是weanable 此時。如果對所有問題的答復是yes, 。通風筒設置應該被減少。對吸入的肌肉力量的評估將幫助引導過程的方向。如果患者有肌肉力量減少導氣管壓力超過5 cm H2O (為貓), 15 cm H2O (為一條小狗), 或15 cm H2O (為一條大狗), 它假設, 患者能容忍一個更加進取的斷絕過程。如果不是, mild. 斷絕過程, 最初地不要求太多患者, 應該被實施。
有許多不同的方法斷絕但他們全都介入在支持的逐漸減退和要求在工作的逐漸增量由患者。您使用的方法取決主要於您的通風筒和患者的能力。斷絕方法包括(在近似次序, 從最少對多數工作要求患者; 雖然有可觀的重疊): 1) 迫使支持(以越來越少的相當數量壓力支持); 2) 斷斷續續的必須的透氣(以減少必須的呼吸); 3) 自發呼吸以連續的正面導氣管壓力; 4) 在集合通風筒週期率的逐漸減退以便動物必須進步地觸發更多呼吸獨自(協助的呼吸以在必需的觸發器努力的逐漸增量); 並且5) 去除患者從通風筒為進步地更長的自發呼吸的試驗。這些不同的斷絕技術的組合是常用在一名唯一患者。
氣管內管、呼吸的電路, 和通風筒一般增量對吸入的流程的抵抗。幾個方式(SIMV 和CPAP) 要求, 動物呼吸通過通風筒。沒有壓力支持, 這增加對吸入的努力的抵抗和增加工作呼吸為患者, 和無法被忽略。
1 。 壓力支持是一個自發呼吸的方式被提供在一些通風筒。患者確定何時快速地開始_發, 多麼_發, 和何時終止_發。通風筒嚮導氣管運用被預先選定的相當數量正面壓力在吸入的階段過程中。氣體流速從通風筒最初地是非常高的為了跟上patient.s 被_發的氣體流速, 當維護preset 接近導氣管壓力。當patient.s 肺填裝, 吸入的流速減少, 並且新氣體流程從通風筒均衡地減少。當流速從通風筒減少到20% 它的峰頂, 通風筒交換對呼氣階段。這是透氣一非常patient 友好的方式因為患者是在各潮汐容量總控制, 假如是小或大, 或快速或慢的。當患者變得堅強和可勝任更多工作呼吸, 相當數量壓力支持可能被減少。
2 。 斷斷續續的必須的透氣(IMV) 方式提供受控呼吸的一個最小的數字從通風筒, 但自發地允許動物對呼吸通過通風筒時間的剩餘。多數IMV 方式同步對patient.s 呼吸的努力(SIMV) 以便機械通風筒呼吸與一名自發患者相符。當斷斷續續的受控呼吸進步地被減少, 患者必須呼吸更獨自。患者必須呼吸通過通風筒、呼吸的電路, 和氣管管的抵抗。
3 。 連續的正面導氣管壓力(CPAP) 是一個自發呼吸的方式以被舉起的導氣管壓力。率和潮汐容量由患者控制當CPAP 保留小導氣管和小窩打開在呼吸之間。這最大化oxygenation 和促進下呼吸的發行對更低的導氣管。患者必須呼吸通過通風筒、呼吸的電路, 和氣管管的抵抗。
4 。 在通風筒週期率的逐漸減退在通風筒裡以協助方式作用, 要求動物進步地觸發它自己的更多呼吸。一旦觸發, 然而, 通風筒完成呼吸在preset 潮汐容量、流速, 和吸入的時間。敏感度控制可能仔細地被調整進步地要求更多努力從患者觸發呼吸。
5 。 通風筒沒有任一類型斷絕方式要求, 耐心從通風被去除為短的自發呼吸的試驗。時間通風筒是進步被增加因為patient.s 情況和力量准許。
問題第二系列瞄準確定多麼恰當動物容忍斷絕過程。對所有問題的一個no. 答復建議, 動物容忍斷絕過程並且一次進一步減少試驗在通風筒支持的水平被擔保。對任何問題的一個yes. 答復建議斷絕失敗和那它大概是必要返回到一個要求較少工作從患者的更加支援的通風筒設置。
得到動物鎮靜劑
鎮靜劑導致呼吸消沉和肌肉弱點。Sedated/anesthetized 患者不會將呼吸並且unsedated 患者和因此更難斷絕。不幸地, 動物必須保留在鎮靜劑在斷絕過程過程中, 直到這樣的時刻, 它是安全分開他們從通風筒和extubate 。它是特別重要, 因此, 在斷絕過程期間, 是肯定運用最少相當數量鎮靜與患者通風筒氣管內管的synchrony 和保留兼容。它是還中意使用短行動或反演性代理以便鎮靜作用儘快終止跟隨extubation 。
內在神經傳送體將容納對長期鎮靜並且撤退這些藥物可能同勵磁和可能奪取聯繫在一起。這是特別可靠對於戊巴比妥, 是頻繁地被使用的藥物為多數透氣規程。補救從短期戊巴比妥麻醉經常是粗礪和亢奮反射; 附屬鎮定藥(苯甲二氮卓, acepromazine) 使這些光滑。補救從中間長度戊巴比妥麻醉(3.4 天) 同煩躁不安和不寬容聯繫在一起對處理; 附屬苯甲二氮卓注入(0.2.0.5 mg/kg/hr) 從時間戊巴比妥被關閉對24 小時在斷絕以後並且extubation 應該使這補救光滑。補救從長時期的麻醉(1+ 幾星期) 同奪取聯繫在一起。這些患者應該開始在苯巴比妥(6 mg/kg q12h) 至少四天在停止戊巴比妥注入前。因為你事先從未知道何時斷絕將發生, 最好及早開始苯巴比妥。它將幫助減少其它藥物的藥量要求在做法期間並且它然後將是那裡您決定開始斷絕戊巴比妥。長期戊巴比妥注入不應該突然被停止以苯巴比妥背景。減少藥量。□天直到藥量是在1 mg/kg/hr 以下, 和然後關閉它。苯甲二氮卓的注入應該開始如果hyperexcitability 或奪取發生。如果更多幫助是需要的, 保持動物被麻醉以propofol 注入(0.1 mg/kg/min) 為24 小時在戊巴比妥被關閉了(之後在戊巴比妥的一個堅固比例代謝了和被消滅了) 期間並且然後讓動物從propofol 恢復) 。
Neuromuscular 阻攔的代理偶爾地被使用了在被通風的動物患者的管理, 並且他們是常用在人的加護病房。Neuromuscular 阻攔的代理取消也許是防護的應該那裡是相互外緣通風筒故障或電路斷開的所有呼吸的能力。撤退neuromuscular 阻攔的代理總不同neuromuscular 封鎖的逆轉聯繫在一起。這的原因不為人所知而是也許同acetylcholine 感受器官的下來章程聯繫在一起在neuromuscular 連接點。總之, neuromuscular 阻攔的代理不是必要的為通風的動物和, 給他們潛在的不利影響, 不被推薦供未受訓練的個體使用。


Weaning an animal off ventilatory support requires special attention since it may be slow to develop the ability to maintain its own ventilation and oxygenation requirements. Severe diffuse pulmonary parenchymal disease heals slowly; gradual withdrawal of support needs to mirror progressive improvement in oxygenating efficiency. The ventilatory muscles undergo disuse atrophy and ventilatory support must be withdrawn slowly so that the animal has time to redevelop muscle strength.
In a sense, the weaning process begins the moment an animal is set up and stable on the ventilator. That is to say, that one is frequently testing the animal during the course of the ventilation procedure by trying slightly less aggressive ventilator settings and then assessing the animal𠏋 response. If there is no deterioration in lung performance, the ventilator settings are decreased a bit more, and so on. If there is unacceptable deterioration in lung performance, the settings are returned to their previous level since it is apparent that the animal is not yet ready to be weaned. After a period of time over which one might expect measurable improvement (but not longer than 24 hours), the process is repeated.
The ability to safely discontinue ventilatory support is always a retrospective assessment. Prospective predictors of 𢘛eanability?are not very reliable and must address the reason for which the animal was initially placed on the ventilator (e.g., don㦙 look at oxygenation parameters if the animal is being ventilated because of tetraplegia).
1. Respiratory center-mediated hypoventilation/apnea is usually associated with other signs of intracranial disease such as coma. These animals do not need to be sedated to be maintained on the ventilator. When these patients regain sufficient consciousness so that they no longer tolerate the ventilation procedure and endotracheal intubation, they probably will have regained sufficient function of their respiratory centers to maintain adequate ventilation. The ventilator settings are progressively decreased to see if the patient can maintain itself.
2. Patients with spinal cord or peripheral neuromuscular disease-mediated hypoventilation should be ventilated via a tracheostomy tube so that they do not have to be sedated/anesthetized. Return of muscle function and strength can then be more easily assessed. Strength of the withdrawal reflex; resistance to appendage flexion; strength of the spontaneous breathing effort; ability to generate a sub-atmospheric pressure greater than 5 to 15 cm H20 (cat to large dog, respectively) when inspiring against a closed airway; and ability to sit up or stand are all signs of possible weanability.
3. Patients with pulmonary parenchymal disease are the most difficult to assess. They may be ready to wean off mechanical ventilation when they require only minimal ventilator settings to generate acceptable arterial oxygenation; oxygenation parameters do not need to be normal, just acceptable, with inspired oxygen concentrations of less than 40%. The ability to maintain a PaCO2 of less than 45 mmHg with a normal-range tidal/minute volume and peak pressures also suggest that the patient may be weanable. The ability to maintain a PaO2 of greater than 80 mmHg with a PEEP < 4 cm H2O and an inspired oxygen of < 40% is also encouraging.
A series of screening questions to assess potential weanability is suggested. A 忛o?answer to any question suggests that the patient may not be weanable at this time. If the answer to all questions is 憘es,?the ventilator settings should be decreased. An assessment of inspiratory muscle strength will help guide the direction of the process. If the patient has the muscle strength to decrease airway pressure more than 5 cm H2O (for a cat), 15 cm H2O (for a small dog), or 15 cm H2O (for a large dog), it is assumed that the patient can tolerate a more aggressive weaning process. If not, a 𢘫ild?weaning process, which does not initially demand too much of the patient, should be implemented.
There are many different methods of weaning but they all involve a gradual decrease in support and require a gradual increase in work by the patient. The method that you use is largely dependent upon the capabilities of your ventilator and the patient. Weaning methods include (in approximate order, from least to most work required of the patient; although there is considerable overlap): 1) pressure support (with decreasing amounts of pressure support); 2) intermittent mandatory ventilation (with decreasing mandatory breaths); 3) spontaneous breathing with continuous positive airway pressure; 4) a gradual decrease in set ventilator cycle rate so that the animal has to trigger progressively more breaths on its own (assisted breathing with a gradual increase in the required trigger effort); and 5) removing the patient from the ventilator for progressively longer spontaneous breathing trials. Combinations of these different weaning techniques are commonly used on a single patient.
The endotracheal tube, the breathing circuit, and the ventilator generally increase the resistance to inspiratory flow. Several modes (SIMV and CPAP) require that the animal breathe through the ventilator. Without pressure support, this adds resistance to the inspiratory effort and increases the work of breathing for the patient, and cannot be ignored.
1. Pressure support is a spontaneous breathing mode offered on some ventilators. The patient determines when to start an inspiration, how fast to inspire, and when to terminate the inspiration. The ventilator applies the pre-selected amount of positive pressure to the airway throughout the inspiratory phase. Gas flow rate from the ventilator is initially very high in order to keep up with the patient𠏋 inspired gas flow rate, while maintaining the preset proximal airway pressure. As the patient𠏋 lungs fill, the inspiratory flow rate decreases, and the fresh gas flow from the ventilator decreases proportionately. When the flow rate from the ventilator decreases to 20% of its peak, the ventilator switches to the expiratory phase. This is a very 𢖯atient-friendly?mode of ventilation because the patient is in total control of each tidal volume, be it small or large, or fast or slow. As the patient becomes stronger and capable of more of the work of breathing, the amount of pressure support can be decreased.
2. Intermittent mandatory ventilation (IMV) modes provide for a minimal number of controlled breaths from the ventilator, but allow the animal to breath spontaneously through the ventilator the rest of the time. Most IMV modes are synchronized to the patient𠏋 breathing efforts (SIMV) so that a mechanical ventilator breath coincides with a spontaneous patient. As the intermittent controlled breaths are progressively decreased, the patient must breath more on its own. The patient has to breath through the resistance of the ventilator, breathing circuit, and tracheal tube.
3. Continuous positive airway pressure (CPAP) is a spontaneous breathing mode at an elevated airway pressure. Both rate and tidal volume are controlled by the patient while the CPAP keeps small airways and alveoli open between breaths. This maximizes oxygenation and facilitates the distribution of the next breath to the lower airways. The patient has to breath through the resistance of the ventilator, breathing circuit, and tracheal tube.
4. A gradual decrease in the ventilator cycle rate in ventilators with an assist-mode function, requires that the animal to trigger progressively more breaths of its own. Once triggered, however, the ventilator finishes the breath at the preset tidal volume, flow rate, and inspiratory time. The sensitivity control can be carefully adjusted to require progressively more effort from the patient to trigger a breath.
5. Ventilators without any type of weaning modes require that the patient be removed from the ventilatory for short spontaneous breathing trials. The length of time off the ventilator is progressing increased as the patient𠏋 condition and strength allows.
A second series of questions is aimed at determining how well the animal is tolerating the weaning process. A 忛o?answer to all questions suggests that the animal is tolerating the weaning process and that a further reduction trial in the level of ventilator support is warranted. A 憘es?answer to any question suggests weaning failure and that it is probably necessary to return to a more supportive ventilator settings which require less work from the patient.
Getting the animal off the sedative drugs
Sedative drugs cause respiratory depression and muscle weakness. Sedated/anesthetized patients will not breath as well as unsedated patients and therefore are more difficult to wean. Unfortunately, animals must remain on sedative drugs throughout the weaning process, until such time that it is safe to disconnect them from the ventilator and extubate. It is especially important, therefore, during the weaning process, to be sure to utilize the least amount of sedation compatible with patient-ventilator synchrony and retention of the endotracheal tube. It is also desirable to use a short-acting or reversible agent so that the sedative effects terminate as soon as possible following extubation.
Endogenous neurotransmitters will accommodate to long-term sedation and withdrawal of these drugs can be associated with excitation and possibly seizures. This is especially true for pentobarbital, which is the frequently used drug for most ventilation procedures. Recovery from short-term pentobarbital anesthesia is often rough and hyper-reflexive; adjunctive tranquilizers (diazepam, acepromazine) will smooth these out. Recovery from intermediate-length pentobarbital anesthesia (3? days) is associated with dysphoria and intolerance to handling; an adjunctive diazepam infusion (0.2?.5 mg/kg/hr) from the time the pentobarbital is turned off to 24 hours after weaning and extubation should smooth this recovery. Recovery from prolonged anesthesia (1+ weeks) is associated with seizures. These patients should be started on phenobarbital (6 mg/kg q12h) at least four days prior to stopping the pentobarbital infusion. Since one never knows in advance when weaning will occur, it is better to start the phenobarbital early. It will help reduce the dose requirement of the other drugs during the procedure and then it will be there when you decide to start weaning the pentobarbital. Long-term pentobarbital infusions should not be stopped abruptly even with a phenobarbital background. Reduce the dose by ?each day until the dose is below 1 mg/kg/hr, and then turn it off. An infusion of diazepam should be started if hyperexcitability or seizures occur. If more help is needed, keep the animal anesthetized with a propofol infusion (0.1 mg/kg/min) for 24 hours after the pentobarbital has been turned off (during which time a substantial proportion of the pentobarbital will have been metabolized and eliminated) and then let the animal recover from the propofol).
Neuromuscular blocking agents have been occasionally used in the management of ventilated animal patients, and they are commonly used in human intensive care units. Neuromuscular blocking agents remove all breathing capabilities which might be protective should there be an inter-rim ventilator malfunction or circuit disconnect. Withdrawal of the neuromuscular blocking agent is not always associated with reversal of the neuromuscular blockade. The reason for this is not known but may be associated with a down-regulation of acetylcholine receptors at the neuromuscular junction. In general, neuromuscular blocking agents are not necessary for ventilating animals and, given their potential adverse effects, are not recommended for use by untrained individuals.

minibabyqq 2007-1-26 02:00

[color=Magenta][size=5][b]Coagulopathies𣶷OTAL [/b][/size][/color]

[size=12px]靈菌是一個共同的臨床介紹在小動物實踐。靈菌混亂通常發生在狗比在貓。靈菌混亂的臨床顯示也許範圍從溫和和self-limited 對威脅生命的出血要求直接治療。動物也許流血由於血管傷害由任一個精神創傷、手術、潰瘍, 和腫瘤造成。在hemostatic 干擾的情況下, 出血性的傾向被誇大依照由自發, multifocal, 和意想不到的嚴厲靈菌舉例證明。
Hemostasis 是對靈菌的複雜生理學反應, 可能被劃分成主要和次要hemostasis 。血管內皮、小片, 和vonWillebrand 因素(vWF) 必需為主要hemostasis 或不穩定的小片插座的形成, 是充足停止血絲靈菌。馮Willebrand 因素, 大血漿蛋白質由內皮綜合, 促進黏附力在小片和subendothelium 之間。以更大的船傷害, 凝固因素並且必要形成一個穩定的纖維蛋白凝塊, 以次要hemostasis 著名。Hemostatic 混亂可能方便地被分類入vasculopathies, thrombocytopenias 、thrombopathias 、vonWillebrand 疾病(vWD), 和coagulopathies, 意識到一些疾病過程起因聯合的hemostatic 瑕疵(即, 傳播的血管內coagulopathy [ DIC ]) 。出血性的介紹也許建議某些hemostatic 混亂和實際測試有時間描繪靈菌傾向。靈菌的起因的一個準確診斷將影響患者的治療和結果。
凝固小瀑布
凝固小瀑布是一系列的enzymatic 反應介入凝固因素, 由羅馬數字表示。這條複雜生物化學的路充當在纖維蛋白的形成的三個舉足輕重的角色從纖維蛋白原:
1 。   纖維蛋白世代的加速度> 10 百萬摺疊。
2 。   纖維蛋白插座大小的章程適當為傷害。
3 。   纖維蛋白凝塊形成的地方化對傷害站點。
凝固小瀑布可能被劃分成合併入共同的路的一個外在和內在系統。當血管牆壁被傷害, 外在凝固系統被組織因素(凝血因子最初地激活導致在subendothelium), 與因素VII 結合。小量的thrombin 生產了通過因素VIIa 看上去充足激活因素XI 對因素夏, 和激活其它輔助因素(因素v, VIII, XIII) 。通過因素夏的行動在因素IX, thrombin 形成被維護。其他聯絡階段凝固因素包括因素XII, prekallikrein 和高分子重Kininogen 和是 [i]活體內[/i] 一點重要在內在系統的活化作用。上面被描述的凝固過程解釋為什麼hemophilic (因素VIII 和IX 短少) 或因素VII 短少動物流血, 但是因素XII 短少動物不。
凝固因素是酵素(絲氨酸proteases), 輔助因素, 或凝固的特殊反應基體落下。多數因素被給羅馬數字從I-XIII, 但編號不是連續的並且沒有因素VI 。鈣(因素Iv) 必需為多數反應和是原因為什麼chelators, 即, 枸櫞酸鹽和EDTA, 被使用為血液彙集和處理血漿或血細胞被分析的地方。凝固小瀑布的所有糖蛋白被綜合在肝臟和流通作為不活潑的前體在血漿。他們需要被激活在船傷害站點(被描述以信件以下他們的羅馬數字) 。維生素K 是需要的為凝固因素II, VII, IX, 和X 的功能綜合。凝固因素的半衰期變化從幾小時(因素VII) 對幾天(纖維蛋白原) 。值得注意的是, 體外凝固因素互作用, 以凝結著名, 進行有些與上面被描述的 [i]活體內[/i] 凝固小瀑布不同, 但是有用的在具體coagulopathies 的證明。在纖維蛋白插座形成以後, 胞漿素原將被激活並且plasmin, 一空泛的protease 將開始劃分纖維蛋白原並且結果在纖維蛋白原病勢漸退和fibrin(-ogen) 分裂產品的纖維蛋白(FSP) 並且D 二聚體形成。
診斷方法
對某人特徵的描述和家史
雖然遺傳性coagulopathies 也許發生在任一養殖, 每個coagulopathy 至今只被報告了在某些養殖。血友病A 和B 發生在許多不同的養殖和是X 染色體recessively 被繼承; 因而, 唯一男性一般是受影響的並且女性是無症狀載體。典型地流血的標誌發生在童年年齡和經常復發, 但不可以被認出直到成年。
歷史
靈菌也許導致(精神創傷, 手術) 或自發地出現。仔細歷史採取也許顯露對毒素(殺鼠劑, 蘑菇) 並且藥物的暴露(warfarin, 肝素) 。它重要辨認具體產品, as, 例如, 不同的殺鼠劑有相當各種各樣的有力。任一其它疾病, 例如, hepatopathies 和癌症的證據, 也許負責對出血。
體格檢查
仔細的臨床評估也許區分在主要和次要hemostatic 瑕疵之間。表面靈菌典型地看以主要hemostatic 混亂。Petechia 和ecchymosis 是thrombocytopenias 和thrombopathias 標記特點。在馮Willebrand 疾病, 流血發生在站點傷害(精神創傷、牙齒疾病, 發情, 食道), 而不是petechia 或ecchymosis 。Coagulopathies 也許同靈菌聯繫在一起唯一或多個站點為洞靈菌描繪譬如hematoma 、hemarthrosis 、hemomediastinum 、和hemoperitoneum 和thorax, 但食道出血和挫傷也許並且發生。其它部下的疾病的標誌也許被認可。
Hemostatic 測試
Hemostatic 測試被表明:
1 。   每當動物過份地流血。
2 。   在手術之前當一個增加的流血的傾向被懷疑。
3 。   對螢幕治療干預。
4 。   為基因掩護在某些養殖或家庭以已知的流血的混亂。
Hemostatic 反常性應該被估計在設立療法前每當可能或至少適當的血樣應該是被收集的預處理。優秀venipuncture 以擯除最初的少數血液(避免小片活化作用和組織因素) 並且延長的壓縮頸部, 隱靜脈或大腿骨靜脈必需。表皮靈菌時間粗暴地估計整體hemostasis 但不被規範化和是痛苦的, 和因此, 沒推薦。一個最小的資料庫包括一個被包裝的細胞容量和總蛋白含量評估。血液汙跡的評估可能提供小片估計和辨認小片大小和聚集並且schistocytes 。結果可能提供程度的某一措施失血和紅血球滲流要求。
主要Hemostasis: 小片和vWF
因為8-15 小片通常被發現每大功率油emersion 微觀領域, 缺乏或編號下限小片建議一嚴厲thrombocytopenia 。出血一般不被觀察除非血小板計數是< 40,000/.l (正常150-500,000/.l) 。小片伴生的抗體的偵查促進支持一免疫斡旋的thrombocytopenia, 但這個測試很少是可利用的。清液滴定量為 [i]Ehrlichia canis [/i]和 [i]E. platy [/i]被表明在某些狀態和國家。schistocytes 出現與thrombocytopenia 一起, 建議血管內的傳播的凝固, 血管內的纖維蛋白擱淺片段紅血球。由於馮Willebrand 疾病是這樣一個共同的溫和的主要hemostatic 瑕疵在狗, 血漿vWF 測量由ELISA 被表明。供選擇地, DNA 測試是可利用的在一些似犬養殖為具體vWD 導致的變化和是有用的為載體的偵查。終於, 根據正常血小板計數和血漿vWF 價值, 長時期的頰黏膜靈菌時光(BMBT) 表明一thrombopathia 。一次性的設備是可利用的, 促進做一個到二標準1 毫米深刻的黏膜切開。小片作用分析儀(PFA100) 是一個簡單的工具功能上估計主要hemostasis 。電子顯微鏡和小片族聚和nucleotide 研究允許小片官能不良的進一步描述特性在專業實驗室。
次要Hemostatic 測試: 凝固測試
但是整體血液凝結的時間測試是厚臉皮和不精確的, 有數規範化的凝固試鏡頭有用為定義coagulopathies 在臨床實踐。試鏡頭估計凝固在試管內, 是有用的, 但現在為人所知不是完全相同和 [i]活體內[/i] 凝固過程。幾乎所有凝固測試估計凝固系統的某些部份的作用在使用新整體血液或新鮮的(結冰的) 血漿引起纖維蛋白在fibrometer 。Recalcified 檸檬酸化的血漿被使用並且許多測試一個patient.s 樣品直接地與同時被獲得的控制或水池血漿(血漿比較從10 個動物) 。總之, 凝固時間(時間對凝結和纖維蛋白形成) 是短的在小動物比在人, 因而測試需要被確認為特殊動物種類。
內在和共同的路在或被激活的凝固時間(行動) 或被激活的部份凝血因子時間以前估計(PTT) 。因素XII 內在小瀑布被白陶土或其他激活被硅藻類地球(celite) 在行動測試和聯絡階段基體在PTT 測試。
外在和共同的路可能由或凝血因子時間(PT) 或[u]我[/u]nduced 由[u]v [/u]itamin[u]K [/u]ntagonism或 bsence的[u]p [/u]rotein估計(PIVKA) 測試。不同的組織因素(thromboplastins) 激活反之將導致纖維蛋白形成的因素VII 。值得注意的是, PIVKA 測試不是具體的為抗凝劑殺鼠劑毒化的偵查, 但查出有用外在和共同的路的任一凝固因素缺乏和是因此不是。
近來行動管測試和PIVKA 測試是唯一的問題的關心測試可利用為臨床實踐, 但是PTT 和PT 測試執行了在參考實驗室。有現在一個新問題的關心是能迅速地確定PTT 和PT 在少量的凝固儀器(SCA2000) (50 .l) 檸檬酸化的整體血液, 因此做使變冷, 迅速分離檸檬酸化的血漿和發貨凍血漿在乾冰對實驗室為最初的凝固掩護多餘。
實際上, 一種合理和簡單的方法使靈菌動物被篩選為coagulopathy 會將首先測量行動或PTT 因為或者測試查出所有coagulopathies (除了遺傳性因素VII 缺乏在小獵犬) 。如果PTT (或法案) 被延長, PT 測試會被表明區分在一個內在和共同的路瑕疵或一聯合的coagulopathy 之間介入幾個凝固因素。
雖然遺傳性coagulopathies 可能被懷疑根據了凝固測試反常性的樣式, 具體要素分析是需要的證實診斷。靈菌公動物與長時期的PTT (或行動) 並且正常PT 可能有血友病A 或B (因素VIII 或IX 缺乏), X 染色體隱性混亂。但是, 因素XI 缺乏同同樣測試反常性聯繫在一起和由一個autosomal 隱性特徵(即Kerry 藍色狗) 繼承。終於, 因素XII 缺乏, 特別共同在家養的shorthair 貓, 和prekallikrein 缺乏不導致明顯PTT (行動) 延長但過份靈菌傾向。
殺鼠劑毒害了是靈菌或是在危險中為靈菌將有延長總計上述凝固測試的動物, 但會有正常thrombin 時光(TT) 。thrombin 時間是獨立維生素K 依賴凝固因素和是一個功能分析用試樣使纖維蛋白原形成纖維蛋白。一次毒理學調查(產品證明, 血液毒素學分析) 也許證實殺鼠劑毒化。適度thrombocytopenia 也許同warfarin 類型殺鼠劑毒化聯繫在一起。
所有肝臟病也許導致各種各樣的coagulopathies 由於被削弱的凝固因素綜合和維生素K 吸收不良。同樣, 傳播的血管內的coagulopathies (DIC), 由於許多不同的混亂同易變地長時期的凝固時間聯繫在一起。有用的對DIC 診斷是schistocytes 的認識, thrombocytopenia 、低antithrombin III 水平、和增加的D 二聚體和纖維蛋白分裂(退化) 產品。最近簡單的成套工具為似犬D 二聚體變得可利用。
療法和監視
上述凝固測試是還有用監測治療干預。肝素猛烈地延長PTT/ACT 和在一點程度上PT 。相反, warfarin 導致PT 和PTT 延長像抗凝劑殺鼠劑。因而, 肝素和warfarin 抗凝劑療法由PTT (行動) 或PT 監測, 各自地。同樣, 維生素K 療法(< 5 mg/kg/d PO 或SC) 應該改正維生素K 缺乏狀態, 可能由或PT 或PTT 測量估計。
滲流支持的作用在靈菌動物以coagulopathies 由凝固試鏡頭和PCV 並且評估。新鮮的結冰的血漿(10 ml/kg 每六個小時) 是適當的為所有coagulopathies, 但是cryoprecipitate (2.5 ml/kg) 是有用的為控制流血在血友病A 和馮Willebrand 疾病。另外, 被包裝的紅細胞或新整體血液單獨能使用改正伴生的貧血症。
為了最好估計patient.s 變化在能力上凝固, 它重要使用同樣技術和理想地同樣operator/laboratory 。這些在被描述的簡單的指南之上應該保證正確診斷和成功的管理動物以出血。[table][tr][td=3,1,766]Hemostatic 測試在臨床實踐。
[/td][/tr][tr][td=1,1,291][b]測試[/b]
[/td][td=1,1,238][b]正常狗[/b]
[/td][td=1,1,238][b]混亂[/b]
[/td][/tr][tr][td=1,1,291]PCV %
[/td][td=1,1,238]37.55%
[/td][td=1,1,238]貧血症; 不是顯然的在最初的少數小時
[/td][/tr][tr][td=1,1,291]總蛋白含量
[/td][td=1,1,238]5.5.7.5 g/dl
[/td][td=1,1,238]Hypoproteinemias 以外在失血
[/td][/tr][tr][td=1,1,291]小片估計
血小板計數
[/td][td=1,1,238]8.15 每油田(1/15,000 ul)
150-400,000/ul
[/td][td=1,1,238]Thrombocytopenias
並且schistocytes
[/td][/tr][tr][td=1,1,291]頰黏膜靈菌時間(BMBT)
[/td][td=1,1,238]< 4 分鐘
[/td][td=1,1,238]Thrombopathias
vWD
[/td][/tr][tr][td=1,1,291]馮Willebrand 因素(vWF)
[/td][td=1,1,238]65.150%
並且變化測試為養殖
[/td][td=1,1,238]馮Willebrand 疾病
[/td][/tr][tr][td=1,1,291]被激活的凝結的時間(行動)
[/td][td=1,1,238]< 110 秒(管)
[/td][td=1,1,238]內在和共同的coagulopathies
[/td][/tr][tr][td=1,1,291]部份凝血因子時間(PTT)
[/td][td=1,1,238]12.16 秒(實驗室*)
54.94 秒(SCA 2000)
[/td][td=1,1,238]內在和共同的coagulopathies
[/td][/tr][tr][td=1,1,291]凝血因子時間
(PT)
[/td][td=1,1,238]10.14 秒(實驗室*)
12.16 秒(SCA 2000)
[/td][td=1,1,238]外在和共同coagulopathy
[/td][/tr][tr][td=1,1,291]蛋白質被維生素K Antagonism/Absence 導致(PIVKA)
[/td][td=1,1,238]< 25 秒
[/td][td=1,1,238]外在coagulopathy,
不具體為warfarin
[/td][/tr][tr][td=1,1,291]Thrombin 時間(TT)
[/td][td=1,1,238]10.12 秒(實驗室*)
[/td][td=1,1,238]Hypofibrinogenemia 功能
[/td][/tr][tr][td=1,1,291]纖維蛋白原
[/td][td=1,1,238]100.300 mg/dl (被沉澱)
[/td][td=1,1,238]Hypofibrinogenemia


[/td][/tr][tr][td=1,1,291]纖維蛋白分裂產品(FSP/FDP)
[/td][td=1,1,238]< 1:5 (實驗室*); < 5 ug/dl (實驗室*)
[/td][td=1,1,238]Fibrin(-ogen) 退化
[/td][/tr][tr][td=1,1,291]D 二聚體
[/td][td=1,1,238]< 250 .g/dl; negative/positive
[/td][td=1,1,238]纖維蛋白退化
[/td][/tr][tr][td=1,1,291]Antithrombin III
[/td][td=1,1,238]90.120% (實驗室*)
[/td][td=1,1,238]低水平以血栓形成
[/td][/tr][/table]Bleeding is a common clinical presentation in small animal practice. Bleeding disorders occur more commonly in dogs than in cats. Clinical manifestations of bleeding disorders may range from mild and self-limited to life-threatening hemorrhage requiring immediate medical attention. Animals may bleed due to vascular injury caused by any trauma, surgery, ulcer, and tumor. In case of hemostatic disturbances, the hemorrhagic tendency is exaggerated as exemplified by spontaneous, multifocal, and unexpected severe bleeding.
Hemostasis is the complex physiologic response to bleeding and can be divided into primary and secondary hemostasis. Vascular endothelium, platelets, and vonWillebrand factor (vWF) are required for primary hemostasis or the formation of the unstable platelet plug, which is sufficient to stop capillary bleeding. Von Willebrand factor, a large plasma protein synthesized by endothelium, facilitates adhesion between platelets and subendothelium. With larger vessel injury, coagulation factors are also needed to form a stable fibrin clot, known as secondary hemostasis. Hemostatic disorders can be conveniently classified into vasculopathies, thrombocytopenias, thrombopathias, vonWillebrand disease (vWD), and coagulopathies, realizing that some disease processes cause combined hemostatic defects (e.g., disseminated intravascular coagulopathy [DIC]). Hemorrhagic presentations may suggest certain hemostatic disorders and practical tests are available to characterize the bleeding tendency. An accurate diagnosis of the cause of bleeding will influence the treatment and outcome of a patient.
Coagulation Cascade
The coagulation cascade is a series of enzymatic reactions involving coagulation factors, denoted by Roman numerals. This complex biochemical pathway plays three pivotal roles in the formation of fibrin from fibrinogen:
1.   Acceleration of fibrin generation > 10 million-fold.
2.   Regulation of fibrin plug size appropriate for injury.
3.   Localization of fibrin clot formation to site of injury.
The coagulation cascade can be divided into an extrinsic and intrinsic system that merges into the common pathway. When blood vessel walls are injured, the extrinsic coagulation system is initially activated by tissue factor (thromboplastin produced in the subendothelium), which combines with factor VII. The small amount of thrombin produced through factor VIIa appears sufficient to activate factor XI to factor XIa, and to activate other cofactors (factors V, VIII, XIII). Through the action of factor XIa on factor IX, thrombin formation is maintained. The other contact phase coagulation factors include factor XII, prekallikrein and High Molecular Weight Kininogen and are [i]in vivo[/i] of lesser importance in the activation of the intrinsic system. The above described coagulation process explains why hemophilic (factor VIII and IX deficient) or factor VII deficient animals bleed, whereas factor XII deficient animals do not.
Coagulation factors are enzymes (serine proteases), cofactors, or substrates of particular reactions of the coagulation cascade. Most factors are given roman numerals from I-XIII, but the numbering is not sequential and there is no factor VI. Calcium (factor IV) is required for most reactions and is the reason why chelators, e.g., citrate and EDTA, are used for blood collection and processing where plasma or blood cells are analyzed. All glycoproteins of the coagulation cascade are synthesized in the liver and circulate as inactive precursors in the plasma. They need to be activated at the site of vessel injury (depicted with letter a following their Roman numeral). Vitamin K is needed for the functional synthesis of the coagulation factor II, VII, IX, and X. The half-lives of the coagulation factors varies from hours (factor VII) to a few days (Fibrinogen). It should be noted that in vitro coagulation factor interaction, known as clotting, proceeds somewhat differently from the above described [i]in vivo[/i] coagulation cascade, but is helpful in identification of specific coagulopathies. Following a fibrin plug formation, plasminogen will be activated and plasmin, an unspecific protease will commence breaking down fibrinogen as well as fibrin which results in fibrinogen lysis and fibrin(-ogen) split product (FSP) as well as D-dimer formation.
Diagnostic Approach
Signalment and Family History
Although hereditary coagulopathies may occur in any breed, each coagulopathy has thus far only been reported in certain breeds. Hemophilia A and B occur in many different breeds and are X-chromosome recessively inherited; thus, only males are generally affected and females are asymptomatic carriers. Signs of bleeding typically occur at an early age and are often recurring, but may not be recognized until adulthood.
History
Bleeding may be induced (trauma, surgery) or appear spontaneously. Careful history taking may reveal exposure to toxins (rodenticides, mushrooms) and drugs (warfarin, heparin). It is important to identify the specific product, as, for example, different rodenticides have quite varied potency. Any evidence of other diseases, for example, hepatopathies and cancer, may be responsible for the hemorrhage.
Physical Examination
Careful clinical evaluation may differentiate between primary and secondary hemostatic defects. Surface bleeding is typically seen with primary hemostatic disorders. Petechia and ecchymosis are hallmark features of thrombocytopenias and thrombopathias. In Von Willebrand disease, bleeding occurs at sites of injury (trauma, dental disease, estrus, gastrointestinal), rather than petechia or ecchymosis. Coagulopathies may be associated with single or multiple sites of bleeding characterized by cavity bleeding such as hematoma, hemarthrosis, hemomediastinum, and hemoperitoneum and 𩣱horax, but gastrointestinal hemorrhage and bruising may also occur. Signs of other underlying diseases may be recognized.
Hemostatic Tests
Hemostatic tests are indicated:
1.   Whenever an animal is bleeding excessively.
2.   Prior to surgery when an increased bleeding tendency is suspected.
3.   To monitor therapeutic interventions.
4.   For genetic screening in certain breeds or families with a known bleeding disorder.
Hemostatic abnormalities should be assessed prior to instituting therapy whenever possible or at least appropriate blood samples should be collected pretreatment. Excellent venipuncture with discarding of first few drops of blood (to avoid platelet activation and tissue factor) and extended compression over jugular, saphenous or femoral vein is required. The cuticle bleeding time crudely assesses overall hemostasis but is not standardized and is painful, and therefore, not recommended. A minimal database includes a packed cell volume and total protein evaluation. Evaluation of a blood smear can provide a platelet estimate and identify platelet size and clumping as well as schistocytes. The results can provide some measure of the extent of blood loss and red blood cell transfusion requirement.
Primary Hemostasis: Platelets and vWF
Since 8-15 platelets are normally found per high power oil emersion microscopic field, an absence or low number of platelets suggests a severe thrombocytopenia. Hemorrhage is generally not observed unless the platelet count is < 40,000/µl (normal 150-500,000/µl). Detection of platelet-associated antibodies further supports an immune-mediated thrombocytopenia, but this test is rarely available. Serum titers for [i]Ehrlichia canis [/i]and [i]E. platy [/i]are indicated in certain states and countries. The presence of schistocytes along with thrombocytopenia, suggests intravascular disseminated coagulation, where intravascular fibrin strands fragment erythrocytes. Because von Willebrand disease is such a common mild primary hemostatic defect in dogs, plasma vWF measurements by ELISA are indicated. Alternatively, DNA testing is available in some canine breeds for specific vWD-causing mutations and is useful for detection of carriers. Finally, in light of normal platelet count and plasma vWF values, a prolonged buccal mucosal bleeding time (BMBT) indicates a thrombopathia. Disposable devices are available that facilitate making one to two standard 1 mm deep mucosal incisions. The platelet function analyzer (PFA100) is a simple tool to functionally assess primary hemostasis. Electron microscopic and platelet aggregation and nucleotide studies allow further characterization of platelet dysfunctions in specialized laboratories.
Secondary Hemostatic Tests: Coagulation Tests[/size]

minibabyqq 2007-1-26 02:01

[color=Magenta][size=5][b]物理療法在獸醫方面Physical Therapy in Veterinary Medicine  [/b][/size][/color]


有很多興趣在似犬物理療法上並且修復和路線被提供在許多上主要會議。有一個證明過程在行動, 將由幾所大學認可, 並且活躍似犬物理與療法相關的研究發生。什麼觸發了這興趣?
有幾個因素考慮:
1 。   公開需求。
2 。   工作狗的誕生; 以需要返回到活動的早先水平。
3 。   被展示的效力在其它種類(人) 。
4 。   增加的優雅在獸醫手術。
5 。   動物長期居住。
6 。   增加價值來獸醫服務。
7 。   潛在的源泉的獸醫收入。
8 。   獎勵對獸醫職員、所有者和動物。
在最近過去, 有一點注意給予張貼有效的關心並且許多動物丟失了對後續跟隨縫合撤除。這, 結合與概念, 動物會使用肢體當它感覺good. 和勉強在獸醫部分敦促早期的流動性, 是限制物理療法的用途和概念的因素。竟管最近前進, 有定期地固定他們的手術後cruciate 患者四個到六個星期的獸醫, 並且這經常做與塑像、括號, 或藤條。早期的行動證明是有效的在催促的補救和限制不用的作用在骨頭、軟骨、periarticular 軟的組織、韌帶, 和腱。
物理療法和修復的目標是返回受影響的部份和動物到充分的作用。我們從賽跑第一次開始了我們的物理療法和修復(PTH) 節目運作靈獅。所有者和教練員勉強投資時候和金錢允許我們修理他們的傷害除非我們能保險他們會回到軌道和會執行在他們的早先水平或會改善。當我們總不是成功的, 我們學會了早期和適當的PTH 的價值。
一個當前的挑戰將證明, PTH 是一樣配受獎賞的在狗像它是在人。有許多研究完成在人展示PTH 的生活方式的價值在更加早期的補救, 再取回, 回歸到運動練習, 和改進的生活水平。有是研究在動物, 著名地在對electrostimulation 的初期用途的Johnson.s 工作中; Levine 和Millis. 從事行動的goniometry, 範圍和超聲波; Steiss 在超聲波; Adamson 在光子療法和水下的踏車; 提及只一些。最近興趣只將刺激調查和研究新範圍。
PTH 措施應該包括在每個手術後計劃。PTH 的好處有:
1 。   增加的血流和淋巴排水設備對被傷害的區域。
2 。   炎症的早期的決議。
3 。   膠原的增加的生產。
4 。   periarticular 收縮的預防。
5 。   正常聯合homeostasis 的促進。
6 。   正常聯合生物力學的促進。
7 。   預防或使肌肉萎縮減到最小。
8 。   正面心理作用為動物和所有者。
有二分明間隔時間在PTH 可能是有用促進充分的手術後補救和返回到作用的補救過程中。為每一個耐心恢復從創傷傷害並且/或者手術那裡是能受益於PTH 並且這些患者包括那些以肥胖病、退化聯接疾病、組織萎縮和殘餘的神經學疾病的十名患者。為本文的目的, 我們將處理崗位trauma/surgery 患者的需要。
第一個階段
逐步採用1 活動開始天手術和典型地介入冰, 行動的被動範圍, 和早期的創傷動員。這個期間從創傷傷害和或手術開始和包含發生在第一三個到四個星期的激動階段和早期創傷癒合。PTH 的目標在這時間期間是使炎症減到最小並且痛苦, 保存行動的聯合範圍, 和防止或進一步使肌肉和軟的組織萎縮減到最小。
階段二
階段2 活動開始因為炎症是解決並且醫治用開始是佔優勢題材在創傷。它非常重要與創傷癒合的世俗方面結合階段二活動。由那, 我們意味申請適當的重音嚮醫治用的組織以便優選他們不非常癒合但, biomechanical 穩定被威脅。理想地, 階段二活動應該平行在抗拉強度的逐漸增量被觀察在創傷。如果你是太進取的與PTH 在這個期間, 失敗可能發生; 相反地, 如果你滯後在PTH 活動, 早期的回歸的目標到作用不是成功的。
結締組織反應對不用和鉗製
為了更好瞭解PTH 需要在補救期間它是適當瞭解方式結締組織反應鉗製和不用。
骨骼肌改變從被減少的重量軸承和裝貨:
1 。 第一類型肌肉纖維和肌肉有第一類型纖維的多人口顯示永久萎縮。這些包括伸張機肌肉和反地心引力的肌肉。
2 。 肌肉力量損失由不僅萎縮但生物化學的變化造成在sarcoplasmic 蜂巢胃上。
3 。 正常狗接受頭蓋骨cruciate 韌帶和直接安定的外科交易接受受影響的肢體肌肉的早期的萎縮, 繼續至少五個星期。萎縮是最重大的在quadriceps 、二頭肌semitendinosus, 和semimembraneous 肌肉小組。
4 。 快速的twitch 蛋白質出現在慢twitch 肌肉纖維表明這些纖維生物化學的轉換。
對鉗製的韌帶變動:
1 。 壓力的減輕是損傷的對膠原和韌帶機械, 生物化學和結構物產。從事五個星期大主教膝蓋的鉗製, 有在最大載荷的39% 減退對失敗(Noyes) 。
2 。 對兔子股骨韌帶脛骨模型的壓力的減輕導致了在裝載的69% 減退對失敗
(求愛 等。) 。
軟骨變動聯繫了被減少的重量軸承和鉗製:
1 。 鉗製創造退化變化在關節軟骨上。那裡對軟骨的proteoglycan 內容, 變薄軟骨, subchondral 骨頭減退在proteoglycan 生產, 和損失的逐漸減少。肢體的鉗製在引伸導致增加的肌肉收縮和改變相似與那些被看見在osteoarthritic 軟骨包括osteophyte 軟骨的形成、原纖維形成作用, 關節軟骨點蝕, 和侵蝕。
骨頭變動聯繫了鉗製和不用:
1 。 鉗製起因減少了骨頭形成, 增加的骨頭吸收並且trabecular 骨頭比表皮骨頭受影響的。鉗製的作用是最發出音的在末端骨頭。
2 。 鉗製(反應階段):
a 。   Stage 1: 六個星期鉗製, 快的損失以近的充分的補救需要8.12 星期。
b 。   Stage 2: 12.32 星期鉗製更加緩慢的損失但更長的補救。
c 。   Stage 3: 大於32 個星期鉗製損失被維護在30.50% 法線。
創傷癒合
那些介入PTH 必須是創傷癒合的學生。例如, 它重要知道, 腱被服從對外科修理只有40% 他們的抗拉強度在四個月。讀者提到標準文本為關於創傷癒合的世俗方面的一次詳細討論。它重要, PTH 活動平行創傷力量的承購在鉗製和癒合的期間。
PTH 形式
當前被使用在獸醫PTH 的形式包括治療超聲波、neuromuscular 刺激、cryotherapy, 熱療法、按摩、治療鍛煉、水生療法, 和行動活動的被動範圍。每個這些形式將被談論在介紹的演講部份。
超聲波
治療超聲波是一種常用的形式在PTH 和被顯示在臨床和科學試驗增加膠原延伸性, 提高膠原改造, 提高膠原生產, 增量熱在深組織, 增量血流, 增量範圍行動, 減少痛苦和肌肉痙孿, 和加速創傷癒合。治療超聲波由應用導致電流通過壓電水晶導致它振動以它的共鳴頻率。水晶起因壓力波浪散發和這些的這些動擺由組織隨後吸收。二個最常用的美國頻率是1.0 兆赫和3.3 兆赫。1 兆赫深深地擊穿和被使用為熱化組織從2.5 cm 詳細。3.3 兆赫頭被使用加熱組織對深度的1.2 cm 。以3.3 兆赫頂頭最大熱引起在2 cm 水平。在許多情況下, 時間組織溫度依然是舉起是短的(在10 分鐘內) 。
美國的熱量作用有:
1 。   組織的增加的新陳代謝率。
2 。   增加的血液和淋巴流程。
3 。   膠原組織(腱、傷痕、肌肉鞘、聯合膠囊, 韌帶的) 增加的延伸性。
4 。   被減少的痛苦和肌肉痙孿。
美國的non-thermal 作用是:
1 。   增加的細胞擴散和細胞膜滲透性。
2 。   膠原和脯胺酸的增加的生產。
3 。   增加的成纖維細胞擴散和活動增量堵嘴綜合。
劑量
美國能量被提供每單位區間的率用Watts/cm 2被表達。強度1.2 W/cm2 被使用在有很多肌肉的區域(譬如大腿) 並且較少強度被使用為其它區域(0.5.1.0 W/cm2) 。連續的美國最好被使用加熱組織, 並且如果可利用, 搏動的交付被使用當美國的non-thermal 作用渴望。
聯結代理
聯結代理是需要的連接美國頭以皮膚為了最大化美國能量的調動在上面組織。水溶膠凝體是適當的。
治療時間和頻率
它重要, 頭髮是被截去的渴望的治療區域。Steiss 表示, 頭髮出現干涉美國能量的吸收並且它是可能燒皮膚如果這不做, 此外頭髮吸收美國能量並且一點對熱化更深的組織是可利用的。時間必要對待區域取決於治療區域的大小和變換裝置頭的大小。你可能估計多少變換裝置頭適合入治療區域並且為每二個頭允許五分鐘。我們典型地做日報或每隔一天治療。
電子刺激
對電子刺激的用途刺激一根周邊神經導致渴望的作用叫做neuromuscular 刺激。電子刺激是一種常用的形式在PTH 和被顯示有效在:
1 。   增長的肌肉力量。
2 。   改進肌肉緊張。
3 。   行動的增長的範圍。
4 。   鎮痛。
5 。   肌肉re-education 。
6 。   減少肌肉痙孿。
當前的型
AC 潮流是常用為肌肉刺激和reeducation 被提供在一個搏動的格式。中頻polyphasic 潮流叫做Russian 刺激。設備被連接到患者通過對或更多電極。他們應該是靈活, 提議低抵抗, 和也許被整理對風俗適合他們將被使用的身體部位。
治療參量
高度是當前的信號波形的大小。舷梯是時候從一開始階段的增加在高度從零的當前的基礎線對高峰高度。信號波形, 搏動的潮流的視覺表示法的形狀, 可能是對稱, 不對稱, 平衡, 失衡, monophasic, 或polyphasic 。頻率, 動擺的率在cycle/second, 被表示為pulses/sec. 開關時間, 表明時間刺激品提供潮流與休眠期比較在收縮之間。
當前的參量為加強:
Millis 和Levine 推薦25.50Hz/sec 頻率以biphasic 信號波形以150.250 微秒的脈衝期間以2.4 秒舷梯時光。
治療鍛煉
所有形式被使用在似犬物理療法, 治療鍛煉經常是最有效的在費用和成就。治療鍛煉(TE) 可能被運用在每個診所和它的用途和實施由one.s 想像力只限制。TE 可能使用保存ROM 和肌肉大量和向醫治用的組織挑戰在補救期間。
一個重要因素承認是需要匹配具體injury/and 或外科修理以適當的鍛煉。我們知道從clinical/research 資料在動物和人中, 隨後而來的頭蓋骨cruciate loss/repair quadriceps 、二頭肌和semimembranosus 去下重大萎縮。當開發一個TE 計劃為一名手術後cruciate 患者, 我們具體地集中這些肌肉。在人, 能力達到膝蓋的充分的引伸是一個渴望的終點, 然而, 由於dog.s 膝蓋, 這的功能角度較不重要。
下面被列出手術後cruciate 修理TE 鍛煉:
1 。   Sit/stand 。
2 。   角落立場。
3 。   8/circle 步行圖。
4 。   輪子置入筒。
5 。   E-stim 。hamstrings/quads 。
6 。   腿筋, 方形字體U.S./stretching 。
7 。   最初的decline 踏車被斜面踏車隨後了而來。
8 。   腿重量。
9 。   proprioception.unbalancing 的改進。

