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minibabyqq 2006-12-28 00:55

[color=Magenta][b][size=5]ENDODONTIC 疾病[/size][/b][/color]   


endodontic 系統是黏漿狀物質組織(血管、神經, 和結締組織) 是在根運河和黏漿狀物質分庭在我們的和我們的患者的牙裡。這個系統供應它需要居住和成熟的生存牙以所有組分。供血為牙出現從血管的下頷骨和上頷骨分支。緊張的供應來自trigeminal 神經的分支。Endodontic 疾病提到任一炎症對叫做pulpitis 的這種 器官。根據侮辱的嚴肅, pulpitis 也許是reverseable 或irreverseable 。Reverseable pulpitis 由少許精神創傷通常造成, 並且牙將生存侮辱。Irreversable pulpitis 歸結於重大pulpitis, 導致牙的死亡。這的同道會是endodontic 系統暴露於口腔為任一個時間的一顆破碎的牙。


殘破的牙是非常共同的發生在狗和貓。他們能打破由於精神創傷(命中由汽車、球, 或岩石) 或由於嚼在堅硬對象。任一顆牙可能打破, 然而一些牙破碎更多比其他人。是殘破的最共同的牙是似犬(犬齒) 牙在狗和貓, 和上部第四顆前臼齒(大牙在上面在後面) 在狗。


在牙破碎之後, 細菌從嘴對黏漿狀物質(根運河) 將能夠存取並且將傳染牙。最終, 牙將死和將成為一個細菌避風港。細菌然後將洩漏通過尖頂(或底部) 牙, 和傳染骨頭在那個區域。最終, 細菌副產物和白細胞酵素將導致骨頭破壞在根要訣附近。其次, 血管在區域將拾起細菌和將傳播它對身體的其它區域。最具體地, 對過濾血液的肝臟和腎臟, 和可能對心臟瓣膜。他們將形成微膿腫在器官, 並且隨時間將減少這些重要器官效率。


這些被傳染的牙是痛苦的, 因為任何人需要根運河可能作證。不幸地, 只非常很少願我們的動物患者展示難受, 如同他們喜歡遭受在沉默。這允許所有者和獸醫忽略問題, 因為it doesn.t 似乎打擾他。但我們現在知道, 這些動物當地影響並且系統地, 並且忽略問題不是一個可行選擇。我有有告訴我的許多客戶寵物由殘破的牙不打擾當它被發現告訴我寵物行動5 年更加年輕二個星期在問題是固定的之後。另外, 我有安排被舉起的肝臟酵素在牙齒工作之時去回到法線在二個星期手術之內的無數患者。

偶爾地, 膿腫在根要訣將得到很壞, 膿腫將發生通過皮膚。這最共同地發生與上部第四顆前臼齒的破裂在狗, 並且它為人所知作為carnassial 膿腫。它可能並且發生次要對一隻膿腫的犬並且多數其它牙。在貓, 膿腫通常歸結於一隻破碎的犬, 但由於鼻子的不足將打開在眼睛之下。抗生素通常將治療問題有一陣子, 但問題不變地將再發生如果觸犯的牙不被處理。  


有三個選擇為處理一顆破碎的牙, 並且忽略它不是 他們的當中一個。和最佳的第一選擇為是否則健康的一顆破碎的牙(沒有牙周疾病或根破裂, 等。) 是標準 根運河療法。這是被傳染的黏漿狀物質被取消的地方並且運河用mendicants 被填裝勸阻未來細菌汙染。這最共同地做在犬在狗和貓, 和上部第四前臼齒和更低的第一槽牙在狗。但是, 任一顆牙可能做在狗。一 重要pulpotomy 可能執行如果破裂是新鮮的並且不嚴厲地被傳染; 這個做法是特別有用的在發育未全的牙破裂(狗和貓少於18 個月年齡) 。

一個最後的選擇, 根據介入的牙, 程度破裂, 和其他疾病禮物, 是 觸犯的牙的提取。為犬齒在狗和貓, 和上部第四顆前臼齒和降低第一槽牙在狗這是的最後的選擇。有我們喜歡避免這個做法當可能時的幾個原因。首先, 照原樣痛苦由於根的大小在我們的動物患者。犬的根是兩次一樣長的和更寬比冠(您能看) 的零件。這是口腔外科和不是簡單的提取在犬特別是。第二, 患者疏鬆牙的作用, 可能是非常重要為嚼在某些情況下。另外, 您能看正牙學問題次要對牙的損失。我們設法避免這在否則健康牙盒。


ENDODONTICS: 黏漿狀物質的治療(神經和血管) 牙。位於在牙裡面。

五基本的類型endodontic 療法:

標準根運河療法
外科根運河療法
直接黏漿狀物質加蓋或重要pulpotomy
間接黏漿狀物質加蓋
Apexification
二這些規程共同地執行在獸醫牙科方面
A) 標準根運河療法

使用在患者與死或害病的牙。最共同地由於破碎的(被傷的) 牙。
為患者與成熟牙(通常大於13 個月年齡) 。
不是緊急狀態
B) 直接黏漿狀物質加蓋或重要Pulpotomy

1 。執行在黏漿狀物質被暴露處, 但可以是健康的並且牙的進一步成熟性渴望。特別是使用在患者在18 個月年齡之下。緊急(在一天或二之內更好地) 做法。

2. 執行當冠(您能看) 的一部分的高度的牙需要被減少或為一個正牙學問題或為解除武裝一條狠毒狗或貓。這些規程是詳細的在他們自己的頁

其它三非常很少執行在獸醫牙科方面

C) 外科根運河療法

1 。非常很少做, 通常只當常規根運河療法失敗或當運河由黏漿狀物質石頭或其它障礙阻攔。
2 。要求切開在一些下頜骨頭齒齦(膠) 組織和撤除暴露牙根(尖頂的) 要訣。要訣被去除, 並且運河被填裝從底部。

D) 間接黏漿狀物質加蓋

1 。共同地使用在人的牙科方面但很少在動物中由於這樣的事實 動物很少得到細菌齲。
2 。執行當瑕疵在牙進入緊挨黏漿狀物質但不是它。
3 。醫藥層數叫做+氧化鈣被安置在瑕疵的底部。這將用於絕緣黏漿狀物質, 並且刺激黏漿狀物質制定更多牙結構。
4 。標準補藥被安置在襯裡

E) Apexification

1 。執行在有價值的一顆死, 發育未全的(未關閉在底部) 牙。
2 。牙被清洗和在標準根運河療法。然後運河用+氧化鈣被填裝刺激牙完成底部(尖頂的) 發展牙。
3 。患者被復校在6 個月的間隔時間確定如果尖頂的關閉發生□。如果它有, 標準根運河療法然後執行。如果沒有一個完全尖頂, +氧化鈣被取消和然後被替換。這個過程被重覆直到有尖頂。
4 。這是沒有一種非常好預測的一個長, 昂貴, 繁瑣 過程。眾多的麻醉劑必需, 並且替換mendicants 。但是, 如果做, 它可能保存牙。

ENDODONTIC DISEASE

The endodontic system is the pulp tissue (blood vessels, nerves, and connective tissue) that are in the root canals and pulp chambers in our and our patients' teeth. This system supplies the living tooth with all components it needs to live and mature. The blood supply for the teeth arises from the mandibular and maxillary branches of the blood vessels. Nervous supply comes from the branches of the trigeminal nerve. Endodontic disease refers to any inflammation to this organ which is called pulpitis. Depending on the severity of the insult, the pulpitis may be reverseable or irreverseable. Reverseable pulpitis is usually caused by a lesser trauma, and the tooth will survive the insult. Irreversable pulpitis is due to significant pulpitis and will result in the death of the tooth. The most common cause of this is a fractured tooth where the endodontic system is exposed to the oral cavity for any length of time.

Fracture of the maxillary fourth premolar results in pulp exposure. This tooth needs endodontic care.







Broken teeth are a very common occurrence in dogs and cats. They can break due to trauma (hit by a car, ball, or rock) or due to chewing on hard objects. Any tooth can break, however some teeth are fractured more than others. The most common teeth that are broken are the canine (fang) teeth in the dog and the cat, and the upper fourth premolar (large tooth on the top in the back) in dogs.  


Teeth with severe damage may benefit from placement of a crown.
After the tooth is fractured, bacteria from the mouth will gain access to the pulp (root canal) and infect the tooth. Eventually, the tooth will die and become a bacterial haven. The bacteria will then leak out through the apex (or bottom) of the tooth, and infect the bone in that area. Eventually, the bacterial byproducts and white blood cell enzymes will cause bone destruction around the root tip. Next, the blood vessels in the area will pick up the bacteria and spread it to other areas of the body. Most specifically, to the liver and kidneys which filter the blood, and possibly to the heart valves. They will form micro-abscesses on the organs, and over time will decrease the efficiency of these vital organs.





These infected teeth are painful, as anyone who has needed a root canal can testify to. Unfortunately, only very rarely will our animal patients show discomfort, as they prefer to suffer in silence. This allows owners and veterinarians alike to ignore the problem, as 𧗽t doesn㦙 seem to bother him? But we now know that these animals are being affected locally as well as systemically, and ignoring the problem is not a viable option. I have had numerous clients who have told me that the pet is not bothered by the broken tooth when it is discovered tell me that the pet acts ? years younger?just two weeks after the problem is fixed. In addition, I have had innumerous patients that have had elevated liver enzymes at the time of dental work go back to normal within two weeks of surgery.

Occasionally, the abscess at the root tips will get so bad that the abscess will break out through the skin. This most commonly occurs with a fracture of the upper fourth premolar in dogs, and it is known as a carnassial abscess. It can also occur secondary to an abscessed canine as well as most other teeth. In cats, the abscess will usually be due to a fractured canine, but due to the shortness of the nose will open below the eye as well. Antibiotics will usually cure the problem for a while, but invariably the problem will reoccur if the offending tooth is not dealt with.  

There are three options for dealing with a fractured tooth, and ignoring it is NOT one of them. The first and best option for a fractured tooth that is otherwise healthy (no periodontal disease or root fracture, etc.) is standard root canal therapy. This is where the infected pulp is removed and the canals filled with mendicants to discourage future bacterial contamination. This is most commonly done in canines in dogs and cats, and the upper fourth premolars and lower first molars in dogs. However, any tooth can be done in a dog. A vital pulpotomy can be performed if the fracture is fresh and not yet severely infected; this procedure is especially useful in fractures of immature teeth (dogs and cats less than 18 months of age).

Completed root canal therapy in a
maxillary fourth premolar.



A final option, depending on the tooth involved, degree of fracture, and any other disease present, is extraction of the offending tooth. For the canine tooth in dogs and cats, and the upper fourth premolar and lower first molar in dogs this is the last option. There are several reasons we prefer to avoid this procedure when possible. First, as it is painful due to the size of the roots in our animal patients. The root of the canine is twice as long and wider than the crown (the part you can see). It is oral surgery and not a simple extraction in canines especially. Secondly, the patient looses the function of the tooth, which can be very important for chewing in some cases. In addition, you can see orthodontic problems secondary to the loss of the tooth. We try to avoid this in cases of otherwise healthy teeth.


ENDODONTICS: Treatment of the pulp (nerves and blood vessels) of the tooth. Located inside the tooth.

Five basic types of endodontic therapy:

Standard root canal therapy
Surgical root canal therapy
Direct pulp capping or vital pulpotomy
Indirect pulp capping
Apexification
Two of these procedures are performed commonly in veterinary dentistry
A) Standard Root Canal Therapy

Used in patients with dead or diseased teeth. Most commonly due to fractured (broken) teeth.
For patients with mature teeth (usually greater than 13 months of age).
Not an emergency
B) Direct Pulp Capping or Vital Pulpotomy

1. Performed in cases where the pulp is exposed, but may be still healthy and further maturation of the tooth is desired. Especially used in patients under 18 months of age. Emergency (within a day or two preferably) procedure.

2. Performed when the height of the crown (part of the tooth you can see) needs to be reduced either for an orthodontic problem or for disarming a vicious dog or cat. These procedures are detailed on their own pages

The other three are performed very rarely in veterinary dentistry

C) Surgical Root Canal Therapy

1. Very rarely done, usually only when conventional root canal therapy fails or when the canal is blocked by a pulp stone or other impediment.
2. Requires an incision in the gingival (gum) tissue and removal of some jaw bone to expose the tip of the tooth root (apex). The tip is removed, and the canal filled from the bottom.

D) Indirect Pulp Capping

1. Used commonly in human dentistry but rarely in animals due to the fact that animals rarely get bacterial caries.
2. Performed when the defect in the tooth gets close to the pulp but not into it.
3. A medicinal layer called calcium hydroxide is placed over the bottom of the defect. This will serve to insulate the pulp, as well as stimulate the pulp to lay down more tooth structure.
4. A standard restorative is placed over the lining

E) Apexification

1. Performed in a dead, immature (has not closed at the bottom) tooth which is very valuable.
2. The tooth is cleaned as in the standard root canal therapy. Then the canal is filled with calcium hydroxide to stimulate the tooth to complete the development of the bottom (apex) of the tooth.
3. The patient is rechecked at 6-month intervals to determine if closure of the apex has occurred. If it has, then standard root canal therapy is performed. If there is not a complete apex, then the calcium hydroxide is removed and replaced. This process is repeated until there is an apex.
4. This is a long, expensive, tedious process which does not have a very good prognosis. Numerous anesthetics are required, as well as replacing the mendicants. However, if done right, it can save the tooth.

minibabyqq 2006-12-28 00:56

[b][size=5][color=magenta]下頜破裂 JAW FRACTURES AND THEIR FIXATION[/color][/size]  
[/b]
[size=12px][align=left]主要方式使下頜破碎是由創傷侮辱(命中在汽車, 秋天以前, 戰鬥) 。但是, 有事例叫做下頜由其它疾病過程減弱的病理性破裂, 並且可能打破以在任一真正的精神創傷之外(吃例如) 。二同道會是 [b][i]先進的牙周疾病[/i][/b] 和 [b][i]惡性口頭腫瘤[/i][/b]。

有下頜破裂的定像的許多技術。類型定像被選擇取決於類型破裂並且外科醫生特選。這個目錄是技術一個簡要的總結和不是完全或詳盡的。我設置了它至於類型破裂和被類型定像隨後了而來可利用。

最共同的類型破裂在貓是下頷骨symphaseal 分離。這不少有地也被看見在狗。最容易的方式固定這破裂是由circum 下頷骨接線。這由安置一根導線在兩塊下顎骨附近在犬之後和拉緊做在皮膚之下在下巴之下。如果下頜是不穩定的圖8 導線可能被安置在犬附近在嘴, 或一個丙烯酸酯的藤條可能被安置進一步穩定分離。

最共同的類型破裂在狗是下頷骨身體破裂, 雖然它不是不凡的在貓或者。有運作為這類型破裂的許多技術, 但我的喜愛是一個丙烯酸酯的藤條。這運作在使用牙旁邊穩定破裂。牙齒丙烯酸酯(相似與環氧) 適用於牙在包含的區域。這使用牙作為崗位握牙對齊。好處對這個定像的形式是, 它是相對地快的並且是非侵入性的, 因為骨頭不是包含的。另外, 撤除不要求外科撤除, 照原樣被切開藤條和去除取消與鑷子。如果破裂是在一邊, 和相當穩定, 槍口可能被使用穩定下頜足夠允許癒合。這是後備的為相對地穩定的破裂。Interdental (在牙之間) 或interossues 架線可能被使用, 根據類型破裂。Interdental 接線是困難的在動物中由於這樣的事實他們沒有脖子對牙, 並且導線可能滑當拉緊。interosseus 導線輕微地更加蔓延性, 和將需要以後外科地被去除。骨頭鍍層很少被使用, 由於困難在避免牙根與定像螺絲。但是, 它可能是有用的當有一個大骨多的瑕疵。外在定像與別針在骨頭附有一個酒吧在嘴之外可能被使用在這些情況。

垂直的ramus 的破裂是相當共同在貓和也被看見在狗。他們可能經常被處理與軟的槍口因為他們肌肉在區域將握下頜相當穩定。如果這不是實際情形, 那麼外科定像與板材或導線可能被使用, 或如果破碎的片斷小它可能被去除。[/align][align=left]上頷骨破裂經常是足夠stabile 由縫合對待軟的組織唯一。如果另外的安定是需要的, 一個丙烯酸酯的藤條、interosseus 或interdental 接線或外部定像可能被使用。 [/align][align=left]病理性破裂非常難對待由於這樣的事實骨頭是非常害病的開始與。破裂從牙周疾病由首先提取觸犯的牙, 和安置通常對待患者在軟的槍口。這通常只不幸地形成纖維狀和不是骨多的聯合。其它選擇隨後而來的提取將試圖外在定像與別針和骨頭嫁接材料, 這5月工作, 但預測不是好的。 [/align][align=left]The main way for a jaw to fracture is by a traumatic insult (hit by car, a fall, fighting). However, there are instances called pathologic fractures where the jaw is weakened by another disease process, and can be broken with out any real trauma (eating for instance). The two most common causes are [b][i]advanced periodontal disease[/i][/b] and [b][i]malignant oral tumors[/i][/b].

There are numerous techniques for the fixation of jaw fractures. The type of fixation selected depends on the type of fracture as well as surgeons preference. This listing is a brief summary of techniques and is not complete or exhaustive. I have set it up as to the type of fracture and followed by the types of fixation available.

The most common type of fracture in the cat is a mandibular symphaseal separation. This is also seen not infrequently in the dog. The easiest way to fix this fracture is by circum-mandibular wiring. This is done by placing a wire around both mandibles just behind the canines and tightening under the skin below the chin. If the jaw is still unstable a figure 8 wire can be placed around the canines in the mouth, or an acrylic splint can be placed to stabilize the separation further.

The most common type of fracture in a dog is a mandibular body fracture, although it is not uncommon in the cat either. There are numerous techniques that work for this type of fracture, but my favorite is an acrylic splint. This works by using the teeth to stabilize the fracture. A dental acrylic (similar to epoxy) is applied to the teeth in the involved area. This uses the teeth as the posts to hold the teeth in alignment. The advantage to this form of fixation is that it is relatively quick and is non-invasive, as the bone itself is not involved. In addition, removal does not require surgical removal, as it is removed by cutting the splint and removing with forceps. If the fracture is on one side, and fairly stable, a muzzle can be used to stabilize the jaw enough to allow healing. This is reserved for relatively stable fractures. Interdental (between the teeth) or interossues wiring can be used as well, depending on the type of fracture. Interdental wiring is more difficult in animals due to the fact that they do not have much of a neck to the tooth, and the wire can slide up when tightened. The interosseus wires are slightly more invasive, and will need to be surgically removed later. Bone plating is rarely used, due to the difficulty in avoiding the tooth roots with the fixation screws. However, it can be useful when there is a large bony defect. External fixation with pins in the bone attached to a bar outside the mouth can be used in these situations as well.

Fractures of the vertical ramus are fairly common in cats and also seen in dogs. They can often be managed with a soft muzzle since they muscles in the area will hold the jaw fairly stable. If this is not the case, then surgical fixations with plates or wires can be used, or if the fractured piece is small it can be removed.[/align][align=left]Maxillary fractures are often stabile enough to be treated by suturing the soft tissues only. If additional stabilization is needed, an acrylic splint, interosseus or interdental wiring or external fixation can be used. [/align][align=left]Pathologic fractures are very difficult to treat due to the fact that the bone is very diseased to begin with. Fractures from periodontal disease are usually treated by first extracting the offending tooth, and placing the patient in a soft muzzle. Unfortunately this usually only forms a fibrous and not a bony union. Another option following extraction is to attempt external fixation with pins and bone grafting material, this MAY work, but the prognosis is not good. [/align][/size]

minibabyqq 2006-12-28 00:58

[color=Magenta][size=5][b]ORAL-NASAL FISTULA   [/b][/size][/color]


這通常是牙周疾病的一個先進的形式。它發生當細菌在匾毀壞上部牙的牙周附件和骨頭直到它到達鼻洞。這是最共同在小養殖狗(Daschunds, 約克夏狗, 馬爾祂, 長捲毛狗) 。它通常歸結於嘴的損失在犬齒的palatal (或裡面) 方面。這的原因是牙的根跑沿著鼻洞, 和被分離從它由唯一骨頭稀薄的板料。牙周疾病將毀壞這個結構與正常附件一起為牙。這導致通信在口腔和鼻子之間。細菌在嘴將導致傳染在鼻洞。臨床標誌是慢性鼻放電(血液或pus), 打噴嚏, 和偶爾地厭食和口臭。這些症狀對抗生素經常是部份地敏感, 但不變地將復發當他們被中斷。這綜合症狀可能並且導致由鼻精神創傷, 癌症, 或偶爾地在牙的提取期間。它可能最著名地並且發生次要對其它牙, 門牙。治療的目標是清除被包裝了入瑕疵的殘骸並且結束通信在口頭和鼻洞之間。這由提取觸犯的牙(如果仍然禮物), 和收穫完成齒齦組織擋水板報道瑕疵。這由創造齒齦組織牙的擋水板在頰(或外部) 表面, 和轉動它在瑕疵和縫合做它到位。如果有一個非常大瑕疵, 或唯一擋水板技術失敗, 一個更加包含的雙重擋水板做法可能執行。這由收穫組織擋水板從上顎和轉動它在瑕疵和首先縫合完成到位。然後做一塊更大的擋水板在面頰邊報道瑕疵和面積, palatal 擋水板被收穫了從。這塊擋水板並且被縫合得到位。這更加困難和蔓延性, 但給更強的修理。


口頭腫瘤

口腔是非常共同領域使癌症發生。在狗有許多良性成長, 然而在貓non-malignant 腫瘤的發生是罕見的。它不可能確定是否損害是良性或惡性由簡單地看它。有譬如骨多的入侵(或缺乏因此) 可能建議惡性或良性腫瘤, 但不一致地某個標誌。另外, 惡性腫瘤非常不同地表現, 並且治療然後會是不同的。為這些原因全部口頭損害應該被抽樣和微小地被審查無論良性看起來。

有發生在嘴的許多類型癌症, 但一些是更加共同。在狗, 最共同的良性腫瘤是一epulid 。這是牙周韌帶的一個良性腫瘤。有許多的其它良性成長, 並且他們分享共同興趣他們是通常有好的被定義的房客, don.t 侵略骨頭或其它組織, don.t metastasize (傳播), 和反應很好外科地被去除。貓非常很少有良性成長在嘴。最共同部分是eosinophillic 肉芽腫或匾, 和牙周炎症。eosinophillic 成長反應很好類皮質激素、外科撤除, 或飲食變動; 牙周損害對一顆觸犯的牙的適當的衛生學或可能提取。

有三份共同的口頭敵意在狗和貓。這些是squamous 細胞癌、fibrosarcomas, 和惡性黑瘤。Squamous 細胞癌非常當地是進取的, 然而傾向於後metastasize 如果根本。他們非常共同地將影響部下的骨頭。這顯然是最共同的腫瘤在貓, 和次要共同性在狗。它共同地被發現在更舊的貓和狗作為一個潰瘍的紅色斑點。次要個共同的腫瘤在狗和貓是fibrosarcoma 。這相似地表現與squamous 細胞, 因為它當地是進取的但不傾向於傳播。並且看起來作為紅色成長, 可能是纖維狀或潰瘍的。這經常被看見在更舊的(> 7.5 年) 公大養殖狗。Melanosarcoma 是最共同的腫瘤在狗, 但非常罕見的在貓。這個腫瘤當地蔓延性, 而且metastasizes 及早在疾病路線。通常當它被診斷的時候, 它已經傳播。它最共同地被看見在有黑暗的被著色的口頭mucosa 的更舊的狗。它可能或黑暗或淺灰色。其它腫瘤少有地被看見在狗是一acanthomatous ameleoblastoma 。這個腫瘤當地是進取的, 但不傾向於傳播。有通常不幸地重大相當數量地方破壞當它被診斷的時候, 然而這個腫瘤反應很好進取的外科切除。

有對待口頭 腫瘤的許多技術 在動物中。療法中流砥柱是外科切除。如果這是可能的, 這是達到治療最有效的手段。有手術的重大問題在惡性腫瘤盒是組織的片斷的大小需要被去除。由於這些腫瘤蔓延性, 他們派出腫瘤細胞的手指入正常組織。這不視覺上或幅射線照相地被看見, 和不可以甚而被診斷在顯微鏡下。保證腫瘤的完全撤除, 外科醫生將去除2 cm 法線出現的組織所有在可看見的腫瘤附近。這是大手術! 但是放射治療、cryosurgery (結冰), 和化療所有被使用了單獨或與手術的組合。



This is usually an advanced form of periodontal disease. It occurs when the bacteria in plaque destroy the periodontal attachment and bone of an upper tooth until it reaches the nasal cavity. This is most common in small breed dogs (Daschunds, Yorkshire Terriers, Maltese, Poodles). It is usually due to loss on the palatal (or inside of the mouth) aspect of the canine teeth. The reason for this is the root of the tooth runs up alongside the nasal cavity, and is separated from it by only a thin sheet of bone. The periodontal disease will destroy this structure along with the normal attachment for the tooth. This results in a communication between the oral cavity and the nose. The bacteria in the mouth will cause an infection in the nasal cavity. Clinical signs are chronic nasal discharge (blood or pus), sneezing, and occasionally anorexia and bad breath. These symptoms are often partially responsive to antibiotics, but will invariably recur when they are discontinued. This syndrome can also be caused by nasal trauma, cancer, or occasionally during extraction of a tooth. It can also occur secondary to other teeth, most notably the incisors.The goal of treatment is to clean out the debris that has been packed into the defect and close the communication between the oral and nasal cavities. This is accomplished by extracting the offending tooth (if still present), and harvesting a flap of gingival tissue to cover the defect. This is done by creating a flap of gingival tissue on the buccal (or outside of the tooth) surface, and rotating it over the defect and suturing it in place. If there is a very large defect, or the single flap technique fails, a more involved double flap procedure can be performed. This is accomplished by first harvesting a flap of tissue from the palate and rotating it over the defect and suturing in place. Then make a larger flap on the cheek side to cover the defect and the area that the palatal flap was harvested from. This flap is also sutured in place. This is more difficult and invasive, but gives a much stronger repair.

ORAL TUMORS

The oral cavity is a very common area for cancer to occur. In dogs there are numerous benign growths, however in cats the incidence of non-malignant tumors is rare. It is impossible to determine whether a lesion is benign or malignant by simply looking at it. There are some signs such as bony invasion (or lack thereof) that can suggest malignant or benign tumors, but not consistently. In addition, malignant tumors behave very differently, and the treatment would then be different as well. For these reasons all oral lesions should be sampled and microscopically examined no matter how benign it appears.

There are many types of cancer that occur in the mouth, but some are much more common. In dogs, the most common benign tumor is an epulid. This is a benign tumor of the periodontal ligament. There are numerous other benign growths as well, and they share in common that they are usually have well defined boarders, don㦙 invade the bone or other tissues, don㦙 metastasize (spread), and respond well to being surgically removed. Cats very rarely have benign growths in the mouth. The most common ones are eosinophillic granulomas or plaques, and periodontal inflammation. The eosinophillic growths respond well to corticosteroids, surgical removal, or diet change; the periodontal lesions to proper hygiene or possibly extraction of an offending tooth.

There are three common oral malignancies in dogs and cats. These are squamous cell carcinoma, fibrosarcomas, and malignant melanomas. Squamous cell carcinomas are very locally aggressive, however tend to metastasize late if at all. They will very commonly affect the underlying bone. This is by far the most common tumor in cats, and the second most common in dogs. It is commonly found in older cats and dogs as an ulcerated red spot. The second most common tumor in dogs and cats is fibrosarcoma. This behaves similarly to squamous cell, in that it is locally aggressive but does not tend to spread. It also appears as a red growth, which can be fibrous or ulcerated. This is often seen in older (>7.5 years) male large breed dogs. Melanosarcoma is the most common tumor in dogs, but very rare in cats. This tumor is locally invasive, but also metastasizes early in the disease course. Usually by the time it is diagnosed, it has already spread. It is most commonly seen in older dogs that have dark pigmented oral mucosa. It can either be dark or light gray. Another tumor seen infrequently in dogs is an acanthomatous ameleoblastoma. This tumor is locally aggressive, but does not tend to spread. Unfortunately there is usually a significant amount of local destruction by the time it is diagnosed, however this tumor responds well to aggressive surgical excision.

There are numerous techniques for treating oral tumors in animals. The mainstay of therapy is surgical excision. If this is possible, it is the most effective means of achieving a cure. The major problem with surgery in malignant tumor cases is the size of the piece of tissue that needs to be removed. Because these tumors are invasive, they send out fingers of tumor cells into the normal tissue. This cannot be seen visually or radiographically, and may not even be diagnosed under the microscope. To ensure complete removal of the tumor, the surgeon will remove 2 cm of normal appearing tissues all around the visible tumor. This is a large surgery! However radiation therapy, cryosurgery (freezing), and chemotherapy have all been used alone or in combination with surgery

minibabyqq 2006-12-28 00:59

[color=Magenta][size=5][b]正牙學器具 ORTHODONTIC APPLIANCES  [/b][/size][/color]


正牙學器具


有許多正牙學器具的形式根據類型問題和操作員特選。以下治療是什麼我發現了工作很好, 然而有許多其它可接受的方法為大多這些問題。

先前crossbite 被對一臺上頷骨擴展器的用途通常改正。這是在極小值三階段做法。在第一參觀期間患者被評估和沉著。整體嘴印象被採取, 和被送到正牙學實驗室為器具的製造。第二次參觀是為器具和指示所有者的黏接關於怎樣調整器具。所有者調整器具直到牙是在正確位置。然後器具被留下到位時期作為保留。這通常不是長的在這些情況下因為重疊牙可能作為一個自然保留。然後患者沉著並且器具被去除並且牙被清洗。曲拱酒吧和有彈性ligatures 或斜面飛機可能被使用以好成功。

Mesial 被打翻的上部犬 (長矛作用) 通常被對待通過橡皮筋。患者沉著並且正牙學托架附有犬並且後部牙(作為船錨為運動) 。經常幾顆牙包括在定住, 或可能導線裡在上頷骨骨頭, 或可能extraoral 船錨(頭飾裡) 。正牙學彈性被舒展在牙之間刺激運動。彈性通常是變動由所有者沒有鎮靜。當牙是在正確位置, 保留階段接著而來避免牙行動回到它的原始位置。

基本的狹窄的犬 orthodontically 被對待通過斜面飛機。這運作在做一個基地旁邊在上顎在上部犬之間和批轉對上部門牙, 和然後創造一條凹線開始在觸犯的牙或牙碰撞上顎的地方, 並且指揮牙對正確地方在嘴。力量是應用的當動物關閉他的嘴。這種器具可能被創造在animal.s 嘴或在模型由一個牙齒實驗室。


正牙學問題

正牙學問題變得流行在我們的狗和貓主要由於有選擇性養殖。他們能發生在任一養殖和在混雜的養殖狗。影響下頜的大小的多數正牙學問題被認為基因, 和受影響的動物不應該被使用為養殖。此時, 牙地點瑕疵唯一被認為non-genetic, 和也許被對待。這也許改變如同更多研究完成。AVMA 和ACVD 的標準是, 所有動物有資格獲得一張健康嘴, 但不是一張完善的嘴。美學不被認為重要在我們的pet.s 牙裡, 除非他們被使用在展示圓環。如果這是實際情形, 嘴通常然後被改正贏取展示。最終目標養殖患者為贏利。因而, 瑕疵傳遞到一個新世代。這就是為什麼標準被寫, 並且改正他們是危害我們的患者。這意味著, 不造成任何衛生問題的咬合不良不應該是固定的, 因為多數正牙學更正是長期和要求許多麻醉的規程。哪些不是在patient.s 最大興趣。如果一個基因問題的正牙學更正被選舉, 患者應該然後是spayed 或閹割了。

這認為那裡是時期, 正牙學更正是在我們的patient.s 最大興趣。

被對待的最共同的正牙學問題是被保留的落葉牙、基地狹窄, crossbite, 被超越的和下前牙突出, 和扭曲的叮咬。

最共同的正牙學問題在小動物患者是被保留的落葉牙。這是特別共同在小養殖狗(馬爾祂, 約克夏狗, 和長捲毛狗) 。乳齒exfoliate 的許多原因的當中一個是, 成人牙施加壓力在乳齒的基地和導致根結構的吸回。在這些情況下, 成人牙正確地不排隊與落葉牙; 因此沒有壓力使乳齒出來。這將導致成人牙偏離對邊, 和有二顆牙那裡。這是一個問題為幾個原因。首先, 成人牙可能噴發入將導致或軟的組織或牙精神創傷的區域。其次, 它可能導致在牙周疾病的增量在區域。這歸結於正常分離的損失在牙之間, 並且事實periodontium 不被允許正確地形成。畸形的periodontium 非常及早將發生(幾天) 在成人牙噴發之後。這不意味充分的爆發, jut, 成人牙能被看見在gumline 之上。這將導致匾和結石組合在區域。終於, 成人牙也許成為衝擊。這個情況由interceptive 畸齒矯正術( 落葉牙的提取) 對待。這應該做當成人牙是看的噴發避免許多問題儘可能。

其它共同的問題是基本的狹窄的更低的犬。這可能歸結於牙或下頜問題。牙品種可能由被保留的落葉更低的犬造成。這歸結於事實成人犬噴發舌(或裡面) 落葉犬。落葉牙將導致成人犬偏離在內。如果有被保留的落葉犬或患者是基本的狹窄以它的落葉齒列, interceptive 畸齒矯正術應該儘快執行有希望地避免問題。成人犬的舌偏差通常將導致palatine 精神創傷和患者難受。下頜品種歸結於一個基因上狹窄的下頜。有二種方式對待這個情況。如果咬合不良是輕微的(通常牙問題), 然後 斜面飛機 或其它正牙學更正可能推出牙。如果問題是適度的對嚴厲, 或有保險設備與上部犬, 那麼 冠截肢術和黏漿狀物質加蓋 通常是最佳的選擇。扭曲的叮咬, 下頜二個一半don.t 增長以同樣率可能並且導致這個問題, 和 冠截肢術 被表明解除軟的組織精神創傷。我們的經驗是非常不報答的在orthodontically 對待扭曲的叮咬。

下前牙突出(更長的更低的下頜) 並且超越(更長的上部下頜) 是共同的問題。下前牙突出的下頜可能是Normal. 為某些養殖(波斯貓、拉薩Apso, 公牛狗, 等。這些情況可能造成問題通過考慮到軟的組織精神創傷由犬是在適當的對準線。被超越的下頜可能導致更低的犬碰撞上部犬或上顎。嚴厲下前牙突出的下頜可能導致嘴唇精神創傷。如果瑕疵是溫和和捉住足夠及早, 問題也許被避免。有時, 下頜差誤只將是臨時的, 並且下頜將想要改正隨時間。但是, 牙齒保險設備不會允許下頜行動。因此, 如果這被發現足夠及早, interceptive 畸齒矯正術 可能由提取執行落葉牙。這將允許下頜行動如果他們要對, 但不會做他們做如此。如果患者已經有它的永久齒列正牙學治療是困難的對不可能。如果牙導致口頭精神創傷, 然後 加冠截肢術並且黏漿狀物質加蓋 是選擇的治療。

Rostrally 被偏移的上部犬由一被保留的落葉上部似犬造成或可能是基因在自然裡。這主要被看見在Shetland sheepdogs 。這可能導致牙周疾病, 並且牙損耗從觸擊更低的牙。這可能被正牙學 帶 改正被牙 、截肢術和黏漿狀物質的提取加蓋 , 或。如果這基因, 患者應該被閹割在執行正牙學更正前。

擁擠並且/或者被轉動的牙共同地被看見在小養殖狗, 特別是bracheocephalic 養殖。他們造成的重大問題是, 他們很大地增加牙周疾病在區域。這些orthodontically 一般不被對待, 然而 提取 他們可能改進動物的整體牙周健康。

先前crossbite 是上部門牙噴發在更低的門牙之後的地方。這通常不是一個問題為患者, 照原樣通常reverse 剪刀和舒適的。這可能被正牙學 器具改正 如果它歸結於牙問題。如果這是下頜問題, 這將是更加困難的並且患者應該被閹割在這個長的過程之前。

後部發怒叮咬是上部第四顆前臼齒是在更低的第一槽牙裡面的地方。這是最共同在大牧羊犬。這個瑕疵的更正是非常困難的和通常不是必要的因為牙適當地起作用在他們的新對準線。There are many forms of orthodontic appliances depending on the type of problem and operator preference. The following treatments are what I have found work well, however there are many other acceptable methods for most of these problems.

Anterior crossbite is usually corrected by the use of a maxillary expander. This is at minimum a three-stage procedure. During the first visit the patient is evaluated and sedated. Whole mouth impressions are taken, and sent to the orthodontic laboratory for fabrication of the appliance. The second visit is for cementation of the appliance and instructing the owner on how to adjust the appliance. The owner adjusts the appliance until the teeth are in the correct position. Then the appliance is left in place for a period of time as a retainer. This is usually not long in these cases as the overlapping of the teeth can act as a natural retainer. Then the patient is sedated and the appliance is removed and the teeth cleaned. Arch bars and elastic ligatures or incline planes can be used as well with good success.

Mesial tipped upper canines (Lance effect) is usually treated by means of elastic bands. The patient is sedated and orthodontic brackets are attached to the canine as well as posterior teeth (to act as an anchor for movement). Often several teeth are included in the anchorage, or possibly wires in the maxillary bone, or possibly extraoral anchors (headgear). Orthodontic elastics are stretched between the teeth to stimulate movement. The elastics are change by the owner usually without sedation. When the tooth is in the correct position, the retention period ensues to avoid the tooth moving back to its original position.

Base narrow canines are orthodontically treated by means of an incline plane. This works by making a base over the palate between the upper canines and forward to the upper incisors, and then creating a groove starting at where the offending tooth or teeth strike the palate, and directing the teeth to the correct place in the mouth. The force is applied when the animal closes his mouth. This appliance can be created in the animal𠏋 mouth or on models by a dental lab.


Before


During


After


The advantages to creating the appliance in the mouth are that it is done in one anesthetic procedure and is slightly less expensive. The advantages to the laboratory-fabricated appliance are that there is less irritation to the palate, and that the appliance can be made to expand to allow the patient to grow. When the tooth is in the right position the appliance is removed and the palate acts as a natural retainer. An expansion device can be made to fit between the lower canines to push them out as well.

Posterior crossbite and rotated teeth are very difficult to treat orthodontically and therefore will not be covered on this page.


ORTHODONTIC PROBLEMS

Orthodontic problems are becoming more prevalent in our dogs and cats mostly due to selective breeding. They can occur in any breed and in mixed breed dogs as well. Most orthodontic problems that effect the size of the jaw are considered genetic, and the affected animals should not be used for breeding. At this time, defects of tooth location only are considered non-genetic, and may be treated. This may change as more studies are done. The standards of the AVMA and ACVD are that all animals are entitled to a healthy mouth, but not a perfect mouth. Aesthetics are not considered important in our pet𠏋 teeth, unless they are used in the show ring. If this is the case, then the mouth is usually being corrected to win shows. The ultimate goal to breed the patient for profit. Thus, the defect is passed on to a new generation. This is why the standards are written, and to correct them is to harm our patients. This means that a malocclusion that is not causing any health problems should not be fixed, as most orthodontic corrections are long term and require numerous anaesthetic procedures. Which is not in the patient𠏋 best interest. If orthodontic correction of a genetic problem is elected, then the patient should be spayed or neutered.

This being said there are times that orthodontic correction is in our patient𠏋 best interest.

The most common orthodontic problems that are treated are retained deciduous teeth, base narrow, crossbite, overshot and undershot, and wry bite.

The most common orthodontic problem in small animal patients is retained deciduous teeth. This is especially common in small breed dogs (Maltese, Yorkshire terriers, and poodles). One of the many reasons the baby teeth exfoliate is that the adult tooth puts pressure on the base of the baby tooth and causes resorption of the root structure. In these cases, the adult tooth does not line up correctly with the deciduous tooth; therefore there is no pressure for the baby tooth to come out. This will cause the adult tooth to be deviated to the side, and have two teeth there. This is a problem for several reasons. First, the adult tooth can erupt into an area that will cause either soft tissue or tooth trauma. Second, it can cause an increase in periodontal disease in the area. This is due to the loss of the normal separation between teeth, as well as the fact that the periodontium is not allowed to form correctly. The malformed periodontium will occur very early (days) after the adult tooth erupts. This does not mean full eruption, jut that the adult tooth can be seen above the gumline. This will cause build up of plaque and calculus in the area. Finally, the adult tooth may become impacted. This condition is treated by interceptive orthodontics (extraction of the deciduous tooth). This should be done as soon as the adult tooth is seen erupting to avoid as many of the problems as possible.

Another common problem is base narrow lower canines. This can be due to a tooth or jaw problem. The tooth variety can be caused by retained deciduous lower canines. This is due to the fact that the adult canines erupt lingual (or inside) the deciduous canines. The deciduous tooth will cause the adult canines to deviate inwards. If there are retained deciduous canines or the patient is base narrow with its deciduous dentition, interceptive orthodontics should be performed as soon as possible to hopefully avoid the problem. The lingual deviation of the adult canines will usually cause palatine trauma and patient discomfort. The jaw variety is due to a genetically narrow jaw. There are two ways to treat this condition. If the malocclusion is slight (usually a tooth problem), then an incline plane or other orthodontic correction can push out the teeth. If the problem is moderate to severe, or there is interlock with the upper canines, then crown amputation and pulp capping is usually the best choice. A wry bite, where the two halves of a jaw don㦙 grow at the same rate can also cause this problem, and crown amputation is indicated to relieve soft tissue trauma. Our experience has been very unrewarding in treating wry bite orthodontically.

Undershot (longer lower jaw) and overshot (longer upper jaw) are common problems as well. Undershot jaws can be 幞ormal?for certain breeds (Persian cats, Lhasa Apso, bull dogs, etc. These conditions can cause problems by allowing for soft tissue trauma by the canines not being in the proper alignment. Overshot jaws can cause the lower canines to strike the upper canine or palate. Severe undershot jaws can cause lip trauma. If the defect is mild and caught early enough, the problem may be avoided. Sometimes, the jaw discrepancy will only be temporary, and the jaws will want to correct over time. However, the dental interlock will not allow the jaw to move. For this reason, if this is discovered early enough, interceptive orthodontics can be performed by extracting the deciduous teeth. This will allow the jaws to move if they want to, but will not make them do so. If the patient already has its permanent dentition orthodontic treatment is difficult to impossible. If the teeth are causing oral trauma, then crown amputation and pulp capping is the treatment of choice.

Rostrally displaced upper canines can be caused by a retained deciduous upper canine or can be genetic in nature. This is mostly seen in Shetland sheepdogs. This can cause periodontal disease, as well as tooth attrition from striking the lower teeth. This can be corrected by extraction of the tooth, amputation and pulp capping, or by orthodontic bands. If this is genetic, the patient should be neutered prior to performing orthodontic correction.

Crowded and/or rotated teeth are commonly seen in small breed dogs, especially the bracheocephalic breeds. The major problem they cause is that they greatly increase periodontal disease in the area. These are generally not orthodontically treated, however extracting them can improve the overall periodontal health of the animal.

Anterior crossbite is where the upper incisors erupt behind the lower incisors. This is usually not a problem for the patient, as it is usually a 𩂈everse scissors?and comfortable. This can be corrected by orthodontic appliance if it is due to a tooth problem. If it is a jaw problem, this will be much more difficult and the patient should be neutered prior to this lengthy process.

Posterior cross bite is where the upper fourth premolar is inside the lower first molar. This is most common in collies. Correction of this defect is very difficult and is usually not necessary as the teeth function properly in their new alignment.

minibabyqq 2006-12-28 01:00

[color=Magenta][b][size=5]牙周疾病 PERIODONTAL DISEASE  [/size][/b][/color]

[size=12px]牙周疾病

[align=left]牙周疾病發生當細菌從嘴形成在牙在物質叫做匾。匾做it.s 方式在gumline 之下和設置在行動惡性循環, 可能最終導致牙損失。細菌在subgingival 匾將藏匿毒素。這些毒素損壞牙周組織, 可能減少附件。但是, 細菌並且將得出一個激動反應從animal.s 齒齦組織。白細胞和其它激動斡旋人將漏在牙周組織外面和入牙周空間(在膠或去骨和牙之間) 。白細胞將發布他們的酵素毀壞細菌侵略者, 但並且將損壞牙的附件。因為這進步, 口袋將得到越□越深。這將減弱骨頭在區域, 和如果它是在更低的下頜它可能減弱它對點導致 [b][i]病理性破裂[/i][/b]。這是最共同在更舊的小養殖狗。這種疾病末端階段是牙損失, 然而疾病造成了問題很好在這之前。

炎症在允許body.s 防禦並且攻擊侵略者的齒齬允許那些侵略者對身體能夠存取。細菌從嘴可能進入血液和運載對身體。研究表示, 這些細菌將由腎臟和肝臟過濾掉, 並且可能導致microabscesses 在這些器官。這導致在這些重要器官的作用的減退在時間期間。另外, 它被建議, 這些細菌可能成為附有心臟瓣膜和導致疾病叫做心內膜炎。另外, 身體必須每天處理這些細菌, 導致慢性疾病狀態。[/align][align=left]牙周疾病的治療是二到三有叉的攻擊。第一步是一 [b][i]詳盡的牙齒預防[/i][/b] 包括繪製和治療計劃。如果沒有當前的牙周口袋, 這將是唯一的治療必要。其次和最重要 [b][i]家庭關心[/i][/b]。這很大地將增加患者的牙周健康, 並且減退專業清潔頻率。如果您有一隻幼小寵物(少於1 年) 您能通常開始以homecare, 首先咨詢您的獸醫。如果您的患者已經有結石, 那麼專業清潔必需允許家庭關心是有效的。如果有當前的牙周疾病, 那麼 [b][i]牙周手術[/i][/b] 也許試圖保存牙。但是, 患者整體健康、費用, 和所有者服從必須被考慮到在做任一牙周手術前。沒有homecare, 牙周手術不應該可能試圖, 並且被介入的牙被提取。[/align][b]PERIODONTAL DISEASE[/b]
[align=left][table=90%][tr][td=2,1,75%][align=left]Periodontal disease occurs when bacteria from the mouth form on the teeth in a substance called plaque. The plaque makes it𠏋 way under the gumline and sets in motion a vicious circle, which can eventually lead to tooth loss. The bacteria in the subgingival plaque will secrete toxins. These toxins damage the periodontal tissues and can decrease the attachment. However, the bacteria will also elicit an inflammatory response from the animal𠏋 gingival tissues. White blood cells and other inflammatory mediators will leak out of the periodontal tissues and into the periodontal space (between the gum or bone and the tooth). The white blood cells will release their enzymes to destroy the bacterial invaders, but will also damage the attachment of the tooth. As this progresses, the pocket will get deeper and deeper. This will weaken the bone in the area, and if it is in the lower jaw it can weaken it to the point of causing a [b][i]pathologic fracture[/i][/b]. This is most common in older small breed dogs. The end stage of this disease is tooth loss, however the disease has caused problems well before this.

