WikiVet English - User contributions [en]

Atrial Standstill

2016-06-25T21:08:37Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
Atrial standstill is the temporary or permanent '''lack of atrial activity''' resulting from a '''failure of atrial depolarisation'''. The ventricles still function normally.

==Aetiology==
The '''atrial muscle fails to depolarise''', despite the production of an impulse from the sinoatrial node. So instead impulses pass from the '''sinoatrial node''' to the '''atrioventricular node''' by '''internodal pathways'''. This produces a '''sinoventricular rhythm'''. This can be caused by '''electrolyte abnormalities''' (especially '''hyperkalaemia''' - which can develop secondary to a number of conditions including [[Hypoadrenocorticism|Addison’s disease]], [[Acute Renal Failure|oliguric renal failure]] and [[Urolithiasis|urethral obstruction]]), '''[[Cardiomyopathy|cardiomyopathies]], [[Muscular Dystrophy|muscular dystrophy]] (causing persistent atrial standstill - most commonly seen in the Springer Spaniel), and drug toxicity'''.

==Clinical Signs==
'''Heart sounds are normal''' on auscultation. As ventricular depolarisation occurs a '''normal pulse''' can be felt. It is common for the heart rate to be '''slow''', at less than 60 beats a minute in small animals.

==Diagnosis==
Diagnosis can be confirmed by '''[[ECG]]''' or '''fluoroscopy'''. With persistent atrial standstill cases, the heart rate will not increase upon administration of atropine. Underlying causes should be investigated, electrolyte abnormalities in particular.

===ECG===
An ECG should show an '''absence of P waves'''. '''Heart rate is regular''' but normally '''slow''', due to the presence of an '''[[Escape Rhythms|escape rhythm]]'''. The '''QRS complexes are normal or slightly wide'''.

It is important to have an artefact-free [[ECG]] of diagnostic quality to confirm atrial standstill.

==Treatment==
Treat the '''underlying cause'''. If this fails to resolve the condition or persistent atrial standstill is diagnosed a '''permanent ventricular pacemaker''' should be implanted.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Illustration/ill00875.asp ECG: persistent atrial standstill in canines]
|flashcards = [[Feline Medicine Q&A 01]] [[Small Animal Soft Tissue Surgery Q&A 08]]
}}

==References==
Gilson, SD (1998) '''Self-Assessment Colour Review Small Animal Soft Tissue Surgery''' '' Manson''

Martin, M (2002) '''ECG interpretation in small animals : 2. Abnormalities in the conduction system''' ''In Practice 2002 24: 194-20''

Sparks, AH & Caney, SMA (2005) '''Self-Assessment Colour Review Feline Medicine''' ''Manson''

{{review}}

{{OpenPages}}
[[Category:Impulse_Conduction_Abnormalities]]
[[Category:Cardiac Diseases - Dog]][[Category:Cardiac Diseases - Cat]]
[[Category:Expert Review]]
[[Category:Cardiology Section]]

Ventricular Tachycardia

2016-06-25T21:07:04Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==

'''Ventricular tachycardia''' (VT) is a '''rhythm disturbance''' classified as '''four or more [[Ventricular Premature Complexes|ventricular premature complexes]] (VPC's) in sequence''', producing a '''rapid''' heart rate. It is a serious condition which has the capability of causing '''[[Ventricular Fibrillation|ventricular fibrillation]]''' and '''sudden death'''. It most commonly occurs secondary to an existing systemic or cardiac abnormality. It is classed as a '''grade 4''' rhythm disturbance because it is '''electrically unstable''' and causes '''haemodynamic compromise'''.

==Small Animals==
It is particularly common in '''Dobermanns''' secondary to '''[[Dilated Cardiomyopathy|Dilated CardioMyopathy]]''' and in the '''Boxer''' secondary to '''Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)'''. The rhythm disturbance is much less common in cats and normally the result of end-stage cardiomyopathy.

===Causes===
* Significant '''structural damage to the heart, heart failure''' or a '''breed specific myopathy'''
* '''Systemic disease''' such as hypoxia, [[Anaemia|anaemia]], electrolyte and acid-base disturbances, [[Hyperthyroidism|hyperthyroidism]] (cats) etc.
* '''Drug reactions'''

===Clinical Signs===
On cardiac auscultation, '''heart rate is abnormally high''' (>160-180 in dogs). There may be signs of '''haemodynamic compromise''' and '''output failure''' such as collapse, hypotension, syncope and congestive heart failure. '''Sudden death''' may be the only presenting sign, especially in predisposed breeds.

===Diagnosis===
The condition can be diagnosed by '''[[ECG]]'''. The ECG shows''' wide and bizarre QRS complexes''' and '''P waves that are not consistently related''' to the QRS complexes. Heart rate is '''high (>160-180 in dogs)'''. QRS complexes can be '''monomorphic''' (similar in appearance with a regular R-R interval) or '''polymorphic''' (variable appearance and irregular R-R interval). A polymorphic appearance is suggestive of a more unstable myocardium. The P-P interval should be regular.

Sustained Ventricular Tachycardia lasts for more than 30 seconds, unsustained VT lasts less than thirty seconds.

===Treatment===
The underlying cause should be identified and treated where possible.

Treatment of the arrhythmia itself is always warranted because V-tach is classed as a grade 4 rhythm disturbance. The aim of treatment is to '''restore a normal sinus rhythm and reduce the ventricular rate''' thus improving cardiac output and preventing sinus arrest.

'''Dog:''' [[Local Anaesthetics|lidocaine]] (1st line of treatment), quinidine or procainamide (2nd line of treatment). Side effects of lidocaine include hypotension and gastrointestinal signs.

'''Cat:''' [[Heart Failure, Treatment|propranolol]] (1st line of treatment), small dose of lidocaine (2nd line of treatment). A high dose of lidocaine can cause neurotoxicity in the cat.

Following 1st line treatment, serum [[Potassium|potassium]] levels should be assessed and corrected if necessary.

===Prognosis===
Prognosis depends on the underlying cause of the arrhythmia and the success of its treatment.

==Large Animals==
Ventricular tacycardia is most likely to be diagnosed and treated in the '''horse'''.

===Causes===

VT normally occurs secondary to '''myocardial disease, endotoxaemia or electrolyte and acid-base abnormalities'''. It can also occur idiopathically.

===Clinical Signs===
Cardiac auscultation should reveal an '''abnormally high heart rate'''. There may also be a history of exercise intolerance and dyspnoea.

===Diagnosis===
The condition can be diagnosed by '''[[ECG]]'''. The ECG shows a '''fast heart rate with wide and bizarre QRS complexes''' and '''P waves that are not consistency related''' to the QRS complexes. QRS complexes can be '''monomorphic''' (similar in appearance with a regular R-R interval) or '''polymorphic''' (variable appearance and irregular R-R interval). A polymorphic appearance is suggestive of a more unstable myocardium. The P-P interval should be regular.

Sustained Ventricular Tachycardia lasts for more than 30 seconds, unsustained VT lasts less than thirty seconds.

===Treatment===
'''Exercise''' should '''not''' be continued whist the horse has VT.

If the cause is thought to be idiopathic then '''box-rest''' and '''steroids''' are the treatment of choice. Otherwise the treatment options are:

*Procainamide (in the conscious horse) or lidocaine (in the unconscious horse)
*Quinidine Gluconate
*Magnesium Sulfate supplementation

===Prognosis===
VT can progress to a '''fatal arrhythmia''' (ventricular fibrillation). Prognosis depends on the underlying cause of the arrhythmia and the success of its treatment.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02646.asp Ventricular tachycardia]
|flashcards = [[Small Animal Emergency and Critical Care Medicine Q&A 02]]
}}

==References==
Dennis, S (2011) '''Ventricular arrhythmias''' RVC Cardiology Elective Course, ''Royal Veterinary College''

Menzies-Gow, N (2001) '''ECG interpretation in the horse''' ''In Practice 2001 23: 454-45''

RVC staff (2009) '''Cardiovascular System''' RVC Intergrated BVetMed Course, ''Royal Veterinary College''

{{review}}

{{OpenPages}}

[[Category:Altered Ventricular Impulse Formations]]
[[Category:Expert Review]]
[[Category:Cardiology Section]]

Haemoabdomen

2016-06-25T21:03:48Z

Michuang0720:

==Description==
Haemoabdomen is defined by a fluid with a haematocrit greater than 10-15%. The cause may be iatrogenic, traumatic or toxic. The most common cause of spontaneous haemoabdomen is a bleeding neoplasm such as haemangiosarcoma or hepatocellular carcinoma.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Lab_test/lab00367.asp Effusion: overview]
}}

==References==
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.

{{unfinished}}
[[Category:Peritoneal_Cavity_-_Traumatic_&_Abnormal_Content]][[Category:To_Do_-_Alimentary]][[Category:To Do - Medium]]
[[Category:Peritoneal Cavity Diseases - Dog]][[Category:Peritoneal Cavity Diseases - Cat]]

Lipoma

2016-06-25T21:01:49Z

Michuang0720:

==Peritoneal==

*'''Lipomas''' - horses
**Arise from mesentery (particularly in horses), omentum (in dogs)
**Can become large and pedunculated (horses)
**May lead to strangulation of intestine
**On cut surface may become friable and necrotic with only the superficial surface remaining viable

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=lipoma Lipoma]
}}

[[Category:Peritoneal_Cavity_-_Neoplastic_Pathology]]

[[Category:Neoplasia]]

[[Category:Peritoneal Cavity Diseases - Horse]]

Mesothelioma

2016-06-25T21:01:03Z

Michuang0720:

[[Image:Peritoneal mesothelioma BioMed by King.jpeg|right|thumb|125px|<center>Peritoneal mesothelioma (Image sourced from BioMed Image Archive with permission)</center>]]

==Peritoneal==

*'''Mesotheliomas'''
**Malignant - implantation rather than metastasis
**Mainly cattle and dogs, occasionally in other species
**Can be congenital in calves
**Arise from serosa of pericardial, [[Pleural Neoplasia|pleural]] and [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavities]]
**Multiple small nodules, may be pedunculated, few milimeters to few centemeters, may present as villous projections
**May be associated with milky or bloody effusions
**Histologically usually appear similar to adenocarcinoma (papillary) or fibrosarcoma (spindle cells)
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=11611 Image of glandular type mesothelioma in a cat from Cornell Veterinary Medicine]

==Pleural==
*Has been found in cat, dog, cow, goat and horse
*Arise from pericardial, pleural and peritoneal surfaces
*May be related to inhalation of asbestos
*Grossly:
**Multiple discrete nodules
*Microscopically:
**Can appear as a carcinoma or fibrosarcoma depending on which tissue, covering or supporting, is predominant in the neoplasm
*Rarely metastasise but are considered malignant

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02568.asp Mesothelioma]
}}

[[Category:Peritoneal Cavity - Neoplastic Pathology]]
[[Category:Peritoneal Diseases - Cattle]][[Category:Peritoneal Cavity Diseases - Dog]]
[[Category:Neoplasia]]
[[Category:To Do - Minor]][[Category:To Do - Respiratory]][[Category:To Do - Alimentary]]

Peritonitis - Cats and Dogs

2016-06-25T21:00:09Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
'''Peritonitis''' is defined as inflammation of the [[Peritoneal Cavity - Anatomy & Physiology|peritoneum]]. The inflammatory response involves vasodilation, [[Exudate|exudation]] of protein-rich fluid, cellular infiltration, pain and, chronically, formation of fibrous adhesion. The disease can be classified into primary and secondary cases.