There is a lot of interest in canine physical therapy and rehabilitation and courses are being offered at many of the major meetings. There is one certification process in motion, which will be sanctioned by several universities, and active canine physical therapy-related research is happening. What has triggered this interest?
There are several factors to consider:
1.   Public demand.
2.   Emergence of the working dog; with need to return to previous level of activity.
3.   Demonstrated efficacy in other species (man).
4.   Increased sophistication in veterinary surgery.
5.   Animals are living longer.
6.   Adds value to veterinary services.
7.   Potential source of veterinary income.
8.   Rewarding to veterinary staff, owner and animal.
In the recent past, there was little attention paid to post operative care and many animals were lost to follow-up following suture removal. This, coupled with the notion that the animal would use the limb when it felt 孄ood?and the reluctance on the part of veterinarians to urge early mobility, were factors that limited the use and concept of physical therapy. In spite of recent advances, there are still veterinary surgeons that routinely immobilize their post-operative cruciate patients for four to six weeks, and this is often done with casts, braces, or splints. Early motion has been shown to be efficacious in hastening recovery and limiting the effects of disuse on bone, cartilage, periarticular soft tissue, ligaments, and tendons.
The goal of physical therapy and rehabilitation is to return the affected part and the animal to full function. We first began our Physical Therapy and Rehabilitation (PTH) program working with racing Greyhounds. Owners and trainers were reluctant to invest the time and money to allow us to repair their injuries unless we could insure that they would return to the track and perform at their previous level or better. While we were not always successful, we learned the value of early and appropriate PTH.
One current challenge is to prove that PTH is as meritorious in the dog as it has been in man. There are many studies done in man demonstrating the value of PTH on earlier recovery, resumption of lifestyle, return to athleticism, and enhanced quality of life. There have been studies in animals, notably Johnson𠏋 work on early use of electrostimulation; Levine and Millis?work on goniometry, range of motion and ultrasound; Steiss on ultrasound; Adamson on photon therapy and the underwater treadmill; to mention only a few. The recent interest will only stimulate new areas of investigation and research.
PTH measures should be included in every post-surgical plan. The benefits of PTH include:
1.   Increased blood flow and lymphatic drainage to the injured area.
2.   Early resolution of inflammation.
3.   Increased production of collagen.
4.   Prevention of periarticular contractions.
5.   Promotion of normal joint homeostasis.
6.   Promotion of normal joint biomechanics.
7.   Prevention or minimize muscle atrophy.
8.   Positive psychological effects for the animal and owner.
There are two distinct intervals in the recovery process where PTH can be useful to facilitate full post-surgical recovery and return to function. For every one patient recovering from a traumatic injury and/or surgery there are ten patients who could benefit from PTH and these patients include those with obesity, degenerative joint disease, tissue atrophy and residual neurologic disease. For purposes of this paper, we will address the needs of the post trauma/surgery patient.
PHASE ONE
Phase 1 activities begin the day of surgery and typically involve icing, passive range of motion, and early wound mobilization. This period begins with the traumatic injury and or surgery and encompasses the inflammatory phase and early wound healing that occurs in the first three to four weeks. The goal of PTH during this time is to minimize inflammation and pain, preserve joint range of motion, and to prevent or further minimize muscle and soft tissue atrophy.
PHASE TWO
Phase 2 activities begin as inflammation is resolving and healing begins to be the predominate theme in the wound. It is very important to combine phase two activities with the temporal aspects of wound healing. By that, we mean applying appropriate stresses to healing tissues so as to optimize their healing but not so much that the biomechanical stability is threatened. Ideally, the phase two activities should parallel the gradual increase in tensile strength observed in the wound. If one is too aggressive with PTH during this period, failure can occur; conversely, if one lags in PTH activities, the goal of early return to function is not accomplished.
RESPONSE OF CONNECTIVE TISSUES TO DISUSE AND IMMOBILIZATION
In order to better understand the needs of PTH during recovery it is appropriate to understand the way connective tissues respond to immobilization and disuse.
Skeletal muscle changes from reduced weight bearing and loading:
1. Type 1 muscle fiber and muscles with a large population of type 1 fibers show perpetual atrophy. These include the extensor muscles and the antigravity muscles.
2. The loss of muscle strength is caused by not only atrophy but biochemical changes in the sarcoplasmic reticulum.
3. Normal dogs undergoing surgical transaction of the cranial cruciate ligament and immediate stabilization undergo early atrophy of the affected limb muscles, which continues for at least five weeks. The atrophy is most significant in the quadriceps, biceps semitendinosus, and semimembraneous muscle groups.
4. The presence of fast twitch proteins in slow twitch muscle fibers indicating a biochemical conversion of these fibers.
Ligament changes to immobilization:
1. Stress reduction is detrimental to the mechanical, biochemical and structural properties of collagen and ligaments. Following five weeks of immobilization of the knee of primates, there was a 39% decrease in maximum load to failure (Noyes).
2. Stress reduction in a rabbit femur ligament tibia model produced a 69% decrease in load to failure
(Woo et al.).
Cartilage changes associated with reduced weight bearing and immobilization:
1. Immobilization creates degenerative changes in the articular cartilage. There a gradual reduction in proteoglycan content of the cartilage, thinning of cartilage, a decrease in proteoglycan production, and loss of subchondral bone. Immobilization of a limb in extension results in increased muscle contraction and changes similar to those seen in osteoarthritic cartilage including osteophyte formation, fibrillation of cartilage, pitting, and erosion of articular cartilage.
Bone changes associated with immobilization and disuse:
1. Immobilization causes decreased bone formation, increased bone absorption and trabecular bone is more affected than cortical bone. The effects of immobilization are most pronounced on distal bones.
2. Immobilization (stages of response):
a.   䒷tage 1: six weeks of immobilization, quick loss with near full recovery requiring 8?2 weeks.
b.   䒷tage 2: 12?2 weeks of immobilization slower loss but longer recovery.
c.   䒷tage 3: Greater than 32 weeks of immobilization loss maintained at 30?0% of normal.
WOUND HEALING
Those involved in PTH must be students of wound healing. For example, it is important to know that tendons subjected to surgical repair only have 40% of their tensile strength at four months. The reader is referred to a standard text for a more in-depth discussion of the temporal aspects of wound healing. It is important that the PTH activities parallel the acquisition of wound strength during the period of immobilization and healing.
PTH Modalities
Modalities that are currently used in veterinary PTH include therapeutic ultrasound, neuromuscular stimulation, cryotherapy, heat therapy, massage, therapeutic exercise, aquatic therapy, and passive range of motion activity. Each of these modalities will be discussed in the lecture portion of the presentation.
Ultrasound
Therapeutic ultrasound is a commonly used modality in PTH and has been shown in clinical and scientific trials to increase collagen extensibility, enhance collagen remodeling, enhance collagen production, increase heat in deep tissues, increase blood flow, increase range of motion, reduce pain and muscle spasm, and accelerate wound healing. Therapeutic ultrasound is produced by applying an electric current through a piezoelectric crystal causing it to vibrate at its resonance frequency. These oscillations of the crystal cause pressure waves to be emitted and these are subsequently absorbed by the tissues. The two most commonly used US frequencies are 1.0 MHz and 3.3 MHz. The 1 MHz penetrates more deeply and is used for heating tissues from 2? cm in depth. The 3.3 MHz head is used to heat tissues to a depth of 1? cm. With the 3.3 MHz head maximum heat is generated at the 2 cm level. In most cases, the amount of time tissue temperatures remain elevated is short (within 10 minutes).
The thermal effects of US include:
1.   Increased metabolic rate of tissues.
2.   Increased blood and lymphatic flow.
3.   Increased extensibility of collagenous tissues (tendons, scars, muscle sheaths, joint capsules, ligaments).
4.   Decreased pain and muscle spasm.
The non-thermal effects of US are:
1.   Increased cell diffusion and cell membrane permeability.
2.   Increased production of collagen and hydroxyproline.
3.   Increased fibroblast proliferation and activity increases GAG synthesis.
Dosage
The rate at which the US energy is delivered per unit area is expressed in Watts/cm2. Intensities of 1? W/cm2 are used in areas that have a lot of muscle (such as the thigh) and less intensity is used for other areas (0.5?.0 W/cm2). Continuous US is best used to heat tissues, and if available, the pulsed delivery is used when the non-thermal effects of US are desired.
Coupling Agent
A coupling agent is needed to connect the US head with the skin in order to maximize transfer of the US energy in top the tissues. Water-soluble gels are advisable.
Treatment time and frequency
It is important that the hair be clipped over the desired treatment area. Steiss has shown that the presence of hair interferes with the absorption of the US energy and it is possible to burn the skin if this is not done, furthermore the hair absorbs the US energy and little is available to heating deeper tissues. The time necessary to treat an area depends on the size of the treatment area and the size of the transducer head. One can estimate how many transducer heads fit into the treatment area and for every two heads allow five minutes. We typically do daily or every other day treatments.
Electrical stimulation
The use of electrical stimulation to stimulate a peripheral nerve to cause the desired effect is called neuromuscular stimulation. Electrical stimulation is a commonly used modality in PTH and been shown efficacious in:
1.   Increasing muscle strength.
2.   Improving muscle tone.
3.   Increasing range of motion.
4.   Pain relief.
5.   Muscle re-education.
6.   Reducing muscle spasms.

minibabyqq 2007-1-26 02:02

[color=Magenta][size=5][b]令人沮喪脊髓疾病 Frustrating Spinal Diseases  [/b][/size][/color]


動物也許提出以介入脊椎或脊髓的各種各樣的疾病。經常, 臨床標誌和診斷評估允許一個具體診斷被做。這最後導致達到臨床標誌的決議的一個適當的治療計劃。動物的某一百分比, 然而, 有難診斷的脊髓疾病, 誤診, 難對待, 或惡劣敏感對可利用的治療。這些箱子可能挫敗為獸醫和所有者。這些疾病被談論在這兒重點放在澄清臨床診斷和計劃對適當的治療。
椎間的盤疾病
椎間的盤疾病(IVD) 依然是脊髓疾病的同道會。就頻率而論, IVD 遇到在臨床實踐, 它是驚奇, 許多診斷和治療的方面為這種疾病是有爭議的。這是適當, 一部分, 對不精確的診斷, 殘缺不全的診斷, 和粗劣的客觀後續評估在治療結果。臨床範圍IVD 變化和是唯一正義起點被澄清的歸結於增加使用橫向(先生或CT) 診斷想像。
二基本的類型椎間的盤疾病被描述; 但是, Hansen.s 分類計劃不反射範圍解剖和pathophysiologic 變動遇到。椎間的盤也許, 和偶爾地擠壓中堅力量anulus 纖維變性的pulposis 或片段, 入脊髓。椎間的盤材料也許來腹上, 側向地, 和背部地說謊對脊髓。例如, 椎間的盤材料也許側向地擠壓從盤, 和遇到和衝擊在退出周邊神經。這後者綜合症狀導致痛苦作為早先認出的主要怨言和是更加共同。
創造一種診斷困境, 一些狗以也許對臨床標誌的盤疾病(特別是Hansen.s 類型Ii) 並且有部下的主要脊髓疾病(即, 退化myelopathy) (多個疾病過程) 貢獻。這些部下的疾病也許有對結果的重大影響跟隨手術。
異常疾病
反常現象介入脊髓或椎骨專欄也許起因於神經系統的管的反常發展。脊髓dysraphism 組分包括脊柱裂(椎骨曲拱的瑕疵融合), meningocele (meninges 伸進通過瑕疵), myelocele (脊髓伸進通過瑕疵), 和meningomyelocele (meninges 和脊髓伸進) 。偶爾地, intramedullary 瑕疵譬如水力發電或syringomyelia 也許伴隨這些其它更加明顯的瑕疵(進一步參見) 。
脊椎的多數先天疾病被認可及早在生活中。偶爾地, 然而, 先天椎骨或脊髓瑕疵不導致脊髓反常性直到成年或以後。這些intraspinal 囊狀反常性也許被錯過與定期myelography 。Intraspinal 反常性經常被發現使用CT/myelography 或想像先生。
這些疾病可能挫敗對待部下的解剖反常性不能是反演性的。另外, 其它部下的疾病可能是當前併發以這些先天不足使準確診斷程度脊髓反常性必要。

Syringomyelia 和hydromyelia
所有intraspinal 繩子反常性, syringomyelia 和hydromyelia 是最流行。Syringomyelia 和hydromyelia 是脊髓的囊狀反常性。Syringomyelia 提到反常洞用液體被填裝內在脊髓的物質。syrinx. 提到這些洞的當中一個。Hydromyelia 提到一個病理性情況為流體的儲積描繪在脊髓的一條擴大的中央運河之內。在這兩個事例, 積累的流體是相似, 如果不相同, 與腦脊髓流體(CSF) 。
導致syringomyelia 和hydromyelia 的病理性機制是多。囊腫形成可能的致病性機制包括脊髓柔膜組織變化在CSF 壓力關係上在脊髓之內(和發生以腦水腫或孔大酒瓶反常性), 中央運河的損失, 狹窄, 和阻礙對CSF 流程通過炎症或腫瘤。每個這些機制是可能的在狗和貓但有明確地被證明。
不聯絡與中央運河的Syrinxes (extracanalicular syrinxes) 在任何水平經常被獲取的歸結於脊髓傷害或損傷從疾病(出血和炎症) 。這些syrinxes 傾向於發生在中央灰色問題或背部和側向白色問題, 可能伴生以變化在血管發行(watershed 區域上) 。其它syringo-/hydromyelia 的重要起因在人是反常CSF 動力學在第四個ventricle/foramen 大酒瓶區域的水平。反常pressure/fluid 動力學也許然後導致脊髓中央運河的氣蝕或擴張。提出的解釋為這包括CSF 的動脈脈動與壓力波浪被傳送對子宮頸繩子和增加的CSF 壓力造成CSF transmedullary 段落從中央運河和硬膜外空間入脊髓柔膜組織。CSF 流程的阻礙從頭蓋骨對脊髓也許導致衝擊脊髓的壓力差別。增加的或有差別的CSF 壓力在脊髓之內也許導致血管妥協對繩子, 削弱多血脈性的排水設備, 和預先處理對parenchymal 損傷。
Hydromyelia 經常同腦水腫聯繫在一起在人。 這很少被報告了在狗, 但是可能的在認出之下。在一個實驗性hydrocephalic 模型在狗, 它被顯示, 以增加的室內的壓力有在壓力的增量在syrinx 洞之內。
人的最近研究以後部窩反常性(指Chiari 畸形), 表示, CSF 的disequilibration 和運動從顱內對脊髓蜘蛛網膜下的空間也許是部下的因素在使永存syringomyelia 。如果孔大酒瓶被阻礙的歸結於後腦的尾部位移, CSF 無法行動或者方向。腦脊髓流體, 無法留出顱內的空間在收縮期間, 導致增加的顱內的壓力。在壓力的脈搏增量被傳送在脊髓下和看來是一個重要因素在使syrinx 洞永存。腦脊髓流體也許進入syrinx 由syrinx 的多微觀連接與蜘蛛網膜下的空間。這些過份壓力脈動逆轉發生在decompressive 手術(craniectomy 和durotomy) 孔大酒瓶以後。
這些畸形頻繁地同腦水腫聯繫在一起並且syringo-/hydromyelias 一致地共同地遇到。CSF 流程的阻礙在孔大酒瓶似乎是這兩種病理變化主要機制。相似的反常性也許發生在狗和其它動物。其它反常性造成腦水腫和一個膨脹的第四個心室也許並且同syringomyelia 聯繫在一起。花花公子步行者綜合症狀在人是一個這樣的例子。以這種疾病, 有後腦的畸形造成a 囊腫像反常性在後腦。側向和第三個心室一致地共同地膨脹。這是一個先天問題被承擔同反常胚胎形成聯繫在一起。相似的綜合症狀的例子被描述了在狗和其它動物。脊髓反常性未被描述, 然而, 受影響的動物脊髓不可以病理性地被審查了。有趣的是, 一定數量的狗和人與syringomyelia 同脊柱側凸聯繫在一起。
syringomelia 診斷可能是困難的, 因為反常性經常不是明顯的跟隨定期myelography 。以腰部射入, 它是有時可能用對比媒介填裝中央運河, 使hydromyelia 明顯。這是對比媒介不填裝syringo-/hydromyelic 洞的inconsistent.if, myelography 也許是正常的或顯示唯一膨脹的脊髓。
其它想像研究, 譬如CT 或磁共振想像先生經常是有用的在建立診斷。磁共振圖像也許好比CT 為定義intraparenchymal 脊髓反常性。
在人, 頭蓋骨子宮頸syringomyelia 的治療有或沒有尾部窩反常性依然是有爭議。被使用了的外科方法包括切開(解壓) syrinx 通過myelotomy, 後部窩解壓通過一suboccipital craniectomy 和伴生的子宮頸椎骨laminectomy, 和syringosubarachnoid 轉軌。在一個報告比較後者二規程, 區別未被發現在耐心小組之間以兩規程是相等地有效的在導致syrinx 崩潰。進一步覆蓋問題, 一些syrinxes 自發地退步了, 造成一些作者對手術表示懷疑的角色作為治療為這個問題。 另外, 直接syrinx 排水設備沒有轉軌, 也許並且是有用的是一些事例。
類型病理學禮物影響治療反應。人的患者與hydromyelia 與腦水腫有關係也許可能受益於ventriculoperitoneal 轉軌, 但是那些與不聯絡與第四個心室的hydromyelia, 不可以。不聯絡與第四個心室的Extracanalicular syrinxes 也許要求直接轉軌。另外, 當這類型syrinx 經常導致對脊髓短文的不可逆的損傷, 整體治療反應不能是一樣有利的像與hydromyelia 。
Wobbler 的綜合症狀
Wobbler.s 綜合症狀包含一定數量的子宮頸椎骨反常性。這些包括椎骨malarticulation/malformation 、盤擠壓、關節小平面肥大, 和韌帶肥大。二類型Wobbler.s 綜合症狀存在。一個人由疾病為尾部子宮頸區域腹壓縮損害描繪從ligamentous 肥大和盤的更舊的Doberman pinschers 舉例證明(通常anulus) 伸進。更加幼小, 大養殖狗譬如了不起的丹麥人, 有一種相似地名為疾病, 但以不同的病理生理學。在這種場合, 背部關節小平面的疾病預先處理對伴生的聯合膠囊和韌帶的肥大, 並且導致脊髓壓縮。相似類型壓縮是罕見的在更舊的狗。
Medical 治療, 包括鍛煉制約, 鎮痛藥, 和corticosteriods, 經常是不充分控制臨床標誌。疾病的一定數量的外科技術被描述了, 建議, 技術不是充分的。這歸結於導致這些疾病對病理生理的機制的相對地粗劣的理解。許多狗有短命的改善跟隨手術, 只有有臨床標誌再現在六個月到一年之內。總之, 許多更舊的狗與腹損害有靜止並且一個動態壓縮組分對他們的疾病。它以及安定外科治療也許被擔保然後似乎合理, 那decompressive 。
在更加幼小, 大狗以背部關節小平面疾病, 一個背部decompressive 做法是適當的。伴生的關節小平面的融合似乎最有利在我們的醫院為長期改善在手術以後。這個小組狗傾向於有更好的長期結果與更舊的狗比較與腹壓縮疾病。在更舊的小組狗, 背部不穩定和聯接失敗對疾病的病理生理學很可能貢獻。不幸地, 當疾病被認可的時候, 腹壓縮是足夠嚴厲的, 脖子的背部引伸導致惡化脊髓壓縮。這動態惡化經常阻止背部定像在引伸。如果, 然而, 疾病能被認可在它的早期, 背部融合也許是有利的在減少疾病的進步。
Lumbosacral 疾病
Lumbosacral 疾病可能提出作為一種診斷困境, 因為這種疾病的臨床標誌也許仿造一定數量的骨盆肢體musculoskeletal 情況。臨床標誌包括痛苦在LS 地區, 糞便並且/或者泌尿無節制的觸診背, 並且更低的馬達神經元(LMN) 簽到骨盆肢體(臀部的區域) 。骨盆肢體震顫也許反射弱點或痛苦。一個痛苦的反應也許看以LS 聯接的背部引伸, 然而, 能也被看見以hip 發育異常。它重要palpate LS 地區當動物側向地recumbent, 因為壓力被安置這裡在一個常設動物與, 例如, coxofemoral 聯合疾病, 也許並且導致痛苦。對壓力的這個痛苦的反應分佈了雖然coxofemoral 區域也許是誤譯在LS 關節痛。一次數字式直腸考試並且被擔保排除intrapelvic 大量。
診斷根據神經壓縮的文獻通過myelography 、epidurography 、diskography 、CT, 或研究先生。dural sac 有時將終止尾部對LS 聯接在更大的狗, 並且壓縮在這個區域也許看與myelography 。Myelography 是還有用排除lumbosacral intumescence 的脊髓損害。由於有經常唯一神經根壓縮以這種疾病, 然而, 這個區域的myelographic 研究充分地不會提供這壓縮。
先進的想像形式(CT 先生) 有提供LS 聯接的一個橫向看法好處, 允許退出神經對foraminal 區域的評估經常是壓縮的。腦脊髓流體分析通常不是有用的, 因為脊髓適當終止了頭蓋骨對壓縮的水平。骨盆肢體和尾巴的肌動電流術(EMG) 並且神經傳導(NCV) 研究也許顯露自發活動一致與去除神經支配或緩慢的傳導速度, 各自地。當這些變動不是具體的為神經壓縮, 這些研究的反常結果趨向對牽連了LMN 疾病作為臨床標誌的起因。
治療介入這個區域的外科解壓並且/或者安定。共同地, 背部laminectomy 和解壓使用釋放被坑害的神經在LS 地區。更加無定論的是對這個區域的外科安定的需要。在我們的經驗, 然而, 不穩定在這聯接對這個區域的退化貢獻, 也許導致臨床標誌再現。因此, 我們決定穩定LS 聯合隨後而來的解壓希望更加迅速地改進臨床標誌和減少再現風險。

Animals may present with a variety of diseases that involve the spine or spinal cord. Often, the clinical signs and diagnostic evaluation allows a specific diagnosis to be made. This ultimately leads to an appropriate treatment plan that brings about resolution of the clinical signs. A certain percentage of animals, however, have spinal diseases that are difficult to diagnose, misdiagnosed, difficult to treat, or poorly responsive to available treatments. These cases can be frustrating for both the veterinarian and owner alike. Some of these diseases are discussed here with an emphasis on clarifying clinical diagnosis and planning for proper treatment.
Intervertebral Disk Disease
Intervertebral disk disease (IVD) remains a common cause of spinal disease. Considering the frequency that IVD is encountered in clinical practice, it is surprising that many aspects of diagnosis and treatment for this disease are controversial. This is due, in part, to inaccurate diagnoses, incomplete diagnoses, and poor objective follow-up evaluations on treatment outcomes. The clinical spectrum of IVD is varied and is only just beginning to be clarified due to increased used of transverse (MR or CT) diagnostic imaging.
Two basic types of intervertebral disk disease are described; however, Hansen𠏋 classification scheme does not reflect the scope of anatomical and pathophysiologic changes encountered. Intervertebral disks may extrude nucleus pulposis or fragments of anulus fibrosis around, and occasionally, into the spinal cord. Intervertebral disk material may come to lie ventrally, laterally, and dorsally to the spinal cord. In some instances, intervertebral disk material may extrude laterally from the disk, and encounter and impinge upon exiting peripheral nerves. This latter syndrome results in pain as a primary complaint and is more common that previously recognized.
Creating a diagnostic dilemma, some dogs with disk disease (especially Hansen𠏋 Type II) also have underlying primary spinal cord disease (e.g., degenerative myelopathy) that may contribute to the clinical signs (multiple disease processes). These underlying diseases may have a significant influence on outcomes following surgery.
Anomalous Diseases
Anomalies involving the spinal cord or vertebral column may result from abnormal development of the neural tube. Components of spinal dysraphism include spina bifida (defective fusion of the vertebral arch), meningocele (protrusion of meninges through the defect), myelocele (protrusion of spinal cord through the defect), and meningomyelocele (protrusion of both meninges and spinal cord). Occasionally, intramedullary defects such as hydro- or syringomyelia may accompany these other more obvious defects (see further).
Most congenital diseases of the spine are recognized earlier in life. Occasionally, however, congenital vertebral or spinal defects do not result in spinal abnormalities until adulthood or later. Some of these intraspinal cystic abnormalities may be missed with routine myelography. Intraspinal abnormalities are more often found using CT/myelography or MR imaging.
These diseases can be frustrating to treat as underlying anatomical abnormalities may not be reversible. Additionally, other underlying diseases can be present concurrent with these congenital defects making accurate diagnosis of the extent of spinal abnormalities imperative.

Syringomyelia and hydromyelia
Of all of the intraspinal cord abnormalities, syringomyelia and hydromyelia are most prevalent. Syringomyelia and hydromyelia are cystic abnormalities of the spinal cord. Syringomyelia refers to abnormal cavities filled with liquid within in the substance of the spinal cord. A 𦽳yrinx?refers to one of these cavities. Hydromyelia refers to a pathologic condition characterized by accumulation of fluid within an enlarged central canal of the spinal cord. In both of these instances, the fluid that accumulates is similar, if not identical, to cerebrospinal fluid (CSF).
The pathologic mechanisms that result in syringomyelia and hydromyelia are multiple. Possible pathogenic mechanisms of cyst formation include changes in CSF pressure relationships within the spinal cord (as occurs with hydrocephalus or foramen magnum abnormalities), loss of spinal parenchyma, stenosis of the central canal, and obstruction to CSF flow via inflammation or tumor. Each of these mechanisms is possible in dogs and cats but have yet to be definitively proved.
Syrinxes that do not communicate with the central canal (extracanalicular syrinxes) at any level are often acquired due to spinal injury or damage from disease (hemorrhage and inflammation). These syrinxes tend to occur in the central grey matter or dorsal and lateral white matter, possibly associated with changes in vascular distribution (𢘛atershed zones?. Another important cause of syringo-/hydromyelia in humans is abnormal CSF dynamics at the level of the fourth ventricle/foramen magnum area. Abnormal pressure/fluid dynamics may then result in spinal cord cavitation or dilation of the central canal. Proposed explanations for this include arterial pulsation of CSF with pressure waves being transmitted to the cervical cord and increased CSF pressures resulting in transmedullary passage of CSF from the central canal and epidural space into the spinal cord parenchyma. Obstruction of CSF flow from the cranium to the spinal cord may result in pressure differentials that impact the spinal cord. Increased or differential CSF pressures within the spinal cord may result in vascular compromise to the cord, impairing venous drainage, and predispose to parenchymal damage.
Hydromyelia is often associated with hydrocephalus in humans. This has been reported rarely in dogs, but is likely under recognized. In an experimental hydrocephalic model in dogs, it was shown that with increased intraventricular pressure there are increases in pressures within the syrinx cavity.
More recent studies of humans with posterior fossa abnormalities (referred to as Chiari malformations), have shown that disequilibration and movement of CSF from the intracranial to the spinal subarachnoid space may be the underlying factor in perpetuating syringomyelia. If the foramen magnum is obstructed due to caudal displacement of the cerebellum, CSF cannot move in either direction. Cerebrospinal fluid, which cannot leave the intracranial space during systole, causes increased intracranial pressure. The pulsatile increase in pressure is transmitted down the spinal cord and appears to be an important factor in perpetuating the syrinx cavity. Cerebrospinal fluid may enter the syrinx by multiple microscopic connections of the syrinx with the subarachnoid space. Reversal of these excessive pressure pulsations occurs after decompressive surgery (craniectomy and durotomy) of the foramen magnum.
These malformations are frequently associated with hydrocephalus and syringo-/hydromyelias are commonly encountered concurrently. Obstruction of CSF flow at the foramen magnum seems to be the primary mechanism of both of these pathologic changes. Similar abnormalities may occur in dogs and other animals. Other abnormalities resulting in hydrocephalus and a dilated fourth ventricle may also be associated with syringomyelia. The Dandy-Walker syndrome in humans is one such example. With this disease, there is a malformation of the cerebellum resulting in a cyst-like abnormality in the cerebellum. The lateral and third ventricles are commonly dilated concurrently. This is a congenital problem assumed to be associated with abnormal embryogenesis. Examples of a similar syndrome have been described in dogs and other animals. The spinal cord abnormalities have not been described, however, the spinal cords of affected animals may not have been examined pathologically. Interestingly, a number of dogs and humans with syringomyelia have associated scoliosis.
The diagnosis of syringomelia can be difficult, as the abnormality is often not apparent following routine myelography. With lumbar injections, it is sometimes possible to fill the central canal with contrast medium, making a hydromyelia apparent. This is inconsistent𡟙f the contrast medium does not fill the syringo-/hydromyelic cavity, myelography may be normal or show only an expanded spinal cord.
Other imaging studies, such as CT or magnetic resonance MR imaging are often more helpful in establishing a diagnosis. Magnetic resonance imaging may be better than CT for defining intraparenchymal spinal cord abnormalities.
In humans, the treatment of cranial cervical syringomyelia with or without caudal fossa abnormalities remains controversial. Surgical approaches that have been employed include incision (decompression) of the syrinx via myelotomy, posterior fossa decompression via a suboccipital craniectomy and associated cervical vertebral laminectomy, and syringosubarachnoid shunting. In one report comparing the latter two procedures, no difference was found between patient groups with both procedures being equally effective in causing syrinx collapse. Clouding the issue further, some syrinxes have spontaneously regressed, resulting in some authors questioning the role of surgery as treatment for this problem. Additionally, direct syrinx drainage without shunting, may also be helpful is some instances.
The type of pathology present influences treatment responses. Human patients with hydromyelia in association with hydrocephalus may be likely to benefit from ventriculoperitoneal shunting, whereas those with hydromyelia that does not communicate with the fourth ventricle, may not. Extracanalicular syrinxes that do not communicate with the fourth ventricle may require direct shunting. Additionally, as this type of syrinx often results in irreversible damage to spinal tracts, overall treatment responses may not be as favorable as with hydromyelia.

minibabyqq 2007-1-26 02:03

[color=Magenta][size=5][b]Cranio 大腦精神創傷 Cranio-Cerebral Trauma  [/b][/size][/color]


頭部受傷, 有或沒有頭骨破裂, 導致直接主要傷害包括, 如果足夠嚴厲, 船中斷和撕毀或擊碎腦子柔膜組織。如果這主要傷害不是足夠嚴厲的導致直接死亡, 次要傷害的發展在以下小時期間, 包括出血、腫鼓、增加的顱內的壓力(ICP) 並且全部, 局部缺血, 可能。臨床工作者是無能為力的在第一傷害期間; 但是, 通過迅速醫療和外科干預, 他也許減慢或扭轉第二個。
第二個傷害機制
組織局部缺血是也許發生在cranio 大腦精神創傷以後的最毀滅的後果。局部缺血歸結於大腦血流的減少(CBF) 。CBF 減少當ICP 增加沒有動脈血壓的伴隨增廣; CBF 也許並且減少當頭蓋骨多血脈性的流出被削弱由於腫鼓、出血, 或子宮頸精神創傷。ICP 開始增加一旦腦脊髓流體(CSF) 並且血液再分配中間轉換能力各自地由CSF 和腦子血管縮小的重吸收或位移用盡。顱內的灌注章程通常被維護通過血管constriction/dilation 在正常腦子。在被傷害的腦子, 這能力也許丟失。PaCO2, 酸鹼度, 和PaO2 影響cerebro vasculature 的自動調節反應。增加的PaCO2 和hypoxemia, 頻繁研究結果在受損傷的患者, 將導致vasodilatation 和將增加ICP 。局部缺血觸發Cushing 反射, 最後保證在CBF 維護, 由增加系統動脈壓力。ICP 最後將增加也是。
腦子腫鼓是增加的ICP 的來源。血液腦子障礙的創傷中斷解釋它的vasogenic 細胞外組分。血管作用的物質的解放和細胞間的副產物的滲透的作用從死的細胞並且將增加它的發展。腦子腫鼓細胞毒素的細胞內組分起因於反常細胞新陳代謝由局部缺血造成。所有分子鏈式反應駕駛到vasogenic 和更加細胞毒素的腫鼓和更高和更高的顱內的壓力。
耐心評估
Cranio 大腦受損傷的患者經常是multi 受損傷的患者。導氣管明顯必須被檢查因為我們看見高的PaCO2 和低PaO2 增加顱內的壓力。尋找主要胸口精神創傷。
患者然後治療為血液動力學的不穩定並且胃腸洞被估計為器官trauma/rupture (脾臟、膀胱、腎臟獨立小分隊, 等) 。大腦低氧症由於hypovolemia 是罕見的由於壓力自動調節, 除非嚴厲內部出血是存在。
終於, 神經學評估狀態被估計; 這將是每小時。雖然較不機械上不穩定比vertebro 髓心精神創傷, 頭部受傷患者必須是處理了以關心。頭被舉起沒有比30.; 這促進多血脈性和CSF 流出從頭骨。知覺狀態、呼吸的樣式、威脅反應、鼻孔敏感性、pupillary 大小和反射、視覺位置和運動、肢體proprioception, 和骨骼馬達作用必須被評估。
知覺的一個被減少的水平(從壓下對神智不清, 昏迷對昏迷) 建議表皮或brainstem (網狀結締組織的激活的系統) 傷害。預測和治療是不同的; 它是根本迅速地區分一supratentorial 從infratentorial 損害。非對稱在威脅反應, 在鼻孔刺激反應, 或在肢體proprioception 沒有其它頭蓋骨神經缺乏, 是傾向於對側半球損害。Stuporous brainstem 被傷害的患者, 顯示多根頭蓋骨神經II 到XII 缺乏, 有一種被守衛的預測。
如果胸口精神創傷未被辨認, 反常性在呼吸樣式是或新陳代謝(酸中毒, 低氧症) 或神經學起源(mesencephalic, 腦乾, 子宮頸) 。apnea 疊更(Cheyne 衝程呼吸作用的) 換氣過度和期間是次要對diencephalic 被減少的PaCO2 快速響應。當腦乾嚴厲地被損壞, 呼吸樣式變得不規則在率和高度和同心跳緩慢聯繫在一起。
伸張機堅硬是UMN 介紹的形式。如果所有四肢體是延長的, 兩個半球是包含的(decerebrate 堅硬); 知覺被修改但PLR 是正常的如果herniation 不是考慮。如果forelimbs 被屈曲並且後方肢體被延伸, 後腦是包含的(decerebellate 堅硬); 知覺被保存但威脅反應也許丟失。
增加的ICP 必須被懷疑當PLR 是反常(或惡化往non-responsive 中等長度範圍或膨脹的學生) 與知覺、伸張機堅硬, 和反常呼吸樣式的惡化平行。指揮雙邊無答復的學生, 對稱或不是, 表明brainstem 傷害。轉折從myosis 到mydriasis 建議一進步損害經常次要次級tentorial occipital herniation 。Pupillary 痲痺歸結於圓鼓的腦子的背部壓力在oculomotor 神經。
Petrosal 骨頭和內耳傷導致也許連續是印象深刻的以動物輾壓在他的邊的周邊或中央前庭標誌。神經學檢查在這些患者最初地是困難的。Proprioception 缺乏在一邊地方化損害對ipsilateral 中央前庭系統。
診斷器械
頭骨射線照相難讀。但是, 破裂線或位移必須被尋找。小腦的傷害與相關occipital 骨頭fracture/displacement 由側向射線照相容易地形象化。這類型精神創傷導致主要不整齊但有一種好預測有或沒有手術。
計算Tomodensitometry (CT) 顯示頭骨破裂和haematomas 。在三個到六個小時以後, 一深刻梗塞導致一個hypodense 區域次要對腫鼓。最大的作用看在三到五天以後。但是, 一些梗塞也許是isodense 和可看見的在對比改進之後在24 到48 個小時以後, 在一個到二個星期以後由於neovascularization 。在二個到三個星期以後, 腫鼓決心和損害成為isodense 。在四個到八個星期以後, 壞死創造氣蝕以密度緊挨腦脊髓流體(CSF) 。Subdural haematomas 不能是一樣罕見的像最初被報告在獸醫文學。圖像密度立刻被減少, 在幾天以後當凝塊組織。Haematomas 成為isodense 在一個月以後。
磁共振圖像(MRI) 是適當的為腦子局部缺血和腫鼓評估。早期的變動是可發現的: hypointense 在T1 衡量了圖像和hyperintense 在T2 裡。順磁的改進與tomodensitometry 是相同的。在出血的情況下, 圖像強度依靠關於血紅蛋白內容和形式(oxy, desoxy 、methemoglobin 、hemochrome, hemosiderin), 它的地點內部或額外erythrocytic, 和圖像的重量。磁共振血管學是做血管學一個非侵入性的方式。CT 和MRI 是適當估計增加的ICP 的間接midline 的標誌由心室的壓縮或非對稱和轉移。
Brainstem 聽覺被召喚的反應(BAER) 是有趣證實petrosal 骨頭或middle/internal 耳朵傷通常與相關前庭標誌。反常結果也許表明需要對於CT 。以ICP 增量, BAER 顯示反演性被減少的高度和增加的潛在因素。這個測試也許有價值預斷。切片檢查法, 外科或超聲波被引導, 允許一個最後的診斷被做。
治療
治療被修改根據神經學狀態、神經學標誌和他們的變動隨時間。一個目標將對待腫鼓。當vasogenic 腫鼓對療法, 細胞毒素的腫鼓是敏感, 一旦創始, 不是。治療因而被指揮在防止局部缺血的創作和減少它的程度和期間由已經工作與藥物在vasogenic 腫鼓禮物和使細胞毒素的腫鼓減到最小來。
雖然hypovolemic 震動不是腦子局部缺血的直接緣由, hypovolemia 減少腦子血流。張力亢進鹽(7.5% NaCl, 35 ml/Kg) 是選擇的解答恢復volemia 。它改進心輸出量, 恢復系統血壓和有一個輕微的脫水的作用在腦組織。膠體(羥乙基澱粉和葡聚糖, 20 ml/Kg) 然後被使用維護血管內的容量。中央血管壓力被監測。
其次, 它是根本保證hypocapnia 和好O2 交付(Pa O2 > 80 mmHg) 。血碳酸過多症(Pa 二氧化碳> 40 毫米百克) 並且低氧症導致vasodilatation, 增加ICP 。插管法是必要的如果患者是不自覺的。氧氣由氧氣籠子交付由鼻導尿管或必須被提供如果患者不是。雖然有效在減少ICP, 進取的換氣過度也許加重低氧症由於過份血管縮小, 也許惡化焦點局部缺血和腫鼓。
第三, 對甘露醇的用途是共同的步在頭蓋骨精神創傷。甘露醇是脫水大腦interstitium 的一個hyperosmolar 分子, 降低ICP 。甘露醇並且減少血液黏度, 促進大腦灌注; 它並且有自由基限制有害分子小瀑布被局部缺血導致的淨化劑能力。在可變的復活以後, 反彈作用的風險對ICP 的減到最小。甘露醇也許理論上是損傷的在活躍靈菌案件或血液腦子障礙的嚴厲破裂, 然而, 這未被證明。想像是唯一的方式查出出血或大腫鼓。但是, 想像設施總不是可利用的。你應該考慮如果患者惡化以時間, 甘露醇是最佳的選擇扭轉過程。被推薦的劑量是0.5 對1g/Kg 20.30 分鐘IV 。它將有一個更長的有利作用如果給在0.25 0.5g/Kg 60 分鐘15 分鐘0.7 mg/Kg 以後potentialized 與furosemide IV,; 但是, 這也許導致更加嚴肅的hyperosmolarity, 也許加重反彈作用。
ICP 測量需要硬膜外, 蜘蛛網膜下或室內的流體被填裝的導尿管和壓力傳感器。監視必要ICP 是無定論的(風險、費用、興趣, 等) 。這大概是一個間接方式監測神經學狀態當患者是昏迷的, 或鎮靜或麻醉必需並且神經學狀態無法不同地被評估。Oxymetry 、腦波記錄儀, 和transcranial 多譜勒儀sonography 被使用在人的醫學。
甲醇prednisolone 協議作為一種自由基淨化劑不被使用在頭部受傷患者。經典corticotherapy 主要使用在neuro 腫瘤學方面對待vasogenic 腫鼓不是有用的反對細胞毒素的腫鼓遇到在第二種傷害類型。副作用不是微不足道的: 他們傾向 糖質新生和維護一個hyperglycemic 狀態知道是有害的。他們傾向嫌氣性細菌新陳代謝和增加穀氨酸水平和神經細胞的死亡。GI 副作用是還重要在已經有一種自主神經系統的不平衡狀態的患者。
導致巴比土酸鹽昏迷(5.15 mg/Kg) 被表明當耐心定向障礙症也許是有害的, 或當ICP 增廣的控制是窮的。呼吸率、血液氣體和動脈壓力必須被監測。Debilitated, 這些患者通常不喝他們的每日水需要。血流比容計、總蛋白含量、電解質和利尿灌注和控制被推薦。
在奪取的情況下, 苯甲二氮卓(0.2 mg/Kg), midazolam, 和苯巴比妥(5.15 mg/Kg) 被使用在IV 一小團或連續的注入。需要追求治療六個月在治癲癇藥物的_蒙以後是有爭議的。
頭部受傷患者有熱量需要在法線之上; 一支nasogastric 管為協助的enteral 營養或腸外營養應該儘快被設立避免慢性高血糖症。
經典護理保健為recumbent 動物必須被提供(頭30. 最大值、眼睛潤滑劑、規則decubitus 變動、膀胱catetherization 、軟的物理療法, 等) 。
手術徵兆是單獨的。線性和被舉起的破裂保守地將被對待並且穩定的沮喪的或trans 靜脈竇破裂。Haematoma 與重大許多作用、滲透的創傷或不穩定的沮喪的破裂外科地將被對待。短的代理巴比土酸鹽被使用為歸納並且isoflurane 是選擇的inhalant 麻醉劑因為它不增加ICP 。
預測
格拉斯哥標度依照被使用在人的醫學不適合與獸醫。知覺pupillary 反射和狀態也許是神經學狀態的一個好晴雨表。消沉和myosis 的協會, uni- 或雙邊, 表明增加的ICP 。大腦herniation 導致副交感神經的刺激和最新痲痺解釋各自myosis 和最新mydriasis 。不規則的呼吸率和無答復的雙邊mydriasis 表明一種粗劣的預測。修改過的格拉斯哥標度增加等級為知覺(1 的水平: 昏迷到6: 戒備), 馬達活動(1MN 到6: 法線), 和腦乾反射(1: 完成痲痺到6: 法線) 。預測是壞從3 到6, 守衛從9.14, 好從15.18 。無痛苦的死亡應該被考慮在患者顯示難處理的奪取或嚴厲呼吸失敗。其他人也許變化莫測地恢復很好, 至少是適當, 自治寵物。