The inflammation in the gingiva that allows the body𠏋 defenses to attack the invaders also allows those invaders to gain access to the body. The bacteria from the mouth can enter the bloodstream and be carried to the bodies. Studies have shown that these bacteria will be filtered out by the kidney and liver, and can cause microabscesses on these organs. This leads to a decrease in function of these vital organs over time. In addition, it has been suggested that these bacteria can become attached to the heart valves and cause a disease called endocarditis. In addition, the body must deal with these bacteria on a daily basis, leading to a state of chronic disease.[/align][align=left]Treatment of periodontal disease is a two to three pronged attack. The first step is a [b][i]thorough dental prophylaxis[/i][/b] including charting and treatment planning. If there is no current periodontal pockets, this will be the only treatment necessary. Next and most important is [b][i]home care[/i][/b]. This will greatly increase the periodontal health of the patient, as well as decrease the frequency of professional cleanings. If you have a young pet (less than 1 year) you can usually start with homecare, however consult your veterinarian first. If your patient has calculus already, then a professional cleaning is required to allow home care to be effective. If there is current periodontal disease, then [b][i]periodontal surgeries[/i][/b] may be attempted to save the teeth. However, the patients overall health, cost, and owners compliance must be taken into account prior to performing any periodontal surgery. Without homecare, periodontal surgery should likely not be attempted, and involved teeth extracted.
[/align][/td][td=1,1,25%][align=center][img=205,155]http://www.avds-online.org/images/resourceimages/periodontaldisease1.jpg[/img]
Periodontal disease associated with the upper canine teeth in cats often produce expansion of the buccal bone and extrusion of the canine tooth coronally.[/align][align=center][img=205,155]http://www.avds-online.org/images/resourceimages/periodontaldisease2.jpg[/img]
Significant tartar associated with overcrowded teeth in a dog.[/align][align=center][img=205,150]http://www.avds-online.org/images/resourceimages/periodontaldisease3.jpg[/img]
Proliferative gingival associated with periodontal disease. These lesions should always be biopsied to rule out neoplasia.[/align][/td][/tr][tr][td=1,1,38%][align=center][img=205,177]http://www.avds-online.org/images/resourceimages/periodontaldisease4.jpg[/img]
Periodontal disease has destroyed the bone associate with this mandibular premolar and molar.[/align][/td][td=1,1,37%][align=center][img=205,155]http://www.avds-online.org/images/resourceimages/periodontaldisease5.jpg[/img]
Bone loss at the furcation of the maxillary fourth premolar is common in advanced periodontal disease in this location.[/align][/td][td=1,1,25%][img=205,155]http://www.avds-online.org/images/resourceimages/periodontaldisease6.jpg[/img]
Plaque, tartar, gum recession and severe gum edema and hyperemia indicative of advanced periodontal disease are present in this patient.
[/td][/tr][/table][/align][/size]

minibabyqq 2006-12-28 01:01

[color=Magenta][size=5][b]先天心臟病疾病體檢Congenital Cardiac Disease Physical Exam  [/b][/size][/color]

[size=12px][color=#000000]心臟病檢查[/color]臨床心臟病考試應該被舉辦以系統的方式。動脈和多血脈性的脈衝、黏膜, 和precordium 應該被評估。心率應該被獲得。臨床考試應該由個體執行以先進的訓練在心臟病診斷。
上證明由獸醫內科美國學院, 心臟病學專業由美國獸醫醫療協會考慮作為臨床熟練的基準為獸醫在臨床心臟病學方面, 並且考試由這個專業委員會Diplomate 被推薦。其它獸醫也許能執行這些考試, 假設他們接受了先進的訓練在subspecialty 先天心臟病。
[b][color=#003399]Ascultation[/color][/b][color=#003399][/color]心臟病聽診應該進行在一個安靜, 無分心環境。動物應該是常設和克制, 但鎮靜劑應該被避免。氣喘必須是受控的並且如果需要, 狗應該被給時刻休息和順應對環境。臨床工作者如果能辨認心臟病閥門區域為聽診。稽查應該逐漸移動聽診器橫跨所有閥門區域和應該還auscultate 在subaortic 區域、上升的主動脈、肺動脈, 和左craniodorsal 心臟病基地。從事左precordium 的考試, 正確的precordium 應該被審查。 [list][*]二尖瓣區域被找出和立刻背部對可觸知的左頂端衝動和由觸診辨認以手指的要訣。聽診器然後被安置在僧帽形的區域和心音被辨認。[*]動脈閥區域是背部和1 或2 肋間的空間頭蓋骨在頂端衝動左面。第二心音將是最強烈的當聽診器被集中在動脈閥區域。私語起源於或放熱對聽診subaortic 範圍是顯然立刻caudoventral 對動脈閥區域。私語起源於或放熱入上升的主動脈將是顯然craniodorsal 對動脈閥, 也許並且射出對正確的頭蓋骨胸部和對頸動脈在脖子。[*]pulmonic 閥門區域是腹和一肋間的空間頭蓋骨對動脈閥區域。私語起源於或放熱入主要肺動脈將是顯然背對pulmonic 閥門在左hemithorax 。[*]tricuspid 閥門區域是一個相對地大區域位於正確的hemithorax, 對面和輕微地頭蓋骨對二尖瓣區域。[*]臨床工作者應該並且auscultate 沿腹正確的precordium (正確的sternal 疆界) 並且是正確的craniodorsal 心臟病疆界。[*]所有心臟病私語或反常聲音應該是著名。私語應該被描述依照下面被表明。[/list][b][color=#003399]心臟病私語的描述[/color][/b][color=#003399][/color]心臟病私語的一個完整描述如果做和記錄在病歷。 [list][*]私語應該被選定作為心臟收縮, 舒張, 或連續。[*]點最大的私語強度應該被表明如上所述。當precordial 興奮是可觸知的, 私語一般將是最強烈的在這振動。[*]私語斷斷續續地只被查出得或是易變的應該是因此表明了。[*]私語的輻射應該被表明[/list][b][color=#003399]心率、心臟節奏, 和鍛煉的作用 [/color][/b][color=#003399][/color]一些心臟私語變得顯然或大聲以變化在自主神經系統的活動、心率, 或心臟病週期長度上。這樣變動也許被鍛煉或其他導致重音。評估心臟私語的重要性在鍛煉以後當前是未解決的。看起來, 一些狗以先天subaortic 狹窄或以動態流出短文阻礙也許有只變得顯然以增加的有同情心的活動的私語或在長時期的心臟病填裝的期間在明顯靜脈竇心率失常期間它應該還注意到之後, 一些正常, 無辜的心臟私語也許增加在強度在鍛煉以後。此外, 氣喘人工製品也許是一個問題在鍛煉以後。 它是很可能審查狗在鍛煉導致增加的敏感性對軟的私語但大概被減少的特異性診斷之後。心臟隨後而來的鍛煉的聽診是在審查的獸醫的謹慎。
此時OFA 不要求一次崗位鍛煉考試在對心臟私語的評估在狗; 但是, 這實踐也許被修改如果明確的資訊變得可利用。

Echocardiographic 檢查echocardiographic 考試應該被舉辦在一件系統的事情。稽查必須能執行二維, 搏動揮動多譜勒儀, 和連續波心臟的多譜勒儀考試。顏色多譜勒儀的可及性是可貴但不根本的為多數考試。echocardiographic 考試應該由個體執行和解釋以先進的訓練在心臟病診斷。
上證明由獸醫內科美國學院, 心臟病學專業由獸醫醫療協會美國學院考慮作為臨床熟練的基準為獸醫在臨床心臟病學方面, 並且考試由這個專業委員會Diplomate 被推薦。其它獸醫也許能執行這些考試提供了他們有適當的設備和接受了先進的訓練在echocardiography 方面。
想像pericardial 空間、兩心房、兩個心室、偉大的船, 和四個心臟病閥門當有必要應該是印象的使用長的軸, 短軸, 頂端, 和有角度的圖像飛機執行心臟的一次完全考試。命名原則應該跟隨那由心臟病學獸醫內科專業美國學院推薦。一個解剖診斷也許是可能的根據二維想像; 但是, 心臟病私語的起源應該並且被評估運用多譜勒儀方法。
多譜勒儀
所有心臟病閥門的多譜勒儀考試應該執行和被記錄。反常流程應該被定量使用搏動的波浪或連續波多譜勒儀技術。價值被獲得應該與參考價值比較。所有鎮定藥的抑制作用或鎮靜劑必須被考慮當測量高峰流程速度。顏色多譜勒儀echocardiography 應該被使用如果可利用估計正常和反常血流樣式。反常流程橫跨心臟病中隔或分流器的證明在偉大的船的水平是最佳由顏色和搏動的波浪多譜勒儀技術的組合完成。典型的echocardiographic 特點共同先天
心臟瑕疵被表明在表一個。
評估特別留意應該被指揮對對流程樣式和速度的評估在左心室出口和下降的主動脈。優選的對準線以血流應該被尋找使準確速度被報告。這也許要求對sub-xiphoid (subcostal) 變換裝置的用途
位置並且左頂端(尾部parasternal) 變換裝置安置。除高峰速度的測量之外使用搏動的或顏色波浪多譜勒儀, 搏動的波浪樣品容量應該逐漸被推進從subaortic 區域入acsending 的主動脈為了辨認突然的加速度在流程速度、動盪, 或大動脈反流。
錄影帶Echocardiographic 研究應該被報告關於錄影帶為隨後分析並且反常研究結果一個書面紀錄應該被輸入病歷。
Echocardiographic 研究結果 [table=98%][tr][size=2][color=#ffffff]先天不足[/color][/size][size=2][color=#ffffff]典型的Auscultatory 特點[/color][/size][size=2][color=#ffffff]診斷Echocardiographic 和多譜勒儀Echocardiographic 特點[/color][/size][/tr][tr][td]專利ductus arteriosus[/td][td]連續的心臟私語以最大的強度在左頭蓋骨背部心臟病基地[/td][td]連續倒退流程從專利ductus arteriosus 入肺動脈[/td][/tr][tr][td]心室氏族的瑕疵[/td][td]心臟收縮的私語以最大的強度在正確的腹precordium; 較不經常最大的強度是在pulmonic 閥門區域和肺動脈[/td][td]氏族的瑕疵可能經常是印象的在多架想像飛機裡。反常, 一般高速度, 心臟收縮的流程橫跨氏族的瑕疵是顯然的。[/td][/tr][tr][td]Atrial 氏族的瑕疵[/td][td]心臟收縮的私語以最大的強度在pulmonic 閥門區域和肺動脈。第二心音也許廣泛被分裂[/td][td]氏族的瑕疵可能一般是印象的在多架想像飛機裡。反常血流也許被辨認橫跨氏族的瑕疵入正確的心房。[/td][/tr][tr][td]Pulmonic 狹窄[/td][td]心臟收縮的私語以最大的強度在pulmonic 閥門區域和肺動脈[/td][td]反常肺閥門和/or subvalvular 解剖學。血流的突然的加速度在正確的心室出口以動盪, 高速度心臟收縮的流程橫跨肺閥門和入主要肺動脈。[/td][/tr][tr][td]Valvular 和subvalvular 大動脈狹窄[/td][td]心臟收縮的私語以最大的強度在subaortic 或動脈閥區域和放熱入上升的主動脈。私語也許並且是突出的在正確的頭蓋骨胸部。[/td][td]反常subvalvular 或大動脈valvular 解剖學也許是顯然的。血流的突然的加速度入左心室流出短文以動盪, 高速度心臟收縮的流程橫跨動脈閥和入上升的主動脈。一致大動脈反流通常是存在。[/td][/tr][tr][td]二尖瓣發育異常[/td][td]心臟收縮的私語以最大的強度在左尖頂和僧帽形的區域[/td][td]二尖瓣用具的反常解剖學。高速度後退心臟收縮的流程橫跨二尖瓣入左心房。一致二尖瓣狹窄也許是存在。[/td][/tr][tr][td]Tricuspid 閥門發育異常[/td][td]心臟收縮的私語以最大的強度在tricuspid 閥門區域[/td][td]tricuspid 閥門用具的反常解剖學。高速度後退心臟收縮的流程橫跨tricuspid 閥門入正確的心房。一致tricuspid 閥門狹窄也許是存在。[/td][/tr][tr][td]正確對左心臟病分流器[/td][td]可變物—一句心臟收縮的私語在左基地經常被查出; 青紫是一個重要臨床標誌[/td][td]反常解剖學與例子有的心臟病畸形關係了: Fallot, 專利ductus arteriosus 四聯劇以肺高血壓, 肺或tricuspid 閥門狹窄以atrial 氏族的瑕疵。正確對左邊轉軌可以相反echocardiography 提供靠多譜勒儀技術並且/或者。[/td][/tr][/table][color=#000000]The Cardiac Exam[/color]The clinical cardiac examination should be conducted in a systematic manner. The arterial and venous pulses, mucous membranes, and precordium should be evaluated. Heart rate should be obtained. The clinical examination should be performed by an individual with advanced training in cardiac diagnosis.
Board certification by the American College of Veterinary Internal Medicine, Specialty of Cardiology is considered by the American Veterinary Medical Association as the benchmark of clinical proficiency for veterinarians in clinical cardiology, and examination by a Diplomate of this specialty board is recommended. Other veterinarians may be able to perform these examinations, provided they have received advanced training in the subspecialty of congenital heart disease.
[b][color=#003399]Ascultation[/color][/b][color=#003399][/color]Cardiac auscultation should be performed in a quiet, distraction-free environment. The animal should be standing and restrained, but sedative drugs should be avoided. Panting must be controlled and if necessary, the dog should be given time to rest and acclimate to the environment. The clinician should able to identify the cardiac valve areas for auscultation. The examiner should gradually move the stethoscope across all valve areas and also should auscultate over the subaortic area, ascending aorta, pulmonary artery, and the left craniodorsal cardiac base. Following examination of the left precordium, the right precordium should be examined. [list][*]The mitral valve area is located over and immediately dorsal to the palpable left apical impulse and is identified by palpation with the tips of the fingers. The stethoscope is then placed over the mitral area and the heart sounds identified.[*]The aortic valve area is dorsal and 1 or 2 intercostal spaces cranial to the left apical impulse. The second heart sound will be most intense when the stethoscope is centered over the aortic valve area. Murmurs originating from or radiating to the subaortic area of auscultation are evident immediately caudoventral to the aortic valve area. Murmurs originating from or radiating into the ascending aorta will be evident craniodorsal to the aortic valve and may also project to the right cranial thorax and to the carotid arteries in the neck.[*]The pulmonic valve area is ventral and one intercostal space cranial to the aortic valve area. Murmurs originating from or radiating into the main pulmonary artery will be evident dorsal to the pulmonic valve over the left hemithorax.[*]The tricuspid valve area is a relatively large area located on the right hemithorax, opposite and slightly cranial to the mitral valve area.[*]The clinician should also auscultate along the ventral right precordium (right sternal border) and over be right craniodorsal cardiac border.[*]Any cardiac murmurs or abnormal sounds should be noted. Murmurs should be described as indicated below.[/list][b][color=#003399]Description of Cardiac Murmurs[/color][/b][color=#003399][/color]A full description of the cardiac murmur should made and recorded in the medical record. [list][*]Murmurs should be designated as systolic, diastolic, or continuous.[*]The point of maximal murmur intensity should be indicated as described above. When a precordial thrill is palpable, the murmur will generally be most intense over this vibration.[*]Murmurs that are only detected intermittently or are variable should be so indicated.[*]The radiation of the murmur should be indicated[/list][b][color=#003399]Effects of heart rate, heart rhythm, and exercise [/color][/b][color=#003399][/color]Some heart murmurs become evident or louder with changes in autonomic activity, heart rate, or cardiac cycle length. Such changes may be induced by exercise or other stresses. The importance of evaluating heart murmurs after exercise is currently unresolved. It appears that some dogs with congenital subaortic stenosis or with dynamic outflow tract obstruction may have murmurs that only become evident with increased sympathetic activity or after prolonged cardiac filling periods during marked sinus arrhythmia It also should be noted that some normal, innocent heart murmurs may increase in intensity after exercise. Furthermore, panting artifact may be a problem after exercise. It is most likely that examining dogs after exercise will result in increased sensitivity to diagnosis of soft murmurs but probably decreased specificity as well. Auscultation of the heart following exercise is at the discretion of the examining veterinarian.
At this time the OFA does not require a post exercise examination in the assessment of heart murmurs in dogs; however, this practice may be modified should definitive information become available.

[color=#000000]The Echocardiographic Exam[/color]The echocardiographic examination should be conducted in a systematic matter. The examiner must be able to perform two-dimensional, pulsed-wave Doppler, and continuous wave Doppler examinations of the heart. The availability of color Doppler is valuable but not essential for most examinations. The echocardiographic examination should be performed and interpreted by individuals with advanced training in cardiac diagnosis.
Board certification by the American College of Veterinary Internal Medicine, Specialty of Cardiology is considered by the American College of Veterinary Medical Association as the benchmark of clinical proficiency for veterinarians in clinical cardiology, and examination by a Diplomate of this Specialty Board is recommended. Other veterinarians may be able to perform these examinations provided they have appropriate equipment and have received advanced training in echocardiography.
[color=#000000]Imaging[/color]The pericardial space, both atria, both ventricles, the great vessels, and the four cardiac valves should be imaged using long axis, short axis, apical, and angled image planes as necessary to perform a complete examination of the heart. Nomenclature should follow that recommended by the American College of Veterinary Internal Medicine Specialty of Cardiology. An anatomic diagnosis may be possible based on two-dimensional imaging; however, the origin of cardiac murmurs should also be evaluated using Doppler methods.
[color=#000000]Doppler[/color]
Doppler examination of all cardiac valves should be performed and recorded. Abnormal flow should be quantified using pulsed wave or continuous wave Doppler techniques. Values obtained should be compared to reference values. The depressant effects of any tranquilizers or sedative must be considered when measuring peak flow velocities. Color Doppler echocardiography should be employed if available to assess normal and abnormal blood flow patterns. Identification of abnormal flow across the cardiac septa or shunts at the level of the great vessels is best done by a combination of color and pulsed wave Doppler techniques. Typical echocardiographic features of common congenital
heart defects are indicated in table one.
[color=#000000]Assessment[/color]Special attention should be directed to the assessment of flow patterns and velocities in the left ventricular outlet and descending aorta. Optimal alignment with blood flow should be sought for accurate velocities to be reported. This may require the use of sub-xiphoid (subcostal) transducer
positions as well as left apical (caudal parasternal) transducer placements. In addition to measurement of peak velocity using pulsed or color wave Doppler, the pulsed wave sample volume should be gradually advanced from the subaortic area into the acsending aorta in order to identify sudden accelerations in flow velocity, turbulence, or aortic regurgitation.
[color=#000000]Videotape[/color]Echocardiographic studies should be reported on videotape for subsequent analysis and a written record of abnormal findings should be entered into the medical record.
[color=#000000]Echocardiographic Findings[/color] [table=98%][tr][size=2][color=#ffffff]Congenital Defect[/color][/size][size=2][color=#ffffff]Typical Auscultatory Features[/color][/size][size=2][color=#ffffff]Diagnostic Echocardiographic and Doppler Echocardiographic Features[/color][/size][/tr][tr][td]Patent ductus arteriosus[/td][td]Continuous heart murmur with maximal intensity over the left cranial dorsal cardiac base[/td][td]Continuous retrograde flow from the patent ductus arteriosus into the pulmonary artery[/td][/tr][tr][td]Ventricular septal defect[/td][td]Systolic murmur with maximal intensity over the right ventral precordium; less often maximal intensity is over the pulmonic valve area and pulmonary artery[/td][td]The septal defect can often be imaged in multiple imaging planes. Abnormal, generally high velocity, systolic flow across the septal defect is evident.[/td][/tr][tr][td]Atrial septal defect[/td][td]Systolic murmur with maximal intensity over the pulmonic valve area and pulmonary artery. The second heart sound may be widely split[/td][td]The septal defect can generally be imaged in multiple imaging planes. Abnormal blood flow may be identified across the septal defect into the right atrium.[/td][/tr][tr][td]Pulmonic stenosis[/td][td]Systolic murmur with maximal intensity over the pulmonic valve area and pulmonary artery[/td][td]Abnormal pulmonary valve and /or subvalvular anatomy. Sudden acceleration of blood flow in the right ventricular outlet with turbulent, high velocity systolic flow across the pulmonary valve and into the main pulmonary artery.[/td][/tr][tr][td]Valvular and subvalvular aortic stenosis[/td][td]Systolic murmur with maximal intensity over the subaortic or aortic valve area and radiating into the ascending aorta. The murmur may also be prominent over the right cranial thorax.[/td][td]Abnormal subvalvular or aortic valvular anatomy may be evident. Sudden acceleration of blood flow into the left ventricular outflow tract with turbulent, high velocity systolic flow across the aortic valve and into the ascending aorta. Concurrent aortic regurgitation is usually present.[/td][/tr][tr][td]Mitral valve dysplasia[/td][td]Systolic murmur with maximal intensity over the left apex and mitral area[/td][td]Abnormal anatomy of the mitral valve apparatus. High velocity retrograde systolic flow across the mitral valve into the left atrium. Concurrent mitral valve stenosis may be present.[/td][/tr][tr][td]Tricuspid valve dysplasia[/td][td]Systolic murmur with maximal intensity over the tricuspid valve area[/td][td]Abnormal anatomy of the tricuspid valve apparatus. High velocity retrograde systolic flow across the tricuspid valve into the right atrium. Concurrent tricuspid valve stenosis may be present.[/td][/tr][tr][td]Right to left cardiac shunt[/td][td]Variable—a systolic murmur at the left base is often detected; cyanosis is an important clinical sign[/td][td]Abnormal anatomy related to the cardiac malformations examples include: tetralogy of Fallot, patent ductus arteriosus with pulmonary hypertension, pulmonary or tricuspid valves stenosis with atrial septal defect. Right to left shunting may be documented by Doppler techniques and/or by contrast echocardiography[/td][/tr][/table][/size]

minibabyqq 2006-12-28 01:02

[color=Magenta][size=5][b]重要PULPOTOMY VITAL PULPOTOMY  [/b][/size][/color]

[size=12px]這個做法與根運河不同因為牙活(重要) 。
這是一個更加容易的做法執行因為唯一頂面(冠狀) 部份被去除。
有二個主要原因, 這個做法執行在獸醫牙科方面: [list=1][*][b][i]冠減少 [/i][/b]。為二個不同原因
a. 正牙學問題導致精神創傷對口頭軟的組織
b. 解除武裝的規程減少損傷由狠毒動物造成。[*][b][i]牙新鮮的破裂[/i][/b]
這做允許牙繼續成熟和獲取力量。這是最可貴的在發育未全的牙裡, 做法執行希望它將保留對生活至關重要或至少長期足夠將成熟(apexify) 並且將接受一個 [b][i]標準根運河做法[/i][/b]。[/list][b]技術[/b]
[list=1][*]前有效的牙齒射線照相被暴露確定成熟水平和如果任何
其它病理學是存在。[*]患者接受一完全牙齒預防(清潔) 並且嘴被漂洗以一種抗菌解答減少細菌汙染。[*]地方麻醉的射入被執行減少痛苦在期間和以後
麻醉。[*]冠被降下(如果需要) 。[*]所有害病的黏漿狀物質組織被去除與高速bur (牙齒鑽子) 。[*]靈菌被控制以不育的紙點在運河允許凝塊形成。[*]+氧化鈣被安置入運河:
這是抗菌的, 和還將激怒黏漿狀物質和將導致它制定牙結構(牙質) 防護層數。這將減少未來細菌汙染的機會。[*]中間層數被安置在+氧化鈣絕緣黏漿狀物質和行動作為一個基地為最後的恢復。[*]最後的補藥被安置在通入站點。[*]手術後射線照相被暴露保證適當的積土。
復校射線照相是重要的在這些規程。有失敗的機會沒有向外臨床標誌。多數寵物將遭受在沉默。[/list]
[b]破舊的牙[/b]

[align=left]有許多起因為破舊的牙在狗或貓。最共同是pruritis (發癢和嚼), 因為頭髮是非常磨蝕。這共同地將導致嚴厲佩帶門牙, 雖然犬可能並且是受影響的。這對gumline, 和偶爾地下面可能一直進步。嚼在網球或其它磨蝕玩具的狗(認為網球作為一個計分的墊), 經常將佩帶他們的更小的前面面頰牙(前臼齒), 和犬的後面方面。這磨蝕won.t 做在一天中, 但嚼每天幾年來可能導致重大穿戴。其它起因嚼在事如籬笆, 將磨損犬的後側方。終於, 咬合不良可能導致二顆牙一起來和佩帶在彼此。 [/align][align=left]破舊的牙看起來像破碎的牙, 但通常不是一個重大問題。如果穿戴慢慢地發生, 牙反應將由制定額外牙結構(牙質) 以回應牙損失保護黏漿狀物質。這與我們的牙反應深洞的方法是相似。如果這發生, 牙一般將停留活, 和不會要求任一種另外的療法。被暴露的牙質在牙中間將弄髒淺棕褐色對中等褐色。儀器不會能進入根運河。[/align][align=left]如果牙是殘破的, 或穿戴發生太快速或繼續太, 牙將變得endodontically 包含。這些牙一般將有黑褐色染黑中心, 將允許儀器入運河。這些牙要求或 [b][i]根運河療法[/i][/b] 或 [b][i]提取[/i][/b]。 [/align][align=left]有事例, 然而, 牙don.t 跟隨上述描述。偶爾, 穿戴可能發生足夠迅速傳染牙, 然而牙將居住足夠長期制定牙質防護層數在它死之前。這些牙將看起來像一顆重要, 被佩帶的牙在外部, 但將是死在裡面。唯一的方式肯定告訴是由牙齒放射學。死的牙將有一條更寬的根運河比他們的重要鄰居。因此, 我推薦射線照相在所有顯著破舊的牙。[/align][align=left]This procedure differs from a root canal in that the tooth is still alive (vital).
It is an easier procedure to perform as only the top (coronal) portion is removed.
There are two main reasons that this procedure is performed in Veterinary Dentistry:[/align][list=1][*][b][i]Crown Reduction [/i][/b]?for two different reasons
a. Orthodontic problems causing trauma to oral soft tissues
b. Disarming procedures to reduce the damage caused by vicious animals.[*][b][i]Fresh fractures of teeth[/i][/b]
This is done to allow the tooth to continue to mature and gain strength. This is most valuable in immature teeth, where the procedure is performed in the hopes that it will remain vital for life or at least long enough to mature (apexify) and accept a [b][i]standard root canal procedure[/i][/b].[/list][b]Technique[/b]
[list=1][*]A pre-operative dental radiograph is exposed to determine maturity level and if any
other pathology is present.[*]The patient receives a complete dental prophylaxis (cleaning) and the mouth is rinsed with an antimicrobial solution to reduce bacterial contamination.[*]A local anesthetic injection is administered to decrease pain during and after
anesthesia.[*]The crown is lowered (if necessary).[*]All diseased pulp tissue is removed with a high-speed bur (dental drill).[*]Bleeding is controlled with sterile paper points in the canal allowing a clot to form.[*]Calcium hydroxide is placed into the canal:
This is antibacterial, and also will irritate the pulp and cause it to lay down a protective layer of tooth structure (dentin). This will decrease the chance of future bacterial contamination.[*]An intermediate layer is placed over the calcium hydroxide to insulate the pulp and act as a base for the final restoration.[*]The final restorative is placed over the access site.[*]A post-operative radiograph is exposed to ensure proper fill.
Recheck radiographs are critical in these procedures. There is a chance of failure without outward clinical signs. Most pets will suffer in silence.[/list][b]WORN TEETH[/b]
[align=center][table=90%][tr][td=1,1,70%][align=left]There are many causes for worn teeth in a dog or cat. The most common is pruritis (itching and chewing), because hair is very abrasive. This will commonly cause severe wearing of the incisors, although the canines can also be affected. This can progress all the way to the gumline, and occasionally below. Dogs that chew on tennis balls or other abrasive toys (think of tennis ball as a scoring pad), will often wear their smaller front cheek teeth (premolars), and the back aspect of the canines. This abrasion won㦙 do much over the course of one day, but chewing every day for years can cause significant wear. Another cause is chewing on things like fences, which will wear down the backside of the canines. Finally, malocclusions can cause two teeth to come together and wear on each other. [/align][/td][td=1,1,30%][align=center][img=255,195]http://www.avds-online.org/images/resourceimages/wornteeth1.jpg[/img]
The wear on this tooth is from the mandibular canine.[/align][/td][/tr][/table][/align]
[align=left]Worn teeth look like fractured teeth, but usually are not a significant problem. If the wear occurs slowly, the tooth will respond by laying down extra tooth structure (dentin) in response to the tooth loss to protect the pulp. This is similar to the way that our teeth respond to deep cavities. If this occurs, the tooth will generally stay alive, and not require any additional therapy. The exposed dentin in the middle of the tooth will stain a light tan to medium brown. An instrument will not be able to enter the root canal. [/align][align=center][table=90%][tr][td=1,1,40%][align=center][img=255,195]http://www.avds-online.org/images/resourceimages/wornteeth2.jpg[/img]
Chronic wear many times results in deposition of reparative dentin, the dark discoloration seen on this tooth. If wear is slow the tooth may survive by this mechanism. Rapid wear rarely produces a significant response and tooth vitality may be compromised.[/align][/td][td=1,1,60%][align=left]If the tooth is broken, or the wear occurs too fast or continues too far, the tooth will become endodontically involved. These teeth will generally have a dark brown to black center, which will allow an instrument into the canal. These teeth require either [b][i]root canal therapy[/i][/b] or [b][i]extraction[/i][/b]. [/align][align=left]There are instances, however, that the teeth don㦙 follow the above descriptions. On occasion, wear can occur quickly enough to infect the tooth, however the tooth will live long enough to lay down a protective layer of dentin before it dies. These teeth will look like a vital, worn tooth on the outside, but will be dead on the inside. The only way to tell for sure is by dental radiology. Dead teeth will have a wider root canal than their vital neighbors. For this reason, I recommend radiographs on all significantly worn teeth.[/align][/td][/tr][/table][/align][/size]

minibabyqq 2006-12-28 01:05

[color=Magenta][size=5][b]一般手肘發育異常資訊General Elbow Dysplasia Information  [/b][/size][/color]

[size=12px]手肘發育異常的三張面孔手肘發育異常是一個一般用語使用辨認一種被繼承的polygenic 疾病在狗手肘。三具體原因論組成這種疾病並且他們能發生獨立地或與互相一道。這些原因論有:
[list=1][*]病理學介入尺骨的中間coronoid (FCP)[*]中間肩髁的Osteochondritis 在肘關節(OCD)[*]Ununited anconeal 過程(UAP)[/list]研究顯示被繼承的 [url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fglossary.html#polygenic][color=#800080]polygenic[/color][/url] 特徵導致這些原因論是獨立互相。臨床標誌介入也許依然是微妙長的時期的瘸。沒人可能預言在什麼年齡瘸將發生在狗由於很大數量的基因和環境因素譬如程度變動重量獲取的嚴肅, 率, 相當數量鍛煉, 等。微妙的變化在步態上也許為培養爪子的外部爪子的過份內部偏差描繪以便它接受較少重量和分佈更加機械的重量在肘關節的外部(側向) 方面從損害位於聯接的裡面。行動的範圍在手肘並且被減少。

評估手肘

[align=center][table=300][tr][td][img=300,262]http://www.offa.org/images/edfig1.gif[/img] [/td][/tr][tr][td][font=Times New Roman, Times, serif][size=2][color=#ffffff][i]正常肘關節的半徑和尺骨的圖示。注意尺骨(有角度的線的) anconeal 過程的光滑的邊際[/i][/color][/size][/font][/td][/tr][/table][/align]手肘發育異常有也許發生單一地或在組合的多被繼承的原因論。這些原因論包括 [b]被分割的中間coronoid (FCP) 尺骨, 中間肩髁的osteochondritis[/b] 和[b] ununited anconeal 過程(UAP)[/b]。最敏感的看法使用診斷次要退化變化在肘關節上是手肘(由OFA 必需和由國際手肘工作團體推薦的圖1) 一個極端被屈曲的medio 側向看法。獸醫放射學家是對尺骨的anconeal 過程的出現感興趣。
當有肘關節的不穩定由於手肘發育異常, 最敏感的幅射線照相的研究結果的當中一個是新骨頭擴散(osteophytes) 在尺骨的anconeal 過程(圖2) 聯繫了次要發展退化聯接疾病。
[align=center][img=200,110]http://www.offa.org/images/edfig2.gif[/img][/align]骨頭擴散是非常微妙的形象化在一些狗, 也許要求對一個特別光源(熱的光的) 用途而不是一個傳統看法箱子診斷它。其它關節炎研究結果譬如硬化在尺骨和骨頭踢馬刺的trochlear 山谷的區域在聯合邊緣並且被報告。如果中間coronoid 的破碎只介入軟骨, 它不可以幅射線照相地被看見但是偶爾地如果骨頭並且被分割, 它可能形象化作為分開的calcific 不透明被疊加在半徑(圖3 和4) 。
[align=center][img=225,110]http://www.offa.org/images/edfig3.gif[/img][/align][align=center][img=225,110]http://www.offa.org/images/edfig4.gif[/img][/align]
分級的手肘為手肘評估, 沒有[b] 等級為幅射線照相地正常手肘[/b]。唯一的介入的成績是為反常手肘以幅射線照相的變動與相關次要退化聯接疾病。像hip 證明, OFA 不會證明正常手肘直到狗是2 年紀。OFA 並且接受初步手肘射線照相。迄今, 沒有長期研究為初步手肘考試如有為臀部, 然而, 初步掩護為手肘與臀部一起可能並且提供可貴的資訊對交配動物者。
[color=#003399][/color][color=#003399][b]等級I 手肘發育異常
[/b][/color]最小的骨頭變動沿尺骨(少於3mm 的) anconeal 過程。
[b][color=#003399][/color][/b][b][color=#003399]等級II 手肘發育異常[/color][/b]
另外的骨頭擴散沿anconeal 過程(3-5 毫米) 並且subchondral 骨頭變動(trochlear 山谷硬化) 。
[b][color=#003399][/color][/b][b][color=#003399]等級III 手肘發育異常 [/color][/b]
井開發了退化聯接疾病以骨頭擴散沿anconeal 過程大於比5 毫米。

The Three Faces of Elbow DysplasiaElbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow of dogs. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:
[list=1][*]Pathology involving the medial coronoid of the ulna (FCP)[*]Osteochondritis of the medial humeral condyle in the elbow joint (OCD)[*]Ununited anconeal process (UAP)[/list]Studies have shown the inherited [url=http://www.offa.org/glossary.html#polygenic][color=#0000ff]polygenic[/color][/url] traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc. Subtle changes in gait may be characterized by excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. Range of motion in the elbow is also decreased.


Evaluating the Elbow

[align=center][table=300][tr][td][img=300,262]http://www.offa.org/images/edfig1.gif[/img] [/td][/tr][tr][td][font=Times New Roman, Times, serif][size=2][color=#ffffff][i]Schematic representation of the radius and ulna of a normal elbow joint. Note the smooth margin of the anconeal process of the ulna (angled line)[/i][/color][/size][/font][/td][/tr][/table][/align]Elbow dysplasia has multiple inherited etiologies which may occur singularly or in combination. These etiologies include [b]fragmented medial coronoid (FCP) of the ulna, osteochondritis of the medial humeral condyle[/b] and[b] ununited anconeal process (UAP)[/b]. The most sensitive view used to diagnose secondary degenerative changes in the elbow joint is an extreme flexed medio-lateral view of the elbow (Figure 1) which is required by the OFA and recommended by the International Elbow Working Group. The veterinary radiologists are most interested in the appearance of the anconeal process of the ulna.
When there is instability of the elbow joint due to elbow dysplasia, one of the most sensitive radiographic findings is new bone proliferation (osteophytes) on the anconeal process of the ulna (Figure 2) associated with secondary developmental degenerative joint disease.
[align=center][img=200,110]http://www.offa.org/images/edfig2.gif[/img][/align]Bone proliferation can be very subtle to visualize in some dogs and may require the use of a special light source (hot light) rather than a traditional view box to diagnose it. Other arthritic findings such as sclerosis in the area of the trochlear notch of the ulna and bone spurs at joint edges are also reported. If fragmentation of the medial coronoid only involves the cartilage, it may not be seen radiographically but occasionally if the bone is also fragmented, it can be visualized as a separate calcific opacity superimposed over the radius (Figures 3 and 4).
[align=center][img=225,110]http://www.offa.org/images/edfig3.gif[/img][/align][align=center][img=225,110]http://www.offa.org/images/edfig4.gif[/img][/align]
Grading ElbowsFor elbow evaluations, there are[b] no grades for a radiographically normal elbow[/b]. The only grades involved are for abnormal elbows with radiographic changes associated with secondary degenerative joint disease. Like the hip certification, the OFA will not certify a normal elbow until the dog is 2 years of age. The OFA also accepts preliminary elbow radiographs. To date, there are no long term studies for preliminary elbow ex>><<ws along with hips can also provide valuable information to the breeder.
[color=#003399][b]Grade I Elbow Dysplasia
[/b][/color]Minimal bone change along anconeal process of ulna (less than 3mm).
[b][color=#003399]Grade II Elbow Dysplasia[/color][/b]
Additional bone proliferation along anconeal process (3-5 mm) and subchondral bone changes (trochlear notch sclerosis).
[b][color=#003399]Grade III Elbow Dysplasia [/color][/b]
Well developed degenerative joint disease with bone proliferation along anconeal process being greater than than 5 mm.[/size]

minibabyqq 2006-12-28 01:07

[color=Magenta][size=5][b]Osteochondritis Dissecans   [/b][/size][/color]


Osteochondritis dissecans, 共同地以OCD 和osteochondrosis dissecans 著名, 是影響聯接在dog’s 身體軟骨的疾病。在任一聯接在身體二骨頭一起來並且運動被允許在他們之間。那裡二根骨頭見面, 軟骨一個格外光滑的區域包括他們的表面。這作為坐墊和保護部下的骨頭。如果任何打亂這光滑的軟骨表面, 聯接的運動變得痛苦。在一條狗與OCD, 這塊軟骨反常地被損壞或增長。代替附有骨頭它蓋子, 它分離或鎮壓, 導致巨大痛苦。在某些情況下, 軟骨小片斷任意終止和漂浮在聯接。軟骨這些片斷不死, 而是寧可繼續增長和增加在大小。這些為人所知作為聯合老鼠。大約15% 所有狗將開發OCD 。這篇文章將包括疾病和它的治療, 將探索一些被懷疑的起因。
誰得到OCD?

OCD 是主要一個問題在大或巨型養殖狗。它被報告了在小狗和貓, 雖然它不是非常共同。它頻繁地影響男性狗2 到5 倍像女性, 很可能由於males’ 更大的大小和增加的重音在聯接。它一般發生當動物在在4 個和8 個月年齡之間, 雖然它能出現在更舊的狗。有儘管是更大的養殖, 減少了疾病的發生包括Doberman Pinscher 、大牧羊犬, 和西伯利亞愛斯基摩的幾養殖。

什麼是OCD 症狀?

症狀是瘸在受影響的肢體。一些狗安排一幾乎沒有引人注目跛行並且其他人無法負擔任一重量在腿。瘸傾向於惡化在鍛煉以後的期間和改善在休息以後。OCD 箱子的七十百分之四發生在肩關節, 11% 在手肘, 和4% 在飛腓節。當它影響前面肩膀, 被變短的forelimb 大步也許著名歸結於勉強對導電線和延伸肩關節。偶爾地, 疾病同時將影響肢體並且狗也許勉強行動。

OCD 怎麼被診斷?

診斷根據歷史、體檢, 和射線照相(X-射線) 。在體檢, 我們注意關節痛。例如, 多數健康狗不顯示抵抗他們的肩關節被屈曲和充分地被延伸。但是, 如果他們有OCD 損害在他們的肩膀, 他們也許抵抗肩膀操作, 也許甚而大聲呼喊在痛苦中當它試圖。另外, 肩關節的這個彎曲和引伸也許惡化瘸。

受影響的聯接的射線照相被採取證實診斷。狗經常沉著以便聯接的充分的放鬆可能被獲得。受影響的聯接和健康聯接的幾觀點在對方被採取為比較。軟骨或聯接老鼠的分離經常被辨認在射線照相。如果射線照相不是確定的而是OCD 仍然被懷疑, 射線照相也許再被採取在2 個到3 個星期。

什麼導致OCD 的形成?

精神創傷對聯接, 遺傳性因素、迅速增長、有限的血流對軟骨, 和營養對OCD 損害的形成貢獻。
OCD 的起因認為是multifactorial 。它被認為, 有對OCD 損害形成貢獻包括精神創傷對聯接、遺傳性因素、迅速增長、有限的血流對軟骨, 和營養的幾個因素。

精神創傷, 是否 慢性 或 深刻, 也許對OCD 損害的形成貢獻。傷害對表面軟骨也許導致軟骨的分離從骨頭或導致在那導致軟骨擋水板形成的供血的減退。

看起來, 有一個基因鏈接在父母和子孫之間和疾病的形成。某些養殖和基因線是可能開發疾病。父母仔細的掩護反對這種疾病被推薦在所有良種畜的選擇期間。

疾病通常發生在迅速增長的期間。所以, 它被建議, 創造迅速增長的營養也許導致在疾病的發生的增量。它建議, 是易受疾病的動物被哺養是低在蛋白質裡和肥胖的, 或他們被哺養有限的方式允許平穩的均勻成長在第一年生活期間的飲食。這種理論也許有優點, 但更加具體的研究需要做在所有一般建議可能提出之前。

OCD 怎麼被對待?

有當前二種方式對待OCD; 保守的藥物治療或損害的外科撤除。保守的治療也許被表明為有OCD 早期的溫和的症狀的狗或具體損害無法被辨認在射線照相的地方。保守的治療包括嚴密的休息4 個到8 個星期。皮帶走被允許但賽跑或演奏不被允許。Anti-inflammatories 和止痛藥譬如緩衝的阿斯匹靈或carprofen (Rimadyl) 也許被表明。(不要給您的貓阿斯匹靈除非由您的獸醫規定。) 另外, 對glucosamine/chondroitin 產品的 用途被建議了, 沒有證實他們的有利用途在這種特殊疾病的潮流研究。保守的治療也許是困難的在也許仍然需要作手術的幼小活躍小狗, 如果症狀不改善。

手術被表明在顯示嚴厲症狀的動物中, 在大損害被辨認在射線照相處, 或當保守的治療失敗。手術是非常直接的。受影響的聯接被打開並且觸犯的擋水板、瑕疵, 或聯合老鼠被去除。有一個非常高成功率為手術並且多數動物充分地恢復沒有任何另外問題。

OCD 怎麼被防止?

預防包括仔細有選擇性養殖那避免育種動物以OCD 的歷史。幼小大和巨型養殖狗不應該接受吃力活動, 特別跳活動。住房在堅硬具體表面與增加的OCD 損害連接了在豬, 也許對問題並且貢獻在狗。提供促進甚而被承受的成長的好平衡的飲食並且被推薦。有當前許多大養殖小狗食物在市場上具體地被做幫助減少骨頭形成問題的發生。當有是沒有證據這些飲食實際上減少這種疾病的發生與其它商業小狗食物比較, 未來研究也許支持他們的用途。

總結

OCD 是影響幼小大和巨型養殖狗的軟骨問題。它歸結於幾個因素包括遺傳學、精神創傷、迅速增長, 和營養。治療是或保守性包括嚴密的休息, 或損壞的軟骨的外科撤除。預防是瞄準的好基因選擇, 被減少的活動, 和仔細哺養。

Osteochondritis dissecans, commonly known as OCD and osteochondrosis dissecans, is a disease of the cartilage that affects the joints in a dog’s body. In any joint in the body two bones come together and movement is allowed between them. Where the two bones meet, an exceptionally smooth area of cartilage covers their surfaces. This acts as a cushion and protects the underlying bone. If anything disrupts this smooth cartilage surface, movement of the joint becomes painful. In a dog with OCD, this cartilage is damaged or grows abnormally. Instead of being attached to the bone it covers, it separates or cracks, causing great pain. In some cases, small pieces of cartilage break off and float free in the joint. These pieces of cartilage do not die, but rather continue to grow and increase in size. These are known as joint mice. Approximately 15% of all dogs will develop OCD. This article will cover the disease and its treatment and will explore some of the suspected causes.
Who gets OCD?

OCD is primarily a problem in large or giant breed dogs. It has been reported in small dogs and cats, though it is not very common. It affects male dogs 2 to 5 times as frequently as females, most likely due to the males’ larger size and increased stress on the joint. It generally occurs when the animal is between 4 and 8 months of age, though it can show up in older dogs. There are several breeds that despite being larger breeds, have decreased incidences of the disease including the Doberman Pinscher, Collie, and Siberian Husky.

What are the symptoms of OCD?

The symptoms are lameness in the affected limb. Some dogs have a barely noticeable limp and others are unable to bear any weight on the leg. The lameness tends to worsen after periods of exercise and improves after rest. Seventy four percent of the cases of OCD occur in the shoulder joint, 11% in the elbow, and 4% in the hock. When it affects the front shoulder, a shortened forelimb stride may be noted due to reluctance to flex and extend the shoulder joint. Occasionally, the disease will affect both limbs simultaneously and the dog may be reluctant to move.

How is OCD diagnosed?

Diagnosis is based on history, physical exam, and radiographs (x-rays). On physical exam, we notice joint pain. For instance, most healthy dogs show no resistance when their shoulder joint is fully flexed and extended. However, if they have an OCD lesion in their shoulder, they may resist shoulder manipulation and may even cry out in pain when it is attempted. In addition, this flexion and extension of the shoulder joint may worsen the lameness.

Radiographs of the affected joint are taken to confirm the diagnosis. The dog is often sedated so that full relaxation of the joint can be obtained. Several views of the affected joint and the healthy joint on the other side are taken for comparison. The separations of the cartilage or joint mice are often identified on radiographs. If the radiographs are not confirmatory but OCD is still suspected, radiographs may be taken again in 2 to 3 weeks.

What causes the formation of OCD?

Trauma to the joint, hereditary factors, rapid growth, restricted blood flow to the cartilage, and nutrition contribute to the formation of OCD lesions.
The cause of OCD is considered to be multifactorial. It is thought that there are several factors that contribute to the formation of OCD lesions including trauma to the joint, hereditary factors, rapid growth, restricted blood flow to the cartilage, and nutrition.

Trauma, whether chronic or acute, may contribute to the formation of OCD lesions. Injury to the surface cartilage may lead to the separation of the cartilage from the bone or cause a decrease in blood supply that leads to cartilage flap formation.

It appears that there is a genetic link between parents and offspring and the formation of the disease. Certain breeds and genetic lines are much more likely to develop the disease. Careful screening of parents against this disease is recommended during the selection of all breeding stock.

The disease usually occurs during periods of rapid growth. Therefore, it has been suggested that nutrition that creates rapid growth may lead to the increase in incidence of the disease. It has been recommended that animals that are susceptible to the disease be fed a diet that is lower in protein and fat, or that they are fed in a limited manner to allow steady even growth during the first year of life. This theory may have merits, but more specific studies need to be done before any general recommendations can be made.

How is OCD treated?

There are currently two ways to treat OCD; conservative medical treatment or surgical removal of the lesion. Conservative treatment may be indicated for dogs that have early mild symptoms of OCD or where a specific lesion cannot be identified on radiographs. Conservative treatment consists of strict rest for 4 to 8 weeks. Leash walking is permitted but no running or playing is allowed. Anti-inflammatories and painkillers such as buffered aspirin or carprofen (Rimadyl) may be indicated. (Do NOT give your cat aspirin unless prescribed by your veterinarian.) In addition, the use of glucosamine/chondroitin products has been suggested, yet there are no current studies that confirm their beneficial use in this particular disease. Conservative treatment may be difficult in young active puppies who may still need to undergo surgery, if the symptoms do not improve.

Surgery is indicated in animals that show severe symptoms, in cases where large lesions are identified on radiographs, or when conservative treatments fail. The surgery is very straightforward. The affected joint is opened and the offending flap, defect, or joint mouse is removed. There is a very high success rate for surgery and most animals recover fully without any further problems.

How is OCD prevented?

Prevention consists of careful selective breeding that avoids the breeding of animals with a history of OCD. Young large and giant breed dogs should not undergo strenuous activity, particularly jumping activities. Housing on hard concrete surfaces has been linked to increased OCD lesions in pigs and may also contribute to problems in the dog. Providing a good balanced diet that promotes even sustained growth is also recommended. There are currently many large breed puppy foods on the market made specifically to help reduce the incidence of bone formation problems. While there has been no evidence that these diets actually reduce the incidence of this disease as compared to other commercial puppy foods, future studies might support their use.

minibabyqq 2006-12-28 01:12

[color=Magenta][size=5][b]類風濕病的關節炎(免疫斡旋的疾病)  [/b][/size][/color]

[size=12px]類風濕病的關節炎最共同地發生在玩具或狗小養殖, 一般在5 和6 年紀之間。

什麼是類風濕病的關節炎?

類風濕病的關節炎是一種免疫斡旋的疾病。這意味著它由免疫系統的過度的反應造成。一個正常免疫系統起反應當身體辨認外國蛋白質譬如蛋白質在細菌的外部。祈求免疫反應的這種雜質稱抗原。身體可能起反應對抗原由生產束縛抗原的蛋白質分子(抗體) 。抗體區域的 組合 或附有抗原稱免疫複合體。

在類風濕病的關節炎, 身體弄錯一些它自己的蛋白質為外國蛋白質。它然後做抗體反對它自己的蛋白質。這些獨特的抗體集體叫做' 類風濕病的因素。' 抗體和蛋白質形成免疫複合體, 然後被放置在聯接。這些複合體觸發處理叫的炎症, 是怎麼身體起反應對傷害。在類風濕病的關節炎情況下, 身體嘗試趕走自己有害免疫複合體, 但設法只創造對聯接的更多損傷。過程然後成為自已永存。最終, 軟骨和甚而骨頭在聯接被磨損。

什麼是類風濕病的關節炎的標誌?

一條狗以類風濕病的關節炎一般有幾聯接影響。動物不總通常是瘸的, 但。瘸也許是溫和或非常嚴厲的對動物無法走的點。有時, 瘸轉移從腿到腿。在某些情況下, 瘸突然進展並且狗並且有胃口熱病和損失。在其它的時候, 類風濕病的關節炎的唯一的標誌是僵硬。

聯接影響是脹大和痛苦的。如果瘸繼續有一段時間了, 那裡也許是肌肉損失在那肢體裡。

一些狗將有其它身體系統影響並且聯接。一些狗以類風濕病的關節炎並且有腎臟疾病、擴大的 淋巴結、扁桃腺炎, 和肺炎。

類風濕病的關節炎怎麼被診斷?