'''Primary peritonitis''' occurs spontaneously without any pre-existing pathological process in the abdomen. In cats, [[Feline Infectious Peritonitis |feline infectious peritonitis]] is the most common cause of primary peritonitis.

'''Secondary peritonitis''' occurs as the result of a pre-existing pathological process within the abdomen. It can be further classified into '''septic''' or '''non-septic''' peritonitis, where septic peritonitis results from direct bacterial infection of the peritoneal cavity. Septic peritonitis is the most common form in the dog and its causes include:
*'''Perforation of the gastro-intestinal tract''' due to foreign bodies, [[Intussusception|intussuscepta]], invasive [[Neoplasia - Pathology|neoplasia]], deep ulceration or dehiscence of surgical wounds or biopsy sites. Peritonitis as a result of wound dehiscence is most likely to occur 3-5 days post-operatively.
*'''Penetration of the abdomen''' by a stick, gunshot or other foreign body.
*Rupture of an infected uterus ('''pyometra'''), [[Biliary Tract Rupture|biliary tract]] or urinary tract.

The bacteria causing septic peritonitis or their products may spread systemically causing sepsis or endotoxaemia.

'''Non-septic''' peritonitis may occur due to the leakage of bile, urine or pancreatic enzymes ('''chemical peritonitis''') or due to the presence of foreign substances such as barium or glove powder ('''physical peritonitis'''). In some cases of urinary tract or biliary tract rupture however, septic peritonitis may occur if the tracts were previously infected.

==Clinical Signs==
The clinical signs are related to the presence of severe inflammation within the body cavity, with or without systemic infection.
*'''Abdominal pain''', manifesting as a reluctance to move due to inflammation of the parietal peritoneum.
*'''Depression''', anorexia and lethargy and non-specific signs of infection or systemic disease.
*[[Vomiting|'''Vomiting''']] and [[Diarrhoea|'''diarrhoea''']] may occur due to alterations in intestinal motility and functional ileus.
*'''Hypotension''' and (septic) [[Shock|'''shock''']] due to effusion of fluid into the peritoneum and systemic vasodilation.
*'''Hypothermia''' or '''hyperthermia'''.

==Laboratory Tests==
===Haematology===
As with any severe inflammatory process, '''leucocytosis''' will occur. Initially, this is caused by '''[[neutrophilia]]''' which may have a left shift or, if very severe, a degenerative right shift. Severe localised inflammation may stimulate a '''leukaemoid response''' with massive mobilisation of neutrophils from the bone marrow pools.

'''Haemoconcentration''' (causing a raised packed cell volume (PCV) and total protein concentration) may occur due to loss of extracellular fluid.

===Biochemistry===
'''Hypoproteinaemia''' may occur due to loss of plasma proteins into the inflammatory [[Exudate|exudate]].

'''Hypoglycaemia''' may occur in cases of septic peritonitis.

Dehydration (which is also responsible for the haemococentration) may also result in pre-renal [[Azotaemia|azotaemia]], increased tissue '''lactate''' production and '''metabolic acidosis'''.

'''Hypokalaemia''' may occur as a result of chronic vomiting and it may contribute to the intestinal ileus which often develops in cases of peritonitis.

==Diagnostic Imaging==
===Radiography===
'''Plain radiographs of the abdomen''' may reveal the presence of free gas in the abdomen ('''pneumoperitoneum''') due to intestinal perforation or bacterial production. The normal serosal detail may be effaced due to the presence of an abdominal effusion and, if a horizontal beam decubitus radiograph is made, a '''fluid line''' may be apparent.

In cases where neoplasia is thought to be the cause of the inflammatory process, thoracic radiograph should be assessed for signs of metastatic disease.

===Ultrasonography===
This modality has a high sensitivity for the detection of free fluid in the abdomen and it may be used to identify some specific causes of peritonitis, including abscesses of organs or [[Biliary Tract Rupture|rupture of the biliary tract]].

Ultrasound scans can also be used to guide '''abdominocentesis'''.

===Other Tests===
Free abdominal fluid can be collected under ultrasound guidance and submitted for cytological analysis. If fluid cannot be obtained on aspiration, '''diagnostic peritoneal lavage''' can be performed by instilling a small volume (~20 ml/kg) of warmed isotonic crystalloid into the abdomen, agitating the abdomen and then re-aspirating this fluid. Grossly, the fluid may contain vegetable fibres if the gastro-intestinal tract has ruptured or it may be evidently green (indicating the presence of bile) or haemorrhagic. On cytological examination, the sample should be assessed for the presence of neutrophils (and other leucocytes) with intracellular bacteria. If motile organisms are observed when examining your sample microscopically, this is a good indication that you have accidentally taken a sample of intestinal contents.

Further possible tests include:
*Measurement of '''amylase''' and '''lipase''' where the cause is suspected to be [[Pancreatitis|pancreatitis]]
*'''Bile''' where [[Biliary Tract Rupture|biliary tract rupture]] is suspected.
*'''Creatinine''' and '''potassium''' if the effusion is thought to be a uroabdomen; creatinine levels in a peritoneal sample that are higher than serum concentrations indicate uroperitoneum.
*'''Glucose''' and '''lactate''' should be measured; where their values are <2.8 mmol/l and >5.5 mmol/l respectively the inflammation is likely to be septic.
Lactate levels are indicative of a hypoxic crisis and levels are occasionally used as a prognostic indicator - rising levels in the face of vigorous treatment of peritonitis seem to be anecdotally more prognostically useful than absolute cut off values. NB. Measurement of lactate on some machines such as hand held blood gas analysers may require a heparin sample.
*Culture is indicated where a bacterial infection is suspected, and should include an anaerobic culture.

In cats with [[Feline Infectious Peritonitis]], the effusion usually has a high protein content (>35g/l) with a high globulin: albumin ratio. There is a variably high cellularity mainly composed of lymphocytes.

==Treatment==
It is vital to identify severe cases promptly as these will require emergency surgical intervention. Any of the following criteria is a major indication for surgery:
*Presence of intracellular bacteria in leucocytes in the abdominal exudate
*Pneumoperitoneum
*Presence of penetrating injuries to the abdomen.

===Medical Management===
====Fluid Therapy====
Aggressive [[Principles of Fluid Therapy|fluid therapy]] with [[Crystalloids|crystalloid]] and [[Colloids|colloid]] should be given on initial presentation to improve haemodynamic parameters and this should be maintained into the peri- and post-operative periods where appropriate and until the patient is normotensive. If the patient remains hypotensive, the use of a vasopressor such as [[Interventional_Agents#Dobutamine|dobutamine]], [[Interventional_Agents#Dopamine|dopamine]] or even [[Interventional_Agents#Vasopressin|vasopressin]] should be considered as animals in septic shock are likely to have systemic peripheral vasodilation.

Glucose and potassium should be supplemented where these parameters are found to be abnormal and, in cases of severe metabolic acidosis, the use of sodium bicarbonate may be considered. This product should be used with care as overdoses may result in overshoot metabolic alkalosis, tissue anoxia due to a left-shift of the haemoglobin-oxygen dissociation curve and paradoxical cerebral acidosis as carbon dioxide (not bicarbonate) crosses the blood brain barrier.

Septic peritonitis can cause [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]] which represents a very large therapeutic challenge. Plasma may be administered to replace used clotting factors and some authors advocate the use of low doses of heparin to prevent further coagulation.

====Antimicrobial Drugs====
Broad spectrum bactericidal antibiotics should be administered and, where possible, the choice of product should then be guided by culture and sensitivity of samples of peritoneal fluid. [[Escherichia coli|''Escherichia coli'']], [[:Category:Clostridium species|''Clostridium spp.'']] and ''[[Enterococcus faecalis]]'' are the species most commonly isolated in cases of septic peritonitis.

===Surgical Management===
Surgical intervention is indicated if the cause of peritonitis is undetermined or if it has been caused by intestinal rupture, intestinal obstruction or mesenteric avulsion. Abdominal lavage is a controversial procedure as it carries a risk of disseminating infection throughout the body and it is therefore indicated in cases of generalised peritonitis but should be used with care in cases of localised peritonitis. A volume of around 200 ml/kg fluid should be used to lavage the abdomen and as much of this fluid as possible should be re-aspirated as its continued presence will hinder the immune system by diluting bactericidal factor and preventing leucocyte migration.

It is beneficial to maintain peritoneal drainage after lavage by either '''open''' or '''closed''' drainage. Open drainage involves leaving part of the abdominal wall loosely sutured so that peritoneal fluid can leak out under gravity. The wound must be dressed under sterile conditions and there is a high risk of ascending infection and of continued protein loss with this technique.

Closed drainage involves implanting a drain into the abdomen (often a '''Jackson Pratt drain''') to which suction can be applied to aspirate fluid from the peritoneal cavity. The drain usually has multiple fenestrations along its length so that it does not become blocked by omentum or fat.