Head trauma, with or without skull fracture, induces immediate primary injury including, if severe enough, vessel disruption and tearing or crushing of brain parenchyma. If this primary injury is not severe enough to induce immediate death, the development of secondary injuries during the following hours, including hemorrhage, edema, increased intracranial pressure (ICP) and over all, ischaemia, might. The clinician is helpless during the first injury; however, through rapid medical and surgical intervention, he may slow or reverse the second one.
The second injury mechanism
Tissue ischaemia is the most devastating consequence that may occur after a cranio-cerebral trauma. Ischaemia is due to reduction of cerebral blood flow (CBF). The CBF decreases when the ICP increases without concomitant augmentation of the arterial blood pressure; the CBF may also decrease when the cranial venous outflow is impaired because of edema, hemorrhage, or cervical trauma. ICP starts to increase once the cerebrospinal fluid (CSF) and blood redistribution buffering capabilities are exhausted respectively by reabsorption or displacement of CSF and brain vasoconstriction. Intracranial perfusion regulation is usually maintained by means of vascular constriction/dilation in a normal brain. In an injured brain, this ability may be lost. PaCO2, pH, and PaO2 influence the autoregulation response of the cerebro-vasculature. Increased PaCO2 and hypoxemia, frequent findings in traumatized patient, will cause vasodilatation and increase ICP. Ischaemia triggers the Cushing reflex, ultimate guarantee in CBF maintenance, by increasing the systemic arterial pressure. ICP will finally increase too.
Brain edema is the source of the increased ICP. The traumatic disruption of the blood brain barrier explains its vasogenic extracellular component. Liberation of vasoactive substances and the osmotic effect of interstitial byproduct from dead cells will also increase its development. The cytotoxic intracellular component of brain edema results from abnormal cell metabolism caused by ischaemia. The all-molecular chain reaction drives to more vasogenic and cytotoxic edema and higher and higher intracranial pressure.
Patient evaluation
Cranio-cerebral traumatized patients are often 𢘫ulti-traumatized?patients. Patency of airways must be checked as we have seen that high PaCO2 and low PaO2 increase intracranial pressure. Look for major chest trauma.
The patient is then treated for hemodynamic instability and the abdominal cavity is assessed for organ trauma/rupture (spleen, bladder, kidney detachment, etc.). Cerebral hypoxia due to hypovolemia is rare because of the pressure autoregulation, unless severe internal hemorrhage is present.
Finally, the neurological assessment status is assessed; this will be hourly. Although less mechanically unstable than vertebro-medullary trauma, the head trauma patient must be handled with care. The head is elevated no more than 30? this facilitates venous and CSF outflow from the skull. State of consciousness, breathing pattern, menace response, nostril sensitivity, pupillary size and reflex, ocular position and movements, limb proprioception, and skeletal motor function must be evaluated.
A decreased level of consciousness (from depressed to delirious, stupor to coma) suggests cortical or brainstem (reticular activating system) injury. The prognosis and the treatment being different; it is essential to rapidly differentiate a supratentorial from an infratentorial lesion. Asymmetry in the menace response, in the nostril stimulation response, or in limb proprioception without other cranial nerve deficit, is in favour of a contralateral hemispheric lesion. Stuporous brainstem injured patients, showing multiple cranial nerve II to XII deficits, have a more guarded prognosis.
If no chest trauma has been identified, abnormalities in respiratory pattern are either of metabolic (acidosis, hypoxia) or neurological origin (mesencephalic, brain stem, cervical). Hyperventilation and periods of apnea alternation (Cheyne-Strokes respiration) is secondary to diencephalic decreased PaCO2 responsiveness. When the brain stem is severely damaged, the respiratory pattern becomes irregular in rate and amplitude and is associated with bradycardia.
Extensor rigidity is a form of UMN presentation. If all four limbs are extended, both hemispheres are involved (decerebrate rigidity); consciousness is altered but PLR are normal if herniation is not a consideration. If the forelimbs are flexed and the rear limbs extended, the cerebellum is involved (decerebellate rigidity); consciousness is preserved but menace response may be lost.
Increased ICP must be suspected when the PLR is abnormal (or deteriorating toward non-responsive midrange or dilated pupils) in parallel with deterioration of consciousness, extensor rigidity, and abnormal respiratory pattern. Direct bilateral unresponsive pupils, symmetrical or not, indicate brainstem injury. Transition from myosis to mydriasis suggests a progressive lesion often secondary to sub-tentorial occipital herniation. Pupillary paralysis is due to dorsal pressure of the swollen brain on the oculomotor nerves.
Petrosal bone and internal ear injury induces peripheral or central vestibular signs that may be impressive with the animal rolling on his side continuously. The neurological exam on these patients is difficult initially. Proprioception deficit on one side localizes the lesion to the ipsilateral central vestibular system.
Diagnostic tools
Skull radiographs are difficult to read. However, fracture lines or displacement must be looked for. Cerebellar injury associated with occipital bone fracture/displacement is easily visualized by a lateral radiograph. This type of trauma induces a major ataxia but has a good prognosis with or without surgery.
Computed Tomodensitometry (CT) shows skull fractures and haematomas. After three to six hours, an acute infarct produces a hypodense area secondary to edema. The maximal effect is seen after three to five days. However, some infarcts may be isodense and visible only after contrast enhancement after 24 to 48 hours, even more after one to two weeks because of neovascularization. After two to three weeks, edema resolves and the lesion becomes isodense. After four to eight weeks, necrosis creates a cavitation with a density close to the cerebrospinal fluid (CSF). Subdural haematomas may not be as rare as originally reported in the veterinary literature. The image density is immediately decreased, even more after a few days when the clot organizes. Haematomas become isodense after a month.
Magnetic Resonance Imaging (MRI) is more suitable for brain ischaemia and edema evaluation. Early changes are detectable: hypointense in T1 weighted images and hyperintense in T2. Paramagnetic enhancement is identical to tomodensitometry. In case of hemorrhage, the image intensity depends about the hemoglobin content and form (oxy, desoxy, methemoglobin, hemochrome, hemosiderin), its location intra or extra erythrocytic, and the weight of the images. Magnetic resonance angiography is a non-invasive way of doing angiography. Both CT and MRI are suitable to assess indirect signs of increased ICP by compression or asymmetry of the ventricles and shift of the midline.
Brainstem auditory evoked response (BAER) is interesting to confirm a petrosal bone or middle/internal ear injury usually associated with vestibular signs. Abnormal results may indicate the need for a CT. With ICP increase, the BAER shows reversible decreased amplitude and increased latency. This test may be of prognostic value. Biopsies, surgical or ultrasound guided, allow a final diagnosis to be made.
Treatment
The treatment is modified according to the neurological status, the neurological signs and their changes over time. One aim is to treat edema. While vasogenic edema is responsive to therapy, cytotoxic edema, once initiated, is not. The treatment is thus directed at preventing the creation of ischaemia and decreasing its degree and duration by working with drugs on the vasogenic edema already present and minimizing the cytotoxic edema to come.
Although hypovolemic shock is not the direct cause of brain ischaemia, hypovolemia decreases brain blood flow. Hypertonic saline (7.5% NaCl , 35 ml/Kg) is the solution of choice to restore volemia. It improves cardiac output, restores systemic blood pressure and has a slight dehydrating effect on brain tissues. Colloids (hydroxyethyl starch and dextran, 20 ml/Kg) are then used to maintain the intravascular volume. Central vascular pressure is monitored.
Second, it is essential to guarantee hypocapnia and good O2 delivery (Pa O2 > 80 mmHg). Hypercapnia (Pa CO2 > 40 mm Hg) and hypoxia induces vasodilatation, which increases ICP. Intubation is necessary if the patient is unconscious. Oxygen delivered by nasal catheter or by oxygen cage must be provided if the patient is not. Although effective in decreasing ICP, aggressive hyperventilation may aggravate hypoxia because of excessive vasoconstriction and may exacerbate focal ischaemia and edema.
Third, the use of mannitol is a common step in cranial trauma. Mannitol is a hyperosmolar molecule that dehydrates the cerebral interstitium, lowering ICP. Mannitol also decreases blood viscosity, promoting cerebral perfusion; it also has free radical scavenger ability which limits the deleterious molecular cascade induced by ischaemia. After fluid resuscitation, the risk of a rebound effect on the ICP is minimized. Mannitol may theoretically be detrimental in cases of active bleeding or severe rupture of the blood brain barrier, however, this has not been proven. Imaging is the only way to detect a hemorrhage or a large edema. However, imaging facilities are not always available. One should consider that if the patient is deteriorating with time, mannitol is the best option to reverse the process. The recommended dosage is 0.5 to 1g/Kg over 20?0 minutes IV. It will have a longer beneficial effect if given at 0.25 to 0.5g/Kg over 60 minutes potentialized with 0.7 mg/Kg of furosemide IV, 15 minutes later; however, this may lead to more serious hyperosmolarity and may aggravate the rebound effect.
ICP measurement necessitates an epidural, subarachnoid or intraventricular fluid filled catheter and a pressure transducer. The necessity of monitoring ICP is still debatable (risk, cost, interest, etc.). It is probably an indirect way to monitor the neurological status when the patient is comatose, or sedation or anesthesia is required and neurological status cannot be evaluated differently. Oxymetry, electroencephalography, and transcranial Doppler sonography are used in human medicine.
The methyl prednisolone protocol as a free radical scavenger is not used in head trauma patients. The classic corticotherapy largely used in neuro-oncology to treat vasogenic edema is not useful against cytotoxic edema encountered in the second injury type. Side effects are not negligible: they favor gluconeogenesis and maintain a hyperglycemic state known to be deleterious. They favor anaerobe metabolism and increase glutamate levels and neuronal death. The GI side effects are also important in patients who already have an autonomic imbalance.

minibabyqq 2007-1-26 02:05

[color=Magenta][size=5][b]大腦和髓心非創傷血管疾病Cerebral and medullary non-traumatic vascular disease  [/b][/size][/color]


有二個原因為什麼非創傷血管損害在獸醫神經學方面不是一樣重要像在人的神經學方面: 1) 動脈粥樣硬化是一罕見familial 或內分泌發現; 並且2) 中央血管混亂補救在動物中大概是更加壯觀的因為動物有一個較不突出的pyramidal 系統。但是, 中央神經系統(CNS) 血管混亂的發生在狗和貓大概共同比什麼被發現在文學因為一個大數字做部份或總補救並且由屍體檢驗從未診斷。
CNS 的Vascularization
基本的解剖學是必要瞭解腦子和脊髓的血管混亂的後果。在狗, 內部carotids 和基部的動脈供應腦子; 他們anastomose 在動脈圈子的水平在洞穴狀靜脈竇之內。一定數量的船出現從動脈圈子, 是終端。rostral, 中間和尾部大腦動脈vascularize 半球。小腦的動脈提供後腦和brainstem 。在貓, 許多分支從上頷骨動脈出現從外在頸動脈替換內部carotids 。
二背部脊髓動脈每脊髓段奔跑在dorsolateral 溝之內和供應血液通過anastomosing 的動脈圓環和輻形動脈, 對白色問題柔膜組織的背部方面。一腹脊髓動脈運行在腹裂痕。它供應腹白色問題由加入anastomosing 的動脈圓環和中央灰色問題通過垂直或中央動脈。這些連續的脊髓動脈由背部和腹radicular 動脈的一個易變的數字供應由椎骨動脈哺養由主動脈和在子宮頸區域。一個anastomotic 內在網路排泄在裂痕之內並且溝, 提供多血脈性的回歸。外在靜脈聯絡與追獵沿硬膜外空間地板在椎骨運河過程中的長度的縱向椎骨靜脈竇。多血脈性的靜脈竇被連接到額外椎骨多血脈性的系統由椎間的靜脈和到basivertebral 靜脈通過osseous 渠道在椎骨。
血管CNS 混亂病理生理學
任一中央神經系統混亂也許導致血管妥協。一個增長的腫瘤也許導致血管崩潰由於許多作用或它也許自發地流血由於易碎的neovascularization 。一深刻圓盤herniation 也許導致靜脈竇破裂和廣泛的hematorrachia 。這些被認為次要血管混亂。主要血管混亂是或創傷或自發的。非創傷血管損害也許是閉塞(embolization) 或出血性的(血管正直破裂) 。他們也許難區分因為結果經常是混雜的損害、兩損害導致組織梗塞, 許多作用從腫鼓, 和各種各樣的程度局部缺血。
臨床介紹
血管混亂的臨床後果取決於船介入(型和大小), 局部缺血的程度和期間, 和parenchymal 感受性對缺氧症。神經元是最敏感的細胞類型對局部缺血, 被oligodendrocytes 跟隨, astrocytes, 和小神經膠質。血管內皮最有抵抗性。在血管損害, 腫鼓是vasogenic 在起源, 由於反常blood/parenchyma 障礙滲透性, 和細胞毒素, 由於細胞低氧症。
缺乏也許變化從簡單的臨時官能不良對死亡由於心肺拘捕。臨床標誌深刻地一般出現(apoplexia.), 是診斷標準的當中一個從其它疾病起始通常是進步在幾個天或星期(傳染, 瘤) 。臨床標誌由於血管損傷穩定和通常退步在24 到72 個小時以後; 這是可歸屬的對許多作用的減少次要對出血和整頓或腫鼓吸回。一個non-progressive 標誌是血管疾病標準。
血管損害的地點重要解釋臨床介紹。以brainstem 介入, 頭蓋骨神經的神經學考試將定義損害的確切的地點和程度。隨prosencephalic 血管損害, 臨床標誌也許變化從簡單的定向障礙症對腦子死亡。單邊的損害將導致ipsilateral 盤旋, hemi 不注意綜合症狀、對側amaurosis 、對側hemiparesia/plegia, 和hypo/anesthesia (面孔和身體) 。表皮神經細胞的功能或結構損害也許導致奪取從焦點對盛大mal 或狀態epilepticus 。血管損害的大小直接地不與神經學標誌或缺乏的強度有關。但是, 更低的馬達神經元細胞身體的破壞有一種更加粗劣的預測。Neurolocalization 也許是困難的由於神志清楚的狀態惡化、反常pupillary 反射, 和乳頭狀的腫鼓也許是存在的增加的顱內的壓力。
以脊髓介入, 臨床介紹將依靠繩子段被損壞。以C1-C5 和T3-L3 介入, 介紹將是UMN 在所有四肢體裡或在後方各自。以C6-T2 和L4-S2 介入, 介紹將是LMN, 各自地在前面肢體或在後方肢體。介紹也許不對稱如果損害不對稱。在這種情況下, 缺乏將是ipsilateral 對損害。
診斷器械
估計凝固缺乏或具體傳染病導致coagulopathy 被表明, 包括CBC 、血小板計數、凝固盤區、rickettsial 血清學、Coombs, 和肝功能測試的驗血, 以及油脂盤區和甲狀腺功能考驗。
Tomodensitometry 是一個非侵入性的想像技術。最初地, 一深刻梗塞導致一個微妙的hypodense 區域由腫鼓造成在三個到六個小時以後。對falx 和心室崩潰的許多作用也許並且是可看見的特別是在三到五天以後。一些梗塞也許是isodense 和是可看見的在碘射入之後。改進看上去在24 到48 個小時和是最顯然在一兩個星期以後特別是在neovascularization 存在的周圍之後。由於是hypodense 的損害在對比成為isodense 在對比之前(和因而惡劣可看見以後), 兩個前和崗位對比圖像必須被審查。在二個到三個星期以後, 腫鼓消失並且損害成為isodense 。在四個到八個星期以後, 壞死導致氣蝕以密度相等地密集對心室系統。Parenchymal 萎縮可能並且是可看見的。出血在損害之內將導致在密度的直接減退, 變得明顯在幾天當凝塊組織和縮回。Hematomas 成為isodense 在一個月以後。
磁共振圖像比tomodensitometry 敏感的。反常性是可看見的在幾小時之內由於水含量變動。梗塞將是hypointense 在T1 和hyperintense 在T2 裡。改進與tomodensitometry 將是相同的。釓提高梗塞由於血管破裂但不提高局部缺血或腫鼓。血紅蛋白起反應作為一個順磁的分子。在出血的情況下, 圖像的強度是次要對血紅蛋白禮物、它的地點(內部或extraerythrocytic), 和機器(在TE 和TR 價值上變化的) 設置的形式。先生並且適用與血管結構的評估由於它的敏感性對各種各樣相關流量的現象。高質量MRAngiography 可能達到和被顯示像常規動脈描記波被獲取完全非侵入性的時尚。
Tomodensitometric 和圖像(地點, 大小, density/intensity, 許多作用, 血液腦子障礙中斷) 先生血管損害不是足夠敏感的排除肯定激動或neoplasic 損害。這些研究結果必須被解釋在臨床上下文。在困難的情況下, 重覆圖像和估計他們的變動也許幫助為最後的診斷。明確的診斷方法依然是損害的切片檢查法。
大腦和髓心非創傷血管疾病
Fibrocartilaginous 栓塞 (FCE) 脊髓是深刻脊髓梗塞綜合症狀由fibrocartilage 的embolization 造成。栓子的來源被假定是被擠壓的椎間的圓盤材料。FCE 被描述了在人、狗和貓。Histopathologic 評估是必要建立FCE 一個明確的診斷。動脈或多血脈性的內在或外在vasculature 也許是包含的。根據組織學上被證實的案件文學回顧在狗, 這深刻non-progressive 脊髓梗塞看上去有高發生在狗大和大的養殖和一種高嗜好為脊髓intumescences 。除組織學上被證實的案件之外, 神經學提及中心看見根據其它橫向myelopathy 的起因排除FCE 的許多被懷疑的案件。這些箱子有深刻non-progressive 官能不良的相似的臨床標誌, 經常與相關精神創傷和鍛煉。但是, 被懷疑的小組包括少量巨人養殖並且更多這些狗有上部馬達神經元介入和原封nociception 。狗臨床標誌大小和嚴肅對所有者選擇無痛苦的死亡大概貢獻在有被證實的損害的狗。
局部缺血neuromyopathy, 次要對尾部主動脈的栓塞, 發生在貓以心肌病和atrial 血栓形成。雖然這是一種更加周邊的緊張的血管疾病, 血栓可能偶爾地位於非常高尾部主動脈導致腎臟和medullar 局部缺血。
似貓的局部缺血的綜合症狀 是單邊的大腦(特別表皮) 梗塞在任一年齡貓。臨床標誌是深刻的並且non-progressive 和大多數完全地解決。中間大腦動脈似乎是經常包含的。腦乾伴隨地或分開地偶爾地是包含的, 或。CT 或MRI 也許顯示梗塞的標誌。損害是局部缺血的壞死, 有時出血性, 雙邊, 或multifocal 。局部缺血的起因是不明的; 心肌病確定地不是一個關鍵系數。Cuterebra 遷移被懷疑。
脈管炎、adventitial 擴散和perivascular 濾滲, 遇到以激動疾病感染(病毒, 細菌, protozoan, rickettsial) 或non-infectious 起源。Thrombophlebitis 細菌起源, 共同在大動物, 是罕見的在寵物。與rickettsial (Ehrlichiosis, Borreliosis) 脈管炎, 神經學標誌也許出現次要對coagulopathy 和傳播的血管內的凝固。Non-infectious meningo-encephalo-myelitis (granulomatous, 養殖具體, arteritis 或類固醇敏感) 也許顯示梗塞由於極端proliferative 脈管炎或自發出血由於血管破裂。
Coagulopathies 不同的起源也許導致腦子或繩子的自發靈菌。免疫斡旋的thrombocytopenia 、遺傳性血友病, 和維生素K 對抗性醉是最共同地遇到。
退化血管疾病 是不凡的在寵物。硫胺缺乏, 今天很少遇到由於工業食物用法, 導致diencephalons 的自發出血。動脈硬化症被描述在寵物是非油脂的形式。動脈硬化症的油脂的形式, 被命名動脈粥樣硬化, 是共同在人, 也許遇到在甲狀腺機能不足的狗。冠狀和腎臟動脈一般是包含的。Hypercholesterolemia 、lipemia 和甲狀腺機能不足是三個最共同的實驗室研究結果。總損害是動脈粥樣硬化、血栓大腦圈子動脈的形成, 和阻礙與相關半球梗塞。先天hyperlipoproteinemia 在微型Schnauzers 並且增加動脈粥樣硬化的流行。這歸結於低密度脂蛋白的一個更大的分數的出現。非油脂的動脈硬化症顯示纖維變性特別是在年邁的動物伴生以amyloidosis 和成礦。動脈硬化症次要對系統高血壓解釋中央標誌遇到在endocrinopathies (低亞硫酸鈉和甲狀腺機能亢進、hyperadrenocorticism, 腎功能不全) 。自發出血也許發生次要對動脈減弱在這些疾病。Hyperlipoproteinemia 或hyperviscosity 能潛在地導致CNS 的parenchymal 局部缺血。
一些 先天或被獲取的血管反常性 深刻地可以decompensate 和導致大出血在腦子或繩子。這可能被發現在動脈瘤或洞穴狀畸形、telangiectasic hemartomas 和動靜脈畸形與相關系統高血壓或較小精神創傷。
一些 CNS 瘤 也許導致深刻惡化由於重大出血。腦下垂體的macroadenoma 是一個例子(腦下垂體的apoplexia) 。
治療可能性
氧氣和協助的透氣是必須維護大腦血流特別是如果顱內的壓力被增加。降低pCO2 由透氣導致正常腦子地區的血管縮小和增加灌注對局部缺血的地區。大腦血流自動調節的損傷也許導致腦子hypoperfusion 或, 相反地, 增加顱內的壓力。緊急治療反對腫鼓和局部缺血必須儘快開始。它重要確定如果靈菌仍然是活躍, 因為對甘露醇的用途不會被表明如果靈菌堅持。它滲透的作用也許增加出血的實際尺寸雖然它也許減少parenchymal 腫鼓的大小和, 同時, 增加大腦血流。如果想像技術不顯示靈菌, 或如果這樣圖像無法被獲取僅惡化是進步, 甘露醇應該被給在1.0 g/Kg 在30 分鐘內IV 在腦子herniation 的情況下, 或慢慢地延長它的有利作用。它應該被0.7 mg/Kg Furosemide 跟隨IV 。
甲醇prednisolone 必須開始在少於八個小時之內保護脊髓柔膜組織免受局部缺血和自由基形成(30 mg/Kg 和然後5.4 mg/Kg/h 在24 小時期間) 如果它將是有利的。短的代理類固醇在一種抗發炎劑量是適當的反對腫鼓。
由於被降下的免疫和經常看與中央神經系統疾病、抗藥性保護、抗酸劑和前列腺素的自主神經系統的消化損傷使用被推薦。苯甲二氮卓、Midazolam 和苯巴比妥被推薦控制奪取活動。Decompressive 手術被推薦在大出血的情況下。
同時, 血管事故的起因一次被確定了, 部下的疾病的治療必須被創始。


There are two reasons why non-traumatic vascular lesions in veterinary neurology are not as important as in human neurology: 1) atherosclerosis is a rare familial or endocrine finding; and 2) recovery of central vascular disorders in animals is probably more spectacular because animals have a less prominent pyramidal system. However, the incidence of central nervous system (CNS) vascular disorders in dogs and cats is probably more common than what is found in the literature as a large number make a partial or total recovery and are never diagnosed by necropsy.
Vascularization of the CNS
Basic anatomy is necessary to understand the consequences of vascular disorders of the brain and spinal cord. In dogs, the internal carotids and the basilar artery supply the brain; they anastomose at the level of the arterial circle within the cavernous sinus. A number of vessels arise from the arterial circle, all of which are terminal. The rostral, middle and caudal cerebral arteries vascularize the hemispheres. The cerebellar arteries supply the cerebellum and the brainstem. In cats, numerous branches from the maxillary artery arising from the external carotid arteries replace the internal carotids.
Two dorsal spinal arteries per spinal cord segment run within the dorsolateral sulci and supply blood through the anastomosing arterial rings and the radial arteries, to the dorsal aspect of the white matter parenchyma. One ventral spinal artery runs in the ventral fissure. It supplies the ventral white matter by joining the anastomosing arterial rings and the central gray matter through vertical or central arteries. These continuous spinal arteries are supplied by a variable number of dorsal and ventral radicular arteries fed by the aorta and by the vertebral arteries in the cervical region. An anastomotic intrinsic network draining within the fissures as well as the sulci, provides venous return. The extrinsic veins communicate with the longitudinal vertebral sinuses that course along the floor of the epidural space throughout the length of the vertebral canal. Venous sinuses are connected to the extra vertebral venous system by intervertebral veins and to the basivertebral veins through osseous channels in the vertebrae.
pathophysiology of vascular CNS disorders
Any central nervous system disorder may at some point cause vascular compromise. A growing tumor may induce vascular collapse because of mass effect or it may bleed spontaneously because of fragile neovascularization. An acute disc herniation may induce a sinus rupture and extensive hematorrachia. These are considered secondary vascular disorders. Primary vascular disorders are either traumatic or spontaneous. Non-traumatic vascular lesions may be occlusive (embolization) or hemorrhagic (rupture of vascular integrity). They may be difficult to differentiate because the result is often a mixed lesion, both lesions inducing tissue infarction, mass effect from edema, and various degrees of ischemia.
Clinical presentation
Clinical consequences of vascular disorders depend on vessel involvement (type and size), degree and duration of ischemia, and parenchymal susceptibility to anoxia. Neurons are the most sensitive cell type to ischemia, followed by oligodendrocytes, astrocytes, and microglia. Vascular endothelium is the most resistant. In vascular lesions, edema is both vasogenic in origin, because of abnormal blood/parenchyma barrier permeability, and cytotoxic, because of cell hypoxia.
Deficits may vary from simple temporary dysfunction to death because of cardio-respiratory arrest. Clinical signs generally appear acutely (弌poplexia?, which is one of the diagnostic criteria from other diseases in which onset is usually progressive over a few days or weeks (infection, neoplasm). Clinical signs due to vascular impairment usually stabilize and regress after 24 to 72 hours; this is attributable to diminution of the mass effect secondary to hemorrhage and reorganization or edema resorption. A non-progressive sign is a criterion of vascular disease.
Location of a vascular lesion is important to explain clinical presentation. With brainstem involvement, neurological examination of the cranial nerves will define the exact location and extent of the lesion. With a prosencephalic vascular lesion, clinical signs may vary from simple disorientation to brain death. A unilateral lesion will induce ipsilateral circling, hemi-inattention syndrome, contralateral amaurosis, contralateral hemiparesia/plegia, and hypo/anesthesia (face and body). Cortical neuronal functional or structural lesions may induce seizures from focal to grand mal or status epilepticus. The size of the vascular lesion is not directly related to the intensity of the neurological signs or deficits. However, the destruction of lower motor neuron cell bodies has a poorer prognosis. Neurolocalization may be difficult because of increased intracranial pressure in which conscious state deterioration, abnormal pupillary reflexes, and papillary edema may be present.
With spinal cord involvement, the clinical presentation will be dependent on the cord segment damaged. With C1-C5 and T3-L3 involvement, the presentation will be UMN in all four limbs or in the rear respectively. With C6-T2 and L4-S2 involvement, the presentation will be LMN, respectively in the front limb or in the rear limbs. The presentation may be asymmetric if the lesion is asymmetric. In such a case, the deficits will be ipsilateral to the lesion.
Diagnostic tools
Blood tests that assess coagulation deficits or specific infectious diseases causing coagulopathy are indicated, including CBC, platelet count, coagulation panel, rickettsial serology, Coombs, and liver function tests, as well as lipid panel and thyroid function test.
Tomodensitometry is a non-invasive imaging technique. Initially, an acute infarct produces a subtle hypodense area caused by edema after three to six hours. A mass effect on the falx and ventricular collapse may also be visible especially after three to five days. Some infarcts may be isodense and are visible only after iodine injection. The enhancement appears after 24 to 48 hours and is most evident after one or two weeks especially in the periphery where neovascularization exists. Because a lesion that is hypodense before contrast becomes isodense after contrast (and thus poorly visible), both pre- and post-contrast images must be examined. After two to three weeks, the edema disappears and the lesion becomes isodense. After four to eight weeks, necrosis induces cavitation with a density equally dense to the ventricular system. Parenchymal atrophy can also be visible. Hemorrhage within the lesion will cause an immediate decrease in density, which becomes more marked over several days as the clot organizes and retracts. Hematomas become isodense after one month.
Magnetic resonance imaging is more sensitive than tomodensitometry. Abnormalities are visible within hours because of water content changes. An infarct will be hypointense in T1 and hyperintense in T2. Enhancement will be identical to tomodensitometry. Gadolinium enhances infarcts because of vascular rupture but does not enhance ischemia or edema. Hemoglobin reacts as a paramagnetic molecule. In case of hemorrhage, the intensity of the image is secondary to the form of hemoglobin present, its location (intra or extraerythrocytic), and the setting of the machine (variation in TE and TR values). MR is also suited for evaluation of vascular structures because of its sensitivity to a variety of flow-related phenomena. High quality MRAngiography can be achieved and be displayed like conventional arteriograms whilst being acquired in a totally non-invasive fashion.
Tomodensitometric and MR images (location, size, density/intensity, mass effect, blood brain barrier disruption) of vascular lesions are not sensitive enough to exclude with certainty inflammatory or neoplasic lesions. These findings must be interpreted in the clinical context. In case of difficulty, repeating the images and assessing their changes may help for final diagnosis. The definitive diagnostic method remains a biopsy of the lesion.
Cerebral and medullary non-traumatic vascular disease
Fibrocartilaginous embolism (FCE) of the spinal cord is a syndrome of acute spinal cord infarction caused by embolization of fibrocartilage. The source of emboli is presumed to be extruded intervertebral disc material. FCE has been described in man, dogs and cats. Histopathologic evaluation is necessary to establish a definitive diagnosis of FCE. Arterial or venous intrinsic or extrinsic vasculature may be involved. Based on a literature review of histologically confirmed cases in dogs, this acute non-progressive spinal cord infarction appears to have a high incidence in large and giant breeds of dogs and a high predilection for the spinal intumescences. In addition to histologically confirmed cases, neurology referral centers see many suspected cases of FCE that are based on the elimination of other causes of transverse myelopathy. These cases have similar clinical signs of acute non-progressive dysfunction, often associated with trauma and exercise. However, the suspected group includes fewer giant breeds and more of these dogs have upper motor neuron involvement and intact nociception. Dog size and severity of clinical signs probably contribute to the owner choosing euthanasia in dogs which have had confirmed lesions.
Ischemic neuromyopathy, secondary to embolism of the caudal aorta, occurs in cats with cardiomyopathy and atrial thrombus formation. Although this is a more peripheral nervous vascular disease, occasionally the thrombus can be located very high in the caudal aorta inducing renal and medullar ischemia.
Feline ischemic syndrome is a unilateral cerebral (especially cortical) infarction in cats of any age. The clinical signs are acute and non-progressive and most of them resolve completely. The middle cerebral artery seems to be most often involved. The brain stem is occasionally involved, either concomitantly or separately. CT or MRI may show signs of infarction. The lesion is an ischemic necrosis, sometimes hemorrhagic, bilateral, or multifocal. The cause of ischemia is unclear; cardiomyopathy is definitely not a key factor. Cuterebra migration has been suspected.

minibabyqq 2007-1-26 02:05

[color=Magenta][size=5][b]獸醫脊髓手術 Veterinary Spinal Surgery  [/b][/size][/color]


這不是這些筆記的作用作為神經外科學的技術一個全面審查; 這些可能被搜集從任何幾本課本的當中一個。相反, 這是我自己的偏心和哲學總結被使用在脊髓傷害的治療在我的外科服務。
解剖學
穩定在椎骨身體之間由周圍的肌組織的關節小平面、椎間的盤、韌帶和腱附件維護。關節小平面是真實的聯接組成由聯合膠囊和關節軟骨。椎間的盤(IVD) 由外面纖維狀殼(環體fibrosus) 並且凝膠狀中心(中堅力量pulposus) 組成。IVD 的主函數是那緩衝器在椎骨終板之間但這並且是一個重要貢獻者對椎骨專欄的旋轉的穩定。
神經學結構遇到在脊髓手術期間包括脊髓, 被劃分成內在灰色問題和外面白色問題。上升的知覺短文ventrolaterally dorso-laterally 位於和下降的馬達短文。背部和腹神經根和背部根神經節出現作為一個唯一側向結構在他們的dural 覆蓋物之內。子宮頸intumescence, 包含細胞身體為上臀結節(脊髓段C6 的神經對T2), 位於椎骨身體C5 區域對T1 。腰部脊髓的intumescence (脊髓段L4 對S3) 並且終止變化在養殖之間和位於從椎骨身體L3 對L6 。
脊髓傷害病理生理學
不管原因論, 脊髓傷害的形式可能被劃分成四個組分: 震蕩、局部缺血的反應、炎症, 和許多作用。
許多作用的撤除是, 以我所見, 外科干預的主要好處。沒有問題那大量導致脊髓組織結果壓縮在作用損失。神經系統的組織壓縮干涉它的地方供血, 妨礙衝動傳輸通過軸突, 可能導致demyelination 。某個時候在壓縮以後起始, 軸突不再將起作用或神經細胞將死。在損傷將是不可逆的什麼點未被提供但在第五天以後, 一些永久神經系統的損傷應該被期望。程度補救被壓縮的嚴肅和期間影響。
脊髓傷害的幅射線照相的診斷和地方化
勘測射線照相和myelographic 評估是診斷形式最常用幫助地方化損害的站點。
反常性共同地被發現在勘測射線照相有:
椎骨身體的病勢漸退暗示一個造形術過程。
骨多的終板的硬化和擴散一致與diskospondylitis 。
椎骨身體的Malalignment 表明精神創傷或先天畸形。
椎間的盤的石灰化與相關盤的退化。
變窄磁盤空間和楔住椎骨終板。
變窄或增加的密度在椎間的孔之內。
變窄小平面清楚的發音。
Myelographic 研究結果將取決於類型損害, 可能一般被分類和:
Extradural (逐漸變細染料專欄往繩子) 由壓縮從dural 管外面, 通常結果盤prolapse 或腫瘤造成椎骨身體。
Intradural/extramedullary 損害阻礙染料流程在dural 管之內但是在脊髓(golf 發球區域配置之外) 。這些同腫瘤聯繫在一起譬如meningiomas 。
Intramedullary 損害導致繩子的剪影的擴大和導致染料專欄逐漸變細從中央運河。溫和的intramedullary 膨脹可能同fibrocartilagenous 栓子聯繫在一起但重大enlargments 是幾乎pathognomonic 為腫瘤在脊髓之內。intramedullary 損害的診斷要求繩子的對稱膨脹是可看見的在側向和ventrodorsal 看法。
脊髓壓縮的外科治療
脊髓的解壓, 在多數臨床患者, 由mass 作用的撤除達到。或改正施加壓力在神經系統的組織的反常解剖學。在這些情況下, 去除周圍的骨多的lamina 或分裂的好處dural 管允許被傷害的繩子脹大是, 以我所見, 最小的好處和增加過份精神創傷來外科手術。造成對繩子的最少醫原性損傷和促進觸犯的大量容易的撤除在thoracolumbar 區域的外科方法, 是pediculectomy 。使用這個技術, 側向地被安置的盤材料或腫瘤被插話在骨頭被去除和脊髓之間。腹上被找出的大量可能直接地看和被取消沒有繩子的過度的操作。Pediculectomy 導致椎骨專欄的最小的不穩定並且側向方法允許所有殘餘的盤的容易的開窗法。在子宮頸區域腹方法和開槽椎骨身體在損害附近幾乎完全被使用為盤prolapse 。這些方法要求損害的精確, preoperative 地方化。有限的曝光他們提供牌子他們不適當當診斷是在疑義。有希望地, 跟隨詳盡的物理和神經學考試, 和幅射線照相的研究、廣泛的laminectomies 或脊髓的一般探險很少將是需要的。
椎間的盤的預防疾病的開窗法是有些有爭議的。許多作者要求對盤prolapse 的再現率的重大減少跟隨開窗法。一些實驗性研究顯示了瑕疵的那創作在環體fibrosus 結果在殘餘的中堅力量pulposus 的持續的炎症和破壞。它並且被推測, 正常身體運動導致剩餘中堅力量被擠壓通過開窗法瑕疵。其他學習(我自己包括) 表明, 殘餘的中堅力量停留unchanged 在盤之內並且環體瑕疵癒合由纖維變性, 防止另外的材料逃命。切環體fibrosus 的腹部份與scalpel 刀片是充分的為子宮頸磁盤空間的搬空。中堅力量的完全撤除從thoracolumbar 盤可能是困難在任一條狗和幾乎不可能的在狗以spondylosis 。對高速毛刺的用途創造開窗法導致被減少的操作時間和中堅力量的更加完全的撤除從thoracolumbar 盤。
椎骨身體的安定不是必要的跟隨定期decompressive 手術為盤prolapse 或腫瘤撤除。創傷fracture/luxations 或先天畸形也許需要受影響的vetebral 身體的某一內部定像。在子宮頸區域, 定像也許介入安置別針或螺絲橫跨小平面清楚的發音, 腹上鍍或別住椎骨身體有或沒有methylmethacrylate 水泥骨架的加法。胸部區域是固有地穩定的然後子宮頸或腰部區域由於肋骨和伴生的肌組織的支持。剛性骨頭板材可能被使用在thoracolumbar 椎骨的側向方面。靈活的(Lubra7) 板材或別針和導線的組合附有背部過程將給一些穩定椎骨L1 L5 。在更低的腰部和sacral 區域, 背部過程是相當短的並且對發怒別針與methylmethacrylate 水泥或別針的用途與靈活的板材的組合也許是需要的。
具體外科疾病不同於盤HERNIATION
sacral 結節的牽引傷害可能發生如果狗和貓得到他們的尾巴被捉住在門或門裡當他們通過他們在充分的飛行。sacrococcygeal 椎骨的分離也許發生造成重大神經系統的損傷。神經根在牽引的站點通常被毀壞造成麻醉劑和被痲痺的尾巴。更加重要地, sacral 結節的神經根也許avulsed 在他們的孔。這傷害將導致作用損失對泌尿膀胱和肛門。
它經常難確定是否動物將恢復充分神經系統的作用為義務尿和糞便控制根據最初的考試。截去頭髮從perineal 區域和映射皮膚感覺極限與一個不可磨滅的標誌, 促進跟隨患者的進展。概括來說, 泌尿膀胱的肛門口氣和控制將恢復如果皮膚感覺回到肛門區域。不顯示知覺水平進步二個星期的那些患者不應該被期望恢復膀胱或腸控制。
Cauda Equina 綜合症狀
由於脊髓停止中間腰部並且cauda equina 的神經繼續入更低的腰部和sacral 區域, 這個區域對傷害是相當有抵抗性。提出歷史範圍從僵硬的步態對動物的勉強對攀登臺階或躍遷。體檢研究結果也許包括被變短的大步、本體感受的缺乏在後面肢體, 粗劣的撤退反射、lumbosacral hyperesthesia, 和極端痛苦在臀部的尾巴或引伸的海拔。勘測射線照相也許顯示lumbosacral spondylosis, 但經常是正常的。Epidurography 、MRI 、CT 和intraosseous venography 使用展示壓縮或cauda equina 或神經根的當中一個退出在lumbosacral 連接點。肌動電流術也許並且建議一個或更多的去除神經支配神經根。它是我的經驗, 所有診斷測試經常是正常的並且動物外科地被探索根據歷史和物理研究結果單獨。反常研究結果不也許是明顯的在手術期間, 但是患者手術後地經常體驗他們的臨床標誌的決議。
一種背部方法被使用, 背部lamina 從L7-S1 和關節小平面被去除被暴露。如果椎骨的操作導致重大行動在關節小平面之間, 關節軟骨被顫動小舌並且K 導線或螺絲transarticularly 被安置得。傳播神經根從midline 也許顯露脫出的盤材料。如果勘測射線照相是暗示的disko-spondylitis, 磁盤空間可能背部地有窗和開化了。椎間的孔由觸診探索以探針和背部地被探索得如果神經根由骨多或纖維狀擴散坑害。肥胖貪佔被採取從地方皮膚下組織被安置使結疤減到最小。
Atlantoaxial 半脫位
這個情況原因論是創傷有或沒有預先處理小室的先天發育不全。背部和腹方法被報告了為外科安定。背部方法是輕微地容易, 但子宮頸椎骨牌子定像的背部lamina 的弱點細。腹方法以發怒別住關節小平面是可靠的在我的手裡。長期預測依然是被守衛的由於在植入管失敗和遷移的潛力。
手術後關心
脊髓手術患者手術後關心像那是相同被使用為盤prolapse 的保守的治療。好護理保健以物理療法和膀胱和腸作用強烈的監視必需。狗窩的充分填料是需要的防止壓力痛處並且對綜合性fleece. 材料的用途被推薦。游泳和水療法不僅幫助保留耐心乾淨, 而且刺激循環對皮膚。在胃潰瘍和大腸穿孔的潛力在神經學上被削弱的患者很好被提供並且對gastroprotectants 的用途被推薦。食道靈菌的證據是禁忌症候對對類皮質激素的用途。同樣, non-steroidal 抗發炎藥物有一點點或沒有地方在脊髓傷害的治療。

It is not the function of these notes to act as a comprehensive review of neuro-surgical techniques; these can be gleaned from any one of several textbooks. Rather, this is a summary of my own bias and the philosophy used in the treatment of spinal injury on my surgical service.
ANATOMY
Stability between the vertebral bodies is maintained by the articular facets, intervertebral disks, ligaments and tendon attachments of the surrounding musculature. The articular facets are true joints composed of joint capsules and articular cartilage. The intervertebral disk (IVD) is composed of an outer fibrous shell (annulus fibrosus) and gelatinous center (nucleus pulposus). The main function of the IVD is that of a shock absorber between the vertebral end plates but it is also an important contributor to the rotational stability of the vertebral column.
The neurologic structures encountered during spinal surgery include the spinal cord, which is divided into the inner gray matter and outer white matter. The ascending sensory tracts are situated dorso-laterally and the descending motor tracts ventrolaterally. The dorsal and ventral nerve roots and dorsal root ganglia appear as a single lateral structure within their dural covering. The cervical intumescence, which contains the cell bodies for the nerves of the brachial plexus (spinal segments C6 to T2), is located in the area of vertebral bodies C5 to T1. The lumbar intumescence (spinal segments L4 to S3) and termination of the spinal cord varies between breeds and is located from vertebral bodies L3 to L6.
PATHOPHYSIOLOGY OF SPINAL CORD INJURY
Regardless of the etiology, the form of spinal cord injury can be divided into four components: Concussion, ischemic reaction, inflammation, and mass effect.
Removal of the mass effect is, in my opinion, the major benefit of surgical intervention. There is no question that a mass causing compression of spinal tissue results in loss of function. Compression of neural tissue interferes with its local blood supply, impedes transmission of impulses through axons and can cause demyelination. Some time after the onset of compression, the axons will no longer function or the nerve cells will die. At what point the damage will be irreversible has not been documented but after the fifth day, some permanent neural damage should be expected. The extent of recovery is influenced by the severity and duration of the compression.
RADIOGRAPHIC DIAGNOSIS AND LOCALIZATION OF SPINAL CORD INJURY
Survey radiographs and myelographic evaluation are the diagnostic modalities most commonly used to help localize the site of the lesion.
Abnormalities commonly found on survey radiographs include:
Lysis of the vertebral bodies suggestive of a neoplastic process.
Sclerosis and proliferation of bony endplates consistent with diskospondylitis.
Malalignment of the vertebral bodies indicating trauma or congenital malformation.
Calcification of the intervertebral disks associated with degeneration of the disks.
Narrowing of the disk space and wedging of the vertebral endplates.
Narrowing or increased density within the intervertebral foramen.
Narrowing of the facet articulation.
Myelographic findings will depend on the type of lesion and can generally be classified as:
Extradural (tapering of the dye column towards the cord) caused by compression from outside the dural tube, usually the result of disk prolapse or tumors of the vertebral bodies.
Intradural/extramedullary lesions obstruct dye flow within the dural tube but are outside the spinal cord (孄olf tee?configuration). These are associated with tumors such as meningiomas.
Intramedullary lesions cause enlargement of the cord's silhouette and result in the dye column tapering away from the central canal. Mild intramedullary swelling can be associated with fibrocartilagenous emboli but significant enlargments are almost pathognomonic for tumors within the spinal cord. The diagnosis of an intramedullary lesion requires the symmetrical swelling of the cord be visible on both the lateral and ventrodorsal view.
SURGICAL TREATMENT OF SPINAL CORD COMPRESSION
Decompression of the spinal cord, in most clinical patients, is achieved by removal of the 𢘫ass effect?or correcting the abnormal anatomy that is putting pressure on the neural tissue. In such cases, the benefit of removing the surrounding bony lamina or splitting of the dural tube to allow the injured cord to swell is, in my opinion, of minimal benefit and adds excessive trauma to the surgical procedure. The surgical approach that causes the least iatrogenic damage to the cord and facilitates the easy removal of an offending mass in the thoracolumbar area, is the pediculectomy. Using this technique, laterally positioned disk material or tumors are interposed between the bone being removed and the spinal cord. Ventrally located masses can be seen directly and removed without undue manipulation of the cord. Pediculectomy results in minimal destabilization of the vertebral column and the lateral approach permits easy fenestration of all remaining disks. In the cervical area the ventral approach and slotting of the vertebral bodies adjacent to the lesion is used almost exclusively for disk prolapse. These approaches require precise, preoperative localization of the lesion. The limited exposure they provide makes them inappropriate when the diagnosis is in doubt. Hopefully, following thorough physical and neurological examination, and radiographic study, extensive laminectomies or general exploration of the spinal cord will seldom be needed.
Prophylactic fenestration of the intervertebral disks is somewhat controversial. Many authors claim a significant reduction in the recurrence rate of disk prolapse following fenestration. Some experimental studies have shown that creation of a defect in the annulus fibrosus results in an on-going inflammation and destruction of the remaining nucleus pulposus. It is also speculated that normal body movements cause the remaining nucleus to be extruded through the fenestration defect. Other studies (my own included) indicate that the residual nucleus stays unchanged within the disk and the annulus defect heals over by fibrosis, preventing the escape of additional material. Incising the ventral portion of the annulus fibrosus with a scalpel blade is adequate for evacuation of cervical disk spaces. Complete removal of the nucleus from thoracolumbar disks can be difficult in any dog and nearly impossible in dogs with spondylosis. The use of a high-speed burr to create the fenestration has resulted in reduced operating time and more complete removal of the nucleus from thoracolumbar disks.
Stabilization of the vertebral bodies is not necessary following routine decompressive surgery for disk prolapse or tumor removal. Traumatic fracture/luxations or congenital malformations may necessitate some internal fixation of the affected vetebral bodies. In the cervical area, fixation may involve placing pins or screws across the facet articulations, plating or pinning the vertebral bodies ventrally with or without the addition of methylmethacrylate bone cement. The thoracic area is innately more stable then the cervical or lumbar areas because of the support of the ribs and associated musculature. Rigid bone plates can be used on the lateral aspect of the thoracolumbar vertebrae. Flexible (Lubra7) plates or a combination of pins and wires attached to the dorsal processes will give some stability to vertebrae L1 to L5. In the lower lumbar and sacral areas, the dorsal processes are quite short and the use of cross pins with methylmethacrylate cement or pins in combination with flexible plates may be needed.
SPECIFIC SURGICAL DISEASES OTHER THAN DISK HERNIATION
Traction injuries of the sacral plexus can occur if dogs and cats get their tails caught in doors or gates when they are passing through them at full flight. Separation of the sacrococcygeal vertebrae may occur causing significant neural damage. The nerves roots at the site of the traction are usually destroyed resulting in an anesthetic and paralyzed tail. More importantly, the nerve roots of the sacral plexus may be avulsed at their foramina. This injury will cause a loss of function to the urinary bladder and anus.
It is often difficult to determine whether the animal will recover adequate neural function for voluntary urine and fecal control based on the initial examination. Clipping the hair from the perineal area and mapping the limits of cutaneous sensation with an indelible marker, facilitates following the patient's progress. As a rule, anal tone and control of the urinary bladder will be regained if cutaneous sensation returns to the anal area. Those patients that show no progression of the sensory level for two weeks should not be expected to regain bladder or bowel control.
Cauda Equina Syndrome
Because the spinal cord stops mid-lumbar and the nerves of the cauda equina continue into the lower lumbar and sacral region, this area is quite resistant to injury. Presenting histories range from a stiff gait to a reluctance of the animal to climb stairs or jump. Physical exam findings may include a shortened stride, proprioceptive deficits in the hind limbs, poor withdrawal reflexes, lumbosacral hyperesthesia, and extreme pain on elevation of the tail or extension of the hips. Survey radiographs may show lumbosacral spondylosis, but are often normal. Epidurography, MRI, CT and intraosseous venography have been used to demonstrate compression of either the cauda equina or one of the nerve roots exiting at the lumbosacral junction. Electromyography may also suggest denervation of one or more of the nerve roots. It has been my experience that often all diagnostic tests are normal and the animal is surgically explored based on the historical and physical findings alone. Abnormal findings may not be apparent during surgery, but patients often experience resolution of their clinical signs postoperatively.
A dorsal approach is used, dorsal lamina is removed from L7-S1 and the articular facets exposed. If manipulation of the vertebrae results in significant motion between the articular facets, the articular cartilage is burred off and K-wires or screws are placed transarticularly. Spreading the nerve roots away from the midline may reveal prolapsed disk material. If survey radiographs are suggestive of disko-spondylitis, the disk space can be fenestrated dorsally and cultured. The intervertebral foramina are explored by palpation with a probe and explored dorsally if the nerve root is entrapped by bony or fibrous proliferation. A fat graft taken from the local subcutaneous tissue is placed to minimize scarring.
Atlantoaxial Subluxation

minibabyqq 2007-1-26 02:06

[color=Magenta][b][size=5]骨髓和它的解釋的實際應用  [/size][/b][/color]