歷史和體檢經常帶領一位獸醫懷疑類風濕病的關節炎。射線照相(X-射線) 被採取和典型地顯示骨頭損失- 骨頭經常出現像孔被猛擊了在它。聯合表面經常是不規則並且骨多的踢馬刺脫去骨頭經常被看見。

特別驗血可能完成尋找類風濕病的因素。不幸地, 類風濕病的因素是有時存在在狗沒有類風濕病的關節炎, 並且沒有所有狗以類風濕病的關節炎測試正面為因素。(A 提示醫學實踐不是確切的科學。)

synovial 流體也許被分析和顯示典型變動。細胞被介入在炎症是存在在大數字, 流體比正常和而不是確切, 流體多雲的通常是更加稀薄的一貫性。

組織的切片檢查法 在聯接之內可能被做和展示典型變動。

獸醫使用資訊從歷史、體檢, 和測試來到類風濕病的關節炎診斷。

類風濕病的關節炎怎麼被對待?

和與人, 許多治療被嘗試了在狗, 以不同程度成功。抗發炎藥物譬如緩衝的阿斯匹靈經常被使用。有時類固醇譬如prednisolone 被使用, 經常根據一個供選擇天依據。壓制免疫系統譬如azathioprine 和cyclophosphamide 的療程被使用得在某些情況下。金射入被使用了在狗以一些成功。寵物仔細的監視在 免疫抑制的 藥物重要。他們將是有傾向對顯現出的傳染, 並且這些藥物有毒性副作用。

嚴密的休息, 及早疾病其間特別是重要。如果狗對治療起反應一個柔和的鍛煉節目可能被起動。它是重要對鍛煉每天為同樣時間。

重量控制並且是治療計劃的一非常重要部份。超重寵物將投入剩餘重音在他們的已經被傷害的聯接。重量獲取是可能的因為寵物經常將是較不活躍的, 因此對飲食的仔細的關注重要。

一些研究員建議脂肪酸補充也許幫助減少一些炎症。

什麼是預測為寵物以類風濕病的關節炎?

這時, 類風濕病的關節炎無法被治療。長期外型為狗以類風濕病的關節炎是一個設法控制標誌和防止進一步傷害對聯接。


Rheumatoid arthritis occurs most commonly in toy or small breeds of dogs, generally between 5 and 6 years of age.

What is rheumatoid arthritis?

Rheumatoid arthritis is an immune-mediated disease. This means it is caused by an overreaction of the immune system. A normal immune system reacts when the body identifies a foreign protein such as proteins on the outside of bacteria. This foreign material which invokes the immune response is called an antigen. The body can react to the antigen by producing protein molecules (antibodies) which bind the antigen. The combination of the antibody bound or attached to the antigen is called an immune complex.

In rheumatoid arthritis, the body mistakes some of its own protein for foreign protein. It then makes antibodies against its own protein. These unique antibodies are collectively called 'rheumatoid factor.' The antibodies and protein form immune complexes, which are then deposited in the joint. These complexes trigger a process called inflammation, which is how the body reacts to injury. In the case of rheumatoid arthritis, the body tries to rid itself of the injurious immune complexes, but manages to only create more damage to the joint. The process then becomes self-perpetuating. Eventually, the cartilage and even the bone in the joint are worn away.

What are the signs of rheumatoid arthritis?

A dog with rheumatoid arthritis generally has several joints affected. The animal is usually lame, but not always. The lameness may be mild or very severe to the point where the animal cannot walk. Sometimes, the lameness shifts from leg to leg. In some cases, the lameness comes on suddenly and the dog also has a fever and loss of appetite. At other times, the only sign of rheumatoid arthritis is stiffness.

The joints affected are swollen and painful. If the lameness has gone on for some time, there may be loss of muscle in that limb.

Some dogs will have other body systems affected as well as the joints. Some dogs with rheumatoid arthritis also have kidney disease, enlarged lymph nodes, tonsillitis, and pneumonia.

How is rheumatoid arthritis diagnosed?

The history and physical exam often lead a veterinarian to suspect rheumatoid arthritis. Radiographs (x-rays) are taken and typically show the loss of bone - the bone often appears like holes have been punched in it. The joint surfaces are often irregular and bony spurs coming off of the bone are often seen.

A special blood test can be done to look for the rheumatoid factor. Unfortunately, rheumatoid factor is sometimes present in dogs without rheumatoid arthritis, and not all dogs with rheumatoid arthritis test positive for the factor. (A reminder that the practice of medicine is not an exact science.)

The synovial fluid may be analyzed and shows characteristic changes. Cells involved in inflammation are present in large numbers, the fluid is usually of a thinner consistency than normal and instead of being clear, the fluid is cloudy.

Biopsies of the tissues within the joint can be made and show characteristic changes.

The veterinarian uses the information from the history, physical exam, and tests to come to a diagnosis of rheumatoid arthritis.

How is rheumatoid arthritis treated?

As with humans, many treatments have been tried in the dog, with varying degrees of success. Anti-inflammatory drugs such as buffered aspirin are often used. Sometimes steroids such as prednisolone are used, often on an alternate day basis. Medications that suppress the immune system such as azathioprine and cyclophosphamide are used in some cases. Gold injections have been used in dogs with some success. Careful monitoring of pet on immunosuppressive drugs is important. They will be more prone to developing infections, and some of these drugs have toxic side effects.

Strict rest, especially early in the course of the disease is important. If the dog responds to treatment a gentle exercise program can be started. It is important to exercise every day for the same amount of time.

Weight control is also a very important part of the treatment plan. Overweight pets will put excess stress on their already injured joints. Weight gain is likely since the pet will often be less active, so careful attention to diet is important.

Some researchers have suggested that fatty acid supplements may help reduce some of the inflammation.

What is the prognosis for pets with rheumatoid arthritis?

At this point, rheumatoid arthritis cannot be cured. The long-term outlook for dogs with rheumatoid arthritis is one of trying to control the signs and prevent further injury to the joint.[/size]

minibabyqq 2006-12-28 01:13

[color=Magenta][b][size=5]被爆裂的先前Cruciate 韌帶Ruptured Anterior Cruciate Ligament   [/size][/b][/color]


膝蓋是有傾向對一定數量的傷害因為任一位足球運動員將告訴您。最共同的膝傷的當中一個在狗是一條被爆裂的cruciate 韌帶。

膝蓋解剖學

膝蓋是由三根骨頭形成的聯接: 股骨(長的骨頭延伸下來從臀部); 脛骨(骨頭在膝蓋和腳腕之間); 並且臏骨(膝蓋骨) 。這些骨頭由一定數量的韌帶一起加入, 是組織堅韌纖維狀帶 。二條韌帶交叉往來在聯接從股骨對脛骨和叫做cruciate 韌帶(cruciate 手段十字架) 。那個往腿的前線稱先前cruciate 韌帶並且那個橫渡在它之後是 後部 cruciate 韌帶。這些韌帶防止股骨和脛骨的末端行動反覆橫跨彼此。

先前cruciate 韌帶的破裂(ACL)

當先前cruciate 韌帶爆裂(被撕毀), 聯接變得不穩定並且股骨和脛骨可能行動反覆橫跨彼此。先前cruciate 韌帶最共同地被撕毀當狗扭轉在他的後腿。扭轉的行動施加許多緊張在韌帶並且它撕毀。這發生如果狗滑倒在溜滑表面, 做一個突然的輪當跑, 或乘汽車經常擊中。肥胖病把許多重量放在膝蓋上並且超重狗傾向於有被爆裂的cruciate 韌帶更多發生。

一條被爆裂的cruciate 韌帶的症狀

爆裂了他們的cruciate 韌帶的狗突然將看上去瘸, 和通常握受影響的腿的腳地面。膝蓋也許成為脹大。及時, 狗也許開始再使用腿, 但瘸經常返回。

一條被爆裂的cruciate 韌帶的診斷

一條被爆裂的cruciate 韌帶的診斷被做通過觀察聯接的反常運動。獸醫將安置一隻手在股骨附近和一個在脛骨附近以精確方式。由施加壓力在膝蓋, 獸醫將感覺骨頭反常地行動什麼稱' 抽屜標誌。' 它叫因為股骨的運動關於脛骨與拉扯和推擠是相似在內閣的抽屜。如果動物是在很多痛苦中, 或非常緊張, 肌肉在膝蓋附近也許是很緊張的, 他們阻止抽屜運動發生。如果獸醫懷疑一條被爆裂的cruciate 韌帶在狗但無法得出抽屜標誌, 狗也許沉重沉著放鬆肌肉和然後被再檢查為抽屜標誌。

設備, 稱' DGY2000, ' 由威斯康辛大學獸醫學校發展查出被舒展的或部份地被撕毀的ACLs 。在這些情況有經常不足的聯合laxity 查出使用做法被描述上面。DGY2000 包括一個平臺以二個移動的片斷。狗的腿被束縛平臺並且股骨被拿著到位當小力量適用於前線和然後脛骨的後面當射線照相(X-射線) 被採取。相當數量的一次確切的測量laxity 在聯接可能然後是堅定的從二射線照相。更加早期的診斷和機會穩定聯接在韌帶的總破裂之前發生有潛力幫助防止痛苦和關節炎在狗。

一條被爆裂的cruciate 韌帶的治療

如果韌帶完全地被撕毀, 狗(特別是一條大狗) 一般被對待以手術。有幾個不同的方法使用修理膝蓋關節當一條先前韌帶被撕毀。他們全都需要使用綜合性縫合材料, 或毗鄰纖維狀組織的部份基本上再創造韌帶。縫合或組織被製作延長從股骨的外部更低的部份對脛骨的裡面上部部份。在手術以後, 狗必須嚴密地被限制2 個星期。將在天10 以前在手術以後, 多數狗接觸受影響的腿的腳趾到地面, 開始負擔最小的重量在腿。一旦狗到達了這點, 它經常非常難保留狗沉寂直到完全癒合發生了。狗必須一般被限於唯一皮帶走為4-6 個另外星期極小值; 確切的時間取決於傷害和矯正做法的程度執行。這鍛煉極端重要防止外科更正撕毀。獸醫的指示關於鍛煉在補救期間應該非常仔細地被遵守。

例如, 如果cruciate 韌帶部份地只被撕毀, 動物更舊, 有能影響癒合的健康狀況, 或所有者不會能保持狗安靜一定數量的星期在手術以後, 藥物治療被使用。這基本上包括控制狗的活動8-12 個星期。游泳和低衝擊鍛煉(走) 依照由獸醫指示也許完成根據一個受控依據, 保持肌肉力量。如果超重, 狗被安置在減少卡路里飲食。Nonsteroidal 抗發炎藥物(NSAIDS) 譬如carprofen, etodolac, meloxicam, deracoxib, 緩衝的阿斯匹靈, 或其它療程經常被使用減少 炎症 在聯接和解除痛苦。(不要給您的貓阿斯匹靈除非由您的獸醫規定。) 產品包含氨基葡萄糖, 軟骨素, perna 淡菜, polysulfated glycosaminoglycans, 並且其它chondroprotective 代理經常被推薦, 。

如果一條狗與一被爆裂的cruciate 不被對待, 嚴厲退化聯接疾病(關節炎) 通常發生。另外, 因為狗傾向受影響的腿, 他一般把更多重量放在未受影響的腿上。它不是異常使狗爆裂先前cruciate 韌帶在那條腿由於增加的重音在腿。

預測

如果狗的鍛煉依照被指示被制約, 並且超重狗回到正常體重, 預測是好的。根據相當數量傷害對膝蓋和時間在問題的傷害和更正之間, 退化聯接疾病也許發生作為寵物年齡。



The knee is prone to a number of injuries as any football player will tell you. One of the most common knee injuries in dogs is a ruptured cruciate ligament.

Knee anatomy

The knee is a joint that is formed by three bones: Femur (the long bone extending down from the hip); Tibia (the bone between the knee and ankle); and Patella (the kneecap). These bones are joined together by a number of ligaments, which are tough fibrous bands of tissue. Two ligaments crisscross in the joint from the femur to the tibia and are called cruciate ligaments (cruciate means cross). The one towards the front of the leg is called the anterior cruciate ligament and the one crossing behind it is the posterior cruciate ligament. These ligaments prevent the ends of the femur and tibia from moving back and forth across each other.

A rupture of the anterior cruciate ligament (ACL)

When the anterior cruciate ligament ruptures (is torn), the joint becomes unstable and the femur and tibia can move back and forth across each other. The anterior cruciate ligament is most commonly torn when the dog twists on his hind leg. The twisting motion puts too much tension on the ligament and it tears. This often occurs if the dog slips on a slippery surface, makes a sudden turn while running, or is hit by a car. Obesity puts too much weight on the knee and overweight dogs tend to have more occurrences of ruptured cruciate ligaments.

Symptoms of a ruptured cruciate ligament

Dogs who have ruptured their cruciate ligament will appear suddenly lame, and usually hold the foot of the affected leg off the ground. The knee may become swollen. In time, the dog may start to use the leg again, but often lameness returns.

Diagnosis of a ruptured cruciate ligament

The diagnosis of a ruptured cruciate ligament is made through observing abnormal movement of the joint. A veterinarian will place one hand around the femur and one around the tibia in a precise manner. By applying pressure on the knee, the veterinarian will feel the bones move abnormally in what is called a 'drawer sign.' It is called that because the movement of the femur in relation to the tibia is similar to pulling and pushing in the drawer of a cabinet. If an animal is in a lot of pain, or very nervous, the muscles near the knee may be so tense that they prevent the drawer movement from occurring. If a veterinarian suspects a ruptured cruciate ligament in a dog but cannot elicit the drawer sign, the dog may be heavily sedated to relax the muscles and then re-examined for the drawer sign.

A device, called the 'DGY2000,' has been developed by the University of Wisconsin School of Veterinary Medicine to detect stretched or partially torn ACLs. In these conditions there is often insufficient joint laxity to detect using the procedure described above. The DGY2000 consists of a platform with two moving pieces. The dog's leg is strapped onto the platform and the femur is held in place while a small force is applied to the front and then the back of the tibia while radiographs (x-rays) are taken. An exact measurement of the amount of laxity in the joint can then be determined from the two radiographs. Earlier diagnosis and a chance to stabilize the joint before total rupture of the ligament occurs has the potential to help prevent pain and arthritis in dogs.

Treatment of a ruptured cruciate ligament

If the ligament is completely torn, the dog (especially a large dog) is generally treated with surgery. There are several different methods used to repair the knee joint when an anterior ligament is torn. They all entail using synthetic suture material, or a portion of adjacent fibrous tissue to basically re-create the ligament. The suture or tissue is made to extend from the outside lower portion of the femur to the inside upper portion of the tibia. After the surgery, the dog must be strictly confined for 2 weeks. By day 10 after surgery, most dogs touch the toe of the affected leg to the ground and will start bearing minimal weight on the leg. Once the dog has reached this point, it is often very difficult to keep the dog quiet until complete healing has taken place. The dog generally has to be restricted to only leash walking for a minimum of 4-6 more weeks; the exact amount of time depends upon the extent of the injury and the corrective procedure performed. This exercise is extremely important to prevent the surgical correction from tearing. The veterinarian's instructions regarding exercise during the recovery period should be followed very carefully.

In some instances, if the cruciate ligament is only partially torn, the animal is older, has medical conditions which could affect healing, or the owners will not be able to keep the dog quiet for a number of weeks after surgery, medical treatment is used. This basically consists of controlling the dog's activity for 8-12 weeks. Swimming and low-impact exercise (walking) may be done on a controlled basis, as instructed by a veterinarian, to keep up muscle strength. If overweight, the dog should be placed on a reduced-calorie diet. Nonsteroidal anti-inflammatory drugs (NSAIDS) such as carprofen, etodolac, meloxicam, deracoxib, buffered aspirin, or other medications are often used to reduce inflammation in the joint and relieve pain. (Do NOT give your cat aspirin unless prescribed by your veterinarian.) Products containing glucosamine, chondroitin, perna mussel, polysulfated glycosaminoglycans, and other chondroprotective agents are often recommended, as well.

If a dog with a ruptured cruciate is not treated, severe degenerative joint disease (arthritis) usually occurs. In addition, because the dog favors the affected leg, he will generally put more weight on the unaffected leg. It is not unusual for the dog to rupture the anterior cruciate ligament on that leg as well because of the increased stress on the leg.

Prognosis

If the dog's exercise is restricted as instructed, and overweight dogs return to normal body weight, the prognosis is good. Depending on the amount of injury to the knee and length of time between the injury and correction of the problem, degenerative joint disease may occur as the pet ages.

minibabyqq 2006-12-28 01:15

[color=Magenta][size=5][b]泌尿無節制 Urinary Incontinence   [/b][/size][/color]


泌尿無節制的起因

在狗, 尿被保留或被存放在膀胱。當狗想要小便, 尿通行證對身體的外部通過一支小管叫尿道。一條正常狗能容易地控制這次行動。泌尿無節制是不隨意或無法控制漏尿從膀胱。尿的少量將漏從尿道當一條incontinent 狗是休息或睡覺, 並且它共同地將被看見舔vulva 或penile 開頭。
尿防止漏在膀胱外面在正常狗由肌肉組織帶 在作為閥門那狗神志清楚地控制膀胱的基地。我們今天知道, 某些激素是重要在這控制。在女性, 女性荷爾蒙 有一個劇烈的作用, 給力量膀胱的肌肉組織。在男性, 睪甾酮有同樣作用。任何並且影響這些激素的水平影響dog’s 能力保留他的尿。

作為狗變老, 這些激素的生產自然地減少。另外, 他們的生產主位置, 卵巢在女性和睪丸在男性, 外科地被去除當狗是spayed 或閹割了。

很少, 泌尿無節制可能發生在更加幼小的動物由於 先天 解剖反常性。少有地, 更舊的狗也許有泌尿無節制由於腫瘤或 珊瑚蟲 在膀胱。神經傷害去到膀胱可能並且導致無節制。

攝護腺疾病也許並且導致無節制。

誰是在危險中?

激素敏感無節制比它是在男性, 和共同在是共同在母狗閹割和spayed 狗比原封一□。更舊的狗傾向於是有傾向對開發這個情況。如果起因是老年齡, 問題通常不看直到狗是八到九年紀。在spayed 女性, 這個問題通常不發生直到他們是三或五年紀。驚奇, 在男性, 不管他們被閹割或不是, 這個情況很少看在狗更加年輕比十年紀。

問題起因於泌尿無節制

狗遭受泌尿無節制有一些共同的次要問題。他們有膀胱傳染的更高的發生。它被相信, 以更加鬆馳的開頭到膀胱, 它是容易對細菌移居尿道和拓殖膀胱。這些狗也許需要是在抗生素直到無節制被處理。

狗與泌尿無節制頻繁地遭受尿燙傷。尿是相當刻薄的, 並且如果它保留與皮膚聯繫長的時期, 它可能導致嚴厲激怒。被燙傷的區域典型地通常 被對待 與抗發炎salves 並且包含抗生素。

不反應100% 療程的狗也許仍然漏尿少量。如果這是實際情形, 狗紕漏或短內褲與吸收劑墊可能被使用浸泡尿。某些人民使用人的一次性的尿布和刪去一個孔為尾巴。

治療

治療為無節制通常不是困難的。Phenylpropanolamine (PPA) 是一個非荷爾蒙療程常用在公和母狗對待無節制。(筆記: 在晚秋天, 1999 年, 聯邦糧食與藥物管理局取締了PPA 至於人的使用。PPA 是可利用的為狗在獸醫公式化。) 因為泌尿無節制的起因一般是激素缺乏, 替換以激素或激素替補也許並且被規定。女性荷爾蒙可能由複合已烯雌酚替換。在每日藥量以後的一個短期, 它通常被給每週一次。在分鐘水平□去□常對待無節制在狗, 副作用是極端罕見的。狗與激素敏感無節制將需要保留在或PPA, 已烯雌酚, 或這些其它藥物的當中一個在他們有生之年。
   



The causes of urinary incontinence

In dogs, urine is retained or stored in the bladder. When the dog wants to urinate, the urine passes to the outside of the body through a small tube called the urethra. A normal dog can easily control this action. Urinary incontinence is involuntary or uncontrollable leaking of urine from the bladder. Small quantities of urine will leak from the urethra while an incontinent dog is resting or sleeping, and it will commonly be seen licking the vulva or penile opening.
Urine is prevented from leaking out of the bladder in normal dogs by a band of muscular tissue at the base of the bladder that acts as a valve that the dog consciously controls. We know today that certain hormones are important in this control. In the female, estrogen has a dramatic effect, giving strength to the muscular tissue of the bladder. In the male, testosterone has much the same effect. Anything that affects the levels of these hormones also affects the dog’s ability to retain his urine.

As a dog ages, the production of these hormones naturally decreases. Additionally, the main sites of their production, the ovaries in the female and the testicles in the male, are surgically removed when the dog is spayed or neutered.

Rarely, urinary incontinence can occur in younger animals due to congenital anatomic abnormalities. Infrequently, older dogs may have urinary incontinence due to tumors or polyps in the bladder. Injury of nerves going to the bladder can also cause incontinence.

Prostate disease may also result in incontinence.

Who is at risk?

Hormone-responsive incontinence is more common in female dogs than it is in males, and more common in neutered and spayed dogs than in intact ones. Older dogs tend to be more prone to developing this condition. If the cause is old age, the problem is usually not seen until the dogs are eight to nine years of age. In spayed females, this problem usually does not occur until they are three or five years of age. Surprisingly, in males, whether they are neutered or not, this condition is rarely seen in dogs younger than ten years of age.

Problems resulting from urinary incontinence

Dogs suffering from urinary incontinence have some common secondary problems. They have a much higher incidence of bladder infections. It is believed that with the more lax opening to the bladder, it is easier for bacteria to migrate up the urethra and colonize the bladder. These dogs may need to be on antibiotics until the incontinence is dealt with.

Dogs with urinary incontinence frequently suffer from urine scalding. Urine is fairly caustic, and if it remains in contact with the skin for long periods of time, it can cause severe irritations. Scalded areas are usually treated topically with anti-inflammatory salves that also contain antibiotics.

Dogs who do not respond 100% to medication may still leak urine in small quantities. If this is the case, dog bloomers or panties with absorbent pads can be used to soak up the urine. Some people use human disposable diapers and cut out a hole for the tail.

Treatment

Treatment for incontinence is usually not difficult. Phenylpropanolamine (PPA) is a non-hormonal medication commonly used in male and female dogs to treat incontinence. (NOTE: In late fall, 1999, the federal Food and Drug Administration had banned PPA for human use. PPA is still available for dogs in a veterinary formulation.) Since the cause of urinary incontinence is generally a hormone deficiency, replacements with hormones or hormone substitutes may also be prescribed. Estrogen can be replaced by the compound diethylstilbestrol. After a brief period of daily doses, it is usually given once a week. At the minute levels used to treat incontinence in dogs, side effects are extremely rare. Dogs with hormone-responsive incontinence will need to remain on either PPA, diethylstilbestrol, or one of these other drugs for the rest of their lives.

minibabyqq 2006-12-28 01:16

[color=Magenta][size=5][b]白內障分類 Cataracts [/b][/size][/color]  


透鏡的最共同的先天疾病是大瀑布。但是, 因為許多大瀑布的形式是可遺傳的(因此先天地事先安排好), 但不要出現直到某個時候在誕生, 大瀑布以後總之將被蓋在被獲取的疾病之下而不是這裡。大多先天疾病被描述這裡是有趣的研究結果, 但是非可治療和無意義的。

無晶狀體
無晶狀體是缺乏透鏡。真實的無晶狀體是極端罕見的和通常同嚴厲拘捕聯繫在一起在視覺發展以便嚴厲microphthalmia 或先天囊狀眼睛是結果。

透鏡的Coloboma
這是由uveal 短文的coloboma 經常伴隨的一個罕見的情況。透鏡將看上去刻凹痕或臨床也許是反常的在形狀, 理論上由於參差不齊的緊張在透鏡膠囊在uveal coloboma 的區域在發展期間。

Microphakia   
透鏡比法線小。它也許是被隔絕的損害或發生作為多個視覺反常現象一部分綜合症狀。如果不已經cataractous 出生時, 它意志以後經常opacify 在生活中。伴隨視覺瑕疵通常阻止這些透鏡撤除為治療目的。

Lenticonus  
在這個情況, 透鏡的表面推出在先前或後部桿以圓錐形形式(Aguirre 和Bistner; Narfstr?and Dubielzig) 。雖然不凡, 它被看見在許多種類。瑕疵在透鏡膠囊經常出現作為透鏡的一個圓瑕疵並且推出的材料也許是不透明的。透鏡膠囊在這些瑕疵區域是微弱的, 經常也許自發地爆裂。

後部lenticonus 也許同堅持hyperplastic 主要玻璃聯繫在一起。

Lenticonus internum 描述延伸到後部外皮的一個反常地形狀的透鏡中堅力量。

被獲取的反常性
大瀑布
大瀑布 是導致透鏡透明度損失和干涉, 因此, 視覺fundus 的視覺透鏡的不透明(包括膠囊) (或形象化) 。它可能是焦點的, 如此不防止視覺通過透鏡, 或散開 , 因而嚴厲地減少的視覺能力甚至矇蔽的清楚的部份 。在一個多孔的水平上, 它同內部和細胞外vacuolation 和蛋白質的地方上皮細胞降雨雪, 損失, 出軌上皮細胞分化或上皮細胞化生聯繫在一起。大瀑布是透鏡的常見病, 簡單地因為透鏡起反應對多數侮辱由opacifying 。雖然這可能是一個被隔絕的情況, 它經常被看見伴生以視覺反常性(van der Woerdt, 等。) 。

發病原理
大瀑布發展發病原理不充分地被瞭解(Kinoshita) 。透鏡纖維透明度由蛋白質的脹大和凝固影響。Opacification 由於水的吸收也許是反演性的如果病理性過程被改正(Fraunfelder 和燒傷) 。Opacification 由於化學變化在蛋白質是不可逆的。這些生物化學的變動經常是具體的為類型大瀑布。通常, 灰的水、百分之, 鈉和鈣被增加, 並且氧氣消耗量、glutathione 、抗壞血酸、鉀、可溶解蛋白質和核黃素被減少。
分類
大瀑布被分類以各種各樣的方式並且分類計劃這種多樣性導致混亂。對疾病過程的理解也許意味深長的比任一份分類計劃。但是, 分類根據形成階段也許是意味深長的因為這描述多數大瀑布進步不管起因(Playter) 。

分類由形成階段:
起初  - 當opacification 的第一證據看。視覺不是受影響的。不透明也許或不能進步。

殘缺不全的 (並且叫發育未全)  - 透鏡主要, 但不完全地是, 不透明。患者也許有一些視覺; tapetal 反射是可看見的。透鏡也許輕微地擴大的歸結於水的吸收。

完全 (並且叫成熟)  - 透鏡是完全不透明的防止的視覺在那隻眼睛。透鏡也許是膨脹的(擴大的由於水的吸收) 。

完成 以收縮 (並且叫做hypermature)    - 殘餘的透鏡纖維是不透明的, 但有減少在這材料裡並且水, 導致在透鏡的大小的減退, 通常通過鋪平。如果膠囊是確切, 患者也許能看通過部份何處一點對沒有表皮材料遺骸的或在透鏡附近如果收縮導致一條更小的直徑。

Morgagnian - 外皮被液化, 但中堅力量不是和不漂浮在外皮(定居以重力) 。
分類根據年齡的依據:
先天 - 禮物出生時。

發展 - 某時顯現出在誕生以後, 但一般在成年之前- 許多可遺傳和營養大瀑布歸入這個類別。
這些有時指' 少年' 大瀑布。這是不幸的因為其他人採取了這對手段具體個體; ' juvenile ' 只描述大瀑布是明顯的年齡。
退化 - 大瀑布形成在正常發展以後。這包括發生由於衰老的大瀑布(叫做' 老態龍鍾的' 大瀑布, 但只作為一個描寫期限) 。
將軍評論對大瀑布
這些申請不管型、起因, 或其它特點。

對光的Pupillary 反應 是正常的 除非有其它問題。光可能擊穿大瀑布和刺激視網膜; 如果大瀑布是異常地密集的, pupillary 反應也許是有些慢吞吞或較不發出音的, 但然而將是存在。

雖然多數大瀑布是進步對某一程度, 您應該從未預言盲目性起始。

總審查整個眼睛在大瀑布的第一標誌以便視網膜和視覺神經的狀態可能建立。這是作為未來參考當大瀑布提取也許被期望。它會是不幸的, 說最少, 去除大瀑布和然後學會患者有視覺神經發育不全或視網膜退化。

使用一mydriatic 為透鏡的考試和總使用一個系統像一個診斷集合, 不是檢眼計的otoscope 零件。

大瀑布的治療是 主要外科的。它應該是顯然的, 然而, 粗劣的視覺由於核或細胞核周圍的區域的不透明能被藥物學地膨脹緩和學生以便視覺可能發生在不透明附近。持久mydriatics, 譬如atropine 投下, 也許被使用保持學生膨脹以極小的努力在客戶部分。如果大瀑布non-progressive, 這也許是所有是需要的。如果它進步, 手術也許被考慮當mydriatic 不再是有用的。

眼內手術介入對專業儀器和技術的用途, 和是在範圍這套之外筆記。大瀑布提取在狗一般被報告是大約70-75% 成功如果有患者的仔細的選擇並且如果規程譬如phacoemulsification 被使用。預測在其它種類是如下: 貓- 好; 馬- 貧寒在成人, 好在駒少於9 個月大(Gelatt, 等。); 大主教- 非常好(容易比在其他人); 牛- 好。

眼內手術要求實踐並且它不建議普通開業醫生嘗試這手術的型除非它將定期地做, 並且在專題培訓之後。

大瀑布提取一般被分類入二型:
Intracapsular - 透鏡的撤除沒有爆裂膠囊。困難在多數非人動物由於zonules 和緊持的牢固的附件對先前玻璃面孔。

Extracapsular - 透鏡的撤除在去除先前膠囊以後。後部膠囊通常被留下到位。
在大瀑布 描述之後不透明的透鏡材料的生產由透鏡上皮細胞忘記了在extracapsular 提取期間。
大瀑布的吸回
在幼小動物(特殊狗少於4 年年紀), 那裡也許是cataractous 透鏡的吸回(Rubin 和Gelatt), 有時對程度充足恢復視覺 ; 視覺回歸是罕見的和通常需要8-12 個月 如果它發生。您臨床將看起皺紋透鏡膠囊  和透鏡的較少伸進通過學生(依照被觀看從邊) 。這發現表明, 透鏡進行吸回。' 外國') 的透鏡蛋白質(丟失通過膠囊發起是易變的在程度的虹膜睫狀體炎, 但通常是溫和的。在多數情況, resorptive 過程和伴隨炎症比幾個月和炎症容易地通常被控制與典型類皮質激素和iridocycloplegics 不持續更多。
大瀑布作為臨床個體
在這個部分被列出一些您也許盼望看的具體類型大瀑布。多數歸結於具體起因, 但一些代表起因未被確定的分明個體(Barnett) 。

玻璃狀的大瀑布 : 不透明後部subcapsular 和膠囊狀, 和排列在大小從針尖對一塊大, 白色匾包含血管。它由瑕疵造成在玻璃狀的船的resorptive 過程和是先天的。通常不進步; mydriatics 也許是有用的如果視覺是受影響的。小玻璃狀的殘餘(沒有透鏡不透明) 被發現在所有動物和共同地是沒有關心。

Y 縫合大瀑布 : 顆粒狀聚集沿Y 縫合的胳膊。不不凡。它重要因為它進步在一些動物並且它也許代表可遺傳的大瀑布的一個變量表達式被看見在金黃獵犬。

堅持pupillary 膜大瀑布  : 這些先前膠囊狀和通常non-progressive 。5月範圍在大小從針尖對大匾。相對地少量患者與堅持pupillary 膜將有大瀑布。嘗試mydriatics 如果視覺是受影響的。外科療法不應該試圖。

新陳代謝的大瀑布: 許多新陳代謝的疾病, 糖尿病mellitus 是最佳的例子 , 導致反過來導致大瀑布的瑕疵透鏡養料。損害開始在赤道表皮或後部subcapsular 地區和迅速地經常首先進步。一旦他們開始, 他們也許推進到完整性不管治療。大瀑布提取可能是成功的如果患者是很好受控的為系統疾病。
在糖尿病mellitus 情況下, 反常地被舉起的血液葡萄糖含量導致增量在葡萄糖裡在透鏡之內。這超載正常葡萄糖路和導致無法逃脫透鏡和結果在流體吸收由透鏡的增加的山梨糖醇(opacification 結果) 。
嚙齒目動物接受麻醉 並且知道開發瞬變大瀑布如果眼皮不被保持閉合(Fraunfelder 和燒傷) 。

毒性大瀑布: 眾多的藥物將導致雙突透鏡的opacities (Sanford 和公爵) 。幸運地, 大多共同的治療代理不看來是cataractogenic 在通常被使用的藥量。 Disophenol, 被使用在對待的hookworm 傳染, 可能導致雙突透鏡的opacities 在藥量臨床不更加高級比被使用, 但這些opacities 通常是反演性的在藥物被中斷之後。

可遺傳: 各種各樣的種類和養殖有素質為cataractogenesis 。在狗一些養殖, 例如, 大瀑布形成是可遺傳的。在其他人, 疾病的可遺傳的本質被懷疑, 但不被證明。
可遺傳的大瀑布一般是明顯的在最初的少數歲月生活之內, 但可能是先天的。各養殖看上去有樣式奇怪對本身。

患者與可遺傳的大瀑布不應該被使用為養殖。如果先天或早期的起始大瀑布發生在不被認為有可遺傳的大瀑布的養殖, 幾件事可能做確定如果大瀑布是可遺傳的。首先, 陛下和水壩可能仔細地被審查為大瀑布的證據; 如果繼承方式隱性, 兩個父母能phenotypically 是法線。下步會是相關個體的家譜和, 如果可能, 考試的仔細的評估。如果父母是正常的並且沒有大瀑布的證據在家譜, 秒鐘聯接能然後完成並且所有子孫審查了。這是不能接受的從我的觀點因為有一個嚴肅的狗人口過剩問題並且測試養殖對問題只貢獻。另外, 如果情況是可遺傳的, 小狗也許是受影響或載體, 也許開發視覺困難或傳遞特徵。簡單地最好不使用可疑的狀態狗為養殖。

下列是養殖一張部份名單知道有或最初地被懷疑有可遺傳的大瀑布, 與起始的年齡, 繼承一起類型不透明和方式, 如果已知。最終進展完成opacification 。
阿富汗 - 4 個月到2 年- 赤道空泡- 可能autosomal 隱性(羅伯特和幫手) 。

美國 斗雞家spaniel  - 先天或在第一4 年之內- 後部subcapsular 或各種各樣的表皮地區- 至少一個形式autosomal 隱性(Yakely) 。

金黃獵犬 - 先天或在第一年之內- 後部, 三角或者沿縫合或subcapsular - 認為是統治的與易變的penetrance (Rubin) 。

微型schnauzer - 先天或在第一年之內- 後部subcapsular 或完全- autosomal 隱性(Barnett) 。

老英國sheepdog - 先天或在第一年之內- 核或表皮- 可能autosomal 隱性(Koch) 。

長捲毛狗(縮樣和玩具) - 在第一3 年之內- 後部subcapsular - autosomal 隱性。

其它似犬養殖 - 有可觀的文學在這個主題; 參見被援引的參考對於更多資訊(Bjerk?and Bergsjo; Gelatt, 等。; Narfstr?/a >; Rubin 和花) 。

貓 - 並非為人所知關於可遺傳的大瀑布。

馬 - 任一隻駒與先天或早期的起始大瀑布應該被認為可疑對有可遺傳的疾病, 但具體不為人所知。摩根馬被顯示有先天核大瀑布哪些可以是可遺傳的在自然(山毛櫸裡, 等。) 。

其它種類 - 大瀑布共同地被看見在其它種類並且他們的遺傳能力在某些情況下被闡明了; 大瀑布認為是可遺傳的或為哪些其它起因未被展示可能被發現在鳥、degus 、老鼠、豬、兔子、鼠, 綿羊和其他人(Barr, 等。; 溪, 等。; Gelatt; Slatter, 等。; Tsai, 等。) 。
複雜或次要大瀑布: 視覺傷害、uveitis 或其它眼內炎症和一些系統病症也許導致大瀑布(Ashton, 等。) 。如果有對透鏡的較小損失並且起因被改良, 不透明大概被形成固定式。如果有週期性uveitis 或如果原始的傷害嚴厲地損壞了透鏡, 不透明也許擴大和最終介入整個透鏡。

治療瞄準消滅起因。Mydriatics 也許是有用的為殘缺不全的大瀑布, 如所描述早先。
透鏡位移(luxation 和半脫位; ectopia lentis)  
部份或完全故障的zonular 附件導致透鏡的位移。如果透鏡保留在patellar 窩它被考慮subluxated; 如果透鏡搬入先前分庭或玻璃, 它是luxated 。

起因
先天- 罕見, 看見以其它先天問題。

創傷- 通常有嚴厲一致眼內損傷因為精神創傷必須是偉大為了劃分正常zonules 。

自發- 最頻繁地看見在狗(wire-haired 狐狸狗、Sealyham 、威爾士和曼徹斯特); 偶爾地在波士頓狗, basset 追逐和斗雞家spaniels 。疾病是可遺傳的和是窮地被開發的zonules 的結果(Curtis 和Barnett) 。透鏡通常不偏移, 然而, 直到個體是2 到5 年年紀。偶爾地看見在馬和貓(Olivero, 等。) 。

次要對其它疾病, 特別是那些導致增加的地球大小, 這樣作為青光眼。在後者案件, zonules 爆裂由於舒展由地球的擴大造成。
標誌和診斷
虹膜將顯示振動或振翼; 這被命名 iridodonesis 和根本上是pathognomonic 為ectopia lentis 。雖然通常容易地看, 它的形象化可能由做促進gonioscopy 。先前分庭也許淺的比法線; 作用也許是不規則因為透鏡也許被掀動造成只虹膜一個區域先前被偏移。評估先前分庭由觀察眼睛從邊。

在自發位移案件在養殖有可遺傳的素質, 它是重要評估相反眼睛為緊急位移的標誌因為兩隻眼睛通常是受影響的。這應該並且被考慮到當給預測客戶。

半脫位: 透鏡保留在patellar 窩。在許多情況下, 透鏡將被轉移在或到一邊下以便有將是aphakic 月牙(沒有透鏡) 學生的區域 ; 如果透鏡未轉移, aphakic 月牙不會是存在。制服室照明和使用一個昏暗的光源促進看aphakic 月牙。一個紫外光來源也許是有用的在 確定透鏡的位置。

Luxation:
先前 luxation  - 透鏡也許審閱學生和在在先前分庭, 它也許摩擦反對角膜和導致角膜腫鼓。通常, 透鏡的赤道疆界直接地看, 或可能由發光強調光從邊當觀察從前線: 在哪裡光被指揮的疆界相對於將發光。 紫外光可能並且被使用。如果角膜是太不透明的, 您不會能做診斷。
透鏡也許簡單地抓緊進行虹膜, 造成極端淺先前分庭。

在許多情況下, 透鏡也許是流動的當仍然附有先前玻璃面孔。
後部luxation - 透鏡的運動也許導致玻璃液化; 這叫做元音融合。透鏡然後可以luxate 入玻璃洞。這通常導致深深地比正常先前分庭, 以被鋪平的虹膜外形。透鏡通常安定對玻璃洞的腹方面。
意義
透鏡位移通常導致適度虹膜睫狀體炎和, 在許多情況下, 它並且導致青光眼(據推測由含水流程阻抗由角度或pupillary 塊) 以地球的擴大。一眼睛擴大的由於青光眼從其他導致也許還有透鏡luxation 。它重要區分主要從次要透鏡位移在擴大的眼睛。狗的養殖是有用的, 狗由主要透鏡位移大概影響。如果青光眼影響只一隻眼睛在非狗養殖, 另一眼睛可能仔細地被審查: 如果這隻眼睛是正常的, luxation 在另一眼睛大概次要。有時透鏡的位置也許提供線索。在主要luxation, 重力腹上會偏移透鏡; 當透鏡被撞出因為zonules 打破了次要對眼睛擴大, 一些zonules 也許更加有抵抗性以便透鏡那時附上; 因而, 如果透鏡背部地附上得, 位移也許是次要對眼睛擴大。

先前透鏡位移可能將導致青光眼。後部luxation 也許由眼睛更好容忍, 但它可能還同青光眼聯繫在一起; 青光眼的原因在a 情況下posteriorly luxated 透鏡不是確切。這些透鏡有潛力任何時候先前luxating 。
治療和預測
透鏡撤除是唯一的合理的治療為自發luxation 或半脫位。及早疾病被診斷和被對待, 更加偉大挽救視覺的機會。如果青光眼是存在與位移一起, 或如果有玻璃退化, 預測是被守衛。如果青光眼是慢性的, 它也許堅持在透鏡撤除以後。

其它類型透鏡luxations 必須被處理根據他們的起因。例如, luxation 次要對青光眼不應該外科地被對待因為位移次要。創傷透鏡位移通常有一種粗劣的預測由於視覺損傷嚴肅。
透鏡破裂
這是一個不凡的情況通常與相關嚴厲精神創傷對眼睛。雖然任一枚針對性的對象或飛彈可能導致破裂在任一個種類, 嚴厲吹動對馬的頭也許導致破裂。

創傷起因是顯然的在許多情況下。在馬與破裂從非滲透的精神創傷, 透鏡外皮也許模仿纖維蛋白在先前分庭。

治療介入透鏡的撤除在撤除也許導致處保存眼睛。在其它案件, 眼睛應該被去除。



Cataract is an opacity of the lens (including the capsule) which results in loss of transparency of the lens and, therefore, interferes with vision (or visualization of the ocular fundus) . It can be focal, thus not preventing vision through clear portions of the lens , or diffuse, thus severely diminishing visual capability or even blinding . On a cellular level, it is associated with intra- and extracellular vacuolation and local precipitation of protein, loss of epithelial cells, aberrant epithelial cell differentiation or epithelial cell metaplasia. Cataract is the most common disease of the lens, simply because the lens reacts to most insults by opacifying. Although it can be an isolated condition, it often is seen associated with ocular abnormalities (van der Woerdt, et al.).

Pathogenesis
The pathogenesis of cataract development is not fully understood (Kinoshita). Lens fiber transparency is affected by swelling and coagulation of protein. Opacification due to the imbibition of water may be reversible if the pathologic process is corrected (Fraunfelder and Burns). Opacification due to chemical changes in the proteins is irreversible. These biochemical changes often are specific for the type of cataract. Generally, water, percent of ash, sodium and calcium are increased, and oxygen consumption, glutathione, ascorbic acid, potassium, soluble protein and riboflavin are decreased.
Classification
Cataracts are classified in various ways and this multiplicity of classification schemes leads to confusion. An understanding of the disease process may be much more meaningful than any classification scheme. However, classification on the basis of stage of formation may be meaningful because this describes the progression of most cataracts regardless of cause (Playter).

Classification by stage of formation:
Incipient  - when first evidence of opacification is seen. Vision is not affected. The opacity may or may not progress.

Incomplete (also called immature)  - lens is largely, but not completely, opaque. The patient may have some vision; a tapetal reflex is visible. The lens may be slightly enlarged due to imbibition of water.

Complete (also called mature)  - lens is totally opaque preventing vision in that eye. The lens may be intumescent (enlarged due to imbibition of water).

Complete with shrinkage (also called hypermature)    - remaining lens fibers are opaque, but there is a reduction in this material as well as water, causing a decrease in the size of the lens, usually through flattening. If the capsule is clear, the patient may be able to see through portions where little to no cortical material remains or around the lens if shrinkage results in a smaller diameter.

Morgagnian - cortex is liquefied, but nucleus is not and floats in the cortex (settles with gravity).
Classification on basis of age:
Congenital - present at birth.

Developmental - develops sometime after birth, but generally before adulthood - many of the heritable and nutritional cataracts fall into this category.
These sometimes are referred to as 'juvenile' cataracts. This is unfortunate because others have taken this to mean a specific entity; 'juvenile' only describes the age at which the cataract was manifest.
Degenerative - cataract formation after normal development. This includes cataracts which occur as a result of senescence (called 'senile' cataracts, but only as a descriptive term).
General comments on cataracts
These apply regardless of type, cause, or other features.

Pupillary responses to light are normal unless there are other problems. Light can penetrate the cataract and stimulate the retina; if the cataract is unusually dense, the pupillary response may be somewhat sluggish or less pronounced, but will nevertheless be present.

Although most cataracts are progressive to some degree, you should never predict the onset of blindness.

Always examine the entire eye at the first sign of cataract so that the status of the retina and optic nerve can be established. This is for future reference when cataract extraction may be anticipated. It would be unfortunate, to say the least, to remove the cataract and then learn the patient had optic nerve hypoplasia or retinal degeneration.

Always use a mydriatic for examination of the lens and use a system like the otoscope part of a diagnostic set, not the ophthalmoscope.

Treatment of cataract is primarily surgical. It should be obvious, however, that poor vision due to an opacity of the nuclear or perinuclear area could be alleviated by pharmacologically dilating the pupil so that vision can occur around the opacity. Long lasting mydriatics, such as atropine drops, may be used to keep the pupil dilated with minimum effort on the part of the client. If the cataract is non-progressive, this may be all that is needed. If it progresses, surgery may be considered when the mydriatic no longer is helpful.

Intraocular surgery involves the use of specialized instruments and techniques, and is beyond the scope of this set of notes. Cataract extraction in the dog generally is reported to be about 70-75% successful if there is careful selection of patients and if procedures such as phacoemulsification are used. Prognosis in other species is as follows: cat - good; horse - poor in adult, good in foal less than 9 months old (Gelatt, et al.); primates - very good (easier than in others); cattle - good.

Intraocular surgery requires much practice and it is not recommended that the general practitioner attempt this type of surgery unless it is to be done routinely, and only after special training.

Cataract extraction is generally classified into two types:
Intracapsular - removal of the lens without rupturing the capsule. Difficult in most nonhuman animals due to firm attachment of zonules and adherence to the anterior vitreous face.

minibabyqq 2006-12-28 01:18

[color=Magenta][size=5][b]Osteosarcoma (骨癌) Osteosarcoma (Bone Cancer)   [/b][/size][/color]


Osteosarcomas 佔只5% 所有似犬 腫瘤, 但80-90% 敵意介入骨頭。共同在大養殖狗, osteosarcoma 是經常要求受影響的肢體截肢術被結合與化療提供臨時安心從 這種 進取的疾病骨頭的進取的癌症。
哪條狗是在危險中為開發osteosarcomas?

Osteosarcomas 一般影響更舊的大或巨型養殖狗。大的養殖在最巨大的風險為開發osteosarcoma 包括了不起的丹麥人、聖徒Bernards, 偉大的比利牛斯、Newfoundlands 、Bernese 山狗, 和愛爾蘭Wolfhounds 。大養殖譬如Rottweilers 、Labradors 、金黃獵犬、牧羊人、Dobermans 、Weimaraners, 和拳擊手並且是在一種增加的風險。這不是一個非常共同的腫瘤在小養殖狗和很少不發生在貓。稱80 磅的狗60 倍可能證明是至少開發osteosarcoma 比狗稱少於75 磅。當更舊的狗通常開發osteosarcomas, 那裡看來是增加的發生在一到二歲中尾隨。馬律狗有osteosarcomas 的增加的發生。

它是未知的為什麼一些狗開發osteosarcomas, 但一種理論建議迅速地增長的細胞被發現在成長板材在骨頭基因上是在變化一種更加巨大的風險。其它理論是, 腫瘤顯現出在精神創傷站點。增加的多孔的活動在破裂或精神創傷的站點能導致癌細胞的發展。現實是, 這兩可以是真實的並且那裡也許是其它起因不被發現。

什麼是osteosarcomas 症狀?

osteosarcomas 症狀經常嚴密同他們的地點聯繫在一起。多數osteosarcomas 顯現出在狗肢體在手肘之下或臨近膝蓋。腫瘤通常形成在或者靠近成長板材。受影響的狗經常將有發出音的骨頭膨脹。 X-射線 經常顯露, 被結合與歷史和養殖, 也許表明osteosarcoma 的發展的一個典型骨頭樣式。這些腫瘤經常導致痛苦在可能首先被查出作為瘸在受影響的肢體的聯接。90% 這些腫瘤將有 轉移 對肺在診斷之時, 但由於轉移的小最初的大小, 少於10% 最初地將出現在胸部X光。由於這轉移的高發生, 所有狗與osteosarcomas 被對待好像他們有轉移對肺不管研究結果在最初的肺X-射線。Osteosarcomas 偶爾地將出現在不同的地點並且其它腫瘤類型可能最初地同樣看來是osteosarcoma 。由於這種可能性, 切片檢查法 總被推薦。黴菌骨頭傳染可能導致相似的症狀和出現在X-射線, 因此黴菌文化經常執行幫助澄清診斷。

什麼是治療為osteosarcoma?

Osteosarcoma 是要求一個進取的治療協議的進取, 高度變形的癌症。一旦腫瘤正面地被辨認了作為osteosarcoma, 受影響的肢體通常被截肢。在腫瘤是在正確的地點的罕見的案件, 一些肢體饒恕的手術做了, 但那通常不是實際情形。在截肢術以後, 化療路線通常開始。最成功的藥物是carboplatin 和cisplatin 。Carboplatin 更加昂貴, 但更加安全和更加容易執行。Doxorubicin 有時被使用。一位合格的獸醫癌症醫師經常是最佳的資訊源並且他或她意識到最新的化療協議。一條狗的估計壽命與一適當地辨認的和被對待的osteosarcoma 很大地變化, 但可能接近一年或長期。

osteosarcoma 是可防止的嗎?