==Prognosis==
Guarded. Peritonitis is a multifactorial disease and the consequence is fatal in most cases. A rapid diagnosis and treatment may improve the prognosis but it is generally poor in cases of septic peritonitis.

{{Learning
|Vetstream = [https://www.vetstream.com/felis/search?s=peritonitis Peritonitis]
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28peritonitis%29+AND+od%3A%28cats%29+ Peritonitis in cats publications]

[http://www.cabdirect.org/search.html?q=title%3A%28peritonitis%29+AND+od%3A%28dogs%29+ Peritonitis in dogs publications]
}}

==References==
*Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) Elsevier Saunders Company
*Fossum, T. W. et. al. (2007) '''Small Animal Surgery (Third Edition)''' ''Mosby Elsevier''
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
*Tilley, L. P. & Smith, F. W. K. (2007) '''Blackwell's Five-minute Veterinary Consult: Canine & Feline (Fourth Edition)''' ''Blackwell Publishing''

For further information on peritonitis see the following In Practice article on SA Peritonitis: [http://inpractice.bvapublications.com/cgi/reprint/26/7/358 maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=haemoabdomen&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT]

{{review}}

{{OpenPages}}

[[Category:Peritoneal_Cavity_-_Inflammatory_Pathology]]
[[Category:Expert Review]][[Category:Peritoneal Cavity Diseases - Cat]][[Category:Peritoneal Cavity Diseases - Dog]]

Peritonitis

2016-06-25T20:59:36Z

Michuang0720:

See also: [[Peritonitis - Cats and Dogs|Peritonitis in Dogs and Cats]]

==Introduction==
Peritonitis refers to [[Inflammation - Pathology|inflammation]] of the [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]] and it may occur in any of the domestic species. Peritonitis represents a considerable therapeutic challenge in any species and frequently carries a very poor prognosis.

==Classification==
Peritonitis may be classified in a number of ways depending on its '''cause''', the nature of the '''inflammatory [[Exudate|exudate]]''' formed, the '''extent''' of the disease and the '''chronicity''' with which it develops.

The inflammation may affect the entire peritoneal cavity ('''generalised''' or '''diffuse''') or it may affect just one part of the cavity ('''localised'''). The formation of fibrous adhesions in chronic peritonitis may isolate the inflammation in one particular area of the cavity.

Different pathological processes result in the formation of different types of inflammatory [[Exudate|exudate]] depending on the degree to which the peritoneal vasculature is damaged and on the types of leucocyte which migrate to the site of the inflammation. The following types of peritonitis are recognised based on the nature of the exudate:
*'''Sero-fibrinous''', as in Glasser’s disease (''[[Haemophilus parasuis]]'') in pigs
*'''Fibrinopurulent''', as with septic peritonitis due to gastro-intestinal perforation or systemic infections such as [[:Category:Pasteurella and Mannheimia species|pasteurellosis in sheep]]
*'''Purulent''', as with [[Rhodococcus equi|''Rhodococcus equi'']] in foals
*'''Haemorrhagic''', as with splenic rupture
*'''Granulomatous''', as with ''[[:Category:Nocardia species|Nocardia]]'' infection in dogs

Peritonitis may occur acutely or it may be a chronic process that reaches an advanced stage before it is diagnosed. In cases of '''acute''' peritonitis, there is likely to be an increased amount of fluid in the peritoneal cavity and roughening of serosal surface of the abdominal organs and [[Peritoneal Cavity - Anatomy & Physiology|parietal peritoneum]] due to the presence of fibrin. Cases of '''chronic''' peritonitis often involve fibrous adhesions between any of the abdominal organs and the omentum, mesentery or [[Peritoneal Cavity - Anatomy & Physiology|peritoneum]].

==Causes of Peritonitis==
Inflammation of the peritoneum may occur as a '''primary''' disease but it is more likely to be '''secondary''' to another pathological process. The inflammation may be '''septic''' if it involves a bacterial infection or it may be '''non-septic'''.

====Physical Peritonitis====
Substances such as '''barium''' contrast agent may cause inflammation if they are allowed to leak into peritoneal cavity. Barium may cause a potentially fatal haemorrhagic peritonitis. '''Glove powder''' from surgical gloves may incite a granulomatous peritonitis.

====Chemical Peritonitis====
Chemical peritonitis occurs when irritant fluids effuse or leak into the peritoneal cavity. [[Biliary Tract Rupture|Rupture of the biliary tract]] results in the leakage of '''bile''' into the abdomen. Initially, this causes few clinical signs but over time, it irritates the visceral and parietal peritoneum and causes them to become inflamed. If the biliary tract is infected at the time of rupture, a septic peritonitis may develop. The parietal peritoneum and abdominal organs are typically stained green by the presence of bile. An image of bile peritonitis in a cat is available [http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=3048 here].

Rupture of the urinary tract causes '''urine''' to spill into the abdomen producing a '''uroabdomen'''. As with bile, the urine irritates the peritoneum after 48-72 hours and causes inflammation but it is likely that the animal will show marked clinical signs of stranguria, anuria and depression before this time. If the urinary tract is infected at the time of rupture, a septic peritonitis may develop.

In small animals with '''[[Pancreatitis|pancreatitis]]''', pancreatic enzymes may leak into the abdomen together with discharge from the necrotic peripancreatic fat. This usually results in a local peritonitis in the cranial abdomen and the animal may show signs of pain when this area is palpated.

[[Chylous Effusion|Chyle]] may cause a mild granulomatous serositis if it accumulates in the abdomen.

====Bacterial Peritonitis====
[[Image:Tubeculous peritonitis.jpeg|thumb|Tuberculous peritonitis with phagocytosis of lymphocytes Sourced from Bristol Biomed with permission]]
The main routes by which bacteria enter the peritoneal cavity are from the gastro-intestinal (GI) tract and from externally. '''Penetrating wounds''' to the abdomen and the introduction of '''foreign bodies''' are likely to introduce bacteria.

GI bacteria may enter the peritoneal cavity after perforation or rupture of the intestine. This may occur due to erosion of the intestinal wall by ulcers or neoplasia or due to rupture after a loop of intestine is strangulated. Rectal tears of the higher grades in horses may also lead to the introduction of bacteria.

Rupture of other infected tracts (including the urinary tract, reproductive tract and biliary tract) may also cause septic peritonitis.

In immature animals in whom the '''umbilicus''' has not fully closed, peritonitis may occur due to ascending infections through this structure. Systemic infections may also enter the peritoneal cavity and cause septic peritonitis.

====Viral Peritonitis====
[[File:FIP Punktat.jpg|thumb|Image of the protein-rich effusion produced in cats with FIP Copyright Kalumet 2006 Wikimedia Commons]]
The 'wet' or effusive form of [[Feline Infectious Peritonitis|'''feline infectious peritonitis''']] is caused by pyogranulomatous inflammation of the venules of the omentum and aprietal and visceral peritoneum. This vasculitis results in the effusion of sero-fibrinous fluid with a high protein and immunoglobulin content and tags of fibrin attach to the [[Peritoneal Cavity - Anatomy & Physiology|peritoneum]] and abdominal organs.

====Parasitic Peritonitis====
The migration of large '''stronglyes''' (particularly ''[[Strongylus vulgaris]]'' in the abdominal vasculature of horses may result in intestinal infarction and septic peritonitis. Severe signs of colic are usually the first sign of this syndrome which typically occurs in late winter/early spring.

The migration of the larvae of the '''liver fluke''' [[Fasciola hepatica|''Fasciola hepatica'']] may produce lesions around the liver that subsequently become inflamed producng a localised peritonitis. Sheep and cattle are most commonly infected by this trematode.

See also [[Peritoneal Cavity - Parasitic Pathology|'''Peritoneal Cavity - Parasitic Pathology''']]

==Consequences of Peritonitis==
Initially, the GI tract of affected animals is hypermotile but this quickly progresses to hypomotility and paralytic ileus. This hypomotility may be appreciable on auscultation in large animals in which borborygmi should normally be audible.

**Ileus - reduces distribution of exudates by intestinal motility
**Fibrinous adhesions may develop
*Impaired CV function and acid-base imbalance
**Due to sequestration of fluid and protein in exudate, hypomotile gut, bacterial exo/endotoxins absorbed directly from [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]] and causing vascular permeability, loss of intestinal absorption
*May resolve, become chronic-active or lead to adhesions.

==Peritonitis in the Domestic Species==
===Dogs and Cats===
See [[Peritonitis - Cats and Dogs]].

===Horses===
Diffuse acute septic peritonitis (as caused by rectal tears or GI rupture) is frequently fatal in horses and affected animals are often euthanased when after a diagnosis is made. Septic peritonitis occurs most commonly due to rupture of the strangulated loops of small intestine or rupture of a stomach distended by fluid refluxed from the duodenum. For an image of acute fibrinous peritonitis in a horse, see[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=6111|here].

In foals, purulent or granulomatous peritonitis may be caused by generalised [[Rhodococcus equi|''Rhodococcus equi'']] infection or fibrinous peritonitis by systemic ''[[Actinobacillus equuli]]'' infection.

Haemorrhage as a consequence of '''castration''' may result in acute non-septic peritonitis.

Peritonitis may also occur secondary to '''parasitic intestinal infarctions''' caused by ''[[Strongylus vulgaris]]'' but this is now rare in the UK due to widespread anthelmintic treatment.

===Cattle===
Peritonitis may occur due to traumatic or iatrogenic perforation of an abdominal organ, usually the [[Reticulum - Anatomy & Physiology|reticulum]] or [[Uterus - Anatomy & Physiology|uterus]]. This produces an acute diffuse fibrinopurulent peritonitis or, in some cases, the inflammation may be confined to a smaller area of the peritoneal cavity by the exuberant formation of fibrous tissue.

[[Traumatic Reticulitis|Traumatic reticuloperitonitis]] occurs when an ingested foreign body becomes lodged in the reticulum and subsequently perforates this organ. This usually produces a localised peritonitis between the reticulum and diaphragm but, in severe cases and in cows around parturition, generalised inflammation may develop. The foreign body me penetrate cranially through the diaphragm and into the pericardial sac. Potential sequelae include acute haemorrhage due to penetration of the left gastro-epiploic artery and vagal indigestion.