徵兆為骨髓評估
基本的徵兆為執行骨髓評估將回答血樣一次定期血液學考試不回答的問題。你不需要採取另外的努力採取骨髓aspirate 和切片檢查法, 如果, 例如, 血液已經清楚表明了免疫斡旋的溶血貧血症, 一個典型的激動反應, 甚至白血病以清楚地診斷特點在EDTA 血液是存在。
最共同的徵兆為骨髓分析是細胞缺乏從一條, 二條或所有三條細胞線。Cytopenias 建議被減少的骨髓作用因此你應該檢查各種各樣的骨髓疾病。這些會是nonregenerative 貧血症、thrombocytopenia 並且/或者白血球減少症。另外, 白血病也許掩藏在marrow.blast 細胞也許是許多的在骨髓但少數或疾風細胞不看在血液(aleukemic 白血病) 。白血病的建議是dysplastic 變動譬如megaloblastic rubricytes 、hypersegmentation, 或罕見的疾風細胞在血液。Hypercalcemia 也許由lymphosarcoma 造成, 也許位於骨髓。血漿細胞骨髓瘤也許由細胞溶解的損害建議由hyperproteinemia 或在脊椎。
骨髓外形
測試外形允許最完全的評估和最佳的結論。外形應該包括完全血液計數(CBC), 骨髓aspirate, 和骨髓切片檢查法。切片檢查法被忽略但經常特別重要當評估cytopenia 和當你期待骨髓的低細胞性。所有太經常, 你安排一惡劣多孔吐氣它是不定的骨髓如果樣品的低細胞性反射骨髓的低細胞性或窮吐氣。CBC 提供優秀定量和形態資訊在骨髓評估之時。aspirate 允許細胞、有差別的計數和myeloid:erythroid (M:E) 比率的優秀形態評估。切片檢查法樣品的一個histologic 部分提供最佳的定量資訊關於骨髓的細胞性和顯露meylofibrosis 和建築樣式。所有三通常一起提供最佳的資訊可能。忽略一兩份經常留下未回答的問題。執行測試幾天在其他也許並且留下一些問題之後。
答復從骨髓評估
通常答復你得到從骨髓吐氣並且切片檢查法是定量的, 以形態資訊關於細胞線在骨髓。典型的答復包括發育不全、增生或myeloid, erythroid, megakaryocytic 和淋巴腺細胞的正常數字。這些變化然後被解釋與細胞數字一道看在血液上。另外的answers/conclusions/diagnoses 根據細胞的成熟和出現被審查。增加的未成熟通常表明hyperplastic/reactive 變動除非極端。30% 疾風細胞出現表明一個急性白血病。Hemosiderin 數額幫助診斷鋼缺乏炎症貧血症(缺席) 或貧血症(被增加) 。
當解釋骨髓報告或讀汙跡, 第一決定應該是是否樣品提供充足的質量充分細胞是骨髓的代表。總意識到, 一個解釋變動從準則在樣品並且一必需首先確定如果樣品充分地代表骨髓。下個因素預言骨髓的細胞性。細胞性由一個histologic 部分最好預言由微粒在aspirate 或。各自的細胞細胞性也許是很密集至於還表明法線對骨髓的增加的細胞性。有差別的計數給各種各樣的細胞類型的百分比, 當與總細胞性的估計比較, 被使用預言細胞線的增生或發育不全。M:E 比率是myeloid 細胞的百分比由erythroid 細胞的百分比劃分。M:E 比率通常是輕微地大於1:1 在狗和貓。淋巴細胞和血漿細胞通常代表大約5% 骨髓細胞。
形態變動通常看增加發育未全的細胞的百分比。非典型形態學出現表明一個dysplastic 過程。發育異常也許被藥物、傳染物質、毒素、營養問題, 或myelodysplastic 或leukemic 疾病導致。似貓的白血病病毒(FeLV) 導致大範圍dysplastic 變化在細胞類型上或改變在各種各樣的細胞的數量: 從nonregenerative 貧血症對erythremic myelosis, 嗜中性白細胞減少症對白血病, 和thrombocytopenia 對megakaryocytic 白血病。因而FeLV 和似貓的免疫缺乏病毒(FIV) 測試被表明在貓任一血液學混亂。
具體骨髓疾病
有許多種疾病列出所有, 但幾個例子隨後而來。發育不全的血細胞減少(發育不全的貧血症, 肥膩骨髓) 是疾病過程損壞了hematopoietic 細胞因此那些細胞是缺席和增加的油脂遺骸的在骨髓。感染起因包括 Ehrlichia canis 、 parvovirus 、FeLV 、FIV 、敗血症和endotoxemia 。毒性起因包括女性荷爾蒙、phenylbutazone 、meclofenamic 酸、trimethoprim sulfadiazine 、奎尼定、griesofulvin 、thiascetarsamide, 和一些化學療法的代理。經常診斷先天。Myelofibrosis 有些相似hematopoietic 細胞被損壞了並且纖維變性替換了正常組織。
似犬純淨的紅細胞發育不全可能是免疫的被斡旋(主要) 或次要對parvovirus 傳染或疫苗在FW 狗或FeLV 在貓。骨髓有非常少量erythroid 細胞餘留, 當其它細胞線是正常的。
Ineffective hematopoiesis 也許難瞭解。樣式看是一條細胞線的缺乏在血液(即, nonregenerative 貧血症) 法線對那條細胞線的增加的數字被發現在骨髓(即, erythroid 增生) 。骨髓細胞性和形態學在cytologic 和histologic 樣品直接地不測量作用。各種各樣化學製品, 感染, 營養, 和其它起因防止甚而細胞的增加的數字在骨髓有效地導致從骨髓被發布的細胞。無效的紅血球生成也許由激動疾病或鋼缺乏造成; 無效的neutropoiesis 也許由藥物(即, 苯巴比妥) 或病毒(即, FeLV) 造成。
白血病是hematopoietic 細胞的一個造形術過程在骨髓。造形術細胞經常看在血液, 給你可能讚賞由看buffy 外套在microhematocrit 管裡從leukemic 患者的命名white 血液。疾風細胞也許被困住到大規模範圍在骨髓並且你也許驚奇看骨髓用血液有那麼少量疾風細胞一個不能排除唯一易反應的淋巴腺細胞出現的疾風細胞被填裝。白血病診斷是一個寬廣的題目但最共同地有30% 疾風細胞在骨髓允許一個容易的基本的診斷。類型具體診斷白血病是有用的在白血病治療在狗和貓很好被接受的國家。

INDICATIONS FOR BONE MARROW EVALUATION
The basic indication for performing a bone marrow evaluation is to answer questions that a routine hematology examination of a blood sample does not answer. One need not take the additional effort to take a bone marrow aspirate and biopsy, if, for example, the blood already clearly indicated an immune mediated hemolytic anemia, a typical inflammatory response, or even a leukemia with clearly diagnostic features in EDTA blood is present.
The most common indications for bone marrow analysis are a deficiency of cells from one, two or all three cell lines. Cytopenias suggest decreased bone marrow function so one should check for various bone marrow diseases. These would be a nonregenerative anemia, thrombocytopenia and/or leukopenia. Additionally, leukemia may be hidden in the marrow𤪳last cells may be numerous in the bone marrow but few or no blast cells are seen in the blood (aleukemic leukemia). Suggestions of leukemia are dysplastic changes such as megaloblastic rubricytes, hypersegmentation, or rare blast cells in the blood. Hypercalcemia may be caused by lymphosarcoma, which may be located in the bone marrow. Plasma cell myeloma may be suggested by hyperproteinemia or by lytic lesions in the spine.
BONE MARROW PROFILE
A profile of tests allows the most complete evaluation and best conclusions. The profile should include a complete blood count (CBC), bone marrow aspirate, and bone marrow biopsy. The biopsy is often neglected but is especially important when evaluating cytopenia and when one expects low cellularity of the bone marrow. All too often, one has a poorly cellular aspirate of bone marrow where it is uncertain if the low cellularity of the sample reflects low cellularity of the bone marrow or a poor aspirate. A CBC gives excellent quantitative and morphologic information at the time of the bone marrow evaluation. An aspirate allows excellent morphologic evaluation of cells, differential count and myeloid:erythroid (M:E) ratio. A histologic section of a biopsy sample gives the best quantitative information on the cellularity of the marrow and reveals meylofibrosis and architectural patterns. All three together usually provide the best information possible. Neglecting one or two parts often leaves unanswered questions. Performing a test several days after the other may also leave some questions.
ANSWERS FROM BONE MARROW EVALUATION
The usual answers one gets from bone marrow aspirates and biopsy are quantitative, with morphologic information on the cell lines in the bone marrow. Typical answers include hypoplasia, hyperplasia or normal numbers of myeloid, erythroid, megakaryocytic and lymphoid cells. These changes are then interpreted in conjunction with the cell numbers seen in blood. Additional answers/conclusions/diagnoses are based on the maturity and appearance of the cells examined. Increased immaturity usually indicates a hyperplastic/reactive change unless extreme. Presence of over 30% blast cells indicates an acute leukemia. Hemosiderin amount helps diagnose iron deficiency anemia (absence) or anemia of inflammation (increased).
When interpreting a bone marrow report or reading a smear oneself, the first decision should be whether the sample provided adequate cells of sufficient quality to be representative of the bone marrow. Always realize that one is interpreting changes from the norm in a sample and one must first determine if the sample represents the bone marrow adequately. The next factor is predicting the cellularity of the bone marrow. Cellularity is best predicted by particles on an aspirate or by a histologic section. Cellularity of individual cells may be so dense as to also indicate normal to increased cellularity of the bone marrow. A differential count gives the percentage of various cell types, which when compared to the estimate of total cellularity, is used to predict hyperplasia or hypoplasia of a cell line. The M:E ratio is the percentage of myeloid cells divided by the percentage of erythroid cells. The M:E ratio is usually slightly greater than 1:1 in dogs and cats. Lymphocytes and plasma cells usually represent about 5% of the marrow cells.
Morphologic changes seen usually are increasing percentages of immature cells. The presence of atypical morphology indicates a dysplastic process. Dysplasia may be induced by drugs, infectious agents, toxins, nutritional problems, or myelodysplastic or leukemic diseases. Feline leukemia virus (FeLV) causes a wide range of dysplastic changes in cell types or alteration in the number of various cells: from nonregenerative anemia to erythremic myelosis, neutropenia to leukemia, and thrombocytopenia to megakaryocytic leukemia. Thus FeLV and Feline immune deficiency virus (FIV) testing is indicated in any hematologic disorder of cats.
SPECIFIC BONE MARROW DISEASES
There are too many diseases to list all, but a few examples follow. Aplastic pancytopenia (aplastic anemia, fatty marrow) is when a disease process has damaged hematopoietic cells so those cells are absent and increased fat remains in the marrow. Infectious causes include Ehrlichia canis, parvovirus, FeLV, FIV, septicemia and endotoxemia. Toxic causes include estrogen, phenylbutazone, meclofenamic acid, trimethoprim-sulfadiazine, quinidine, griesofulvin, thiascetarsamide, and some chemotherapeutic agents. Often the diagnosis is idiopathic. Myelofibrosis is somewhat similar in that hematopoietic cells have been damaged and fibrosis has replaced normal tissue.
Canine pure red cell aplasia can be immune mediated (primary) or secondary to parvovirus infection or vaccine in dogs or FeLV of FW in cats. The bone marrow has very few erythroid cells remaining, while other cell lines are normal.
狢neffective hematopoiesis may be difficult to understand. The pattern seen is a deficiency of a cell line in blood (e.g., nonregenerative anemia) yet normal to increased numbers of that cell line are found in the bone marrow (e.g., erythroid hyperplasia). Bone marrow cellularity and morphology in cytologic and histologic samples do not directly measure function. Various chemical, infectious, nutritional, and other causes prevent even increased numbers of cells in the marrow from effectively producing cells that are released from the marrow. Ineffective erythropoiesis may be caused by inflammatory diseases or iron deficiency; ineffective neutropoiesis may be caused by drugs (e.g., phenobarbital) or viruses (e.g., FeLV).
Leukemia is a neoplastic process of hematopoietic cells in the bone marrow. The neoplastic cells are often seen in the blood, giving the name 𢘛hite blood?which one can appreciate by looking at buffy coats in microhematocrit tubes from leukemic patients. The blast cells may be trapped to a great extent in the bone marrow and one may be surprised to see a bone marrow filled with blast cells where the blood had so few blast cells that one could not rule out only the presence of reactive lymphoid cells. The diagnosis of leukemia is a broad topic but most commonly there are over 30% blast cells in the bone marrow to allow an easy basic diagnosis. Specific diagnosis of types of leukemia is useful in countries where treatment of leukemia in dogs and cats is well accepted.

minibabyqq 2007-1-26 02:07

[color=Magenta][size=5][b]子宮頸椎骨的透視Perspective on Cervical Vertebral  [/b][/size][/color]


各種各樣的疾病情況影響子宮頸脊髓造成神經學缺乏和傷殘為動物。建立一個精確診斷必需勸告所有者關於可能的治療選擇和預測。許多子宮頸疾病早期的路線也許相似, 做診斷測試的委託人建立診斷。
尾部子宮頸spondylomyelopathy (CCSM) 共同地指Wobblers 綜合症狀和子宮頸椎骨instability.(1) 病理性反常性與尾部子宮頸spondylomyelopathy 交往可能大致被劃分成二個小組根據年齡在介紹。幼小狗(了不起的丹麥人少於二年紀) 典型地有椎骨畸形以伴隨導致脊髓compression.(2,3) 中年狗的次要軟的組織變動(Doberman Pinschers 四到10 年紀) 有脊髓壓縮由於背部環體纖維變性肥大或Hansen 類型2 盤rupture.(1-3) 許多狗其它養殖被診斷了與CCSM 並且他們典型地是大或巨人breeds.(2,3)
關於CCSM 的討論的第一部份依照被看見將集中於疾病在中年狗(典型地Doberman Pinscher) 與背部環體纖維變性或Hansen 類型II 盤疾病的肥大。多數狗與CCSM 將被提出以逐漸惡化以時間的一個緩慢的進步起始(65%).(1) 狗百分之二十將有疾病一個緩慢的進步起始以一深刻惡化臨床標誌當15% 比females.(1,4) 年齡在介紹變化從1.5 到12 年紀將有臨床標誌一個深刻起始沒有早先問題noted.(1) 男性有CCSM 的更高的發生, 以狗多數分成四到八年年齡group.(1,4) 狗大養殖可能大多影響與disease.(1,4)
一條受影響的狗的提出的情況範圍從後方腿的溫和的不整齊對nonambulatory tetraparesis, 用多數狗有適度地嚴厲能走paraparetic 狀態。不整齊將開始在後方腿和不會是顯然的在前面腿直到後方腿至少是適度地動轉失調的。深刻地受影響的狗典型地被提出nonambulatory 或最好微弱地迴廊。
所有者將訴說顫抖的不平穩的步態在後方腿, 也許注意狗knuckles 。在後方腳。受影響的狗將有一個低頭和脖子姿勢和一般抵抗子宮頸脊椎的引伸。子宮頸痛苦典型地不是存在在這些狗, 雖然一個小數字將陳列溫和的子宮頸痛苦在脖子操作。狗與CCSM 傾向於走以僵硬的stilted 步態在前面腿。
神經學測試將變化根據脊髓壓縮嚴肅。典型的狗將顯示本體感受安置, 跳躍, 和hemiwalking 的缺乏對後方腿。神經學反常性對前面腿缺席或較不嚴厲的比對後方腿不同於為更加嚴厲地受影響的狗。神經學缺乏可能由延伸使更壞脖子。Myotactic 反射將是正常的對hyperreflexic 對後方腿。Myotactic 反射對前面腿是典型地正常的, 雖然他們是堅硬執行由於伸張機口氣。由於壓縮lesion(s) 的地點在C5-6 和C6-7, 你會期待更低的馬達神經元反射對前面腿, 但這些典型地不是明顯的。發怒伸張機反射將是存在如果損害是慢性的。
CCSM 一個根據推定的診斷被做根據歷史、對某人特徵的描述, 和神經學標誌。CCSM 案件提及應該儘快完成建立一個明確的診斷和允許外科更正執行。一個明確的診斷可能用myelography.if myelography 只被做可能執行, 這些箱子提及可能被做在一個明確的診斷的創立以後。
應該執行為CCSM 被懷疑的案件的診斷workup 包括子宮頸脊椎的簡單的射線照相與myelography 和脊髓流體分析一起。Myelography 應該包括側向, ventrodorsal, 和線性牽引看法。脖子的伸直過度看法被勸阻由於造成對脊髓的另外的神經學損傷的可能性。脊髓流體分析執行排除激動疾病。因為大多這些狗是Doberman pinschers, 篩選為甲狀腺機能不足和馮Willebrand 的疾病並且進行與完全血液計數和生物化學的掩護一起。
狗簡單的影片射線照相與CCSM 也許顯示變窄磁盤空間、spondylosis, 對椎骨身體的形狀變動, 和打翻椎骨。打翻椎骨不是在哪裡損害是located.(1) 側向myelographic 看法顯示的可靠的顯示腹壓縮損害經常位於在C5.6 並且/或者脊髓的C6.7. A 背部壓縮之間從ligamentum flavum 也許並且是存在。加寬側向染料專欄也許看在ventrodorsal myelographic 投射在壓縮區域。側向牽引myelographic 看法將展示如果壓縮損害是動態或靜止在自然裡。動態壓縮損害是存在多半時間, 當靜態損害是不凡的在中年狗。如果脊髓的壓縮改善在線性牽引, 損害被認為動態壓縮損害。如果壓縮損害不改善在線性牽引, 它被認為壓縮的一個靜態形式。不同的外科治療必需為問題的更正, 依靠是否壓縮靜態或動態。
對待CCSM 二個方法是醫療療法和手術。醫療管理被表明只如果所有者財政是無法或不願意的安排手術做, 或如果動物有會阻止手術的其它主要衛生問題。醫療管理介入對待狗以類皮質激素和鍛煉制約; 做法典型地提供唯一臨時改善。以時間, 醫療上治療的患者的神經學狀態傾向於惡化。
為脊髓的靜態腹壓縮損害, 二個外科選擇是可利用的。首選是背部laminectomy 壓縮觸犯的區域。這個做法運載神經學上使狗的一次重大機會壞在手術以後, 至少暫時。另一選擇是一個腹子宮頸解壓做法相似與做法被使用取消Hansen 第一類型盤材料。一個被倒置的錐體解壓技術(標準腹解壓技術的修改) 被描述的脊髓的腹解壓減少病態與標準腹decompressive procedure.(5) 交往
為動態腹脊髓壓縮, 一個修改過的分心安定技術使用一個interbody polymethyl 異丁烯酸插座是choice.(4) 這個做法用途作者的做法每polymethyl 異丁烯酸插座拿著椎骨在一個分散的位置如此解壓脊髓。cancellous 骨頭貪佔被安置沿椎骨的腹方面手術後地導致椎骨的spondylosis 到occur.(4), 狗被安置在一個身體塑像四個到八個星期允許椎骨的腹融合發生。
手術後關心為有分心安定技術的狗將取決於他們的神經學狀態。非能走狗將要求可觀的護理保健, 包括保持他們乾燥和將清洗, 確信, 他們接受適當的營養和可變的進水閘, 並且修復。被填塞的臥具譬如蛋條板箱泡沫或waterbeds 將幫助防止decubital 痛處。走的推車是無價的在修復這patients.(5) 為能走患者, 食物並且水應該取得到在一個被舉起的位置因為他們無法吃從一個碗在地板上。這些狗必須並且是限於從對臺階的用途除非協助, 由於風險下落。皮帶走被鼓勵促進肌肉發展和協調。塑像一次被去除, 鞔具被使用代替衣領為狗的生活的剩餘。
預測為狗被對待以修改過的分心修改技術是非常good.(4) 狗的百分之九十有一個成果以這個做法, 與50% 認為是完全地normal.(4) 三個月是平均時間對最大的改善, 雖然一些狗將佔去比是nonambulatory 在手術之時有優選的補救的一次更加粗劣的機會的10 months.(4) 狗是nonambulatory 在手術之時的迴廊dogs.(4) 狗通常不會回到正常神經學狀態, 但有一次合理的機會的是一隻功能寵物。
了不起的丹麥人是狗養殖最共同地受影響以椎骨畸形類型損害。其它大養殖狗可能並且影響以這個疾病的形式。這個Wobblers 疾病的形式典型地看在幼小狗在6.24 月年齡之間。標誌慢慢地臨床是進步並且所有者不能最初地認為問題存在因為他們認為它歸結於小狗粗笨。不整齊開始在後方腿, 也許進步影響前肢。所有者將訴說顫抖的incorodinate 步態與knuckling 腳一起。所有者也許並且聽見釘子小塊在地板或邊路上。痛苦典型地不是存在。神經學測試將變化根據脊髓壓縮嚴肅。典型的狗將顯示本體感受安置, 跳躍, 和hemiwalking 的缺乏對後方腿。神經學反常性對前面腿缺席或較不嚴厲的比對後方腿不同於為更加嚴厲地受影響的狗。神經學缺乏可能由延伸使更壞脖子。Myotactic 反射將是正常的對hyperreflexic 對後方腿。Myotactic 反射對前面腿是典型地正常的雖然他們是堅硬執行由於伸張機口氣。Wobblers 疾病一個根據推定的診斷被做根據歷史、對某人特徵的描述, 和神經學標誌。
診斷工作是同一樣為中年狗以Wobblers 疾病。簡單的射線照相、myelogram, 和脊髓流體分析應該執行。是有用的其它想像技術是CT 掃瞄和MRI 。典型地, 脊髓壓縮多個區域被辨認在子宮頸脊椎。脊髓的壓縮歸結於椎骨的畸形以促進妥協脊髓的次要變動。被認可的反常性包括椎骨運河、畸形關節過程以退化變動, 背部環體纖維變性的肥大ligamentum flavum 和聯接膠囊, 和肥大的狹窄。動態和靜態損害可能是存在。意志壓縮顯著很少被改進與牽引, 然而。
手術的目標是解壓脊髓和抵制任一固有不穩定。由於壓縮的典型的環型本質, 一背部laminectomy 執行。咬邊lamina 的邊將釋放脊髓的側向邊。一背部laminectomy 也許導致更多不穩定由於組織的本質被去除或被分開。小平面的螺絲和導線定像被設法抵銷不穩定。磁盤空間的融合從一種腹方法可能並且被設法消滅不穩定。歷史上, 預測為幼小狗以Wobblers 疾病不是好的。在密蘇里大學, 我們結合背部laminectomy 、滯後小平面的螺絲定像, 和腹interbody 融合改正這些狗。早期的成功令人鼓舞。

A variety of disease conditions affect the cervical spinal cord resulting in neurological deficits and disability for the animal. Establishing a precise diagnosis is required to advise the owner about possible treatment options and prognosis. The early course of many cervical diseases may be similar, making diagnostic testing mandatory to establish a diagnosis.
Caudal cervical spondylomyelopathy (CCSM) is commonly referred to as Wobblers syndrome and cervical vertebral instability.(1) The pathological abnormalities associated with caudal cervical spondylomyelopathy can be roughly divided into two groups based on the age at presentation. Young dogs (Great Danes less than two years of age) typically have vertebral malformation with accompanying secondary soft tissue changes that cause spinal cord compression.(2,3) Middle-aged dogs (Doberman Pinschers four to 10 years of age) have spinal cord compression as a result of hypertrophy of the dorsal annulus fibrosis or Hansen type 2 disk rupture.(1-3) Numerous other breeds of dogs have been diagnosed with CCSM and they typically are large or giant breeds.(2,3)
The first part of the discussion of CCSM will focus on the disease as seen in the middle-aged dog (typically Doberman Pinscher) with the hypertrophy of the dorsal annulus fibrosis or Hansen type II disk disease. Most dogs with CCSM will be presented with a slow progressive onset that gradually worsens with time (65%).(1) Twenty percent of dogs will have a slow progressive onset of the disease with an acute worsening of the clinical signs while 15% will have an acute onset of clinical signs with no previous problems noted.(1) Males have a higher incidence of CCSM than females.(1,4) Age at presentation varies from 1.5 to 12 years of age, with the majority of the dogs falling into the four to eight year old age group.(1,4) Most of the large breeds of dogs can be affected with disease.(1,4)
The presenting condition of an affected dog will range from mild ataxia of the rear legs to nonambulatory tetraparesis, with most dogs having a moderately severe ambulatory paraparetic status. The ataxia will start in the rear legs and not be evident in the front legs until the rear legs are at least moderately ataxic. Acutely affected dogs typically are presented nonambulatory or at best weakly ambulatory.
The owner will complain of a wobbly unsteady gait in the rear legs and may notice that the dogs 恾nuckles over?on the rear feet. Affected dogs will generally have a low head and neck posture and resist extension of the cervical spine. Cervical pain is typically not present in these dogs, though a small number will exhibit mild cervical pain on neck manipulation. Dogs with CCSM tend to walk with a stiff stilted gait in the front legs.
Neurologic testing will vary depending on the severity of spinal cord compression. The typical dog will show proprioceptive placing, hopping, and hemiwalking deficits to the rear legs. Neurologic abnormalities to the front legs will be absent or less severe than to the rear legs other than for the more severely affected dogs. Neurologic deficits can be made worse by extending the neck. Myotactic reflexes will be normal to hyperreflexic to the rear legs. Myotactic reflexes to the front legs are typically normal, though they are hard to perform due to extensor tone. Because of the location of the compressive lesion(s) at C5-6 and C6-7, one would expect lower motor neuron reflexes to the front legs, but these typically are not apparent. Cross extensor reflexes will be present if the lesion is chronic.
A presumptive diagnosis of CCSM is made based on history, signalment, and neurologic signs. Referral of CCSM cases should be done as soon as possible to establish a definitive diagnosis and to allow surgical correction to be performed. A definitive diagnosis can only be made with myelography𡟙f myelography can be performed, referral of these cases can be made after establishment of a definitive diagnosis.
The diagnostic workup that should be performed for suspected cases of CCSM includes plain radiographs of the cervical spine along with myelography and spinal fluid analysis. Myelography should include lateral, ventrodorsal, and linear traction views. Hyperextension views of the neck are discouraged because of the possibility of causing additional neurologic damage to the spinal cord. A spinal fluid analysis is performed to rule out inflammatory disease. Since most of these dogs are Doberman pinschers, screening for hypothyroidism and Von Willebrand's disease is also performed along with complete blood count and biochemical screening.
Plain film radiographs of dogs with CCSM may show narrowing of the disk space, spondylosis, shape changes to the vertebral body, and tipping of the vertebra. Tipping of the vertebrae is not a reliable indicator of where the lesion is located.(1) The lateral myelographic view will show a ventral compressive lesion most often located between C5? and/or C6?. A dorsal compression of the spinal cord from the ligamentum flavum may also be present. A widening of the lateral dye columns may be seen on the ventrodorsal myelographic projection over the area of compression. The lateral traction myelographic view will demonstrate if the compressive lesion is dynamic or static in nature. Dynamic compressive lesions are present most of the time, while static lesions are uncommon in the middle-aged dog. If the compression of the spinal cord improves on linear traction, the lesion is considered a dynamic compressive lesion. If the compressive lesion does not improve on linear traction, it is considered a static form of compression. Different surgical treatments are required for correction of the problem, depending on whether the compression is static or dynamic.
The two methods of treating CCSM are medical therapy and surgery. Medical management is indicated only if the owner is unable financially or unwilling to have surgery performed, or if the animal has other major health problems which would preclude surgery. Medical management involves treating the dog with corticosteroids and exercise restriction; the procedure typically provides only temporary improvement. With time, the neurologic status of the medically treated patient tends to worsen.
For static ventral compressive lesions of the spinal cord, two surgical options are available. The first option is dorsal laminectomy over the offending area of compression. This procedure carries a significant chance of making the dog worse neurologically after surgery, at least on a temporary basis. The other choice is a ventral cervical decompression procedure similar to the procedure used to remove Hansen type 1 disk material. An inverted cone decompression technique (a modification of the standard ventral decompression technique) has been described for ventral decompression of the spinal cord to decrease the morbidity associated with the standard ventral decompressive procedure.(5)
For dynamic ventral spinal cord compression, a modified distraction-stabilization technique using an interbody polymethyl methacrylate plug is the author's procedure of choice.(4) This procedure uses a plug of polymethyl methacrylate to hold the vertebrae in a distracted position thus decompressing the spinal cord. A cancellous bone graft is placed along the ventral aspect of the vertebrae to cause a spondylosis of the vertebrae to occur.(4) Postoperatively, the dog is placed in a body cast for four to eight weeks to allow ventral fusion of the vertebrae to occur.
Postoperative care for dogs that have had the distraction-stabilization technique will depend on their neurologic status. Non-ambulatory dogs will require considerable nursing care, including keeping them dry and clean, making sure that they receive proper nutritional and fluid intake, and rehabilitation. Padded bedding such as egg-crate foam or waterbeds will help prevent decubital sores. Walking carts are invaluable in rehabilitation of these patients.(5) For ambulatory patients, food and water should be available in an elevated position because they cannot eat from a bowl on the floor. These dogs must also be restricted from use of stairs unless assisted, because of the risk of falling. Leash walking is encouraged to promote muscle development and coordination. Once the cast is removed, a harness is used instead of a collar for the rest of the dog's life.
Prognosis for dogs treated with the modified distraction-modification technique has been very good.(4) Ninety percent of the dogs had a successful outcome with this procedure, with 50% considered to be completely normal.(4) Three months is the average time to maximal improvement, though some dogs will take up to 10 months.(4) Dogs that are nonambulatory at the time of surgery have a poorer chance of optimal recovery than ambulatory dogs.(4) Dogs that are nonambulatory at the time of surgery usually will not return to a normal neurologic status, but have a reasonable chance of being a functional pet.
The Great Dane is the breed of dog most commonly affected with the vertebral malformation type of lesion. Other large breed dogs can also be affected with this form of the disease. This form of the Wobblers disease is seen in young dogs typically between 6?4 months of age. Clinically signs are slowly progressive and the owner may not initially recognize that a problem exists because they think that it is due to puppy clumsiness. Ataxia starts in the rear legs and may progress to affect the forelegs. The owner will complain of a wobbly incorodinate gait along with knuckling of the feet. The owner may also hear the nails scrap on the floor or sidewalk. Pain typically is not present. Neurologic testing will vary depending on the severity of spinal cord compression. The typical dog will show proprioceptive placing, hopping, and hemiwalking deficits to the rear legs. Neurologic abnormalities to the front legs will be absent or less severe than to the rear legs other than for the more severely affected dogs. Neurologic deficits can be made worse by extending the neck. Myotactic reflexes will be normal to hyperreflexic to the rear legs. Myotactic reflexes to the front legs are typically normal though they are hard to perform due to extensor tone. A presumptive diagnosis of Wobblers disease is made based on history, signalment, and neurological signs.
The diagnostic work-up is the same as for the middle aged dog with Wobblers disease. Plain radiographs, myelogram, and spinal fluid analysis should be performed. Other imaging techniques that are helpful are CT scans and MRI. Typically, multiple areas of spinal cord compression are identified in the cervical spine. Compression of the spinal cord is due to malformation of the vertebrae with secondary changes that further compromise the spinal cord. Abnormalities that are recognized include stenosis of the vertebral canal, malformation of the articular processes with degenerative changes, hypertrophy of the ligamentum flavum and joint capsule, and hypertrophy of the dorsal annulus fibrosis. Both dynamic and static lesions can be present. Rarely will compression be significantly improved with traction, however.
The goals of surgery are to decompress the spinal cord and counteract any inherent instability. Because of the typical annular nature of the compression, a dorsal laminectomy is performed. Under-cutting the sides of the lamina will free up the lateral side of the spinal cord. A dorsal laminectomy may lead to more instability due to the nature of the tissue removed or detached. Screw and wire fixation of the facets has been tried to offset the instability. Fusion of the disc space from a ventral approach can also be tried to eliminate the instability.?Historically, the prognosis for young dogs with Wobblers disease has not been good. At the University of Missouri, we have combined dorsal laminectomy, lag screw fixation of the facets, and ventral interbody fusion to correct these dogs. Early success has been encouraging.

minibabyqq 2007-1-26 02:08

[color=Magenta][size=5][b]頭蓋骨Cruciate 短少Traditional Repair Techniques  [/b][/size][/color]


解剖學
抑止聯接是複雜, diarthroidial 聯接包括femoropatellar 和femorotibial 清楚的發音。抑止聯接有由各種各樣的韌帶和腱壓抑並且聯合膠囊和肌肉的六個自由程度(彎曲, 引伸、varus 和valgus 測角, 內部和外在自轉) 。狗的抑止有110 度的行動的正常範圍, 範圍從150 度在充分的引伸對40 度在充分的彎曲。抑止由quadriceps 肌肉小組擴大; 臏骨是一根sesamoid 骨頭在用於改進肌肉腱單位的機械利益的quadriceps 腱之內。quadriceps 小組包括rectus fomoris 、vastus medialis 、vastus intermedius, 和vastus lateralis 。這些肌肉起源於接近股骨和骨盆, 和插入通過patellar 韌帶在tibial tuberosity 。長的數字式伸張機肌肉並且擔當未成年人抑止伸張機。抑止由semimembranosus/semitendinosus 肌肉屈曲。popliteal 肌肉是抑止板轉器。
頭蓋骨和尾部cruciate 韌帶是抑止聯接的主要安定器。頭蓋骨cruciate 起源於側向大腿骨髁和插入物的中間邊在頭蓋骨中間tibial 高原。它由二份組成: craniomedial 和caudolateral 帶。craniomedial 帶是緊的在彎曲並且引伸, 但是, 更大的caudolateral 帶是緊在引伸和寬鬆在彎曲。尾部cruciate 起源於中間大腿骨髁和插入物的側向邊於脛骨的popliteal 窩。它由一條頭蓋骨和尾部帶組成。頭蓋骨帶是緊的在彎曲並且尾部帶是緊的在引伸。cruciate 韌帶擔當抑止的主要限制和限制頭蓋骨尾部行動、內部自轉, 和伸直過度。
中間和側向抵押韌帶是還抑止的重要安定器。中間抵押韌帶起源於末端中間大腿骨髁和插入物在接近中間脛骨。側向抵押韌帶起源於末端側向大腿骨髁和插入物在腓骨的頭。這些韌帶用於限制varus (側向抵押) 並且valgus (中間抵押) 不穩定。側向抵押韌帶變得寬鬆當抑止被屈曲並且允許脛骨內部轉動。當抑止是延長的, 側向抵押韌帶拉緊和轉動外在地脛骨對它的正常重量空頭處境。這為人所知作為screw 家庭機制。
中間和側向menisci 是C. 擔當抑止的主要安定器fibrocartilage 的被塑造的楔子。側向半月板綁住對脛骨由cranio- 和caudolateral meniscotibial 韌帶, 對股骨與meniscofemoral 韌帶, 和到中間半月板intermeniscal 韌帶。中間半月板綁住對脛骨由cranio- 和caudomedial meniscotibial 韌帶和到側向半月板intermeniscal 韌帶。中間半月板並且附有中間抵押韌帶和caudomedial 聯合膠囊。
頭蓋骨Cruciate 破裂
1926 年頭蓋骨cruciate 韌帶破裂的第一報告在狗在, 但不是直到50 年代外科更正第一報告被描述了。從那以後, 頭蓋骨cruciate 短少膝蓋的修理的許多外科技術被報告了在一個技術的literature.(1) 選擇頭蓋骨cruciate- 短少膝蓋的修理的應該根據許多標準包括大小、狗的年齡、和傷害的作用, 慢性和外科醫生特選。修理技術被分類像額外關節和內部關節。額外關節修理是那些穩定聯接從境外聯合膠囊和包括招牌lata 鱗狀重疊、側向retinacular 鱗狀重疊(DeAngelis 縫合), 和fibular 頂頭交叉點。內部關節技術使用某一類貪佔材料解剖上替換頭蓋骨cruciate 韌帶
所有外科手術為CCL 不穩定從抑止聯接的徹底的探險開始通過一種側向parapatellar 方法。所有內部關節結構被審查。最共同的傷害共存與CCL 破裂是一滴淚花在中間半月板的尾部墊鐵(以後被談論) 。尾部cruciate 韌帶(CaCL) 並且抵押韌帶並且被審查, 並且長的數字式伸張機和popliteus 的腱。被爆裂的CCL 和任何殘餘的原封CCL 的殘餘的樹樁被去除。它假設, 殘餘的原封CCL 或被損壞或將變完全地爆裂如果留下。如果中間半月板的尾部墊鐵被損壞, 只有損壞的部份被去除。
額外關節修理技術
招牌Lata 鱗狀重疊
鱗狀重疊提到重疊二層像瓦片或木瓦。招牌lata 的鱗狀重疊影響將採取任何鬆馳在招牌lata 外面如此拉緊組織。拉緊招牌lata 因而穩定聯接由使脛骨的頭蓋骨翻譯和內部自轉減到最小。這個技術, 作為安定單一手段, 1966 年1969 年第一次被報告了並且以後被修改被增加Lembert sutures.(2,3) 招牌lata 鱗狀重疊第二層數最適當地被使用作為附屬對其它方法抑止安定, 不應該被使用作為安定單一方法。
Lembert 和Mayo 床墊縫合樣式是主要類型縫合樣式被使用成鱗狀招牌lata 。能吸收的縫合, 譬如Vicryl 或PDS, 是更喜歡的縫合材料類型。縫合安置開始末端和進行在一個接近方向。緊張被判斷, 在安置第一縫合之前, 由多少招牌lata 的邊緣將重疊。必須非常被保重對不是地方緊張在組織, 一側向patellar luxation 導致。
側向Retinacular 鱗狀重疊
1970 年側向retinacular 鱗狀重疊為安定頭蓋骨cruciate 短少抑止第一次被報告了由DeAngelis 和Lau 。這個技術共同地指DeAngelis technique.(4) 這個技術最初包括安置重的nonabsorbable 縫合材料在側向fabella 附近到臏骨韌帶的末端三分之一。縫合材料對應於正常頭蓋骨cruciate 韌帶的取向當它遊遍聯接除了縫合是在聯合膠囊外面。這個技術的眾多的改動做了包括安置縫合通過孔操練了tibial tuberosity 並且增加相似的被指揮的縫合從二縫合的joint.(5) 安置的中間邊從側向抵押韌帶來臏骨和一縫合從fabella 來臏骨韌帶並且被描述了為抑止stabilization.(5)
側向retinacular 鱗狀重疊被使用了為所有狗的大小抑止的安定。典型地, 側向retinacular 鱗狀重疊運作最好為狗40.45 磅或較少在重量。易變的結果遇到當狗的大小增加。招牌lata 鱗狀重疊一般執行除這個技術之外進一步穩定聯接。
重的nonabsorbable 縫合材料(尼龍, 結辮的聚酯) 被使用為側向retinacular 鱗狀重疊。不鏽鋼導線典型地並且是used.(7), 縫合被拉緊與抑止被擴大和脛骨外在地被轉動。多個結是需要的鞏固縫合。通過縫合通過一個孔在tibial tuberosity 大概准許更好停住為縫合。在時間期間, 所有這些縫合打破或鬆懈。有希望地縫合維護聯合穩定直到periarticular 纖維變性穩定聯接。最共同的手術後複雜化以這個技術是膨脹和排水設備從縫合。這兩複雜化被報告發生在18% 和21% cases.(3,9) 中
Fibular 頂頭交叉點
Fibular 頂頭交叉點是使用側向抵押韌帶穩定抑止聯接的一個額外關節修理技術。(10) 側向抵押韌帶運行從股骨的側向epicondyle 到fibular 頭。在fibular 頭的頭蓋骨交叉點以後, 側向抵押韌帶的取向被改方向接近那頭蓋骨cruciate 韌帶。頭蓋骨抽屜行動和聯接的過份內部自轉由側向抵押韌帶的這個取向防止。這個做法可能被使用為任一狗的大小與或頭蓋骨cruciate 韌帶的深刻或慢性破裂。Fibular 頂頭交叉點特別適用與狗以一個內部關節技術不是中意的抑止的骨關節炎。頭蓋骨cruciate 破裂慢性在修理之前被報告不影響臨床結果在修理以後以這個技術。(10) 其它fibular 頂頭交叉點的好處是更短的恢復時間與內部關節techniques.(10) 比較
外科手術介入切開fibular 頭的ligamentous 附件對脛骨以便fibular 頭可能cranially 被移置。fibular 頭被移動今後向點, 抽屜標誌被消滅了。fibular 頭然後綁到脛骨上與K 導線和緊張帶wire.(10)
手術後地, 腿被安置在軟被填塞的繃帶10.14 天。狗的活動是有限的為第一月和然後慢慢地增加的第二個月。這個做法的長期臨床評估表明, 90% 狗有一優秀或fibular 頂頭交叉點的好result.(11) 研究評估表示, 技術沒有控制頭蓋骨抽屜行動或旋轉的不穩定, 不是成功的在恢復肢體作用, 和沒有防止側向抵押韌帶的聯合degeneration.(12) 重大伸長發生了第一3 個星期在手術以後。(13) 抵押韌帶的僵硬被增加隨時間, however.(13) 清楚地那裡是在臨床上的一個區別和研究評估至於多麼有效的fibular 頂頭交叉點是。最共同的複雜化與相關fibular 頂頭交叉點是fibular 頭的醫原性破裂intraoperatively (12.5%) 並且seroma 形成(10.7%) 在fibular 頭手術後。被報告了包括導線破損的其它複雜化並且撕毀側向抵押ligament.(10) Pin 鬆懈和對腓骨神經的遷移、尾部膝狀的動脈的損傷, 和撕裂是其它可能的複雜化。
內部關節修理技術
有fascial, patellar 韌帶, 或非生物貪佔被拉扯通過抑止聯接的許多規程在這種情況下CCL 的自然作用被仿造嚴密。多數這些規程執行通過一種側向parapatellar 方法並且聯接被探索和debrided 和在extraarticular 規程。under 和在做法一般是這些規程代表和最常用。這個做法運用自生的貪佔包括patellar 韌帶的側向1/3 並且招牌lata 從側向大腿。這貪佔由切準備它的側向, 中間, 和接近附件, 留給它末端上附上。貪佔然後被拉扯在intermeniscal 韌帶之下和通過聯合over 它由縫合或骨頭螺絲和尖洗衣機停住側向大腿骨髁的上面。聯接定期地是閉合的。這貪佔將減弱在第一二個星期期間在手術以後, 爾後將獲取力量。它到達preoperative 力量六個星期在手術以後。支持繃帶是必要的六個星期在手術以後。其它intraarticular 規程運用碳纖維、同種異體移植從patellar 韌帶, 或其它自生的貪佔; 但是, 基本的做法是相同。