不看起來, osteosarcoma 是可防止的。由於一些強的養殖交互作用, 有的任一條養殖線osteosarcoma 的歷史應該被審查嚴密在養殖前。不幸地, 我們不完全地瞭解osteosarcoma 的起因, 但有希望地當我們的知識改善, 我們能繼續提供更加有效的治療和早期診斷測試。

Osteosarcomas account for only 5% of all canine tumors, but 80-90% of malignancies involving the bone. Much more common in large breed dogs, osteosarcoma is an aggressive cancer of the bone that often requires amputation of the affected limb coupled with chemotherapy to provide temporary relief from this aggressive disease.
Which dogs >><<

Osteosarcomas generally affect older large or giant breed dogs. The giant breeds >><<eat Danes, Saint Bernards, Great Pyrenees, Newfoundlands, Bernese Mountain Dogs, and Irish Wolfhounds. Large breeds such as Rottweilers, Labradors, Golden Retrievers, Shepherds, Dobermans, Weimaraners, and Boxers are also at an increased risk. It is not a very common tumor in small breed dogs and rarely occurs in cats. Dogs that weigh over 80 pounds have been shown to be at least 60 times more likely to develop an osteosarcoma than dogs weighing less than 75 pounds. While older dogs more commonly develop osteosarcomas, there does appear to be an increased incidence in one to two year old dogs as well. Male dogs have an increased incidence of osteosarcomas.

It is unknown why some dogs develop osteosarcomas, but one theory suggests that the rapidly growing cells found at the growth plates in the bones are genetically >><<ased cellular activity at the site of a fracture or trauma could result in the development of cancer cells. The reality is that both of these may be true and there may be other causes not yet discovered.

What are the symptoms of osteosarcomas?

The symptoms of osteosarcomas are often closely associated with their location. Most osteosarcomas develop on the limbs of dogs below the elbow or near the knee. The tumors usually form at or near the growth plates. Affected dogs will often have a pronounced bone swelling. X-rays often reveal a characteristic bone pattern that, coupled with history and breed, may indicate the development of an osteosarcoma. These tumors often produce pain in the joint that can first be detected as lameness in the affected limb. Up to 90% of these tumors will have metastasis to the lungs at the time of diagnosis, but because of the small initial size of the metastases, less than 10% will initially show up on a chest x-ray. Because of this high incidence of metastasis, all dogs with osteosarcomas are treated as if they have metastasis to the lungs regardless of the findings on the initial lung x-rays. Osteosarcomas will occasionally show up at different locations and likewise other tumor types can initially appear to be an osteosarcoma. Because of this possibility, a biopsy is always recommended. Fungal bone infections can produce similar symptoms and appearance on an x-ray, so a fungal culture is often performed to help clarify the diagnosis.

What is the treatment for osteosarcoma?

Osteosarcoma is an aggressive, highly metastatic cancer that requires an aggressive treatment protocol. Once the tumor has been positively identified as an osteosarcoma, the affected limb is usually amputated. In rare cases where the tumor is in the right location, some limb-sparing surgeries have been performed, but that is not usually the case. After the amputation, a course of chemotherapy is usually begun. The most successful drugs have been carboplatin and cisplatin. Carboplatin is more expensive, but safer and easier to administer. Doxorubicin is sometimes used as well. A qualified veterinary oncologist is often the best source of information and he or she will be aware of the newest chemotherapy protocols. The life expectancy of a dog with a properly identified and treated osteosarcoma varies greatly, but can approach a year or longer.

Is osteosarcoma preventable?

It does not appear that osteosarcoma is preventable. Because of some strong breed correlations, any breed line that has a history of osteosarcoma should be examined closely prior to breeding. Unfortunately, we do not completely understand the cause of osteosarcoma, but hopefully as our knowledge improves, we can continue to provide more effective treatments and early diagnostic tests.

minibabyqq 2006-12-28 01:20

[color=Magenta][size=5][b]白內障手術 Cataract Surgery  [/b][/size][/color]

[size=12px][table=98%][tr][td=2,1][align=center][size=+3]大瀑布手術:
[size=+2][size=+3][size=+2]當前的科技目前進步水平[img=219,179]http://www.veterinaryvision.com/pictures/liu2.jpg[/img][/align][align=left]大瀑布是盲目性的主導的起因在狗。雖然他們也許顯現出由於視覺精神創傷或炎症, 大瀑布最頻繁地發生在純血統狗, 他們幾乎總被繼承。起始的年齡是易變的, 通常從5-8 年紀。[/align]
幾年前, 我們被教等待直到大瀑布"成熟" (造成盲目性) 做手術。以最近前進在大瀑布撤除的技術, 它變得有利做手術及早, 如此避免複雜化與相關透鏡導致的uveitis 和次要青光眼。手術單邊地經常現在做沒有等兩個透鏡變得完全地不透明。在任何情況下, 這總是最佳執行一次最初的考試足夠及早形象化fundus 肯定, 沒有一致視網膜退化的證據。
[size=+2][size=+2]外科技術 當前, 大瀑布被extracapsular 提取或phacoemulsification 去除或。兩個技術留給後部透鏡膠囊原封為一個眼內透鏡的安置。Extracapsular 提取介入180 度切開在周邊角膜以透鏡外皮和中堅力量的先前透鏡膠囊和手工表示的撤除。這個技術是必要的在非常密集的大瀑布撤除。Phacoemulsification 運用超聲波波浪破壞大瀑布以透鏡片段的同時灌溉和志向。這個技術好處是:
[list][*]更小的角膜切開[*]維護先前分庭以對角膜內皮的較少損傷[*]透鏡片段更加詳盡的撤除。[/list]Phacoemulsification 是最有用的在更軟的(較不成熟) 透鏡撤除。高成功率(90.2%) 與相關phacoemulsification 鼓勵了大瀑布更加早期的撤除。
[/td][/tr][tr][td=2,1]
[img=216,264]http://www.veterinaryvision.com/pictures/cataract.jpg[/img]  






[/td][/tr][tr][td=2,1][align=center][img=290,264]http://www.veterinaryvision.com/pictures/lens_iol.jpg[/img][/align][/td][/tr][tr][td=2,1][size=+2][size=+2]眼內透鏡 在不複雜的大瀑布提取以後單獨, 視覺被改進既使透鏡不被替換。這導致什麼叫做"功能視覺" 。患者能一般駕駛沒有碰到事但經常有困難以深度知覺和演奏與玩具。替換眼內透鏡被使用了跟隨大瀑布撤除在人從50 年代。在玻璃或聯絡是不切實際的我們的動物患者, 對眼內更正的需要是偉大的。折射力量需要由地球的軸向長度, 角膜的曲度, 和替換透鏡的地點確定在眼睛之內。在人, 16-18 diopters 透鏡一般被使用; 測量在狗眼睛表明, 40-43 diopters 透鏡必需。因而, 狗站立從對替換眼內透鏡的用途很大地有益於。眼內透鏡經常被做polymethylmethacrylate 的光學部份(PMMA) 以靈活的haptics 修理透鏡在膠囊狀的袋子之內。複雜化跟隨眼內透鏡安放是不凡和不通常伴生的以替換透鏡的出現。視覺表現的評估, 雖然必要主觀, 表明顯著改善的視覺當替換透鏡被使用。
在膠囊狀的袋子是不穩定的(處和與a luxated 透鏡) 它是可能種入直接地然後被縫合入ciliary 溝的替換透鏡。這個做法成為通常執行和導致很大地改善的視敏度。
Phacoemulsification 錄影帶可利用我們有一盤短的(大約10 分鐘) 教育錄影帶關於phacoemulsificaiton 為大瀑布提取。這個做法好處被談論並且回答多數常問問題關於前和手術後關心。實際手術的英尺長度被攝製通過經營的顯微鏡說明技術包括替換眼內透鏡的安放。敘述被設計容易地被瞭解和也許是有用的對客戶考慮這個做法。請打電話給我們的辦公室請求拷貝。
[img=412,266]http://www.veterinaryvision.com/pictures/eyedrawing-cataract.gif[/img][/td][/tr][/table][table=98%][tr][td=2,1][align=center][size=+3]Cataract Surgery:
[size=+2]The Current State of the Art[img=219,179]http://www.veterinaryvision.com/pictures/liu2.jpg[/img][/align][align=left]Cataracts are a leading cause of blindness in dogs. Although they may develop as a result of ocular trauma or inflammation, cataracts occur most frequently in purebred dogs, where they are nearly always inherited. The age of onset is variable, usually from 5-8 years of age.[/align]
Years ago, we were taught to wait until a cataract "matures" (resulting in blindness) to perform surgery. With recent advances in techniques for cataract removal, it has become advantageous to perform surgery earlier, thus avoiding complications associated with lens-induced uveitis and secondary glaucoma. Now surgery is more often performed unilaterally without waiting for both lenses to become completely opaque. In any case, it is always best to perform an initial examination early enough to visualize the fundus to be certain that there is no evidence of concurrent retinal degeneration.
[size=+2]Surgical Techniques Currently, cataracts are removed either by extracapsular extraction or phacoemulsification. Both techniques leave the posterior lens capsule intact for placement of an intraocular lens. Extracapsular extraction involves a 180 degree incision in the peripheral cornea with removal of the anterior lens capsule and manual expression of the lens cortex and nucleus. This technique is necessary in the removal of very dense cataracts. Phacoemulsification utilizes ultrasound waves to break up the cataract with simultaneous irrigation and aspiration of the lens fragments. The advantages of this technique are:
[list][*]smaller corneal incision[*]maintaining the anterior chamber with less damage to the corneal endothelium[*]more thorough removal of lens fragments.[/list]Phacoemulsification is most useful in the removal of softer (less mature) lenses. The high success rates (90.2%) associated with phacoemulsification have encouraged earlier removal of cataracts.
[/td][/tr][tr][td=2,1]
[img=216,264]http://www.veterinaryvision.com/pictures/cataract.jpg[/img]  






[/td][/tr][tr][td=2,1][align=center][img=290,264]http://www.veterinaryvision.com/pictures/lens_iol.jpg[/img][/align][/td][/tr][tr][td=2,1][size=+2]Intraocular lenses Following uncomplicated cataract extraction alone, vision is improved even if the lens is not replaced. This resulted in what has been called "functional vision". Patients can generally navigate without bumping into things but often have difficulty with depth perception and playing with toys. Replacement intraocular lenses have been used following cataract removal in humans since the 1950s. In our animal patients where glasses or contacts are impractical, the need for intraocular correction is even greater. The refractive power needed is determined by the axial length of the globe, the curvature of the cornea, and the location of the replacement lens within the eye. In humans, a lens of 16-18 diopters is generally used; measurements in dog eyes indicates that a lens of 40-43 diopters is required. Thus, dogs stand to benefit greatly from use of a replacement intraocular lens. Intraocular lenses are most often made of an optical portion of polymethylmethacrylate (PMMA) with flexible haptics to fix the lens within the capsular bag. Complications following intraocular lens implantation are uncommon and not usually associated with the presence of the replacement lens itself. Evaluations of visual performance, although necessarily subjective, indicate significantly improved vision when a replacement lens is used.
Even in cases where the capsular bag is unstable (as with a luxated lens) it is still possible to implant a replacement lens which is then directly sutured into the ciliary sulcus. This procedure is becoming more commonly performed and has resulted in greatly improved visual acuity.
Phacoemulsification Videotape AvailableWe have a short (approximately 10 minutes) educational videotape about phacoemulsificaiton for cataract extraction. The advantages of this procedure are discussed as well as answering the most frequently asked questions about the pre- and post-operative care. Footage of an actual surgery filmed through the operating microscope illustrates the technique including implantation of a replacement intraocular lens. The narration is designed to be easily understood and may be helpful to clients considering this procedure. Please call our office to request a copy.
[img=412,266]http://www.veterinaryvision.com/pictures/eyedrawing-cataract.gif[/img][/td][/tr][/table][/size]

minibabyqq 2006-12-28 01:23

[color=Magenta][size=5][b]腎臟移植 Kidney Transplantation   [/b][/size][/color]


NFORMATION 為寵物所有者
下列是關於腎臟移植的一些總說明。各個盒單獨地被對待, 和不能遵守這些指南。當每一努力被做保持這資訊準確, 它絕不是完全的。

腎臟失敗在貓
慢性腎臟失敗(慢性腎衰竭, CRF) 是疾病的當中一個帶領的起因在更舊的貓, 雖然它可能並且發生在幼小貓。它由各種各樣的問題造成; 同道會的當中一個是腎臟功能部件, 稱nephrons, 逐個停止運作的老化變動。其它nephrons 將完成額外工作由點決定, 補償nonfunctioning 部分, 但那裡來點當他們無法跟上, 並且這是腎臟疾病的標誌變得明顯。其它腎臟失敗的起因包括傳染、毒素, 和癌症。

慢性腎臟失敗治療
腎臟失敗的治療包括許多不同的方面。在嚴厲案件, 住院治療給靜脈內流體對"充足" 是必要的, 在腎臟之外。當情況是更加穩定的, 可變的治療可能在家被給以皮膚下(在皮膚之下) 流體的形式。其它治療包括特別飲食與被減少的蛋白質和磷、療程防止磷吸收, 激素替換與貧血症交戰, 和反潰瘍療程為噁心。這些措施幫助貓與腎臟失敗感受更好和活更長, 但腎臟疾病繼續進步。

移植作為一種治療為CRF
腎臟移植可能幫助對待疾病由提供一個健康腎臟執行所有正常作用。在成功的移植以後, 只二個療程是需要的防止腎臟的rejection 。

誰可能有腎臟移植?
移植會是適當的為有腎臟疾病從老化或先天缺陷的貓, 或幾其它類型腎臟疾病如果他們由傳染或癌症不造成。貓被考慮為移植將審閱一連串測試確定沒有使這種治療複雜化的暗藏的問題。

誰無法有腎臟移植?
有傳染的貓無法有移植因為他們會傳染被移植的腎臟和會導致它失敗。同樣適用為多數種腎臟癌症。被感染似貓的白血病病毒或似貓的免役缺陷病毒的貓並且不是適當的因為免疫鎮壓必要防止他們攻擊新腎臟使他們非常不適。有其它疾病除腎臟、特別是心臟或食道疾病之外的貓, 傾向於不是足夠強的安全地作必需的手術。由於困難在壓制免疫系統沒有過份副作用, 移植在狗不是現在可以得到的。

新腎臟何處來自?
貓(和人們和狗, 太) 像必要的正常生活能有正常腎臟作用以只一個正常腎臟一半, 因此一隻健康貓能捐贈一個整個腎臟和仍然有兩倍同等數量腎臟作用。貓的家庭接受被移植的腎臟必需採取施主貓和給它終身家。我們的腎臟捐款人是需要家的貓。他們廣泛地被篩選了為任一疾病或傳染。



被移植的腎臟外科解剖學。 被移植的腎臟的船附有主動脈和cavdal venacava 。當地腎臟剩下到位

準備好手術
在確定以後, 貓是一名好候選人為移植, 手術預定。幾天在預定的手術之前, 貓應該被承認醫院為靜脈內可變的療法和完成最後測試。一個兼容腎臟捐款人將被辨認, 並且對捐款人的最後的測試將被完成在這些少量天期間, 還。

手術
移植介入去除一個腎臟從一隻健康施主貓, 安置它在腹部在接收者附近的鼠蹊區域, 和附有它血管導致腿。接收者的自然二個腎臟通常剩下到位。接收貓必須然後被安置在療程防止免疫系統rejecting 新腎臟。一支哺養的管被安置在手術之時, 對幫助直到貓的胃口返回(通常在月之內) 。



病後調養在醫院
監視在手術包括觀看腎臟作用、療程的血液貧血症的水平, 水平, 和各種各樣的其它方面之後。多數貓將停留在醫院1 個到2 個星期在手術以後。

長期關心
貓用一個被移植的腎臟必須接受他們的醫學每日兩次, 每天, 防止新腎臟的rejection 。在手術之後, 每週復校與狩醫要求檢查腎臟價值和療程水平在血液。當時間繼續, 復校逐漸被減少對一次每3 個月。

結果
大約75% (三喪失四得到移植手術的) 貓生存和被送在家從醫院。一些貓將有複雜化在第一六個月, 並且大約60% 被移植的貓居住對6 個月在手術以後。複雜化的率減少在第一六個月以後(雖然複雜化是可能的在任一點), 並且40% 貓仍然去強在3 年以後, 並且有是6-10 年崗位手術的幾隻貓。

費用
在動物醫療中心, 費用為手術和時間在醫院在手術附近估計花費大致$8000 。後續關心, 包括療程和復校參觀估計爾後花費大約$4000 第一年, 和大概$3000 每年。

移植不是適當的為所有情況。一些貓有防止它的疾病。這是一個昂貴的做法。一些所有者沒有時候帶來貓為頻繁後續考試。一些貓每日兩次沒有態度適當為終身藥片管理和頻繁旅行對狩醫為考試和血液測試。為那些, 然而, 符合所有要求, 腎臟移植可能是給更長, 更加健康的生活否則不會是可能的做法。

NFORMATION FOR PET OWNERS
The following is some general information about kidney transplantation. Each case is treated individually, and may not adhere to these guidelines. While every effort is made to keep this information accurate, it is by no means complete.

Kidney failure in cats
Chronic kidney failure (chronic renal failure, CRF) is one of the leading causes of disease in older cats, although it can occur in young cats also. It is caused by a variety of problems; one of the more common causes is an aging change where the functional units of the kidney, called the nephrons, one by one stop working. The other nephrons will do extra work up to a point, to make up for the nonfunctioning ones, but there comes a point when they can't keep up, and this is when signs of kidney disease become apparent. Other causes of kidney failure include infection, toxins, and cancer.

Chronic kidney failure treatment
Treatment of kidney failure includes many different aspects. In severe cases, hospitalization to give intravenous fluids is necessary, to "flush" out the kidneys. When the situation is more stable, fluid treatment can be given at home in the form of subcutaneous (under the skin) fluids. Other treatments include special diets with reduced protein and phosphorus, medications to prevent phosphorus absorption, hormone replacement to combat anemia, and anti-ulcer medications for nausea. These measures help the cat with kidney failure feel better and live longer, but the kidney disease continues to progress.

Transplantation as a treatment for CRF
Kidney transplantation can help treat the disease by providing a healthy kidney to perform all of the normal functions. After successful transplantation, only two medications are needed to prevent rejection of the kidney.

Who can have a kidney transplant?
Transplantation would be suitable for >><<y disease if they are not caused by infection or cancer. A cat being considered for transplantation will go through a battery of tests to make sure there are no hidden problems that would complicate this treatment.

Who cannot have a kidney transplant?
Cats who have infection cannot have transplants because they would infect the transplanted kidney and cause it to fail. The same holds true for most kinds of kidney cancer. Cats who are infected with the feline leukemia virus or the feline immunodeficiency virus are also not suitable because the immune suppression necessary to prevent them from attacking the new kidney makes them very ill. Cats who have other disease in addition to the kidney, especially heart or gastrointestinal disease, tend not to be strong enough to safely undergo the required surgery. Because of the difficulties in suppressing the immune system without excessive side effects, transplantation in dogs is not currently available.

Where does the new kidney come from?
Cats (and people and dogs, too) can have normal kidney function with only one half of one normal kidney, so a healthy cat can donate an entire kidney and still have twice as much kidney function as is necessary for a normal life. The family of the cat receiving the transplanted kidney are required to adopt the donor cat and give it a lifetime home. Our kidney donors are cats who need a home. They have been extensively screened for any disease or infection.



Surgical anatomy of transplanted kidney. The vessels of the transplanted kidney are attached to the aorta and cavdal venacava. The native kidneys are left in place

Getting ready for surgery
After determining that a cat is a good candidate for transplantation, the surgery is scheduled. Several days before the scheduled surgery, the cat should be admitted to the hospital for intravenous fluid therapy and to complete the final testing. A compatible kidney donor will be identified, and the final tests on the donor will be completed during these few days, also.

The surgery
The transplantation itself involves removing one kidney from a healthy donor cat, placing it in the abdomen near the groin region of the recipient, and attaching it to the blood vessels leading to the leg. The recipient's natural two kidneys are usually left in place. The recipient cat must then be placed on medications to prevent the immune system from rejecting the new kidney. A feeding tube is placed at the time of surgery, to help until the cat's appetite returns (usually within the month).



Aftercare in the hospital
Monitoring after surgery includes watching the kidney function, blood levels of the medications, level of anemia, and a variety of other aspects. Most cats will stay in the hospital for 1 to 2 weeks after surgery.

Long term care
Cats with a transplanted kidney must receive their medicines twice a day, every day, to prevent rejection of the new kidney. Immediately after surgery, weekly rechecks with the vet are required to check on the kidney values and the medication levels in the bloodstream. As time goes on, the rechecks are gradually decreased to once every 3 months.

Outcome
About 75% (three out of four) of cats who get a transplant surgery survive and are sent home from the hospital. Some cats will have complications in the first six months, and about 60% of transplanted cats live to 6 months after surgery. The rate of complications decreases after the first six months (although complications are possible at any point), and 40% of cats are still going strong after 3 years, and there are a few cats who are 6-10 years post surgery.

Cost
At the Animal Medical Center, the cost for the surgery and the time in the hospital around surgery is estimated to cost roughly $8000. Follow-up care, including medications and recheck visits is estimated to cost around $4000 for the first year, and probably $3000 per year thereafter.

Transplantation is not appropriate for all situations. Some cats have diseases that prevent it. It is an expensive procedure. Some owners do not have the time to bring the cat in for frequent follow-up examinations. Some cats do not have an attitude appropriate for lifelong twice daily pill administration and frequent trips to the vet for examination and blood testing. For those, however, which do meet all the requirements, kidney transplantation can be a procedure that gives a longer, healthier life that would not otherwise be possible.

minibabyqq 2006-12-28 01:25

[color=Magenta][size=5][b]Coccidia (球蟲病): 腹瀉的起因Coccidia (Coccidiosis): A Cause of Diarrhea   [/b][/size][/color]


什麼是coccidia?


Coccidia 是小 protozoans (one-celled 有機體) 最共同地倍增在狗和貓小腸短文, 在小狗和小貓少於六個月年齡, 在免疫系統 被壓制 的成人動物, 或在被注重用其它方式的動物中(即; 改變在歸屬, 其它疾病禮物) 。

在狗和貓, 多數coccidia 是類稱 Isospora。 Isospora canis 和 I. ohioensis 是種類經常遇到在狗。不管哪個種類是存在, 我們一般提到疾病作為球蟲病。作為小狗變老, 他傾向於開發自然 免疫 對coccidia 的作用。作為成人, 他不能運載coccidia 在他的肚腑裡, 和流灑了 囊腫 在排匯物, 但體驗惡劣效果。

coccidia 怎麼被傳送?

小狗不被負擔以coccidia 有機體在他的肚腑裡。但是, 一旦出生, 小狗頻繁地暴露於他的母親的排匯物, 並且如果母親是 流出傳染性囊腫 在她的排匯物, 幼小動物可能然後將咽下他們並且coccidia 將顯現出在他們的肚腑之內。從幼小小狗, 通常那些少於六個月年齡, 沒有免疫對coccidia, 有機體再生產在了不起的數字和寄生於幼小動物的肚腑。經常, 這有嚴厲作用。

從對coccidia 的暴露在排匯物對病症的起始是大約13 天。是不適從coccidia 的多數小狗, 因此, 二星期年齡和更舊。雖然多數傳染是傳播的結果從母親, 這總不是實際情形。任一隻被傳染的小狗或小貓是傳染性的對其它小狗或小貓。在助長設施, 風雨棚、動物醫院, 等, 它是明智隔絕那些被傳染從那些不是。

什麼是球蟲病症狀?

動物的主要標誌遭受以球蟲病是腹瀉。腹瀉也許是溫和的對嚴厲根據傳染的水平。血液和黏液也許是存在, 特別是在先進的案件。嚴厲地受影響的動物也許並且嘔吐, 丟失他們的胃口, 成為脫水, 和例如, 模子從疾病。

多數被傳染的小狗由作者遇到是在四個到十二個星期年齡組。球蟲病的可能性應該總被考慮當寬鬆凳子或腹瀉遇到在這年齡組。微觀糞便檢查由獸醫將查出囊腫證實診斷。

什麼是風險?

雖然許多案件是溫和的, 它不是不凡看嚴厲, 血淋淋的腹瀉結果在失水和均勻死亡。這是最共同在是不適或傳染與其它寄生生物、細菌, 或病毒 的動物中。球蟲病是非常傳染性的, 特別是在幼小小狗之中。整個狗窩也許成為沾染, 與許多年齡組小狗同時影響。

什麼是球蟲病的治療?

值得一提的是, 重音充當在球蟲病的發展的一個角色。它不是不凡為一隻表面上健康小狗到達在他的新家和開發腹瀉幾天以後導致coccidia 診斷。如果小狗是在新家少於十三天, 那麼他有coccidia 在他到達了之前。記住, 潛伏期(從暴露到病症) 是大約十三天。如果小狗是以他的新所有者幾個星期, 對coccidia 的暴露很可能然後發生了在動物到達了在新家之後。

幸運地, 球蟲病是可治療的。藥物譬如 sulfadimethoxine (Albon®) 並且 trimethoprim sulfadiazine (Tribrissen®) 是有效的在coccidia 的治療和預防。由於這些藥物不殺害有機體, 而是寧可禁止他們的再生產能力, coccidia 的排除從肚腑不迅速。由停止原生動物的能力再生產, 時刻允許為小狗的自己的免疫開發和去除有機體。

球蟲病怎麼被防止或被控制?

由於coccidia 由載體動物排匯物 傳播, 它是非常重要對實踐嚴密的衛生。所有糞便材料應該被取消。安置需要是這樣, 食物和水無法成為沾染與排匯物。乾淨的水應該一直被提供。多數殺菌劑不運作很好反對coccidia; 排匯物的焚化, 和蒸汽清潔、浸沒在開水裡, 或10% 氨解答是最佳的方法殺害coccidia 。Coccidia 可能承受結冰。

蟑螂和飛行能機械上運載coccidia 從一個地方到另一個。老鼠和其它動物能咽下coccidia 和當由狗殺害和吃, 例如, 能傳染狗。所以, 昆蟲和嚙齒目動物控制是非常重要在防止球蟲病。

狗和貓的coccidia 種類不傳染人。
   




What are coccidia?


Coccidia are small protozoans (one-celled organisms) that multiply in the intestinal tracts of dogs and cats, most commonly in puppies and kittens less than six months of age, in adult animals whose immune system is suppressed, or in animals who are stressed in other ways (e.g.; change in ownership, other disease present).

In dogs and cats, most coccidia are of the genus called Isospora. Isospora canis and I. ohioensis are the species most often encountered in dogs. Regardless of which species is present, we generally refer to the disease as coccidiosis. As a puppy ages, he tends to develop a natural immunity to the effects of coccidia. As an adult, he may carry coccidia in his intestines, and shed the cyst in the feces, but experience no ill effects.

How are coccidia transmitted?

A puppy is not born with the coccidia organisms in his intestine. However, once born, the puppy is frequently exposed to his mother's feces, and if the mother is shedding the infective cysts in her feces, then the young animals will likely ingest them and coccidia will develop within their intestines. Since young puppies, usually those less than six months of age, have no immunity to coccidia, the organisms reproduce in great numbers and parasitize the young animal's intestines. Oftentimes, this has severe effects.

From exposure to the coccidia in feces to the onset of the illness is about 13 days. Most puppies who are ill from coccidia are, therefore, two weeks of age and older. Although most infections are the result of spread from the mother, this is not always the case. Any infected puppy or kitten is contagious to other puppies or kittens. In breeding facilities, shelters, animal hospitals, etc., it is wise to isolate those infected from those that are not.

What are the symptoms of coccidiosis?

The primary sign of an animal suffering with coccidiosis is diarrhea. The diarrhea may be mild to severe depending on the level of infection. Blood and mucous may be present, especially in advanced cases. Severely affected animals may also vomit, lose their appetite, become dehydrated, and in some instances, die from the disease.

Most infected puppies encountered by the authors are in the four to twelve week age group. The possibility of coccidiosis should always be considered when a loose stool or diarrhea is encountered in this age group. A microscopic fecal exam by a veterinarian will detect the cysts confirming a diagnosis.

What are the risks?

Although many cases are mild, it is not uncommon to see severe, bloody diarrhea result in dehydration and even death. This is most common in animals who are ill or infected with other parasites, bacteria, or viruses. Coccidiosis is very contagious, especially among young puppies. Entire kennels may become contaminated, with puppies of many age groups simultaneously affected.

What is the treatment of coccidiosis?

It should be mentioned that stress plays a role in the development of coccidiosis. It is not uncommon for a seemingly healthy puppy to arrive at his new home and develop diarrhea several days later leading to a diagnosis of coccidia. If the puppy has been at the new home for less than thirteen days, then he had coccidia before he arrived. Remember, the incubation period (from exposure to illness) is about thirteen days. If the puppy has been with his new owner several weeks, then the exposure to coccidia most likely occurred after the animal arrived at the new home.

Fortunately, coccidiosis is treatable. Drugs such as sulfadimethoxine (Albon®) and trimethoprim-sulfadiazine (Tribrissen®) have been effective in the treatment and prevention of coccidia. Because these drugs do not kill the organisms, but rather inhibit their reproduction capabilities, elimination of coccidia from the intestine is not rapid. By stopping the ability of the protozoa to reproduce, time is allowed for the puppy's own immunity to develop and remove the organisms.

How is coccidiosis prevented or controlled?

Because coccidia is spread by the feces of carrier animals, it is very important to practice strict sanitation. All fecal material should be removed. Housing needs to be such that food and water cannot become contaminated with feces. Clean water should be provided at all times. Most disinfectants do not work well against coccidia; incineration of the feces, and steam cleaning, immersion in boiling water, or a 10% ammonia solution are the best methods to kill coccidia. Coccidia can withstand freezing.

Cockroaches and flies can mechanically carry coccidia from one place to another. Mice and other animals can ingest the coccidia and when killed and eaten by a dog, for instance, can infect the dog. Therefore, insect and rodent control is very important in preventing coccidiosis.

The coccidia species of dogs and cats do not infect humans.

minibabyqq 2006-12-28 01:26

[color=Magenta][b][size=5]雄激素小組促合成類固醇The Androgen Group-Anabolic Steroids   [/size][/b][/color]


這些化合物與男性激素睪甾酮有關。他們指促合成類固醇因為他們導致新蛋白質的形成。如同我們陳述了前面, 他們由運動員經常濫用設法增加力量和肌肉大量。他們的用途在似犬醫學, 當少有, 與這些和相似的物產有關。
促合成類固醇進來液體形式為射入和片劑為口服。二最常用在似犬醫學是stanozolol (Winstrol-V) 並且nandrolone (DecaDurabolin) 。

是病的長期或是通過嚴厲的動物, 致衰弱的傷害經常推斷了弱點和萎縮的肌肉。在一些, 這進步了對動物能走甚至不再站立的點。他們的身體是正義太奔跑下來, 並且沒有一些外部刺激, 他們也許簡單地放棄意願居住。

促合成類固醇是有時有用的在這些情況。療法也許需要幾個星期。療程可能是最有用的如果獸醫認可情況在許多力量丟失之前。促合成類固醇協助身體在收復它的肌肉大量由修造新蛋白質, 是肌肉纖維主要組成部分。另外, 他們幫助加強現有的肌肉。

在一些這些同樣案件, 促合成類固醇頻繁地被使用刺激debilitated 或恢復的患者的胃口。達到這個作用通常需要幾天對幾個星期療法為重大的變動。

促合成類固醇是還有用的在對待某些類型 貧血症。貧血症是規定使用描述更低比紅血球(RBCs 的) 正常數字。在骨髓停止生產新RBCs 的某些案件, 促合成類固醇的管理將刺激這個系統和將帶來這些細胞的數量回到正常水平。他們並且為人所知稍微刺激 白細胞和小片 (協助凝結) 的微小的細胞的生產在血液。在這些情況, 促合成類固醇是有用的只在增加這些細胞的數量。 他們不增加細胞的能力對作用。

腎臟失敗經常帶來在貧血症因為這些器官也許不生產物質erythropoietin 。它的正常作用將監測RBCs 的水平在身體和刺激骨髓增加生產當RBC 數字是太降低。在它的缺席, 促合成類固醇經常是有用的在背面這貧血症的作用。他們不導致新erythropoietin 被生產; 他們只替換它的作用。

在許多情況, 促合成類固醇不提供好處被描述這裡。不管哪個特殊產品被使用, 它經常是不可能扭轉情況禮物。這些不是可能保存每名debilitated 或嚴厲地不適的患者的奇蹟藥物, 但在一些他們能幫助。

依照陳述, 這些療程與睪甾酮相關緊密地並且許多問題與相關他們的用法由男性激素的正常行動帶來。他們能導致熱週期和仿製架置行為的停止在女性。在男性, 他們被發現增加攝護腺疾病的發生和某些 疝氣 和腫瘤由正常睪甾酮水平造成在更舊的公狗。正常精液生產經常被打亂, 與少量新細胞被形成。無這些問題被認為重大在這些情況下, 許多患者已經是在生活或死亡情況。

促合成類固醇並且導致水保留並且這可能導致另外的複雜化在腎臟或心力衰竭患者。這些產品增加鈣的吸收由小腸短文和並且導致腎臟保留鈣在正常尿生產期間。這兩次行動導致過份地高的鈣水平在可能是慘敗的對正常心臟作用的血液。這可能迅速是致命的在那些以已經failing 心臟。
   



These compounds are related to the male hormone testosterone. They are referred to as the anabolic steroids because they cause the formation of new proteins. As we stated before, they are often abused by athletes trying to increase strength and muscle mass. Their use in canine medicine, while infrequent, is related to these and similar properties.
Anabolic steroids come in liquid forms for injection and tablets for oral administration. Two of the most commonly used in canine medicine are stanozolol (Winstrol-V) and nandrolone (DecaDurabolin).

Animals th>><<generalized weakness and atrophied muscles. In some, this has progressed to the point where the animals can no longer walk or even stand. Their bodies are just too run down, and without some outside stimulation, they simply may give up the will to live.

Anabolic steroids are sometimes useful in these situations. The therapy may take several weeks. The medications can be most helpful if the veterinarian recognizes the condition before too much strength is lost. Anabolic steroids assist the body in regaining its muscle mass by building new proteins, which are the primary constituent of muscle fibers. Additionally, they help strengthen existing muscles.

In some of these same cases, anabolic steroids are frequently used to stimulate the debilitated or recovering patient's appetite. To achieve this effect usually requires several days to several weeks of therapy for significant changes.

The anabolic steroids are also useful in treating certain types of anemia. Anemia is the term used to describe lower than normal numbers of red blood cells (RBCs). In certain cases where the bone marrow has stopped producing new RBCs, administration of anabolic steroids will stimulate this system and bring the number of these cells back to normal levels. They also are known to stimulate the production of white blood cells and platelets (tiny cells in blood that assist in clotting) to a lesser degree. In these situations, the anabolic steroids are useful only in increasing the numbers of these cells. They do not increase the ability of the cells to function.

Kidney failure often brings on anemia because these organs may fail to produce the substance erythropoietin. Its normal function is to monitor the level of RBCs in the body and to stimulate the bone marrow to increase production when RBC numbers are too low. In its absence, anabolic steroids are often useful in reversing the effects of this anemia. They do not cause new erythropoietin to be produced; they only replace its function.

In many situations, the anabolic steroids fail to provide the benefits described here. Regardless of which particular product is used, it is often impossible to reverse the condition present. These are not miracle drugs that can save every debilitated or severely ill patient, but in some they can help.

As stated, these medications are closely related to testosterone and many of the problems associated with their usage are brought on by the normal actions of the male hormones. They can cause cessation of heat cycles and imitation mounting behavior in females. In males, they have been found to increase the incidence of prostate disease and certain hernias and tumors that are caused by normal testosterone levels in older male dogs. Normal sperm production is often disrupted, with few new cells being formed. None of these problems are considered significant in these cases, as many of the patients are already in a life or death situation.

Anabolic steroids also cause water retention and this can cause additional complications in kidney or heart failure patients. These products also increase the absorption of calcium by the intestinal tract and cause the kidneys to retain calcium during normal urine production. Both of these actions lead to excessively high calcium levels in the blood which can be disastrous to normal heart function. This can be quickly fatal in those with already failing hearts.

minibabyqq 2006-12-28 01:27

[color=Magenta][size=5][b]Baylisascaris procyonis (Raccoon Roundworm)   [/b][/size][/color]


現在這您沒聽見的蛔蟲, 和您從未有希望地將見面。但如果您, 它是嚴肅的。 Baylisascaris procyonis 是浣熊蛔蟲。它不導致嚴厲疾病在浣熊除了在也許開發小腸阻礙的年輕人。真正的危險是它傳染人或狗。在人, 它導致一個情況叫做' 神經系統的幼蟲migrans, ' 或' 腦脊髓nematodiasis 。' 這是一種罕見的疾病, 但是嚴肅和經常致命的。
除狗和人以外, 有哺乳動物的17 個其它種類和能擔當B. procyonis 的中間主人 鳥 的19 個 種類。在浣熊, B. procyonis 居住在小腸。在人、狗, 和中間主人裡, B. procyonis 侵略身體器官、中央神經系統(CNS), 和眼睛。

怎樣共同性是 B. procyonis?

一位研究員建議 B. procyonis 傳染佔5% 嚙齒目動物死亡在被傳染的浣熊是共同的造林地。
B. procyonis 被發現遍及北美洲。在中西部, 浣熊的結束一半被學習被騷擾了。B. procyonis 的 流行 減少從北對南方的州。

什麼是生命週期在浣熊?

成人蠕蟲居住在浣熊的小腸和下是棚子在排匯物的蛋。在3-4 個星期以後在環境裡, 蛋變得傳染性。幼小浣熊能成為由吃傳染這些蛋。蛋孵化, 顯現出成 幼蟲 和成熟入成人在小腸。

更舊的浣熊通常成為由吃傳染一個中間主人譬如被感染幼蟲的老鼠、灰鼠, 或鳥。這些中間主人成為了由咽下傳染傳染性蛋從環境或或許通過修飾如果他們的毛皮成為了沾染與稠黏的蛋。在中間主人, 幼蟲孵化從蛋在肚腑和移居對各種各樣的 組織。大約5-7% 幼蟲移居對中間主人的腦子。幼蟲那裡造成大面積損壞。這些害病的動物是容易的犧牲者, 和當由浣熊殺害和吃, 幼蟲從中間主人被發布在浣熊的肚腑。這些幼蟲顯現出成成人和然後下蛋。

B. procyonis 起因疾病在人和狗?

當人們或狗偶然地咽下 B. procyonis 蛋, 幼蟲孵化和然後移居。傷害對人和狗是大面積損壞的結果由移居幼蟲造成。當幼蟲移居通過主人的組織, 他們增長大在大小, 雖然他們微觀。他們的相對地大大小導致可觀的機械損傷當他們移居並且主人的身體導致一個非常強烈的激動反應。這些激動反應是損傷的主要起因在CNS 。

騷擾獾的幾個 Baylisascaris , 臭鼬、漁夫、貂, 和熊的其它種類可能導致疾病在人。
當很大數量的幼蟲被咽下, CNS 疾病的可能性增加。嚴厲疾病症狀可能顯現出在2-4 個星期攝取之內。疾病症狀包括進步對昏迷和死亡的協調喪失、 慵倦 和昏迷。

疾病可能並且發生如果幼蟲移居對眼睛。標誌包括畏光(輕的敏感性) 並且視覺損失。幼蟲移居通過其它身體器官能導致症狀譬如熱病、擴大的 肝臟, 和 呼吸 問題。

因為浣熊也許被發現在農村和城市佈局, 在人的傳染的潛力是高的。人的傳染同woodpiles 和汙染的煙囪聯繫在一起。保留浣熊作為寵物造成直接威脅。野生生物rehabilitators 運作與浣熊和幼兒以粗劣的衛生學並且是可能被暴露。

傳染與B. procyonis 怎麼 被診斷?

在浣熊, 蛋, 是相似在大小和形狀與狗和貓蛔蟲, 被發現在排匯物。

在人和 家畜, 幼蟲也許被看見在眼睛的視網膜在眼科檢查期間。否則, 診斷被做通過歷史, 臨床標誌, 和血清學測試。

什麼是治療為 B. procyonis 傳染?

這是真正地可怕部份。有當前沒有治療為 B. procyonis 傳染在人或家畜。既使治療以後被辨認, 它的好處將有價值可疑的因為許多損害由移居幼蟲已經造成是永久。

如果幼蟲被看見在視網膜, 它是有時可能毀壞他們通過laser 療法。但, 再, 許多損傷是永久並且眼力也許或不能改善。

浣熊在修復, 或否則限制應該被對待每1-2 個星期為3-4 種治療與任何共同的wormers 使用對待蛔蟲在狗, 即, piperazine 、pyrantel pamoate, 和fenbendazole 。ivermectin 效力是未知的。

什麼可能做防止狗和人成為傳染?

記得, 蛋必須是在環境裡3-4 個星期在他們是傳染性的之前。如此, 新鮮的浣熊排匯物不包含傳染性蛋。傳染性蛋被發現在瓦解和已經也許是較不顯然的在環境裡的糞便材料裡。像狗和貓蛔蟲的蛋, B. procyonis 蛋可能生存幾年來在環境裡和對所有共同的殺菌劑是有抵抗性。

保留浣熊作為寵物可能擺在一個重大健康危害。浣熊恢復原狀或被限制為其它原因應該是在一個worming 節目如上所述。對浣熊被限制的區域的人和家畜通入應該是限於。浣熊應該quarantined 從其它動物在可能被清洗和容易地decontaminated 的籠子。籠子由浣熊使用不應該被使用為其它種類。

浣熊排匯物應該被取消和被毀壞的日報。個體清洗籠子應該穿手套和橡膠起動。防護工作服應該被穿著和被洗滌在近的開水和漂白。

小汙染的區域可能被對待與二甲苯和對氨基苯甲酸二50:50 混合物。這是一種危害解答, 應該由訓練的個體只使用。漂白的解答不會殺害蛋, 而是將去除他們稠黏的防護外套。汙穢大範圍最好decontaminated 使用一個便攜式的丙烷火炬。

當清洗也許被沾染了與浣熊排匯物, 譬如haylofts, 壁爐, 和頂樓的區域, 使用一次性的衣裳、手套, 和塵土面具。被取消的材料應該被燒。不要使用汙染的秸桿在庭院。建立熱的火在壁爐可能decontaminate 壁爐和煙囪。煙囪蓋帽被勸告防止浣熊能夠存取。



Now here is a roundworm you do not hear that much about, and hopefully you will never meet. But if you do, it is serious. Baylisascaris procyonis is a roundworm of raccoons. It does not cause severe disease in raccoons except in the young who may develop intestinal obstructions. The real hazard is when it infects humans or dogs. In man, it causes a condition called 'neural larva migrans,' or 'cerebrospinal nematodiasis.' This is a rare disease, but is serious and often fatal.
Besides dogs and humans, there are 17 other species of mammals and 19 species of birds that can serve as intermediate hosts of B. procyonis. In raccoons, B. procyonis lives in the small intestine. In man, dogs, and intermediate hosts, B. procyonis invades body organs, the central nervous system (CNS), and the eyes.

How common is B. procyonis?

One researcher suggests that B. procyonis infections account for 5% of rodent deaths in woodlots where infected raccoons are common.
B. procyonis is found throughout North America. In the Midwest, over half of the raccoons studied were infested. The prevalence of B. procyonis decreases from northern to southern states.

What is the life cycle in raccoons?

Adult worms live in the small intestine of raccoons and lay eggs that are shed in the feces. After 3-4 weeks in the environment, the eggs become infective. Young raccoons can become infected by eating these eggs. The eggs hatch, develop into larvae and mature into adults in the small intestine.

Older raccoons usually become infected by eating an intermediate host such as a mouse, squirrel, or bird that is infected with the larvae. These intermediate hosts became infected by ingesting the infective eggs from the environment or perhaps through grooming if their fur had become contaminated with the sticky eggs. In the intermediate host, larvae hatch from the eggs in the intestine and migrate to various tissues. About 5-7% of the larvae migrate to the brain of the intermediate host. There the larvae cause extensive damage. These diseased animals are easy prey, and when killed and eaten by the raccoon, the larvae from the intermediate host are released in the raccoon's intestine. These larvae develop into adults and then lay eggs.

How does B. procyonis cause disease in humans and dogs?

When people or dogs accidentally ingest B. procyonis eggs, the larvae hatch and then migrate. Injury to humans and dogs is a result of the extensive damage caused by the migrating larvae. As the larvae migrate through the host's tissues, they grow much larger in size, though they are still microscopic. Their relatively large size results in considerable mechanical damage as they migrate and the host's body produces a very strong inflammatory response. These inflammatory reactions are a major cause of damage in the CNS.

Several other species of Baylisascaris that infest badgers, skunks, fishers, martens, and bears can cause disease in man.
When large numbers of larvae are ingested, the possibility of CNS disease increases. Severe signs of disease can develop within 2-4 weeks of ingestion. Signs of disease include loss of coordination, lethargy and stupor that progresses to coma and death.

Disease can also occur if the larvae migrate to the eye. Signs include photophobia (light sensitivity) and vision loss. Larvae migrating through other body organs can produce symptoms such as fever, enlarged liver, and respiratory problems.

Since raccoons may be found in both rural and urban settings, the potential for human infection is high. Human infections have been associated with woodpiles and contaminated chimneys. Keeping raccoons as pets poses a direct threat. Wildlife rehabilitators working with raccoons and young children with poor hygiene are also more likely to be exposed.

How is infection with B. procyonis diagnosed?

In the raccoon, the eggs, which are similar in size and shape to the roundworms of dogs and cats, are found in the feces.

In man and domestic animals, the larvae may be seen in the retina of the eye during an ophthalmologic exam. Otherwise, the diagnosis is made through history, clinical signs, and serologic testing.

What is the treatment for B. procyonis infection?

This is the really scary part. There is currently no treatment for B. procyonis infection in man or domestic animals. Even if a treatment is later identified, its benefit will be of questionable value since much of the damage already done by the migrating larvae is permanent.

If larvae are seen in the retina, it is sometimes possible to destroy them through laser therapy. But, again, much of the damage is permanent and eyesight may or may not improve.

Raccoons in rehabilitation, or otherwise confined should be treated every 1-2 weeks for 3-4 treatments with any of the common wormers used to treat roundworms in dogs, e.g., piperazine, pyrantel pamoate, and fenbendazole. The efficacy of ivermectin is unknown.

What can be done to prevent dogs and humans from becoming infected?

Remember that the eggs must be in the environment 3-4 weeks before they are infective. So, fresh raccoon feces do not contain infective eggs. Infective eggs are found in fecal material that is already disintegrating and may be less obvious in the environment. Like eggs of the roundworms of dogs and cats, B. procyonis eggs can survive for years in the environment and are resistant to all common disinfectants.

Keeping raccoons as pets can pose a significant health hazard. Raccoons being rehabilitated or confined for other reasons should be on a worming program as described above. Human and domestic animal access to areas where raccoons are confined should be restricted. Raccoons should be quarantined away from other animals in cages that can be easily cleaned and decontaminated. Cages used by raccoons should not be used for other species.

Raccoon feces should be removed and destroyed daily. Individuals cleaning the cages should wear gloves and rubber boots. Protective coveralls should be worn and washed in near boiling water and bleach.

Small contaminated areas can be treated with a 50:50 mixture of xylene and ethanol. This is a hazardous solution and should only be used by trained individuals. Solutions of bleach will NOT kill the eggs, but will remove their sticky protective coats. Large areas of contamination are best decontaminated using a portable propane torch.

When cleaning areas that may have been contaminated with raccoon feces, such as haylofts, fireplaces, and attics, use disposable clothes, gloves, and a dust mask. Removed material should be burned. Do not use contaminated straw on gardens. Building a hot fire in a fireplace can decontaminate the fireplace and chimney. Chimney caps are advised to prevent raccoons from gaining access.

minibabyqq 2006-12-28 01:28

[color=Magenta][size=5][b]腎小球性腎炎 Glomerulonephritis   [/b][/size][/color]


多半時間當腎臟疾病被談論, "腎功能不全" 或"慢性腎臟失敗" 是主題。在這個情況腎臟丟失它的能力保存身體的水當它取消身體的每日毒素組合。很多水必需做足夠的尿。過份水消耗量看如同一個早期的標誌。減重接著而來。古典新陳代謝的變動結果。

Glomerular 疾病是完全地不同的。

小球是微觀腎臟區域那過濾器毒素。它的工作將從血液去除所有小新陳代謝的毒素和把更大的分子(具體地血液蛋白質留在) 在他們屬於的血液。小球分離尿從血液。優化以後發生沿電解質是平衡的腎臟的tubules 但最初過濾發生在成千上萬小球做腎臟。

當glomerular 疾病存在, 孔被猛擊在這個濾清系統允許某人的身體需要繼續輸入尿流程和小便忘卻的大分子。在腎小球性腎炎, 這是慢性炎症那導致孔在濾清系統。免疫系統的慢性刺激導致流通的一點兒antibody/antigen 叢。這些叢黏附在他們引起更多炎症和最終入一個小孔小球的濾清膜。

診斷怎麼被做?