Local chronic peritonitis, abscesses containing usually ''[[Actinomyces pyogenes]]''

Other less common causes of peritonitis in cattle include:
*Fibrinopurulent peritonitis after umbilical infection in calves
*Fibrinous peritonitis in calves with septicaemic [[Escherichia coli|colibacillosis]]
*Serofibrinous peritonitis associated with sporadic bovine encephalomyelitis
*Diffuse fibrinohaemorrhagic peritonitis with clostridial haemoglobinuria caused by ''[[Clostridium haemolyticum]]''
*Localised peritonitis in [[Septicaemia and Enteritis, Bacterial|clostridial enterotoxaemia]] caused by [[Clostridium perfringens type B|''Clostridium perfringens'' type B]] and [[Clostridium perfringens type C|type C]] and [[Clostridium septicum|''Cl. septicum'']] ('''Braxy''')

===Sheep===
Fibrinopurulent peritonitis may occur in postpartum ewes that develop septic metritis due uterine contamination at parturition or retention of a lamb or a portion of the placenta.

Serofibrinous peritonitis may occur in diseases caused by [[:Category:Mycoplasmas|''Mycoplasma spp'']].

Peritonitis may also occur after penetration of the intestines by larvae of [[Oesophagostomum|''Oesophagostomum columbianum'']].

===Goats===
Acute fibrinous peritonintis may be caused by infection with [[Mycoplasma mycoides subsp. mycoides|''Mycoplasma mycoides'']].

===Pigs===
Diffuse fibrinopurulent peritonitis may occur with severe systemic infections of ''[[Actinomyces pyogenes]]'', [[Escherichia coli|''Escherichia coli'']] or other bacterial organisms.

Serofibrinous peritonitis occurs in '''Glasser’s disease''' caused by ''[[Haemophilus parasuis]]'' as part of a more severe polyserositis affecting the pleural cavity, pericardium and synovial spaces. Serofibrinous peritonitis may also be caused by infection with [[:Category:Mycoplasmas|''Mycoplasma spp'']] or septicaemias caused by ''[[Streptococcus suis]]'' type 2.

Acute gelatinous haemorrhagic peritonitis may occur as part of a systemic disease caused by ''[[Bacillus anthracis]]'' ('''Anthrax''')

{{Learning
|Vetstream = [https://www.vetstream.com/felis/search?s=peritonitis Peritonitis]
|flashcards = [[Cytology Q&A 15]]
}}

== References ==

The following images are available: [http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=1262 Image of acute fibrinous peritonitis from Cornell Veterinary Medicine] [http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=11598 Image of FIP by Cornell Veterinary Medicine]

{{unfinished}}
[[Category:To_Do_-_Alimentary]][[Category:To Do - Major]] [[Category:Peritoneal_Diseases_-_Cattle]] [[Category:Donkey]] [[Category:Peritoneal_Diseases_-_Sheep]] [[Category:Alimentary_Diseases_-_Goat]] [[Category:Alimentary_Diseases_-_Pig]] [[Category:Alimentary_Diseases_-_Birds]] [[Category:Peritoneal_Cavity_-_Inflammatory_Pathology]] [[Category:Peritoneal_Cavity_Diseases_-_Horse]]

Steatitis

2016-06-25T20:57:49Z

Michuang0720:

{{OpenPagesTop}}
Also Known As: '''''Yellow Fat Disease'''''

==Introduction==
'''Steatitis''' is also known as ''''yellow fat disease''''. It occurs in many species including cats, reptiles and mink. It is not seen in ruminants.

The condition occurs in animals fed on a '''fat-laden diet''',''' high in polyunsaturated fat and low in tocopherols'''. This causes an '''[[Inflammation|inflammatory response]]''' of '''adipose tissue''' due to '''oxidative damage'''. [[Vitamin E Deficiency|Vitamin E deficiency]] is thought to contribute to the condition.

==Clinical Signs==
The animal normally presents with '''firm nodules in subcutaneous tissue''' that are '''yellow or orange in colour'''. Mink may also present with abnormal locomotion and sudden death.

==Treatment & Prevention==
The condition is '''vitamin E responsive''', therefore affected animals should be treated with oral or injectable vitamin E supplementation and fed on a '''low fat diet'''.

The condition is prevented by feeding an '''appropriate diet''' (low in polyunsaturated fat) and supplementing the diet with '''vitamin E'''.

==Prognosis==
If the condition is recognised when the signs are mild, then prognosis is good - with complete reversal of signs. More chronic lesions are harder to treat as they may be walled off by a dense capsule of fibrocollagenous [[Connective Tissue Histology resource|connective tissue]].

{{Learning
|Vetstream = [https://www.vetstream.com/felis/Content/Disease/dis02911.asp Skin: panniculitis]
|flashcards = [[Reptiles and Amphibians Q&A 05]]
}}

==External Links==
* [http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=595 Image of yellow fat disease in a cat from Cornell Veterinary Medicine]

==References==
Frye, FL & Williams, DL (1995) '''Self-Assessment Colour Review - Reptiles & Amphibians''' ''Manson''

Merck & Co (2009) '''The Merck Veterinary Manual''' (Ninth Edition), ''Merial''

{{review}}

{{OpenPages}}

[[Category:Peritoneal_Cavity_-_Degenerative_Pathology]]
[[Category:Alimentary Diseases - Cat]]
[[Category:Snake Diseases]]
[[Category:Expert Review]]
[[Category:Expert Review - Exotics]]

Transudate

2016-06-25T20:55:30Z

Michuang0720:

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==Introduction==
Transudates are a type of [[:Category:Effusions|effusion]] that has a low cellularity and a low protein content. Transudates occur due to imbalances in the [[Blood Pressure Physiology#Capillary Fluid Shift Mechanism |'''Starling forces''']], of which the two principal examples are hydrostatic pressure and plasma oncotic pressure (or colloid osmotic pressure). The following causes of transudate effusions are therefore recognised:
*'''Reduced plasma oncotic pressure''' may occur if plasma proteins are lost. Albumin contributes 75% of the total oncotic pressure so [[Hypoalbuminaemia|'''hypoalbuminaemia''']] is the major cause of transudate effusions.
*'''Increased hydrostatic pressure''' may occur with inappropriate activation of the renin-angiotensin-aldosterone system (RAAS), as in congestive heart failure and portal hypertension. Both diseases commonly result in high-volume ascites, although this is more often composed of a [[Modified Transudate|modified transudate]].

==Diagnosis==
===Clinical Signs===
Effusions may occur in any of the major body cavities, causing ascites, hydrothorax or pericardial effusion. '''Ascites''' is often of a high volume. An abdominal fluid thrill will often be palpable and the abdomen may appear to be grossly swollen.

'''Hydrothorax''' will cause coughing, tachypnoea and dyspnoea if severe. Dullness will be evident on thoracic percussion if a pleural effusion has developed and the heart sounds will be muffled on auscultation.

'''Pericardial effusion''' may be sufficiently severe to cause cardiac tamponade and right-sided heart failure. The heart sounds will be muffled on auscultation and there may be hepatojugular reflux, a jugular pulse or signs of left-sided forward failure. In horses and cattle, it is much more likely that '''ventral oedema''' will be observed in animals with liver failure (causing hypoalbuminaemia) or congestive [[Heart Failure|heart failure]].

===Diagnostic Imaging===
Effusions are easily diagnosed by '''ultrasonography''' and this modality may also be used to guide fine needle aspiration to obtain a sample of the fluid. Effusions also produce a distinctive pattern on '''plain radiographs''':
*With pericardial effusion, the heart may appear to be generally enlarged with a globular shape. There may be a crisp cardiac silhouette (as the heart is moving within a stationary bag of fluid) and a hypovascular lung pattern due to pulmonary underperfusion.
*With ascites, there is a loss of serosal detail due to the presence of fluid in the abdominal cavity. This appearance may also occur with large abdominal masses and in emaciated animals.
*With pleural effusions, the lung lobes are contracted and lobulation is evident. Areas of peripheral radio-opacity should be evident, especially peripherally in the chest.

===Cytology===
Definitive diagnosis of the type of effusion relies on collection of a sample and subsequent cytological analysis. A refractometer is frequently used to measure the specific gravity of the fluid. The following findings would be expected for a transudate:
{| cellpadding="10" cellspacing="0" border="1"
| Appearance
| Clear, colourless fluid
|-
| Specific gravity
| <1.018
|-
| Total protein
| < 25g/l
|-
| Nucleated cells
| <0.5 x 10e9/L, of which the most common are [[Mesothelial cells|mesothelial cells]], [[Macrophages|macrophages]] and low numbers of non-degenerate neutrophils.
|}

==Treatment==
In general, it is not advisable to drain effusions unless they are causing clinical signs as the procedures are invasive and drainage of large volumes of fluid will further deplete body protein reserves. Neverthless, pleural and pericardial effusions should be drained to stabilise an animal with dyspnoea or signs of heart failure.

The [[Hypoalbuminaemia|management of hypoalbuminaemia is discussed here]].