Anatomy
The stifle joint is a complicated, diarthroidial joint consisting of a femoropatellar and a femorotibial articulation. The stifle joint has six degrees of freedom (flexion, extension, varus and valgus angulation, internal and external rotation) that are constrained by various ligaments and tendons as well as the joint capsule and muscles. The dog's stifle has a normal range of motion of 110 degrees, ranging from 150 degrees in full extension to 40 degrees in full flexion. The stifle is extended by the quadriceps muscle group; the patella is a sesamoid bone within the quadriceps tendon that serves to improve the mechanical advantage of the muscle-tendon unit. The quadriceps group consists of the rectus fomoris, vastus medialis, vastus intermedius, and vastus lateralis. These muscles originate from the proximal femur and pelvis, and insert via the patellar ligament on the tibial tuberosity. The long digital extensor muscle also serves as a minor stifle extensor. The stifle is flexed by the semimembranosus/semitendinosus muscles. The popliteal muscle is a stifle rotator.
The cranial and caudal cruciate ligaments are primary stabilizers of the stifle joint. The cranial cruciate originates from the medial side of the lateral femoral condyle and inserts on the cranial medial tibial plateau. It is composed of two parts: the craniomedial and caudolateral bands. The craniomedial band is tight in flexion and extension, whereas, the larger caudolateral band is tight in extension and loose in flexion. The caudal cruciate originates from the lateral side of the medial femoral condyle and inserts in the popliteal fossa of the tibia. It is composed of a cranial and caudal band. The cranial band is tight in flexion and the caudal band is tight in extension. The cruciate ligaments serve as primary constraint of the stifle and limit cranial-caudal motion, internal rotation, and hyperextension.
The medial and lateral collateral ligaments are also important stabilizers of the stifle. The medial collateral ligament originates from the distal medial femoral condyle and inserts on the proximal medial tibia. The lateral collateral ligament originates from the distal lateral femoral condyle and inserts on the head of the fibula. These ligaments serve to limit varus (lateral collateral) and valgus (medial collateral) instability. The lateral collateral ligament becomes loose when the stifle is flexed and allows the tibia to rotate internally. As the stifle is extended, the lateral collateral ligament tightens and externally rotates the tibia to its normal weight bearing position. This is known as the 𦽳crew home mechanism.?/p> The medial and lateral menisci are 鏠?shaped wedges of fibrocartilage that serve as primary stabilizers of the stifle. The lateral meniscus is secured to the tibia by the cranio- and caudolateral meniscotibial ligaments, to the femur with the meniscofemoral ligament, and to the medial meniscus by the intermeniscal ligament. The medial meniscus is secured to the tibia by the cranio- and caudomedial meniscotibial ligaments and to the lateral meniscus by the intermeniscal ligament. The medial meniscus is also attached to the medial collateral ligament and to the caudomedial joint capsule.
Cranial Cruciate Rupture
The first report of a cranial cruciate ligament rupture in the dog was in 1926, but it was not until the 1950s that the first report of surgical correction was described. Since then, numerous surgical techniques for repair of the cranial cruciate-deficient knee have been reported in the literature.(1) Selection of a technique for repair of the cranial cruciate- deficient knee should be based upon numerous criteria including size, age, and function of the dog, chronicity of the injury and surgeon preference. Repair techniques are classified as extra-articular and intra-articular. Extra-articular repairs are those that stabilize the joint from outside of the joint capsule and include fascia lata imbrication, lateral retinacular imbrication (DeAngelis suture), and fibular head transposition. Intra-articular techniques use some sort of graft material to anatomically replace the cranial cruciate ligament
All surgical procedures for CCL instability begin with a thorough exploration of the stifle joint through a lateral parapatellar approach. All intra-articular structures are examined. The most common injury coexisting with a CCL rupture is a tear in the caudal horn of the medial meniscus (discussed later). The caudal cruciate ligament (CaCL) and collateral ligaments are also examined, as well as the tendons of the long digital extensor and popliteus. The remaining stumps of the ruptured CCL and any remaining intact CCL are removed. It is assumed that the remaining intact CCL either is damaged or will become completely ruptured if left. If the caudal horn of the medial meniscus is damaged, only the damaged portion is removed.
Extra-articular Repair Techniques
Fascia Lata Imbrication
Imbrication refers to the overlapping of two layers like tiles or shingles. The affect of imbrication of the fascia lata is to take any slack out of the fascia lata thus tightening the tissue. The tightening of the fascia lata thus stabilizes the joint by minimizing the cranial translation and internal rotation of the tibia. This technique, as the sole means of stabilization, was first reported in 1966 and later modified in 1969 by adding a second layer of Lembert sutures.(2,3) Fascia lata imbrication is most appropriately used as an adjunct to other methods of stifle stabilization and should not be used as the sole method of stabilization.
The Lembert and Mayo-Mattress suture patterns are the main type of suture patterns used to imbricate the fascia lata. An absorbable suture, such as Vicryl or PDS, is the preferred suture material type. Suture placement starts distal and proceeds in a proximal direction. Tension is judged, before placing the first suture, by how much the edges of the fascia lata will overlap. Care must be taken to not place so much tension on the tissue that a lateral patellar luxation is produced.
Lateral Retinacular Imbrication
Lateral retinacular imbrication for stabilization of the cranial cruciate deficient stifle was first reported in 1970 by DeAngelis and Lau. This technique is commonly referred to as the DeAngelis technique.(4) This technique originally consisted of placing a heavy nonabsorbable suture material around the lateral fabella to the distal one-third of the patella ligament. The suture material corresponds to the orientation of the normal cranial cruciate ligament as it travels through the joint except that the suture is outside of the joint capsule. Numerous modifications of this technique have been made including placing the suture through a hole drilled in the tibial tuberosity and adding a similar directed suture from the medial side of the joint.(5) Placement of two sutures from the lateral collateral ligament to the patella and one suture from the fabella to the patella ligament has also been described for stifle stabilization.(5)
Lateral retinacular imbrication has been used for stabilization of the stifle of all sizes of dogs. Typically, lateral retinacular imbrication works best for dogs 40?5 pounds or less in weight. Variable results are encountered as the size of the dog increases. Fascia lata imbrication generally is performed in addition to this technique to further stabilize the joint.
Heavy nonabsorbable suture material (nylon, braided polyester) is used for lateral retinacular imbrication. Stainless steel wire has also been used.(7) Typically, the suture is tightened with the stifle extended and the tibia externally rotated. Multiple knots are needed to secure the suture. Passing the suture through a hole in the tibial tuberosity probably allows better anchoring for the suture. Over time, all of these sutures break or loosen. Hopefully the sutures maintain joint stability until periarticular fibrosis stabilizes the joint. The most common postoperative complications with this technique are swelling and drainage from the suture. These two complications are reported to occur in 18% and 21% of cases.(3,9)
Fibular Head Transposition
Fibular head transposition is an extra-articular repair technique that uses the lateral collateral ligament to stabilize the stifle joint.(10) The lateral collateral ligament runs from the lateral epicondyle of the femur to the fibular head. After cranial transposition of the fibular head, the orientation of the lateral collateral ligament is redirected to approximate that of the cranial cruciate ligament. Cranial drawer motion and excessive internal rotation of the joint are prevented by this orientation of the lateral collateral ligament. This procedure can be used for any size of dog with either acute or chronic ruptures of the cranial cruciate ligament. Fibular head transposition is particularly suited for dogs with osteoarthritis of the stifle where an intra-articular technique is not desirable. Chronicity of cranial cruciate rupture prior to repair has been reported not to affect clinical results after repair with this technique.(10) Another benefit of fibular head transposition is the shorter recovery time compared to intra-articular techniques.(10)
The surgical procedure involves cutting the ligamentous attachments of the fibular head to the tibia so that the fibular head can be transposed cranially. The fibular head is moved forward to a point that the drawer sign has been eliminated. The fibular head is then secured to the tibia with K-wires and a tension band wire.(10)
Postoperatively, the leg is placed in a soft-padded bandage for 10?4 days. The dog's activity is limited for the first month and then slowly increased over the second month. Long-term clinical evaluation of this procedure indicated that 90% of the dogs had an excellent or good result.(11) Research evaluation of fibular head transposition showed that the technique did not control cranial drawer motion or rotational instability, was not successful in restoring limb function, and did not prevent joint degeneration.(12) Significant elongation of the lateral collateral ligament occurred over the first 3 weeks after surgery.(13) Stiffness of the collateral ligament increased over time, however.(13) Clearly there is a difference in the clinical and research evaluation as to how effective fibular head transposition is. The most common complications associated with fibular head transposition was iatrogenic fracture of the fibular head intraoperatively (12.5%) and seroma formation (10.7%) over the fibular head postoperatively. Other complications that have been reported include wire breakage and tearing of the lateral collateral ligament.(10) Pin loosening and migration, damage to the peroneal nerve, and laceration of the caudal geniculate artery are other possible complications.
Intra-articular Repair Techniques
There are numerous procedures in which a fascial, patellar ligament, or non-biologic graft is pulled through the stifle joint in such a way that the natural function of the CCL is closely mimicked. The majority of these procedures are performed through a lateral parapatellar approach and the joint is explored and debrided as in the extraarticular procedures. The 𠀾nder-and-over?procedure is generally the representative of these procedures and is the most commonly used. This procedure utilizes an autogenous graft including the lateral 1/3 of the patellar ligament as well as the fascia lata from the lateral thigh. This graft is prepared by incising its lateral, medial, and proximal attachments, leaving it attached distally. The graft is then pulled under the intermeniscal ligament and through the joint 㺸ver the top?of the lateral femoral condyle where it is anchored by sutures or a bone screw and spiked washer. The joint is closed routinely. This graft will weaken during the first two weeks after surgery and will gain strength thereafter. It reaches preoperative strength six weeks after surgery. A support bandage is necessary for six weeks after surgery. Other intraarticular procedures utilize carbon fibers, allografts from patellar ligament, or other autogenous grafts; however, the basic procedure is the same.

minibabyqq 2007-1-26 02:09

[color=Magenta][size=5][b]動物按摩脊柱治療  [/b][/size][/color]


按摩脊柱治療者和操縱療法最近集成了常規獸醫。這些療法有: 按摩脊柱治療者、Osteopathy 、Myofascial 發行(軟的組織唯一), 和按摩。按摩脊柱治療者從希臘cheir. 意思手和praxis. 意思實踐被獲得, 暗示, 這是實踐完成用手。它被定義作為藝術並且dysrelationships 的診斷和更正科學在神經系統和脊髓專欄之間通過手工脊髓manipulation.(1) 由於按摩脊柱治療者的AVMA 政策闡明, 一位被准許的獸醫必須被介入在診斷, 規定, 和動物的監督的按摩脊柱治療者治療。提及必須被做對一位獸醫以畢業後的訓練或誰是一位被准許的按摩醫生, 並且在依照以狀態實踐行動。按摩脊柱治療者關心是一種全部方法對許多馬和狗的健康和性能問題。按摩脊柱治療者不替換傳統獸醫和手術, 而是提供關心一個供選擇的方法。按摩脊柱治療者集中於健康和適當作用脊髓專欄。
脊髓專欄包括一個複雜結構組成由骨頭、韌帶、肌肉、神經、血管, 和lymphatics 。它提供支持中央神經系統的框架, 內臟的保護, 和保護。
主要挑戰的當中一個在集成的按摩脊柱治療者在獸醫方面是術語被使用在人的按摩脊柱治療者, 是外國對獸醫。例如, 半脫位的定義是完全地不同的對獸醫和按摩醫生, 導致許多誤解和辯論。你需要看當前的定義為了更好瞭解按摩脊柱治療者概念。這些定義和概念演變。按摩脊柱治療者馬達單位被定義作為二塊毗鄰椎骨和他們伴生的結構, 包括韌帶血管, 聯接、肌肉, 和椎間的孔內容。從按摩脊柱治療者透視, 椎骨半脫位複合體被定義作為一disrelationship 在椎骨段之間與接觸椎骨有關係, 造成正常biomechanical 和神經學作用干擾。二個主要干擾起因於這disrelationship 。你是一個kinesiopathic 組分造成馬達單位的運動病理學(亢奮或低亞硫酸鈉機動性) 。秒鐘是一個neuropathic 組分造成神經系統的組分的病理學(神經系統的作用的幫助或禁止) 。
半脫位的起因包括創傷傷害, 手術後複雜化, 相應一致, 多餘重量, 遺傳性, 或先天不足。是富挑戰性使獸醫瞭解的其它概念是調整或操作。調整被定義作為一根short 槓桿, 高速, 快推力用具體力量被應用在一個具體方向嚮一塊具體椎骨和被設計提供最大的力量以最小的組織損傷。操作分佈力量對多段通過long 槓桿, 緩慢的速度, 非推了技術。這些全部根據Wolf.s 法律, structure 跟隨作用。換句話說, 功能問題在實際結構瑕疵之前。
半脫位複合體病理生理學包括脊髓神經根或脊髓壓縮, vertebrobasilar 動脈不足、somatovisceral 官能不良, 和被減少的流動性。獸醫按摩脊柱治療者研究是有限的。多數最近研究由凱文・Hausler 博士開展了在康奈爾獸醫學校, 他提供馬脊椎流動性和展示馬脊髓運動跟隨按摩脊柱治療者調整。
按摩脊柱治療者考試技術包括靜態觸診、行動觸診, 和步態評估。靜態觸診評估背部和橫向spinous 過程對稱。對稱被評估從左到右, 頭蓋骨對尾部, 背部對腹, 並且看肌組織的對稱, 尋找任一肌肉萎縮、駝背(蟑螂後面), 或脊柱側凸。評估並且包括檢查熱、痛苦、肌肉緊張, 和痙孿。行動觸診包括行動的活躍和被動範圍的評估在椎骨馬達單位。側向彎曲、軸向自轉、彎曲, 和引伸全部被評估。
在考試以後, 調整和操作嚮適當的區域被申請。輔助關心也許包括針刺, 肌肉弛緩劑, 休息, 按摩, 舒展鍛煉、laser 療法、超聲波, 或磁性療法。
按摩脊柱治療者關心也許是聯合入常規伴侶動物實踐為預防醫療保健, 運動醫學為敏捷性試驗狗, 工作狗, 並且其他人。它也許被使用作為附屬為後面和脖子痛的治療或對待次要報償對主要問題譬如hip 發育異常。進一步研究是需要的提供行動機制、徵兆和獸醫按摩脊柱治療者的局限和禁忌症候。附加培訓節目需要被開發。科羅拉多獸醫州立大學學院提供這種類第一節目在美國獸醫學校。未來按摩脊柱治療者將包括它以專業方式作為獸醫的整體部分。

Chiropractic and manipulative therapies have recently been integrated into conventional veterinary medicine. These therapies include: Chiropractic, Osteopathy, Myofascial Release (soft tissue only), and Massage. Chiropractic is derived from the Greek 𡤧heir?meaning hand and 𢖯raxis?meaning practice, implying that it is a practice done by hand. It is defined as the art and science of diagnosis and correction of dysrelationships between the nervous system and the spinal column through manual spinal manipulation.(1) The AVMA policy on chiropractic states that a licensed veterinarian must be involved in diagnosing, prescribing, and supervising chiropractic treatment of animals. Referrals must be made to a veterinarian with post-graduate training or who is a licensed chiropractor, and in conformance with state practice acts. Chiropractic care is a holistic approach to many of the health and performance problems of the horse and dog. Chiropractic does not replace traditional veterinary medicine and surgery, but provides an alternative method of care. Chiropractic focuses on the health and proper functioning of the spinal column.
The spinal column consists of a complex structure composed of bones, ligaments, muscles, nerves, blood vessels, and lymphatics. It provides a framework of support, protection of the central nervous system, and protection of internal organs.
One of the major challenges in integrating chiropractic in veterinary medicine is the terminology used in human chiropractic, which is foreign to veterinarians. For example, the definition of a subluxation is completely different to a veterinarian and a chiropractor, leading to numerous misunderstandings and debates. One needs to look at current definitions in order to better understand chiropractic concepts. These definitions and concepts are evolving as well. The Chiropractic Motor Unit is defined as two adjacent vertebrae and their associated structures, including ligaments blood vessels, joints, muscles, and the contents of intervertebral foramen. From a chiropractic perspective, a vertebral subluxation complex is defined as a disrelationship between a vertebral segment in association with contiguous vertebrae, resulting in disturbance of normal biomechanical and neurologic function. Two main disturbances result from this disrelationship. One is a kinesiopathic component resulting in pathology of movement of the motor unit (hyper or hypo mobile). The second is a neuropathic component resulting in pathology of the neural component (facilitation or inhibition of neural function).
Causes of subluxations include traumatic injury, postoperative complications, conformation, excess weight, hereditary, or congenital defects. Another concept that is challenging for veterinarians to understand is an adjustment or manipulation. An adjustment is defined as a 𦽳hort-lever, high-velocity, quick thrust?with specific force applied in a specific direction to a specific vertebra and designed to deliver maximal force with minimal tissue damage. Manipulation distributes the force to multiple segments via 𢡠ong-lever, slow velocity, non-thrust?techniques. These are all based on Wolf𠏋 Law that 𦽳tructure follows function.?In other words, that functional problems precede actual structural defects.
The pathophysiology of subluxation complexes includes compression of spinal nerve roots or the spinal cord, vertebrobasilar arterial insufficiency, somatovisceral dysfunction, and decreased mobility. Veterinary chiropractic research is limited. Most recent research has been conducted by Dr. Kevin Hausler at Cornell Veterinary School, where he documented mobility of the equine spine and demonstrated equine spinal movement following a chiropractic adjustment.
Chiropractic examination techniques include static palpation, motion palpation, and gait evaluation. Static palpation evaluates the symmetry of both dorsal and transverse spinous processes. Symmetry is evaluated from left to right, cranial to caudal, dorsal to ventral, as well as looking at symmetry of the musculature, looking for any muscle atrophy, kyphosis (roach back), or scoliosis. Evaluation also includes checking for heat, pain, muscle tone, and spasms. Motion palpation includes evaluation of active and passive range of motion in vertebral motor units. Lateral flexion, axial rotation, flexion, and extension are all evaluated.
After the examination, adjustments and manipulations are applied to appropriate areas. Ancillary care may include acupuncture, muscle relaxants, rest, massage, stretching exercises, laser therapy, ultrasound, or magnetic therapy.
Chiropractic Care may be integrated into a conventional companion animal practice for preventive health care, sports medicine for agility trial dogs, working dogs, as well as others. It may be used as an adjunct for the treatment of back and neck pain or to treat secondary compensation to primary problems such as hip dysplasia.?Further research is needed to document the mechanisms of action, indications and limitations and contraindications of veterinary chiropractic. Additional training programs need to be developed. Colorado State University College of Veterinary Medicine is offering the first program of this kind at a U.S. veterinary school. The future of chiropractic is to include it in a professional manner as an integral part of veterinary medicine.

minibabyqq 2007-1-26 02:10

[color=Magenta][size=5][b]口頭解剖學和繪製 Oral Anatomy and Charting [/b][/size][/color]

[size=12px]對牙科的理解要求口頭組織、兩顆牙和支撐結構的結構和作用的了悟。這對牙齒病理學和療養的欣賞是根本的。牙齒患者實踐上變化從traditional. 寵物, 譬如狗和貓, 對小herbivores 。
口頭解剖學
接近下頜是咀嚼的主要肌肉: temporalis 肌肉、masseter, 和pterygoid (側向和中間) 。激動所有四是下頷骨神經, 是trigeminal 神經的唯一的馬達分支。
唯一的肌肉張開下頜是digastricus 。唯一rostral 腹部innervates 通過trigeminal 的下頷骨分支當尾部腹部innervates 通過面部(C7) 神經。
口腔被分裂成前庭和口腔適當。在口腔之內適當是堅硬上顎、軟的上顎、舌頭, 和嘴的地板。重要性的骨頭對口腔的是尖銳骨頭、下顎骨, 和上顎骨。插口在包含牙的所有這些骨頭裡被命名齒齦音過程。下顎骨包括二根骨頭由強的纖維狀聯接rostrally 加入被命名下頷骨symphysis 。下顎骨包含一水平和垂直的ramus 。水平的ramus 包括symphyseal 區域和身體當垂直的ramus 包括coronoid 過程、condylar 過程, 和有角過程。舌頭是結構由內在和外在肌肉和作用組成作為採取流體和固體入嘴和有重要作用在修飾和vocalisation 的結構。
牙齒解剖學: 牙和附件
牙解剖組分將被談論根據他們的結構和作用。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]搪瓷。[/b] 搪瓷是96% 無機, 主要hydroxyapatite 水晶, 以4% 水和纖維狀有機材料。這是最堅硬的物質在身體和報道冠的外部表面唯一。搪瓷包括hydroxyapatite 水晶六角棱鏡或標尺由一個用水泥塗的有機矩陣相連。搪瓷由ameloblasts 形成在牙芽之內在爆發之前。它是有能力在僅僅非常有限的修理上當損壞一次牙噴發了。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]牙質。 [/b]牙質是牙的主要支撐結構和是第二個堅硬組織在身體在搪瓷以後。它70% 礦物和非細胞當hydroxyapatite 水晶和30% 有機作為水、膠原和黏多糖。主要結構是dentinal tubule, 延長從外在表面對黏漿狀物質。有大約30,000.40,000 tubules 每毫米2, 可能傳達痛苦給黏漿狀物質如果牙質被暴露。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]齒齦音骨頭。 [/b]根被裝箱在下頜的齒齦音過程。最密集的骨頭排行小窩和叫cribriform 板材。它幅射線照相地是顯然的如同一條白色線叫lamina dura 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]牙骨質[/b] 報道搪瓷自由根和為牙周韌帶提供歸屬點。相似在構成裡與被編織的骨頭它是45-50% 無機, 主要當hydroxyapatite 水晶, 和50-55% 有機材料。牙骨質是有能力在形成、破壞, 和修理上。它被養育從船在牙周韌帶之內。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]牙周韌帶。[/b] 由拉緊的膠原纖維捆綁組成(叫做他們被困住在牙骨質和齒齦音骨頭裡) 停住對牙和齒齦音骨頭的牙骨質的Sharpey.s 纖維。血管廣泛膨脹和均勻地被分佈在牙周韌帶與是能傳送熱、寒冷、痛苦, 和壓力除proprioception 之外在某一種類的神經一起。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]黏漿狀物質。[/b] 這活組織在牙之內位於黏漿狀物質分庭和根運河。它innervated 和vascularised 和很好包括結締組織、神經、淋巴和血管、膠原, 和undifferentiated 儲備mesenchymal 細胞(即, odontoblasts) 。Odontoblasts 線黏漿狀物質洞和分支入牙質tubules 。這些分支, 與美好的神經末梢一起, 導致牙質是敏感的對溫度和痛苦。odontoblasts 放下次要牙質和減少黏漿狀物質洞在大小作為動物年齡。黏漿狀物質被養育通過船進入和留下根運河在頂端三角洲和, 偶爾地, 通過輔助運河。
齒齬和圍攏
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]附加的齒齬。[/b] 附上齒齬緊緊是追隨者對subgingival 結締組織和骨頭通過深rete 釘。它是keratinised 承受剝去的和撕毀的食物重音。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Mucogingival 連接點(MGJ) 。[/b] 這是連接點在口腔的軟, 肉多黏液膜和堅韌, 膠原富有齒齬之間。MGJ 保留固定式通過生活雖然齒齬在它附近也許改變在高度由於增生、後退或附件損失。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]自由齒齦。[/b] 自由齒齬形成齒齦邊際可看見在檢查期間。它圍攏牙的冠。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]齒齦溝。[/b] 在牙和自由齒齦邊際之間是齒齦溝。這是圍攏牙的空隙。溝的正常深度是0.5 毫米到1 毫米在貓和1.3 毫米在狗。概括來說1mm 為貓和1.2 毫米在狗可能被認為正常。溝襯裡皮膜迅速地更新自己每4.6 天與6.12 天比較為口頭皮膜。溝沐浴在crevicular 流體裡, 包含許多免疫的元素。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Junctional 皮膜。[/b] 在溝的底部是junctional 皮膜(或上皮附件), 是很重要在牙周疾病控制。這附上齒齦組織對牙使用hemidesmosomes 。
牙類型和作用
masticatory 力量在狗估計是300 到800 psi 因為被動叮咬力量用突然的地方化的叮咬力量當攫取下頜關閉了儘量30,000 到80,000 psi 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]門牙。[/b] 使用為切口, 挖出, 採摘對象和修飾。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]犬。[/b] 使用為藏品犧牲者, 大幅度削減和撕毀當戰鬥和行動作為搖籃為舌頭。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]前臼齒。[/b] 使用為藏品, 運載和打破食物小片斷。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]槽牙。[/b] 使用為研食物入小片斷與平的咬合桌。
牙編號: Triadan
修改過的Triadan 系統提供編號牙一個一致的方法橫跨另外動物種類。系統根據豬的永久齒列, 有11 顆牙在各個象限: 三顆門牙、一隻犬、四顆前臼齒和三槽牙。總和是44 顆牙。同樣框架為所有種類存在但其它種類也許有缺掉牙從演變, 和在這些情況下, 數字作為這只要某些規則被遵循。
修改過的 Triadan 系統的[b]第一個數字[/b]表示象限: [table][tr][td=1,1,459]正確的上部永久= 1
[/td][td=1,1,459]正確上部落葉= 5
[/td][/tr][tr][td=1,1,459]左上部永久= 2
[/td][td=1,1,459]左上部落葉= 6
[/td][/tr][tr][td=1,1,459]左更低的永久= 3
[/td][td=1,1,459]左更低落葉= 7
[/td][/tr][tr][td=1,1,459]正確的更低的永久= 4
[/td][td=1,1,459]正確更低落葉= 8
[/td][/tr][/table][b]其次和第三個數字[/b] 表示牙位置在象限之內, 用序列總開始在midline 。
系統依靠確定地標、[i]fours [/i]所謂的[i]rule 和nines. 。[/i] 犬齒總是第號四當禮物。第一槽牙總是第號九當禮物。另外, carnassials 總是上部第四顆前臼齒和更低的第一槽牙。在貓, 牙數字被減少, 對carnassials 的用途因為地標可觀地將幫助。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 中央門牙總是01 與以下門牙02 和03 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 犬(當禮物) 總是04 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 前臼齒(當禮物) 是05 到08 。上部carnassials 在食肉動物總是最後上部前臼齒, 必須因此是或108 或208 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 槽牙(當禮物) 是09 到011 。更低的carnassials 在食肉動物總是第一槽牙, 必須因此是或309 或409
繪製
為什麼您需要繪製您的牙齒案件圖表?
1 。 繪製是根本記錄健康並且/或者疾病出現以可能現在和以後被使用的形式。在它的最簡單的形式, 它是必要的為medico-legal 保護原因知道什麼牙和病理學是存在在治療開始了之前。
2 。 成功或的治療否則不可能測量隨時間沒有適當的資訊收集在最初的治療。
3 。 這臨床是好習性顯現出。客戶經常被打動當採取對聚集他們能容易地瞭解和使用起他們的作用在口腔的維護的資訊的時候。
許多不同的圖存在在狩醫牙齒文學。使用一適合您的目的。主要圖被談論在本文期間被使用以感恩的允許從Pharmacia 動物健康。
怎麼繪製
繪製嘴圖表開始在邊uppermost 。這是最佳使用microcassette 記錄器和以後抄錄為速度和潔淨:
1 。 計數牙和注意失蹤或額外牙。
2 。 確定平實結石正如每傳奇。(0=none 對3 = 100% 蓋子)
3 。 確定齒齦炎症的水平正如每傳奇。使用直言的perio 探針, 奔跑探針圍繞頰溝柔和地確定程度齒齦炎症。保重不使用許多頂端壓力或通過同樣方式twice.you 不要希望創造無存在的損傷。
4 。 注意所有主要反常性可看見: 破碎的牙、搪瓷瑕疵、瘤, 和損耗以三重牙質曝光。
5 。 任意: 使用透露解答確定匾的地點和水平。這步有用多數在診療室考試崗位操作。適用於頰表面與被浸泡的棉花芽。二重奏128 。(Virbac) 包含二種染料; 桃紅色儲蓄表明發育未全的匾和紫色是成熟, 礦化的匾。
在最初的結垢以後:
1 。 審查各顆牙溝在六個地點極小值: 三頰和三palatal/lingual 。使用畢業的探針在牙的長的軸在一個頂端方向。施加沒有比一盎司壓力。使用探針如同您的眼睛在膠線和感受之下為被錯過的subgingival 結石, 反常坑和消沉在根表面和牙周口袋; 描述深度和地點。
2 。 注意牙的地點被提取在這個做法由橫渡在牙之外在圖表和橫渡在箱子之外。
3 。 注意其它重要特點譬如: a) 齒齦後退和根furcation exposure.draw 新新行在頰圖表; b) caries.draw 地點; c) 搪瓷defects.draw 地點; d) 流動teeth.use 索引正如每編碼鍵; e) 其它重大損害(即, 破碎的冠或尖頂、磨蝕站點, FORL.s 在貓等。)
4 。 注意治療performed.fillings, 根飛行, 提取、口袋管理和齒齦擋水板, 和根運河。

An understanding of dentistry requires an awareness of the structure and function of oral tissues, both the teeth and supporting structures. This is fundamental to the appreciation of dental pathology and treatment regimens. Dental patients in practice vary from 懀raditional?pets, such as dogs and cats, to small herbivores.
ORAL ANATOMY
The main muscles of mastication that close the jaws are: temporalis muscle, masseter, and pterygoid (lateral and medial). Innervation of all four is the mandibular nerve, which is the only motor branch of the trigeminal nerve.
The only muscle to open the jaw is the digastricus. Only the rostral belly innervates via the mandibular branch of the trigeminal while the caudal belly innervates via the facial (C7) nerve.
The oral cavity itself is split into the vestibule and the oral cavity proper. Within the oral cavity proper are the hard palate, soft palate, tongue, and the floor of the mouth. The bones of importance to the oral cavity are the incisive bone, mandibles, and maxillae. The sockets in all these bones that contain the teeth are termed alveolar processes. The mandibles comprise of two bones joined rostrally by a strong fibrous joint termed the mandibular symphysis. The mandible contains a horizontal and vertical ramus. The horizontal ramus comprises the symphyseal area and the body while the vertical ramus comprises the coronoid process, condylar process, and the angular process. The tongue is a structure comprised of both intrinsic and extrinsic muscles and functions as the structure that takes fluids and solids into the mouth and has important functions in grooming and vocalisation.
DENTAL ANATOMY: THE TOOTH AND ATTACHMENTS
The anatomical components of teeth will be discussed in terms of their structure and function.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Enamel.[/b] Enamel is 96% inorganic, mainly hydroxyapatite crystals, with 4% water and fibrous organic material. It is the hardest substance in the body and covers the exterior surface of the crowns only. The enamel consists of hexagonal prisms or rods of hydroxyapatite crystals held together by a cementing organic matrix. Enamel is formed by ameloblasts within the tooth bud before eruption. It is capable of only very limited repair when damaged once the tooth has erupted.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Dentine. [/b]Dentine is the main supporting structure of the tooth and is the second hardest tissue in the body after enamel. It is 70% mineral and acellular as hydroxyapatite crystals and 30% organic as water, collagen and mucopolysaccharide. The main structure is the dentinal tubule, which extends from the external surface to the pulp. There are some 30,000?0,000 tubules per mm2, which can transmit pain to the pulp if the dentine is exposed.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Alveolar bone. [/b]The roots are encased in the alveolar processes of the jaws. The densest bone lines the alveolus and is called the cribriform plate. It may be seen radiographically as a white line called the lamina dura.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Cementum[/b] covers the enamel free roots and provides a point of attachment for the periodontal ligament. Similar in composition to woven bone it is 45-50% inorganic, primarily as hydroxyapatite crystals, and 50-55% organic material. Cementum is capable of formation, destruction, and repair. It is nourished from vessels within the periodontal ligament.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Periodontal Ligament.[/b] Comprised of taut collagen fibre bundles (called Sharpey𠏋 fibres where they are trapped in cementum and alveolar bone) that are anchored to the cementum of the tooth and the alveolar bone. Blood vessels are widely dilated and evenly distributed in the periodontal ligament along with nerves that are capable of transmitting heat, cold, pain, and pressure in addition to proprioception in some species.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Pulp.[/b] This living tissue within the tooth is located in the pulp chambers and root canals. It is well innervated and vascularised and comprises connective tissue, nerves, lymph and blood vessels, collagen, and undifferentiated reserve mesenchymal cells (e.g., odontoblasts). Odontoblasts line the pulp cavity and branch into the dentine tubules. These branches, together with the fine nerve endings, cause the dentine to be sensitive to temperature and pain. Theodontoblasts lay down secondary dentine and reduce the pulp cavity in size as the animal ages. The pulp is nourished via vessels entering and leaving the root canal at the apical delta and, occasionally, via accessory canals.
GINGIVA AND SURROUNDS
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Attached gingiva.[/b] The attached gingiva is tightly adherent to the subgingival connective tissue and bone via deep rete pegs. It is keratinised to withstand the stress of ripping and tearing food.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Mucogingival junction (MGJ).[/b] This is the junction between the soft, fleshy mucus membrane of the oral cavity and the tough, collagen rich gingiva. The MGJ remains stationary through life although the gingiva around it may change in height due to hyperplasia, recession or attachment loss.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Free gingival.[/b] Free gingiva forms the gingival margin visible during exam. It surrounds the crown of the tooth.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Gingival sulcus.[/b] Between the tooth and the free gingival margin is the gingival sulcus. It is the crevice that surrounds the tooth. The normal depth of the sulcus is 0.5 mm to 1 mm in cats and 1? mm in dogs. As a rule 1mm for cats and 1? mm in dogs can be considered normal. The sulcus lining epithelium renews itself rapidly every 4? days compared to 6?2 days for oral epithelium. The sulcus is bathed in crevicular fluid, which contains many of the elements of immunity.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Junctional epithelium.[/b] At the bottom of the sulcus is thejunctional epithelium (or epithelial attachment), which is so important in the control of periodontal disease.This attaches the gingival tissues to the tooth using hemidesmosomes.
Teeth Types and Function
The masticatory forces in the dog have been estimated to be 300 to 800 psi as passive bite force with a sudden localised bite force when snapping the jaws shut of as much as 30,000 to 80,000 psi.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Incisors.[/b] Used for cutting, scooping, picking up objects and grooming.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Canines.[/b] Used for holding prey, slashing and tearing when fighting and act as a cradle for the tongue.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Premolars.[/b] Used for holding, carrying and breaking food into small pieces.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] [b]Molars.[/b] Used for grinding food into small pieces with flat occlusal tables.
Tooth Numbering: Triadan
The modified Triadan system provides a consistent method of numbering teeth across different animal species. The system is based on the permanent dentition of the pig, which has 11 teeth in each quadrant: three incisors, one canine, four premolars and three molars. The grand total is 44 teeth. The same framework exists for all species BUT other species may have missing teeth from evolution, and in these cases, the numbers take this into account as long as certain rules are followed.
[b]First digit[/b] of the modified Triadan system denotes the quadrant: [table][tr][td=1,1,459]Right upper permanent = 1
[/td][td=1,1,459]Right upper deciduous = 5
[/td][/tr][tr][td=1,1,459]Left upper permanent = 2
[/td][td=1,1,459]Left upper deciduous = 6
[/td][/tr][tr][td=1,1,459]Left lower permanent = 3
[/td][td=1,1,459]Left lower deciduous = 7
[/td][/tr][tr][td=1,1,459]Right lower permanent = 4
[/td][td=1,1,459]Right lower deciduous = 8
[/td][/tr][/table][b]Second and third digits[/b] denote the tooth position within the quadrant, with the sequence always starting at the midline.
The system relies on definite landmarks, the so-called [i]𩂈ule of fours and nines.?/i> The canine teeth are always number four when present. The first molars are always number nine when present. In addition, the carnassials are always the upper fourth premolars and lower first molars. In cats, where tooth numbers are reduced, the use of the carnassials as landmarks will help considerably.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] The central incisor is always 01 with the following incisors 02 and 03.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] The canines (when present) are always 04.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] The premolars (when present) are 05 to 08. The upper carnassials in carnivores are always the last upper premolar, therefore must be either 108 or 208.
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] The molars (when present) are 09 to 011. The lower carnassials in carnivores are always the first molar, therefore must be either 309 or 409
CHARTING
Why do You Need to Chart Your Dental Cases?
1. Charting is essential to record the presence of health and/or disease in a form that can be used now and later. At its very simplest form, it is necessary for medico-legal protection reasons to know what teeth and pathology was present before treatment was started.
2. The success or otherwise of treatments is impossible to gauge over time without the proper information gathered at initial treatment.
3. It is clinically a good habit to develop. The client is often impressed by the time taken to gather information that they can easily understand and use to play their part in the maintenance of the oral cavity.
Many different charts exist in the vet dental literature. Use one that suits your purposes. The main chart discussed during this paper is used with grateful permission from Pharmacia Animal Health.
How to Chart
Chart the mouth starting at the side uppermost. It is best to use a microcassette recorder and transcribe later for speed and cleanliness
[/i][/size]

minibabyqq 2007-1-26 02:11

[color=Magenta][size=5][b]犬眼睛的被繼承的疾病Inherited Disease of the Canine Eye  [/b][/size][/color]

介紹
被繼承的視覺疾病光譜在家譜狗的世界介入許多養殖和所有眼睛的部份。疾病類型和發生像助長大眾化地理上變化, 。當前, 這是代表試圖疾病控制最有效的方式的規則臨床考試, 但在將來, 基於DNA 的基因測試將充當一個越來越重大角色。1995 年, 大約12,000 條狗被審查了在正式控制計劃之下在英國, 記錄整體錯誤率的4.23% 。在之下捐款在一些區域意味, 準確發生形象為一些疾病很少不幸地是可利用的。當然, 臨床考試有它的限制, 可能只證實基因型直接地在疾病面前。為將來DNA 基於的測試諾言將允許基因型的準確決心在臨床是法線在考試的時期的狗。但是, 不問診斷機制, 成功的疾病控制意味遺傳性疾病作為養殖問題和批發捐款採納對當前的控制計劃必需如果這樣計劃將證明成功。
疾病以繼承被證明的機制
被繼承的或主要視覺疾病也許是存在作為先天不足或也許臨床顯現出在青年期或以後在生活中。繼承確切的方式可以或不可以被定義了, 但被標記的養殖素質清楚地展示一個基因基地。先天主要視覺疾病在狗包括視網膜發育異常、大牧羊犬眼睛反常現象(CEA), 大瀑布, 和pupillary 膜的元素的主要玻璃(PHPV) 並且元素堅持(PPM) 。先天青光眼 就其本身而言 不被繼承, 僅goniodynesis, iridocorneal 或排水設備角度的反常發展, 被繼承在某些養殖並且這先天不足也許預先處理對主要角度關閉青光眼, 通常在中年或更舊的狗。幾類型進步視網膜萎縮發現起源在視網膜的光感受器單位的先天反常性, 但伴生的疾病不它的臨床露面直到幾個月年齡。顯現出在誕生以後的被繼承的疾病, 包括各種各樣的眼皮和其它附件問題、遺傳性大瀑布(HC), 透鏡luxation (LL), 主要青光眼(頁), 進步視網膜萎縮(PRA), 和視網膜顏料epithelelial 營養失調(RPED, 正式CPRA) 。
1 。視網膜發育異常
視網膜發育異常描述反常分化結果在neuroretinal 摺疊和玫瑰華飾形成、退化或非附件裡的那些被繼承的情況。作用範圍從視域的沒有引人注目的損傷通過對盲目性。所有RD 的形式被認為簡單的隱性特徵。簡單的摺疊也許是線性, Y 被塑造或通報和結果從視網膜, neuroretina 的神經系統的部份的非附件, 對部下的視網膜顏料皮膜在那個區域。有光感受器擴散和RPE 元素的複雜的摺疊指玫瑰華飾。摺疊也許由易變的程度視網膜獨立小分隊和退化伴隨。
在英國R.D. 被記錄了在Bedlington 狗, 騎士國王查爾斯・Spaniel, 匈牙利Puli, 拉布拉多獵犬, Rottweiler 、Sealyham 狗、美國斗雞家Spaniel 和英國Springer Spaniel 。它潛在的存在作為一種被繼承的疾病當前被調查在另外八養殖包括看除簡單的neuroretinal 摺疊之外在騎士國王查爾斯Spaniel 、金黃獵犬和拉布拉多獵犬的地理形式。
2 。大牧羊犬眼睛反常現象
大牧羊犬眼睛反常現象享受高發生在粗礪的大牧羊犬並且Shetland Sheepdog 養殖在英國, 但也被看見在光滑的大牧羊犬和疆界大牧羊犬。它最近被記錄了在非大牧羊犬養殖, Lancashire Heeler 。再, 疾病認為被繼承作為一個簡單的隱性特徵和陳列pleiomorphism 。所有受影響的狗展示脈絡膜發育不全在變化的程度上, 與大約30% 由視覺圓盤和仙子乳頭狀的sclera 的colobomatous 瑕疵另外影響。盲目性通常看在大約6% 受影響的眼睛中由於或先天neuroretinal 非附件或neuroretinal 獨立小分隊早期的起始在第一二到三年生活之內。出血可能使提出的臨床圖片複雜化。疾病控制由事實多達陳列脈絡膜發育不全的ophthalmoscopic 標誌在六個星期年齡的30% 那些小狗, 掩沒這損害由染色在成人fundus, 所謂的go 法線現象複雜化。因而, 表現型看上去正常但, 當然, 基因型是那疾病。因而斷定疾病控制必須開始以廢棄物掩護為go 法線的組合並且載體抵銷了先天存在好處和繼承一個知道的機制。
3 。堅持Hyperplastic 主要
堅持Hyperplastic 主要玻璃歸結於胎兒血管供應的元素的保留對透鏡, tunica vasculosis lentis 。損害被看見是易變的相當數量維管組織的匾在後部透鏡膠囊和可能的後部表皮大瀑布。對視域的作用可能範圍從□什麼對盲目性。害病的透鏡的撤除可能由任一血管介入複雜化。堅持pupillary 膜是同樣起源, 但tunica vasculosis lentis 的先前部份的這時候殘餘子線保留附有虹膜, 也許偶爾地干涉視域由於伴生的透鏡或角膜opacities 。再, 對視域的任一作用是易變的, 但大瀑布提取是可能的, 但是角膜不透明不是可治療的。
4 。遺傳性大瀑布
遺傳性大瀑布也許是先天地存在作為核不透明或也許易變地顯現出根據位置、程度和年齡在年輕和變老的成人從大約6.8 月到九年紀。當前, 大約17 養殖影響在英國與波士頓狗和微型Schnauzer 每個影響以二類型被繼承的大瀑布。HC 的可能性當前被調查在狗另外八養殖。
大瀑布被定義如同透鏡並且/或者它的膠囊的任一不透明。因而, 臨床特點看範圍從針頭標記對總透鏡不透明。更大大瀑布, 更加嚴厲對視域的作用。先天大瀑布通常是靜態的, 允許視覺通過透鏡的成人表皮部份。, 它可能醫療上經常被處理並且手術也許從未證明必要。遺傳性大瀑布在年輕人和成人狗也許或不能導致盲目性根據介入的相當數量透鏡。例如, 金黃獵犬的後部極性大瀑布是靜態的, 但在5% 受影響的狗中, 有隨後表皮opacitation 並且手術是必要恢復視域。在西伯利亞愛斯基摩和挪威Buhund, 大瀑布通常被限制對後部外皮, 但相當數量變動是易變的並且手術很少證明必要。在受影響的養殖過程中, 這是大瀑布的樣式與指揮診斷往遺傳性損害介入一起的年齡。分化主要從次要大瀑布通常容易地達到, 和當然, 根本根據疾病控制。
5 。透鏡luxation
透鏡luxation 是透鏡的位移或脫臼從它的位置在先前面孔的玻璃由於它的suspensory 用具的退化。多數患者, 透鏡搬入學生或先前分庭造成次要青光眼。透鏡luxation recessively 遺傳在幾狗養殖和疆界大牧羊犬和通常影響狗在三到四年紀。不幸地, premonitory 標誌是短命的; 青光眼的出現口授診斷。通常有幾天的滯後對幾星期在第二眼睛介入和它在在出現玻璃在學生或明顯的iridodenesis 的這時間期間之前(虹膜打顫) 看。青光眼由透鏡的撤除對待, 但這樣的手術必須迅速被完成如果視域將被保存並且慢性青光眼被避免。
6 。進步視網膜萎縮
進步視網膜萎縮包括一定數量的被繼承的neuroretinal 退化, 一些歸結於主要光感受器發育異常, 其他人歸結於光感受器退化, 未確定的原因論。當前, 十五養殖被介入在PRA 故事在英國並且它可能的存在被調查在另外六養殖。所有類型PRA 被繼承當隱性特徵和所有由增加的tapetal 反射性和血管退化ophthalmoscopically 描繪。起始的年齡變化, 但共計盲目性是共同的終點。例如, 愛爾蘭安裝員的rod/cone 發育異常導致盲目性在八個到12 個月年齡, 微型長捲毛狗或斗雞家Spaniel 的rod/cone 退化不能展示臨床作用直到受影響的狗是五或六年紀。原因論完全地只被瞭解為愛爾蘭安裝員並且它是可能開發一個基於DNA 的測試辨認瑕疵基因在這養殖。這樣的測試為其它類型PRA 當前不存在並且疾病控制由載體和晚起始迷惑。除愛爾蘭安裝員、微型長捲毛狗, 和斗雞家Spaniel 之外, PRA 被描述了在粗礪的大牧羊犬、微型長頭髮的Dachshund 、Elkhound 、微型Schnauzer 、玩具長捲毛狗、切塞皮克灣獵犬、拉布拉多獵犬、美國斗雞家Spaniel, 英國Springer Spaniel, 西藏Spaniel, 西藏狗, 和威爾士(羊毛衫) Corgi 。次要大瀑布是普遍的在許多受影響的狗。
7 。視網膜顏料上皮營養失調
視網膜顏料上皮營養失調歸結於視網膜顏料上皮細胞的無能提供營養素給neuroretina 並且, 那裡接著而來次要光感受器退化。它的作用主要被限制對視網膜的non-pigmented 部份在tapetal fundus 之內並且, 受影響的狗很少丟失他們的周邊視覺。最初的ophthalmoscopic 變動是淺褐色的顏料焦點出現在tapetal fundus 之內。組織學顯示出, 焦點歸結於積累的lipopigment 在視網膜顏料上皮細胞之內。lipopigment 是phagocytosed 積累在這些細胞之內細胞質的光感受器外面段材料, 而不是由lyzosomal 活動被劃分和重新傳布入neuroretina 為新外面段生產。這是停止光感受器充分營養由視網膜顏料皮膜和導致他們的退化顏料的持續的儲積。這退化ophthalmoscopically 看作為增加的tapetal 反射性; 儘量18 個月到二年可能通過在顏料焦點的最初的出現和引人注目的增加的反射性之間。由於被著色的視網膜顏料上皮細胞依然是相對地免疫對lipopigment 儲積, 受影響的狗有效地只丟失他們的中央視覺。例如, 狗與一個固定式對象碰撞, 但查出運動。RPED 被查出儘早17 個月年齡, 但不能一次露面直到第九年生活。繼承機制是未知的並且這與一個可能的晚起始一起可能使疾病控制困難。
RPED 當前被描述在疆界大牧羊犬, Briard, 粗礪的大牧羊犬, 光滑的大牧羊犬, 金黃獵犬, 拉布拉多獵犬, Shetland Sheepdog, 斗雞家Spaniel, 英國Springer Spaniel 並且威爾士Corgi 養殖在英國和它可能的繼承在波蘭人低地Sheepdog 被調查。最近的工作在斗雞家Spaniel 養殖表示, 這種疾病同血漿阿爾法維生素E 聯繫在一起的低水平並且, 被繼承的瑕疵可能是肝臟被獲得的維生素E 調動作用的缺乏。
8 。主要青光眼
主要青光眼歸結於固有瑕疵在含水排水設備路之內。開放角度青光眼是不凡的在似犬人口, 但角度關閉青光眼, 結果對一goniodysgenesis 有梳狀的韌帶的反常分化, 被繼承在狗幾養殖。這種後者疾病為視域和痛苦突然的起始損失描繪由於ciliary 裂縫的自發關閉。goniodysgenesis 可能被查出在四個到六個月年齡由gonioscopy 並且疾病被描述了在Basset 追逐, 平的上漆的獵犬、西伯利亞愛斯基摩、美國斗雞家Spaniel, 斗雞家Spaniel, 和威爾士Springer Spaniel 在英國。它可能的存在作為一個被繼承的瑕疵, 但不一定同樣原因論, 當前被調查在Dandie Dinmont 狗、Elkhound, 了不起的丹麥人, 匈牙利Vizsla, 金黃獵犬, 英國Springer Spaniel, 和威爾士狗。
結論
被繼承的疾病控制是交配動物者和他的責任養殖社會, 但獸醫行業和全國狗窩俱樂部有他們的角色扮演。只要眼睛, 這樣的控制根據規則臨床考試, 特別良種畜。在將來, DNA 基於的測試將充當一個越來越重大角色, 但為禮物和直接將來, 疾病的了悟和對正式證明計劃的用途代表疾病控制最重大的特點。一種被繼承的疾病的出現是不僅一個問題為受影響的狗, 而且一個問題為整體養殖, 並且, 管理措施必須由整體養殖接受工作在一致。定期考試和結果的出版物在開放登記是根本的如果被繼承的疾病的傳播將denied 。
Introduction
The spectrum of inherited ocular disease in the world of the pedigree dog involves many breeds and all parts of the eye. Both disease type and incidence vary geographically, as does breed popularity. Currently, it is regular clinical examination which represents the most effective way of attempting disease control, but in the future, the DNA-based genetic tests will play an increasingly significant role. In 1995, some 12,000 dogs were examined under the official control scheme in the UK, recording an overall failure rate of 4.23%. Under-subscription in some areas means that unfortunately accurate incidence figures for some of the diseases are rarely available. Of course, clinical examination has its limitations and can only confirm genotype directly in the presence of disease. For the future the promise of DNA based tests will allow the accurate determination of genotype in the dog which is clinically normal at time of examination. However, irrespective of the mechanism of diagnosis, successful disease control means the acceptance of hereditary disease as a breed problem and wholesale subscription to the current control schemes is required if such schemes are to prove successful.
Diseases with Proven Mechanisms of Inheritance
Inherited or primary ocular disease may be present as a congenital defect or may develop clinically in adolescence or later in life. The exact mode of inheritance may or may not have been defined, but marked breed predisposition clearly demonstrates a genetic base. The congenital primary ocular diseases in the dog include retinal dysplasia, Collie Eye Anomaly (CEA), cataract, and the persistence of elements of the primary vitreous (PHPV) and elements of the pupillary membrane (PPM). Congenital glaucoma per se is not inherited, but goniodynesis, abnormal development of the iridocorneal or drainage angle, is inherited in certain breeds and this congenital defect may predispose to primary angle closure glaucoma, usually in middle-aged or older dogs. Several types of progressive retinal atrophy find origin in congenital abnormality of the photoreceptor units of the retina, but the associated disease does not make its clinical appearance until several months of age. The inherited diseases which develop after birth, include the various eyelid and other adnexal problems, hereditary cataract (HC), lens luxation (LL), primary glaucoma (PG), progressive retinal atrophy (PRA), and retinal pigment epithelelial dystrophy (RPED, formally CPRA).
1. Retinal Dysplasia
Retinal Dysplasia describes those inherited conditions in which abnormal differentiation results in neuroretinal fold and rosette formation, degeneration or non-attachment. The effect ranges from no noticeable impairment of sight through to blindness. All forms of RD are considered simple recessive traits. A simple fold may be linear, Y shaped or circular and results from the non-attachment of the neural part of the retina, the neuroretina, to the underlying retinal pigment epithelium in that area. Complicated folds in which there is a proliferation of photoreceptor and RPE elements are referred to as rosettes. Folds may be accompanied by variable degrees of retinal detachment and degeneration.
In the United Kingdom R.D. has been recorded in the Bedlington Terrier, the Cavalier King Charles Spaniel, the Hungarian Puli, the Labrador Retriever, the Rottweiler, the Sealyham Terrier, the American Cocker Spaniel and the English Springer Spaniel. Its potential presence as an inherited disease is being investigated currently in another eight breeds including a geographic form that is seen in addition to simple neuroretinal folds in the Cavalier King Charles Spaniel, the Golden Retriever and the Labrador Retriever.
2. Collie Eye Anomaly
Collie Eye Anomalyenjoys high incidence in the Rough Collie and Shetland Sheepdog breeds in the U.K, but is also seen in the Smooth Collie and the Border Collie. It was recently recorded in a non-collie breed, the Lancashire Heeler. Again, the disease is considered to be inherited as a simple recessive trait and exhibits pleiomorphism. All affected dogs demonstrate choroidal hypoplasia to varying extent, with some 30% being additionally affected by colobomatous defects of the optic disc and peri-papillary sclera. Blindness is seen in approximately 6% of affected eyes as the result of either congenital neuroretinal non-attachment or the early onset of neuroretinal detachment usually within the first two to three years of life. Haemorrhage can complicate the presenting clinical picture. Disease control is complicated by the fact that as many as 30% of those puppies which exhibit the ophthalmoscopic signs of choroidal hypoplasia at six weeks of age, mask this lesion by pigmentation in the adult fundus, the so called 孄o normal?phenomenon. Thus, the phenotype appears normal but, of course, the genotype is that of disease. It follows that disease control must start with litter screening for a combination of 孄o normal?and carrier offset the advantages of congenital presence and a known mechanism of inheritance.
3. Persistent Hyperplastic Primary
Persistent Hyperplastic Primary vitreous is due to the retention of elements of the foetal vascular supply to the lens, the tunica vasculosis lentis. The lesions seen are variable amounts of fibrovascular plaque on the posterior lens capsule and possible posterior cortical cataract. The effect on sight can range from nothing to blindness. Removal of the diseased lens can be complicated by any vascular involvement. Persistent pupillary membrane is of the same origin, but this time remnant strands of the anterior part of the tunica vasculosis lentis remain attached to the iris and may occasionally interfere with sight as the result of associated lens or corneal opacities. Again, any effect on sight is variable, but cataract extraction is possible, whereas corneal opacity is not treatable.
4. Hereditary Cataract
Hereditary Cataract may be congenitally present as a nuclear opacity or may develop variably in terms of position, extent and age in both young and ageing adults from approximately 6? months to nine years of age. Currently, some 17 breeds are affected in the UK with the Boston Terrier and the Miniature Schnauzer each being affected with two types of inherited cataract. The possibility of HC is currently being investigated in another eight breeds of dog.
Cataract is defined as any opacity of the lens and/or its capsule. Thus, the clinical features seen range from pinhead marks to total lens opacity. The larger the cataract, the more severe the effect on sight. Congenital cataract is usually static, allowing vision through the adult cortical portion of the lens. As such, it can often be managed medically and surgery may never prove necessary. Hereditary cataract in young and adult dogs may or may not cause blindness depending on the amount of lens involved. For example, the posterior polar cataract of the Golden Retriever is static, but in 5% of affected dogs, there is subsequent cortical opacitation and surgery is necessary to restore sight. In the Siberian Husky and the Norwegian Buhund, the cataract is usually confined to the posterior cortex, but the amount of change is variable and surgery seldom proves necessary. Throughout the affected breeds, it is the pattern of the cataract together with age of involvement that directs the diagnosis towards a hereditary lesion. Differentiation of primary from secondary cataract is usually easily achieved, and of course, essential in terms of disease control.
5. Lens luxation
Lens luxation is the displacement or dislocation of the lens from its position on the anterior face of the vitreous due to the degeneration of its suspensory apparatus. In most patients, the lens moves into the pupil or the anterior chamber resulting in secondary glaucoma. Lens luxation is recessively inherited in several Terrier breeds and the Border Collie and usually affects dogs at three to four years of age. Unfortunately, the premonitory signs are short lived; the presence of the glaucoma dictates the diagnosis. Usually there is >><<hat the presence of vitreous in the pupil or marked iridodenesis (iris tremble) is seen. The glaucoma is treated by removal of the lens, but such surgery must be completed quickly if sight is to be preserved and chronic glaucoma avoided.
6. Progressive Retinal Atrophy
Progressive Retinal Atrophy covers a number of inherited neuroretinal degenerations, some of which are due to primary photoreceptor dysplasia, whilst others are due to photoreceptor degeneration of, as yet, undetermined aetiologies. Currently, fifteen breeds are involved in the PRA story in the United Kingdom and its possible presence is being investigated in another six breeds. All types of PRA are inherited as recessive traits and all are characterised ophthalmoscopically by increased tapetal reflectivity and blood vessel degeneration. The age of onset varies, but total blindness is the common endpoint. For example, the rod/cone dysplasia of the Irish Setter results in blindness at eight to 12 months of age, whilst the rod/cone degeneration of the Miniature Poodle or Cocker Spaniel may not demonstrate clinical effect until the affected dog is five or six years of age. Aetiology is only completely understood for the Irish Setter and it has been possible to develop a DNA-based test to identify the defective genetic material in this breed. No such test currently exists for the other types of PRA and disease control is confounded by carriers and late onset. In addition to the Irish Setter, the Miniature Poodle, and the Cocker Spaniel, PRA has been described in the Rough Collie, Miniature Long-Haired Dachshund, Elkhound, the Miniature Schnauzer, Toy Poodle, Chesapeake Bay Retriever, Labrador Retriever, American Cocker Spaniel, English Springer Spaniel, Tibetan Spaniel, Tibetan Terrier, and Welsh (Cardigan) Corgi. Secondary cataract is commonplace in many affected dogs.
7. Retinal Pigment Epithelial Dystrophy