腎臟的切片檢查法技術上是需要的absolutely 證實這個診斷但尿測試通常是充足感到確信glomerular 疾病是存在。蛋白質損失在尿是明顯的在定期尿分析。小量的蛋白質在尿不是反常的, 特別是如果尿很好被集中, 但如果它似乎像相當數量蛋白質願是更多比什麼是期望的進一步然後測試是需要的。尿文化排除潛在膀胱傳染是有用的, 因為炎症由膀胱傳染引起將增加蛋白質來尿。測試稱"尿protein:creatinine 比率" 可能執行在尿樣更加有效地定量相當數量蛋白質損失。

如果protein:creatinine 比率充足地被舉起, 這表明對小球和那手段或腎小球性腎炎或情況的損傷叫做amyloidosis 。唯一腎臟的切片檢查法可能確定哪些是存在; 但是, 在amyloidosis (腎臟由惡性反常蛋白質滲入叫做澱粉質食物) 的地方預測是很窮和疾病進步很迅速, 對治療的反應可能建議哪個情況是存在。

重要驗血對筆記是白蛋白水平。白蛋白是非常重要血液蛋白質負責任對運載許多其它biochemicals 在血液附近。當這蛋白質被發現降低在掩護驗血, 它重要確定為什麼白蛋白可能丟失(小便) 在glomerular 疾病, 丟失在小腸短文在某些GI 疾病, 或簡單地在之下被生產在肝臟病。一個低白蛋白水平也許要訣關閉對早檢測在glomerular 疾病, 並且當它被發現尿protein:creatinine 比率應該完成。如果血液白蛋白水平下降太低, 腫鼓(可變的儲積) 結果, 典型地在更低的肢。

什麼可能導致腎小球性腎炎?

慢性地刺激免疫系統的任一件事可能導致這種腎臟損傷。一些共同的可能的起因是:

長期被忽略的嚴厲牙齒疾病
巨蟹星座
Heartworm 傳染
Ehrlichia 傳染(一種滴答作響出生的疾病)
Lyme 疾病(其它滴答作響出生的疾病)
似貓的白血病病毒傳染
似貓的感染腹膜炎
Pyometra (膿腫的子宮體)
心內膜炎(細菌傳染在心臟)
慢性地被激起的皮膚
免疫斡旋的疾病(譬如lupus)
慢性胰腺炎
前列腺炎(被激起的攝護腺)
腎小球性腎炎可能並且是什麼稱先天, 意味那儘管搜尋, 根本原因無法被發現。

臨床標誌/症狀

多數動物以腎小球性腎炎丟失重量並且胃口。腸胃不適是共同。大約70% 患者將進步對更加古典的慢性腎衰竭, 巨大地惡化最後預測。

glomerular 疾病嚴厲案件, 複雜化稱Nephrotic Syndrome 可能導致由於極端泌尿蛋白質損失。有腎變病綜合症狀病人顯現出:

高血壓
傾向形成反常血塊
腫鼓(膨脹) 特別是腿
(腎變病綜合症狀被定義作為組合: 1) 重大蛋白質損失在尿; 2) 低清液白蛋白; 3) 腫鼓或其它反常可變的儲積; 或4) 被舉起的血液膽固醇。

對待這種疾病

可能做在對待的腎小球性腎炎的最重大的事是辨認抗原來源和消滅它如果它是可能做如此。這意味著寬廣測試也許是需要的篩選為條件被列出以上。

對待的glomerular 炎症的下個最重要的方面是免疫系統的鎮壓。這意味著療程譬如cyclophosphamide, 或cyclosporine 。如果部下的情況是類皮質激素敏感(即, 風濕甾酮衍生物被表明) 某事像強體松也許然後幫助但強體松在許多情況下不是一個好選擇。慢性類皮質激素用途導致Cushing 的綜合症狀, 可能增加風險反常凝結(thromboembolism) 。尿protein:creatinine 比率可能被監測為進展。如果比率增加, 這會表明, 免疫鎮壓不幫助並且療程應該被改變甚至被中斷。

治療的第三部份是關於防止免疫複合體黏附對精美glomerular 膜。阿斯匹靈管理是最簡單的方式完成這加上阿斯匹靈低藥量並且減少傾嚮往過份血液凝結。有當前研究進展中關於使用Ω3 脂肪酸補充進一步協助治療這個分支, 但具體治療推薦未解決。

治療的第四個部份介入一個小組藥物叫做血管緊縮素轉換的酵素抗化劑(或簡單地一點抗化劑) 。Enalapril 當前是唯一一個被批准用於狗但許多一點抗化劑可利用歸結於寬用途在人的醫學。一點抗化劑是有用的他們減少蛋白質損失和保存腎臟作用。進一步, 他們能幫助下降高血壓。有一點抗化劑的問題是, 他們固有地下降血流對腎臟, 可能是問題如果利尿藥一致地被使用, 和在心力衰竭。在許多情況下glomerular 疾病, 這不是問題。

在更舊的時期, 補充蛋白質被推薦補嘗泌尿蛋白質損失。這從那以後被發現實際上使蛋白質損失更壞和不再被推薦。


Most of the time when kidney disease is discussed, "renal insufficiency" or "chronic kidney failure" is the subject. In this condition the kidney loses its ability to conserve the body's water as it removes the body's daily toxin build up. Large amounts of water are required to make enough urine. Excessive water consumption is seen as an early sign. Weight loss ensues. Classical metabolic changes result.

Glomerular disease is completely different.

The glomerulus is the microscopic kidney area that filters toxins. Its job is to remove all the small metabolic toxins from the blood stream and leave the larger molecules (specifically blood proteins) in the blood stream where they belong. The glomerulus separates urine from blood. Fine-tuning occurs later on along the kidney's tubules where electrolytes are balanced but the initial filtering takes place in the millions of glomeruli making up the kidneys.

When glomerular disease exists, holes are punched out in this filtration system allowing large molecules that one's body needs to keep entering the urine flow and be urinated away into oblivion. In glomerulonephritis, it is chronic inflammation that leads to the holes in the filtration system. A chronic stimulation of the immune system leads to circulating bits of antibody/antigen clumps. These clumps stick in the filtration membranes of the glomerulus where they generate more inflammation and eventually into a small hole.

How Is Diagnosis Made?

Technically a biopsy of the kidney is needed to absolutely confirm this diagnosis but usually urine testing is sufficient to feel confident that glomerular disease is present. Protein loss in the urine is apparent on a routine urinalysis. A small amount of protein in urine is not abnormal, especially if the urine is well concentrated, but if it seems like the amount of protein may be more than what is expected then further testing is needed. A urine culture to rule out a latent bladder infection is helpful, as the inflammation generated by a bladder infection will add protein to the urine. A test called a "urine protein:creatinine ratio" can be performed on the urine sample to quantify the amount of protein loss more effectively.

If the protein:creatinine ratio is sufficiently elevated, this indicates damage to the glomeruli and that means either glomerulonephritis or a condition called amyloidosis. Only a biopsy of the kidney can determine which is present; however, in amyloidosis (where the kidney is infiltrated by a malignant abnormal protein called amyloid) prognosis is so poor and the progression of disease so rapid that response to treatment can suggest which condition is present.

An important blood test to note is the albumin level. Albumin is a very important blood protein responsible for carrying numerous other biochemicals around the bloodstream. When this protein is found to be low on a screening blood test, it is important to determine why. Albumin can be lost (urinated away) in glomerular disease, lost in the intestinal tract in certain GI diseases, or simply under-produced in liver disease. A low albumin level may be the tip off to early detection in glomerular disease, and when it is found a urine protein:creatinine ratio should be done. If the blood albumin level drops too low, edema (fluid accumulation) results, typically in the lower extremities.

What Can Cause Glomerulonephritis?

Any thing that chronically stimulates the immune system can cause this kind of kidney damage. Some common possible causes are:

Long ignored severe dental disease
Cancer
Heartworm infection
Ehrlichia infection (a tick-borne disease)
Lyme disease (another tick-borne disease)
Feline Leukemia virus infection
Feline Infectious Peritonitis
Pyometra (abscessed uterus)
Endocarditis (bacterial infection in the heart)
Chronically inflamed skin
Immune-mediated diseases (such as lupus)
Chronic pancreatitis
Prostatitis (inflamed prostate)
Glomerulonephritis can also be what is called idiopathic, which means that despite searching, the underlying cause cannot be found.

Clinical Signs / Symptoms

Most animals with glomerulonephritis lose weight as well as appetite. Upset stomach is common. Approximately 70% of patients will progress to the more classical chronic renal failure, which tremendously worsens the ultimate prognosis.

In severe cases of glomerular disease, a complication called Nephrotic Syndrome can result due to the extreme urinary protein loss. Patients with nephrotic syndrome develop:

High blood pressure
Tendency to form abnormal blood clots
Edema (swelling) especially of the legs
(Nephrotic syndrome is defined as the combination of: 1) significant protein loss in urine; 2) low serum albumin; 3) edema or other abnormal fluid accumulation; or 4) elevated blood cholesterol level.

Treating this Disease

The most significant thing that can be done in treating glomerulonephritis is to identify the antigen source and eliminate it if it is possible to do so. This means broad testing may be needed to screen for the conditions listed above.

The next most important aspect of treating glomerular inflammation is suppression of the immune system. This means medications such as cyclophosphamide, or cyclosporine. If the underlying condition is corticosteroid responsive (i.e., the cortisone derivatives are indicated) then something like prednisone might help but in most cases prednisone is not a good choice. Chronic corticosteroid use can lead to Cushing's syndrome and can increase the risk of abnormal clotting (thromboembolism). The urine protein:creatinine ratio can be monitored for progress. If the ratio increases, this would indicate that immune suppression is not helping and that medication should be changed or even discontinued.

The third part of treatment is about preventing the immune complexes from sticking to the delicate glomerular membranes. Aspirin administration is the simplest way to accomplish this plus low doses of aspirin also reduce the tendency towards excessive blood clotting. There is currently research in progress about using omega 3 fatty acid supplementation to further assist in this branch of treatment, but specific treatment recommendations have not yet been worked out.

The fourth portion of treatment involves a group of drugs called angiotensin converting enzyme inhibitors (or simply ACE inhibitors). Enalapril is currently the only one approved for use in dogs but numerous ACE inhibitors are available due to wide use in human medicine. The ACE inhibitors are helpful in that they reduce protein loss and preserve renal function. Further, they can help drop high blood pressure. The problem with the ACE inhibitors is that they inherently drop blood flow to the kidney, which can be a problem if diuretics are used concurrently, as in heart failure. In most cases of glomerular disease, this is not an issue.

In older times, supplementing protein was recommended to compensate for the urinary protein loss. This has since been found to actually make the protein loss worse and is no longer recommended.

minibabyqq 2006-12-28 01:29

[color=Magenta][size=5][b]銅存貯疾病(銅Hepatotoxicosis)Copper Storage Disease (Copper Hepatotoxicosis)   [/b][/size][/color]


似犬銅hepatotoxicosis, 並且叫做銅存貯疾病, 是由銅過份儲積造成在 肝臟的 情況。它更加頻繁地發生在狗某些養殖。這可能是, 留給未經治療, 可能是致命的一種嚴肅的疾病。
誰是在危險中?

似犬銅hepatotoxicosis 最共同地影響Bedlington 狗、Doberman Pinscher 、Skye 狗, 和西部高地白色狗。Bedlington 狗患 慢性 肝炎 由於導致銅保留在肝臟而不是從身體被消滅的一個被繼承的新陳代謝的瑕疵。在美國, 多達66% Bedlington 狗可以是受影響的。

Doberman Pinscher 是在一種增加的風險為開發慢性肝炎和 肝病。一個基因依據被懷疑由於高頻率在這養殖。肝臟銅含量被增加在許多, 但沒有所有受影響的狗。增加的銅也許是偶發事件發現或這養殖也許有肝臟損傷在更低的銅水平比其它養殖。

慢性肝炎和肝病聯繫了銅儲積在肝臟被報告了在基因上相關Skye 狗。它被推測是膽汁分泌物 混亂 。

西部高地白色狗是在開發慢性肝炎和肝病增加的風險。剩餘肝臟銅儲積是一個熟悉的特徵, 但繼承方式未建立。許多西部高地白色狗增加了肝臟銅水平, 但不是在程度上, 臨床病症看。

什麼是起因?

銅的剩餘儲積在肝臟也許由銅反常捆綁造成對某些蛋白質在銅的肝臟或反常分泌物在膽汁。

什麼是症狀?

狗以銅存貯疾病顯示症狀的範圍根據相當數量對肝臟的損傷。症狀也許包括靈菌從膠或鼻孔、 腹水, 黃疸, 嘔吐, 腹瀉, 和減重。 銅的深刻發行從肝臟也許導致紅血球破壞導致 貧血症、hemoglobinemia (自由 血紅蛋白 在血液), 和hemoglobinuria (血紅蛋白在尿) 。

銅存貯疾病怎麼被診斷?

狗症狀和養殖將導致一位獸醫懷疑銅存貯疾病。驗血也許表明在肝臟酵素的增量譬如 清液 胺基代丙酸aminotransferase (參見 肝臟混亂症狀和診斷) 。肝臟 切片檢查法 是必要的為一個明確的診斷和確定相當數量銅禮物。

什麼是治療?

治療包括對青黴胺的用途結為螯合物(困境) 並且增加銅的泌尿排泄。鋅醋酸鹽幫助束縛銅防止它的吸收。受影響的狗被安置在低銅飲食, 更好地以少於0.5 PPM 銅。額外 維生素E 被供應如同一種 抗氧化 療法幫助減少對肝臟的損傷。 維生素C 應該被避免在狗以銅儲積因為它也許增加對肝臟的銅的損傷。對銅結為螯合物的代理的用途在Doberman Pinscher 是有爭議的因為疾病傾向於進步既使銅水平被減少對法線。

銅存貯疾病怎麼被防止?

疾病的排除從養殖在高風險開發它取決於能顯示怎麼它被繼承和然後去除運載基因從助長節目的那些狗。一個基因標記為銅toxicosis 在Bedlington 狗被辨認了。肝臟登記被形成了為是未受影響的依照由肝臟切片檢查法確定被採取在一年紀以後的Bedlington 狗。


Canine copper hepatotoxicosis, also called copper storage disease, is a condition that is caused by an excessive accumulation of copper in the liver. It occurs more frequently in certain breeds of dogs. It can be a serious disease that, left untreated, can be fatal.
Who is at risk?

Canine copper hepatotoxicosis most commonly affects the Bedlington Terrier, Doberman Pinscher, Skye Terrier, and West Highland White Terrier. Bedlington Terriers develop chronic hepatitis as a result of an inherited metabolic defect that causes copper to remain in the liver rather than be eliminated from the body. In the United States, as many as 66% of Bedlington Terriers may be affected.

The Doberman Pinscher is >><<and cirrhosis. A genetic basis is suspected because of the high frequency in this breed. Liver copper concentrations are increased in many, but not all affected dogs. The increased copper may be an incidental finding or this breed may have liver damage at lower copper levels than other breeds.

Chronic hepatitis and cirrhosis associated with copper accumulation in the liver has been reported in genetically related Skye Terriers. It is speculated to be a disorder of bile secretions.

West Highland White Terriers are at increased risk of developing chronic hepatitis and cirrhosis. Excess liver copper accumulation is a familiar trait, but the mode of inheritance has not been established. Many West Highland White Terriers have increased liver copper levels, but not to an extent that clinical illness is seen.

What are the causes?

The excess accumulation of copper in the liver may be caused by an abnormal binding of copper to certain proteins in the liver or abnormal secretion of copper in the bile.

What are the symptoms?

Dogs with copper storage disease show a range of symptoms depending on the amount of damage to the liver. Symptoms may include bleeding from the gums or the nostrils, ascites, jaundice, vomiting, diarrhea, and weight loss. Acute release of the copper from the liver may result in red blood cell destruction causing anemia, hemoglobinemia (free hemoglobin in the blood), and hemoglobinuria (hemoglobin in the urine).

How is copper storage disease diagnosed?

The symptoms and breed of dog will cause a veterinarian to suspect copper storage disease. Blood tests may indicate an increase in the liver enzymes such as serum alanine aminotransferase (see Symptoms and Diagnosis of Liver Disorders). A liver biopsy is necessary for a definitive diagnosis and to determine the amount of copper present.

What is the treatment?

Treatment includes the use of penicillamine to chelate (bind) and increase urinary excretion of copper. Zinc acetate helps to bind copper preventing its absorption. Affected dogs are placed on a low copper diet, preferably with less than 0.5 PPM of copper. Extra Vitamin E is supplied as an antioxidant therapy to help reduce damage to the liver. Vitamin C should be avoided in dogs with copper accumulation because it may increase the copper's damage to the liver. The use of copper chelating agents in the Doberman Pinscher is controversial since the disease tends to progress even if copper levels are decreased to normal.

How is copper storage disease prevented?

Elimination of the disease from breeds at high risk of developing it depends on being able to show how it is inherited and then to remove those dogs who carry the gene from breeding programs. A genetic marker for copper toxicosis in the Bedlington Terrier has been identified. A liver registry has been formed for Bedlington Terriers who are unaffected as determined by liver biopsy taken after one year of age

minibabyqq 2006-12-28 01:31

[color=Magenta][size=5][b]對脊髓作用的Electrophysiological 評估   [/b][/size][/color]


脊髓官能不良是共同的問題在獸醫神經學方面。脊髓狀態的一個相當精確評估可能被獲取通過臨床評估。的確, 神經纖維以清楚地不同的卑鄙軸突直徑執行幾個臨床可測試性的作用。更大軸突, 更加敏感的它是對病理性過程。結果, proprioception 、馬達命令和愚鈍的痛苦被分級的失蹤平行繩子損害增長的嚴肅。愚鈍的(深深, 燒) 痛苦由有毒刺激(價格1977) 應該出現從unmyelinated (c) 纖維的活化作用。1 預測可能被公式化根據了這臨床分級和經驗大身體被獲取以早先案件。臨床分級的系統限制了精確度因為它是不連續和主觀的。而且, 它取決於動物的觀察, 氣質可能修改反應。

除確定損害的嚴肅之外, 臨床評估並且瞄準確定問題的地點。想像充當在地方化引起損害的一個主要角色但依靠宏觀損害的出現。但是, 脊髓官能不良可能發起於一個純淨地功能問題, 無法由想像地方化, 即脊髓震動。並且, 它可能出現從微觀損害譬如激動損害或梗塞。相反地, 那裡可能是不解釋功能損傷和不是因此毫不相關的幅射線照相的損害。終於, 當前, 想像有唯一在估計多數繩子官能不良嚴肅的一個少量的角色。

有限制臨床考試的一些具體因素:

1 。 接近低能者 可能難分類, 特別是那些以輕微或斷斷續續的神經學損傷和那些, 在光譜的相反結尾, 那到達了prognostically 相關的疆界在出現或缺乏愚鈍的痛苦悟性之間。

2 。一些疑義可能出現患者遭受 超過一個身體系統疾病: 例如, cauda equina 壓縮和一致hip osteoarthrosis 。

3 。決定必須有時做出與 不合作, stoic 患者 甚至在 昏迷或被麻醉的患者。

4 。患者也許遭受 二種一致神經學疾病。老狗以一致退化myelopathy 和盤伸進有時遇到; 動物以臨床標誌表明一損害有時有二幅射線照相的損害。在這樣患者, 一次功能測試能是有用的在確定是否幅射線照相地辨認的損害的確是標誌的起因, 或確定哪些二損害是很可能是起因。

補全臨床考試和想像技術的規程能有價值與這些局限打交道。這樣規程應該合理地容易和齋戒執行和應該提供清楚答復。一些被召喚的潛在的錄音也許湧出幫助這個過程。

被召喚的潛力是任一個電子活動由可激發的細胞引起以回應遙遠的刺激。關於脊髓作用, 二個方法被評估了用於可能的臨床獸醫: somatosensory 被召喚的潛力(SSEP) 2-15 和馬達召喚了潛力(MEP) 。16-21 Somatosensory 被召喚的潛力被記錄在脊椎和頭骨以回應一根周邊知覺或混雜的神經的刺激。開汽車被召喚的潛力被記錄在肢體肌肉裡以回應頭或脊椎的磁性刺激。

本文的目的將熟悉讀者SSEP 錄音。它首先是必要描述某些技術和生理因素關於人為緊張的組織刺激和關於記錄從可激發的組織。在那以後, 這些方法臨床相關性以各種各樣的脊髓問題可能被回顧。

周邊神經刺激為SSEP 錄音

這種同樣刺激品像被使用為周邊神經系統評估, 或馬達神經傳導、反覆stimulations 或知覺electroneuronography 被使用在得出somatosensory 潛力。這些刺激品提供長方形脈衝在二個電極之間。

刺激電極設置

通常, 針電極被安置在線沿神經, 即, 在"雙極" 設置, 將是更加高效率的因為潮流是可能流經神經纖維比如果電極是在從神經的一個距離("monopolar" 設置) 。軸突膜將被去極化在最消極的電極(負極之下) 因為它帶來額外和內部axonal 潛力離彼此較近。axonal 膜可能是hyperpolarised 在最正面的電極之下造成"傳導anodal" 塊; 因而, 負極應該被安置離錄音電極較近比陽極。

刺激強度: 名詞性的詞對有效

刺激由刺激品交付是在電子反饋控制之下克服組織的短路的作用被插話在電極和神經之間瞄準。例如, 一個恆定的電壓單位需要當前的峰頂加強矩形波的顯著上升和秋天。恆定的現有數量, 以反饋控制在電壓並且是可利用的。

不管類型刺激品, 有效的刺激到達神經減少如同距離在電極和神經增量之間。結果, 刺激強度實際上被提供對神經比有名無實的刺激總是較少(即刺激設置設備) 。它是有利定義刺激強度由一個生理作用譬如強度必要觀察門限反應, 或給最大的肌肉潛力的強度當一根混雜的神經被使用。由於恆定的聯繫在有名無實和有效的電壓之間, 使用這參考電壓的倍數或分數允許變化刺激強度的作用的準確決心。

刺激強度: 神經纖維的補充

增加刺激強度吸收更多神經纖維。更大神經纖維的直徑, 更加敏感的它是對刺激。的確, 大直徑纖維有更低的縱向抵抗並且更加當前流經他們。概括來說, 大輸入纖維突觸在大高次纖維。

SSEP 的研究由tibial 神經刺激召喚和被記錄在T13/L1 顯示出, 潛力的被測量的特徵(第一峰頂的潛在因素和高度) 迅速地到達了穩定的價值當刺激強度被增加了, 雖然信號波形進一步改變了。 22 結果, 脊椎記錄的SSEP 似乎相對地厚臉皮對零錢在刺激強度在這點之上。

刺激期間

刺激期間是妥協在時間之間需要克服神經纖維和周圍的組織電容物產, 50 m s 極小值, 和得出同步齊射必要在神經; 100 ms 是刺激期間廣泛被應用。神經纖維的電容並且與它的直徑有關。為指定的潮流, 潛在的變動是慢的在大纖維。它是可能優先地吸收大纖維通過對低強度的用途, 長的期間刺激。

刺激頻率

刺激頻率不應該被增加在5 赫茲之上從神經衝動導致可能持續十倍毫秒傳入(主要輸入去極化劑, 墊的) 的禁止。結果, 增長的刺激頻率可能降低反應的高度。頭皮記錄的SSEP 的高度也許被刺激率修改在2 赫茲23 和脊椎記錄的SSEP 的晚組分之上由刺激率在4 赫茲之上。3

候選人神經為刺激

各種各樣的神經被刺激了, 包括知覺, 肌肉和被混合的神經。肢體神經(tibial, 腓骨, cubital 和輻形神經) 經常被使用, 僅pudendal 和尾骨的神經並且被使用了。接近刺激吸收更多纖維, 和給更大的潛力。但接近刺激反射, 和直接地導致肌肉活動還與混雜的神經。4 刺激在腕或tarsus 妥協之上在激活纖維的一個充足的數字和避免剩餘肌肉活動之間。Neuromuscular 阻攔也許是有用的當肌肉人工製品問題無法被解決。

神經系統的發電器

一根周邊神經的充分刺激同時去極化軸突的數字。被去極化的區域在中心(和並且被繁殖周邊地) 並且可能被記錄作為一個 複合動作電位 從電極被安置沿神經。周邊神經活動並且召喚複合動作電位在脊髓短文。周邊神經刺激並且導致突觸神經的活動在脊髓, 首先在脊髓段接受軸突從被刺激的神經。突觸神經的活動導致複合動作電位上升的脊髓短文的傳播, 並且是可錄的。上升的活動導致突觸神經的活動在中堅力量在骨髓和反過來被傳遞對更高的中心, 包括突觸並且被激活的大腦外層。突觸神經的活動在所有水平是可錄的和並且反射被召喚的活動的到來在突觸和細胞的健康負擔突觸。它重要強調這些基本的區別: 複合動作電位是行動, 旅行沿被激活的軸突, 但是突觸神經的潛力是固定, 固定事件。 他們指 領域潛力, (或有時作為"水槽來源潛力") 。

Somatosensory 神經系統的路

第一他們到達的等級知覺纖維大方地分支在脊髓段灰色問題並且分支也許cranially 和尾部遊遍幾段在終止之前。另外, 許多纖維從皮膚和聯接感受器官送一個分支在背部專欄由骨髓決定沒有synapsing 在脊髓段。終端從小組Ia 肌肉傳入登高在背部專欄幾繩子段在傳遞在Clarke 的專欄之前。24, 25 A 拷貝這後者資訊旅行在二次纖維在dorsolateral fasciculus 。26 痛苦感覺並且運載一部分在dorso 側向fasciculus 。27

資訊從身體的後面肢體和尾部一半被表達對突觸在髓心(nn. 薄肌和z) 和側向子宮頸中堅力量。從那裡路decussates 在骨髓和rostrally 繼續在中間蹄繫到達丘腦, 主要ventrocaudolateral 中堅力量。28-30 終端的一個大分數從克拉克的專欄(背部spino 小腦的短文) 到達後腦。26

對於資訊從forelimb 和頭蓋骨身體部位, 克拉克的專欄的角色和子宮頸, 薄肌和z 中堅力量由楔形和側向楔形的中堅力量演奏。31 從丘腦, 資訊被傳遞對主要somato-sensory 外皮, 圍繞在冠狀溝在食肉動物。32

dorsolateral fasciculus 和背部專欄引起脊椎記錄的SSEP 的最早期的偏折。但是, 腹繩子, 包括不適被定義的spino-thalamic 短文非大主教哺乳動物, spino-tectal 和spino 網狀結締組織的路, 以及腹spino 小腦的短文, 也許對最新偏折貢獻脊椎被記錄9月。33,34 背部專欄和dorsolateral fasciculus 並且是主要重要為頭皮記錄的SSEP 。但是, 腹繩子也許貢獻。35

複合動作電位

動作電位旅行沿神經纖維。地方化的潛在的變動在神經纖維導致一個潛在的變化在周圍的媒介上。傳染媒介可能同去極化劑聯繫在一起, 並且潛力在周圍的媒介的遙遠的點可能被計算。36 傳染媒介以相反極性同repolarisation 聯繫在一起和跟隨嚴密第一傳染媒介。這兩次電子事件(去極化劑的組合被repolarisation 跟隨) 提升典型, triphasic positive/negative/positive 波浪當動作電位接近, 通過, 和旅行從錄音點(無花果1) 。複合動作電位是更或較少同步的貢獻的總和從纖維用不同的短文。複合動作電位在狗的周邊神經裡被塑造了。37 複合動作電位的一個重要特徵是, 它的潛在因素增加當錄音點是進一步從刺激站點。它的高度和配置(信號波形) 是更加恆定的雖然組分分散作用被觀察以更加遙遠的錄音地點由於在傳導速度上的區別在不同的直徑之中軸突。

重要地, 記錄的潛力的配置可能改變用一個可預測的方式由於生理學或病理性起因。如果動作電位接近但不到達錄音點的水平, 即, 當由損害阻攔, 只有正面偏折將被記錄。如果動作電位通過由但被阻攔小的過去錄音站點, 正面消極波浪將被記錄38 (無花果2) 。這兩個"被召喚的傷害潛力的" 方面(EIP) 可能被使用為臨床目的。15

結束("在附近") 領域潛力

在灰色問題, 動作電位旅行唯一短的距離。領域潛力的高度將減少如同記錄的點從來源被移動。但是, 它重要注意到, 領域潛力潛在因素不改變以錄音點的距離從潛力的來源。預言方式突觸, 枝狀突起、細胞身體和軸突可能影響一個遙遠的錄音電極是更加困難的。但是, 根據纜繩潛力, 我們可能期望的原則和一樣資訊遊遍往錄音電極在由傳播之前被取消軸突終端將給monophasic 正面潛力。相反地, 資訊旅行從錄音電極將給消極潛力(無花果2) 。

興奮突觸導致當前的流程在中轉神經元裡。這些潮流使潛力一個附近的電極更加消極。生理學者使用深度microelectrodes 講話當前的水槽為這觀察。潮流並且漏在神經元外面由某一距離決定創造是相對地更加正面的一個細胞外區域, 導致當前的來源的概念(禁止突觸並且創造一個當前的來源) 。水槽被記錄在interneurones 和來源附近身體和枝狀突起某處沿他們的軸突。錄音電極離水槽較近有消極潛力但是錄音電極離來源較近有正面潛力。"水槽來源潛力" 被使用如同接近的領域潛力同義詞。

如果軸突在灰色問題被安置在同樣方向, 他們各自的貢獻summate 並且潛力可能被記錄從距離。他們說形成一個開放領域。如果他們傳送資訊以各種各樣的方向, 各自的貢獻也許取消和不會被記錄從距離; 他們說形成一個閉合的領域。

遠的領域潛力

遠的領域潛力可能被記錄在某些情況之下。他們與接近的領域潛力分享特徵的有一個固定的潛在因素沒有問題錄音電極的地點, 但他們不發起於中堅力量。他們起因於事實中等圍攏潛在的來源是不同源亦不無限的, 依照被假設為塑造的化合物動作電位。六起因為遠的領域潛力被辨認了和被塑造了。39 個 變化在媒介的傳導性, 在容量指揮大小或在神經纖維的方向上是經常被認可的起因。遠的領域潛力被使用為臨床目的在人的患者; 他們使成為可能監測作用幾點沿somatosensory 路以一個固定的電極設置。40, 41 他們可能通常被記錄在狗雖然具體研究未被出版在這個種類。

距離的作用在錄音點和發電器之間。

記錄的潛力的高度迅速地減少作為距離在錄音電極和發電器增量之間。錄音電極應該被插入一樣緊密儘可能對發電器沒有危及緊張的組織, 在interarcuate 韌帶或lamina 級例如。實際上, 這是被測量的區別在二個電極潛力之間。 在一個monopolar 設置, 一個電極(錄音電極) 儘可能坐一樣緊密對發電器但是第二個(參考電極) 坐一樣很遠儘可能。但是, 移動這個第二個電極的好處減少以距離。一個大間極距離可能做錄音人工製品。但是, 這樣設置是需要的當尋找領域潛力。

在一個雙極設置, 兩個電極坐在發電器附近。這個設置不被期望給最大的高度, 並且被觀察的偏折的解釋是被複雜化(無花果3) 。努力應該被做保留距離在發電器和錄音電極常數之間, 不僅使高度可比較而且因為它修改複合動作電位被測量的潛在因素。 42

錄音從緊張的組織

有差別的放大器。

有差別的放大器普遍地被使用在臨床neurophysiology 方面。一個有差別的放大器看起來像二個放大器一起被修造當鏡像; 這些第一階段產品然後被混合。有是完全地等效的二輸入, 除了他們影響唯一產品在相反方向。因此, 產品與電位差是比例在二輸入之間。

過濾

它是損傷的放大潛力由不起源於發電器在研究之下的電極和導線查出; 他們是遮暗渴望的信號的正義"噪聲" (電子或生理學) 。放大器的能力reject 這些"共同方式" 潛力不是無限的。過濾是有用的在減少"噪聲。另外, 高頻率過濾器是需要的在下步之前, 模擬對數字式轉換, 否則會引起人工製品(現象叫做"混淆現象") 。但是, 過份過濾將降低, 將變形和將壓制信號的一些組分, 可能使測量無意義。結果, 它是明智保持過濾器窗口一樣開放儘可能。我們使用一個窗口從20 赫茲對4 千赫在脊椎記錄了SSEP 和10 赫茲到2 千赫為頭皮記錄的SSEP 。高頻率極限是多餘地高的在這個後者案件: 信號波形有主要低頻率內容並且300 赫茲經常被使用在其它laboraatories 。

類似物對數字式(廣告) 轉換和信號平均

信號在研究之下是在 mv 範圍甚至更低。電子和生理學噪聲是同樣數量級。"信號平均" 被使用查出信號在噪聲之中。錄音被抽樣在高頻率, 每30 ms 例如, 並且價值被存放。對刺激的反應, 和信號處理, 是"時間被鎖" 對刺激。刺激被重覆並且連續試驗的各樣品點的價值增加。各樣品價值由二潛力做成: 你是價值在那信號的片刻在研究中並且秒鐘是貢獻從噪聲。前有同樣標誌和價值在各次試驗(因為是時間被鎖) 當標誌和秒鐘的價值是一次任意事件。以連續總和, 信號高度增長並且噪聲趨嚮往零。但是, 這個趨向, 也許被表達作為"針對噪音的信號ratio"(S/N), 不是線性和S/N 的改善進步地逐漸消失。

它是可能控制在實時S/N 的改善。當各樣品點的價值增加在各次試驗以後在一個存儲器, 他們可能增加和連續地被減去在其它存儲器。改變標誌在各連續試驗取消時間鎖著的信號的貢獻當任意貢獻仍然趨嚮往零。殘餘的噪聲的這演算由"plus/minus" 方法增加一個客觀標準當尋找信號以非常低高度。43 的確, S/N 合計一如果信號不是存在。稽查能安置極限, 例如S/N 更低比1.2, 決定, 無回應存在。統計論據在這樣價值之後辯論。44

錄音電極: 哪些是哪些?

錄音(探索, 激活, 不同) 電極坐在被承擔的發電器附近並且參考(不活潑, 冷漠) 電極是遙遠從這臺發電器。如果稽查想要錄音電極的潛力的陽被顯示作為向下偏折在屏幕和印表機, 他必須連接錄音電極到放大器的倒置的輸入。這個設置被使用在EMG 和多數工作與SSEP, 但定期地不被使用為一些知覺被召喚的潛力即, 聽覺被召喚的潛力。這是正義的大會事情。(陽被顯示向上在本論文的所有辨別目標。)

當錄音電極像在幾工作關於頭皮記錄的SSEP 在狗5-7 選定是緊挨互相 , 一個電極"錄音" 和另一"參考" 是, 實際上, 有些任意的。這解釋差誤在作者之中關於頭皮記錄的SSEP 極性揮動的一部分。

4 脊椎記錄的SSEP 在原封動物

進行從尾部對rostral, 對SSEP 的四貢獻被記錄沿脊椎可能被認可。在L7-S1 水平, 根組分被記錄; 在尾部腰部區域, 繩子背潛力是突出的, 並且在rostral 水平, 登高的被召喚的潛力(AEP) 可能被跟隨; 另外, 髓心組分可能被記錄在池優秀大學畢業生3,4,12,46 (無花果 4) 的 水平。

脊椎記錄了SSEP 高度可能被同時雙邊刺激增加。12 早期的峰頂的高度迅速地到達最大值當刺激強度被上升, 雖然最新峰頂可能爾後增加。22 最早期的事件對麻醉深度不是敏感的。4

根組分

根組分不是非常與潛力不同被記錄在神經樹幹附近。這是發起於cauda equina 神經根的一個複合動作電位, 並且通常由三連續正面消極偏折做成。它可能被查出在二到三最尾部的椎間的空間之上當它與interneuronal 組分合併。它的峰頂潛在因素增加地增加在rostral 錄音。

繩子背潛力

繩子背潛力最好被記錄在lumbosacral 擴大。它被做一個相對地短的複合動作電位, 並且叫triphasic 潛力, 在interneuronal 組分之前和與它合併。這潛力發起於接踵而來的axones 上升的collaterals 。 45

interneuronal 組分的高度比那多次大的根組分和登高的被召喚的潛力。它的峰頂潛在因素不變化, 但是高度減少當錄音電極搬走。這接近的領域潛力被彌補一個長的期間消極峰頂被更長的期間blunted 正面波浪跟隨。消極峰頂(動作電位旅行從錄音電極) 發起於幾個地方在脊髓灰色問題根據這種傳入(低或高門限皮膚, 肌肉) 被刺激。46 增加刺激的力量召喚凹進長的正面波浪的最新消極波浪。這個峰頂的期間歸因於廣泛傳遞或反覆生火45。晚正面波浪跟隨大, 消極interneuronal 組分起源於主要輸入去極化劑(墊) (動作電位旅行往錄音電極) 。這是部份地或完全地阻攔突觸神經的傳輸在軸突終端在背部墊鐵灰色問題的一個神經原突觸前的禁止機制。47 這個高度廣義過程過濾掉一些輸入(當postsynaptic 禁止行動在所有輸入) 。它是允許有機體應付資訊剩餘伸手可及的距離它的一幾個中央禁止機制。

登高召喚了潛力

AEP 有一個複合動作電位的特徵。它是小高度和組分分離(分散劑) 如同錄音cranially 試圖。它可能難記錄在頭蓋骨胸部區域和在子宮頸區域由於發現一個適當的錄音電極位置困難。這是特別真實的在大狗。13 發電器電極距離可能是大的在這些區域並且錄音可能要求。

傳導登高的被召喚的潛力的速度價值被出版了。7-9,14 平均值變化了從66 m/s 到127 m/s 。幾源泉的在AEP 傳導速度的測量上變化被辨認了。錄音電極的深度有對被測量的潛在因素的影響依照已經被提及。如果錄音電極地點被使用為傳導速度測量跨過lumbosacral 擴大, 突觸神經的延遲被合併在cranially 被測量的潛在因素, 因此減少故意的速度。 12 快速, synaptically 被延遲的資訊旅行在dorsolateral 臍帶追上更加緩慢, 不間斷的資訊旅行在背部專欄。這介紹一個變化在發生在一個易變的地點沿thoracolumbar 區域的最大傳導速度上, 根據狗的大小。 4 終於, 上升的纖維直徑逐漸變細以距離; 因而, 傳導速度, 減少在子宮頸區域。48

刺激forelimb 神經提升一個interneuronal 組分在脊髓子宮頸擴大水平, 並且cranially, 對登高召喚了潛力, 可能由髓心組分遮暗。2

髓心組分

在池優秀大學畢業生的水平, 組分出現從中堅力量在骨髓可能被記錄。2,11 它被做一個消極峰頂被正面波浪跟隨。這接近的領域潛力也許發起於子宮頸和髓心中堅力量。貢獻從楔形的中堅力量被展示了在貓。 49 資訊傾沒從背部地坐的中轉中堅力量對更腹的中間蹄系。信號波形應該由機制造成相似與那些引起interneuronal 組分: 傳遞在interneurons 和墊裡。47

頭皮記錄的SSEP 在原封狗

這些潛力可能被記錄使用頭皮電極為探索和參考電極。並且, 遠的領域潛力可能被記錄與一個extracephalic 參考電極當使用同樣頭部地點為探索的電極。最早期的接近的領域潛力(P18 和N 30) 是最大在nasion 和前囟門之間。他們的高度迅速地減少如果錄音電極搬走(無花果5) 。他們保留同樣出現沒有問題參考電極(脖子的鼻子或基地的要訣的位置) 。13 從什麼知道關於somatotopic 投射在主要somatosensory 外皮, 記錄midline, 對側對被刺激的神經, 可能給更大的P18-N30 潛力。但是, 關於錄音位置地點的作用的系統的研究在狗未被出版。更長的潛在因素positive/negative 潛力可能被記錄在沉著或只被麻醉用麻醉劑的動物中。5,6 後者潛力由巴比土酸鹽壓制和對被鹵化的麻醉劑是相當敏感的。50 第一偏折的信號波形被這種鎮靜或麻醉修改。6 除對鎮靜劑和麻醉劑的易變的用途之外, 錄音電極地點, 經常雙極型, 變化了在現有的研究之中, 做比較困難。

高度的個人間的增殖率和第一波浪的潛在因素不是像與脊椎記錄了SSEP 一樣。潛在因素當然與身體尺寸有關, 但高度被影響也是。參考價值為潛在因素和高度作為身體尺寸功能是可利用的。13

SSEP 在狗以脊髓壓縮

有唯一觀察的一個有限的數字關於SSEP 變化在狗上以自然地被獲取的脊髓疾病。4,9,14,51 這與研究對比與豐富的文學在SSEP 變化在實驗性地被給予的脊髓損害在實驗室種類上和在人之後。

SSEP 頭蓋骨對繩子損害和AEP 傳導速度通過損壞的區域

頭皮比脊椎記錄的SSEP 記錄了SSEP 有抵抗性當實驗性繩子損害嚴肅增加。52 頭皮的觀察記錄了SSEP 或他們的再出現期望功能補救參加一系列狗以自然地被獲取的脊髓壓縮,51 結果一致與子宮頸繩子的實驗性壓縮的觀察在狗。53 在另中研究介入狗以自然地被獲取的脊髓壓縮, 14 傳導通過損壞的區域不能被查出與脊椎記錄的SSEP 在40% 狗中以等級3 臨床傷殘(paraplegic, 以某一義務馬達活動禮物) 並且在等級4 狗中(paraplegic 的70 % 以某一痛苦悟性禮物) 。頭皮記錄的SSEP 是有抵抗性以潛力可錄在所有等級3 狗和在60% 等級4 狗中。結果, 案件的一個相當大的比例應該被考慮作為假的陰性以這些測試與臨床評估比較。頭皮記錄的SSEP 不是可錄的在狗沒有痛苦悟性(等級5) 。當疏忽記錄SSEP 從頭和缺乏不一定運載絕望功能預測愚鈍的痛苦悟性一樣, 任一活動錄音頭蓋骨對損害運載一種好預測。 4

脊椎記錄的SSEP 一個有趣的特點是發現被召喚的傷害潛力(EIP) 能被記錄在有焦點損害的多數狗。

AEP 的分散作用記錄了頭蓋骨對老損害14 或緩慢生長大量(無花果6) 是顯然的。這些特點可能有價值當你老, 臨床沈默和一個深刻, 當代損害共存在thoraco 腰部區域: 當代你大概是緊挨EIP; 並且AEP 的期間增加的頭蓋骨到老一個(無花果7, 無花果8) 。

AEP 傳導速度的重大減少橫跨損壞的繩子區域被發現在動轉失調, 能走患者。14 實驗工作顯示出, 被承受的壓縮典型地導致潛在因素變動craniad 對被承受的壓縮。54 傳導速度的比橫跨損壞的區域與SSEP 的期間被記錄從更多一個頭蓋骨站點使用評估脊髓損害嚴肅在狗。9 然而, cranially 記錄的SSEP 實際上是EIP 在嚴厲地受影響的狗在這項研究中。混亂使這企圖無用。

與焦點損害對比, 在散開神經學問題譬如退化radiculomyelopathy, AEP 也許被期望進步地丟失高度並且成為更分散作為錄音站點cranially 被移動。但是, 困難在獲得可解釋的錄音在大狗胸部區域可能使這難令人信服地展示。

被召喚的傷害潛力

EIP craniad 的發生對繩子損害很好被描述了從實驗工作在貓。55 它並且被使用了如同一個intraoperative 地方化的工具為深刻子宮頸脊髓傷害56 和在子宮頸脊髓腫瘤撤除57 期間 在人。

不同於SSEP 被記錄從頭, EIP 有一個傾向是大的在更加嚴厲的案件。EIP 的研究介入25 條狗以自發脊髓壓縮被進行了。15 研究的目標將尋找一個最大的傳導塊地點。的確, EIP 信號波形變動被發現取決於錄音電極的地點相對傳導塊地點(無花果2) 。錄音站點被安置了每5 到10 毫米跟隨變化在EIP 配置上。最大的傳導塊被承擔是在二個電極中間記錄EIP 的變動從biphasic 對monophasic 。這點, 被測量在射線照相與錄音電極到位, 總是尾部對脊髓壓縮的實際幅射線照相的地點。距離在最大的傳導塊和脊髓壓縮之間是大的在最受影響的狗, 大概反射損傷的尾部傳播由次要損害現象造成。這次距離測量也許允許一進一步分級在狗之中沒有痛苦悟性, 某事是完全地不可及的以臨床考試。在這項研究中, 統計區別不能被發現在狗之間以臨床成績4 和5, 但是樣本大小為等級4 相當小。距離, 傳導塊對機械壓縮, 迄今是最有為的客觀預斷標準在嚴厲脊髓壓縮。

對SSEP 的其它臨床用途

SSEP 被使用了作為上臀結節問題評估, 58 的一診斷部份 為臀部的神經的功能監視在hip 手術59 期間 和在狗的評估以cauda equina 綜合症狀。60

有未解決對頭皮記錄的SSEP 的一個潛在的用途在腦子問題。髓心組分能被使用在這些情況下作為內部控制和排除一致脊髓介入。

minibabyqq 2006-12-28 01:32

[color=Magenta][size=5][b]NEUROMUSCULAR 混亂影響幼小狗和貓   [/b][/size][/color]


Neuromuscular 疾病是馬達單位的混亂和包括neuromuscular 傳輸neuropathies (神經元的混亂包括細胞身體、軸突、Schwann 細胞和myelin), 混亂, myopathies (肌肉纖維的混亂), 和neuromyopathies (神經元和肌肉纖維混亂) 。疾病聯繫了每個這些組分被描述了在幼小狗和貓少於6 個月年齡。neuromuscular 混亂的原則臨床標誌被推斷或地方化的肌肉弱點。弱點也許由局部痲痺體現或痲痺、步態反常性和與鍛煉相關的弱點、咽下困難、dysphonia 、呼吸困難, 或反流。肌肉萎縮、發育不良、肥大和骨骼殘疾也許是存在。neuromuscular 疾病診斷依靠詳盡的物理和神經學考試, 具體血清學測試, electrophysiological 評估, 和考試優選地處理肌肉和周邊神經切片檢查法。除那些之外有感染或免疫斡旋的原因論, 早期的起始neuromuscular 混亂是, 總之, 養殖相關和繼承。具體治療當前不是可利用的並且預測為補救一般是窮的。這些可遺傳的混亂遺傳學的認識和研究為交配動物者提供可貴的資訊, 應該最後導致分子分析用試樣為受影響的狗和臨床正常載體的偵查。

NEUROPATHIES - 神經細胞的細胞身體

遺傳性馬達神經元疾病。 被繼承的馬達神經元疾病在動物中為脊髓和brainstem 的腹墊鐵細胞的進步退化描繪。這廣泛地被學習了在布里坦尼spaniels 1,2 和被描述了作為一種統治被繼承的更低的馬達神經元疾病被認可以三形式: 加速(弱點在1 個月年齡以前注意與 tetraparesis 在3-4 個月年齡以前), 中間體(弱點被注意在4-6 個月年齡與tetraparesis 在2-3 年紀), 和慢性(慢慢地進步) 。除狗也許生存很好入成人生活的慢性形式之外, 預測是窮的並且tetraparesis 和tetraplegia 顯現出在一個到六個月年齡內。其它受影響的養殖包括尖,3 條 瑞典拉普蘭狗, 4 和rottweilers 。5,6 在rottweilers, 臨床標誌被描述了在四個星期年齡以迅速地進步tetraplegia 、震顫、megaesophagus 、廣義肌肉萎縮, 和骨盆肢體伸張機堅硬 (圖1)。一隻影響的小貓被描述了以弱點當前在4 個星期年齡。7 種 被繼承的馬達神經元疾病是難以處置的。

知覺Neuronopathy。幾養殖, 包括 長髮dachshunds8 和 英國尖,9 影響了以神經細胞的細胞身體和知覺神經纖維損失。繼承被描述了像autosomal 隱性在兩養殖。在 英國尖, 主要知覺神經元的缺乏在成長或分化也許是包含的。主要知覺神經元損失同對弄髒的著名的減少聯繫在一起物質P, 斡旋nociception 的一個興奮代理。這損失是最明顯的在脊髓背部墊鐵的表面laminae 。知覺官能不良的臨床標誌佔優勢包括骨盆肢體不整齊, 神志清楚的proprioception, 沮喪的痛苦感覺, patellar hyporeflexia 損失, 並且自已切斷自已切斷也許是主要臨床標誌起點在6 個月年齡之前。

NEUROPATHIES - 周邊神經

進步axonopathy 在 拳擊手。autosomal 隱性神經病以臨床進步不整齊, 被減少的或缺席反射, 本體感受的損失、被減少的肌肉緊張和弱點起點在骨盆肢體和進步的標誌對胸部肢體, 被描述了在拳擊手開始在1-2 個月年齡。10 軸突在周邊和中央神經系統被擴大。骨盆肢體不整齊也許是存在儘早2 個月年齡。Hyporeflexia 是存在以彎曲的保留。一中央axonopathy 並且被描述了在幼小拉布拉多獵犬。11