Inappropriate activation of the RAAS is best treated with the diuretic spironolactone (a potassium sparing diuretic) because this prevents aldosterone from acting on Na/K pumps in the distal convoluted tubules and collecting ducts of the renal nephrons. Frusemide (a loop diuretic) may be used later if aldosterone does not produce satisfactory results. The underlying cause of the increased hydrostatic pressure should also be addressed.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=transudate transudate]
|flashcards = [[Cytology Q&A 13]]
}}

{{review}}

{{OpenPages}}

[[Category:Effusions]]
[[Category:Expert_Review]]

Exudate

2016-06-25T20:54:27Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
An exudate is a type of effusion that has a high cell count and protein content. It is often associated with [[Inflammation - Pathology|inflammation]] in the body cavities because changes to the endothelium during this process allow protein-rich fluid to escape from the vasculature and because leucocytes migrate out to the site of disease. As with any type of inflammation, the exudate may occur in response to a bacterial infection ('''septic''') or it may be sterile ('''non-septic'''). The presence of infection and purulent material in the chest cavity is termed '''pyothorax'''. Commons causes of exudates are:
Septic exudates
*Pyothorax may be caused by:
**'''Penetrating wounds''' to the thorax, including bites, bullet wounds and stick injuries.
**'''[[Rupture of the Oesophagus]]'''.
**'''Migrating foreign bodies''', particularly grass awns in hunting dogs.
**Severe forms of '''bacterial pneumonia''' that break into the pleural cavity.
*Septic peritonitis may be caused by:
**'''Penetrating wounds''' to the abdomen.
**'''Rupture of the intestine''', spilling luminal contents into the peritoneal cavity. This may be caused by trauma, strangulation, obstruction, ulceration or deeply infiltrative neoplasia.
**'''Rupture of an infected uterus (pyometra)''' or pyosalpinx with discharge of pus from the fimbriae of the oviducts into the abdomen.
**'''Rupture of an infected urinary tract'''.
*'''Septic [[Pericarditis|pericarditis]]''', which is much more common in farm animals and leads to the production of a purulent [[Pericardial Effusion|pericardial fluid]].
Non-septic exudates
*In the abdomen, '''chemical peritonitis''' induced by the prolonged presence of urine or bile will lead to the conversion of a [[Modified Transudate|modified transudate]] into an exudate. Bile peritonitis is characterised by a distinctive green discolouration of the parietal peritoneum and abdominal organs.
*'''[[Pancreatic Necrosis, Acute|Acute necrotic pancreatitis]]''' is associated with necrosis of the peripancreatic fat and discharge of enzymes and other factors into the abdomen.
*'''Neoplasia''' may produce exudates if they have large necrotic portions.
*Infection with '''[[Feline Infectious Peritonitis|Feline Infectious Peritonitis Virus]]''' may cause the development of either an exudate or a modified transudate.

==Diagnosis==
===Clinical Signs===
Exudates may occur in any of the major body cavities. In the '''abdomen''', there may be signs of abdominal pain (due to the underlying cause of the effusion), an abdominal fluid thrill or a palpable mass. 
In the '''chest''', a pleural effusion (including pyothorax) may cause tachypnoea and dyspnoea if severe. Dullness will be evident on thoracic percussion if a pleural effusion has developed and the heart sounds will be muffled on auscultation. 
'''Pericardial effusions''' may be sufficiently severe to cause '''[[Cardiac Tamponade|cardiac tamponade]]''' and right-sided [[Heart Failure|heart failure]]. The heart sounds will be muffled on auscultation and there may be hepatojugular reflux, a jugular pulse or signs of left-sided forward failure. The exudate of a chronic septic pericarditis undergoes organisation and replacement with fibrous tissue which bridges the visceral and parietal pericardia. This results in a '''restrictive pericarditis''' with clinical signs similar to cardiac tamponade. Infections which penetrate deeply into the cardiac muscle may cause '''[[Myocarditis|myocarditis]]''' with disruptions of the normal conduction pathways and resultant dysryhthmias. 
Septic processes may be accompanied by more general signs of infection, including '''pyrexia''', depression, lethargy and anorexia. Highly inflammatory exudates may cause severe pain when they damage the parietal pleura or peritoneum. Affected animals may be reluctant to walk and will stand with a typical 'tucked-up' posture.

===Diagnostic Imaging===
Effusions are easily diagnosed by '''ultrasonography''' and this modality may also be used to guide fine needle aspiration to obtain a sample of the fluid. Effusions also produce a distinctive pattern on '''plain radiographs''':

With '''pericardial effusion''', the heart may appear to be generally enlarged with a globular shape. There may be a crisp cardiac silhouette (as the heart is moving within a stationary bag of fluid) and a hypovascular lung pattern due to pulmonary underperfusion.

With '''ascites''', there is a loss of serosal detail due to the presence of fluid in the abdominal cavity. This appearance may also occur with large abdominal masses and in emaciated animals. Pneumoperitoneum may occur if the gut has ruptured or, in the case of pancreatitis, there may be an area of localised peritonitis (resembling 'ground glass') in the cranial abdomen.

With '''pleural effusions''', the lung lobes are contracted and lobulation is evident. Areas of peripheral radio-opacity should be evident, especially peripherally in the chest.

'''Pyothorax''' may be diagnosed and treated by '''thoracoscopy''', the passage of an endoscope into the pleural space. This technique is especially useful in the detection of loculation, the formation of septa of fibrous tissue that divided the effusion into pockets of fluid.

===Cytology===
Definitive diagnosis of any effusion relies on collection of a sample and cytological analysis. A refractometer can be used to measure the specific gravity of the fluid. The following features are typical of an exudate:
{| cellpadding="10" cellspacing="0" border="1"
| Appearance
| Turbid or flocculent red, yellow or white (purulent) fluid
|-
| Specific gravity
| > 1.018
|-
| Total protein
| > 30g/L
|-
| Nucleated cells
| >3 x 10e9/L, mainly comprising non-degenerate or degenerate [[Neutrophils|neutrophils]], [[Macrophages|macrophages]], [[Lymphocytes - Introduction|lymphocytes]] or [[Eosinophils|eosinophils]] (with parasites)
|}

With a septic exudate, the neutrophils are more likely to be present and intracellular (phagocytosed) bacteria may be visible.

In '''horses''', enterocentesis (or paracentesis) is often performed as part of a [[:Category:Colic Diagnosis in the Horse|colic work-up]]. The following findings are considered to be abnormal and may lend support to a decision to manage the case surgically:
{| cellpadding="10" cellspacing="0" border="1"
| Appearance
| *Yellow/green fluid containing plant fibres suggests that the gut has ruptured, giving the horse a hopeless prognosis as endotoxic shock will develop very rapidly. *Blood-tinged fluid suggests that an area of the gut wall is compromised, probably due to ischaemia. Since it is a much more acute process, the appearance of the peritoneal fluid deteriorates more rapidly in horses with strangulations than in those with simple obstructions.
|-
| Total protein content
| >20 g/l
|-
| Total cell count
| >20 x 10e9, especially if degenerate neutrophils or bacteria are present.
|}

==Treatment==
Specific treatment is dependent on the cause of the effusion. For further details, see the following sections:
*[[Peritonitis]]
*[[Feline Infectious Peritonitis]]
*[[Pericarditis]]
*[[Pancreatitis|Pancreatitis]]
*[[Rupture of the Oesophagus]]

{{Learning
|Vetstream = [https://www.vetstream.com/felis/search?s=exudate Exudate]
|flashcards = [[Cytology Q&A 16]]
}}

{{review}}

{{OpenPages}}

[[Category:Effusions]]
[[Category:Expert_Review]]

Chylous Effusion

2016-06-25T20:53:23Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
[[File:Chyle.jpg|right|200px|thumb|<center>Chylous effusion (Courtesy of B. Stanikova)</center>]]
Chylous effusions are predominantly composed of chyle, the lymphatic fluid that flows through the lacteals of the small intestine and the thoracic duct in the chest. Effusions occur when the normal flow of lymph is disrupted, either by alterations in the pressure gradient between the lymphatic and systemic venous systems or by physical disruption of the lymphatic vessels. Chyle resembles milk and it is composed chiefly of fat globules (chylomicrons) with a high lymphocytic cellularity. The vast majority of chylous effusions occur in the chest (producing chylothorax) but chylous ascites may occur. The major causes of chylous effusions are:
*Reduction of the pressure gradient from the lymphatic system to the major veins
**'''Right-sided backward heart failure''' caused by [[Cardiac Tamponade|cardiac tamponade]], heartworm (''[[Angiostrongylus vasorum]]'' or ''[[Dirofilaria immitis]]''), [[Tricuspid Valve Dysplasia|tricuspid dysplasia]] or [[Cardiomyopathy|cardiomyopathy]].
**'''Intrathoracic masses''' impeding venous return to the heart. Commons types of mass are thymoma and thymic lymphoma.
*Direct disruption of lymphatic flow
**'''Rupture of the thoracic duct''' due to trauma or thoracic surgery
**'''Erosion of lymphatics''' by neoplasia. The most common tumours to cause chylothorax are lymphoma, mesothelioma and tumours of the chest wall (e.g., chondrosarcomas of the ribs).
**'''Lung lobe torsion'''
**'''[[Lymphangiectasia]]''' may produce chylothorax or chylous ascites. Lymphangiectasia may be intestinal, thoracic or generalised and all forms may cause chylothorax.
*'''Idiopathic''' chylothorax may develop, especially in Afghan hounds.

==Diagnosis==
===Clinical Signs===
Effusions may occur in the thorax and, occasionally, the abdomen. This causes:
*'''Ascites''', with which an abdominal fluid thrill will often be palpable and the abdomen may appear to be grossly swollen.
*'''Chylothorax''' causing coughing, tachypnoea and dyspnoea if severe. Dullness will be evident on thoracic percussion if a pleural effusion has developed and the heart sounds will be muffled on auscultation.

===Diagnostic Imaging===
Effusions are easily diagnosed by '''ultrasonography''' and this modality may also be used to guide fine needle aspiration to obtain a sample of the fluid. Effusions also produce a distinctive pattern on '''plain radiographs''':
*With ascites, there is a loss of serosal detail due to the presence of fluid in the abdominal cavity. This appearance may also occur with large abdominal masses and in emaciated animals.
*With pleural effusions, the lung lobes are contracted and lobulation is evident. Areas of peripheral radio-opacity should be evident, especially peripherally in the chest.

===Cytology===
Definitive diagnosis of the type of effusion relies on collection of a sample and subsequent cytological analysis. A refractometer is frequently used to measure the specific gravity of the fluid. The following findings would be expected for a chylous effusion:

{| cellpadding="10" cellspacing="0" border="1"
| Appearance
| Opaque, milky but may be stained with blood resulting in a 'strawberry milkshake' appearance
|-
| Specific gravity
| > 1.017
|-
| Total protein
| > 30g/l (variable)
|-
| Nucleated cells
| 1.5 - 20 x 10e9/L of which the majority are small [[Lymphocytes - Introduction|lymphocytes]], mature [[Neutrophils|neutrophils]] and variable numbers of [[Macrophages|macrophages]].
|}

===Other Tests===
'''Pseudochyle''' is a type of fluid which has the same milky appearance as chyle but is actually composed of cellular debris, cholesterol micelles and lecithin globulin complexes. Pseudochyle may represent an inflammatory or neoplastic process and, although rare in animals, it may be associated with [[:Category:Mycobacterium species|''Mycobacterium'']] infection. True chyle may be identified in the following ways:
*Chyle has a higher triglyceride concentration than plasma but a lower cholesterol concentration and it has a triglyceride: cholesterol ratio (C:T) of <1. Pseudochyle has a higher cholesterol concentration than plasma but a lower triglyceride concentration.
*When chyle is left to stand overnight, an upper 'cream' layer will become evident due to the presence of chylomicrons in the fluid, whereas pseudochyle will remain homogenous.
*The '''ether clearance test''', in which a drop of ether was added to chyle to dissolve the lipid component, is no longer considered to be a reliable test for chylous effusions.
*Sudan III stain may be used to identify lipid droplets

==Treatment==
Effusions should be drained if they are causing clinical signs (of dyspnoea with chylothorax) but otherwise should be left as drainage will deplete body protein reserves. The thoracic duct can be ligated to prevent the development of chylothorax but this is not always successful and it may be difficult to identify the vessel.