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[color=Magenta][size=5][b]眼科考試The Ophthalmic Examination  [/b][/size][/color]


患者的考試從距離
第一部份, 和大概眼科考試的被忽略的部份, 將詳細檢查患者從距離。許多重要反常性最容易地看以仔細的遙遠的檢查。問題要求是: 1) 什麼是患者的精神狀態和整體姿勢? 瞎的動物廣泛典型地握眼睛開放為增加輕的刺激對視網膜。2) 有是對稱對眼睛和軌道嗎? 改變那影響立場並且地球的大小最容易地被查出這樣; 區分地球擴大(buphthalmos) 從地球伸進(眼球突出) 是困難的以結束檢查, 但應該是容易以仔細的遙遠的考試。3) 有是對稱對面孔和眼皮嗎? Blepharospasm 、ptosis, 和面部droop. 應該被評估。4) 有是正常共軛眼睛運動當動物勘測它的環境? 視覺激動和能動性的反常性由遙遠的考試容易地只查出。並且, 考慮如果動物眨眼完全地和以規則頻率。這是唯一的方式查出lagophthalmos, 佔許多角膜疾病在brachycephalic 養殖。
通過患者的仔細的察視從距離, 您疏忽地評估了幾乎所有頭蓋骨神經眼科重要(頭蓋骨神經II, III, IV, v, VI, 和VII) 。清單為遙遠的檢查: 視覺、精神狀態、地球和軌道對稱、對稱對adnexa 和面部結構, 眨眼特徵, 和視覺能動性。
Adnexa 的考試
附件考試從Schirmer 的淚花測試開始。Schirmer 的淚花測試應該完成對有盡職、標誌炎症, 或角膜疾病的任一隻眼睛(沒有禁忌症候為這個做法) 。淚花測試是特別重要在角膜潰瘍盒。淚花小條的安置的地點在眼皮裂痕安排一點影響在結果。在不合作的患者, 眼皮也許手工被拿著閉合。平均狗應該生產20 毫米wetting 在60 秒, 和平均貓輕微地。價值10 毫米被認為正常。價值在5 和10 毫米之間表明sicca 的可能性, 當價值< 5 毫米是診斷的。密碼為好附件考試是放大。雖然任一個擴大化的透鏡也許被使用, 我更喜歡的方法將使用otoscope 的透鏡; 這個透鏡是足夠強有力的查出幾乎所有共同的反常性和容易操作。唯一的事更好是裂縫燈biomicroscope 。清單為附件檢查: distichiasis 、trichiasis 、宮外的纖毛、外國身體在第三眼皮之下, 濾泡形成、conjunctival 血管視覺放電變動(炎症和壅塞), 字符, 眼皮瘤、chalazions, 和眼瞼炎。
角膜的考試
熒光素染料保留選擇代理為查出角膜潰瘍。它重要, 剩餘熒光素周到地被灌溉從cul de sac 避免混淆被癒合的潰瘍與激活一□; 熒光素將合併epithelialized stromal 瑕疵。如果熒光素吸收發生, 區別完全對部份上皮細胞損失由弄髒的強度; 在表面角膜炎病例皮膜可能微弱地弄髒, 雖然真實的潰瘍是缺席的。紫外或鈷藍色被過濾的光是有用的但很少必要。角膜然後被審查為其它opacities 譬如腫鼓、顏料, 和vascularization 。
船應該被分類根據了深度(表面船以樹時尚分支, 能被看見橫渡異色邊緣, 更深的船擁有一種刷子類型疆界和從sclera 湧現) 。Proliferative 血管損害有時遇到在小動物角膜。在許多情況下, 他們是次要對慢性激怒, 或同醫治用的潰瘍聯繫在一起。如果緊挨異色邊緣, 主要激動損害應該被考慮(特別是在狗, 即, 纖維狀histiocytoma 、慢性表面角膜炎, pannus) 。終於, 角膜被審查為通常是傷痕, dystrophies, 或新陳代謝滲入的白色opacities 。如果密集的白色不透明是存在, 角膜被審查為依附虹膜組織(虹膜黏連) 。這樣損害指一依附leukoma 。清單為角膜檢查: 潰瘍、腫鼓、vascularization 、顏料、激動大量, 和白色opacities (傷痕, dystrophies, 和新陳代謝滲入) 。
先前分庭和先前烏韋阿島的考試
最共同地被忽略的先前分庭反常性是含水火光。含水火光(plasmoid 含水) 發生當血液含水障礙減弱了。雖然最共同地由於炎症, 血液含水障礙的故障並且發生以眼內瘤。含水火光的偵查重要因為這頻繁地是眼內疾病的唯一的明確的標誌。當疾病過程打亂虹膜血管, 高分子重蛋白質被允許對先前分庭的通入。通常透明含水幽默變得透明; 但是, 含水蛋白質可能只被查出以光學原則的正確應用。
看含水火光一個強烈和焦點光源必須舉行緊密(1 cm) 對角膜表面。一個直接檢眼計最好設置了在白光它的最小的圓開口, 和對它的最高的光強度, 工作(筆光是不充分為這個做法) 。含水火光是存在如果光束是可看見的在先前分庭。其它反常先前分庭內容包括化膿滲出液(hypopyon), 血液(hyphema), 和造形術大量。這些反常性的偵查由審查促進先前分庭以放大從世俗異色邊緣, 垂直對視覺軸。它是只從微妙的變化在先前分庭深度上, 表示透鏡位移, 可能被查出的這透視。
當審查虹膜, 反常性尋找是dyscoria 、anisocoria 、虹膜膨脹、變化在虹膜顏色(heterochromia 上), 虹膜囊腫、堅持pupillary 膜、虹膜黏連, 和萎縮。ciliary 身體的考試可能在完全mydriasis 的幫助下只被完成。清單先前分庭和先前uveal 檢查: 含水火光, 先前分庭深度, hypopyon, hyphema, 虹膜黏連, 虹膜囊腫, 虹膜萎縮, heterochromia, 堅持pupillary 膜, 虹膜膨脹。
Mydriasis 和Fundus 反射
Tropicamide (Mydriacyl。) 是選擇代理; 二下落被逐漸灌輸在五周詳間隔時間生產持續3.5 小時的mydriasis 在20 分鐘之內。青光眼是唯一的禁忌症候對膨脹學生。fundus 反射的考試是最簡單仍然最有用的方法為估計視覺媒介的清晰。使用一個直接檢眼計設置在0 diopters, 光被反射從視覺fundus 被觀看從距離12.18 英寸。
被反射的光的質量看隨動物的養殖和外套顏色類型變化; 動物與tapetum 將有明亮的fundus 反射黃色, 橙色, 或綠色, 當那些沒有tapetum 通常有紅色fundus 反射(由脈絡膜船導致) 。不管顏色, fundus 反射應該是一致的在學生過程中, 和免於變型。由審查fundus 反射, 臨床工作者能準確地估計相當數量光到達視網膜, 和因此估計視域的質量。例如, 在動物提出了以盲目性怨言被懷疑歸結於大瀑布, 有合理地正常fundus 反射, 盲目性不能歸因於透鏡opacification 。同樣原則適用於opacification 任何地方在眼睛, 包括角膜, 先前分庭, 透鏡, 和玻璃之內。一旦不透明被辨認了, 它較詳細地被審查使用其它技術。
透鏡的考試
裂縫燈biomicroscope 被設計為審查透鏡; 但是, 為幾乎所有實用目的, 透鏡可能充分地被審查與一個直接檢眼計和otoscope 。透鏡檢查的第一部份發生當評估fundus 反射。如果不透明遮暗fundus 反射被懷疑是在透鏡, 它的地點由排除最容易地核實角膜和先前分庭結構的opacification 如上所述。fundus 反射然後使用地方化不透明在透鏡之內。由於透鏡中堅力量是緊挨地球的旋轉的軸, 透鏡opacities (大瀑布的) 定向運動表明他們的地點; 行動地球運動的方向的opacities 是在透鏡, 那些的先前部份看上去保留固定式被找出在中心(核), 和那些在對面行動是在後部部份。如果大瀑布被發現, 透鏡的先前膠囊被審查為不規則性(觀察垂線對動物視覺軸) 與otoscope 。變化在透鏡的位置上應該被查出了當審查先前分庭。但是, 微妙的透鏡位移也許由一個小月牙被塑造的區域只見證在是無透鏡材料的學生之內(aphakic 月牙); aphakic 月牙由觀看最容易地並且查出fundus 反射。終於, 透鏡膠囊被審查為被遵守的uveal 組織(後部虹膜黏連, 先天顏料殘餘), 堅持pupillary 膜, 和玻璃狀的動脈殘餘出現。清單為透鏡檢查: 大瀑布、透鏡位移、堅持pupillary 膜、玻璃狀的動脈殘餘, 和虹膜黏連。
視覺Fundus 的考試
Mydriasis 是absolutely 必要的當評估視覺fundus 。Ophthalmoscopy 也許做與或者二個技術, 直接或間接。以直接方法(直接檢眼計), 您觀看fundus 的一個真正的圖像在距離1.2 cm 從眼睛。以間接方法(間接檢眼計) fundus 的一個被倒置的圖像看從距離一到二英尺從眼睛。什麼是實用區別在這兩個技術之間? 間接ophthalmoscopy 提供視覺fundus 的一個寬看法的最重要的區別是當以直接方法唯一一個非常小範圍可能被觀看。在多數眼科學課本, 直接方法被描述像更加容易。
但是, 我不同意這斷言。由於patient.s 眼睛經常行動, 它採取可觀的經驗看所有fundus 的部份當觀看這樣小表面。以間接方法, 辨認反常區域更加容易的這樣fundus 的一個大部份能被看見。間接ophthalmoscopy 並且導致一個圖像以可觀的景深, 使它容易告訴如果損害被上升或被壓下。不利間接ophthalmoscopy 是, 圖像被倒置。fundus 反射首先被觀看從距離12.18 英寸(透鏡diopter 設置0) 。行動向距離1.2 cm 從patient.s 角膜和從視覺孔頭開始觀看fundus, 首先開始。混亂存在關於對直接檢眼計的不同的力量透鏡的用途。為大多數我們儀器將保留集合在0 diopters 。
在一些小動物, 由於他們的近視, 透鏡設置-1 到-3 也許提供一個更加清楚的圖像。當其它透鏡被使用之時, 是估計fundic 損害的高度或深度; 如果損害被上升它將進入焦點以一個更加正面的透鏡設置, 和如果壓下將進入焦點以一個更加消極的設置。3 diopters 區別表明大約1 毫米的深度變動。更加正面的(+8 到+20 diopter) 設置可能被使用審查更加表面的結構在眼睛; 但是, 因為這些透鏡小和提供一個有限的看法, 大otoscope 透鏡更加容易使用為這些結構。當做間接ophthalmoscopy fundus 反射首先被觀看與或者一個直接檢眼計被設置在0 diopters 、一明亮的penlight, 或transilluminator (Finhoff) 從距離1.2 英尺從眼睛。一清楚的反射被觀察, 拿著一個間接透鏡大約1 cm 從patient.s 眼睛。fundus 現在將是視線內。增加放大由慢慢地移動透鏡從眼睛; 導致最大放大的距離取決於透鏡的屈光的力量(那些與更小的數字產物最巨大的放大) 。

Examination of the Patient From a Distance
The first part, and probably the most overlooked portion of the ophthalmic examination, is to scrutinize the patient from distance. Many important abnormalities are most easily seen with a careful distant exam. The questions to ask are: 1) What is the mental status and overall posture of the patient? The blind animal typically holds the eyes widely open in an attempt to increase light stimulation to the retina. 2) Is there symmetry to the eyes and orbits? Changes that affect position and size of the globe are most easily detected in this manner; differentiating globe enlargement (buphthalmos) from globe protrusion (exophthalmos) can be difficult with close inspection, but should be easy with careful distant examination. 3) Is there symmetry to the face and eyelids? Blepharospasm, ptosis, and facial 𡞫roop?should be evaluated. 4) Is there normal conjugate eye movement as the animal surveys its environment? Abnormalities of ocular innervation and motility are only easily detected by distant examination. Also, consider if the animal blinks completely and with regular frequency. This is the only way to detect lagophthalmos, which accounts for much of the corneal disease in brachycephalic breeds.
Through careful scrutiny of the patient from a distance, you will have inadvertently evaluated nearly all cranial nerves of ophthalmic importance (cranial nerves II, III, IV, V, VI, and VII). Checklist for distant exam: vision, mental status, globe and orbital symmetry, symmetry to adnexa and facial structures, blink characteristics, and ocular motility.
Examination of the Adnexa
Adnexal examination begins with Schirmer's tear test. The Schirmer's tear test should be done to any eye in which there is discharge, signs of inflammation, or corneal disease (there is no contraindication for this procedure). The tear test is especially important in cases of corneal ulceration. The location of placement of the tear strip in the palpebral fissure has little affect on the result. In uncooperative patients, the eyelids may be manually held closed. The average dog should produce 20 mm wetting in 60 seconds, and the average cat slightly less. Values over 10 mm are considered normal. Values between 5 and 10 mm indicate the possibility of sicca, while values < 5 mm are diagnostic. The password for good adnexal examination is magnification. Although any magnifying lens may be used, the method I prefer is to use the lens of an otoscope; this lens is powerful enough to detect nearly all common abnormalities and is easy to manipulate. The only thing better is a slit lamp biomicroscope. Checklist for the adnexal exam: distichiasis, trichiasis, ectopic cilia, foreign bodies under third eyelid, follicle formation, conjunctival vascular changes (inflammation and congestion), character of ocular discharge, eyelid neoplasms, chalazions, and blepharitis.
Examination of the Cornea
Fluorescein dye remains the agent of choice for detecting corneal ulcers. It is important that excess fluorescein be thoroughly irrigated from the cul de sac to avoid confusing healed ulcers with active ones; fluorescein will pool in epithelialized stromal defects. If fluorescein absorption occurs, distinguish complete versus partial epithelial cell loss by intensity of the staining; in cases of superficial keratitis the epithelium is likely to faintly stain, although true ulceration is absent. Ultraviolet or cobalt blue-filtered light is helpful but rarely necessary. The cornea is then examined for other opacities such as edema, pigment, and vascularization.
Vessels should be categorized based on depth (superficial vessels branch in tree fashion and can be seen crossing the limbus, deeper vessels possess a brush type border and emerge from the sclera). Proliferative-vascular lesions are sometimes encountered in the corneas of small animals. In most cases, they are secondary to chronic irritation, or are associated with healing ulcers. If close to the limbus, primary inflammatory lesions should be considered (especially in dogs, e.g., fibrous histiocytoma, chronic superficial keratitis, pannus). Finally, the cornea is examined for white opacities that usually are scars, dystrophies, or metabolic infiltrates. If a dense white opacity is present, the cornea is examined for adherent iris tissue (synechia). Such a lesion is referred to as an adherent leukoma. Checklist for corneal exam: ulceration, edema, vascularization, pigment, inflammatory masses, and white opacities (scars, dystrophies, and metabolic infiltrates).
Examination of the Anterior Chamber and Anterior Uvea
The most commonly overlooked anterior chamber abnormality is aqueous flare. Aqueous flare (plasmoid aqueous) occurs when the blood-aqueous barrier has been compromised. Although most commonly due to inflammation, breakdown of the blood-aqueous barrier also occurs with intraocular neoplasms. Detection of aqueous flare is important because it is frequently the only definitive sign of intraocular disease. When a disease process disrupts iris blood vessels, high molecular weight proteins are allowed access to the anterior chamber. The normally transparent aqueous humor becomes transparent; however, aqueous protein can only be detected with the correct application of optical principles.
To see aqueous flare an intense and focal light source must be held close (1 cm) to the corneal surface. A direct ophthalmoscope set at its smallest circular aperture of white light, and to its highest light intensity, works best (a pen light is inadequate for this procedure). Aqueous flare is present if the light beam is visible in the anterior chamber. Other abnormal anterior chamber contents include purulent exudate (hypopyon), blood (hyphema), and neoplastic masses. The detection of these abnormalities is facilitated by examining the anterior chamber with magnification from the temporal limbus, perpendicular to the visual axis. It is only from this perspective that subtle changes in anterior chamber depth, indicative of lens displacement, can be detected.
When examining the iris, abnormalities to look for are dyscoria, anisocoria, iris swelling, changes in iris color (heterochromia), iris cysts, persistent pupillary membranes, synechia, and atrophy. Examination of the ciliary body can only be accomplished with the aid of complete mydriasis. Check list anterior chamber and anterior uveal exam: aqueous flare, anterior chamber depth, hypopyon, hyphema, synechia, iris cysts, iris atrophy, heterochromia, persistent pupillary membranes, iris swelling.
Mydriasis and the Fundus Reflex
Tropicamide (Mydriacyl?/sup>) is the agent of choice; two drops instilled at five minute intervals produces mydriasis in 20 minutes which lasts for 3? hours. Glaucoma is the only contraindication to dilating the pupils. Examination of the fundus reflex is the most simple and yet useful methods for estimating the clarity of the ocular media. Using a direct ophthalmoscope set on 0 diopters, the light reflected from the ocular fundus is viewed from of distance of 12?8 inches.
The quality of reflected light seen varies with the breed and coat color type of the animal; animals with a tapetum will have a bright fundus reflection of yellow, orange, or green, while those without a tapetum usually have a red fundus reflection (produced by the choroidal vessels). Regardless of the color, the fundus reflex should be uniform throughout the pupil, and be free of aberrations. By examining the fundus reflex, the clinician can accurately estimate the amount of light reaching the retina, and thereby estimate the quality of sight. For example, in an animal presented with the complaint of blindness suspected to be due to cataracts, which has a reasonably normal fundus reflex, blindness cannot be attributed to lens opacification. The same principle applies to opacification anywhere within the eye, including the cornea, anterior chamber, lens, and vitreous. Once an opacity has been identified, it is examined in more detail using other techniques.
Examination of the Lens
The slit lamp biomicroscope is designed for examining the lens; however, for almost all practical purposes, the lens can be examined adequately with a direct ophthalmoscope and otoscope. The first part of the lens exam occurs when evaluating the fundus reflex. If an opacity obscuring the fundus reflex is suspected to be in the lens, its location is most easily verified by ruling out opacification of corneal and anterior chamber structures as described above. The fundus reflex is then used to localize the opacity within the lens. Because the lens nucleus is close to the rotational axis of the globe, the directional movement of lens opacities (cataracts) indicates their location; opacities that move in the direction of globe movement are in the anterior portion of the lens, those that appear to remain stationary are centrally located (nuclear), and those that move opposite are in the posterior portion. If cataracts are found, the anterior capsule of the lens is examined for irregularities (viewing perpendicular to the animals visual axis) with the otoscope. Changes in position of the lens should have been detected when examining the anterior chamber. However, subtle lens displacement may only be evidenced by a small crescent shaped area within the pupil that is devoid of lens material (aphakic crescent); aphakic crescents are also most easily detected by viewing the fundus reflex. Finally, the lens capsule is examined for the presence of adhered uveal tissue (posterior synechia, congenital pigment remnants), persistent pupillary membranes, and hyaloid artery remnants. Checklist for lens exam: cataracts, lens displacement, persistent pupillary membranes, hyaloid artery remnants, and synechia.

minibabyqq 2007-1-26 02:13

[color=Magenta][size=5][b]視覺表面的疾病Diseases and Immunity of the Ocular Surface  [/b][/size][/color]


介紹
視覺表面包括主要淚花影片、角膜, 和內眼膜。盒蓋用於保護眼睛和塗淚花在視覺表面, 和必須因而被認為視覺表面的整體部分。影響視覺表面的疾病幾乎一定將影響盒蓋正盒蓋疾病也許有一個深刻作用在視覺表面。淚花影片是視覺表面的主要未指明的防禦系統並且眼睛的第一折射層數。另外, 它維護一一致角膜表面和提供營養素和氧氣對角膜。所以, 瞭解和保存適當的淚花作用是一個根本組分為優選的視覺健康在我們的患者。keratoconjunctivitis sicca 的研究(KCS) 並且典型cyclosporine 的發展為那種疾病的治療深刻地影響了影響視覺表面對視覺表面免疫和疾病的我們的理解。
視覺表面的免疫學
瞭解視覺表面的免疫學防禦系統允許臨床工作者更好瞭解視覺表面混亂和治療病理生理學被使用解決他們。雖然事件順序在防禦機制是複雜的, 它是可能分類他們入二個主要類別, 輸入和傳出弧。輸入弧是主人recognizes. 觸犯的抗原, 和傳出弧代表具體反應反對他們的系統由。
角膜是有些immunologically 被賦予特權的站點。因為它缺乏vascularization 和淋巴排水設備。抗原與視覺表面聯繫因此最初地主要被處理在內眼膜抗原提出細胞(的地方APC.s) 與主要組織相容性複合體II (MHC-II) 分子在他們的表面困境抗原。Conjunctival 同淋巴腺組織(CALT), 巨噬細胞聯繫在一起, 並且Langerhans. 細胞從limbal 區域全部作為APC.s 。CALT 接受抗原為介紹對流通的T 淋巴細胞(T 幫手細胞), 並且淋巴渠道排泄它對地方淋巴結。專業皮膜躺在上面CALT 與相對地平的皮膜不同在毗鄰區域因為它延長了microvillae, 援助在抗原捕獲暴露於視覺表面。Langerhans. 細胞和巨噬細胞束縛抗原對他們的表面或為介紹對流通的T 幫手細胞或運載他們通過淋巴渠道對排泄的淋巴結。另外, 對伽瑪干擾素的暴露由被激活的淋巴細胞生產可能導致角膜和lacrimal 葡萄核的上皮細胞顯示MHC-II 和功能作為APC.s 。因而, 當疾病進步, 越□越寄主細胞變得介入host.s 免疫反應的補充對抗原的。在地方淋巴結, B 和T 淋巴細胞被刺激激增和區分。爾後, B 淋巴細胞移居對lacrimal 和輔助lacrimal 封墊皮膜當T 淋巴細胞移居回到sensitization 範圍收集在內眼膜的submucosa 。
B 細胞被刺激乘以B 細胞成長因素並且然後生產抗體由B 細胞分化析因。被激活的T 幫手細胞藏匿這些因素。抗體具體地束縛與刺激它的生產因此B 淋巴細胞遷移對lacrimal 組織為表面的地方生產提供的抗原當它被傷害或激動過程(即, 角膜vascularization) 破壞。
T 淋巴細胞也許被劃分成3 個子集: 幫手T 細胞、兇手T 細胞, 和遏抑器T 細胞。被激活的幫手T 細胞變換成lymphoblasts 並且, 在激增在地方以後淋巴結依照已經被談論移居對內眼膜的submucosa 。被激活的淋巴細胞和巨噬細胞生產是可溶解蛋白質充當在免疫反應多孔的事件的許多重要角色並且允許相對地少量被激活的細胞吸收和控制很大數量的使非敏感的淋巴細胞和巨噬細胞的lymphokines 。lymphokines 包括Interleukin 1, Interleukin 2, 巨噬細胞遷移禁止因素、巨噬細胞激活的因素、趨化性因素, 和免疫干擾素。兇手T 細胞是細胞毒素的對被抗原侵略了或損壞了和發生在傳染和瘤形成的外國細胞或寄主細胞。遏抑器T 細胞減慢免疫反應當扣人心弦的起因被控制了。
補全活化作用和干擾素的生產是免疫反應的另外的組分。補全活化作用結果在導致細胞膜中斷貢獻對多孔的死亡通過抗體斡旋的和細胞免疫enzymatic 反應的小瀑布。干擾素可能干涉某些病毒的複製當被傳染的細胞導致導致它。由於它的低分子重量, 它可能散開入毗鄰細胞保護他們。對阿爾法干擾素的典型和口頭用途主張了在堅持或嚴厲Herpes felis keratoconjunctivitis 的 治療在貓, 但也許是最有效的當使用及早在深刻傳染。
視覺表面免疫和疾病
當免疫系統負責對保護主人, 眼睛是一個非常敏感結構和窮地經常經歷在疾病反應的面孔。以下例子是熟悉對所有獸醫, 將用於刺激進一步研究嚮其它疾病瞭解和申請這知識, 視覺和系統。
Keratoconjunctivitis sicca 古典地被看待如同視覺表面的疾病由含水淚花分泌物缺乏造成。多原因論被認可和包括傷害對lacrimal 封墊或第三眼皮的封墊的他們的激動、藥物毒力(sulfa 藥物是最共同地包含的), 藥物或做法導致的(次要對麻醉、輻射, 或atropine 或抗組胺的管理), 外科切除或慢性prolapse, 先天官能不良、遺傳、慢性炎症(blepharoconjunctivitis 或keratoconjunctivitis), 和免疫斡旋的疾病(或自動免疫或allergic/hyperimmune) 。對典型cyclosporine 的發展和用途為KCS 集中注意於前3 個類別, 佔多數盒。的確, 遺傳性因素和慢性炎症像清楚的從程度養殖predispositionparallels 的樣式過敏癩密切被栓對免疫官能不良。
負責對型I 過敏症) 的集中IgE (可能很大地被增加在conjunctival 血漿細胞裡在 過敏keratoconjunctivitis。氨基酸感受器官是存在在視覺表面並且conjunctival 帆柱細胞的degranulation 由IgE 斡旋發布可能然後束縛對視覺表面和施加它的地方作用, 沒有對精美組織是特別親切的氨基酸。因而以慢性未管制的遺傳性過敏症, 角膜和內眼膜體驗漸增和經常進步損傷, 本身促進進一步免疫反應的補充的損傷。
對herpetic keratoconjunctivitis 的 免疫學反應 主要是T 細胞被斡旋, 並且在某些情況下, 可以要求鎮壓與抗病毒療法一道為了維護正常角膜作用。許多獸醫眼科醫生相信, 有一種交互作用在herpetic 傳染在貓和嗜伊紅的角膜炎之間 發生, 對類皮質激素療法通常是敏感。
慢性keratoconjunctivitis (pannus) 發生主要用德語牧羊人和為表面角膜和內眼膜的濾滲描繪與淋巴細胞、顏料, 和維管組織的組織。它廣泛被認可作為要求終身控制由免疫抑壓代理的每日管理的一個免疫斡旋的問題(主要類皮質激素和cyclosporine) 。
Mooren.s 潰瘍 是潰瘍介入周邊角膜stroma 在人; 相似的發生被注意了在狗和認為是免疫的被斡旋以回應沉澱在周邊角膜的抗原抗體複合體。接著而來的主人反應導致keratomalacia 或熔化包含的角膜。
CYCLOSPORINE 在獸醫眼科學方面
Cyclosporine (CsA) 行動主要在免疫反應的輸入胳膊在出現抗原和細胞的動員的認識期間在反應。它施加它的活動在淋巴細胞但不干涉吞噬細胞或hemopoietic 乾細胞, 因此它較不經常同機會主義的傳染聯繫在一起比其它代理。它防止lymphokine 發行和T 細胞、B 細胞和monocytes 的隨後擴散和活化作用。它, 然而, 不阻攔遏抑器T 細胞因此它下來調控免疫反應傾向於容忍。行動機制在抵抗對lacrimal 分泌物的禁止作用由paracrine neurohormones 由淋巴細胞藏匿在lacrimal 和輔助lacrimal 封墊依然是殘缺不全地瞭解。
近來(1995 的秋天), cyclosporine 的眼科準備未被銷售, 並且它被配製了在油裡當對口頭產品的一個額外標籤用途意欲為系統免疫鎮壓。最初地, 它準備了在一種2% 解答在橄欖油裡, 但激怒是問題。隨後, 玉米油被替代了在公式化和很好被容忍了在多數患者。偶爾地激怒根據2% 解答也許發生, 並且在這些情況下, 一種1% 公式化在玉米油裡也許是較不惱人的當有效在刺激的淚花分泌物。這樣公式化現在是在使用中大約10 年和很好被容忍了以少量副作用。但是, 有臨床工作者應該知道的一些重大關心。
對這些公式化的典型用途可能導致cyclosporine 的系統吸收在足夠偉大成水平被測量, 並且在淋巴細胞活化作用的可測量的減退被提供了(Gilger, 等, 1995 年和1996) 。臨床標誌未被注意在這些患者, 但是臨床工作者運用這些公式化應該意識到在互作用或協同作用的作用的潛力與一致地被使用的療程。另外, 程度吸收從皮膚接觸在人是未知的但應該被考慮, 特別是在是immunocompromised 的所有者。
或許最偉大的令人擔心的事圍繞不育和產品穩定的問題。沾染玉米油解答在用途期間由人的患者被提供了。在人的角膜移植患者的研究中使用典型2% cyclosporine 被配製在玉米油裡在不育的情況下, 瓶被分與了對患者在瓶的最初的文化沒有顯露細菌成長之後。在他們之時復校在25.30 天, 82% 之間瓶是正面的為細菌成長。 Klebsiella spp. 是存在在46%, 帚形菌屬 spp 在31%, 和 葡萄球菌 spp 在27% 。(D.Alessandro, 等。 投資。Ophthalmol 。力。Sci 。 35(4), 1994) 。
療程的溢出是偶爾的怨言從所有者, 並且某些人民反對盒蓋和面孔的含油。 Mallasezia spp 也許偶爾地利用這樣一個油膩的環境。
Optimmune。, cyclosporine 的一種0.2% 軟膏公式化, 1995 年由Schering Schering-Plough 介紹了在美國和現在被批准了用於動物在25 個國家。它很好被容忍, 並且它長時期的聯絡時間與眼睛允許更低的集中是有效的在刺激的淚花生產和壓制表面視覺免疫一些混亂。雖然關於它的作用的研究對淋巴細胞活化作用未被進行, 它最小地被吸收入血液, 並且系統副作用不是著名在臨床試驗期間。由於軟膏不支持細菌成長, 汙穢不是問題。一些客戶也許有困難以應用, 特別是如果他們的狗是進取的或不合作或他們的手工手巧由傷殘或年齡相關的體弱減弱。在比較研究中, 軟膏是相等地有效的在生產淚花與公式化比較在油裡, 但一些獸醫眼科醫生報告他們的臨床經驗是它是較不有效的。能對區別貢獻的因素包括單獨變異、粗劣的客戶遵照軟膏, 或一個過早的開關從軟膏對下落。

INTRODUCTION
The ocular surface is comprised primarily of the tear film, cornea, and conjunctiva. The lids serve to protect the eye and spread the tears over the ocular surface, and thus must be considered an integral part of the ocular surface. Diseases that affect the ocular surface will almost certainly affect the lids just as lid diseases may have a profound effect on the ocular surface. The tear film is the primary nonspecific defense system of the ocular surface as well as the first refractive layer of the eye. In addition, it maintains a uniform corneal surface and provides nutrients and oxygen to the cornea. Therefore, understanding and preserving proper tear function is an essential component for optimal ocular health in our patients. The study of keratoconjunctivitis sicca (KCS) and the development of topical cyclosporine for the treatment of that disease have profoundly influenced our understanding of the ocular surface immunity and the diseases that affect the ocular surface.
IMMUNOLOGY OF THE OCULAR SURFACE
Understanding the immunological defense systems of the ocular surface allows the clinician to better understand the pathophysiology of ocular surface disorders and the treatments employed to resolve them. Although the sequences of events in the defense mechanisms are complex, it is possible to classify them into two major categories, the afferent and efferent arcs. The afferent arc is the system by which the host 𩂈ecognizes?offending antigens, and the efferent arc represents the specific reactions against them.
The cornea is somewhat of an 𧗽mmunologically privileged site?in that it lacks vascularization and lymphatic drainage. Antigens contacting the ocular surface therefore are primarily processed initially in the conjunctiva where antigen-presenting cells (APC𠏋) with major histocompatibility complex II (MHC-II) molecules on their surface bind antigen. Conjunctival associated lymphoid tissue (CALT), macrophages, and Langerhans?cells from the limbal region all act as APC𠏋. The CALT receives antigen for presentation to circulating T-lymphocytes (T-helper cells), and lymphatic channels drain it to regional lymph nodes. Specialized epithelium overlying the CALT differs from the relatively flat epithelium in adjacent areas in that it has elongated microvillae, which aids in the capture of antigens exposed to the ocular surface. Langerhans?cells and macrophages bind antigens to their surface either for presentation to circulating T-helper cells or to carry them through the lymphatic channels to the draining lymph nodes. In addition, exposure to gamma interferon produced by activated lymphocytes can induce epithelial cells of the cornea and lacrimal acini to display MHC-II and function as APC𠏋. Thus, as the disease progresses, more and more host cells become involved in recruitment of the host𠏋 immune responses to antigens. In the regional lymph nodes, B and T lymphocytes are stimulated to proliferate and differentiate. Thereafter, the B-lymphocytes migrate to lacrimal and accessory lacrimal gland epithelium while the T lymphocytes migrate back to the area of sensitization to collect in the submucosa of the conjunctiva.
The B-cells are stimulated to multiply by B-cell growth factor and then to produce antibodies by B-cell differentiation factor. Activated T-helper cells secrete these factors. Antibodies bind specifically with the antigen that stimulated its production so the migration of the B-lymphocytes to the lacrimal tissue provides for the local production of surface when it is breached by injury or inflammatory processes (e.g., corneal vascularization).
T lymphocytes may be divided into 3 subsets: helper T cells, killer T cells, and suppressor T cells. Activated helper T cells transform into lymphoblasts and, after proliferating in the regional lymph nodes migrate to the submucosa of the conjunctiva as already discussed. The activated lymphocytes and macrophages produce lymphokines which are soluble proteins that play many vital roles in the cellular events of the immune response and which allow relatively few activated cells to recruit and control a great number of non-sensitized lymphocytes and macrophages. The lymphokines include Interleukin 1, Interleukin 2, macrophage migration-inhibition factor, macrophage activating factor, chemotactic factor, and immune interferon. Killer T cells are cytotoxic to foreign cells or host cells that have been invaded or damaged by antigens as occurs in infection and neoplasia. Suppressor T cells slow the immune response when the exciting cause has been controlled.
Complement activation and the production of interferon are additional components of the immune response. Complement activation results in a cascade of enzymatic reactions that result in disruption of cell membranes contributing to cellular death via both antibody-mediated and cell-mediated immunity. Interferon can interfere with the replication of certain viruses when infected cells are induced to produce it. By virtue of its low molecular weight, it can diffuse into adjacent cells protecting them. Topical and oral use of alpha interferon has been advocated in the treatment of persistent or severe Herpes feliskeratoconjunctivitis in cats, but may be most effective when used early in acute infections.
Ocular Surface Immunity and Disease
While the immune system is responsible for protecting the host, the eye is a very sensitive structure and often fares poorly in the face of the disease response. The following examples are familiar to all veterinarians and will serve to stimulate further study to understand and apply this knowledge to other diseases, ocular and systemic.
Keratoconjunctivitis sicca is classically regarded as a disease of the ocular surface caused by a deficiency of aqueous tear secretion. Multiple etiologies are recognized and include injury to the lacrimal glands or their innervation, drug toxicity (sulfa drugs being most commonly involved), drug or procedure induced (secondary to anesthesia, radiation, or the administration of atropine or antihistamines), surgical excision or chronic prolapse of the gland of the third eyelid, congenital dysfunction, heredity, chronic inflammation (blepharoconjunctivitis or keratoconjunctivitis), and immune mediated disease (either autoimmune or allergic/hyperimmune). The development and use of topical cyclosporine for KCS has focused attention on the last 3 categories, which account for the majority of cases. Indeed, both hereditary factors and chronic inflammation are tied inextricably to immune dysfunction as is clear from the degree to which the pattern of breed predispositionparallels that of allergic skin disease.?
The concentration of IgE (which is responsible for type I hypersensitivity) can be greatly increased in conjunctival plasma cells in allergic keratoconjunctivitis. Histamine receptors are present on the ocular surface and the degranulation of conjunctival mast cells mediated by IgE releases histamine which can then bind to the ocular surface and exert its local effects, none of which are particularly kind to the delicate tissue. Thus with chronic uncontrolled atopy, the cornea and conjunctiva experience a cumulative and often progressive damage, damage that itself facilitates the recruitment of further immune responses.
The immunological response to herpetic keratoconjunctivitis is largely T-cell mediated, and in some cases, may require suppression in conjunction with antiviral therapy in order to maintain normal corneal function. Many veterinary ophthalmologists believe that there is a correlation between herpetic infections in cats and the occurrence of eosinophilic keratitis, which is usually responsive to corticosteroid therapy.
Chronic keratoconjunctivitis (pannus) occurs primarily in German Shepherds and is characterized by infiltration of the superficial cornea and conjunctiva with lymphocytes, pigment, and fibrovascular tissue. It is widely recognized as an immune mediated problem that requires lifelong control by the daily administration of immune suppressive agents (primarily corticosteroids and cyclosporine).
Mooren𠏋 ulcers are ulcerations involving the peripheral corneal stroma in humans; similar occurrences have been noted in dogs and are believed to be immune mediated in response to antigen-antibody complexes that precipitate in the peripheral cornea. The ensuing host response results in keratomalacia or melting of the involved cornea.
CYCLOSPORINE IN VETERINARY OPHTHALMOLOGY
Cyclosporine (CsA) acts primarily on the afferent arm of the immune response during the recognition of the presence of antigen and the mobilization of cells in response. It exerts its activity on lymphocytes but does not interfere with phagocytes or the hemopoietic stem cells, so it is less often associated with opportunistic infections than other agents. It prevents lymphokine release and the subsequent proliferation and activation of T-cells, B-cells and monocytes. It does not, however, block suppressor T-cells so it down-regulates the immune response in favor of tolerance. The mechanisms of action in countering the inhibitory effect on lacrimal secretion by paracrine neurohormones secreted by lymphocytes in the lacrimal and accessory lacrimal glands remain incompletely understood.
Until recently (Fall of 1995), no ophthalmic preparation of cyclosporine was marketed, and it was compounded in oil as an extra label use of the oral product intended for systemic immune suppression. Initially, it was prepared in a 2% solution in olive oil, but irritation was a problem. Subsequently, corn oil was substituted in the formulation and was well tolerated in most patients. Occasionally irritation by 2% solutions may occur, and in such cases, a 1% formulation in corn oil may be less irritating while still effective in stimulating tear secretion. Such formulations have now been in use for approximately 10 years and have been well tolerated with few side effects. However, there are some significant concerns of which the clinician should be aware.
The topical use of these formulations can result in the systemic absorption of cyclosporine in great enough levels to be measured, and a measurable decrease in lymphocyte activation has been documented (Gilger, et. al., 1995 and 1996). No clinical signs were noted in these patients, but clinicians utilizing these formulations should be aware of the potential for interactions or synergistic effects with concurrently used medications. In addition, the degree of absorption from skin contact in humans is unknown but should be considered, especially in owners who are immunocompromised.
Perhaps the greatest cause for concern revolves around the issue of sterility and product stability. Contaminated of corn oil solutions during use by human patients has been documented. In a study of human cornea transplant patients using topical 2% cyclosporine compounded in corn oil under sterile conditions, the bottles were dispensed to the patients after initial cultures of the bottles revealed no bacterial growth. At the time of their rechecks between 25?0 days, 82% of the bottles were positive for bacterial growth. Klebsiella spp. was present in 46%, Pseudomonas spp in 31%, and Staphylococci spp in 27%. (D𡒶lessandro, et. al.. Invest. Ophthalmol. Vis. Sci. 35(4), 1994).