Laryngeal 痲痺polyneuropathy 複合體。 廣義polyneuropathy 與相關laryngeal 痲痺和megaesophagus 被描述了在幾條幼小 Dalmatian 狗。12 當繼承方式不是堅定的, 一個autosomal 隱性樣式被懷疑。臨床標誌起始是從4-6 個耐力、進步laryngeal stridor 、聲音變動、呼吸困難、青紫在情節嚴厲呼吸困難期間, 和崩潰月年齡和包括的呼吸困厄和損失。預測被守衛了對貧寒。具體治療不是可利用的並且受控養殖被建議了。laryngeal 痲痺polyneuropathy 複合體最近也被描述了在幼小rottweiler 狗以吸入的stridor 起點在11-13 個星期年齡。13 其它養殖被描述以laryngeal 痲痺的遺傳性形式包括 bouviers des Flandres14 和可能年輕 西伯利亞愛斯基摩和愛斯基摩雜種。(Shelton, 未出版的觀察。)

Niemann 採摘疾病。 一demyelinating 的polyneuropathy 也許同聯繫在一起Niemann 採摘疾病, 一種autosomal 隱性lysosomal 存貯疾病為缺乏sphingomyelinase 描繪 (圖2)。三隻 暹羅貓在2 個和5 個月年齡之間以這種疾病被描述了。15 個 神經學標誌包括進步tetraparesis 和不整齊、palmigrade 和plantigrade 姿態、罰款廣義震顫, 和減少了或缺席反射。適度hepatosplenomegaly 並且被描述了。有實際上每個身體系統的普遍濾滲與擴張的顆粒狀巨噬細胞。疾病是進步和致命的沒有治療可利用。

主要Hyperoxaluria 。 深刻弱點 (圖3) 和腎衰竭被描述了在相關 貓從不列顛與相關主要hyperoxaluria (L 甘油的aciduria), 類似於主要hyperoxaluria 類型II 在人。16 個 臨床標誌成為了明顯的起點在5 個月年齡。繼承一個autosomal 隱性方式被建議了。所有被報告的貓死了在1 年紀之前儘管根據症狀的療法為急性腎衰竭。

糖朊存貯疾病類型IV 。 糖朊分支的酵素的缺乏被報告了在三隻幼小相關挪威森林貓。17 個 臨床標誌包括廣義肌肉震顫 和弱點進步對變得明顯在大約5 個月年齡的tetraplegia 。嚴厲廣義肌肉萎縮和攣縮是存在在無痛苦的死亡之時。反常糖朊的儲積(圖4) 和嚴厲退化也許被發現在CNS 、PNS 、骨骼肌和心臟。

NEUROPATHIES - SCHWANN 細胞瑕疵

被繼承的肥大性神經病 - 肥大性神經病被描述了作為autosomal 隱性馬達神經病在 西藏mastiffs 。18 個 病理性研究結果包括被減少的密度myelinated 神經纖維、普遍demyelination, 和早期的蔥電燈泡形成以較少axonal 退化在周邊神經和神經根。肌動蛋白像細絲積累了在Schwann 細胞細胞質。最初的研究的結果表明了一個Schwann 細胞瑕疵。臨床標誌出現在動物中從7-10 個星期年齡和迅速地包括進步廣義弱點、hyporeflexia 、hypotonia, 和dysphonia 。Electrodiagnostic 研究顯露了一適度對對神經傳導速度的嚴厲減少。預測被守衛並且治療不是可利用的。

Hypomyelinating polyneuropathy 在 金黃獵犬 - 周邊神經系統的Hypomyelination 被描述了在金黃獵犬littermates 。骨盆 肢體不整齊的15 個臨床標誌是存在在5-7 個星期年齡以骨盆肢體的綁架和hocks 的增加的彎曲之間造成一次蹲下的出現。溫和的骨盆肢體肌肉萎縮和弱點被描述了以"兔寶寶hopping" 步態當跑。馬達神經傳導速度明顯被減少了。Histopathological 和形態測量學的分析提供了hypomyelination 。治療不是可利用的。在動物中被跟隨一年, 臨床標誌的進步或改善未被描述。

NEUROMUSCULAR 傳輸混亂

Myasthenia Gravis 。 Myasthenia gravis (鎂) 是neuromuscular 傳輸混亂起因於或acetylcholine 感受器官(先天鎂) 缺乏或一個 自動免疫的反應反對感受器官(被獲取的鎂) 。兩個鎂的形式可能發生在狗少於6 個月年齡。 先天鎂被描述了在 傑克・Russell 狗 20 (圖5), springer spaniel,21 和 光滑的狐狸狗。22 臨床弱點起始在在6-9 個星期年齡。反流從megaesophagus 是易變的。被獲取的鎂, 以相似的臨床標誌, 也許發生在狗在3-4 個月年齡(Shelton, 未出版) 。在被獲取的鎂裡, 動物臨床是法線在臨床標誌之前起始。

先天鎂診斷由在肌肉力量的改善做由短行動的膽鹼酯抑制劑藥物edrophonium 氯化物(Tensilon, 0.1 mg/kg Iv) 的靜脈內管理。減少量的示範在肌肉動作電位跟隨扭轉與膽鹼酯抑制劑的反覆神經刺激服麻醉劑並且支持診斷。診斷的確認由被減少的acetylcholine 感受器官(AChR) 集中的示範做由新鮮的結冰的肋間的肌肉組織的生物化學的量化。 被獲取的鎂診斷由清液AChR 抗體出現的示範做由immunoprecipitation 放射免疫測定。23

治療中流砥柱為先天鎂是膽鹼酯抑制劑藥物。Pyridostigmine 溴化物(Mestinon, 0.5-3.0 mg/kg BID-TID, PO) 也許是有效的在控制臨床標誌, 雖然藥物抵抗以慢性治療也許發生。治療為被獲取的鎂是相似與一些狗要求類皮質激素(0.5 mg/kg q 24 h, PO) 或其它免疫抑制的藥物的加法。預測被守衛對貧寒在先天鎂裡和好對守衛在被獲取的鎂裡根據疾病和一致志向肺炎的嚴肅。

neuromuscular 傳輸其它混亂。 雖然不凡在狗, 被預先形成的外毒素的攝取 紡錘狀細菌屬botulinum 可以導致溫和的面部肌肉、咽、食道和下頜的弱點對嚴厲鬆弛tetraplegia 以缺席脊髓反射和弱點。診斷由歷史, 臨床, 和electrodiagnostic 評估建議和由毒素的證明證實在材料被咽下或在受影響的動物清液、排匯物, 或嘔吐物。治療是主要支援和預測通常有利在狗。

壁虱痲痺, 由神經毒素造成由某一壁虱的種類引起, 導致鬆弛, 無熱的上升的馬達痲痺在狗, 與recumbancy 在24-72 個小時。反射丟失以痛苦感覺的保存。以壁虱撤除和支援關心, 有通常補救在1-3 天之內。

慢性有機磷酸鹽(操作) 毒力也許導致脖子的堅持ventroflexion 在幼小貓和廣義弱點在狗和貓, 沒有嘔吐, 腹瀉、分泌唾液, 和miosis 的經典自主神經系統的標誌。診斷根據歷史對操作, 低血漿acetylcholinesterase 水平, 和一個decremental 反應的最近用途跟隨反覆神經刺激。治療包括沐浴去除任何殘餘的操作和口頭diphenhydramine (4 mg/kg 每8 個小時) 。補救通常將需要3-6 個星期。

MYOPATHIES

肌肉Dystrophies 。 肌肉營養失調(MD) 是提到一個大小組被繼承的和進步地致衰弱的肌肉混亂為骨骼肌的退化描繪的一個一般用語。在人超過20 種疾病被描繪了根據了基因並且臨床特點。23 X 連接的和autosomal 隱性繼承樣式被描述了在人。在狗和貓, X 連接的形式很好被描繪。

似犬X 連接的MD - X 連接的肌肉營養失調被描述了在幾養殖包括金黃獵犬,25 條 愛爾蘭狗, 26 薩莫耶特人,27 隻 微型schnauzer,28 位 比利時Groenendaeler 牧羊人,29 rottweilers,30 德國短髮尖,31 和 Pembroke 威爾士corgis 。32 個 臨床標誌出現在6-9 個星期年齡和首先包括進步弱點、僵硬的步態、肌肉萎縮和攣縮。清液肌酸kinase (CK) 水平被舉起和明顯也許被查出儘早1-2 天年齡。典型形態損害是存在在肌肉切片檢查法包括肌肉壞死、吞噬作用、再生、肥大、endomysial 纖維變性和myofiber 成礦。 臨床, X 連接的MD 診斷由展示做明顯減少在或缺乏蛋白質 dystrophin 由immunohistochemical (圖6.A 、b) 或分子方法。預測是窮的因為具體治療不是可利用的。心肌病一致地是存在在X 連接的MD 並且更舊的dystrophic 狗也許死於心力衰竭。33

似貓的X 連接的MD - X 連接的MD 的一個肥大性形式被描述了在幼小家養的shorthair 貓。34,35 與萎縮對比當前在狗, 疾病在貓為肌肉肥大描繪以潛在地致死的複雜化。36 臨床標誌是存在在 大約3 個月年齡和包括肌肉肥大 (圖7), 僵硬, 和被減少的敏捷性。舌肥大也許是存在以無能關閉嘴和修飾 (圖7) 。 反流也許是存在由於膜片的嚴厲肥大。清液CK 明顯被舉起。典型形態損害包括重大endomysial 纖維變性是存在在肌肉切片檢查法標本 (圖8)。 Dystrophin 明顯被減少或完全缺席在immunohistochemical 分析用試樣。預測是窮的並且治療不是可利用的。

Rottweiler 狗末端Myopathy - 雖然沒描繪一樣完全地像X 連接的dystrophic 混亂, 一familial 末端myopathy 最近被描述了在幼小Rottweiler 狗。37 當一個確切的繼承樣式未被確定, 多條狗在廢棄物也許是受影響的。所有被認可的狗迄今養殖了在南加利福尼亞。臨床標誌是存在在6-8 個星期年齡和包括的末端附屬物的弱點由姿勢反常性見證範圍從被展開的數字 (tarsal 和腕骨聯接的圖9) 和hyperflexion 對plantigrade 和palmigrade 姿態 (圖10)。診斷由electrophysiologic 測試和myopathic 反常性的histologic 示範證實在末端肢體肌肉包括gastrocnemius 。具體治療不是可利用的。

新陳代謝的myopathies

線粒體myopathy - 一myopathy 為粗劣的鍛煉容忍描繪以嚴厲新陳代謝的酸中毒的發展, 和乳汁和丙酮酸酸血症隨後而來的鍛煉被描述了在 Clumber 38 和 蘇克塞斯 39 spaniels 從英國和最近被辨認了在這些同樣養殖狗從美國(Shelton, 未出版) 。生物化學的分析在蘇克塞斯spaniel 從英國展示了一個瑕疵在 丙酮酸鹽氧化作用由於丙酮酸鹽dehydrogenase 缺乏。39 一線粒體myopathy 與修改過的 細胞色素c oxidase 活動和被減少的線粒體mRNA 並且被描述了在老英國sheepdog littermates 以鍛煉不寬容。40,41 線粒體混亂的評估要求被舉起的休息或崗位鍛煉血漿lactate 和丙酮酸鹽含量的示範, 和線粒體的光和電子顯微鏡評估在肌肉切片檢查法部分之內。精確描述特性依靠專業生物化學的分析用試樣和分子研究。

糖朊新陳代謝瑕疵 - 這個小組相對地不凡的混亂起因於糖朊新陳代謝天生錯誤以糖朊像材料的儲積在肌肉和其它組織之內。debranching 酵素amylo 1,6 glucosidase 的瑕疵(glycogenosis 類型Iii) 被報告了用 德語牧羊人和 Akitas 以肌肉弱點顯然在2 個月年齡。42,43 胃腸膨脹也許並且是存在由於hepatomegaly 起因於糖朊像材料的證言。phosphofructokinase 缺乏(型VII 糖朊 存貯疾病的) 一個autosomal recessively 被繼承的形式被描述了在年輕 英國springer spaniels 44 在大約8 個月年齡。提出臨床標誌由補償的溶血貧血症、血管內的hemolysis, 和hemoglobinuria 主要地組成了沒有公開肌肉弱點。雖然清液CK 集中也許溫和地被舉起, 缺乏突出的肌肉弱點很可能反射似犬骨骼肌的高度氧化本質。一個相似的情況發生在 斗雞家spaniel 。45 分子測試是現在可以得到的為受影響的狗和臨床正常載體的偵查。

Myotonic myopathies

Myotonia 被定義當活躍肌肉收縮堅持的狀態在義務努力或刺激停止了之後。先天myotonia 以臨床標誌起始在大約2 個月年齡被描述了用 食物食物,46 Staffordshire 狗,46 和 了不起的丹麥人,47 和最近在5 個月年齡在二隻 家養的shorthair 貓。48 僵硬通常是存在在休息以後和典型地消失在鍛煉("溫暖的" 現象以後) 。接近肢體肌肉、舌頭, 和脖子的肥大也許是存在。笑渦結果跟隨肌肉撞擊聲。 診斷由反覆放電的典型火車出現打蠟和減少在頻率導致"潛水轟炸機" 聲音通常證實。肌肉切片檢查法通常是正常或展示唯一溫和的myopathic 變動。

最近, myotonic 混亂以起波紋的和典型electrophysiological 反常性 (myotonic 放電) 被觀察了在微型Schnauzers (圖11) 在大約6 個星期年齡。50 接近肢體肌肉被標記的肥大是存在。舌頭僵住和推出從嘴 (圖12)。咽下困難和過份分泌唾液是共同。面部dysmorphism, 被描述作為額嘴形狀對下頜, 是存在在一些受影響的狗。與發生在chow-chow 的myotonia 對比, 僵硬看上去惡化隨後而來的鍛煉代替改善。肌肉形態學是平凡的(Shelton, 未出版) 。治療不是現在可以得到的。

其它遺傳性Myopathies。

遺傳性myopathy 拉布拉多獵犬- 一遺傳性myopathy 由弱點臨床描繪、明顯缺乏在骨骼肌大量, 反常姿勢和步態, 和鍛煉不寬容廣泛發生在這養殖。51 腱反射是一般被減少或缺席的以正常proprioception 。受影響的動物是黑和黃色外套顏色的男性和女性。臨床標誌, 由寒冷、興奮, 和鍛煉加重, 是顯然的在3 個月年齡以前和通常穩定在6 個月和1 年紀之間。繼承證明是一個簡單的autosomal 隱性方式。52

清液CK 集中也許是在正常極限內或溫和地舉起了。Electromyographic 評估也許顯示自發活動包括原纖維形成作用潛力、正面鋒利的波浪, 和異常的高頻率放電。神經傳導速度是正常的並且沒有對反覆神經刺激的decremental 反應。診斷這myopathy 由新結冰的肌肉切片檢查法部分的評估證實包括纖維鍵入。 當原始的報告這myopathy 描述了型II 肌肉纖維缺乏,51 大範圍形態特點也許被觀察在肌肉切片檢查法從受影響的狗建議那裡也許是超過一混亂影響這養殖幼小狗。Neuropathic 特點是存在在一些狗, 當在其他人myopathic 和dystrophic 特點佔優勢。這混亂部下的原因論, 是否myopathic 或neuropathic, 未被澄清。治療不是現在可以得到的。雖然受影響的狗不是適當的為工作, 他們也許是可接受的房子寵物當臨床標誌穩定在6 個月和1 年紀之間。因為這disorder(s) 分子瑕疵未被辨認並且一次診斷測試不是可利用的為臨床正常heterozygous 載體的證明, 交配動物者應該從他們育種的節目消滅受影響的小狗的父母或兄弟姐妹。

Nemaline 標尺myopathy - Nemaline 標尺被描述了與一先天 myopathy 有關係在家庭貓 53 和在一隻幼小藍色merle 疆界大牧羊犬。54 起始臨床簽署被報告的貓開始了在大約6 個月年齡和包括了溫和的弱點和勉強被處理, 進步對震顫和肌肉萎縮。臨床簽到疆界大牧羊犬, 顯然在14 個星期年齡、包括的震顫、鍛煉不寬容、僵硬和stilted 步態, 和肌肉萎縮 (圖13)。新結冰的肌肉切片檢查法部分的Histochemical 評估使用修改過的Gomori trichrome 汙點展示了出現許多標尺 (圖14)。弱點是進步, 最後造成四肢癱瘓。治療不是現在可以得到的。Nemaline 標尺並且被描述了與一嚴厲進步myopathy 有關係在一條年輕 柔滑的狗以臨床標誌顯然在12 個星期年齡包括咽下困難, 堵塞, 僵硬的hindlimb 步態和彎成拱狀的姿態。55

核心myopathy - 一被繼承的myopathy, 開始在大約6 個月年齡, 被描述了用 了不起的丹麥人在英國 (圖15)。臨床標誌開始在大約6 個月 年齡從進步肌肉浪費, 鍛煉不寬容、廣義身體由興奮惡化的震顫和崩潰。56 診斷這myopathy 依靠 肌肉顯示明確定義的黑暗弄髒的中心地區在許多myofibers 之內的切片檢查法部分評估, 一致與核心 (圖16)。具體治療不是可利用的此時。

張力亢進的myopathies - 電子沈默張力亢進的myopathy 起點在大約3 個月年齡被描述了在 騎士查爾斯國王spaniels 在英國,57,58 並且肌肉切片檢查法被評估了從2 影響的littermates 從澳洲(Shelton, 未出版) 。所有被描述的狗有由"鹿偷偷靠近的" 行動在之前鍛煉和興奮導致的"崩潰的" 的歷史。在所有4 肢體的肌肉伸張機口氣的增量是顯然的在崩潰期間的時期以補救發生在大約10 分鐘之內。治療與苯甲二氮卓沒有導致改善。混亂的進步未被報告並且安定或改善也許發生。當線粒體和membranous 反常性形態上被發現了在肌肉切片檢查法之內, 這具情況遺骸的發病原理陰暗。

張力亢進的混亂為myoclonus 和伸張機堅硬描繪被描述了在 拉布拉多獵犬。59 個 臨床標誌, 發生在6 個星期年齡, 包括附屬物和軸向肌肉的斷斷續續的刺激敏感收縮, 並且廣義收縮創始由義務運動。治療試驗以苯甲二氮卓和clonazepam 不是有效的。

肌肉hypertonicity (蘇格蘭獵犬抽瘋) 與相關姿勢和活動困難和為肌肉hypertonicity 發作描繪被描述了在蘇格蘭狗狗。60,61 個 臨床標誌也許被觀察在小狗在6-8 個星期年齡。明顯骨盆肢體伸張機堅硬也許導致狗下落當跑和嚴肅也許是這樣步行是不可能的。繼承一個autosomal 隱性方式被建議。methylsergide 的管理(0.1-0.6 mg/kg 口頭) 是有效的在辨認溫和地受影響的狗以抽瘋顯然在2 個小時和作用之內持續8 個小時。苯甲二氮卓(0.5 到1.5 mg/kg 口頭三次每日) 可以被使用在受影響的狗的治療。

混雜被繼承的myopathies - 其它被繼承的myopathies 疏散案件報告是在文學。 一autosomal 隱性myopathy 被描述了在德文郡rex 貓。62,63 個 臨床標誌被觀察在1 個和6 個月年齡之間和包括廣義附屬物的脖子的弱點、ventroflexion, megaesophagus, 和肩胛骨的背部伸進與正常反射和正常CK 。Dystrophic 變動被描述了在肌肉切片檢查法部分。迄今, pathogenetic 機制負責任對德文郡rex myopathy 依然是未知。 familial polysystemic 混亂介入dyserythropoiesis, polymyopathy 和心臟病反常性並且被描述了在3 條相關的springer spaniel 狗。64 名單將繼續增長當最近被認可的養殖具體myopathies 被辨認。

激動myopathies

Masticatory 肌肉myositis (MMM) - 這免疫被斡旋, 焦點激動myopathy 有選擇性地影響咀嚼的肌肉, 可能發生在狗少於6 個月年齡。臨床標誌包括某一masticatory 肌肉萎縮或膨脹的組合和反常下頜作用, 由有限的下頜流動性一般體現。清液CK 集中也許是正常的或溫和地舉起了。 實驗室診斷由流通的抗體的偵查做反對型2M 纖維 (圖17), 一種獨特的纖維類型禮物只在咀嚼的肌肉。65,66 肌肉切片檢查法的評估依照由相當數量myofiber 破壞和纖維變性確定是必要的為診斷的確認和在預測為下頜作用和肌肉大量回歸。類皮質激素免疫抑制的劑量應該被使用直到下頜作用恢復正常並且清液CK 是在參考範圍之內。劑量應該然後被減少直到保持狗免於臨床標誌的最低的供選擇天劑量被到達。這種劑量應該繼續在一個另外的4-6 個月因為臨床標誌將再發生如果治療太很快被停止或一種不充分的劑量最初地被使用。

Dermatomyositis 在大牧羊犬狗和Shetland sheepdogs - Familial 似犬dermatomyositis 被報告了在大牧羊犬狗 67 和在Shetland sheepdogs 。皮炎的 68 個臨床標誌佔優勢 (圖18), 開始在大約8-10 個星期年齡。肌肉疾病的臨床標誌包括廣義肌肉萎縮、僵硬的步態、咽下困難和megaesophagus 也許發生在嚴厲地受影響的狗並且溫和地受影響的狗也許無症狀。Dermatomyositis 被顯示有一個autosomal 統治繼承樣式在大牧羊犬狗。

感染polymyositis - 激動myopathy (myositis), polyneuropathy, 和multifocal 神經學疾病也許被發現在幼小小狗被感染 弓形體gondii 和 Neospora caninum 。 69,70 個 臨床標誌也許是存在儘早4 個星期年齡和包括進步paraparesis 和"兔寶寶hopping" 步態以進步對骨盆肢體伸直過度 (圖19) 並且 肌肉萎縮。進步對骨盆肢體伸直過度是更加可能的當傳染顯現出在4 個月年齡之前。71 清液CK 集中通常被舉起。清液和CSF 抗體的被舉起的集中反對 N. caninum 和 T. gondii 支持傳染出現。肌肉和周邊神經切片檢查法應該證實polymyositis 和周邊神經病診斷。偶爾地有機體被發現在肌肉切片檢查法部分之內。治療包括氯林肯黴素 72 和sulfadiazine 和trimethoprim 。73 當一些改善也許被注意在神經學作用, 骨盆肢體伸直過度的完全決議未被報告發生。
Neuromuscular diseases are disorders of the motor unit and include neuropathies (disorders of the neuron including the cell body, axon, Schwann cell and myelin), disorders of neuromuscular transmission, myopathies (disorders of the muscle fiber), and neuromyopathies (disorders of both neurons and muscle fibers). Diseases associated with each of these components have been described in young dogs and cats less than 6 months of age. The principle clinical sign of neuromuscular disorders is generalized or localized muscle weakness. Weakness may be manifested by paresis or paralysis, gait abnormalities and exercise-related weakness, dysphagia, dysphonia, dyspnea, or regurgitation. Muscle atrophy, hypotrophy, hypertrophy and skeletal deformities may be present. The diagnosis of neuromuscular diseases is dependent on thorough physical and neurological examinations, specific serological testing, electrophysiological evaluations, and examination of optimally processed of muscle and peripheral nerve biopsies. With the exception of those having an infectious or immune-mediated etiology, neuromuscular disorders of early onset are, in general, breed related and inherited. Specific treatments are currently not available and the prognosis for recovery is generally poor. Recognition and study of the genetics of these heritable disorders provide valuable information for breeders and should ultimately result in molecular assays for detection of affected dogs and clinically normal carriers

minibabyqq 2006-12-28 01:33

[color=Magenta][size=5][b]EXTERNAL FIXATOR TO CORRECT SPINAL FRACTURE/LUXATION   [/b][/size][/color]


M所有外科技術被描述了為似犬脊髓專欄的修理並且/或者安定跟隨精神創傷[1-8] 。各個技術有它自己獨特的套被報告的好處和不利[1, 4, 8] 。脊髓外在fixator 系統被描述這裡 使用正面外形被插入入每個身體四塊毗鄰椎骨的結束穿線的別針在試驗孔操練以適當的大小的位元之後。八個別針被使用, 與一個別針被安置在各 各個椎骨身體的 邊。別針在各塊椎骨然後附有金屬 脊髓fixator 曲拱 以定像螺栓並且四曲拱一起然後連接使用穿線的連接桿。這個技術相對地容易使用和有幾好處。較少軟的組織解剖是需要的因為椎骨的身體不充分地被暴露在手術期間, 如此減少損壞重要結構和保存對脊椎貢獻的周圍的肌肉和他們的附件的危險[ 5, 8 的] 穩定這個技術其它好處有: 植入管撤除舒適; 沒有干涉如果一背部laminectomy 是必要的; 充分安定供應嚮破裂癒合發生; 並且能力調整fixator 在手術後期間沒有外科干預[8] 。外在fixator 可能嚮更低的胸部和腰部脊椎被申請和由患者很好容忍。

技術的應用要求椎骨解剖學詳盡的知識保證適當的別針安置。對皮膚安置的仔細的關注是必要的當別針被插入入椎骨身體減少緊張和手術後別針的可能性-短文sepsis 。所有者必須是被指示和努力在適當的手術後別針管理。

這個案件報告的目的將描述對一個外在fixator 系統的用途在三條狗以 創傷脊髓不穩定。

材料和方法:

狗: 所有狗 提到了獸醫弗吉尼亞馬里蘭地方學院的教的醫院為被懷疑的脊髓不穩定跟隨精神創傷。脊髓官能不良診斷次要對精神創傷和椎骨運河不穩定根據主要研究結果從神經學考試和慣例造影。在狗1, flexion/extension 射線照相並且被獲得展示動態不穩定。在狗1 和2, 脊髓壓縮形象化使用計算tomography.a 。被重新排版的CT 圖像引起了使用一臺遠程診斷工作站。b

外科技術: 狗被安置了在sternal recumbency 和為對脊椎的一種背部方法準備了, 與切開被集中在不穩定區域。在外科曝光以後, fracture/luxation 臨時地舉行了在減少與Kirschner 導線被安置橫跨受影響的椎骨身體的關節小平面。一背部laminectomy 執行得如果需要保證減少並且/或者從椎骨運河去除圓盤或骨頭片段。一個試驗孔然後操練了入椎骨的身體的頭蓋骨部份在450 個 角度對背部脊椎。孔通過了兩件椎骨外皮, 使用接近正面外形別針內在直徑被使用的鑽頭。在腰部椎骨輔助部件處理並且橫向過程被使用了作為地標並且在胸部脊椎輔助部件過程和肋骨頭被使用了作為地標。深度測量儀被使用測量試驗孔的深度並且這個措施被標記了在正面外形末端穿線的別針與一個不育的標誌。一個試驗孔相似地被做了在椎骨身體的對側邊。試驗孔在對側邊被做在椎骨的尾部部份為了保留別針從干涉互相在他們的安置期間。

在完成所有飛行員孔, 皮膚和周圍的肌組織被拉扯了對切開的中心並且毛巾鑷子被使用臨時地拿著切開被關閉。第號15 scalpel 刀片被使用做小皮膚切開起一個詞條門戶作用對於別針。一個6.5 毫米鑽子指南插入入詞條門和通過周圍的肌組織保留別針的螺紋從捲入周圍的軟的組織在所有案件。別針被安置了入椎骨身體使用一個低速, 高扭矩鑽子。這個做法被重覆了直到所有八個別針被安置了。別針的適當的安置通過皮膚和肌組織允許皮膚的關閉以一點緊張在切開線和軟的組織圍攏別針。

頭蓋骨fixator 曲拱然後綁住到二個頭蓋骨別針對定像螺栓的用途, 被最尾部的脊髓曲拱的安置跟隨對二個最尾部的定像別針。最初地, 一根穿線的連接桿在各脊髓專欄的邊被使用連接頭蓋骨和尾部脊髓fixator 曲拱。在頭蓋骨和尾部脊髓曲拱綁到穿線的連接桿上之前, 殘餘的二fixator 曲拱通過了通過連接桿, 但未綁到定像別針上。這允許切開被關閉定期時尚。隨後而來的皮膚關閉殘餘的二脊髓曲拱綁到定像別針上使用定像螺栓。一根另外的穿線的連接桿被安置在任何一方脊髓專欄完成定像。手術後射線照相被製作, 估計別針椎骨運河的安置和對準線。海綿部份的一次性外科刷子被收集了和被安置了在skin/pin 接口附近對皮膚的減退micromotion 圍攏別針。脊髓曲拱然後被包裹了與被熔鑄的填料和狩醫套d。張貼有效地, 別針管理每日兩次包括的別針外科海綿的清潔用一種0.05% chlorhexidine 解答和安置在別針附近防止micromotion 在pin/skin 接口直到粒化組織形成了在別針附近。狗並且是被執行的口頭抗生素10 天防止別針短文sepsis 。

結果:

狗1: 一條2 年老27.3 公斤母原封德國牧羊人狗被提出了對提到的獸醫在乘汽車以後被擊中。在介紹狗是paraplegic 以深刻的痛苦悟性當前在後方肢體。分裝式脊髓反射在骨盆肢體被誇大了並且hyperpathia 發生了 在thoracolumbar (T-L) 連接點的區域的觸診 。側向脊髓射線照相顯露了半脫位在T12-T13 。動物是methylprednisolone 丁二酸鹽e (MPSS) IV 被執行的30mg/kg 和提到我們的醫院。

神經學考試顯露了截癱, 缺席皮膚trunci 反射尾部對T-L 連接點和hyperreflexia 在骨盆肢體。肛門口氣是正常和橫渡-伸張機反射不是顯然的在骨盆肢體。痛苦悟性是存在在骨盆肢體、perineum 和尾巴的數字。這些研究結果被解釋了作為表明損害某處在T3-L3 脊髓段。

狗綁到藍球板上並且側面和脊椎的VD (水平的射線) 射線照相 被獲得了。這些顯露了一個倒塌的磁盤空間在T12-T13 和T13 相對T12. (無花果1a) (腳註的輕微的腹 位移關於圖)。位移被改進以引伸和惡化與脊椎(圖1b) 計算X線體層照相術(CT 的) 彎曲 顯露了軟的組織大量在腹椎骨運河之內據推測導致T12 lamina 脊髓的一hyperdense (圖2.a) 位移腹壓縮入脊髓運河並且是顯然的(圖2b)

在手術, 一背部laminectomy 顯露了圓盤材料和很多出血在脊髓運河之內。T11 、T12 、T13 和L1 的脊髓定像進行了, 如上所述。手術後射線照相展示了正確fixator 安置和改進了T12-13. (圖3) 的對準線九天跟隨狗的馬達作用在骨盆肢體改進了的手術並且狗是只適度地動轉失調的。狗從醫院被釋放了十天跟隨手術並且所有者被指示一次每週拉緊穿線的連接桿的定像螺栓和堅果。六個星期跟隨狗的神經學狀態很大地改善了 的手術, 以唯一溫和的不整齊可看見在步行。別針短文癒合了沒有排水設備或鬆懈的證據。脊髓射線照相顯露, 減少被維護了在T12-T13 並且別針鬆懈的證據不是可看見的。所有者報告, 狗容忍了外在fixator 設備為六個星期期間沒有任何複雜化(無花果3c, 3d)The 動物沉著了並且外在fixator 被去除了。手術後射線照相展示了T12-13 椎骨的好對準線(圖4) 所有者被指示贍養狗在籠子休息之下為另外的3 個星期。六個月跟隨手術提到的獸醫報告, 狗看來免於所有神經學缺乏。

狗2

一條4 年老39.3 公斤公原封德國牧羊人狗被提出了對提到的獸醫在乘汽車以後被擊中。在介紹動物是paraparetic 以被誇大的分裝式脊髓反射在骨盆肢體。胸部射線照相顯露了椎骨的嚴厲肺挫傷和半脫位L1-L2 。狗被給了一公升分泌乳汁的槍手的解答 f IV, 500 毫克MPSS e IV, 1000 毫克Cephazolin g IV 和12 butorphanol h 毫克 平方和第二天提到了我們的醫院。

在介紹對VMTH 動物是在嚴厲呼吸困厄和立刻被安置了在氧氣籠子。它很好反應了氧氣。側向胸部影片顯露了嚴厲肺挫傷與L1-L2 椎骨身體的半脫位一起。神經學缺乏被限於骨盆肢體。反常性注意了包括一nonambulatory paraparesis 、被誇大的分裝式脊髓反射在骨盆肢體和hyperpathia 在TL 地區。這些標誌表明了損害在T3-L3 地區。狗被固定了在藍球板和被對待了為肺挫傷直到椎骨身體的外科安定L1-L2 能進行。在最初之後介紹對VMTH 狗四天有輕微的改善在馬達作用在骨盆肢體和被視為能承受一般麻醉。

前有效的射線照相展示了L1-2 椎骨身體的半脫位, 以L2 的 腹位移椎骨身體相對L1. (圖5) 背部平面CT 顯露了L2. 的左側向位移(圖6) 瀘頂骨矢狀合縫的平面CT 顯露了L1-2 椎骨運河狹窄由於L2 lamina (圖7) 的cranioventral位移

在手術, t他半脫位被修理了使用二6 孔3.5 毫米被限制的聯絡動態壓縮板材(LCDCP), 一塊板材被安置在任何一方L1 andL2 椎骨身體。一背部laminectomy 執行了為脊髓解壓。切開被關閉了定期時尚和狗從手術沒有事故恢復。

手術後射線照相顯露了L1-2 椎骨身體的改善的對準線。跟隨手術狗六天顯示了改善的馬達作用在骨盆肢體, 能走以毛巾支持。跟隨手術狗從醫院十天被釋放了並且所有者被指示繼續狗的籠子剩餘6 個星期。三個星期跟隨手術 所有者報告, 狗運行在後院和突然失去的馬達作用到後面腿。在介紹對VMTH 一次神經學考試顯露了骨盆肢體和缺乏的馬達作用被誇大的分裝式反射和損失深刻的痛苦悟性在 兩骨盆肢體裡。射線照相顯露了T13-L1 半脫位和鬆懈2nd 和正確的 LCDCP. 的3 個rd 螺絲(圖8) 所有者是消息靈通 粗劣的預測但決定有外科安定執行了。

在手術一種背部方法被做暴露T12-L4 椎骨段並且半脫位臨時地舉行了在減少與Kirschner 導線被駕駛橫跨椎骨關節小平面T13-L1 。正面外形別針被安置了在T12 、T13 、L3 和L4 椎骨身體。LCDCP 的所有螺絲被重新拉緊了。四脊髓fixator 曲拱和 4 根穿線的連接桿被使用穩定半脫位在T13-L1 。手術後射線照相顯露了T13-L1 和L1-2. (圖9) 充分對準線動物從手術沒有事故恢復。跟隨手術動物仍然十天沒有深刻的痛苦悟性在骨盆肢體並且所有者決定有動物euthanized 由於財政限制。沒有複雜化與相關脊髓外在fixator 在無痛苦的死亡之時。

狗3

一4 年老18.4 公斤男性被閹割的Shar-Pei 被提出了對提到的獸醫在乘汽車以後被擊中。在介紹狗是能走但動轉失調的在骨盆肢體以被誇大的分裝式脊髓反射。體檢是平凡的, 除了上述的神經學缺乏。脊椎的側向射線照相顯露了椎骨的半脫位L1-L2 。其它反常性未被發現。狗被對待了以0.2 mg/kg butorphanol IV, 30 mg/kg MPSS e IV 和l 公升分泌乳汁的槍手的解答 f IV 。狗第二天提到了我們的醫院為進一步評估。

在介紹, 狗有一非能走paraparesis, 但有輕微的馬達作用和 被誇大的分裝式脊髓反射在骨盆肢體。脊椎的側向和ventrodorsal 射線照相顯露了L1-L2 椎骨(圖10 的)fracture/subluxation。T13 肋骨的發育不全並且被注意了。胸部和胃腸射線照相沒有顯露反常性。

狗然後被麻醉了, 安置在sternal recumbency 並且對椎骨身體的一種背部方法L1-L2 被做了。正面外形末端穿線的別針被安置了在椎骨身體T13 、 L1 、L2 和L3 。四脊髓曲拱和四根穿線的連接桿被使用完成fixator 。手術後地, 有正確fixator 安置和L1-L2 (圖11 的)改善的對準線。

二天跟隨手術狗能在毛巾支持的幫助下走。關於第三天跟隨手術它注意到, 狗有他的腹股溝區域重大膨脹。狗似乎壓下並且胃腸ultrasonography 顯露了尾部胃腸疝氣與被禁閉的膀胱和肚腑。一試探性celiotomy 顯露了prepubic 腱破裂。腸的被禁閉的段被切除了並且小腸接合執行了。prepubic 腱由縫合修理了prepubic 腱對陰部的骨頭。切開被關閉了定期時尚和狗從手術沒有事故恢復。跟隨他試探性celiotomy 狗從醫院三天被釋放了。提到的獸醫報告, 二天跟隨狗死於胃膨脹和volvulus 的放電。

討論:

外在定像為椎骨instability/fracture 的安定被表明對尾部腰部脊椎、fracture/luxations 次要對discospondylitis 和破裂的款待不穩定由內部定像[ 5, 8-10 ] 不容易地穩定。內部骨骼fixators, "fixateurs 實習生", 被描述了至於使用在人和獸醫[ 9-11 方面] 。內部骨骼fixators 不利包括過早鬆懈鉗位和主要腐蝕如果鉗位不是構成和fixator 別針或連接桿一樣。另外這個做法要求大植入管容量, fracture/luxation 的手術後操作無法發生, 並且最後, 第二手術必需為植入管[ 9-12 的] 撤除。

對外在fixators 的用途為脊髓專欄破裂的安定早先被報告了在獸醫文學為尾部腰部破裂修理在狗[ 13 ] [ 8 ] 。一個技術使用型II Kirschner-Ehmer 設備的組合並且spinous 過程鍍層和另一被報告的技術使用唯一型II Kirschner-Ehmer 設備為尾部lumbar 的安定fracture/luxations 。遇到的主要手術後複雜化是別針短文sepsis, 然而; 這個問題是解決的隨後而來的適當的抗藥性療法和別針管理。設備被使用在這個報告證明了簡單執行, 但可能的不利是這個技術要求preoperative 計劃。

別針骨頭接口是最重要的站點所有外在定像[ 5 ] 。在箱子被報告這裡所有別針被安置了在椎骨身體在一個試驗孔操練了之後。一個試驗孔接近, 但不超出定像別針的內在直徑被創造了在椎骨身體。Pre-drilling 一個試驗孔被顯示改進最初的別針穩定和減少也許導致過份骨頭吸回和過早別針鬆懈的損傷[ 2 ] 。鬆懈別針未遇到在狗1, 有脊髓外在fixator 到位為一共計6 個星期。

Pin 短文sepsis 並且同對外在fixators 的用途聯繫在一起。為了減少別針短文sepsis, 別針的安置通過皮膚和肌組織需要適當地執行防止緊張發生在別針附近。這被完成了在這些情況下由仔細的intraoperative 計劃。手術後別針衛生學如上所述導致了令人滿意的結果在□一條狗生存足夠長期是情報的。

外在脊髓定像設備被使用在箱子提出了提供了充足的穩定和這裡允許椎骨的適當的重新排列和安定。fixator 的手術後操作未必需對脊髓專欄的改善的對準線在任何箱子, 而是能容易地執行了。fixator 被安置了在尾部胸部和頭蓋骨腰部椎骨沒有複雜化。所有狗容忍了外在fixator 在手術後期間並且脊髓曲拱的獨特的設計允許狗是舒適的當在側向recumbency 。早先報告的不利, 型II Kirschner-Ehmer 設備被使用[ 即, 8, 13 ], 是, 動物被迫說謊在連接桿當安置在側向recumbency 。脊髓曲拱當前進來想成為的圈子的二不同大小, 220 和140 毫米曲拱。220mm 脊髓曲拱有19 個均勻地間隔的孔並且140mm 脊髓曲拱有15 個均勻地間隔的孔。這種配置允許定像螺栓的安置連接定像別針, 允許定像別針被安置用不同的dorsoventral 飛機。定像別針應該被安置在同樣craniocaudal 飛機為了減少緊張和彎曲定像別針在他們綁到脊髓定像曲拱上之後。孔在曲拱並且允許穿線的連接桿的安置完成fixator 。fixator 可能還被使用在壓縮破裂, 由跨過包含的椎骨身體。這項原則被使用了在狗2, fixator 被安置跨過luxation 在椎骨身體T13-L1 自從板材的一個椎骨身體被使用修理早先subluxated 椎骨身體L1-L2 。

使用一個不穩定的似犬死屍脊椎模型, 步行者, 等。(步行者TM, 等Proc 。獸醫矯形手術27th 年會, 2000) 表示, 四個或八個別針脊髓曲拱外在定像比原封脊椎極大(p<0.05) 僵硬的在彎曲和引伸。同樣學習, 沒有在僵硬上的重大區別在脊髓曲拱修建和polymethylmethacrylate(PMMA) 內部定像。定像設備被使用在這個報告與型Ib (單邊biplanar 的) 外在骨骼fixator 是可比較的。 後者配置包括二根 T ype I一半別針唯一連接桿s被安置在90 度互相和被連接在他們的接近和末端末端形成一個bi 平面框架。型Ib 修建對剪和彎曲的力量比型是有抵抗性II 配置[ 14-16 ] 。在早先獸醫報告, 型II 外在骨骼fixators 被使用了有或沒有spinous 過程鍍層。Dorsoventral 彎曲是主要力量的當中一個需要被抵制跟隨脊髓安定, 因此; 型Ib 比型II 外在骨骼fixator 有利的。別針和連接桿分享力量在型Ib 外在fixators, 但是在型II 別針是幾乎所有被服從對整個裝載[ 14, 15 ] 。所以, 型Ib fixators 是可適用的對軸向地是槽櫪但不穩定的在彎曲的破裂。

雖然只一條狗到位有fixator 六個星期, 所有狗容忍了它在手術後期間並且所有者報告狗1 很好容忍了它在整個六個星期。椎骨半脫位的減少和定像與外在脊髓fixator 被證明是安定一個有效的方法。這些箱子的手術後管理是辛苦強烈的, 也許阻止它的用途在一些患者。fixator 是可利用的在可能容納狗大和小養殖的二大小。fixator 的撤除在半脫位癒合了之後可能進行使用鎮靜單獨。我們結束脊髓fixator 是有用的為fracture/luxations 的安定在這個區域thoracolumber 連接點的。
Many surgical techniques have been described for repair and/or stabilization of the canine spinal column following trauma [1-8]. Each technique has its own unique set of reported advantages and disadvantages [1, 4, 8]. The spinal external fixator system described here employs positive-profile end-threaded pins that are inserted into the bodies of each of four adjacent vertebrae after pilot holes are drilled with an appropriate sized bit. Eight pins are used, with one pin being placed on each side of each vertebral body. The pins in each vertebra are then attached to a metallic spinal fixator arch with fixation bolts and the four arches are then linked together using threaded connecting rods. This technique is relatively easy to use and has several advantages. Less soft tissue dissection is needed since the bodies of the vertebrae are not fully exposed during the surgery, thus reducing the danger of damaging vital structures and preserving surrounding muscles and their attachments that contribute to the stability of the spine. [5, 8] Other advantages of this technique include: ease of implant removal; no interference if a dorsal laminectomy is necessary; provision of adequate stabilization for fracture healing to occur; and the ability to adjust the fixator in the postoperative period without surgical intervention [8]. The external fixator can be applied to both the lower thoracic and lumbar spine and is well tolerated by the patient.

Application of the technique requires a thorough knowledge of vertebral anatomy to ensure proper pin placement. Careful attention to skin placement is necessary when pins are inserted into the vertebral body to reduce tension and the possibility of postoperative pin-tract sepsis. Owners must be instructed and diligent in proper postoperative pin management.

The purpose of this case report is to describe the use of an external fixator system in three dogs with traumatic spinal instability.

Materials and Methods:

Dogs: All dogs were referred to the Teaching Hospital of the Virginia-Maryland Regional College of Veterinary Medicine for suspected spinal instability following trauma. The diagnosis of spinal cord dysfunction secondary to trauma and vertebral canal instability was based primarily on findings from the neurologic examination and routine radiography. In dog 1, flexion/extension radiographs were also obtained to demonstrate dynamic instability. In dogs 1 and 2, spinal cord compression was visualized using computed tomography.a. Reformatted CT images were generated using a remote diagnostic workstation.b

Surgical technique: Dogs were positioned in sternal recumbency and prepared for a dorsal approach to the spine, with the incision centered over the area of instability. After surgical exposure, the fracture/luxation was held in reduction temporarily with Kirschner wires placed across the articular facets of the affected vertebral bodies. A dorsal laminectomy was performed if necessary to assure reduction and/or remove disc or bone fragments from the vertebral canal. A pilot hole was then drilled into the cranial portion of the body of the vertebrae at a 450 angle to the dorsal spine. The hole passed through both vertebral cortices, using a drill bit that approximated the inner diameter of the positive profile pin to be used. In the lumbar vertebrae the accessory processes and the transverse processes were used as landmarks and in the thoracic spine the accessory processes and the rib heads were used as landmarks. A depth gauge was used to measure the depth of the pilot hole and this measure was marked on the positive profile end threaded pin with a sterile marker. A pilot hole was made in the contralateral side of the vertebral body in a similar fashion. The pilot hole on the contralateral side was made in the caudal portion of the vertebrae in order to keep the pins from interfering with each other during their placement.

Upon completing all the pilot holes, the skin and surrounding musculature were pulled to the center of the incision and a towel forceps was used to temporarily hold the incision closed. A number 15 scalpel blade was used to make a small skin incision to serve as an entry portal for the pin. A 6.5 mm drill guide was inserted into the entry portal and through the surrounding musculature to keep the threads of the pin from entangling the surrounding soft tissues in all cases. The pin was placed into the vertebral body using a low speed, high torque drill. This procedure was repeated until all eight pins were placed. Proper placement of the pins through the skin and musculature allowed closure of the skin with little tension on the incision line and soft tissues surrounding the pins.