A '''low fat diet''' will reduce the production of chyle as fewer fat globules are absorbed in the small intestine and lymphatic flow is reduced. This is the same rationale for the use of a low fat diet in lymphangiectasia.

'''Rutin''' is a benzopyrone drug used for the treatment of lymphoedema in humans and it may have value in the management of chylothorax, if it can be obtained. It is thought to stimulate the phagocytosis of chylomicrons by tissue macrophages.

If a tumour is found to be causing the clinical signs, resection may be attempted.

{{Learning
|Vetstream = [https://www.vetstream.com/felis/search?s=chylous Chylous effusion]
|flashcards = [[Feline Medicine Q&A 11]] [[Small Animal Emergency and Critical Care Medicine Q&A 03]]
|literature search = [http://www.cabdirect.org/search.html?q=%22Chylous+Effusion%22 Publications involving chylous effusion]
}}

{{review}}

{{OpenPages}}
[[Category:Effusions]]
[[Category:Expert_Review]]

Exocrine Pancreatic Insufficiency

2016-06-25T20:50:51Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''EPI — Pancreatic Exocrine Insufficiency'''''

==Introduction==
'''Exocrine pancreatic insufficiency (EPI)''' is a syndrome characterised by insufficient secretion of digestive enzymes by the exocrine portion of the pancreas. Most commonly EPI occurs following the progressive reduction in pancreatic mass caused by pancreatic acinar atrophy or chronic pancreatitis. EPI may also occur secondary to excessive gastric acid secretion (excess acid affects the activity and production of the pancreatic enzymes) or severe protein malnutrition (decreased synthesis of pancreatic enzymes). Concurrent diabetes mellitus and pancreatic hypoplasia have also been documented as causes in the dog.

The Pancreas has a considerable functional reserve and a large proportion needs to be non-functional to show signs of EPI. In the dog EPI is mostly caused by [[Pancreatic Atrophy, Exocrine| Exocrine Pancreatic Atrophy]] or [[Pancreatic Atrophy, Exocrine|Pancreatic Acinar Atrophy (PAA)]]. In the cat EPI is usually associated with [[Pancreatitis|chronic pancreatitis]].

==Signalment==
EPI is most common in the dog, German Shepherd dogs and rough collies are over-represented. Many other breeds however can also be affected by EPI.

EPI can occur in cats as a result of [[Pancreatitis|chronic pancreatitis]] and also occasionally in calves with [[Pancreatic Hypoplasia|pancreatic hypoplasia]]. In contrast, '''horses''' with very little pancreatic tissue develop '''hypoinsulinism''' but rarely EPI.

<big>'''[[Exocrine Pancreatic Insufficiency - Dog|Exocrine Pancreatic Insufficiency in the dog]]

'''[[Exocrine Pancreatic Insufficiency - Cat|Exocrine Pancreatic Insufficiency in the cat]]</big>

{{Learning
|Vetstream = [https://www.vetstream.com/felis/search?s=exocrine Exocrine pancreatic insufficiency (EPI)]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Exocrine+Pancreatic+Insufficiency%22&occuring1=title&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&x=37&y=15&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Exocrine pancreatic insufficiency publications]
}}

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2)

Sturgess, K. (2003) '''Notes on Feline Internal Medicine''' Blackwell Publishing.

Tams, T.R. (2003) '''Handbook of Small Animal Gastroenterology''' (2nd edition) Saunders.

{{review}}

{{OpenPages}}

[[Category:Pancreas_-_Pathology]]
[[Category:Pancreatic Diseases - Cattle]]
[[Category:Expert_Review]]

Pancreatitis

2016-06-25T20:49:37Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
[[Image:Pancreatitis.jpg|right|thumb|200px|<center>Pancreatitis (Image sourced from Bristol Biomed Image Archive with permission)</center>]]
Pancreatitis occurs following activation of digestive enzymes within the [[Pancreas - Anatomy & Physiology|pancreas]] leading to autodigestion of the gland. Can be referred to as acute or chronic pancreatitis.

'''Acute''' pancreatitis is rapid onset inflammation of the pancreas with little or no pathological changes occurring post recovery. This may completely resolve or 'wax and wane' in the future.

'''Chronic''' pancreatitis is continued inflammation leading to irreversible pathological changes (fibrosis, atrophy) and possible decreases in function.

The specific cause is usually idiopathic but several risk factors exist including:

A '''Nutritional''' basis which refers to obesity, low protein and high fat diets, feeding of ethionine and hypertriglyceridaemia.

'''Drugs and toxins''' including L-asparginase, oestrogen, azathioprine, potassium bromide, furosemide, thiazide diuretics, salicylates, [[Tetracyclines|tetracyclines]], [[Sulphonamides|sulphonamides]], vinca alkaloids, zinc toxicosis, cholinesterase inhibitor insecticides, cholinergic agonist and hypercalcaemia.

'''Pancreatic duct obstruction''' which is caused by biliary calculi, sphincter spasm, duct wall oedema, duodenal wall oedema, neoplasia, parasites, trauma and iatrogenic reasons.

'''Duodenal juice reflux, pancreatic trauma, ischaemia and reperfusion''' which includes duodenal juice reflux into the pancreatic duct, surgical intervention, [[shock]], [[Regenerative and Non-Regenerative Anaemias|anaemia]], venous occlusion and hypotension.

'''Other''' risk factors include parasitic (babesiosis), viral, mycoplasmal, end stage renal disease, liver disease and auto-immune diseases.

Cats mainly suffer from mild chronic interstitial pancreatitis.

== Acute Haemorrhagic Pancreatitis ==

This term is often interchangeable with [[Pancreatic Necrosis, Acute|acute pancreatic necrosis]] or '''acute pancreatitis'''. The condition can be mild or severe, non-fatal or fatal. It usually occurs as a sudden onset condition, often after ingestion of a meal rich in fat, but this depends on what species the condition occurs.

The [[Pancreas - Anatomy & Physiology#Endocrine|Islets of Langerhans]] may become involved thus causing the signs if insulin insufficiency. Pancreatitis may be initiated by trauma which initiates the leakage of enzymes. It can also present as recurrent acute pancreatitis - repeated inflammation with minimal permanent pathology. In the disease process, proteolytic degradation of pancreatic parenchyma, vascular damage and haemorrhage occur as well as necrosis of fat by lipolytic enzymes in the pancreas and surrounding omentum. These changes are concentrated at the periphery of lobules and infiltration by leukocytes indicates inflammation. In mild cases oedema of the interstitial tissue occurs. In more severe cases the [[Pancreas - Anatomy & Physiology|pancreas]] is haemorrhagic and oedematous with greyish white areas of necrosis and this may be interspersed with normal parenchyma. The [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]] may contain blood-stained fluid sometimes with droplets of fat. Due to these large amounts of necrotic debris, infection by microorganisms from the [[Alimentary System Overview - Anatomy & Physiology|GIT]] is likely, causing abscesses.

=== Cats and Dogs===

See [[Pancreatitis - Cat]] and [[Pancreatitis - Dog]]

=== Other Animals ===

In '''horses''', necrosis and inflammation results due to migration of parasites, usually strongyle larvae, releasing pancreatic enzymes causing autodigestion. Destructive granulomatous pancreatitis is a part of multisystemic eosinophilic epitheliotrophic syndrome.

In '''pigs''' suppuration of the pancreas can occasionally arise as an extension from nearby infection, eg. peritonitis and perforated oesophageal ulcers.

== Chronic Interstitial Pancreatitis ==

Chronic pancreatitis often occurs following ongoing inflammation with progression to irreversible damage and impaired function. There is usually fibrosis and reduction in acinar mass. This condition can occur in all species as a consequence of obstruction of the pancreatic ducts, [[Vitamin A Deficiency|vitamin A deficiency]] may predispose to this. The condition is most common in the dog, but also in cat, horse and cattle. The [[Pancreas - Anatomy & Physiology#Endocrine|islets of Langerhans]] tend to be preserved. If chronic pancreatitis persisits it can lead to [[Exocrine Pancreatic Insufficiency]] (EPI). In cats, chronic pancreatitis can also lead to [[Diabetes Mellitus]] developing.

=== Cats and Dogs===

See [[Pancreatitis - Cat]] and [[Pancreatitis - Dog]]

=== Other Animals ===

'''In sheep'''

Necrosis of [[Pancreas - Anatomy & Physiology#Exocrine|exocrine pancreatic cells]] followed by fibrosis can be caused by zinc toxicosis. Focal pancreatitis may occur during [[Foot_and_Mouth_Disease|Foot and Mouth disease]] resulting in [[DM|diabetes mellitus]] during recovery.

'''In horses'''

Chronic pancreatitis can occur sporadically and is usually a consequence of [[Pancreas - Parasitic Pathology|parasitic migration]] or from ascending bacterial infection of pancreatic ducts. It can occur alongside '''chronic eosinophilic gastroenteritis''' and is usually clinically silent. Organ tends to be replaced by scar tissue.

'''In cattle'''

Focal pancreatitis may occur during [[Foot_and_Mouth_Disease|Foot and Mouth disease]] resulting in [[DM|diabetes mellitus]] during recovery. 