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[color=Magenta][size=5][b]眼疾病和手術Diseases and Surgery of the Eyelids  [/b][/size][/color]


介紹
盒蓋不僅是極端重要對視覺表面和作用的健康保護免受精神創傷, 而且提供淚花影片的發行在眼睛。它因此重要, 眼皮的疾病是受控的在重大結疤干涉他們的作用之前。結構眼皮瑕疵應該被改正以退回解剖學儘可能與法線接近的規程。由於盒蓋的多數包括皮膚, 盒蓋的激動疾病也許被處理因為他們會是為皮膚。在短時間我們有在這個會議上, 我們將尋求集中於可能共同地被使用改正他們盒蓋和方法的最重要的結構瑕疵。
解剖考慮
眼皮的皮膚是相對地稀薄和韌勁的當與皮膚在別處比較在身體。由於許多的眼皮的tarsal 板材動物是較不好的被發展比在人, 盒蓋邊際是極端重要為維護眼皮裂痕的正常形狀和作用。另外, meibomian 或tarsal 封墊倒空通過跑盒蓋邊際中部的長度並且這些封墊油脂分泌物是重要為淚花影片的保存的小開頭。所以, 一個重要眼皮的考慮在疾病和手術是盒蓋邊際的正直的維護每當可能。
orbicularis oculi 肌肉包圍眼皮裂痕和作用關閉裂痕當它收縮。中間眼皮韌帶和翻悔者anguli oculi lateralis 肌肉作用中間和側向地停住orbicularis 各自地。這些中間和側向附件用於保存眼皮裂痕的省略形狀。他們進一步防止裂痕變得圓在orbicularis 的攣縮期間為眨眼睛和盒蓋關閉。在加法, orbicularis oculi 有插入入lacrimal sac 的側向牆壁的纖維, 並且纖維的攣縮和放鬆對淚花的運動貢獻通過sac 通過所謂的lacrimal 泵浦。
當眨眼睛發生, 上部盒蓋是更加流動的和旅行一個更加了不起的距離在角膜比更低的盒蓋。另外, 因為更低的盒蓋自然地傾向於下垂輕微地從地球, 溫和的entropion 和trichiasis 更好被容忍當他們影響更低的盒蓋比鞋幫。上部盒蓋應該因而接受重要性在重建規程並且特別留意應該將維護上部盒蓋邊際和相應一致指向。
盒蓋主要供血出現從中間和側向canthi 。所以, 必須被保重在手術保證供血對盒蓋被維護。當擋水板被塑造從盒蓋在重建手術, 他們的中間或側向pedicles 應該是至少4.6 毫米在寬度保證, 擋水板有充分灌注。
lacrimal punctae 和小管起作用排泄淚花入lacrimal sac 並且更低的斑點比鞋幫重要在這個作用。至少更低的斑點和小管的保存是因而重要性在介入中間眼角的盒蓋手術。
一個一般經驗法則是, 瑕疵介入25% 盒蓋邊際也許主要是閉合的。在一些養殖以euryblepharon (macroblepharon) 並且外翻, 這百分比可能是儘量33% 。因為我們將談論, 這可能是極端重要在處理大盒蓋瑕疵和瘤。
BASIC 外科原則
和以所有事, 困難的問題可能由打破經常解決他們下來更加簡單的任務或步。幾個簡單的外科技術可能嚮更加困難的盒蓋問題的決議被申請。
經常出現問候年齡盒蓋規程應該執行的一個問題當幼小動物有一個盒蓋瑕疵(colobomas 、entropion 、外翻、distichiasis, 等。) 。。總之, 理想的情況會將等待直到至少一年紀當大多數面部相應一致的成熟性發生□。但是, 在次要損傷的潛力對視覺表面必須採取優先次序高於一切, 並且任一個措施必要應該被採取防止角膜潰瘍並且/或者結疤。因而, 更加嚴厲的盒蓋瑕疵是更加偉大的是對及時外科干預的需要。
經常臨床工作者被面對以介入盒蓋邊際的腫瘤或瑕疵。對cruciate 縫合的用途(更好地6-0 聚丙烯或尼龍) 保證優選的關閉盒蓋邊際瑕疵以組織的排除轉移沒有角膜激怒風險從縫合結。
當手術或撕裂影響lacrimal 小管, 重建可能由cannulation 援助使用silastic 管材。這可能由單絲縫合的最初的段落促進通過小管或nasolacrimal 輸送管。管材也許通過在縫合和然後被拉扯通過輸送管依照被談論在演講。pigtail. 探針也許被使用以極大好處, 特別是當cannulating 小管。對這臺儀器的用途和它的局限將被談論。
在獸醫方面, 我們有一個傾向想要立即做一切完成更正在一手術期間和避免多麻醉。但是, 外科醫生應該記得, 它比它將替換總更加容易去除更多組織什麼丟失。在整容手術, 它也許是更好達到更正通過幾個逐漸更正比冒險結束更正並且/或者過份結疤。所有者應該被製作知道, 次要調整規程也許是需要的達到優選的結果因此關於有所有者的問題的詳盡的討論是根本的。
DISTICHIASIS 的更正
眾多的技術沉重主張了的distichiasis 的治療與區別受撫養者在外科醫生特選、可利用的設備, 和居住訓練用不同的區域。明顯地, 額外鞭子不造成問題的案件不要求治療, 和當epiphora 是唯一的標誌, 每一努力應該被做排除其它起因在distichiasis 的治療被承擔之前。技術經常主張包括, 受影響的盒蓋邊際的簡單的外翻, electroepilation (特別是當很小數量的鞭子是存在), cryoablation 以和沒有鞭子濾泡的切除, 和鞭子濾泡的laser 燒蝕。一一致的教學在多數作者之中是, 盒蓋邊際不應該被分裂依照主張為疾病在人。這樣分裂邊際減弱它和對也許是嚴厲的不規則性和結疤貢獻。另外, 觸犯的鞭子並且/或者隨後trichiasis 再現是共同以盒蓋分裂。同樣, 任一個技術應該避免對盒蓋邊際的過份損傷。最共同的療法的好處和不利將被談論。

大眼皮瑕疵的更正
大眼皮瑕疵的更正不管他們的起源擺在面對眼科外科醫生的最富挑戰性的手術的當中一個。最共同地被使用的技術包括推進和旋轉的擋水板(菱形和pedicle) 從毗鄰皮膚和十字架盒蓋擋水板。推進和旋轉的擋水板更加容易執行但不允許眼皮邊際的重建當上部眼皮瑕疵是存在。發怒盒蓋擋水板使用更低的盒蓋邊際改正上部盒蓋的瑕疵。但是, 這樣擋水板是更加複雜的做和要求手術在至少二個階段。這些選擇和他們的好處和不利詳細將被談論。
MACROBLEPHARON 的更正的技術
Macroblepharon 可能收效在entropion 和外翻面前在同樣眼睛。根據嚴肅, 對療法的幾種不同的方法也許被使用。在演講, 我們將考慮說明不同的技術範圍從簡單的canthal 關閉對rhomboid canthoplasty 的選擇的案件。

選擇為外翻的更正
依靠是否外翻是主要和相關對過份盒蓋長度並且/或者缺乏盒蓋口氣或次要對結疤, 不同的方法對更正也許被使用。為結疤, Wharton 瓊斯(V 對Y) blepharoplasty 也許是更喜歡, 但其它盒靠盒蓋縮短和技術最好對待改進盒蓋口氣。這些技術和他們的徵兆將被說明正像時間准許。

選擇為ENTROPION 的更正
entropion 的更正是或許最共同地被教的盒蓋手術和或許最簡單執行。Shar Peis 和養殖與重的面部摺疊可能提出臨床工作者以富挑戰性困境。我們將談論簡單盒蓋添加被表明並且何時申請更加先進的技術。


INTRODUCTION
The lids are extremely important to the health of the ocular surface and function not only to protect against trauma, but also to provide for the distribution of the tear film over the eye. It is therefore important that disease of the eyelids be controlled before significant scarring interferes with their function. Structural eyelid defects should be corrected with procedures that return the anatomy to as close to normal as possible. Because the majority of the lid consists of skin, inflammatory diseases of the lids may be managed much as they would be for the skin. In the short time we have in this session, we will seek to focus on the most important structural defects of the lids and the methods that can be commonly employed to correct them.
ANATOMIC CONSIDERATIONS
The skin of the eyelids is relatively thin and pliable when compared to the skin elsewhere on the body. Because the tarsal plate of the eyelid of many of animals is less well developed than in man, the lid margins are extremely important for maintaining the normal shape and function of the palpebral fissure. In addition, the meibomian or tarsal glands empty through small openings that run the length of the middle of the lid margin and the lipid secretion of these glands is important for preservation of the tear film. Therefore, one of the important considerations in diseases and surgery of the eyelids is the maintenance of the integrity of the lid margins whenever possible.
The orbicularis oculi muscle encircles the palpebral fissure and functions to close the fissure when it contracts. The medial palpebral ligament and the retractor anguli oculi lateralis muscle function to anchor the orbicularis medially and laterally respectively. These medial and lateral attachments serve to preserve the elliptical shape of the palpebral fissure. They further prevent the fissure from becoming circular during contracture of the orbicularis for blinking and lid closure. In addition, the orbicularis oculi has fibers that insert into the lateral wall of the lacrimal sac, and contracture and relaxation of the fibers contribute to movement of tears through the sac via the so-called lacrimal pump.
When blinking occurs, the upper lid is more mobile and travels a greater distance over the cornea than the lower lid. In addition, because the lower lid naturally tends to sag slightly away from the globe, mild entropion and trichiasis are better tolerated when they affect the lower lid than the upper. The upper lid should thus receive a higher priority in reconstructive procedures and special attention should be directed toward maintaining the upper lid margin and conformation.
The major blood supply of the lids arises from the medial and lateral canthi. Therefore, care must be taken in surgery to assure the blood supply to the lids is maintained. When flaps are fashioned from the lids in reconstructive surgeries, their medial or lateral pedicles should be at least 4? mm in width to ensure that the flaps have adequate perfusion.
The lacrimal punctae and canaliculi function to drain the tears into the lacrimal sac and the lower punctum is more important than the upper in this function. Preservation of at least the lower punctum and canaliculus is thus a high priority in lid surgeries that involve the medial canthus.
A general rule of thumb is that defects involving up to 25% of the lid margin may be closed primarily. In some breeds with euryblepharon (macroblepharon) and ectropion, this percentage can be as much as 33%. As we will discuss, this can be extremely important in managing large lid defects and neoplasms.
BASIC SURGICAL PRINCIPLES
As with all things, difficult problems can often be solved by breaking them down into simpler tasks or steps. Several simple surgical techniques can be applied to the resolution of more difficult lid problems.
One question that often arises regards the age at which lid procedures should be performed when young animals have a lid defect (colobomas, entropion, ectropion, distichiasis, etc.).?In general, the ideal situation would be to wait until at least a year of age when most of the maturation of facial conformation has occurred. However, the potential for secondary damage to the ocular surface must take precedence above all else, and any measure necessary should be taken to prevent corneal ulceration and/or scarring.?Thus, the more severe the lid defect is the greater is the need for prompt surgical intervention.
Often the clinician is confronted with tumors or defects that involve the lid margin. The use of a cruciate suture (preferably 6-0 polypropylene or nylon) assures optimal closure of lid margin defects with elimination of tissue shifting without risk of corneal irritation from the suture knot.
When surgery or lacerations affect the lacrimal canaliculi, reconstruction can be aided by the cannulation using silastic tubing. This can be facilitated by initial passage of a monofilament suture through the canaliculi or the nasolacrimal duct. The tubing may then be passed over the suture and pulled through the ducts as discussed in the lecture. A 𢖯igtail?probe may be used with great benefit, especially when cannulating the canaliculi. The use of this instrument and its limitations will be discussed.
In veterinary medicine, we have a tendency to want to do everything at once to accomplish correction during one surgery and avoid multiple anesthesias. However, the surgeon should remember that it is always easier to remove more tissue than it is to replace what is lost. In plastic surgery, it may be better to achieve correction through several gradual corrections than to risk over correction and/or excessive scarring. The owner should be made aware that secondary adjustment procedures might be needed to achieve optimal results so thorough discussion of the problem with the owner is essential.
CORRECTION OF DISTICHIASIS
Numerous techniques have been advocated for the treatment of distichiasis with differences dependent heavily on surgeon preference, available equipment, and residency training in different areas. Obviously, cases in which the extra lashes are causing no problems require no treatment, and when epiphora is the only sign, every effort should be made to rule out other causes before treatment of distichiasis is undertaken. Techniques most often advocated include, simple eversion of the affected lid margin, electroepilation (especially when small numbers of lashes are present), cryoablation with and without excision of the lash follicles, and laser ablation of lash follicles. One consistent teaching among most authors is that the lid margins should not be split as advocated for the disease in humans. Such splitting of the margins weakens it and contributes to irregularities and scarring which may be severe. In addition, recurrence of offending lashes and/or subsequent trichiasis is common with lid splitting. Similarly, any technique should avoid excessive damage to the lid margins. The advantages and disadvantages of the most common therapies will be discussed.

CORRECTION OF LARGE EYELID DEFECTS
The correction of large eyelid defects regardless of their origin poses one of the most challenging surgeries that confront the ophthalmic surgeon. The most commonly employed techniques include advancement and rotational flaps (rhomboid and pedicle) from adjacent skin and cross lid flaps. The advancement and rotational flaps are easier to perform but do not allow reconstruction of the eyelid margin when an upper eyelid defect is present. The cross lid flap uses the lower lid margin to correct defects of the upper lid.?However, such flaps are more complex to perform and require surgery in at least two stages. These alternatives and their advantages and disadvantages will be discussed in detail.
TECHNIQUES FOR CORRECTION OF MACROBLEPHARON
Macroblepharon can result in the presence of both entropion and ectropion in the same eye. Depending on the severity, several different approaches to therapy may be employed. In the lecture, we will consider selected cases that illustrate the different techniques ranging from simple canthal closure to rhomboid canthoplasty.

ALTERNATIVES FOR THE CORRECTION OF ECTROPION
Depending upon whether ectropion is primary and related to excessive lid length and/or lack of lid tone or secondary to scarring, different approaches to correction may be employed. For scarring, the Wharton-Jones (V to Y) blepharoplasty may be most preferred, but other cases are best treated by lid shortening and techniques to improve lid tone. These techniques and their indications will be illustrated as time allows.

ALTERNATIVES FOR THE CORRECTION OF ENTROPION
Correction of entropion is perhaps the most commonly taught lid surgery and is perhaps the simplest to perform. Shar Peis and breeds with heavy facial folds can present the clinician with challenging predicaments. We will discuss when simple lid tacking is indicated and when to apply more advanced techniques.

minibabyqq 2007-1-26 02:15

[color=Magenta][size=5][b]Glaucoma.Is 有效的治療 Glaucoma𦎾s Effective Treatment a Reality  [/b][/size][/color]


介紹
許多固有困難遇到在所有被馴化的種類在青光眼的管理範圍從困難在診斷對視網膜神經節細胞死亡的預防。臨床經驗單獨口授期望的粗劣的預測為視域, 但機制的最近了悟幾乎一定介入了ganglionopathy 清楚地表明充分neuroprotection 也許從未達到。不僅是可能的療法仍然臆想, 但什麼的早期的發生大概是neurodegeneration 的自已繁殖過程使有效的療法特別困難在我們對待的種類。我們現有的療法必須當前未達到標記和實用困難與相關對流出設施的評估, 療法準確監視和外科技術的複雜所有組合迷惑預測。它是邏輯的角度關閉青光眼可能由碳anhydrase 禁止有效地從未對待單獨, 借自己對這種治療方法的那些青光眼經常被診斷當神經節細胞死亡已經是視域廣泛和損失不可避免。忽略的因素在所有青光眼是視網膜神經節細胞的退化, 因而neuroprotection 通過有效的視覺低血壓症是我們運用任一種療法的根本要求。但是, 我們經常是太晚在設立那種療法和雖然我們也許包含伴生的痛苦和難受, neuroretinal 退化的過程當前裝於罐中不被扭轉亦不被停止。多數我們能達到通過眼內壓力的充分減少(IOP) 將減慢這個過程下來和保留視域長期。
什麼我們瞭解由期限glaucoma? 。它簡單地被定義了如同視覺組織破壞的過程由IOP 的被承受的海拔造成在它的正常生理極限之上。這是那的具體作用被舉起的壓力在回報青光眼緊急狀態視覺神經的複合零件。normal 緊張和low 緊張青光眼的存在在人弄髒了這個簡單的定義為這些診斷發現起源在視覺神經退化的臨床相似性看兩個與被舉起的IOP 和其他有關係非壓力相關的因素譬如圓盤局部缺血或視網膜excitotoxicity。 它可能與唯一作用甚而被爭論, 上升在IOP 被看見在主要open-angle 青光眼在人是作用而不是起因, 由當前的療法被估計和對待。幸運地, open-angle 青光眼限制了發生在被馴化的種類, 為了很少是我們診斷它早期的存在和因而禁止神經節細胞退化及早在過程中。有證據表明, 反常性在神經節細胞作用存在在小獵犬, 以被繼承的主要open-angle 青光眼在海拔在IOP 發生之前, 並且有強的誘惑使用這證據建議IOP 改變自己純淨地是一個次要特點到另一個, 不清楚, 疾病過程。
只在有可示範主要的那些青光眼或導致的瑕疵在含水流出通過iridocorneal 角度能我們說, 被舉起的壓力上升直接地負責對接著而來的神經節細胞死亡。即使如此, 這樣的知識不保證有效的治療控制。它保留難定義ciliary 和周邊先前synechiae 形成的程度由一先前uveitis 造成後部synechiae 形成對療法通常是有抵抗性。在透鏡luxation, 這是pupillary 塊由導致ciliary 裂縫和唯一早期的lensectomy 意志恢復充分含水流出的崩潰透鏡的先前運動達到。在主要角度關閉青光眼, 我們描述可能的先天素質和生理pupillary 塊作為可能的扣人心弦的因素在含水流出的深刻停止從先前分庭, 但這樣的考慮不排除其它原因論。再, 缺乏病因論細節使減血壓療法困難, 並且固有複雜化對外科技術通常被運用, 使預測不定。但是, 它是可能的, 我們看的所有青光眼歸結於生理地不相容的上升的維護在IOP, 並且這是那的特徵被舉起的IOP, 提示了咨詢, 是否他們是痛苦、episcleral 壅塞、角膜腫鼓、地球擴大, 或瑕疵視覺。根據臨床圖片, 我們簡單地記錄被舉起的IOP, 診斷青光眼, 和設置關於治療沿著傳統減血壓線, 以知識, 對IOP 的有效, 長期減少將接近最佳我們能達到。有充足的實驗性證據顯示出, 神經節細胞退化的過程, 是否這是壞死或apoptosis, 開始在上升的最初的少數小時之內在IOP, 並且一次觸發, 這個過程無法被停止。因而, 預測為視域必須總當前是窮的, 以任一種減血壓療法的減輕的影響易變地被表達從一名患者到另一個。
機制和類型青光眼
有幾個分類系統被使用描述青光眼在被馴化的種類和可觀的討論關於期限的妥帖被運用。Congenital. 口授存在出生時並且primary. 提到那裡也許是先天素質的被繼承的青光眼。有混亂在期限narrow 角度和closed 角度之間。兩個依照由gonioscopy 估計提到入口的寬度對ciliary 裂縫。在主要青光眼, 一個先天地變窄的角度也許預先處理對更加容易的關閉, 但有是困難在查明如果IOP 舉起在實際關閉之前。它是可能的, 兩個期限簡單地是同樣先天反常性的漸進性。因而, 兩個用語被使用, 並且他們的擁護者蒼勁地辯解他們的用法。值得注意的是, 期限goniodysgenesis 。共同地被使用得意味狹窄的角度或梳狀的韌帶發育異常或兩個。它的用途由我們的gonioscopic 觀察限制, 但實質上, 這個期限應該包括說謊在梳狀的韌帶之外的水平ciliary 裂縫的其它反常性。
青光眼可能使其它視覺疾病過程複雜化譬如uveitis, 透鏡luxation, 瘤形成並且大瀑布和這裡期限次要被使用。治療要求創始的疾病和注意的兩個決議對導致上升在壓力的變動的。
發病原理
在我們的患者, 所有青光眼為被舉起的IOP 描繪, 雖然海拔的水平也許變化。在海拔最初地是低的那些青光眼(即, 開放角度青光眼, melanocytic 青光眼) 並且一些次要青光眼, 視網膜神經節細胞和視覺神經損傷是慢的進步。在角度關閉青光眼突然的高上升在IOP 經常回報眼睛窗簾, 無容置疑地主要由於axoplasmic 流程的停止在lamina cribrosa 的水平。
視網膜神經節細胞退化也許是壞死, 但可能性這是apoptosis 由上升觸發在IOP 是振振有詞, 和硝酸氧化物和穀氨酸的各自角色是值得的討論。以下觀察是當前的青光眼辯論的一部分根據發病原理和可能的療法。
局部缺血
在人的研究中, 它廣泛被接受, 組織局部缺血有一個零件演奏在發生在青光眼視覺圓盤損傷的_蒙或進步。血流的自動調節在圓盤之內是一個根本機制在營養維護並且海拔在IOP 可能干涉自動調節。
硝酸氧化物
假說, 硝酸氧化物(沒有) 被介入在視網膜神經節細胞軸突的退化是最吸引人的為幾個原因。一些硝酸氧化物synthase isoforms 的明顯的章程和歸納(第) 在astrocytes 在視覺神經頭之內當有IOP 的海拔清楚地被展示了並且有清楚的證據沒有毒力對軸突。沒有和endothelin 看上去並且被介入在IOP 的章程和在視覺血流的模塊化, 沒有被介入在apoptosis 。
穀氨酸
穀氨酸水平被舉起在玻璃大主教, 犬, 並且兔子青光眼患者和視網膜神經節細胞層數是非常易受穀氨酸毒力。Excitotoxicity 可能導致神經細胞的apoptosis; excitotoxicity 的斡旋是由N 甲醇D aspartate (NMDA) 類型的刺激穀氨酸感受器官。NMDA 感受器官的overstimulation 無法導致增加了水平和複合體和潛在地惡性循環。NMDA 導致的excitotoxicity 的預防代表一個潛在的機制為neuroprotection 。
Apoptosis
可能性, 被編程的細胞死亡可能由axoplasmic 流程的壓力導致的失敗觸發長期被假設了, 和簡單地根據營業因素的疏忽到達神經節細胞身體。但是, 有借自己對它可能的考慮在青光眼, 包括角色和穀氨酸導致的excitotoxicity 的其它方面對apoptosis 。
治療...
成功總要求對有效的療法的用途和雖然幾原因論被介入在青光眼複合體, absolute 定列式在療法選擇是相當數量主要並且/或者導致的變動在iridocorneal 角度之內。被舉起的IOP 的醫療鎮壓可能試圖使用四類型藥物: 含水形成遏抑器; miotics; uveoscleral 流出enchancers; 並且hyperosmotic 代理。所有四共同地被使用在似犬青光眼的治療, 第一三當緊急治療和在長期控制當hyperosmotic 代理是無價的作為緊急狀態和preoperative 治療。藥物, neuroprotection 代理第五個類別, 開始湧現作為重要可能的加法對醫療療法。
A. 含水形成遏抑器
碳anhydrase 抗化劑傳統上被使用在狗和以困難在貓。對beta-adrenergic 阻攔的代理的供選擇的用途仍然被評估為兩個種類。
i) 碳anhydrase 抗化劑
Acetazolamide (Diamox; Lederle) 。50 的口頭藥量率到75 毫克每公斤應該被使用並且劑量應該是二到三次每日。視覺副作用不看, 但是深刻過量用藥或長期療法也許導致新陳代謝的酸中毒, 由不適、vomition 和腹瀉最初地通常表明。
Dichlorphenamide (Daranide; 默克、Sharpe 和Dohme) 提供了一個有用的選擇對acetazolamide 因為它由較少新陳代謝的酸中毒伴隨。10 的藥量率到12 毫克每公斤每日更喜歡二或三次為狗。鉀取盡由具體療程防止由補充鉀濃食物或。百分之二dorzolamide HCl (Trusopt; 默克) 一典型碳anhydrase 抗化劑和brinzolamide (Azopt-Alcon) 會看來是作為有效和是較不惱人。
(ii) Beta-adrenergic 阻攔的代理。 Timolol maleate (Timoptol; 默克・Sharpe 和Dohme) 。用法在小動物患者不被表明因為商業準備的低集中使它無效在狗和貓。百分之四的集中加上由任一看得出的程度必需減少正常犬IOP 。其它這樣代理被使用在人是betaxolol HCl, carteolol HCl, levobunolol HCl 和metipranolol 。timolol 和dorzolamide 的組合被銷售作為Cosopt (默克, 銳利和Dohme), 但經驗在狗並且貓是有限的。
(iii) Alpha2.adrenoreceptor 苦悶者。 二種這樣藥物是現在可以得到的。Apraclonidine (Iopidine) 窮地減少含水分泌物在狗但brimonidine 酒石酸(Alphagan 裡; Allergan) 似乎是更多effective.(30) 它導致較不過敏反應, 大概增加uveoscleral 流出和是還neuroprotective 。這種藥物能證明有價值可觀的對獸醫但長期效力研究必需估計它潛在的用途在狗和貓。
B. Miotics
Miotic 藥物是或者parasympathomimetics, 生產直接刺激(糞膽鹼) iridal 肌組織(即, carbachol 和pilocarpine), 或膽鹼酯抑制劑抗化劑間接地生產miosis 由acetylcholine 活動(即demacarium 溴化物的) potentiation 。Pilocarpine 是或許miotic 經常被使用在似犬青光眼的治療。它應該記住雖然潛力增加流出設施存在, 患者一定保留了某一trabecular meshwork 作用。有害地, pilocarpine 可能蜇並且它可能對iritis 恢復活動和貢獻。Demacarium 溴化物有價值特殊在維護長期miosis 在後部主要透鏡luxation 的管理, 但它的商業生產現在停止了。 Latanoprost (Xalatan.Pharmacia 和Upjohn)也許證明有價值相似的, 雖然這個前列腺素F2 類似物主要使用改進uveoscleral 流出。它並且生產長期行動的miosis 並且在沒有一種長的代理miotic 準備時, 它的用途在狗與後部主要透鏡luxation 能證明無價。
C. Uveoscleral Outflow 改進物
Latanoprost 增加流出的率由uveoscleral 路線。它是有效的反對是存在在細胞外矩陣的peptides, 使肌肉更加多孔。Brimonidine 酒石酸並且增加uveoscleral 流出但機制為這活動未被定義。
D. Hyperosmotic Agents
對IOP 的減少可能由增加有效地和迅速地導致血漿的osmolality 在ciliary 循環之內導致一個滲透壓梯度橫跨blood/aqueous 障礙在ciliary 皮膜之內。Hyperosmotic 代理有價值當緊急療法。他們的用途preoperatively 是根本附屬對青光眼手術, 為了外科paracentesis 作用是較不重大的當IOP 是降低, 並且對被充塞的地球的總血液容量的總值減少很大地促進手術的施行。甘露醇、丙三醇和尿素定期地被使用, 所有三是有效的在1.0 到1.5 g 每公斤體重。
Neuroprotection 和Neuroregeneration
IOP 的海拔無容置疑地是最重大的觸發器因素為glaucomatous 視覺神經病並且降下IOP 對一個正常或低質水平是根本因素在治療。但是, 第和穀氨酸成水平的觀察被舉起在他們被介入在視網膜神經節細胞壞死或apoptosis 提高了neuroprotective 療法和甚而neuroregeneration 的可能性的青光眼和。因而第抗化劑、扣人心弦的氨基酸反對者、穀氨酸感受器官反對者、apoptosis 抗化劑和鈣渠道預鍛模全部潛在地被介入在未來青光眼療法的發展。鈣渠道預鍛模也許使被削弱的microcirculation 降低的作用到視覺神經頭潛在地增長的流出設施在trabecular 細胞的水平。
外科療法
達到IOP 的充分減少困難對似犬青光眼通過醫療手段現在可以得到提示了對幾個外科技術的用途在這個種類。對含水生產的減少可能由cyclodestruction 達到運用cryosurgery 、熱或laser 。相當數量ciliary 身體損傷必須是充足保證, 平衡被收復在總值被削弱的含水生產並且任何含水排水設備之間是可能的。再開閉合的ciliary 裂縫由cyclodialysis 介入劃分倒塌的裂縫組織和synechiae 分離ciliary 身體從部下的sclera, 允許先前分庭變得匯合以suprachoroidal 空間。某一疏忽控制青光眼歸結於裂縫的隨後關閉由手術後黏附力的迅速形成。
在狗, 倒塌的ciliary 裂縫的外科旁路由一個corneoscleral (limbal) 環鋸手術技術最容易地達到或由iridencleisis 或與周邊iridectomy 被結合。這些技術准許含水通過直接地從先前分庭對它由血管和淋巴元素吸收當前的subconjunctival 組織。兩個也許最初地但短期證明成功, 纖維蛋白也許遮沒sclerostomy 創傷並且長期控制也許由sclerostomy 和subconjunctival 組織纖維變性denied 。
分流器(或gonioimplant)手術為IOP 控制提供一種現實方法為它抵制subconjunctival 纖維變性的作用在某種程度上。幾類型分流器存在: 那些有或沒有閥門。令人滿意的結果也許被獲得使用一根單件silastic 排水設備植入管包括一支先前分庭管和一條附上大表面皮帶。分流器准許含水被牽制免受先前分庭對顯現出在皮帶附近的大subconjunctival 傷痕sac 。這個技術的進一步修改造成更小的gonioimplants 和更加簡單的手術將是可能的使用成纖維細胞抗化劑藥物。簡單sclerostomy 也許在將來是非常是必要提供耐心有效的長期IOP 控制。


Introduction
The many inherent difficulties encountered in all domesticated species in the management of glaucoma range from difficulty in diagnosis to the prevention of retinal ganglion cell death. Clinical experience alone dictates the expected poor prognosis for sight, but recent awareness of the mechanisms almost certainly involved the ganglionopathy clearly indicates that adequate neuroprotection might never be achieved. Not only are possible therapies still conjecture, but the early occurrence of what is probably a self-propagating process of neurodegeneration renders effective therapy particularly difficult in the species we treat. Currently our existing therapies must fall short of the mark and the practical difficulties associated with the assessment of outflow facility, the accurate monitoring of therapy and the complexity of surgical techniques all combine to confound the prognosis. Whilst it is logical that angle-closure-glaucomas can never be treated effectively by carbonic anhydrase inhibition alone, those glaucomas which do lend themselves to this kind of therapeutic approach are often diagnosed when ganglion cell death is already extensive and loss of sight inevitable. The overriding factor in all glaucoma is the degeneration of the retinal ganglion cell, thus neuroprotection through effective ocular hypotension is the essential requirement of any therapy we utilise. However, we are often too late in instituting that therapy and although we may contain associated pain and discomfort, the process of neuroretinal degeneration currently can neither be reversed nor stopped. The most we can achieve through the adequate reduction of intraocular pressure (IOP) is to slow this process down and retain sight for longer periods.
What do we understand by the term 孄laucoma??It has been simply defined as the process of ocular tissue destruction caused by a sustained elevation of the IOP above its normal physiological limits. It is the specific effect of that elevated pressure upon the composite parts of the optic nerve that renders glaucoma an emergency. The existence of 忛ormal tension?and 𢡠ow tension?glaucomas in man has blurred this simple definition for these diagnoses find origin in the clinical similarities of the optic nerve degeneration seen both in association with elevated IOP and other non-pressure related factors such as disc ischaemia or retinal excitotoxicity. It can even be argued that the rise in IOP seen in primary open-angle glaucoma in man is effect rather than cause, with only the effect being assessed and treated by current therapies. Fortunately, open-angle glaucoma has limited incidence in the domesticated species, for seldom are we in a position to diagnose its early presence and thus inhibit ganglion cell degeneration early in the process. There is evidence to indicate that abnormality in ganglion cell function exists in Beagles, with inherited primary open-angle glaucoma before the elevation in IOP occurs, and there is strong temptation to use this evidence to suggest that the IOP changes themselves are purely a secondary feature to another, as yet ill-defined, disease process.
Only in those glaucomas in which there is demonstrable primary or induced defect in aqueous outflow through the iridocorneal angle can we say that the elevated pressure rise is directly responsible for the ensuing ganglion cell death. Even so, such knowledge does not ensure effective therapeutic control. It remains difficult to define the extent of the ciliary and peripheral anterior synechiae formation caused by an anterior uveitis whilst posterior synechiae formation is usually resistant to therapy. In lens luxation, it is the pupillary block achieved by the anterior movement of the lens that causes the collapse of the ciliary cleft and only early lensectomy will restore adequate aqueous outflow. In primary angle-closure glaucoma, we describe possible congenital predisposition and physiological pupillary block as the probable exciting factors in the acute cessation of aqueous outflow from the anterior chamber, but such consideration does not exclude other >><<and inherent complications to the surgical techniques usually utilized, render prognosis uncertain. However, it is likely that all the glaucomas we see are due to maintenance of a physiologically incompatible rise in IOP, and it is the characteristics of that elevated IOP, which have prompted the consultation, whether they be pain, episcleral congestion, corneal oedema, globe enlargement, or defective vision. Based on the clinical picture, we simply record the elevated IOP, diagnose glaucoma, and set about treatment along the traditional hypotensive lines, with the knowledge that effective, long-term reduction in the IOP will approach the best we can achieve. There is sufficient experimental evidence to demonstrate that the process of ganglion cell degeneration, whether it be necrosis or apoptosis, starts within the first few hours of the rise in IOP, and that once triggered, this process cannot be stopped. Thus, currently the prognosis for sight must always be poor, with the moderating influence of any hypotensive therapy being variably expressed from one patient to another.
MECHANISMS AND TYPES OF GLAUCOMA
There are several classification systems used to describe glaucoma in the domesticated species and considerable discussion concerning the appropriateness of the terms utilised. 鏠ongenital?dictates a presence at birth and 𢖯rimary?refers to inherited glaucoma to which there may be congenital predisposition. There is confusion between the terms 忛arrow angle?and 𡤧losed-angle.?Both refer to the width of the entrance to the ciliary cleft as assessed by gonioscopy. In primary glaucoma, a congenitally narrowed angle may predispose to easier closure, but there has been difficulty in ascertaining if IOP elevates prior to actual closure. It is likely that both terms are simply gradations of the same congenital abnormality. Thus, both terms are used, and their proponents vigorously justify their usage. It should be noted that the term 孄oniodysgenesis?is used commonly to mean narrow angle or pectinate ligament dysplasia or both. Its use is limited by our gonioscopic observations, but in essence, this term should cover other abnormalities of the ciliary cleft which lie beyond the level of the pectinate ligament.
Glaucoma can complicate other ocular disease processes such as uveitis, lens luxation, neoplasia and cataract and here the term secondary is used. Treatment demands both resolution of the initiating disease and attention to the changes that induce the rise in pressure.
PATHOGENESIS
In our patients, all glaucomas are characterised by an elevated IOP, although the level of elevation may vary. In those glaucomas in which the elevation is initially low (i.e., open angle glaucoma, melanocytic glaucoma) and some secondary glaucoma, retinal ganglion cell and optic nerve damage are slow to progress. In angle- closure glaucoma the sudden high rise in IOP often renders the eye blind, undoubtedly primarily due to a cessation of axoplasmic flow at the level of the lamina cribrosa.
Retinal ganglion cell degeneration may be necrosis, but the possibility that it is apoptosis triggered by the rise in IOP is plausible, and the respective roles of nitric oxide and glutamate are worthy of discussion. The following observations are part of the current glaucoma debate in terms of pathogenesis and possible therapy.
Ischaemia
In human studies, it has been widely accepted that tissue ischaemia has a part to play in the initiation or progression of the optic disc damage that occurs in glaucoma. The autoregulation of blood flow within the disc is an essential mechanism in the maintenance of nutrition and an elevation in IOP can interfere with autoregulation.
Nitric Oxide
The hypothesis that nitric oxide (NO) is involved in the degeneration of retinal ganglion cell axons is most appealing for several reasons. The apparent up-regulation and induction of some nitric oxide synthase isoforms (NOS) in astrocytes within the optic nerve head when there is an elevation of IOP has been clearly demonstrated and there is clear evidence of NO toxicity to the axons. NO and endothelin appear to be involved in the regulation of IOP and in the modulation of ocular blood flow, with NO also being involved in apoptosis.
Glutamate
Glutamate levels are elevated in the vitreous of primate, canine, and rabbit glaucoma patients and the retinal ganglion cell layer is very susceptible to glutamate toxicity. Excitotoxicity can result in neuronal apoptosis; the mediation of excitotoxicity is by the stimulation of the N-methyl-D aspartate (NMDA) type of glutamate receptor. The overstimulation of the NMDA receptors can lead to increased NO levels and a complex and potentially vicious circle. Prevention of NMDA-induced excitotoxicity represents a potential mechanism for neuroprotection.

minibabyqq 2007-1-26 02:16

[color=Magenta][size=5][b]切片檢查法原則和外科腫瘤學Overview of Biopsy Principles and Surgical Oncology  [/b][/size][/color]


最重要的步的當中一個在癌症患者的管理是一個準確切片檢查法標本的獲得和解釋。切片檢查法不僅將提供一個診斷而且它將幫助預言生物行為, 援助在確定類型和程度治療應該買得起。
共同目標以任一個切片檢查法技術是獲得足夠的造形術組織建立一個準確診斷。哪個做法使用將由您的目標經常確定為大量的事例、站點, 設備可利用, 患者的一般狀態, 和個人特選和經驗。一個準確組織診斷應該被獲得 在 治療之前為以下二個原因:
如果治療方式(手術對輻射對化療, 等。) 或程度治療(保守對進取的切除術) 由知道會修改腫瘤類型。切片檢查法特別重要如果手術是在一個困難的地點(即, 末端肢、尾巴、或頭和脖子) 為重建或如果提出的做法運載重大病態(即, maxillectomy 或截肢術) 。
如果所有者自願對待他們的寵物由腫瘤類型知識會修改和因此, 預測, 切片檢查法是中意的在主要治療干預之前。
總指導路線為組織獲得和定像
1 。 incisional 或針切片檢查法的適當的表現 不增加轉移的率。另一方面, 癌細胞也許允許沾染組織圍攏大量, 使切除術更加困難。切片檢查法站點應該計劃以便它能隨後被去除與整個大量一起。
2 。 避免包含只潰瘍或被激起的組織的切片檢查法。
3 。 幾個樣品從一大量比一個唯一樣品是可能產生一個準確診斷。
4 。 小切片檢查法不應該被獲得與electrocautery, 因為它傾向於扭屈(由自溶或極化) 多孔的建築學。
5 。 如果切除邊際的評估渴望, 這是最佳如果外科醫生標記標本(美好的縫合或墨水在可疑的邊緣) 或遞交邊際在一個分開的容器。
6 。 組織一般被固定在10% 緩衝的中性甲醛水裡與一份組織對十份固定。
7 。 組織比1 厘米或它不深深地將固定不應該厚實的。大大量可能被削減成適當的大小的片斷和代表部分遞交或被切像一個麵包, 留下一個邊緣原封, 允許定像。在定像以後(二到三天), 組織可能被郵寄以組織1:1 比與甲醛水。
8 。 詳細的 歷史應該伴隨所有切片檢查法請求!
切片檢查法方法
組織獲得通常半新方法是針拳打切片檢查法、incisional 切片檢查法, 和excisional 切片檢查法。所有有徵兆根據一定數量的可變物譬如腫瘤大小、潰瘍地點、敵意出現, 和可能。
結果的解釋
pathologist.s 工作將確定: 。1) 腫瘤對沒有腫瘤, 2) 良性對惡性, 3) histologic 型、4) 等級(如果可利用和臨床相關), 和5) 邊際(如果excisional) 。。許多陷阱可能發生使最終結果不精確。潛在的錯誤可能發生在任一個診斷的水平並且它是由臨床工作者決定負責案件解釋切片檢查法結果的充分的意思。一樣高像10% 切片檢查法結果不精確的在臨床重大感覺。如果切片檢查法結果不關聯以臨床情節, 幾個選擇是可能的:
1 。 告訴病理學家和表達您的對切片檢查法結果的關心。這資訊交換應該是有用的為兩個黨和不被視為作為冒犯對pathologist.s 當局或專門技術。它也許導致:
a 。   Re 區分可利用的組織或石蠟塊。
b 。   特別汙點為某些可能的腫瘤類型(即, 對甲苯胺藍色為帆柱細胞) 。
c 。   第二個觀點由其它病理學家。
2 。 如果腫瘤是存在在患者, 和特別, 如果廣泛變化的選擇為療法存在, 第二個(或第三) 切片檢查法應該執行。
一個仔細地執行的, 遞交的, 和被解釋的切片檢查法也許是最重要的步在管理和病人的隨後預測有癌症。所有腫瘤太經常不遞交為histologic 評估在撤除以後因為the 所有者沒有想支付它... 切片檢查法不應該是一個選舉所有者決定。由於增加medicolegal 關心, 這不是醫療求知慾單獨腫瘤類型那命令知識。
外科腫瘤學
大多數堅實腫瘤在動物中將被對待以手術。手術可能使用防止癌症(即, ovariohysterectomy 在幼小狗防止乳房癌症的最新發展), 診斷癌症(切片檢查法), 提供緩和(壞死的口頭腫瘤撤除在一條狗以轉移), debulk 腫瘤提高對輻射或化療的反應, 或手術可能被使用以治病的意向。
像輻射和化療, 手術可能由藥量執行。常用的藥量是intralesional (轟擊在脂肪瘤之外), 少量(在pseudocapsule, 經常留下微觀殘餘的疾病), 寬的(超出1 cm 邊際), 和基礎(整個隔間, 即, 截肢術) 。。腫瘤站點、腫瘤等級、腫瘤階段, 和種類影響確定需要的外科藥量。如果治病的專心手術做了, 它是必要適當地遞交整個標本(被修理和被著墨) 為對等級的撤除(邊際) 評估和充足。。殘缺不全的邊際要求直接re 干預與第二手術、輻射, 或化療而不是等不可避免的地方再現和可能的轉移。進取的外科切除術譬如mandibulectomy, maxillectomy, orbitectomy, 鼻planum 切除術, 截肢術, 肢體饒恕, 肋骨撤除, 和hemipelvectomy 一般被容忍很好以可接受的化妝用品和功能結果。對痛覺缺失的適當的關注, 麻醉, 和手術後支持對一個成果是重要的。


One of the most important steps in the management of the cancer patient is the procurement and interpretation of an accurate biopsy specimen.?Not only will the biopsy provide a diagnosis but also it will help predict biologic behavior, which aids in determining the type and extent of treatment that should be afforded.
The common goal with any biopsy technique is to procure enough neoplastic tissue to establish an accurate diagnosis.?Which procedure to use will often be determined by your goals for the case, site of the mass, equipment available, general status of the patient, and personal preference and experience.?An accurate tissue diagnosis should be attained before treatment for the following two reasons:
If the type of treatment (surgery vs. radiation vs. chemotherapy, etc.) or the extent of treatment (conservative vs. aggressive resection) would be altered by knowing the tumor type.?A biopsy is particularly important if the surgery is in a difficult location (e.g., distal extremity, tail, or head and neck) for reconstruction or if the proposed procedure carries significant morbidity (e.g., maxillectomy or amputation).
If the owners?willingness to treat their pet would be altered by knowledge of tumor type and therefore, prognosis, a biopsy is desirable before major therapeutic intervention.
General Guidelines for Tissue Procurement and Fixation
1. The proper performance of an incisional or needle biopsy does not increase the rate of metastasis.?On the other hand, cancer cells may be allowed to contaminate the tissues surrounding the mass, making resection more difficult.?The biopsy site should be planned so that it may be subsequently removed along with the entire mass.
2. Avoid biopsies that contain only ulcerated or inflamed tissues.
3. Several samples from one mass are more likely to yield an accurate diagnosis than a single sample.
4. Small biopsies should not be obtained with electrocautery, as it tends to deform (by autolysis or polarization) the cellular architecture.
5. If evaluation of margins of excision is desired, it is best if the surgeon marks the specimen (fine suture or ink on questionable edges) or submits margins in a separate container.
6. Tissue is generally fixed in 10% buffered neutral formalin with one part tissue to ten parts fixative.
7. Tissue should not be thicker than 1 centimeter or it will not fix deeply. Large masses can be cut into appropriate sized pieces and representative sections submitted or sliced like a loaf of bread, leaving one edge intact, to allow fixation.?After fixation (two to three days), tissue can be mailed with a 1:1 ratio of tissue to formalin.
8. A detailed history should accompany all biopsy requests!
Biopsy Methods
The more commonly used methods of tissue procurement are needle punch biopsy, incisional biopsy, and excisional biopsy.?All have indications depending on a number of variables such as tumor size, location, presence of ulceration, and likelihood of malignancy.
Interpretation of Results
The pathologist𠏋 job is to determine:?1) tumor vs. no tumor, 2) benign vs. malignant, 3) histologic type, 4) grade (if available and clinically relevant), and 5) margins (if excisional).?Many pitfalls can take place to render the end result inaccurate.?Potential errors can take place at any level of diagnosis and it is up to the clinician in charge of the case to interpret the full meaning of the biopsy result. As high as 10% of biopsy results are inaccurate in a clinically significant sense.?If the biopsy result does not correlate with the clinical scenario, several options are possible:
1. Call the pathologist and express your concern over the biopsy result.?This exchange of information should be helpful for both parties and not looked upon as an affront to the pathologist𠏋 authority or expertise.?It may lead to:
a.   Re-sectioning of available tissue or paraffin blocks.
b.   Special stains for certain possible tumor types (e.g., toluidine blue for mast cells).
c.   A second opinion by another pathologist.
2. If the tumor is still present in the patient, and particularly, if widely varied options exist for therapy, a second (or third) biopsy should be performed.
A carefully performed, submitted, and interpreted biopsy may be the most important step in management and subsequent prognosis of the patient with cancer.?All too often tumors are not submitted for histologic evaluation after removal because 懀he owner did not want to pay for it.? Biopsies should not be an elective owner decision.?Because of increasing medicolegal concerns, it is not medical curiosity alone that mandates knowledge of tumor type.
Surgical Oncology
The vast majority of solid tumors in animals will be treated with surgery.?Surgery can be used to prevent cancer (e.g., ovariohysterectomy in young dogs prevents later development of mammary cancer), diagnose cancer (biopsy), provide palliation (removal of necrotic oral tumor in a dog with metastasis), debulk a tumor to enhance response to radiation or chemotherapy, or surgery can be used with curative intent.
Just like radiation and chemotherapy, surgery can be administered by dose.?The commonly used doses are intralesional (shelling out a lipoma), marginal (on the pseudocapsule, often leaves microscopic residual disease), wide (in excess of 1 cm margins), and radical (entire compartment, e.g., amputation).?Tumor site, tumor grade, tumor stage, and species affected determine the needed surgical dose.?If curative intent surgery has been performed, it is imperative to properly submit the entire specimen (fixed and inked) for assessment of grade and adequacy of removal (margins).?Incomplete margins require immediate re-intervention with a second surgery, radiation, or chemotherapy rather than waiting for the inevitable local recurrence and possible metastasis.?Aggressive surgical resection such as mandibulectomy, maxillectomy, orbitectomy, nasal planum resection, amputation, limb sparing, rib removal, and hemipelvectomy are generally tolerated well with acceptable cosmetic and functional outcomes.?Proper attention to analgesia, anesthesia, and postoperative support are vital to a successful outcome.

minibabyqq 2007-1-26 02:16

[color=Magenta][size=5][b]放射治療 When is Radiation Therapy Really Indicated  [/b][/size][/color]