The most cranial fixator arch was then secured to the two most cranial pins by the use of fixation bolts, followed by placement of the most caudal spinal arch to the two most caudal fixation pins. Initially, one threaded connecting rod on each side of the spinal column was used to connect the cranial and caudal spinal fixator arches. Before the cranial and caudal spinal arches were secured to the threaded connecting rod, the remaining two fixator arches were passed through the connecting rod, but not secured to the fixation pins. This allowed the incision to be closed in a routine fashion. Following skin closure the remaining two spinal arches were secured to the fixation pins using fixation bolts. One additional threaded connecting rod was placed on either side of the spinal column to complete the fixation. Postoperative radiographs were made, to assess pin placement and alignment of the vertebral canal. The sponge portions of disposable surgical scrub brushes were collected and placed around the skin/pin interface to decrease micromotion of the skin surrounding the pins. The spinal arches were then wrapped with cast padding and Vet Wrapd. Post operatively, pin management consisted of twice daily pin cleaning with a 0.05% chlorhexidine solution and placement of surgical sponges around the pins to prevent micromotion at the pin/skin interface until granulation tissue formed around the pin. Dogs also were administered oral antibiotics for 10 days to prevent pin tract sepsis.

minibabyqq 2006-12-28 01:34

[color=Magenta][size=5][b]Cervicothoracic 脊髓綜合症狀聯繫了 Ehrlichia canis 。   [/b][/size][/color]

總結和診斷

狗提到我們的醫院以不整齊的早先歷史的一隻粗礪的大牧羊犬被描述得這裡。狗以前被發現了一個星期緊挨一條繁忙的路和被採取了對一間地方動物庇護所。提到的獸醫懷疑臨床標誌的一個創傷起源。我們的體格檢查顯露了一條溫和地lethargic 和動轉失調的狗。神經學考試顯露了cervicothoracic 脊髓綜合症狀, 與更低的馬達神經元簽到在前部的腿並且上部馬達神經元簽到後方腿。尾部子宮頸區域的簡單的X-射線看上去顯示被減少的C6-C7 椎間的空間, 一致與神經學考試。但是, 反常性未被發現在myelography 。CSF 被採取在myelography 之時提出了變動特點meningitis/meningoencephalitis 。CSF 的間接immuneflourescence 是正面的為 E.canis。

雖然描述, 腦膜炎不是E.canis 的一個典型的介紹, 亦不是E.canis 每腦膜炎的典型的起因。另外, 腦膜炎經常被認為導致multifocal 標誌; 但是, 這個案件提出了標誌與焦點損害兼容。


治療和後續。

Imidocarb dipropionate, 皮膚下, 兩次, 以14 天之間。

巨大改善5 天在第一射入以後; 完全補救每星期在第二imidocarb dipropionate 射入以後。

討論

腦膜炎是meninges 1 的炎症, 和由腦炎2 通常 伴隨。 傳統上, 它被認為有multifocal 神經學標誌 1,3; 但是, 在研究中由Tipold 完成在瑞士, 1995 年狗的三分之二以被證明的腦膜炎被提出了與標誌的焦點而不是multifocal 神經學損害。同樣研究表示, 臨床標誌(系統和神經學) 的腦膜炎是相當空泛的不管原因論, 回報診斷meningitis/meningoencephalitis 非常困難 1。

當有輔助診斷測試2,3 的臨床標誌和結果 , 特別是CSF 分析, 與meningitis/meningoencephalitis 是一致的, 幾CNS 的激動疾病的起因必須排除。有差別的診斷在南西部歐洲應該包括 弓形體gondii 、Neospora caninum 、立克次休屬微生物rickettsii 、Ehrlichia canis 、Criyptoccocus neoformans, 慍怒病毒傳染腦膜炎和先天激動混亂像granulomatous meningoencephalomyelitis, 和類固醇敏感腦膜炎arteritis 。所以CSF 分析是根本到達診斷。這分析應該包括, WBC 計數和差別、蛋白質含量和血清學 1。 其它可能的測試是文化和敏感性和免疫球蛋白G 比率。也許是有用的輔助測試包括電腦化的X線體層照相術、磁共振圖像, 和腦子切片檢查法 1。

在這種情況下, 有CSF 分析一致與inflammatory/infectious 過程, CSF 的血清學為這個區域的最共同的感染起因執行了。正面滴定量被獲得了證實ehrlichiosis 診斷。

抗體的偵查反對 E. canis 是被考慮高特異性和敏感性。或清液或CSF 可能被測試為抗體由間接熒光分析用試樣。滴定量1:10 或偉大以間接螢光分析用試樣測試被認為正面。測試也許是消極的及早在疾病 4,5。

E. canis 是滴答作響出生的細胞內細菌在家庭 Ehrlichiaceae 4,6。它被傳達給狗由棕色狗壁虱 Rhipicephalus sanguineus 4,5。CNS 損害為一lymphoplasmacytic meningoencephalitis 描繪介入meninges 、大腦外層和brainstem 5。 在一個易變的孵出階段以後, 疾病也許審閱三個被描述的階段: 一深刻一個通常持續二個到四個星期以未指明的標誌, 被一個臨床症狀不顯的階段跟隨, 和第三個階段以更加嚴厲的症狀。神經學標誌出現在後者階段 4 。

它是不凡的為狗遭受疾病提出神經學標誌, 仍然那 E. canis 同幾神經學綜合症狀聯繫在一起。 4,5,8。神經學標誌起因於有機體導致的脈管炎、主人免疫反應和haemorrhagic 素質 3。這些標誌會包括奪取, 前庭官能不良、更低的motoneuron 疾病和腦膜炎, 作為在這種情況下 4,8。

狗遭受似犬monocytic ehrlichiosis 提出神經學疾病通常顯示系統標誌譬如熱病, 眼科反常性, 蒼白mucosae, 呼吸標誌。4,7,8,9。 非神經學標誌是足夠通常使臨床工作者懷疑疾病, 特別是在區域以疾病的大流行。診斷由發現通常證實正面 E。canis 清液滴定量 4,8,9。

選擇的治療是或doxycicline (在10 - 20 mg/kg, PO 出價), 或imidocarb dipropionate (5-7 毫克, SC 或IM; 2 射入, 2 個星期分開), 兩個以非常好結果。 4,5,8,9 。 治療選擇依靠具體案件; Doxycycline 通常是第一個選擇在房子被保留的狗, 但是imidocarb dipropionate, 要求二痛苦的射入, 是應用的在每日管理是行不通或不便的處。

SUMMARY and DIAGNOSIS

A Rough Collie dog referred to our hospital with a previous history of ataxia is described here. The dog had been found a week before close to a busy road and taken to a local animal shelter. The referring veterinarian suspected a traumatic origin of the clinical signs. Our physical examination revealed a mildly lethargic and ataxic dog. Neurological examination revealed a cervicothoracic spinal cord syndrome, with lower motor neuron signs in the fore legs and upper motor neuron signs in the rear legs. Plain X-rays of the caudal cervical area appeared to show a decreased C6-C7 intervertebral space, consistent with the neurological examination. However, no abnormality was found on myelography. CSF taken at the time of myelography presented changes typical of meningitis/meningoencephalitis. Indirect immuneflourescence of the CSF was positive for E.canis.

Although described, meningitis is not a typical presentation of E.canis, nor is E.canis a typical cause of meningitis. In addition, meningitis is often regarded as causing multifocal signs; however, this case presented signs compatible with a focal lesion.


Treatment and Follow-up.

Imidocarb dipropionate, subcutaneous, twice, with 14 days in between.

Great improvement 5 days after the first injection; completely recovery a week after the second imidocarb dipropionate injection.

DISCUSSION

Meningitis is inflammation of the meninges1, and usually is accompanied by encephalitis 2. Traditionally, it has been considered to have multifocal neurological signs 1,3; however, in a study done by Tipold in 1995 in Switzerland, two thirds of the dogs with proven meningitis were presented with signs of focal rather than multifocal neurological lesion. The same study showed that clinical signs (both systemic and neurological) of meningitis are rather unspecific regardless of the aetiology, rendering the diagnosis of meningitis/meningoencephalitis very difficult 1.

When there are clinical signs and results of ancillary diagnostic tests 2,3, especially CSF analysis, are consistent with meningitis/meningoencephalitis, several causes of inflammatory disease of the CNS must be ruled out. The differential diagnosis in south west Europe should include Toxoplasma gondii, Neospora caninum, Rickettsia rickettsii, Ehrlichia canis, Criyptoccocus neoformans,, distemper virus infection meningitis and idiopathic inflammatory disorders like granulomatous meningoencephalomyelitis, and steroid responsive meningitis-arteritis. Therefore a CSF analysis is essential to reach a diagnosis. This analysis should include, WBC count and differential, protein content and serology 1. Other possible tests are culture and sensitivity and immunoglobulin-G ratio. Ancillary tests that may be useful include computerized tomography, magnetic resonance imaging, and brain biopsy 1.

In this case, having a CSF analysis consistent with an inflammatory/infectious process, serology of the CSF for the most common infectious causes of this area was performed. A positive titer was obtained confirming a diagnosis of ehrlichiosis.

The detection of antibodies against E. canis is is considered of high specificity and sensitivity. Either serum or CSF can be tested for antibody by indirect fluorescence assay. A titer of 1:10 or greater with the indirect fluorescent assay test is considered positive. The test may be negative early in the disease 4,5.

E. canis is a tick-borne intracellular bacterium in the family Ehrlichiaceae 4,6. It is transmitted to dogs by the brown dog tick Rhipicephalus sanguineus 4,5. CNS lesions are characterized by a lymphoplasmacytic meningoencephalitis involving the meninges, cerebral cortex and brainstem 5. After a variable incubation phase, the disease may go through three described stages: an acute one that usually lasts two to four weeks with non-specific signs, followed by a subclinical phase, and a third phase with more severe symptoms. Neurological signs appear in the latter phase 4.

It is uncommon for dogs suffering the disease to present neurological signs, notwithstanding that E. canis has been associated with several neurological syndromes. 4,5,8. Neurological signs result from organism-induced vasculitis, the host immune response and the haemorrhagic diathesis 3. These signs would include seizures, vestibular dysfunction, lower motoneuron disease and meningitis, as in this case 4,8.

Dogs suffering canine monocytic ehrlichiosis presenting neurological disease usually show as well systemic signs such as fever, ophthalmic abnormalities, pale mucosae, respiratory signs.4,7,8,9. Non-neurological signs are usually enough for the clinician to suspect the disease, especially in areas with high prevalence of the disease. The diagnosis is usually confirmed by finding positive E.canis serum titers 4,8,9.

The treatment of choice is either doxycicline (at 10 - 20 mg/kg, PO bid), or imidocarb dipropionate (5-7 mg, SC or IM; 2 injections, 2 weeks apart), both with very good results. 4,5,8,9. The choice of treatment depends on the specific case; Doxycycline is usually first choice in house-kept dogs, whereas imidocarb dipropionate, that requires two painful injections, is applied in cases where daily administration is impracticable or inconvenient.

minibabyqq 2006-12-28 01:35

[color=Magenta][size=5][b]狗 顯示KL5UVER-BUCY SYNDROME-LIKE 行為   [/b][/size][/color]


摘要: 過份週期性奪取, 譬如狀態epilepticus (SE) 並且/或者群奪取, 被顯示導致癲癇的(次要) 腦損傷(EBD) 在實驗性研究和人的癲癇的患者中。EBD 導致各種各樣的關於行為(心理) 並且/或者神經學官能不良。在這個報告, 被診斷了和被對待了與治癲癇藥物的一條癲癇的狗顯示了關於行為的變動相似與Kl5uver-Bucy 綜合症狀, 起因於雙邊limbic 損害在大主教在嚴厲SE 以後。EBD 早先案件在小動物s 顯示了憤怒reaction/aggression 或是euthanized 在恢復從SE 之前。我們報告在這兒顯示分明臨床和病理性相似性對大主教Kl5uver-Bucy 綜合症狀的一條狗, 包括人的患者。

n 8 年和9 個月大, ovariohysterectomized 女性威爾士corgi 稱10.6 公斤提到了日本獸醫和動物學大學的動物醫療中心(AMC-NVAU) 為關於行為的問題, 開始在狀態epilepticus (SE 以後) 。狗有最初的奪取在2 年紀, 和1-3 次一個隨後奪取頻率每月。在1 個月在最初的奪取以後, 狗被服從了對物理, 血液學(CBC 和清液化學), 和神經學考試, 並且計算X線體層照相術和清液似犬慍怒病毒(CDV) 抗體滴定量 其它獸醫醫院。這些考試顯示了正常研究結果, 並且先天癲癇症一個試探性診斷 被做了。 治癲癇藥物(AED) 療法與苯巴比妥(鉛: 3-8 mg/kg 、PO 、q12h) 和鉀溴化物(KBr: 30 mg/kg 、PO, q24h) 被創始了。 但是, 奪取頻率極大沒有改善(1-3 次每月) 。這條狗奪取通常開始了像部份, 包括分泌唾液, 注視, 鉗製和頭震顫, 被次要廣義補劑抽筋的奪取跟隨。 在interictal 期間, 狗是服從對所有者的家庭, 但有一個怯懦的字符和通常咆哮在或被威脅的陌生人。

在是之前提到的AMC-NVAU, 所有者二個月發現了狗在SE; SE 持續了至少3 個小時直到她把帶對其它獸醫醫院。SE 繼續了在住院治療期間大約1 個小時在苯甲二氮卓的靜脈內射入以後, 被戊巴比妥跟隨。

在恢復從SE 以後, 狗沒有認可她的所有者, 沒有vocalize, 和改變她的個性到是服從和友好的對大家。 狗沒有起反應對叫或任何噪聲, 和由 任何大聲的聲音未震驚。另外, 狗吃了任何東西在她附近譬如毛巾、鞋子、凳子, 等(12點活字) 。

關於行為的標誌堅持了直到提及對AMC-NVAU 。在入場那裡, 歷史顯露, 定期接種(包括CDV 和狂犬病) 並且filarial prophylaxes 執行了每年。AED 療法與鉛(6 mg/kg 、PO, q12h) 並且KBr (30 mg/kg 、PO, q24h) 繼續了直到入場, 和奪取未被觀察在SE 以後情節。狗的一般出現是正常的並且反常性未被發現在體格檢查中。神經學考試顯露了關於行為的標誌被描述在正溫和的雙邊本體感受的缺乏之上在骨盆肢體和疏忽起反應對所有聲音。CBC 、清液化學、血液氣體、電解質、胸部射線照相, 和心電圖是正常的; 著名地, 沒有在阿爾卑斯的增量由於鉛 療法。

Brainstem 聽覺被召喚的潛力(BAEP), 被記錄使用被召喚的潛在考試系統 被表明brainstem 聽覺路雙邊是正常的。

腦波記錄儀(EEG) 執行了以參考和雙極派生。b 在錄音the 狗期間是非常安靜和昏昏欲睡的沒有鎮靜。 分散並且/或者同步paroxysmal 放電譬如釘、polyspikes, 和鋒利的波浪背部地雙邊是許多的在世俗和頭頂骨地區 (圖1)。

磁共振圖像(MRI) 使用一個1.5 Tesla MRI 系統c 執行了在一般麻醉之下。相稱和形成氣穴的壞死的損害延長 從amygdalae 對側向世俗耳垂被查出了作為hyperintensities 在T2 被衡量的圖像(T2WI) 並且hypointensities 在流體變稀的反向補救(天才) 並且T1 衡量了圖像(T1WI) 。在這些損害附近, 即雙邊在pyriform, 世俗和頭頂骨外皮和雙邊 在海怪, hyperintensities 被查出了在T2WI 和天才, 並且hypointensities 被查出了在T1WI (圖2)。這些損害由釓未提高。

在MRI 之時, 腦脊髓流體(CSF) 由cisternal 刺收集了。具體反常性未被發現, 除了神經元具體enolase 輕微增量(NSE: 25 ng/mL, 參考範圍< 15 ng/mL) 。CDV 抗體和抗原未被查出在CSF 。

在MRI 考試以後, 無痛苦的死亡被執行了按照由所有者要求。屍體檢驗和histopathological 考試執行了。在腦子的總考試中, pyriform 耳垂的表面和世俗耳垂的腹部份被發現雙邊被壓下。 Histopathologically 、amydalae 、parahippocampal gyri 和extratemporal 外皮顯示了廣泛, 雙邊對稱壞死和形成了cavitary 損害可看見在MRI 。 (圖3)。神經細胞的損失、pyknosis 、和neuropile 稀薄與肥胖裝載巨噬細胞和astrocytic 擴散被觀察了在pyriform, parahippocampal 和世俗耳垂的殘餘的外皮。在海怪, 有 嚴厲神經細胞的損失和pyknosis, 與astrocytosis 在CA3, 4, 和1 pyramidal 細胞層數中 (圖4)。加州2 和齒狀gyrus 顯示了輕微的損傷。沒有反常性在其它腦子地區, 並且包括身體並且/或者perivascular 打的建議的病毒並且/或者non-suppurative 腦炎未被查出。此外, immunohistochemistry 使用CDV monoclonal 抗體 d 執行了和顯示了一個消極結果。

過份週期性奪取被顯示導致癲癇的腦損傷(EBD), 由難處理的人的癲癇症和各種各樣的 實驗性動物模型的研究許多案件展示了。Hippocampal 硬化(HS) 或mesial 世俗硬化(MTS) 是典型的EBDs 和被看見在kainic 酸(鉀) 導致的模型1-5 和在難處理的人的世俗耳垂癲癇症。6, 7 另一方面, EBD 發生在狗是有爭議的因為不同的報告不建議或具體病理性研究結果在幾個案件先天癲癇症8-11 或相似的研究結果作為HS/MST12-15。

早先, 我們學習了似犬模型鉀導致的複雜部份狀態epilepticus4,5。在那些研究中, 雖然鉀被注射了入單邊的amygdala 和早期部份奪取開始在被注射的amygdala, 次要廣義奪取和對側部份奪取以次要廣義奪取頻繁地被觀察了在SE 期間。雙邊延長的壞死在amygdala 形成cavitary 損害和典型的HS 被觀察了。那些結果建議, 似犬部份奪取, 特別是limbic 奪取, 容易推斷並且似犬limbic 系統有一種更高的敏感性對奪取活動。MRI 和病理性研究結果在當前案件與那些確切地是相似被觀察在似犬鉀模型。當前, excitotoxicity 理論認為是一個病理生理的機制EBD1-3。最近, Mellena 等報告了MRI 反常性4 個相似的案件跟隨週期性奪取19, 並且Mariani 等報告了polioencephalomalacia 相似的事例使用MRI 和病理性研究結果20。他們發現了相稱並且/或者不對稱的limbic 損害和並且建議excitotoxicity 從嚴厲奪取也許是那些損害的起因。

與excitotoxicity 理論一起, HS 病理生理的機制被調查了在鉀模型使用嚙齒目動物和貓2, 3 。最近, Buckmaster 等被調查的HS, 包括生苔纖維發芽在難處理的癲癇症在狗使用Timm 汙點和, 根據他們的研究結果, 被建議, HS 和世俗耳垂癲癇症不是似犬癲癇症11 的同道會。雖然我們沒有調查生苔纖維, 組織學研究結果在當前案件的海怪與那些是一致的HS 在實驗性模型和人的癲癇症。所以我們建議HS 導致在狗根據奪取類型並且/或者SE 。

其它研究建議了polioencephalomalacia 在limbic 系統, 然而, 許多案件同CDV 腦炎16-19 聯繫在一起。當前案件臨床, 病理性地和immunohistochemically 是卓越的從CDV 。雖然CDV 腦炎是似犬表皮壞死的同道會, 其它起因存在。大腦梗塞、低氧症、化工毒力和其它類型s 腦炎被建議了作為可能的起因17, 20,21 。大腦梗塞單邊地通常發生, 並且梗塞的證據未被觀察在當前案件。另外, 低氧症和化學製品毒力不是顯然的從她的歷史和病理學。其它類型腦炎包括壞死的meningoencephalitis 和未知慢ly- 進步病毒或產生免疫的腦炎。壞死的meningoencephalitis (NME), 亦稱Pug 狗腦炎, 為深刻描繪對慢性進步大腦壞死, 也許由自動免疫的機制22造成, 並且發生在一些養殖除Pug 狗23,24 之外。NME 慢性壞死的損害與觀察是相似在這種情況下。但是, NME 顯示進步神經學官能不良, 並且granulomatous 損害包括perivascular 袖口典型地被觀察。所以, 可能性, 我們的情況有NME 是極端降低。蒙加馬利和李10 和Gredal25 報告了intraneuronal 包括相似與Lafora 的身體在癲癇的小獵犬狗。Lafora 的身體被觀察在人的Lafora 疾病顯示myoclonic 癲癇症。一條被報告的小獵犬狗顯示了進步myoclonus, 並且沒有顯示表皮壞死25。當前狗的奪取不myoclonic, 並且包括屍體 未被發現。最近, 到人, 非herpetic 和non-paraneoplastic limbic 腦炎受到了很多關注26-28。這limbic 腦炎認為是一種自動免疫的疾病和並且顯示對類固醇療法的好反應。但是, 這種疾病的起因未建立並且沒有這種疾病報告在獸醫方面。

有趣的是, 在當前案件, 腦子官能不良的臨床標誌與"Kl5uver-Bucy 綜合症狀" 是相似(KBS), 和是一致的以雙邊傷害對amygdalae 和世俗耳垂。KBS 由Kl5uver 報告起因於雙邊世俗葉切除術在猴子和Bucy 在30 年代之內和是官能不良的一個臨床標誌在amygdalae 和世俗耳垂在動物和人中。 29, 30 KBS 為以下關於行為的變動描繪: 1) ` 精神盲目性的, 是無能認可和評估對象; 2) ` hyperorality ', 是攝取和吃不適當的對象(12點活字); 3) ` hypersexuality ' 往性別並且/或者另外種類; 4) ` 修改過的情感行為', 為對敵人並且/或者周圍的恐懼placidity 和損失描繪。少量報告提供了關於行為的變動在對amygdalae 的損傷以後在狗和貓。田中・等報告了憤怒反應當amygdala 被激發在一個似貓的hippocampal 鉀模型31。Caldwell 和少許32 和Mariani 等。20 並且被報告侵略在狗與杏仁狀和hippocampal 損害。這些進取的行為認為是似是而非的症狀由 適度amygdala 和其它limbic 系統結構的損傷或刺激造成。雖然我們詳細沒有評估案件, 我們的早先鉀被對待的狗並且改變他們的行為是服從在CPSE9 以後。臨床簽到當前案件, 恐懼反應包括的損失對大聲的聲音竟管所有者正常聽覺作用、12點活字和不承認, 是相似以KBS 被報告在猴子和人。但是, hypersexuality 未被觀察。關於行為的變動和polyphagia 是AEDs 33 的知名的副作用。我們無法完全地排除藥物學地導致 KBS 像關於行為的變化在出席案件上因為AEDs 的清液水平未被測量在SE 前後。但是, AED 療法在SE 未被修改從早先藥量之後, 和狗從未顯示了修改過的行為s 在SE 之前。一種潛在可能性存在, 狗的 敏感性對AEDs 由病理變化提高了。

對作者的知識, 這是KBS 第一 被報告的事例在狗。 根據postictal 或interictal 行為的更加詳細的觀察, KBS 在狗也許被認可在慢性腦炎, 譬如NME 和CDV, 除EBD 之外。情感和行為的 進一步研究在狗和貓, 臨床, neuroanatomically 和neuropathologically, 是必要的。

Abstract: Excessive recurrent seizures, such as status epilepticus (SE) and/or cluster seizures, have been shown to induce epileptic (secondary) brain damage (EBD) in experimental studies and human epileptic patients. EBD results in various behavioral (psychological) and/or neurological dysfunctions. In this report, an epileptic dog that had been diagnosed and treated with antiepileptic drugs showed behavioral changes similar to Klüver-Bucy syndrome, which results from bilateral limbic lesion in primates after severe SE. Previous cases of EBD in small animals have shown rage reaction/aggression or were euthanized before recovering from SE. We report here a dog that showed distinct clinical and pathological similarities to Klüver-Bucy syndrome of primates, including human patients.

An 8-year and 9 months old, ovariohysterectomized female Welsh corgi weighing 10.6 kg was referred to the Animal Medical Center of Nippon Veterinary and Animal Science University (AMC-NVAU) for behavioral problems, which began after status epilepticus (SE). The dog had an initial seizure at 2 years of age, and a subsequent seizure frequency of 1-3 times per month. At 1 month after the initial seizure, the dog was subjected to physical, hematological (CBC and serum chemistry), and neurological examinations, as well as computed tomography and serum canine distemper virus (CDV) antibody titer another veterinary hospital. These examinations showed normal findings, and a tentative diagnosis of idiopathic epilepsy was made. Antiepileptic drug (AED) therapy with phenobarbital (PB: 3-8 mg/kg, PO, q12h) and potassium bromide (KBr: 30 mg/kg, PO, q24h) was initiated. However, the seizure frequency did not improve significantly (1-3 times per month). The seizures of this dog usually began as partial, consisting of salivation, gazing, immobilization and head tremor, followed by a secondary generalized tonic-clonic seizure. During the interictal period, the dog was obedient to the owner’s family, but had a cowardly character and usually barked at or threatened strangers.

Two months before being referred to AMC-NVAU, the owner found the dog in SE; SE lasted at least 3 hours until she was taken to another veterinary hospital. The SE continued during hospitalization for about 1 hour after intravenous injection of diazepam, followed by pentobarbital.

After recovering from SE, the dog did not recognize her owners, did not vocalize, and changed her personality to being obedient and friendly to everyone. The dog did not react to calling or any noise, and was not startled by any loud sounds.In addition, the dog ate anything around her such as towels, shoes, stool, etc. (pica).

The behavioral signs persisted until referral to AMC-NVAU. On admission there, the history revealed that routine vaccinations (including CDV and rabies) and filarial prophylaxes had been performed every year. AED therapy with PB (6 mg/kg, PO, q12h) and KBr (30 mg/kg, PO, q24h) had been continued until admission, and no seizures had been observed after the episode of SE. The dog’s general appearance was normal and no abnormalities were found on physical examination. Neurological examinations revealed the behavioral signs described above plus mild bilateral proprioceptive deficits in the pelvic limbs and failure to react to any sounds. CBC, serum chemistry, blood gases, electrolytes, thoracic radiographs, and electrocardiogram were normal; notably, there was no increase in ALP as a result of PB therapy.

Brainstem auditory evoked potentials (BAEP), recorded using an evoked potential examination systema indicated the brainstem auditory pathways were normal bilaterally.

Electroencephalography (EEG) was performed with both referential and bipolar derivations.b During recording the dog was very quiet and drowsy without sedation. Sporadic and/or synchronous paroxysmal discharges such as spikes, polyspikes, and sharp waves were numerous bilaterally in the temporal and parietal regions dorsally (Fig. 1).

Magnetic resonance imaging (MRI) using a 1.5 Tesla MRI systemc was performed under general anesthesia. Symmetric and cavitating necrotic lesions extending from the amygdalae to the lateral temporal lobes were detected as hyperintensities on T2-weighted images (T2WI) and hypointensities on fluid-attenuated inversion recovery (FLAIR) and T1-weighted images (T1WI). Around these lesions, i.e. bilaterally in the pyriform, temporal and parietal cortices and bilaterally in the hippocampi, hyperintensities were detected on T2WI and FLAIR, and hypointensities were detected on T1WI (Fig. 2). These lesions were not enhanced by gadolinium.

At the time of the MRI, cerebrospinal fluid (CSF) was collected by cisternal puncture. No specific abnormalities were found, except a mild increase of neuron-specific enolase (NSE: 25 ng/mL, reference range < 15 ng/mL). CDV-antibody and antigen were not detected in the CSF.

After the MRI examination, euthanasia was carried out as requested by the owner. Necropsy and histopathological examinations were performed. On gross examination of the brain, the surfaces of the pyriform lobes and the ventral parts of the temporal lobes were found to be depressed bilaterally. Histopathologically, the amydalae, parahippocampal gyri and extratemporal cortices showed extensive, bilaterally symmetrical necrosis and formed the cavitary lesions visible on MRI. (Fig. 3). Neuronal loss, pyknosis, and neuropile rarefaction with fat-laden macrophages and astrocytic proliferation were observed in the remaining cortex of the pyriform, parahippocampal and temporal lobes. In the hippocampi, there was severe neuronal loss and pyknosis, with astrocytosis in CA3, 4, and 1 of the pyramidal cell layer (Fig. 4). CA 2 and the dentate gyrus showed slight damage. There were no abnormalities in other brain regions, and inclusion bodies and/or perivascular cuffing suggesting virus and/or non-suppurative encephalitis were not detected. Furthermore, immunohistochemistry using CDV monoclonal antibody d was performed and showed a negative result.

Excessive recurrent seizures have been shown to produce epileptic brain damage (EBD), which has been demonstrated by many cases of intractable human epilepsy and the studies of various experimental animal models. Hippocampal sclerosis (HS) or mesial temporal sclerosis (MTS) are typical EBDs and are seen in kainic acid (KA) induced models1-5 and in intractable human temporal lobe epilepsy.6, 7 On the other hand, the occurrence of EBD in the dog has been controversial because different reports suggest either no specific pathological findings in several cases of idiopathic epilepsy8-11 or similar findings as HS/MST12-15.

Previously, we studied the canine model of KA-induced complex partial status epilepticus4,5. In those studies, although KA was injected into the unilateral amygdala and the partial seizures of early stage started at the injected amygdala, secondary generalized seizures and contralateral partial seizures with secondary generalized seizures were observed frequently during SE. Bilateral extended necrosis in the amygdala forming a cavitary lesion and typical HS were observed. Those results suggested that canine partial seizures, especially limbic seizures, are easy to generalize and that the canine limbic system has a higher sensitivity to seizure activity. MRI and pathological findings in the present case are exactly similar to those observed in the canine KA model. At present, the excitotoxicity theory is believed to be a pathophysiological mechanism of EBD1-3. Recently, Mellena et al. reported 4 similar cases of MRI abnormalities following recurrent seizures19, and Mariani et al. reported a similar case of polioencephalomalacia using MRI and pathologic findings20. They also found symmetric and/or asymmetric limbic lesions and suggested that excitotoxicity from severe seizures might be the cause of those lesions.

Along with the excitotoxicity theory, the pathophysiological mechanism of HS has been investigated in KA-models using rodents and cats2, 3 . Recently, Buckmaster et al. investigated HS, including mossy fiber sprouting in intractable epilepsy in dogs using Timm stain and, based on their findings, suggested that HS and temporal lobe epilepsy are not common causes of canine epilepsy11. Although we did not investigate the mossy fibers, the histological findings in the hippocampi of the present case are consistent with those of HS in experimental models and human epilepsy. Therefore we suggest that HS is induced in dogs depending on the seizure type and/or SE.

minibabyqq 2006-12-28 01:36

[color=Magenta][size=5][b]Megakaryocytes 在狗   [/b][/size][/color]


Megakaryocytes 在正常 狗 有各種各樣的核形式。最共同的變異是一唯一大的multilobed 中堅力量 或一個被分割的中堅力量包括不規則的核耳

垂由 chromatin 子線加入。被誇大的分割(hyperseg- mentation) 中堅力量發生在很小數量的megakaryocytes 。Megakaryocytes 以倍數分開

的中堅力量少有地 被觀察。在一項1 mo 毒素學研究中在幼小成人小獵犬 狗 與PNU-100592, 一個新oxazolidinone 抗菌代理, 在megakaryocyt

es 的 數量的大增量與hypersegmented 中堅力量並且倍數分開的中堅力量被觀察了。小組手段 血小板計數輕微地被減少了為多數PNU 10059

2 被對待的小組。Siderocytes 被觀察了在周邊血液汙跡, 並且圓環sideroblasts 是存在在骨髓汙跡。最小對溫和的毒理學損害被觀察了在大

腸、 直腸、腎臟、肝臟, 和睪丸, 主要在高藥量小組。PNU-100592 也許是有用的在endomitosis 的章程的研究 在megakaryocytopoiesis 期間

在狗。 骨髓; endomitosis; 黏膜萎縮; sideroblasts; siderocytes; 毒素學.




介紹 深刻monoblastic 白血病, 和先天dyserythro- megakaryocyte 是一個大多元體細胞以或者 poietic 貧血症(1, 18, 19, 24, 25, 27) 。 一唯

一大lobulated 中堅力量或一個被分割的中堅力量 在這個報告, 我們描述在數字包括的不規則的核 耳垂的大增量由megakaryocytes 棗樹子線

加入與hypersegmented 中堅力量和 chromatin 。被誇大的分割(hypersegmenta- 倍數分開的中堅力量在 狗 從1 mo 毒素學 tion) 中堅力量發

生在很小數量的兆 研究中與一個新oxazolidinone 抗菌代理, PNU- karyocytes 。Megakaryocytes 與倍數分離nu- 100592 。對最佳我們的知

識, 相似的obser- clei 少有地不被觀察。Megakaryocytes 在正常 vation 被報告了在 狗 由於曝光 狗 有一語氣ploidy 16.N (54%) 與17% 8N

對xenobiotic 。 並且16% 32N (3) 。ploidy 數字不關聯 以核lobulations (20, 22 的) 數量; 但是, megakaryocyte DNA 內容與megakaryocyt

e 大小有關並且因此對讚成PNU-100592 靜脈內被執行對 小獵犬小片的最後的數量 duced (17, 21, 22) 。在megakaryocyte 核狗 ,7lsexlgrou

p, 在0 (車控制), 12.5, 40, 和形態學上 變化被報告在 狗 每日兩次包括karyorrhexis 在125 條mglkg (0, 25, 80, 和250 mglkglday) 狗 以實驗

性免疫thrombocytopenia, hy- 為1 mo 。車控制如此是一不育的等滲的 polobulation 在 狗 以Pelger-Huet 反常現象, 和 lution 包含檸檬酸鈉

和葡萄糖在酸鹼度4.8 。 倍數分開的中堅力量在4N promegakaryocyte 狗 被獲得了從馬歇爾農場, 公司。 階段, 偶爾地被觀察在法線 被增加

以回應thrombocyto- 在藥量的_蒙的變異(北部羅斯, NY ) 並且是在10 和 11 mo 老狗之間但。四條 狗/sex/group 是sac- penia (12-14) 。me

gakaryocytes 的一個增加的數字 rificed 和審查了1 天在最後藥量以後, 並且 與hypersegmented 中堅力量並且megakaryocytes 與 殘餘的 狗

(3lsexlgroup) 被犧牲了在 多個分開的中堅力量被報告了在人的pa- 30 天補救期間之後。血樣是被收集的 tients 以各種各樣的混亂包括kala aza

r, mye- 在藥量_蒙之前和在研究天8, 15, 22, 29, 36, 43, 50, 和57 。完全血細胞計數是每 * 地址書信: 約翰E. 隆德, 全世界毒素學, 被形成在

Technicon H-1 儀器。屍體檢驗是 Pharmacia & Upjohn, Inc., 7000 Portage 路, Kalamazoo, 密執安 4900 1 。 執行了在所有 狗, 和標準套組



Megakaryocytes in normal dogs have a variety of nuclear forms. The most common variations are a single large multilobed nucleus or a se

gmented nucleus consisting of irregular nuclear lobes joined by strands of chromatin. Exaggerated segmentation (hyperseg- mentation)

of the nucleus occurs in a small number of megakaryocytes. Megakaryocytes with multiple separate nuclei are infrequently observed. In

a 1-mo toxicology study in young adult beagle dogs with PNU-100592, a new oxazolidinone antibacterial agent, a large increase in the n

umber of megakaryocytes with hypersegmented nuclei and multiple separate nuclei was observed. The group mean platelet count was s

lightly decreased for most PNU-100592-treated groups. Siderocytes were observed on peripheral blood smears, and ring sideroblasts wer

e present on bone marrow smears. Minimal to mild toxicologic lesions were observed in the large intestine, rectum, kidneys, liver, and tes

tes, primarily in the high-dose group. PNU-100592 may be useful in the study of the regulation of endomitosis during megakaryocytopoie

sis in the dog. Bone marrow; endomitosis; mucosal atrophy; sideroblasts; siderocytes; toxicology Keywords. lodysplastic syndromes, acut

e myelogenous leukemia, INTRODUCTION acute monoblastic leukemia, and congenital dyserythro- The megakaryocyte is a large polyploi

d cell with either poietic anemia (1, 18, 19, 24, 25, 27). a single large lobulated nucleus or a segmented nucleus In this report, we descr

ibe a large increase in the num- consisting of irregular nuclear lobes joined by strands of ber of megakaryocytes with hypersegmented nu

clei and chromatin. Exaggerated segmentation (hypersegmenta- multiple separate nuclei in dogs from a 1-mo toxicology tion) of the nucl

eus occurs in a small number of mega- study with a new oxazolidinone antibacterial agent, PNU- karyocytes. Megakaryocytes with multipl

e separate nu- 100592. To the best of our knowledge, no similar obser- clei are infrequently observed. Megakaryocytes in normal vation

has been reported in dogs as a result of exposure dogs have a modal ploidy of 16N (54%) with 17% 8N to a xenobiotic. and 16% 32N

(3). The ploidy number does not correlate with the number of nuclear lobulations (20, 22); however, megakaryocyte DNA content is rel

ated to megakaryocyte size and therefore to the eventual number of platelets pro- PNU-100592 was administered intravenously to beag

le duced (17, 21, 22). Variations in megakaryocyte nuclear dogs, 7lsexlgroup, at 0 (vehicle control), 12.5, 40, and morphology reported

in dogs include karyorrhexis in 125 mglkg twice daily (0, 25, 80, and 250 mglkglday) dogs with experimental immune thrombocytopenia,

hy- for 1 mo. The vehicle control was a sterile isotonic so- polobulation in dogs with the Pelger-Huet anomaly, and lution containing sodiu

m citrate and dextrose at pH 4.8. multiple separate nuclei at the 4N promegakaryocyte The dogs were obtained from Marshall Farms, In

c. stage, a variation that is observed occasionally in normal (North Rose, NY) and were between 10 and 11 mo old dogs but that is incre

ased in response to thrombocyto- at the initiation of dosing. Four dogs/sex/group were sac- penia (12-14). An increased number of meg

akaryocytes rificed and examined 1 day after the last dose, and the with hypersegmented nuclei and megakaryocytes with remaining do

gs (3lsexlgroup) were sacrificed after a multiple separate nuclei have been reported in human pa- 30-day recovery period. Blood samples

were collected tients with a variety of disorders including kala azar, mye- prior to dose initiation and on study days 8, 15, 22, 29, 36, 43,

50, and 57. Complete blood cell counts were per- * Address correspondence to: John E. Lund, Worldwide Toxicology, formed on a Tec

hnicon H-1 instrument. A necropsy was Pharmacia & Upjohn, Inc., 7000 Portage Road, Kalamazoo, Michigan 4900 1. performed on all do

gs, and a standard set of tissues was

minibabyqq 2006-12-28 01:43

[color=Magenta][b][size=5]Opioids-- 鎮痛藥可利用   [/size][/b][/color]


Opioids-- 是最強有力的鎮痛藥可利用, 以行動在周邊, 脊髓和supraspinal 水平。有4 類型opioid 感受器官, 以多感受器官子型。 Mu 感受器官導致最深刻的痛覺缺失, 和可能導致幸福感、呼吸消沉、物理依賴性和心跳緩慢。 Kappa 感受器官觸發少許鎮痛藥反應, 和也許導致miosis 、鎮靜和煩躁不安。 三角洲 感受器官調整mu 感受器官活動。 斯格碼 感受器官提供一點對沒有痛覺缺失。他們負責對許多不利影響與相關opioids (煩躁不安, 幻覺, 呼吸和血管舒縮的刺激) 。一些調查員分類斯格碼感受器官作為phencyclidine, 而不是opioid, 感受器官。
Opioids 可能作為 苦悶者 (困境和刺激感受器官), 反對者 (困境和塊或禁止活動), 部份苦悶者 (困境和較不比充分刺激, 但以活動在某些感受器官子型), 和 混雜的agonist/antagonists (刺激一些感受器官當阻攔其他人) 。

Opioids 是有用的在各種各樣的慢性地痛苦的情況(雖然他們也許有有限的有效率以某種neuropathic 痛苦的形式) 。為慢性痛苦管理的目的, 各種各樣的opioids 的只口頭和transdermal 版本將被考慮在以下討論中。

純淨的mu 苦悶者 提供最佳的痛覺缺失, 而且有潛力導致副作用(心跳緩慢、低血壓症、鎮靜、呼吸消沉, 泌尿保留, 嘔吐, 排糞, 便秘) 。他們的用途對短期"搶救" 痛覺缺失最好被限制, 雖然某些混亂(特別是癌症痛苦) 也許要求連續用法在疾病的最新階段。以慢性用途, 容忍經常顯現出, 需要進步地大劑量達到一個鎮痛藥作用。

嗎啡sulfate (CII) 是可利用的在口頭片劑、膠囊和液體準備。一個建議的藥量範圍在狗是0.5-2.0 mg/kg QID (一些狗體驗不能接受的便秘在藥量超出1 mg/kg) 。貓被藥量了以液體形式在0.2-0.5 mg/kg TID-QID, 但多數貓強烈煩惡口味。

可待因並且被使用了作為一個口頭mu 苦悶者, 雖然它比嗎啡通常較不有效的。它是最共同地可利用的與acetaminophen 的組合作為CIII 準備, 和一般被藥量在狗在可待因部份TID-QID (它的1-2 mg/kg 不應該被使用在貓與acetaminophen 的組合由於致命methemoglobinemia 風險) 。

芬太奴是可利用的作為一個transdermal 補釘(Duragesic -- CII) 在25, 50, 75 和100 ug/hour 力量。一些研究建議75 個和100 個ug 補釘不能提供一致的血漿水平; 25 個和50 個ug 補釘的組合可能使用達到適當的藥量(2-4 ug/kg) 在狗。在貓> 2.5 公斤, 整體25 ug 補釘被使用; 如果< 2.5 公斤, 塑料依託的一半包括膠凝體被去除(不要切開補釘) 。

Duragesic 補釘提供非常好背景痛覺缺失, 雖然他們偶爾地需要用口頭mu 苦悶者被補充。在狗, 起始時間是12-36 個小時, 以作用的72 個小時期間。貓傾向於有更加快速的起始時光(5-8 個小時) 並且更長的(120 個小時) 期間。副作用也許包括inappetance 、agitation/dysphoria 、鎮靜和極高熱(貓) 。

部份mu 苦悶者 束縛在mu 感受器官但部份地只激活他們。Buprenorphine (CIII) 是樣本藥物在這類; 它是適度地昂貴但非常安全的, 導致少量副作用和最小的鎮靜。Buprenorphine 有巨大親合力為mu 感受器官, 和競爭地將禁止純淨的mu 苦悶者從束縛。這物產使它有用為"扭轉" 嗎啡的作用或芬太奴如果有害後果出現, 當仍然維護痛覺缺失的水平。

對痛覺缺失的天花板作用存在與部份苦悶者, 使他們較不有用為嚴厲痛苦。Buprenorphine 是有趣在那增加藥量延長痛覺缺失的期間, 當程度鎮痛根本上依然是未改變。30 ug/kg 藥量(0.030 mg/kg) 將提供~ 8-10 個小時痛覺缺失, 和40 ug/kg (0.040 mg/kg) 也許生產儘量12 個小時痛苦控制。行動起始是相當慢的(~ 30 分鐘當指定的IV, 60 分鐘IM, transmucosal 或transdermal) 。

Buprenorphine 不是可利用的作為一種口頭準備(重大first-pass 作用使它不活潑), 但是它的親油性自然借自己對吸收橫跨皮膚或黏膜。配製藥房可能生產PLO (pleuronic 卵磷脂organogel, 或transdermal 膠凝體) 為應用在pinna 的內在表面或被刮的皮膚在脖子在狗和貓。供選擇地, 貓鹼性唾液酸鹼度考慮到優秀transmucosal 吸收當可注射的藥物被給在嘴(它不應該與風味糖漿被混合, 和吞下將撤消它; 可注射的形式是無味和由貓很好容忍) 。研究未被進行在transmucosal 用法在狗, 雖然他們的唾液酸鹼度是離那人較近, 生物相容性在黏膜管理以後是唯一~ 30% 。

混雜的agonist/antagonists 像butorphanol (CIV) 不被認為有用在慢性痛苦的管理。First-pass 作用毀壞一些藥物, 並且痛覺缺失認為是相對地短命的(1-2 個小時) 。由於這些藥物是kappa 苦悶者和mu 反對者, 鎮痛經常是比優選為慢性難受。但是, 發自內心的nociception 認為是敏感對kappa agonism, 帶領一些尿科醫師主張butorphanol 的用途在慢性膀胱痛苦中(FLUTD) 。

   
1)   BUPRENORPHINE

a)      分類

i)        Opioid

(1)   極端高親合力部份mu 苦悶者

(2)   一些kappa 對抗性

(3)   類III

b)      總說明

i)        好所有在鎮痛藥附近使溫和減輕痛苦免於任何期望的不受歡迎的作用

(1)   狗逸事報告接受0.2 mg/lb IV 根據為幾藥量的一個QID 依據沒有消極後果(M. Richey, DACVA)

ii)       最小, 如果有, 鎮靜作用

iii)     Buprenorphine 有一個被延遲的起始

(1)   30 分鐘對高峰作用當指定的IV

(2)   45 到60 分鐘對高峰作用當指定的IM

iv)     作用的期間被藥量影響

(1)   3 個到4 個小時在0.010 mg/kg (0.005 mg/lb) 藥量

(2)   6 個到8 個小時在0.020 mg/kg (0.010 mg/lb) 藥量

(3)   8 個到10 個小時在0.030 mg/kg (0.015 mg/lb) 藥量

(4)   10 個到12 個小時在0.040 mg/kg (0.020 mg/lb) 藥量

c)      Advantages/Recommended 用途

i)        一般軟的組織手術

ii)       輕的矯形手術

iii)     在 貓, 研究表示, 生物相容性是相同是否指定的IV, IM, 或通過頰口頭mucosa (生物相容性是窮的從GI 短文- 給sublingually 或在側向面頰囊)

(1)   這transmucosal 吸收被似貓的唾液鹼性酸鹼度影響

(a)    有, 沒有支持對於有效的口頭吸收由狗

(2)   優秀選擇為家庭鎮痛藥管理在貓

d)      警告資訊

(1)   難扭轉 如果 不受歡迎的作用出現

(2)   會被預計對抗其它純淨的mu 苦悶者像嗎啡、hydromorphone 、芬太奴, 和oxymorphone

e)      劑量資訊

(1)   尾隨- 0.010 到0.040 mg/kg (0.005 - 0.02 mg/lb) IM 或IV

(2)   貓- 0.010 到0.040 mg/kg (0.005 - 0.02 mg/lb) IM, IV, 或 Tramsmucosally

f)       費用

i)        減輕在藥量範圍- 上流的末端在上部藥量範圍

2)   BUTORPHANOL

a)      分類

i)        Opioid

(1)   混雜的agonist/antagonist 以主要競爭的活動在kappa 感受器官

(a)    通常對抗性在mu 感受器官

b)      總說明

i)        好所有在鎮痛藥附近為溫和的痛苦免於任何期望的不受歡迎的作用

ii)       少許, 或沒有呼吸消沉在臨床藥量

iii)     作用的期間是30 分鐘到1 個小時在狗和1 個到3 個小時在貓

c)      Advantages/Recommended 用途

i)        一般軟的組織手術

ii)       有效為發自內心(軟的組織) 比體壁(矯形) 鎮痛藥

d)      警告資訊

i)        作用的短期

(1)   狗- 30 分鐘到1 個小時

(2)   貓- 1 個到3 個小時

ii)       大劑量可能導致興奮和煩躁不安

e)      劑量資訊

i)        狗& 貓

(1)   0.2 到0.4 mg/kg (0.1 到0.2 mg/lb) IV, IM, SC

(a)    0.2 mg/kg (0.1 mg/lb) 是最共同地選擇的藥量

f)       費用

i)        減輕(對上流如果給每隔幾個小時)

3)   DURAMORPH®

a)      分類

i)        防腐劑釋放嗎啡

ii)       純淨的mu opioid 苦悶者

b)      總說明

i)        一種具體準備至於硬膜外使用

c)      Advantages/Recommended 用途

i)        硬膜外痛覺缺失

d)      警告資訊

i)        單一用途的10 個毫克(10 機器語言) 小瓶和2 個毫克(2ml) 小瓶- 不要保存殘餘的meds

e)      劑量資訊

i)        硬膜外用途

(1)   狗& 貓- 0.1 mg/kg (0.045 mg/lb 。)

(a)    1 cc 每10 公斤

f)       費用

i)        適度地高- 重大副產品

4)   芬太奴

a)      分類

i)        一個純淨的mu 苦悶者

b)      總說明

i)        作用的期間是30 到45 分鐘

c)      Advantages/Recommended 用途

i)        短期痛覺缺失

(1)   優秀作為內部有效"完成" 鎮痛藥

ii)       歸納代理當與benzodiazepine 結合

iii)     CRI 鎮痛藥用途

d)      警告資訊

i)        看氣喘和肌肉堅硬

e)      劑量資訊

i)        歸納

(1)   看苯甲二氮卓& Opioid 部分在歸納協議之下為細節

ii)       痛覺缺失

(1)   一小團- 0.002 mg/kg (0.001 mg/lb)

(2)   CRI - 0.001 到0.004 mg/kg/hr (0.005 到0.002 mg/lb/hr)

(3)   Duragesic 補釘- 根據重量

  

患者
藥量
芬太奴內容

小狗** (< 5kg) & 貓
25 mcg/hr
2.5 毫克

狗: 5-10 公斤
25 mcg/hr
2.5 毫克

狗: 10-20 公斤
50 mcg/hr
5 毫克

狗: 20-30 公斤
75 mcg/hr
7.5 毫克

狗: > 30 毫克
100 mcg/hr
10 毫克


  

(a)    小狗和貓, 使用25 mcg/hr 補釘但只暴露補釘的.

(b)    為更小的貓考慮暴露補釘的.