{{Learning
|Vetstream = [https://www.vetstream.com/felis/search?s=pancreatitis Pancreatitis]
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22pancreatitis%22%29+AND+%28od%3A%28cats%29+OR+title%3A%28dogs%29%29&fq=sc%3A%22ve%22 Pancreatitis in cats and dogs publications]
}}

{{Chapter}}
{{Mansonchapter
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761115_sample.pdf
|chaptername = Acute Pancreatitis
|book = Clinical Medicine of the Dog and Cat, 2nd edition
|author = Michael Schaer
|isbn = 9781840761115
}}

==References==

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) '''Bovine Medicine''' (Second edition), ''Blackwell Publishing''

Bertone, J. (2006) '''Equine Geriatric Medicine and Surgery''', ''Elsevier''

Blood, D.C. and Studdert, V. P. (1999) '''Saunders Comprehensive Veterinary Dictionary''' (2nd Edition), ''Elsevier Science''

Brown, C.M, Bertone, J.J. (2002) '''The 5-Minute Veterinary Consult- Equine''', Lippincott, ''Williams & Wilkins''

Cowart, R.P. and Casteel, S.W. (2001) '''An Outline of Swine diseases: a handbook,''' ''Wiley-Blackwell''

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat''' Volume 2 (Fifth Edition), ''W.B. Saunders Company''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2), ''W.B. Saunders Company''

Fossum, T. W. et. al. (2007) '''Small Animal Surgery''' (Third Edition), ''Mosby Elsevier''

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition),''' ''BSAVA''

Jackson, G.G. and Cockcroft, P.D. (2007) '''Handbook of Pig Medicine,''' ''Saunders Elsevier''

Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students University of Liverpool'''

Merck & Co (2008) '''The Merck Veterinary Manual''' ''Merial''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine''' (Fourth Edition) ''Mosby Elsevier''

Sturgess, K. (2003) '''Notes on Feline Internal Medicine''' ''Blackwell Publishing''

Tilley, L.P. and Smith, F.W.K.(2004) '''The 5-minute Veterinary Consult''' (Third edition) Lippincott, ''Williams & Wilkins''

{{review}}

{{OpenPages}}

[[Category:Pancreas_-_Inflammatory_Pathology]][[Category:Pancreatic Diseases - Dog]][[Category:Pancreatic Diseases - Cat]]

[[Category:Pancreatic_Diseases_-_Pig]] [[Category:To_Do_-_Review]] [[Category:Pancreatic_Diseases_-_Horse]][[Category:Pancreatic_Diseases_-_Sheep]]

Pancreatic Nodular Hyperplasia

2016-06-25T20:48:39Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
'''Nodular hyperplasia''' is seen as hard pale elevations of the exocrine tissue of the pancreas in older dogs, cats and cattle. It is of no clincal significance but must be distinguished from malignant neoplasia. It is a common incidental finding but the cause is unknown.

==Signalment==
Older dogs, cats and cattle.

==Diagnosis==
There are no adverse clinical signs associated with the condition, it is an incidental finding. Nodular hyperplasia can be distinguished from neoplasia by ultrasonography, radiography and biopsy. The gross appearance is of white lobules or plaques projecting from the surface which are usually firmer than normal pancreatic tissue and do not distort adjacent tissue and are non-encapsulated. The microscopic appearance is similar to the normal glandular tissue, with non-encapsulated aggregates of acinar cells.

{{Learning
|Vetstream = [https://www.vetstream.com/felis/Content/Disease/dis00188.asp Pancreas: neoplasia]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=pancrea*&occuring1=title&rowId=2&options2=AND&q2=nodular&occuring2=title&rowId=3&options3=AND&q3=hyperplasia&occuring3=title&x=42&y=10&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Pancreatic Nodular Hyperplasia publications]
}}

==References==
* Blood, D.C. and Studdert, V. P. (1999) '''Saunders Comprehensive Veterinary Dictionary (2nd Edition)''' ''Elsevier Science''

{{review}}

{{OpenPages}}

[[Category:Pancreas - Hyperplastic and Neoplastic Pathology]][[Category:Pancreatic Diseases - Dog]][[Category:Pancreatic Diseases - Cat]][[Category:Pancreatic Diseases - Cattle]]
[[Category:Expert_Review - Small Animal]][[Category:Expert Review - Farm Animal]]

Insulinoma

2016-06-25T20:46:55Z

Michuang0720:

{{OpenPagesTop}}

==Introduction==
[[Image:Islet cell tumour.jpg|right|thumb|100px|<center>Islet cell tumour (Image sourced from Bristol Biomed Image Archive with permission)</center>]]
'''Insulinomas''' are slow growing, well-encapsulated, functional tumours of the [[Pancreas - Anatomy & Physiology#Endocrine|beta cells]] of the pancreatic islets. They secrete inappropriately high amounts of [[Pancreas - Anatomy & Physiology#Insulin|insulin]], irrespective of the serum glucose concentration. They are often malignant, with a high metastatic rate to regional lymph nodes, [[Liver - Anatomy & Physiology|liver]] and omentum. 60% of insulinomas are carcinomas, which are more likely to be endocrinologically active whereas the others are adenomas.

Blood glucose concentration is normally maintained within a narrow homeostatic range because several tissues are able to use only glucose as an energetic substrate. These tissues are particularly affected by the hypoglycaemia which occurs with hyperinsulinaemia and they include neurones, blood cells, renal medullary cells and fibroblasts in healing wounds. The release of hormones antagonistic to insulin (such as glucagon, growth hormone, glucocorticoids and catecholamines) also contributes to the pathogenesis and clinical signs observed in animals with insulinoma.

==Signalment==
Insulinomas occur most commonly in middle-aged or older dogs of the larger breeds. There is no sex predilection and the condition occurs less commonly in cats. Older cattle may rarely develop insulin-secreting tumours.

==Diagnosis==
===Clinical Signs===
The following signs are related primarily to '''hypoglycaemia''' but the release of catecholamines during episodes of hypogylcaemia may be contributory:
*'''Collapse'''
*'''Seizures'''
*'''Muscle tremors and weakness'''
*'''Ataxia'''
*'''Lethargy and depression'''
*'''Exercise intolerance'''

These signs may be intermittent early in the course of the disease, but they become more frequent and sustained with time. In between hypoglycaemic episodes, the animals often appear to be normal. Hypoglycaemic episodes may occur shortly after feeding (as insulin secretion is stimulated) or a long time after feeding (as the animal cannot maintain its blood glucose in the acceptable range) and they may also be associated with exercise or excitement.

A presumptive diagnosis can be made on the basis of '''Wipple's triad''', which refers to the presence of:
*Clinical signs associated with hypoglycaemia
*Fasting hypoglycaemia
*Amelioration of clinical signs with the administration of glucose

===Laboratory Tests===
====Biochemistry====
*'''Hypoglycaemia''' which should be a persistent finding during fasting.
*'''Serum ALT and ALK''' are often elevated but the significance of these findings is not known.

====Other Tests====
*'''Serum insulin concentration''' is usually elevated in the face of profound hypoglycaemia, with an '''insulin: glucose ratio''' of >4.2 considered to be diagnostic for insulinoma.
*'''Serum fructosamine levels''' can also be assessed to gauge whether the animal has been persistently hypoglycaemic over the previous 2-3 weeks. A level <250-350 umol/l is suggestive of insulinoma

===Pathology===
Collection and examination of a biopsy is needed for definitive confirmation of the diagnosis. The following features may be identified: usually single, or less often multiple, small (1-3cm) spherical nodules, yellow to dark red, in one or more lobes.

Histologically, small islets of acinar tissue are sometimes present within the neoplasm.

Pancreatic beta cells can readily be identified using immunocytochemistry.

===Diagnostic Imaging===
====Radiography====
Thoracic radiographs may be used to identify any pulmonary metastases, but it is uncommon for insulinomas to metastasise to the lungs.

====Ultrasonography====
Occasionally, it may be possible to visualise the location of the neoplasm on the [[Pancreas - Anatomy & Physiology|pancreas]] as a hypoechoic nodule. However, this may not always be possible, especially if the tumour is very small. Metastases to [[Lymph Nodes - Anatomy & Physiology|lymph nodes]] and [[Liver - Anatomy & Physiology|liver]] can sometimes be identified but suspected hepatic metastases should always be biopsied.

==Treatment==
===Emergency Stabilisation===
In the event of a hypoglycaemic episode, a bolus of 50% dextrose solution should be given immediately by the intra-venous route. Glucose syrup can also be rubbed onto the gums of an affected animal or a meal could be provided and this approach may reduce the risk of rebound hypoglycaemia encountered with administration of 50% dextrose solution. Intra-venous fluid therapy can then be maintained using 2.5% dextrose solution.

===Medical Management===
This is suitable for patients in which surgery has been declined or when clinical signs recur after surgical treatment due to the presence of metastases. A suitable regime would include:
*'''Small and frequent meals''' (3-6 times/day) of with high fat and protein content and some complex carbohydrate.
*'''Exercise restriction'''.
*[[Steroids|'''Glucocorticoids''']] such as prednisolone prescribed to increase hepatic gluconeogenesis and to decrease cellular glucose uptake.
*'''Diazoxide''', an oral hyperglycaemic drug, used to inhibit pancreatic insulin secretion and tissue glucose uptake.
*'''Octreotide''', a somatostatin analogue which reduces the synthesis of insulin but which is rarely used for management of insulinomas.

===Surgical Management===
A '''partial pancreatectomy''' is suitable for patients with a solitary tumour and any suspected metastases may be removed or biopsied during the procedure. An intra-operative ultrasound scan can be performed if the mass is not evident when the pancreas has been exposed. Possible post-operative complications include:
*'''Persistent hypoglycaemia''', probably due to the presence of unidentified metastases.
*[[Pancreatitis|'''Pancreatitis]]''' or '''[[Diabetes Mellitus|Diabetes mellitus]]''' due to disruption to the pancreatic parenchyma during the procedure.
*'''Epilepsy''' and '''diffuse polyneuropathy''' due to chronic hypoglycaemia.
*'''Duodenal necrosis and perforation''' as the cranial pancreatico-duodenal artery may be disrupted when the right limb of the pancreas is dissected away from the duodenum.