放射治療技術
可觀的知識被獲取了在過去10 年關於最佳的方式執行放射治療。指南為總藥量、藥量的大小每分數, 和整體時間現在被開發。在更加早期的天獸醫放射治療, 它是普遍給相對地大分數(4.5 Gy) 三天每星期, 為一共計10 個分數(45 Gy 總藥量) 。我們現在知道這總藥量是太降低, 並且分數大小太大。它並且知道, 治療時間的延長是不利的並且每日分數的管理現在是普遍的。
大分數大小預先處理對嚴肅的複雜化在慢慢地激增正常組織, 譬如脊髓或心臟。這些複雜化是生活威脅和限制也許規定輻射的藥量。由使用更小的藥量每分數, 這些複雜化的可能性在慢慢地激增組織可能避免。對更小的分數大小的用途需要整體時刻的延長規定充足地大總藥量。這將增加重音在動物所有者和治療費用但捷徑在這個基本的事實附近不是現實的。
增加強度藥量管理由給小分數, 但每天, 也許增加複雜化頻率在迅速地激增組織, 譬如皮膚。不幸地, 腫瘤表現像一個迅速地激增組織並且它一般不是可能可能給輻射藥量控制腫瘤和沒有一些可示範的變化在激增正常組織上。幸運地, 雖然臨時地discomforting, 這些反應在迅速地激增組織癒合和一般不限制也許規定對患者輻射的藥量。
治療時間的延長允許腫瘤擴散在治療期間。這擴散增加的腫瘤clonogens 的數量必須由輻射消炎。為擴散的生物依據在被延長的治療計劃期間是損傷的對腫瘤的輻射反應是無可爭辯的並且多餘的治療的空白在治療或延長應該被避免。
典型的明確的放射治療協議在獸醫方面介入3.0 Gy 分數的每日管理為總藥量57-60 Gy 。
政策制定
當你考慮治療選擇為腫瘤, 典型地只一種形式被選擇。經常這是一個壞決定, 使永久地方控制腫瘤不可能。第一療法被執行應該是優選的療法, 並且這也許需要形式的組合。清楚地, 組合療法比一種唯一療法最初地昂貴的, 但在對待週期性腫瘤, 可觀的另外的費用將被招致。另外, 週期性腫瘤是加工困難的對永久地方控制並且最佳的機會為治療腫瘤是優選的療法的管理第一次腫瘤被對待。
應該被考慮的腫瘤因素當選擇最初的療法是: 1) 地點; 2) 容量; 3) 等級; 並且4) histologic 型。許多個體安置最大的數額意義在histologic 型, 但其它三個因素經常充當在確定反應的一個更大的角色對療法。
何時使用任一種唯一形式, 殺害少於10% 腫瘤細胞導致腫瘤可看見更小的一個部份反應, 但仍然總明顯。殺害99% 細胞典型地導致沒有腫瘤的總證據的一個完全反應。但是, 這相當數量細胞殺害是離治療很遠的地方。假設, 腫瘤包含1010 個 細胞(不是一個不合情理的假定) 。如果你殺害99% 1010 個 細胞, 有108 個 (100,000,000 個) 細胞餘留。清楚地, 這個腫瘤復發。一個完全反應暫時平息臨床工作者入認為, 一種有效的療法被執行了。堅實腫瘤療法應該是瞄準的永久地方控制, 不簡單地獲得一個完全反應。這要求細胞殺害10 到12 日誌, 不僅二或三。
放射治療效力單獨
少量宏觀腫瘤可能非常被控制以放射治療單獨。一些例子是: 1) acanthomatous epulides; 2) 齒齦癌(似犬); 3) 小成績II 帆柱細胞腫瘤; 並且4) transmissible 性愛tumors.(4,5,9,10) 這張小名單是腫瘤容量的結果是最大的因素貢獻對放射治療的失敗對控制腫瘤。增加腫瘤容量的惡劣效果發生在驚奇小腫瘤volumes.(5) 因而, 為完全外科切除不是可能的總腫瘤, 療法的組合應該被考慮作為最重要的療法而不是嘗試一較不進取, 和無效, 治療。
手術和放射治療
手術和放射治療的組合是最有效的癌症治療選擇的當中一個可利用對獸醫。對這個組合的優選的用途要求周道的預先計劃和通信在所有包含的黨之中並且緊持對好外科oncologic 原則。手術可能是半新或者在放射治療, 和那裡是徵兆為各個序列前後。這不會被談論在這兒, 但是更多資訊是available.(7)
由手術和輻射的明智的組合, 各種各樣的堅實腫瘤永久地方控制也許達到。這些有: 1) 等級I 和II 帆柱細胞腫瘤; 2) 似犬和似貓的軟的組織肉瘤; 並且3) 混雜軟的組織腫瘤譬如甲狀腺, perianal 腫瘤、耳道tumors.(3,6) 手術的組合和輻射也許並且是有利的為似犬鼻腫瘤, 但可能性為永久地方控制不是高的。
化療和放射治療
化療和放射治療的組合在放射治療清楚地是優越單獨為一些人的腫瘤。臨床試驗提供這項原則在獸醫方面未執行。然而, 在理論上這也許是有用的在一些患者。問題與不確定性預定關係二個代理、可能的化療藥量減少, 和意想不到的毒力。
一些化學療法的代理是實際radiosensitizers, 但實際上, 你應該期待唯一疊加性互作用 in-vivo 。 以疊加性, 增加的反應是合理的期望如果化療殺害由輻射不會殺害的細胞。被使用與輻射的組合在獸醫方面的代理包括cisplatin 、carboplatin, 和doxorubicin 。
化療增加了來手術和放射治療的組合在似犬鼻腫瘤、似貓的疫苗聯繫的肉瘤, 和高等級似犬軟的組織肉瘤的治療。結果提供這些組合優勢不是可利用的。
化療與輻射的組合並且被使用在似犬黑瘤。似犬黑瘤細胞為大容量描繪積累和修理非殺生輻射損傷。因而, 由於他們的大修理容量, 相似與慢慢地激增正常組織如上所述, 有是試驗使用輻射大分數藥量, 有時與化療的組合。這些試驗證明, 主要腫瘤的完全反應是可能的在許多patients.(1,2) 轉移遺骸的每嚴重的問題。
緩和放射治療
經常, 患者有機會為明確的控制是非常降低不管形式或形式被使用的腫瘤。許多這些患者能受益於緩和放射治療。緩和放射治療意向是discomforting 臨床標誌的緩解與相關腫瘤, 不是延長生存。這意向必須表明完全對寵物所有者。緩和輻照區域介入少量分數(典型地1.5 的) 管理以更大的藥量每分數(4.8 Gy) 比被使用在明確的輻照區域。緩和輻照區域被使用了為骨頭的治療並且軟的組織腫瘤以一些成功和在osteosarcoma, 因素與相關久寬恕時間被辨認了(8) 。這些包括骨頭的介入的長度和程度腫瘤病勢漸退。
總結
交付的輻射的技術方面知識治療地, 和腫瘤的輻射與組織, 和行為的互作用的生物方面, 可觀地增加了在過去10 年。任一種唯一形式的局限很好被瞭解。有也許被控制以放射治療的一些腫瘤, 但許多最好被對待以形式的組合。它重要, 第一療法執行了是absolute 最佳的療法。輻射有在標誌的緩和的一個角色與相關先進的骨頭和軟的組織腫瘤。

Radiation Therapy Technique
Considerable knowledge has been gained in the past 10 years about the best way to administer radiation therapy. Guidelines for total dose, the size of dose per fraction, and overall time are now developed. In earlier days of veterinary radiation therapy, it was commonplace to give relatively large fractions (4.5 Gy) three days per week, for a total of 10 fractions (45 Gy total dose). We now know this total dose is too low, and the fraction size is too big. It is also known that prolongation of treatment time is disadvantageous and administration of daily fractions is now commonplace.
Large fraction sizes predispose to serious complications in slowly proliferating normal tissues, such as spinal cord or heart. These complications are life threatening and limit the dose of radiation that may be administered. By using smaller doses per fraction, the probability of these complications in slowly proliferating tissues can be avoided. Use of smaller fraction sizes necessitates prolongation of overall time to administer a sufficiently large total dose. This will increase stress on animal owners and the expense of treatment but shortcuts around this basic fact are not realistic.
Increasing the intensity of dose administration by giving small fractions, but on a daily basis, may increase the frequency of complications in rapidly prolifer>><<sue and it is not generally possible to give a dose of radiation likely to control the tumor and not have some demonstrable change in proliferating normal tissue. Fortunately, although temporarily discomforting, these reactions in rapidly proliferating tissues heal and do not generally limit the dose of radiation that may be administered to the patient.
Prolongation of treatment time allows tumor proliferation during treatment. This proliferation increases the number of tumor clonogens that must be sterilized by the radiation. The biologic basis for proliferation during protracted treatment schemes being detrimental to radiation response of the tumor is indisputable and unnecessary gaps in treatment or prolongation of treatment should be avoided.
Typical definitive radiation therapy protocols in veterinary medicine involve daily administration of 3.0 Gy fractions for a total dose of 57-60 Gy.
Decision Making
When one considers therapeutic options for a tumor, typically only one modality is chosen. Often this is a bad decision, making permanent local control of the tumor impossible. The first therapy administered should be the optimal therapy, and this may entail combinations of modalities. Clearly, combination therapy will initially be more expensive than one single therapy, but in treating recurrent tumors, considerable additional expense will be incurred. Additionally, recurrent tumors are more refractory to permanent local control and the best chance for curing the tumor is administration of the optimal therapy the first time the tumor is treated.
The tumor factors that should be considered when selecting the initial therapy are: 1) location; 2) volume; 3) grade; and 4) histologic type. Many individuals place the greatest amount of significance on histologic type, but the other three factors often play a bigger role in determining response to therapy.
When using any single modality, killing less than 10% of the tumor cells will result in a partial response where the tumor will be visibly smaller, but still grossly apparent. Killing 99% of the cells will typically result in a complete response where there is no gross evidence of the tumor. However, this amount of cell killing is far from a cure. Assume that a tumor contains 1010 cells (not an unreasonable assumption). If one kills 99% of 1010 cells, there are 108 (100,000,000) cells remaining. Clearly, this tumor is going to recur. A complete response lulls the clinician into thinking that an effective therapy has been administered. Therapy of solid tumors should be aimed at permanent local control, not simply obtaining a complete response. This requires killing 10 to 12 logs of cells, not just two or three.
Efficacy of Radiation Therapy Alone
Very few macroscopic tumors can be controlled with radiation therapy alone. Some examples are: 1) acanthomatous epulides; 2) gingival carcinomas (canine); 3) small grade II mast cell tumors; and 4) transmissible venereal tumors.(4,5,9,10) This small list is the result of tumor volume being the biggest factor contributing to the failure of radiation therapy to control tumors. The detrimental effect of increasing tumor volume occurs at surprisingly small tumor volumes.(5) Thus, for gross tumors where complete surgical excision is not possible, combinations of therapy should be considered as the first-line therapy rather than trying a less aggressive, and ineffective, treatment.
Surgery and Radiation Therapy
The combination of surgery and radiation therapy is one of the most effective cancer treatment options available to veterinarians. Optimal use of this combination requires thoughtful preplanning and communication among all involved parties as well as adherence to good surgical oncologic principles. Surgery can be used either before or after radiation therapy, and there are indications for each sequence. This will not be discussed here, but more information is available.(7)
By judicious combination of surgery and radiation, permanent local control of various solid tumors may be achieved. These include: 1) grade I and II mast cell tumors; 2) canine and feline soft tissue sarcomas; and 3) miscellaneous soft tissue tumors such as thyroid, perianal tumors, ear canal tumors.(3,6) The combination of surgery and radiation may also be beneficial for canine nasal tumors, but the probability for permanent local control is not high.
Chemotherapy and Radiation Therapy
The combination of chemotherapy and radiation therapy is clearly superior to radiation therapy alone for some human tumors. Clinical trials documenting this principle in veterinary medicine have not been performed. Nevertheless, in theory this may be useful in some patients. Problems relate to the uncertainties of scheduling of the two agents, possible chemotherapy dose reductions, and unexpected toxicity.
Some chemotherapeutic agents are actual radiosensitizers, but in reality, one should expect only an additive interaction in vivo. Even with additivity, increased response is a reasonable expectation if chemotherapy kills cells that would not have been killed by radiation. Agents that are used in combination with radiation in veterinary medicine include cisplatin, carboplatin, and doxorubicin.
Chemotherapy has been added to the combination of surgery and radiation therapy in treatment of canine nasal tumors, feline vaccine associated sarcomas, and high-grade canine soft tissue sarcomas. Results documenting the superiority of these combinations are not yet available.
Chemotherapy in combination with radiation is also used in canine melanoma. Canine melanoma cells have been characterized by a large capacity to accumulate and repair sublethal radiation damage. Thus, because of their large repair capacity, similar to slowly proliferating normal tissues as described above, there have been trials using large fractional doses of radiation, sometimes in combination with chemotherapy. These trials have proven that complete response of the primary tumor is possible in many patients.(1,2) Metastasis remains a serious issue.
Palliative Radiation Therapy
Often, patients have tumors where the chance for definitive control is very low regardless of the modality or modalities used. Many of these patients can benefit from palliative radiation therapy. The intent of palliative radiation therapy is alleviation of discomforting clinical signs associated with the tumor, not prolongation of survival. This intent must be made perfectly clear to the pet owner. Palliative irradiation involves administration of fewer fractions (typically 1?) with larger doses per fraction (4? Gy) than employed in definitive irradiation. Palliative irradiation has been used for treatment of bone and soft tissue tumors with some success and in osteosarcoma, factors associated with long remission times have been identified (8). These include length of bone involved and degree of tumor lysis.
Summary
The knowledge of technical aspects of delivering radiation therapeutically, and the biologic aspects of interaction of radiation with tissue, and behavior of the tumor, has increased considerably in the past 10 years. The limitations of any single modality are well understood. There are some tumors that may be controlled with radiation therapy, but many are best treated with a combination of modalities. It is important that the first therapy administered be the absolute best therapy. Radiation has a role in palliation of signs associated with advanced bone and soft tissue tumors.

minibabyqq 2007-1-26 02:17

[color=Magenta][size=5][b]犬淋巴瘤預斷因素和治療 [/b][/size][/color]

[size=12px]似犬淋巴瘤
預斷因素
1 。 表現型(淋巴細胞後裔): 最重要的預斷因素迄今被辨認是是否瘤出現從B 細胞後裔或T 細胞後裔。幾大回顧展回顧認為, T 細胞淋巴瘤是可能失敗比是B 細胞腫瘤。至少T 細胞被獲得的腫瘤的一半是幫手T 細胞(CD4+), 藏匿副甲狀腺像激素和是因而, hypercalcemic 。總之, 只20% 所有狗以淋巴瘤是T 細胞起源, 殘餘80% B 細胞腫瘤代表很大數量的狗。在這個小組心頭, 對化療的反應並且是非常不同。進一步描述responding. 手段從non 反應。B 細胞淋巴瘤是必要的。
2 。 頭蓋骨Mediastinal Lymphadenopathy: 任一lymphadenopathy 出現在頭蓋骨縱隔之內被辨認了作為結果的其它消極預報因子在一項大回顧展研究中。這個協會被觀察了以溫和的(小) mediastinal 介入和並且被發現unassociated 以表現型(即, 作用是相等地強的在B 和T 細胞之內類別) 。
3 。 世界衛生組織階段和Substaging: 狗以階段I.III 比狗以階段IV/V 被發現有對治療的更好的反應。狗以他們的腫瘤(熱病、消沉、coagulopathies, GI 症狀的) 系統顯示比狗是可能失敗沒有病症(substage A 的標誌對B) 。
4 。 性別: 原封公狗由幾位調查員比其它性別發現是在死亡更高的風險。睪甾酮的角色在chemosensitivity 不是好的被描繪。
5 。 細胞擴散狀態: 數字細胞活躍循環和細胞擴散(加倍的時間的) 率被審查了在幾項不同的研究中為與結果的相關性。資料被混合了在這些研究中。
表1: 對因素的多維分佈的分析被辨認像重大為寬恕(REM) 並且(Surv) [table][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][/td][td=3,1,64][/td][td=6,1,128][b]所有狗(n=162)[/b]
[/td][td=4,1,64][/td][td=3,1,90][/td][td=4,1,90][/td][td=1,1,13]
[/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][b]REM[/b] [/td][td=4,1,90][/td][td=3,1,64][/td][td=5,1,90][/td][td=3,1,90][b]Surv[/b] [/td][td=4,1,90][/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]因素
[/td][td=2,1,90]p
[/td][td=1,1,90]Rel 風險
[/td][td=4,1,90]CI
[/td][td=3,1,64][/td][td=5,1,90]p
[/td][td=3,1,90]Rel 風險
[/td][td=4,1,90]CI
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]B 卷T
[/td][td=2,1,90]0002
[/td][td=1,1,90]2.6
[/td][td=4,1,90]1.6-4
[/td][td=3,1,64][/td][td=5,1,90]002
[/td][td=3,1,90]2.2
[/td][td=4,1,90]1.4-3.5
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]世界衛生組織
[/td][td=2,1,90]0006
[/td][td=1,1,90]2.1
[/td][td=4,1,90]1.4-3.2
[/td][td=3,1,64][/td][td=5,1,90]003
[/td][td=3,1,90]1.9
[/td][td=4,1,90]1.2-3.0
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]Cr Med
LN
[/td][td=2,1,90]008
[/td][td=1,1,90]1.7
[/td][td=4,1,90]1.1-2.4
[/td][td=3,1,64][/td][td=5,1,90]007
[/td][td=3,1,90]1.7
[/td][td=4,1,90]1.2-2.5
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96][b]中間[/b]
[/td][td=1,1,77][/td][td=3,1,128]160 v 。60 天
[/td][td=3,1,65][/td][td=3,1,64][/td][td=3,1,64][/td][td=7,1,141]335 v 。157 天
[/td][td=4,1,90][/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][/td][td=3,1,64][/td][td=3,1,64][/td][td=3,1,64][/td][td=5,1,90][/td][td=4,1,90][/td][td=3,1,77]
[/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][/td][td=3,1,64][/td][td=6,1,128][b]B 細胞唯一(n=129)[/b]
[/td][td=4,1,64][/td][td=3,1,90][/td][td=4,1,90][/td][td=1,1,13]
[/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][b]REM[/b] [/td][td=4,1,90][/td][td=3,1,64][/td][td=5,1,90][/td][td=3,1,90][b]Surv[/b] [/td][td=4,1,90][/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]因素
[/td][td=2,1,90]p
[/td][td=1,1,90]Rel 風險
[/td][td=4,1,90]CI
[/td][td=3,1,64][/td][td=5,1,90]p
[/td][td=3,1,90]Rel 風險
[/td][td=4,1,90]CI
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]B5 (> 75%)
[/td][td=2,1,90]0002
[/td][td=1,1,90]2.8
[/td][td=4,1,90]1.6-5
[/td][td=3,1,64][/td][td=5,1,90]0054
[/td][td=3,1,90]2.3
[/td][td=4,1,90]1.3-4.3
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]世界衛生組織
[/td][td=2,1,90]014
[/td][td=1,1,90]2.1
[/td][td=4,1,90]1.2-4.1
[/td][td=3,1,64][/td][td=5,1,90]-
[/td][td=3,1,90]-
[/td][td=4,1,90]-
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]卷B
[/td][td=2,1,90]015
[/td][td=1,1,90]1.9
[/td][td=4,1,90]1.1-3.1
[/td][td=3,1,64][/td][td=5,1,90]-
[/td][td=3,1,90]-
[/td][td=4,1,90]-
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]
[b]中間[/b]
[/td][td=1,1,77][/td][td=4,1,141]
203 v 。125 天
[/td][td=3,1,64][/td][td=3,1,64][/td][td=3,1,64][/td][td=7,1,142]
375 v 。200 天
[/td][td=2,1,64][/td][/tr][/table]表2: 完成反應(CR) 率、進步自由生存(PFS.days) 並且整體生存(Surv.days) 為狗被對待以組合化療以淋巴瘤各種各樣的immunophenotypic 類別 [table=90%][tr][td=1,1,156][b]免役[/b]
[b]表現型(n)[/b]
[/td][td=1,1,93][align=center][b]CR 率[/b]
[b](%)[/b][/align][/td][td=2,1,248][align=center][b][u]所有狗[/u][/b]
[b]PFS 。Surv[/b][/align][/td][td=2,1,248][align=center][b][u]Dog.s 達到的CR[/u][/b]
[b]PFS 。Surv[/b][/align][/td][/tr][tr][td=1,1,156]些T (27)
[/td][td=1,1,93][align=center]67%[/align][/td][td=1,1,124][align=center]52a[/align][/td][td=1,1,124][align=center]153 a[/align][/td][td=1,1,124][align=center]60 a[/align][/td][td=1,1,124][align=center]168 a[/align][/td][/tr][tr][td=1,1,156]任何B (119)
[/td][td=1,1,93][align=center]81[/align][/td][td=1,1,124][align=center]160[/align][/td][td=1,1,124][align=center]330[/align][/td][td=1,1,124][align=center]188[/align][/td][td=1,1,124][align=center]385[/align][/td][/tr][tr][td=1,1,156]... B5 低(57)
[/td][td=1,1,93][align=center]79[/align][/td][td=1,1,124][align=center]125b[/align][/td][td=1,1,124][align=center]202 b[/align][/td][td=1,1,124][align=center]155 b[/align][/td][td=1,1,124][align=center]245 b[/align][/td][/tr][tr][td=1,1,156]... B5 準則(23)
[/td][td=1,1,93][align=center]83[/align][/td][td=1,1,124][align=center]203 b[/align][/td][td=1,1,124][align=center]385 b[/align][/td][td=1,1,124][align=center]232 b[/align][/td][td=1,1,124][align=center]420 b[/align][/td][/tr][/table][i]日誌等級和Wilcoxon 統計< 0.0001 在T 細胞淋巴瘤和任何B.cell 淋巴瘤類別之間。 b 採伐等級和Wilcoxon 統計< 0.05 為比較在B5(low) 和B5(Normal) 之間B 細胞淋巴瘤類別。[/i]
似貓的淋巴瘤
預斷因素
1 。 階段: 似貓的淋巴瘤古典地被演出根據一份相似的計劃作為那在狗。另外, 程度疾病(liver/spleen 的龐大的腫瘤介入或巨型的胃腸介入) 被認為另外的援助在估計對常規療法的潛在的反應。貓以龐大的階段III 或IV 疾病也許不經常達到一個完全寬恕(50%) 比貓沒有廣泛的腫瘤負擔(90%) 。貓的介紹以系統病症並且是一個消極預斷因素和在狗。
2 。 FeLV antigenemia: 除FeLV 傳染之外的消極作用, FeLV 傳染的其它顯示也許限制用途進取的療法, 也許要求堅固支援療法(血液組分管理和營養協助) 。
[b]6 。 [/b]形態成績在小腸, infiltrative 疾病。
7 。 [b]對最初的療法的反應是或許最可靠的預斷因素[/b]。雖然這要求承諾從所有者創始治療和維護治療一個充足的期間確定反應, 這時間表經常不是超過四個到八個星期。最初地達到一個完全寬恕的貓也許繼續有耐久的寬恕, 延長超過12-18 個月。鼓勵貓所有者以淋巴瘤試圖治療和設置論點四個到八個星期跟隨治療將給好處貓, 不冒險堅固毒力或費用。
[indent][table=90%][tr][td][b][u]分級法標準[/u][/b][/td][td][b][u]預斷因素Med Surv [/u][/b][/td][td][u][b](mo.s)[/b][/u] [/td][tr][td]演出I      唯一淋巴結, 腫瘤(胸線或extranodal)[/td][td][/td][td][/td][/tr][tr][td]階段II     地方淋巴結, 膜片的一邊。[/td][td]對療法的反應[/td][td][/td][/tr][tr][td]唯一, resectable GI 根瘤
[/td][td]CR[/td][td]7[/td][/tr][tr][td]階段III    廣義lymphadenopathy 。[/td][td]PR[/td][td]2.5[/td][/tr][tr][td]Unresectable/multiple GI 根瘤
[/td][td]階段[/td][td][/td][/tr][tr][td]階段IV 。    肝臟並且/或者脾臟介入。[/td][td]I, II [/td][td]7.6[/td][/tr][tr][td]硬膜外介入
[/td][td]III, IV, V[/td][td]3.0[/td][/tr][tr][td]+/- 階段III 。
[/td][td]FeLV 狀態[/td][td][/td][/tr][tr][td].[/td][td]Neg[/td][td]9[/td][/tr][tr][td]階段v     血液並且/或者骨髓介入。[/td][td]Pos[/td][td]4.2[/td][/tr][tr][td]多或infiltrative extranodal 介入。
[/td][td]FeLV Neg/ 階段I, ii[/td][td]17.5[/td][/tr][tr][td](肺, CNS) 。
[/td][td]GI.well 被區分 [/td][td]> 18[/td][/tr][tr][td]+/- 階段III 或IV 。
[/td][td][/td][td][/td][/tr][tr][td]另外的考慮: Substage a 對b
廣泛的腫瘤負擔(organomegaly)

[/td][td][/td][td][/td][/tr][/table][/indent]對療法的一般推薦
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 導致一個完全寬恕是治療的最重要的方面。幾個歸納協議存在並且所有者應該被鼓勵包括這個組分在療養既使較不進取的維護療法被選舉。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 組合化療比唯一代理化療有效的。但是, 每個的活動唯一必須為人所知在並網之前入多代理協議。對強體松的用途單獨被認為緩和療法, 並且實際上, 可以使能力降低到組合協議的隨後有效率。所以, 創始組合療法在短時間之內跟隨診斷而不是起動強體松幾個星期以以後設立藥物的剩餘的意圖。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] doxorubicin 的並網入組合協議供給一個重大好處對許多狗淋巴瘤。這種化合物要求更加廣泛的監視和知識關於潛在的副作用的管理。但是, 它當前被推薦作為療養的組分, 除非禁忌症候對它的用途存在。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 眾多的協議存在並且數可能被發現總之課本。一般反應和生存為許多共同的協議下面是列出的。記得, 每個數字這裡是一個中點沒有任一個唯一預斷類別的考慮。具體資料為小組狗以prognostically 分明特徵被對待以組合協議位於桌上面。
[indent][table=90%][tr][td=3,1][b]治療協議比較為似犬淋巴瘤。[/b][/td][/tr][tr][td][u]治療。[/u][/td][td][u]寬恕時間[/u][/td][td][u]生存時間[/u][/td][/tr][tr][td]未經治療。[/td][td]-[/td][td]~ 30 天[/td][/tr][tr][td]強體松[/td][td]20-40 天[/td][td]30-120 天[/td][/tr][tr][td]警察[/td][td]150 天[/td][td]200 天[/td][/tr][tr][td]L-AspPCOM[/td][td]132 天[/td][td]219 天[/td][/tr][tr][td]基於Adriamycin[/td][td].~ 240 天。[/td][td].~ 365 天[/td][/tr][tr][td][u]COAP 。[/u][/td][td][u]180 天[/u][/td][td][u]220 天[/u][/td][/tr][tr][td=3,1][i]C = Cyclophosphamide, O = Oncovin. (vincristrine), P = 強體松, 。M = Methotrexate, A = 胞嘧啶Arabinoside, L Asp = L-asparaginase[/i][/td][/tr][/table][/indent][img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 另外的化學療法的代理知道是有效的為似犬淋巴瘤:
CCNU (CeeNU 或Lomustine), 。。Mechlorethamine (Mustargen) 。
Procarbazine (Matulane), Chlorambucil (Leukeran) 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 貓以低檔, infiltrative, 小腸淋巴瘤:
強體松(5 毫克q12 PO 或q24h) 加上Chlorambucil (2 毫克PO EOD) 。
[img=8,8]http://www.vin.com/Images/Icons/Bullet1.gif[/img] 其它考慮:
一半身體放射療法跟隨化療。
唯一GI 根瘤有或沒有腸繫膜lymphadenopathy 或infiltrate.consider 手術被化療隨後了而來。
孤零零, extranodal 淋巴瘤(皮膚, CNS 、盯鏡, 等)
FelV (+) 。地方控制以手術或輻射加上系統化療。
FelV (-) 。地方控制唯一(手術或輻射) 。


  
Canine Lymphoma
Prognostic Factors
1. Phenotype (lymphocyte lineage): The most important prognostic factor identified to date is whether the neoplasm arises from a B-cell lineage or a T-cell lineage. Several large retrospective reviews have concluded that T-cell lymphomas are more likely to fail than are B-cell tumors. At least half of the T-cell derived tumors are helper T cells (CD4+), secrete parathyroid-like hormone and are thus, hypercalcemic. Overall, only 20% of all dogs with lymphoma are of T-cell origin, the remaining 80% of B-cell tumors represent a large number of dogs. Within this group, the response to chemotherapy is also very diverse. Means of further delineating 𩂈esponding?from 忛on-responding?B-cell lymphoma is necessary.
2. Cranial Mediastinal Lymphadenopathy: The presence of any lymphadenopathy within the cranial mediastinum was identified as another negative predictor of outcome in a large retrospective study. This association was observed with even mild (small) mediastinal involvement and was also found to be unassociated with phenotype (i.e., the effect was equally strong within the B and T cell categories).
3. WHO Stage and Substaging: Dogs with stage I𦎾II were found to have better response to treatment than were dogs with stage IV/V. Dogs with systemic manifestations of their tumor (fever, depression, coagulopathies, GI symptoms) were more likely to fail than dogs without signs of illness (substage A vs. B).
4. Gender: Intact male dogs have been found by several investigators to be at higher risk of death than other genders. The role of testosterone on chemosensitivity is not well characterized.
5. Cell proliferation status: The number cells actively cycling and the rate of cell proliferation (doubling time) has been examined in several different studies for relevance to outcome. Data has been mixed in these studies.
TABLE 1: Multivariate analysis of factors identified as significant for remission (Rem) and (Surv) [table][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][/td][td=3,1,64][/td][td=6,1,128][b]All Dogs (n=162)[/b]
[/td][td=4,1,64][/td][td=3,1,90][/td][td=4,1,90][/td][td=1,1,13]
[/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][b]Rem[/b] [/td][td=4,1,90][/td][td=3,1,64][/td][td=5,1,90][/td][td=3,1,90][b]Surv[/b] [/td][td=4,1,90][/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]Factor
[/td][td=2,1,90]p
[/td][td=1,1,90]Rel Risk
[/td][td=4,1,90]CI
[/td][td=3,1,64][/td][td=5,1,90]p
[/td][td=3,1,90]Rel Risk
[/td][td=4,1,90]CI
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]B v. T
[/td][td=2,1,90].0002
[/td][td=1,1,90]2.6
[/td][td=4,1,90]1.6-4
[/td][td=3,1,64][/td][td=5,1,90].002
[/td][td=3,1,90]2.2
[/td][td=4,1,90]1.4-3.5
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]WHO
[/td][td=2,1,90].0006
[/td][td=1,1,90]2.1
[/td][td=4,1,90]1.4-3.2
[/td][td=3,1,64][/td][td=5,1,90].003
[/td][td=3,1,90]1.9
[/td][td=4,1,90]1.2-3.0
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]Cr Med
LN
[/td][td=2,1,90].008
[/td][td=1,1,90]1.7
[/td][td=4,1,90]1.1-2.4
[/td][td=3,1,64][/td][td=5,1,90].007
[/td][td=3,1,90]1.7
[/td][td=4,1,90]1.2-2.5
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96][b]Median[/b]
[/td][td=1,1,77][/td][td=3,1,128]160 v. 60 days
[/td][td=3,1,65][/td][td=3,1,64][/td][td=3,1,64][/td][td=7,1,141]335 v. 157 days
[/td][td=4,1,90][/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][/td][td=3,1,64][/td][td=3,1,64][/td][td=3,1,64][/td][td=5,1,90][/td][td=4,1,90][/td][td=3,1,77]
[/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][/td][td=3,1,64][/td][td=6,1,128][b]B-Cell Only (n=129)[/b]
[/td][td=4,1,64][/td][td=3,1,90][/td][td=4,1,90][/td][td=1,1,13]
[/td][/tr][tr][td=1,1,96][/td][td=2,1,90][/td][td=1,1,90][b]Rem[/b] [/td][td=4,1,90][/td][td=3,1,64][/td][td=5,1,90][/td][td=3,1,90][b]Surv[/b] [/td][td=4,1,90][/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]Factor
[/td][td=2,1,90]p
[/td][td=1,1,90]Rel Risk
[/td][td=4,1,90]CI
[/td][td=3,1,64][/td][td=5,1,90]p
[/td][td=3,1,90]Rel Risk
[/td][td=4,1,90]CI
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]B5 (>75%)
[/td][td=2,1,90].0002
[/td][td=1,1,90]2.8
[/td][td=4,1,90]1.6-5
[/td][td=3,1,64][/td][td=5,1,90].0054
[/td][td=3,1,90]2.3
[/td][td=4,1,90]1.3-4.3
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]WHO
[/td][td=2,1,90].014
[/td][td=1,1,90]2.1
[/td][td=4,1,90]1.2-4.1
[/td][td=3,1,64][/td][td=5,1,90]-
[/td][td=3,1,90]-
[/td][td=4,1,90]-
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]A v. B
[/td][td=2,1,90].015
[/td][td=1,1,90]1.9
[/td][td=4,1,90]1.1-3.1
[/td][td=3,1,64][/td][td=5,1,90]-
[/td][td=3,1,90]-
[/td][td=4,1,90]-
[/td][td=2,1,26]
[/td][/tr][tr][td=1,1,96]
[b]Median[/b]
[/td][td=1,1,77][/td][td=4,1,141]
203 v. 125 days
[/td][td=3,1,64][/td][td=3,1,64][/td][td=3,1,64][/td][td=7,1,142]
375 v. 200 days
[/td][td=2,1,64][/td][/tr][/table]TABLE 2: Complete response (CR) rate, progression free survival (PFS䤥ays) and overall survival (Surv䤥ays) for dogs treated with combination chemotherapy in various immunophenotypic categories of lymphoma [table=90%][tr][td=1,1,156][b]Immuno[/b]
[b]Phenotype (n)[/b]
[/td][td=1,1,93][align=center][b]CR rate[/b]
[b](%)[/b][/align][/td][td=2,1,248][align=center][b][u]All Dogs[/u][/b]
[b]PFS?Surv[/b][/align][/td][td=2,1,248][align=center][b][u]Dog𠏋 achieving CR[/u][/b]
[b]PFS?Surv[/b][/align][/td][/tr][tr][td=1,1,156]Any T (27)
[/td][td=1,1,93][align=center]67%[/align][/td][td=1,1,124][align=center]52a[/align][/td][td=1,1,124][align=center]153 a[/align][/td][td=1,1,124][align=center]60 a[/align][/td][td=1,1,124][align=center]168 a[/align][/td][/tr][tr][td=1,1,156]Any B (119)
[/td][td=1,1,93][align=center]81[/align][/td][td=1,1,124][align=center]160[/align][/td][td=1,1,124][align=center]330[/align][/td][td=1,1,124][align=center]188[/align][/td][td=1,1,124][align=center]385[/align][/td][/tr][tr][td=1,1,156]??B5 Low (57)
[/td][td=1,1,93][align=center]79[/align][/td][td=1,1,124][align=center]125b[/align][/td][td=1,1,124][align=center]202 b[/align][/td][td=1,1,124][align=center]155 b[/align][/td][td=1,1,124][align=center]245 b[/align][/td][/tr][tr][td=1,1,156]??B5 Norm (23)
[/td][td=1,1,93][align=center]83[/align][/td][td=1,1,124][align=center]203 b[/align][/td][td=1,1,124][align=center]385 b[/align][/td][td=1,1,124][align=center]232 b[/align][/td][td=1,1,124][align=center]420 b[/align][/td][/tr][/table][i]a[/i][i] Log Rank and Wilcoxon statistic < 0.0001 between T-cell lymphoma and any of the B櫘ell lymphoma categories. b Log Rank and Wilcoxon statistic < 0.05 for comparison between B5(low) and B5(Normal) categories of B-cell lymphomas.[/i]
Feline Lymphoma
Prognostic Factors
1. Stage: Feline lymphoma is classically staged according to a similar scheme as that in dogs. In addition, the extent of disease (bulky tumor involvement of liver/spleen or massive abdominal involvement) is considered an additional aid in assessing potential response to conventional therapy. Cats with bulky stage III or IV disease may fail to achieve a complete remission more often (50%) than cats without extensive tumor burdens (90%). Presentation of cats with systemic illness is also a negative prognostic factor as in dogs.
2. FeLV antigenemia: In addition to negative effect of FeLV infection, other manifestations of the FeLV infection may limit the use aggressive therapy and may require substantial supportive therapy (blood component administration and nutritional assistance).
[b]6. [/b]Morphologic grade in intestinal, infiltrative disease.
7. [b]Response to initial therapy is perhaps the most reliable prognostic factor[/b]. Although this requires commitment from the owner to initiate treatment and maintain the treatment for a sufficient period to determine response, this time frame is often not more than four to eight weeks. Cats that achieve a complete remission initially may continue to have durable remissions, extending for more than 12-18 months. Encouraging the owner of cat with lymphoma to attempt treatment and setting a decision point four to eight weeks following the treatment will give the benefit to the cats and does not risk substantial toxicity or expense.
[/size]

minibabyqq 2007-1-26 02:18

[color=Magenta][size=5][b]關心在動物腫瘤學方面Palliative Care in Companion Animal Oncology [/b][/size][/color]

[size=12px]世界衛生組織定義緩和關心當疾病對治病的治療不是敏感患者的The 活躍總關心。痛苦控制, 其它症狀, 和心理社會和精神問題, 是至高無上的。緩和關心的目標是最佳的生活水平的成就為患者和他們的家庭。獸醫腫瘤學和緩和關心的目標很好總被排列了因為生活水平有是忽略的關心為動物接受癌症治療。近似一半所有動物以癌症將死由於疾病和最將要求症狀或痛苦控制。對緩和關心的需要在獸醫腫瘤學方面已經是偉大的, 但可能將繼續增加因為領域更好定義徵兆為治病和緩和療法和認為一些緩和關心的方面可能是聯合入治病的療法為了創造癌症管理連續流。為討論的目的, 治病的療法的定義將是主要和任一種變形的疾病的中間控制至少一年以常規療法為一種指定的腫瘤類型。患者以無法是受控的為這個任意終點的腫瘤也許被認為有資袼緩和治療。但是, 對緩和干預和類型的需要干預被使用是巨大辯論。規定緩和治療舒適也許制約未來療法或妨害進展往一種治病的治療。緩和關心的概念在人和獸醫腫瘤學方面是需要嚴謹研究。圖如下說明一種治療決定算法根據概念的治病對緩和主要控制。 [table][tr][td=1,1,560][table][tr][td][table][tr][td][img=550,353]http://www.vin.com/ImageDBPub/IM05000/IMC02853.gif[/img]
[/td][/tr][/table][/td][/tr][/table][/td][td=1,1,5][/td][/tr][/table]主要緩和療法... 。。
主要療法為緩和目的是成功的為了控制各種各樣的症狀。症狀與相關先進的癌症包括植物生長的作用的物理中斷譬如語言困難、裡急後重、尿痛和呼吸困難, 和症狀與相關新陳代謝或paraneoplastic sequelae 對癌症譬如貧血症、惡病質性、低血糖症, 或hypercalcemia 。所有這些也許導致難受、憂慮或痛苦除有機反常性之外。如果症狀同大量的物理出現聯繫在一起, 它一般假設, 大量的減少將改進兩種有機症狀和使伴生痛苦以大量。主要療法為緩和包括手術、化療, 和放射療法。主要療法的目標在一個緩和設置不同的比在一個治病的設置。緩和外科debulking 不意欲包括大正常組織邊際。緩和放射治療是藥量的組合與相關一點深刻正常組織作用。緩和化療被執行試圖根瘤的減少或安定改進生活水平。支援療程譬如抗生素、凳子軟化劑, anti-emetics, 和其他人被交付對舒適症狀或有或沒有主要療法。也許是必要的支援規程包括滲流、thoracentesis 、cystostomy tubes/valves 、營養支持通過哺養的管, 等。multimodality 療法(手術加上化療或緩和輻射加上化療) 也許是適當的在某些事例。但是, 某些組合是疑難, 譬如緩和輻射和手術。
痛苦管理
痛苦可能被定義作為令人不快的知覺或情感經驗與相關實際或被期望的組織損傷。痛苦是癌症的恐懼的複雜化在人。大約40% 有癌症人的病人遭受痛苦並且80% 以先進的癌症有痛苦。痛苦控制在人和動物成為了一個主要臨床焦點在最近五年。痛苦認識在動物中要求接近的觀察。Vocalization 是一次非常晚事件為動物以回應痛苦。生理學變化在心率、呼吸率, 和學生大小(mydriasis 上) 是早期的標誌。姿勢標誌譬如勉強躺下和胃腸守衛是還早期的標誌。不安定性和變動從是交互式的對隱退也許是引人注目的。痛苦可能被分類像或深刻或慢性。劇痛也許伴隨規程譬如手術或輻照區域。地方麻醉劑, 合適對鎮定藥的用途, 並且先發制人的痛苦管理一般是充足的。慢性痛苦要求一種更加全面的方法, 經常介入藥物和nonpharmcologic 鎮痛藥戰略的組合。 [table][tr][td=1,1,560][table][tr][td][table][tr][td][img=550,203]http://www.vin.com/ImageDBPub/IM05000/IMC02854.gif[/img]
[/td][/tr][/table][/td][/tr][/table][/td][td=1,1,5][/td][/tr][/table]腫瘤的主要治療可能導致對痛苦的直接減少既使腫瘤不反應由對容量的減少。放射治療的鎮痛藥有效率很好被提供在骨疼痛、轉移, 和CNS 瘤形成的治療。在人, 周邊神經的輻照區域為perineal 痛苦和肝輻照區域(2,000.3,000 GY) 為膠囊狀的膨脹是有效和很好容忍。主要化療的作用在癌症痛苦經常被觀察當治療同對腫瘤大小的減少聯繫在一起。手術可能解除痛苦和難受從問題譬如膿腫或潰瘍的表面大量、GI 阻礙、CNS 壓縮和不穩定的骨多的結構。主要療法的好處應該斟酌反對好處的風險、住院治療、恢復時間, 和期望的期間。
對具體鎮痛藥代理的用途是頻繁為有與癌症相關的痛苦病人。Glucocorticosteroids 慷慨地被使用了為動物以癌症希望增長的胃口、心情, 和福利。具體痛苦的情況聯繫了以知道反應類固醇有的腫瘤: 被上升的顱內的壓力、深刻脊髓壓縮、變形的骨疼痛、neuropathic 痛苦由於濾滲或壓縮由腫瘤, 根據症狀的lymphedema, 和肝膠囊狀的膨脹。Non-Opioid 鎮痛藥通常是管理第一線在人。藥量的逐步升級確定鎮痛藥活動對2X 正常藥量近似地被認為最大值。Nonsteroidals 譬如carprofen 並且piroxicam (0.3 mg/kg pl q 24 小時) 一般是選擇最初的藥物在這個類別。如果不足的痛覺缺失達到以non-opioids, opioid 的一個口頭形式與Tylenol (Tylenol 4 經常被使用和經常被結合與60 毫克可待因被藥量在1.2 mg/kg q6.8h PO, 根據可待因組分) 。在貓, 口頭butorphanol (0.2.1.0 mg/cat q6.12h PO) 也許被使用作為唯一療法。嗎啡片劑或嗎啡塞劑也許並且被使用。Transdermal 芬太奴管理是非常有用的為先發制人的鎮痛和持續的鎮痛從慢性痛苦。伴侶動物很少被承受在長期opioid 麻醉劑為慢性痛苦。許多選擇為痛苦療程的管理現在存在在人長時間譬如存在的平方口岸、植入管, 等。在一些情況, 長時期的痛苦控制在狗或貓也許被表明。
針刺、按摩脊柱治療者管理和物理療法也許被合併痛苦的藥物管理提高整體福利。

The world health organization defines palliative care as 孏he active total care of patients whose disease is not responsive to curative treatment. Control of pain, of other symptoms, and of psychological social and spiritual problems, is paramount. The goal of palliative care is achievement of the best quality of life for patients and their families.?The goals of veterinary oncology and palliative care have always been well aligned since quality of life has been the overriding concern for animals undergoing cancer treatment. Approximately half of all animals with cancer will die because of the disease and most will require symptom or pain control. The need for palliative care in veterinary oncology is already great, but will likely continue to increase as the field better defines the indications for curative and palliative therapy and recognizes that some aspects of palliative care can be integrated into curative therapies in order to create a continuum of cancer management. For purposes of discussion, the definition of curative therapy will be median control of the primary and any metastatic disease for at least one year with conventional therapy for a given tumor type. Patients with tumors that cannot be controlled for this arbitrary endpoint may be considered eligible for palliative treatment. However, the need for palliative intervention and the type of intervention used is of great debate. The ease of prescribing palliative treatments may restrict future therapies or hinder progress toward a curative treatment. The concept of palliative care in both human and veterinary oncology is in need of rigorous study. The figure below illustrates a treatment decision algorithm based on the concept of curative vs. palliative primary control. [table][tr][td=1,1,560][table][tr][td][table][tr][td][img=550,353]http://www.vin.com/ImageDBPub/IM05000/IMC02853.gif[/img]
[/td][/tr][/table][/td][/tr][/table][/td][td=1,1,5][/td][/tr][/table]Primary Palliative Therapy???
Primary therapy for palliative purposes is accomplished in order to control a variety of symptoms. Symptoms associated with advanced cancers includes physical disruption of vegetative functions such as dysphasia, tenesmus, dysuria and dyspnea, and symptoms associated with metabolic or paraneoplastic sequelae to cancer such as anemia, cachexia, hypoglycemia, or hypercalcemia. All of these may induce discomfort, anxiety or pain in addition to organic abnormalities. If symptoms are associated with physical presence of a mass, it is generally assumed that reduction of the mass will improve both organic symptoms and pain associated with mass. Primary therapy for palliation includes surgery, chemotherapy, and radiotherapy. The goals of primary therapy in a palliative setting are different than in a curative setting. Palliative surgical debulking is not intended to include large normal tissue margins. Palliative radiation therapy is a combination of doses associated with little acute normal tissue effects. Palliative chemotherapy is administered to attempt reduction or stabilization of nodules to improve quality of life. Supportive medications such as antibiotics, stool softeners, anti-emetics, and others are delivered to ease symptoms either with or without primary therapy. Supportive procedures that may be necessary include transfusions, thoracentesis, cystostomy tubes/valves, nutritional support via feeding tube, etc. Even multimodality therapy (surgery plus chemotherapy or palliative radiation plus chemotherapy) may be appropriate in certain instances. However, certain combinations are problematic, such as palliative radiation and surgery.
Pain Management
Pain can be defined as an unpleasant sensory or emotional experience associated with actual or anticipated tissue damage. Pain is the most feared complication of cancer in humans. Approximately 40% of human patients with cancer suffer from pain and 80% with advanced cancer have pain. Pain control in humans and animals has become a major clinical focus in the last five years. Pain recognition in animals requires close observation. Vocalization is a very late event for animals in response to pain. Physiologic changes in heart rate, respiratory rate, and pupil size (mydriasis) are early signs. Postural signs such as reluctance to lie down and abdominal guarding are also early signs. Restlessness and a change from being interactive to reclusive may be noticeable as well. Pain can be categorized as either acute or chronic. Acute pain may accompany procedures such as surgery or irradiation. Local anesthetics, appropriate use of tranquilizers, and pre-emptive pain management is generally sufficient. Chronic pain requires a more comprehensive approach, often involving a combination of pharmacologic and nonpharmcologic analgesic strategies. [table][tr][td=1,1,560][table][tr][td][table][tr][td][img=550,203]http://www.vin.com/ImageDBPub/IM05000/IMC02854.gif[/img]
[/td][/tr][/table][/td][/tr][/table][/td][td=1,1,5][/td][/tr][/table]Primary treatment of the tumor can cause a direct reduction in pain even if the tumor does not respond by reduction in volume. The analgesic effectiveness of radiation therapy is well documented in the treatment of bone pain, metastases, and CNS neoplasia. In humans, irradiation of peripheral nerves for perineal pain and hepatic irradiation (2,000?,000 cGy) for capsular distention is effective and well tolerated. The effect of primary chemotherapy on cancer pain is most often observed when treatment is associated with reduction in tumor size. Surgery can relieve pain and discomfort from problems such as abscessed or ulcerated superficial masses, GI obstruction, CNS compression and unstable boney structures. The benefits of primary therapy should be weighed against the risks, hospitalization, recovery time, and expected duration of benefit.
Use of specific analgesic agents is frequent for patients with cancer-related pain. Glucocorticosteroids have been used generously for animals with cancer in hopes of increasing appetite, mood, and well-being. Specific painful conditions associated with tumors that are known to respond to steroids include: raised intracranial pressure, acute spinal cord compression, metastatic bone pain, neuropathic pain due to infiltration or compression by tumor, symptomatic lymphedema, and hepatic capsular distention. Non-Opioid analgesics are usually the first line of management in humans. Escalation of the dose to determine analgesic activity to approximately 2X the normal dose is considered the maximum. Nonsteroidals such as carprofen and piroxicam (0.3 mg/kg pl q 24 hrs) are generally the initial drugs of choice in this category. If insufficient analgesia is achieved with non-opioids, an oral form of opioid is often used and is most often combined with Tylenol (Tylenol 4 with 60 mg codeine dosed at 1? mg/kg q6?h PO, based on the codeine component). In cats, oral butorphanol (0.2?.0 mg/cat q6?2h PO) may be used as single therapy. Morphine tablets or morphine suppositories may also be used. Transdermal fentanyl administration has been very useful for both pre-emptive pain relief and ongoing pain relief from chronic pain. Companion animals are rarely sustained on long-term opioid narcotics for chronic pain. Many alternatives exist now for administration of pain medication in humans for prolonged periods such as indwelling SQ ports, implants, etc. In some situations, prolonged pain control in dogs or cats may be indicated.
Acupuncture, chiropractic management and physical therapy may be incorporated into pharmacologic management of pain to enhance overall well being.[/size]
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