(c)    從未切開補釘

(d)    截去頭髮越緊密越好在計劃的補釘站點沒有激怒皮膚。柔和地抹區域一兩次以輕微地被挫傷的紗取消寬鬆頭髮。讓區域乾燥溫暖的補釘對體溫。取消依託和嚮皮膚應用補釘。牢固地舉行反對皮膚用手2 充分的分鐘。白色磁帶和Kling 紗被使用蓋和支持補釘當可能時。

f)       費用

i)        低落每IV 用途

ii)       上流每補釘

5)   HYDROMORPHONE
a)      分類

i)        純淨的mu 苦悶者

(1)   類II

b)      總說明

i)        作用的期間是4 個到6 個小時

ii)       考慮有相似的整體物產當與oxymorphone 比較雖然較不有力

c)      Advantages/Recommended 用途

i)        將軍premed 為麻醉的候選人在所有類別

ii)       通常氣喘比oxymorphone

iii)     不同於嗎啡, 不應該導致瞬變低血壓症

(1)   IV 用途 不同氨基酸發行聯繫在一起

d)      警告資訊

i)        心跳緩慢是共同

ii)       嘔吐是共同在IM 管理以後

iii)     有適度鎮靜協同作用在hydromorphone 和acepromazine 之間在狗

(1)   Acepromazine 藥量應該被保留在藥量範圍的末端

iv)     有一個傾向使貓被鼓動除非 更高的 Acepromazine 藥量被使用

e)      劑量資訊

i)        狗- 0.01 到0.4 mg/kg (0.05 - 0.20 mg/lb) IV, IM

(1)   通常0.1 到0.2 mg/kg (0.05 到0.10 mg/lb)

ii)       貓- 0.05 到0.2 mg/kg (0.025 - 0.10 mg/lb) IV, IM

(1)   通常0.05 到0.1 mg/kg (0.025 到0.05 mg/lb)

iii)     歸納

(1)   IV 歸納#2 - 與芬太奴、hydromorphone, 或oxymorphone 被結合- 最有用為狗

(a)    參見苯甲二氮卓& Opioid 部分在歸納協議之下為細節

iv)     維護

(2)   IV 維護- 最有用為狗

(a)    參見苯甲二氮卓& Opioid 部分在維護協議之下為細節

v)      硬膜外藥量

(1)   0.03 到0.10 mg/kg (0.015 到0.05 mg/lb)

f)       費用

i)        低

6)   嗎啡SULFATE

a)      分類

i)        一個純淨的mu opioid 苦悶者

b)      總說明

i)        作用的期間是4 個到6 個小時

c)      Advantages/Recommended 用途

i)        將軍premed 適當為健康動物

ii)       最常用與acepromazine 、阿爾法2 苦悶者, 或benzodiazepine 的組合sedative/tranquilizer

iii)     比能達到與hydromorphone 或oxymorphone 提供更加偉大的鎮靜

d)      警告資訊

i)        更高的劑量可能導致心跳緩慢和呼吸消沉

ii)       可能導致瞬變減血壓比hydromorphone 、芬太奴, 或oxymorphone

iii)     經常導致嘔吐和排糞當指定的IM 或SC

iv)     IV 用途同氨基酸發行聯繫在一起

(1)   這認為是瞬變低水平關心和一般是不太可能的如果慢慢地執行

v)      有重大鎮靜協同作用在嗎啡和acepromazine 之間在狗

(1)   Acepromazine 藥量必須適當地被減少

vi)     應該小心地被使用在貓如果sedative/tranquilizer 不被使用

e)      劑量資訊

i)        狗- 0.5 到1.0 mg/kg (0.25 到0.50 mg/lb) SC, IM, 或慢慢地IV

(1)   Acepromazine 藥量會是末端- 0.005 到0.040 mg/kg (0.0025 到0.020 mg/lb)

ii)       貓- 0.25 到0.5 mg/kg (0.125 到0.25 mg/lb) SC, IM, 或慢慢地IV

(1)   Acepromazine 藥量必須是更高的末端- 0.06 到0.1 mg/kg (0.03 到0.05 mg/lb)

iii)     其他用途

(1)   恆定的率注入- 參見關於CRIs 的部分

(2)   硬膜外- 參見關於epidurals 的部分

f)       費用

i)        低

7)   NALOXONE

a)      分類

i)        opioid 反對者

b)      總說明

i)        一短行動, 純淨的反對者

c)      Advantages/Recommended 用途

i)        扭轉opioid 療程的不需要的作用

(1)   可能使用小藥量部份地扭轉opioid 作用

ii)       作用的期間是1 個到3 個小時

d)      警告資訊

i)        通常短期比多數opioid 苦悶者

(1)   逆轉作用也許消減在苦悶者被清除了從身體之前

(2)   Redosing 也許是必要的在1 個到3 個小時以後如果不受歡迎的苦悶者影響返回

ii)       Buprenorphine 作用不能是雙面布料由於高約束親合力

iii)     Butorphanol 不能扭轉一樣完全地像純淨的Mu opioid 苦悶者

e)      劑量資訊

i)        狗& 貓-).02 對0.1 mg/kg (0.01 到0.05 mg/lb) IM 或IV

(1)   給故意的藥量的1/4 每3 - 4 分鐘直到渴望的作用達到

f)       費用

i)        適度地低

8)   OXYMORPHONE

a)      分類

i)        一個純淨的Mu opioid 苦悶者

b)      總說明

i)        作用的期間是4 個到6 個小時

c)      Advantages/Recommended 用途

i)        將軍premed 為麻醉的候選人在所有類別

ii)       減血壓患者

(1)   不同於嗎啡, 不應該導致瞬變低血壓症

iii)     更高的風險患者當風險嘔吐需要減到最小

d)      警告資訊

i)        心跳緩慢是共同

ii)       噪聲過敏症也許是問題

iii)     有適度鎮靜協同作用在oxymorphone 和acepromazine 之間在狗

(1)   Acepromazine 藥量必需保持了在藥量範圍的末端

iv)     如果小心地被使用在貓如果sedative/tranquilizer 不被使用

e)      劑量資訊

i)        狗- 0.05 到0.2 mg/kg (0.025 - 0.050 mg/lb) IM, IV

ii)       貓- 0.025 到0.05 mg/kg (0.01 - 0.025 mg/lb) IM, IV

(1)   組合與acepromazine 0.06 到0.10 mg/kg (0.03 到0.05 mg/lb)



   
Dr. Dave Thompson
   
1)   BUPRENORPHINE

a)      Classification

i)        Opioid

(1)   Partial mu agonist of extremely high affinity

(2)   Some kappa antagonism

(3)   Class III

b)      General Information

i)        Good all around analgesic for mild to moderate pain free of any expected undesirable effect

(1)   Anecdotal reports of dogs receiving 0.2 mg/lb IV on a QID basis for several doses without negative consequences (M. Richey, DACVA)

ii)       Minimal, if any, sedative effect

iii)     Buprenorphine has a delayed onset

(1)   30 minutes to peak effect when given IV

(2)   45 to 60 minutes to peak effect when given IM

iv)     Duration of effect is influenced by dose

(1)   3 to 4 hours at 0.010 mg/kg (0.005 mg/lb) dose

(2)   6 to 8 hours at 0.020 mg/kg (0.010 mg/lb) dose

(3)   8 to 10 hours at 0.030 mg/kg (0.015 mg/lb) dose

(4)   10 to 12 hours at 0.040 mg/kg (0.020 mg/lb) dose

c)      Advantages/Recommended use

i)        General soft tissue surgery

ii)       Light orthopedic surgery

iii)     In cats, studies have shown that bioavailability is the same whether given IV, IM, or via buccal oral mucosa (bioavailability is poor from GI tract – give sublingually or in lateral cheek pouch)

(1)   This transmucosal absorption is influenced by the alkaline pH of feline saliva

(a)    There is, as yet, no support for effective oral absorption by the dog

(2)   Excellent option for home analgesic management in cats

d)      Cautionary Information

(1)   Difficult to reverse if undesirable effects arise

(2)   Would be expected to antagonize other pure mu agonists like morphine, hydromorphone, fentanyl, and oxymorphone

e)      Dosage Information

(1)   Dogs – 0.010 to 0.040 mg/kg (0.005 – 0.02 mg/lb) IM or IV

(2)   Cats - 0.010 to 0.040 mg/kg (0.005 – 0.02 mg/lb) IM, IV, or Tramsmucosally

f)       Cost

i)        Moderate at low end of dose range - high at upper dose range

2)   BUTORPHANOL

a)      Classification

i)        Opioid

(1)   A mixed agonist/antagonist with primary agonistic activity at the kappa receptor

(a)    Generally antagonistic at the mu receptor

b)      General Information

i)        Good all around analgesic for mild pain free of any expected undesirable effect

ii)       Little, or no respiratory depression at clinical doses

iii)     Duration of effect is 30 minutes to 1 hour in dogs and 1 to 3 hours in cats

c)      Advantages/Recommended use

i)        General soft tissue surgery

ii)       More effective for visceral (soft tissue) than somatic (orthopedic) analgesic

d)      Cautionary Information

i)        Short duration of effect

(1)   Dogs - 30 minutes to 1 hour

(2)   Cats - 1 to 3 hours

ii)       Higher doses can produce excitement and dysphoria

e)      Dosage Information

i)        Dog & Cats

(1)   0.2 to 0.4 mg/kg (0.1 to 0.2 mg/lb) IV, IM, SC

(a)    0.2 mg/kg (0.1 mg/lb) is the most commonly selected dose

f)       Cost

i)        Moderate (to high if given every few hours)

3)   DURAMORPH®

a)      Classification

i)        Preservative free morphine

ii)       Pure mu opioid agonist

b)      General Information

i)        A specific preparation for epidural use

c)      Advantages/Recommended use

i)        Epidural analgesia

d)      Cautionary Information

i)        Single use 10 mg (10 ml) vials and 2 mg (2ml) vials - do not save residual meds

e)      Dosage Information

i)        Epidural use

(1)   Dog & Cat - 0.1 mg/kg (0.045 mg/lb.)

(a)    1 cc per 10 kg

f)       Cost

i)        Moderately high – significant wastage

4)   FENTANYL

a)      Classification

i)        A pure mu agonist

b)      General Information

i)        Duration of effect is 30 to 45 minutes

c)      Advantages/Recommended use

i)        Short-term analgesia

(1)   Excellent as an intra-operative “top up” analgesic

ii)       Induction agent when combined with a benzodiazepine

iii)     CRI analgesic use

d)      Cautionary Information

i)        May see panting and muscle rigidity

e)      Dosage Information

i)        Induction

(1)   See Diazepam & an Opioid section under Induction protocols for details

ii)       Analgesia

(1)   Bolus – 0.002 mg/kg (0.001 mg/lb)

(2)   CRI – 0.001 to 0.004 mg/kg/hr (0.005 to 0.002 mg/lb/hr)

(3)   Duragesic patch – based upon weight

  

Patient
Dose
Fentanyl Content

Small Dogs ** (<5kg) & Cats
25 mcg/hr
2.5 mg

Dogs: 5-10 kg
25 mcg/hr
2.5 mg

Dogs: 10-20 kg
50 mcg/hr
5 mg

Dogs: 20-30 kg
75 mcg/hr
7.5 mg

Dogs: >30 mg
100 mcg/hr
10 mg


  

(a)    Small dogs and cats, use the 25 mcg/hr patch but only expose ½ of the patch

(b)    For even smaller cats consider exposing ¼ of the patch

(c)    Never cut the patch

(d)    Clip hair as closely as possible at planned patch site without irritating the skin. Gently wipe area once or twice with slightly dampened gauze to remove loose hair. Let area dry. Warm patch to body temperature. Remove backing and apply patch to skin. Hold firmly against skin with hand for 2 full minutes. White tape and Kling gauze are used to cover and support the patch when possible.

f)       Cost

i)        Low per IV use

ii)       High per patch

5)   HYDROMORPHONE
a)      Classification

i)        Pure mu agonist

(1)   Class II

b)      General Information

i)        Duration of effect is 4 to 6 hours

ii)       Considered to have similar overall properties when compared to oxymorphone although less potent

c)      Advantages/Recommended use

i)        General premed for anesthetic candidates in all categories

ii)       Generally less panting than oxymorphone

iii)     Unlike Morphine, should not cause transient hypotension

(1)   IV use is not associated with histamine release

d)      Cautionary Information

i)        Bradycardia is common

ii)       Vomiting is common after IM administration

iii)     There is moderate sedative synergism between hydromorphone and acepromazine in the dog

(1)   Acepromazine doses should be kept at the lower end of the dose range

iv)     There is a tendency for cats to be agitated unless higher Acepromazine doses are used

e)      Dosage Information

i)        Dog – 0.01 to 0.4 mg/kg (0.05 - 0.20 mg/lb) IV, IM

(1)   Generally 0.1 to 0.2 mg/kg (0.05 to 0.10 mg/lb)

ii)       Cats – 0.05 to 0.2 mg/kg (0.025 - 0.10 mg/lb) IV, IM

(1)   Generally 0.05 to 0.1 mg/kg (0.025 to 0.05 mg/lb)

iii)     Induction

(1)   IV induction #2 - combined with fentanyl, hydromorphone, or oxymorphone – most useful for dogs

(a)    See Diazepam & an Opioid section under Induction Protocols for details

iv)     Maintenance

(2)   IV maintenance – most useful for dogs

(a)    See Diazepam & an Opioid section under Maintenance Protocols for details

v)      Epidural dose

(1)   0.03 to 0.10 mg/kg (0.015 to 0.05 mg/lb)

f)       Cost

i)        Low

6)   MORPHINE SULFATE

a)      Classification

i)        A pure mu opioid agonist

b)      General Information

i)        Duration of effect is 4 to 6 hours

c)      Advantages/Recommended use

i)        General premed suitable for healthy animals

ii)       Most commonly used in combination with acepromazine, an alpha-2 agonist, or a benzodiazepine sedative/tranquilizer

minibabyqq 2006-12-28 01:44

[color=Magenta][size=5][b]NSAID 為慢性地痛苦的患者 [/b][/size][/color]  


NSAID 的-- 依然是療法中流砥柱為慢性地痛苦的患者。行動他們的主要方式將阻攔前列腺素生產由束縛和禁止cyclooxygenase (考克斯) 。當這個作用的結果是主要對炎症和周邊nociceptor sensitization 的減少, 有一些證據, NSAID 的有一次中央鎮痛藥行動, 雖然確切的機制依然是不明。
Cyclooxygenase 發生在至少2 isoforms: COX1 (結構性), 斡旋前列腺素形成負責任對GI 黏膜保護、hemostasis 和腎臟血流, 並且COX2 (可誘導), 摧化前列腺素生產作為激動斡旋人。這是一點太簡單的事, 因為COX2 可能充當在禁止COX2>COX1 被認為選擇藥物在這類的一些情況的一個homeostatic 角色(潰瘍癒合, 腎臟血流維護在重音期間, prostacyclin 生產), 但總之NSAID 的。這些經常指COX2 優先或有選擇性的代理。

各種各樣的selective/preferential NSAID 的是可利用的至於使用在狗, 包括carprofen (2.2 mg/kg 出價或4.4 mg/kg SID), etodolac (10-15 mg/kg SID), deracoxib (1-2 mg/kg SID 至於慢性使用), meloxicam (0.2 mg/kg 在天1, 然後0.1 mg/kg SID), 和tepoxalin (20 mg/kg SID 在天一個, 然後10 mg/kg SID) 。雖則在理論上他們所有是相等地有效的, 一些患者出現反應更好一另; 因而, 疏忽達到一個鎮痛藥作用與一種藥物不暗示缺乏對所有NSAID 的反應。

小心應該行使當使用NSAID 的在貓。在肝生物轉化上的區別可能導致長時期的半衰期和在毒力的潛力。另外, 少量研究非常被進行了審查對這些化合物的似貓的反應。看上去很好被容忍在貓的一個少數NSAID 的是meloxicam (0.1 mg/kg SID 3-5 天, 然後0.1 mg/CAT/q 24-72 個小時長期) 。由於巨大變異在各自的貓之中存在關於新陳代謝, 這是推薦他們嚴密被監測為不利影響當在長期療法。

在所有患者, NSAID 的應該被避免在腎臟或肝官能不良、coagulopathies 、GI 混亂、震動、hypotension/hypovolemia 、hypoalbuminemia 或懷孕面前。狗和貓在慢性療法應該階段性地被監測為改變在血液學或生物化學的參量, 並且他們的所有者應該被指示觀看為GI 翻倒的標誌, 改變在胃口和PU/PD 。
1)   CARPROFEN

a)      分類

i)        COX2 有選擇性的NSAID

b)      總說明

i)        有效的anti-inflammatory/analgesic 一般免於重大GI 副作用

c)      Advantages/Recommended 用途

i)        短期用途為劇痛

ii)       長期用途在慢性痛苦中為寬容患者

d)      警告資訊

i)        和與任一NSAID, GI 副作用可能是堅固的

(1)   中斷用途如果GI 標誌顯現出

ii)       避免用途在:

(1)    組合與類皮質激素

(a)    潛在地增加的ulcerogenic 作用

(2)   腎臟妥協的有肝疾病病人, 被脫水的或減血壓患者, 患者, 懷孕, 有已存在GI 疾病病人, coagulopathies

iii)     監測似犬患者肝臟酵素在慢性療法

e)      劑量資訊

i)        狗- 2.20 mg/kg (1.0 mg/lb) SC 、PO 出價或4.4 mg/kg (2.0 mg/lb) SC, PO SID

ii)       貓 - 1 到2.0 mg/kg (0.45 到0.90 mg/lb) SC 一次唯一

f)       費用

i)        適度

2)   DERACOXIB

a)      分類

i)        coxib 組COX2 有選擇性的NSAID

b)      總說明

i)        有效的anti-inflammatory/analgesic 一般免於重大GI 副作用

c)      Advantages/Recommended 用途

i)        短期用途為劇痛

ii)       長期用途在慢性痛苦中為寬容患者

d)      警告資訊

i)        和與任一NSAID, GI 副作用可能是堅固的

(1)   中斷用途如果GI 標誌顯現出

ii)       避免用途在:

(1)    組合與類皮質激素

(a)    潛在地增加的ulcerogenic 作用

(2)   腎臟妥協的有肝疾病病人, 被脫水的或減血壓患者, 患者, 懷孕, 有已存在GI 疾病病人, coagulopathies

iii)     監測似犬患者肝臟酵素在慢性療法

e)      劑量資訊

i)        狗- 1 到2 mg/kg PO SID 為一般痛苦管理

(1)   3 到4 mg/kg PO SID 7 天為深刻外科痛苦

ii)       貓- 對deracoxib 的用途不被推薦此時

f)       費用

i)        適度地高

3)   ETODOLAC

a)      分類

i)        COX2 有選擇性的NSAID

b)      總說明

i)        有效的anti-inflammatory/analgesic 一般免於重大GI 副作用

c)      Advantages/Recommended 用途

i)        短期用途為劇痛

ii)       長期用途在慢性痛苦中為寬容患者

d)      警告資訊

i)        和與任一NSAID, GI 副作用可能是堅固的

(1)   中斷用途如果GI 標誌顯現出

ii)       避免用途在:

(1)    組合與類皮質激素

(a)    潛在地增加的ulcerogenic 作用

(2)   腎臟妥協的有肝疾病病人, 被脫水的或減血壓患者, 患者, 懷孕, 有已存在GI 疾病病人, coagulopathies

iii)     監測似犬患者肝臟酵素在慢性療法

e)      劑量資訊

i)        狗- 10 到15 mg/kg (4.8 到6.8 mg/lb) PO SID

ii)       貓- 對etodolac 的用途不被推薦此時

f)       費用

i)        適度地低

4)   KETOPROFEN

a)      分類

i)        NSAID

b)      總說明

i)        有效的anti-inflammatory/analgesic 以重大GI 副作用如果半新長期

c)      Advantages/Recommended 用途

i)        長代理鎮痛藥可注射至於 唯一藥量 崗位操作使用

(1)   作用的期間是12 個到18 個小時

(2)   唯一藥量崗位操作用法證明是免於所有副作用關心在正常狗和貓

d)      警告資訊

i)        避免長期用途

(1)   GI 副作用可能是堅固的

ii)       避免用途與類皮質激素的組合

(1)   潛在地增加的ulcerogenic 作用

iii)     避免在腎臟妥協的患者

iv)     避免在被脫水的或減血壓患者

e)      劑量資訊

i)        狗- 2.0 mg/kg (0.9 mg/lb) SC 一次唯一

ii)       貓- 2.0 mg/kg (0.9 mg/lb) SC 一次唯一

f)       費用

i)        非常低

5)   MELOXICAM

a)      分類

i)        COX2 有選擇性的NSAID

b)      總說明

i)        有效的anti-inflammatory/analgesic 一般免於重大GI 副作用

c)      Advantages/Recommended 用途

i)        短期用途為劇痛

ii)       長期用途在慢性痛苦中為寬容患者

(1)   這NSAID 看上去適當用於較長期貓

(a)    貓, 更加比狗, 需要被監測嚴密在療法期間

d)      警告資訊

i)        和與任一NSAID, GI 副作用可能是堅固的

(1)   中斷用途如果GI 標誌顯現出

ii)       避免用途在:

(1)    組合與類皮質激素

(a)    潛在地增加的ulcerogenic 作用

(2)   腎臟妥協的有肝疾病病人, 被脫水的或減血壓患者, 患者, 懷孕, 有已存在GI 疾病病人, coagulopathies

iii)     監測似犬患者肝臟酵素在慢性療法

e)      劑量資訊

i)        狗- 0.2 mg/kg (0.1 mg/lb) IV, SC, PO SID 在天一個然後0.1 mg/kg (0.05 mg/lb) IV, SC, PO SID

ii)       貓- 0.1 mg/kg (0.05 mg/lb) SC, PO 3 到5 天, 然後0.1 毫克 總藥量 PO SID 每24 到72 個小時如果長期用途必需

(1)   您能使用meloxicam 瓶(而不是包括的注射器) 準確地藥量這種藥物。

(a)    1 下落從 瓶 是藥物0.05 毫克

f)       費用

i)        適度

NSAID’s -- remain the mainstay of therapy for chronically painful patients. Their principal mode of action is to block prostaglandin production by binding and inhibiting cyclooxygenase (COX). While the result of this effect is mainly a reduction in inflammation and peripheral nociceptor sensitization, there is some evidence that NSAID’s have a central analgesic action as well, though the exact mechanism remains unclear.
Cyclooxygenase occurs in at least 2 isoforms: COX1 (constitutive), which mediates formation of prostaglandins responsible for GI mucosal protection, hemostasis and renal blood flow, and COX2 (inducible), which catalyzes production of prostaglandins that act as inflammatory mediators. This is a bit of an oversimplification, as COX2 can play a homeostatic role in some situations (ulcer healing, maintenance of renal blood flow during stress, prostacyclin production), but in general NSAID’s that inhibit COX2>COX1 are considered the drugs of choice in this class. These are often referred to as COX2 preferential or selective agents.

A variety of selective/preferential NSAID’s are available for use in dogs, including carprofen (2.2 mg/kg BID or 4.4 mg/kg SID), etodolac (10-15 mg/kg SID), deracoxib (1-2 mg/kg SID for chronic use), meloxicam (0.2 mg/kg on day 1, then 0.1 mg/kg SID), and tepoxalin (20 mg/kg SID on day one, then 10 mg/kg SID). Though in theory they should all be equally efficacious, some patients appear to respond better to one over another; thus, failure to achieve an analgesic effect with one drug does not imply lack of response to all NSAID’s.

Caution should be exercised when employing NSAID’s in cats. Differences in hepatic biotransformation can lead to prolonged half-lives and the potential for toxicity. Additionally, very few studies have been performed examining the feline response to these compounds. One of the few NSAID’s that appears to be well tolerated in cats is meloxicam (0.1 mg/kg SID for 3-5 days, then 0.1 mg/CAT/q 24-72 hours long-term). Because tremendous variation among individual cats exists in regard to metabolism, it’s recommended they be monitored closely for adverse effects when on long-term therapy.

In all patients, NSAID’s should be avoided in the presence of renal or hepatic dysfunction, coagulopathies, GI disorders, shock, hypotension/hypovolemia, hypoalbuminemia or pregnancy. Dogs and cats on chronic therapy should be monitored periodically for alterations in hematological or biochemical parameters, and their owners should be instructed to watch for signs of GI upset, alterations in appetite and PU/PD.
1)   CARPROFEN

a)      Classification

i)        A COX2 selective NSAID

b)      General Information

i)        Effective anti-inflammatory/analgesic generally free of significant GI side effects

c)      Advantages/Recommended use

i)        Short term use for acute pain

ii)       Long term use in chronic pain for tolerant patients

d)      Cautionary Information

i)        As with any NSAID, GI side-effects can be substantial

(1)   Discontinue use if GI signs develop

ii)       Avoid use in:

(1)    Combination with corticosteroids

(a)    Potentially increased ulcerogenic effect

(2)   Renal compromised patients, dehydrated or hypotensive patients, patients with hepatic disease, pregnancy, patients with pre-existing GI disease, coagulopathies

iii)     Monitor liver enzymes of canine patients on chronic therapy

e)      Dosage Information

i)        Dogs – 2.20 mg/kg (1.0 mg/lb) SC, PO BID or 4.4 mg/kg (2.0 mg/lb) SC, PO SID

ii)       Cats – 1 to 2.0 mg/kg (0.45 to 0.90 mg/lb) SC one time only

f)       Cost

i)        Moderate

2)   DERACOXIB

a)      Classification

i)        A coxib class COX2 selective NSAID

b)      General Information

i)        Effective anti-inflammatory/analgesic generally free of significant GI side effects

c)      Advantages/Recommended use

i)        Short term use for acute pain

ii)       Long term use in chronic pain for tolerant patients

d)      Cautionary Information

i)        As with any NSAID, GI side-effects can be substantial

(1)   Discontinue use if GI signs develop

ii)       Avoid use in:

(1)    Combination with corticosteroids

(a)    Potentially increased ulcerogenic effect

(2)   Renal compromised patients, dehydrated or hypotensive patients, patients with hepatic disease, pregnancy, patients with pre-existing GI disease, coagulopathies

iii)     Monitor liver enzymes of canine patients on chronic therapy

e)      Dosage Information

i)        Dogs – 1 to 2 mg/kg PO SID for general pain management

(1)   3 to 4 mg/kg PO SID for up to 7 days for acute surgical pain

ii)       Cats – use of deracoxib is not recommended at this time

f)       Cost

i)        Moderately high

3)   ETODOLAC

a)      Classification

i)        A COX2 selective NSAID

b)      General Information

i)        Effective anti-inflammatory/analgesic generally free of significant GI side effects

c)      Advantages/Recommended use

i)        Short term use for acute pain

ii)       Long term use in chronic pain for tolerant patients

d)      Cautionary Information

i)        As with any NSAID, GI side-effects can be substantial

(1)   Discontinue use if GI signs develop

ii)       Avoid use in:

(1)    Combination with corticosteroids

(a)    Potentially increased ulcerogenic effect

(2)   Renal compromised patients, dehydrated or hypotensive patients, patients with hepatic disease, pregnancy, patients with pre-existing GI disease, coagulopathies

iii)     Monitor liver enzymes of canine patients on chronic therapy

e)      Dosage Information

i)        Dogs – 10 to 15 mg/kg (4.8 TO 6.8 mg/lb) PO SID

ii)       Cats – use of etodolac is not recommended at this time

f)       Cost

i)        Moderately low

4)   KETOPROFEN

a)      Classification

i)        An NSAID

b)      General Information

i)        Effective anti-inflammatory/analgesic with significant GI side effects if used long term

c)      Advantages/Recommended use

i)        Long acting analgesic injectable for single dose post-op use

(1)   Duration of effect is 12 to 18 hours

(2)   Single dose post-op usage has been shown to be free of any side-effect concerns in normal dogs and cats

d)      Cautionary Information

i)        Avoid long term use

(1)   GI side effects can be substantial

ii)       Avoid use in combination with corticosteroids

(1)   Potentially increased ulcerogenic effect

iii)     Avoid in renal compromised patients

iv)     Avoid in dehydrated or hypotensive patients

e)      Dosage Information

i)        Dogs – 2.0 mg/kg (0.9 mg/lb) SC one time only

ii)       Cats – 2.0 mg/kg (0.9 mg/lb) SC one time only

f)       Cost

i)        Very low

5)   MELOXICAM

a)      Classification

i)        A COX2 selective NSAID

b)      General Information

i)        Effective anti-inflammatory/analgesic generally free of significant GI side effects

c)      Advantages/Recommended use

i)        Short term use for acute pain

ii)       Long term use in chronic pain for tolerant patients

(1)   This NSAID appears more suitable for longer term use in cats

(a)    Cats, even more so than dogs, need to be monitored closely during therapy

d)      Cautionary Information

i)        As with any NSAID, GI side-effects can be substantial

(1)   Discontinue use if GI signs develop

ii)       Avoid use in:

(1)    Combination with corticosteroids

(a)    Potentially increased ulcerogenic effect

(2)   Renal compromised patients, dehydrated or hypotensive patients, patients with hepatic disease, pregnancy, patients with pre-existing GI disease, coagulopathies

iii)     Monitor liver enzymes of canine patients on chronic therapy

e)      Dosage Information

i)        Dogs – 0.2 mg/kg (0.1 mg/lb) IV, SC, PO SID on day one then 0.1 mg/kg (0.05 mg/lb) IV, SC, PO SID

ii)       Cats – 0.1 mg/kg (0.05 mg/lb) SC, PO for 3 to 5 days, then 0.1 mg total dose PO SID every 24 to 72 hours if long term use is required

(1)   You can use the meloxicam bottle (rather than the included syringe) to accurately dose this drug.

(a)    1 drop from the bottle is 0.05 mg of drug

f)       Cost

i)        Moderate

minibabyqq 2006-12-28 01:46

[color=Magenta][size=5][b]KETAMINE-鎮痛藥藥物  [/b][/size][/color]


恆定的率注入(CRI) 的鎮痛藥藥物是改進耐心舒適一個簡單和有效的手段。各種各樣的公式化可能被使用作為恆定的率注入; 協議被選擇取決於患者和程度痛苦被體驗或被期望。一些常用的藥物包括以下:

1) KETAMINE -- NMDA (N 甲醇D aspartate) 感受器官是存在在脊髓和某些區域的背部墊鐵在腦子之內。強烈並且/或者慢性有毒輸入對背部墊鐵細胞(由C 纖維主要地斡旋) 導致去除鎂從NMDA 感受器官和他們的活化作用由穀氨酸。這導致脊髓神經元(在神經元生火的巨大和期間的增量的長時期的去極化劑), 導致"放大作用" 痛苦反應。這是中央sensitization (在脊髓神經元的激發性的增量的過程的一重大部份) 並且也許導致痛覺過敏(對痛苦的刺激的一個過份反應) 並且allodynia (對通常非痛苦的刺激的一個痛苦的反應) 。

它是欣然明顯的, 阻攔(對抗) NMDA 感受器官將幫助使過份地痛苦的反應減到最小。另外, 研究建議那對抗這些感受器官改進opioid 感受器官敏感性, 減少opioid 容忍和使反彈痛覺過敏減到最小(明顯增加的痛苦現象的發展當opioids 被撤出) 。

Ketamine 是NMDA 感受器官的最常用的反對者在獸醫方面。當它的作用作為一種分離的麻醉劑在標準藥量是知名的, 活動一個新領土發生當它被提供在次級麻醉劑藥量。在恆定的率注入藥量, ketamine 阻攔感受器官活動沒有導致任何分離或其他不利影響。

值得注意的是, microdose ketamine CRI 不應該被使用作為痛覺缺失單一手段。它意欲增添其它止痛藥, 和應該總被使用與opioids 或其它鎮痛藥一道。

2) 嗎啡 -- 當與ketamine 結合在恆定的率注入, 重大痛覺缺失達到。嗎啡的穩定水平幫助避免一些"峰頂並且谷" 影響看見以opioids 的prn 管理。另外, 它的用途(作為"肩扛" 麻醉的維護流體) intraoperatively 用於減少相當數量麻醉的氣體必需, 可能是有用的在減少低血壓症風險。

它可能被使用在貓在藥量的光譜的末端(更高的速率也許導致重大煩躁不安和勵磁) 。

當其它opiods 可能用嗎啡被替代, 我們決定只包括資訊為一個其它mu 苦悶者, 芬太奴, 在藥量的資訊部分。這參考不意欲是所有CRI 選擇詳盡的回顧但起堅實而是基本的參考作用對於那些增加CRI 痛覺缺失來他們的實踐。

3) LIDOCAINE -- lidocaine 的加法有幾個好處。為intractable/very 嚴厲痛苦, 它補充說來痛覺缺失和鎮靜。Lidocaine 被報告有一些cytoprotective 作用, 譬如也許是有用的在防止reperfusion 傷害) 的微弱的鈣渠道禁止(, 和能極大幫助在案件以潛力為DIC 或先生, 包括GDV 的和脾切除術) 的被減少的嗜中性chemotaxis 和小片族聚(。並且, lidocaine 有一些活動在防止腸塞痛(潛在地有用為enterotomies) 。

lidocaine 的各種各樣的劑量率主張了。在狗, 率一樣低像10 ug/kg/minute (0.6 mg/kg/hour) 提供痛覺缺失, 雖然它也許佔去50 ug/kg/minute (3 mg/kg/hour) 為充分的cytoprotective 和反腸塞痛作用。直到進一步資料是可利用的, lidocaine 的用途在貓無法被推薦, 由於在毒力的潛力, 通常被體現作為奪取和嚴厲心跳緩慢。

   


CRI 藥量的資訊



KETAMINE (100 mg/ml) - 2 到20 ug/kg/minute (0.12 到1.2 mg/kg/hr) 。

·         一最初0.25 到0.50 mg/kg IV 一小團被給非常慢慢地迅速地達到藥物的最初的治療血液水平(當CRI 意欲維護, 或, 增量血液水平) 。疏忽規定這"裝貨" 藥量導致過份延遲在藥物到達治療水平。

·         Ket/val 歸納和telazol 歸納兩個提供充分裝貨藥量(tiletamine 提供NMDA 對抗性和ketamine 一樣) 。

·         2 到20 ug/kg/min = 0.002 到0.020 mg/kg/min 。

嗎啡 (15 mg/ml) - 2 到6 ug/kg/minute (0.12 到0.36 mg/kg/hr) 。

·         如果早先mu 苦悶者未被給, 執行0.5 mg/kg 嗎啡IM (或Iv) 迅速地非常慢慢地達到最初的治療血液水平。

·         嗎啡是輕敏感的。  確定注射器或IV 袋子被蓋保護嗎啡免受光當使用長期嗎啡CRIs 。

·         2 到6 ug/kg/min = 0.002 到0.006 mg/kg/min 。

LIDOCAINE (20 mg/ml) - 10 到50 ug/kg/minute (0.6 到3.0 mg/kg/hr) 。

·         最初1 mg/kg IV 一小團被給迅速地達到最初的治療血液水平。

·         假使的2% lidocaine 的容量這是, 稀釋劑的相似的容量應該被去除 在 所有其它藥物增加之前。

·         Lidocaine 是輕敏感的也是。確定注射器或IV 袋子被蓋保護lidocaine 免受光當使用長期lidocaine CRIs 。

·         10 到50 ug/kg/min = 0.010 到0.050 mg/kg/min 。

  

總說明

·         所有三種藥物定期地被使用在狗和在任一個組合。

·         貓- 對 嗎啡的 定期用途CRIs 在貓不是共同。但這可能是一個有效的選擇如果似貓的患者嚴密被監測為dysphoric 趨向。總開始在opiod CRI 藥量範圍的末端。

·         貓- 直到更多資料被獲得, lidocaine 的用途在貓無法被推薦的 歸結於潛在的毒力問題。如果它被使用在貓, 不要超出10 ug/kg/minute, 和仔細地監測為奪取活動和心臟病反常性(心跳緩慢) 。10 ug/kg/min = 0.010 mg/kg/min 。

·         它是共同使用一個ketamine 唯一CRI 袋子在幾名患者, 交換IV 引伸線在患者之間。當嗎啡增加來CRI, 袋子致力那名唯一患者。數量嗎啡被勾畫和數額未使用仔細地被記錄在受控藥物日誌。

·         Ketamine/morphine/saline 解答證明是穩定的至少4 天。

·         D5W 並且其它流體是可接受的稀釋劑。

  

  

  


例子似貓或似犬KETAMINE 食譜

  

T他簡單的食譜根據10 到20 ml/kg/hr 的定期支援可變的率。

這是被推薦的開始的食譜為那些新對CRI 鎮痛藥。

以下食譜可能被使用在狗和貓。   

  

KETAMINE: 增加60 毫克ketamine (0.6 機器語言) 來1000 機器語言流體

·         交付以正常麻醉支援可變的率的10 ml/kg/hr = 10 ug/kg/min 或0.6 mg/kg/hr 。

·     這份食譜假設, ketamine 集中是100 mg/ml

  

總說明

·         率可能被加倍對20 ml/kg/hr 交付20 ug/kg/min 或1.2 mg/kg/hr 。

·         如果更高的可變的率是需要的, 增加第二條可變的線適應患者的需要。

·         記住裝貨藥量要求被選派以上。   

  

  


例子似貓或似犬MK 食譜

  

T他簡單的食譜根據最後的dilution/kg/hr 流體率的一1 機器語言。

以下食譜可能被使用在狗和貓。


  

KETAMINE: 60 mg/500 機器語言= 0.6 ml/500 機器語言 稀釋劑 = 1.2 ml/1000 機器語言 稀釋劑

·         交付以1ml/kg/hr 可變的率= 2 ug/kg/min 或0.12 mg/kg/hr   

·      這份食譜假設, ketamine 集中是100 mg/ml

嗎啡: 60 mg/500 機器語言= 4 ml/500ml = 8 ml/1000 機器語言

·         交付以1ml/kg/hr 可變的率= 2 ug/kg/min 或0.12 mg/kg/hr   

·      這份食譜假設, 嗎啡含量是15 mg/ml

  

總說明

·         它容易然後輸入患者的重量(在公斤) 在注入泵浦為適當的最初的可變的率。

·         狗- 可變的率可能被增加由3 ml/kg/hr 決定沒有超出劑量指南為或者藥物。

·         貓- 可變的率被增加由3 ml/kg/hr 決定但也許導致不需要的煩躁不安在醒的似貓的患者。嚴密監測得和減少率如果煩躁不安發生。

·         用嗎啡替代芬太奴在藥量equipotent 對嗎啡藥量上面增加:

.         芬太奴(0.05 mg/ml): 0.6 mg/500 機器語言= 12 ml/500 機器語言稀釋劑= 24 ml/1000 機器語言稀釋劑。

.  交付以1ml/kg/hr 可變的率= 0.02 ug/kg/min 或0.0012 mg/kg/hr

這         是的. 假使芬太奴的容量, 稀釋劑的相似的容量應該被取消 在 所有其它藥物增加之前。

.         為狗, 可變的率可能 被增加由3 ml/kg/hr 決定 依照被注意以上。

·         記住裝貨藥量要求被選派以上。


  



例子似犬MLK 食譜

  

T他簡單的食譜根據最後的dilution/kg/hr 流體率的一1 機器語言。

以下三種藥物可能被使用在任一個組合為狗。

為擅長CRI 計算器看支撐材料

  

KETAMINE: 60 mg/500 機器語言= 0.6 ml/500 機器語言 稀釋劑 = 1.2 ml/1000 機器語言 稀釋劑

·         交付以1ml/kg/hr 可變的率= 2 ug/kg/min 或0.12 mg/kg/hr   

·      這份食譜假設, ketamine 集中是100 mg/ml

嗎啡: 60 mg/500 機器語言= 4 ml/500ml 稀釋劑 = 8 ml/1000 機器語言 稀釋劑

·         交付以1ml/kg/hr 可變的率= 2 ug/kg/min 或0.12 mg/kg/hr   

·      這份食譜假設, 嗎啡含量是15 mg/ml

LIDOCAINE: 500 mg/500 機器語言= 25 ml/500 機器語言 稀釋劑 = 50 ml/1000 機器語言 稀釋劑

·         交付以1ml/kg/hr 可變的率= 17 ug/kg/min 或1.0 mg/kg/hr   

·      這份食譜假設, lidocaine 集中是20 mg/ml

  

總說明

·         請輸入患者的重量(在公斤) 在注入泵浦為適當的最初的可變的率。

·         不要忘記從稀釋劑袋子取消容量相等與lidocaine 容量 在 增加任何之前藥物對CRI 計劃。

·         記住裝貨藥量要求被選派以上。

·         狗- 可變的率可能被增加由3 ml/kg/hr 決定沒有超出劑量指南為任何藥物(不問藥物組合) 。

·         貓- 直到更多資料被獲得, lidocaine 的用途在貓無法被推薦的歸結於潛在的毒力問題。如果它被使用在貓, 不要超出10 ug/kg/minute, 和仔細地監測為奪取活動和心臟病反常性(心跳緩慢) 。

.         LIDOCAINE (20 mg/ml): 300 mg/500 機器語言稀釋劑= 15 ml/500 機器語言稀釋劑= 30 ml/1000 機器語言稀釋劑

.  交付以1ml/kg/hr 可變的率= 10 ug/kg/min 或0.6 mg/kg/hr

·         用嗎啡替代芬太奴在藥量equipotent 對嗎啡藥量上面增加:

.         芬太奴(0.05 mg/ml): 0.6 mg/500 機器語言= 12 ml/500 機器語言稀釋劑= 24 ml/1000 機器語言稀釋劑。

.  交付以1ml/kg/hr 可變的率= 0.02 ug/kg/min 或0.0012 mg/kg/hr

這         是的. 假使芬太奴的容量, 稀釋劑的相似的容量應該被取消 在 所有其它藥物增加之前。

.         為狗, 可變的率可能 被增加由3 ml/kg/hr 決定 依照被注意以上。







另外的CRI 藥物和藥量

  

芬太奴 - 0.02 到0.06 ug/kg/minute (0.0012 到0.0036 mg/kg/hr) 。

·         作用的  芬太奴的期間  是只大約30 分鐘。不受歡迎的作用不會徘徊只要當嗎啡、hydromorphone, 或oxymorphone 被使用

·         如果早先mu 苦悶者未被給, 執行0.003 mg/kg 芬太奴IM 或IV 迅速地達到最初的治療血液水平。

·         假使這是芬太奴的容量, 稀釋劑的相似的容量應該被去除 在 所有其它藥物增加之前。

·         0.02 到0 。06 ug/kg/min = 0.00002 到0.00006 mg/kg/min 。
A constant rate infusion (CRI) of analgesic drugs is a simple and effective means of improving patient comfort. Various formulations can be used as a constant rate infusion; the protocol chosen depends on the patient and the degree of pain experienced or anticipated. Some of the commonly used drugs include the following:

1) KETAMINE -- NMDA (N-methyl-D-aspartate) receptors are present in the dorsal horn of the spinal cord and certain areas within the brain. Intense and/or chronic noxious input to the dorsal horn cells (mediated principally by C-fibers) results in the removal of magnesium from the NMDA receptors and their activation by glutamate. This causes prolonged depolarization of spinal neurons (an increase in the magnitude and duration of neuron firing), which leads to an “amplification” of the pain response. This is a significant part of the process of central sensitization (an increase in the excitability of spinal neurons) and may result in hyperalgesia (an excessive response to a painful stimulus) and allodynia ( a painful response to a normally non-painful stimulus).

It is readily apparent that blocking (antagonizing) the NMDA receptors will help to minimize excessively painful responses. Additionally, studies suggest that antagonizing these receptors improves opioid receptor sensitivity, reduces opioid tolerance and minimizes the development of rebound hyperalgesia (the phenomenon of markedly increased pain when opioids are withdrawn).

Ketamine is the most commonly used antagonist of NMDA receptors in veterinary medicine. While its effects as a dissociative anesthetic at standard doses are well known, a new realm of activity occurs when it is delivered at sub-anesthetic doses. At constant rate infusion doses, ketamine blocks receptor activity without causing any dissociative or other adverse effects.

It should be noted that a microdose ketamine CRI should not be used as a sole means of analgesia. It is intended to augment other pain relievers, and should always be used in conjunction with opioids or other analgesics.

2) MORPHINE -- When combined with ketamine in a constant rate infusion, significant analgesia is achieved. The steady-state levels of morphine help to avoid some of the “peak and valley” effects seen with prn administration of opioids. Additionally, its use intraoperatively (as a “piggyback” onto anesthetic maintenance fluids) serves to reduce the amount of anesthetic gas required, which can be useful in decreasing the risk of hypotension.

It can be used in cats at the low end of the dosing spectrum (higher rates may induce significant dysphoria and excitation).

While other opiods can be substituted for morphine, we have elected to only include information for one other mu agonist, fentanyl, in the dosing information section. This reference is not intended to be an exhaustive review of all CRI options but to serve as a solid but basic reference for those adding CRI analgesia to their practice.

3) LIDOCAINE -- The addition of lidocaine has several benefits. For intractable/very severe pain, it adds to the analgesia and sedation. Lidocaine is reported to have some cytoprotective effects, such as weak calcium channel inhibition (which may be helpful in preventing reperfusion injury), and reduced neutrophil chemotaxis and platelet aggregation (which could help significantly in cases with the potential for DIC or SIRS, including GDV’s and splenectomies). Also, lidocaine has some activity in preventing ileus (potentially useful for enterotomies).

Various dosage rates of lidocaine have been advocated. In dogs, rates as low as 10 ug/kg/minute (0.6 mg/kg/hour) provide analgesia, though it may take up to 50 ug/kg/minute (3 mg/kg/hour) for the full cytoprotective and anti-ileus effects. Until further data is available, lidocaine’s use in cats cannot be recommended, due to the potential for toxicity, usually manifested as seizures and severe bradycardia.

   


CRI DOSING INFORMATION



KETAMINE (100 mg/ml) - 2 to 20 ug/kg/minute (0.12 to 1.2 mg/kg/hr).

·         An initial 0.25 to 0.50 mg/kg IV bolus is given to rapidly achieve initial therapeutic blood levels of the drug (while the CRI is intended to maintain, or very slowly, increase blood levels). Failure to administer this "loading" dose will result in an excessive delay in the drug reaching therapeutic levels.

·         Ket/val inductions and telazol inductions both provide adequate loading doses (tiletamine provides the same NMDA antagonism as ketamine).

·         2 to 20 ug/kg/min = 0.002 to 0.020 mg/kg/min.

MORPHINE (15 mg/ml) - 2 to 6 ug/kg/minute (0.12 to 0.36 mg/kg/hr).

·         If no previous mu agonist has been given, >><< rapidly achieve initial therapeutic blood levels.

·         Morphine is light sensitive.  Make sure the syringe or IV bag is covered to protect the morphine from light when using long-term morphine CRIs.

·         2 to 6 ug/kg/min = 0.002 to 0.006 mg/kg/min.

LIDOCAINE (20 mg/ml) - 10 to 50 ug/kg/minute (0.6 to 3.0 mg/kg/hr).

·         An initial 1 mg/kg IV bolus is given to rapidly achieve initial therapeutic blood levels.

·         Given the volume of 2% lidocaine this is, a similar volume of the diluent should be removed BEFORE any other drugs are added.

·         Lidocaine is light sensitive too. Make sure the syringe or IV bag is covered to protect the lidocaine from light when using long-term lidocaine CRIs.

·         10 to 50 ug/kg/min = 0.010 to 0.050 mg/kg/min.

  

GENERAL INFORMATION

·         All three drugs are used routinely in dogs and in any combination.

·         Cats - the routine use of morphine CRIs in cats is not common. But it can be an effective option if the feline patient is monitored closely for dysphoric trends. Always start at the low end of the opiod CRI dose range.

·         Cats - until more data is obtained, lidocaine’s use in cats cannot be recommended due to potential toxicity issues. If it is used in cats, do not exceed 10 ug/kg/minute, and monitor carefully for seizure activity and cardiac abnormalities (bradycardia). 10 ug/kg/min = 0.010 mg/kg/min.

·         It is common to use a ketamine only CRI bag over several patients, switching IV extension lines between patients. When morphine is added to the CRI, the bag is dedicated to that single patient. The amount of morphine drawn up and the amount unused is carefully recorded in the controlled drug logs.

·         Ketamine/morphine/saline solutions have been shown to be stable for at least 4 days.

·         D5W as well as other fluids are acceptable diluents.

  

  

  


EXAMPLE FELINE OR CANINE KETAMINE RECIPE

  

This simple recipe is based on routine supportive fluid rates of 10 to 20 ml/kg/hr.

This is the recommended starting recipe for those new to CRI analgesics.

The following recipe can be used in dogs and cats.   

  

KETAMINE: Add 60 mg ketamine (0.6 ml) to 1000 ml fluids

·         Deliver at normal anesthesia supportive fluid rate of 10 ml/kg/hr = 10 ug/kg/min or 0.6 mg/kg/hr.

·     This recipe assumes that the ketamine concentration is 100 mg/ml

  

GENERAL INFORMATION

·         Rate can be doubled to 20 ml/kg/hr to deliver 20 ug/kg/min or 1.2 mg/kg/hr.

·         If higher fluid rates are needed, add a second fluid line to meet the patient’s need.

·         Remember the loading dose requirement detailed above.   

  

  


EXAMPLE FELINE OR CANINE MK RECIPE

  

This simple recipe is based on a 1 ml of the final dilution/kg/hr fluid rate.

The following recipe can be used in dogs and cats.


  

KETAMINE: 60 mg/500 ml = 0.6 ml/500 ml diluent = 1.2 ml/1000 ml diluent

·         Deliver at 1ml/kg/hr fluid rate = 2 ug/kg/min or 0.12 mg/kg/hr   

·      This recipe assumes that the ketamine concentration is 100 mg/ml

MORPHINE: 60 mg/500 ml = 4 ml/500ml = 8 ml/1000 ml

·         Deliver at 1ml/kg/hr fluid rate = 2 ug/kg/min or 0.12 mg/kg/hr   

·      This recipe assumes that the morphine concentration is 15 mg/ml

  

GENERAL INFORMATION

·         It’s easy then to just enter the patient's wt (in kg) in the infusion pump for the proper initial fluid rate.

·         Dogs – fluid rates can be increased up to 3 ml/kg/hr without exceeding the dosage guidelines for either of the drugs.

·         Cats – fluid rates can be increased up to 3 ml/kg/hr but may cause unwanted dysphoria in awake feline patients. Monitor closely and reduce rate if dysphoria occurs.

·         To substitute fentanyl for morphine at a dose equipotent to the morphine dose above add:

§         FENTANYL (0.05 mg/ml): 0.6 mg/500 ml = 12 ml/500 ml diluent = 24 ml/1000 ml diluent.

¨  Deliver at 1ml/kg/hr fluid rate = 0.02 ug/kg/min or 0.0012 mg/kg/hr

§         Given the volume of fentanyl this is, a similar volume of the diluent should be removed before any other drugs are added.

§         For dogs, the fluid rate can be increased up to 3 ml/kg/hr as noted above.

·         Remember the loading dose requirements detailed above.
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