==Prognosis==
This is related to the WHO stage of the tumour at diagnosis. An animal with a stage I and II neoplastic process could expect a median survival time of 18 months but this falls to only 6 months for an animal with stage III disease. Patients which undergo surgery to remove an insulinoma have a better prognosis than those treated medically but the condition will recur invariably after surgical removal. Those animals which show a recurrence of clinical signs after surgery may then be treated medically, an approach that produces a significant increase in median survival time (from approximately 2 years to 4 years).

{{Learning
|Vetstream = [https://www.vetstream.com/felis/Content/Disease/dis02122.asp Insulinoma]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=Insulinoma&occuring1=title&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&x=44&y=8&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Insulinoma publications]
}}

==References==
*Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition) ''W.B. Saunders Company''.
*Fossum, T. W. et. al. (2007) '''Small Animal Surgery (Third Edition)''' ''Mosby Elsevier''
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
*Polton, G. A., White, R. N., Brearley, M. J. and Eastwood, J. M. (2007) '''Improved survival in a retrospective cohort of 28 dogs with insulinoma''' ''Journal of Small Animal Practice'' 48:151-156 [http://www3.interscience.wiley.com/cgi-bin/fulltext/117961667/PDFSTART]

{{review}}

{{OpenPages}}

[[Category:Pancreas_-_Hyperplastic_and_Neoplastic_Pathology]][[Category:Endocrine_System_-_Pathology]]
[[Category:Neoplasia]][[Category:Pancreas_-_Hyperplastic_and_Neoplastic_Pathology]][[Category:Endocrine_System_-_Pathology]]

[[Category:Endocrine Diseases - Dog]][[Category:Neurological Diseases - Dog]][[Category:Pancreatic Diseases - Dog]]
[[Category:Endocrine Diseases - Cat]][[Category:Neurological Diseases - Cat]][[Category:Pancreatic Diseases - Cat]]
[[Category:Expert_Review]]

Exocrine Pancreatic Neoplasia - Dogs and Cats

2016-06-25T20:45:00Z

Michuang0720:

==Introduction==
Primary pancreatic tumours are rare (accounting for less than 0.5% of all cancers in the dog), however the pancreas is also a site for metastasis from particularly gastro-intestinal neoplasms. Primary tumours include:
* [[Carcinoma#Pancreatic|Carcinomas]]
* Adenocarcinomas
* [[Adenoma#Pancreatic|Adenomas]]

It is important to make the distinction between pancreatic neoplasia and [[Pancreatic Nodular Hyperplasia|pancreatic nodular hyperplasia]] which frequently occurs in older dogs and cats and is non-significant.

==Signalment==
[[Carcinoma#Pancreatic|Carcinomas]]:
* Usually female dogs with a mean age of 10 years
* Spaniels and Airedale terriers may have breed predispositions

<gallery>
Image:Cocker_spaniel.jpg‎|'''English Cocker Spaniel''' Ellen Levy Finch (2004) WikiMedia Commons

Image:Airedale_Terrier.jpg|'''Airedale Terrier''' Pleple2000 (2006) WikiMedia Commons
</gallery>
* Affected cats have a mean age of 12 years

==Description==
Aetiology is idiopathic. [[Adenoma#Pancreatic|Adenomas]], although they do not metastasise and are frequently small and focal, can compress the surrounding pancreas. [[Carcinoma#Pancreatic|Carcinomas]] are aggressive with local invasion of the stomach or duodenum and metastasis to the liver, regional lymph nodes (hepatic and splenic), lungs, periotoneal surface and other abdominal organs usually occurring prior to a diagnosis being reached. Other complications include blockage of the common bile duct and [[Exocrine Pancreatic Insufficiency|exocrine pancreatic insufficiency]]. [[Pancreatitis|Pancreatitis]] can also occur where pancreatic atrophy results in tumour necrosis and an inflammatory response.

==Diagnosis==
===Clinical Signs===
Non-specific including:
* Lethargy
* Weight loss - marked in cats
* Anorexia - marked in cats
* Vomiting
* Diarrhoea
* Constipation
* Abdominal pain/distension due to mass effect or abdominal effusions
* Jaundice - if biliary obstruction
* Alopecia - as a paraneoplastic syndrome, occurring ventrally, facially and on the limbs in cats with adenocarcinoma
Such signs may also occur with concurrent [[Pancreatitis|pancreatitis]]. Alternatively clinical signs may reflect those of metastatic disease.

===Physical Examination===
In cats, an abdominal mass may be palpable.

===Haematology and Biochemistry===
Potential abnormalities include:
* Mild anaemia
* Neutrophilia
* Elevated hepatic enzymes or bilirubinaemia - if there is cholestasis or biliary obstruction
* Hyperglycaemia - If there is concurrent beta cell destruction
* Hypokalaemia

===Plain and Contrast Radiography===
Plain abdominal radiography may reveal a mass or mottled appearance on account of local peritonitis. In addition, there may be diplacement of the descending duodenum and pylorus. Where there is peritoneal metastasis and effusion loss of serosal detail and increased radiodensity may be observed. Thoracic radiography is also advised for pulmonary metastases.

Positive contrast radiography can be used to evaluate gastric emptying which can be delayed with pancreatic neoplasia. Compression or invasion of the duodenum may also be seen.

===Ultrasonography===
Provides information on the extent of the tumour and its invasiveness. A guided fine needle aspirate may be taken at this time, however, cytological examination is often unrewarding as pancreatic tumour cells do not exfoliate well.

===Exploratory Celiotomy===
Excising the whole tumour if operable or taking a sample via shave biopsy or crush ligation allows histopathological confirmation.

==Treatment==
===Surgery===
Usually at the time of diagnosis adenocarcinomas have already metastasised or local invasion has already taken place. If metastasis has no yet occurred surgical resection may be attempted with care to avoid iatrogenic trauma to the vascular supply to the proximal duodenum and obstruction of the main pancreatic duct. Total pancreatectomy and pancreaticoduodenectomy (Whipple's procedure) are not advised. Tumours of the body or base of the pancreas are inoperable. Gastrojejunostomy (gastrointestinal bypass) may be performed for short term palliation. Small pancreatic adenomas may be removed via partial pancreatectomy.

===Chemotherapy===
Not recommended.

===Radiotherapy===
Not recommended.

==Prognosis==
Poor for adenocarcinomas on account of their invasiveness and early metastasis. Survival time is less than 1 year for such tumours regardless of treatment.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis01111.asp Pancreas: neoplasia of the exocrine pancreas (adenocarcinoma)]
}}

==References==
* Morris J, Dobson J (2001) Gastrointestinal Tract, in Small Animal Oncology, Blackwell Science, pp 140-142
* Liptak J. M, Withrow S.J, (2007), Cancer of the Gastrointestinal Tract, in Withrow and MacEwen's Small Animal Clinical Oncology, fourth edition, Eds Withrow S.J, Vail D.M, Missouri, Saunders Elsevier, pp 479-480
[[Category:Pancreas_-_Hyperplastic_and_Neoplastic_Pathology]][[Category:Pancreatic Diseases - Dog]][[Category:Pancreatic Diseases - Cat]]
[[Category:To_Do_-_Clinical]]
[[Category:Neoplasia]]

Cholelithiasis

2016-06-25T20:41:24Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''Biliary calculi — Gallstones — Gall Stones — Choleliths — Cholecystolithiasis — Choledocholithiasis'''''

==Introduction==
Cholelithiasis is rare but occurs in '''all animals'''.

Choleliths may be of '''minute size''', like grains of sand, or they may be '''large and solitary'''.

In dogs and cats, most stones consist of '''calcium salts and bilirubinate''' (pigment stones).

Stones vary in weight and fragility depending upon their composition. They are sometimes concentrically laminated and often faceted. They are composed of a varying mixtures of materials to include salts of bilirubin, calcium carbonate, calcium phosphate and glycoproteins.

When stones occur in the gallbladder this is called '''cholecystolithiasis''', and when they occur in the bile duct it is called '''choledocholithiasis'''.

==Pathogenesis==
Potential causes include:
:'''bile stasis'''
:'''cholecystitis'''
:'''change in bile composition'''

Stones can form in the absence of infection, but clinical disease usually results when the biliary system containing stones becomes infected or obstructed.

Dogs with pigment gallstones suffer from '''gallbladder inflammation and mucus hypersecretion''' from soluble factors in the bile that inflame the gallbladder wall.

==Clinical Signs==
Cholelithiasis is '''often asymptomatic'''.

Clinical disease presents as: '''[[jaundice]], vomiting, anorexia, weight loss and dehydration'''.

Signs may be mild, transitory or recurrent.

'''Acholic faeces''' indicate complete bile duct obstruction, which can lead to persistent abdominal pain.

==Diagnosis==
Cholelithiasis should be considered as a possible diagnosis if obstructive [[icterus]] is present.

'''Radiography''': will detect radioopaque calculi (50% at most)

'''Ultrasonography''': will detect radiolucent calculi and enables examination of the liver parenchyma.

'''Haematology and biochemistry''' reveal extrahepatic [[Biliary Tract Obstruction|biliary tract obstruction]]: raised AST and ALP, increased [[bilirubin]].

==Treatment==
Animals may need no treatment if they are asymptomatic.

'''Surgical removal''' is the treatment of choice for clinical cases.

'''Cholecystotomy or choledochotomy''' enable stone removal, but bile duct patency must be checked and is vital for a successful surgical outcome.

The treatment of choice is '''cholecystectomy''', as secondary changes of inflammation, fibrosis and necrosis of the gallbladder are common, and removing the gallbladder elimiates a potential source of disease and a reservoir for subsequent stone formation.

Bile should be '''cultured and antibiotic sensitivity testing''' should be performed to ensure adequate antimicrobial cover.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre60060.asp Gall bladder disease: overview] [https://www.vetstream.com/canis/Content/Illustration/ill80945.asp Cholelith picture]
|flashcards = [[Small Animal Soft Tissue Surgery Q&A 18]]
}}

==References==
Pasquini, C. (1999) '''Tschauner's Guide to Small Animal Clinics''' ''Sudz Publishing''

Slatter, D. (2002) '''Textbook of small animal surgery''' ''Elsevier Health Sciences''

Carlyle, T. (1997) '''Veterinary pathology''' ''Wiley-Blackwell''

Merck and Co (2008) '''Merck Veterinary Manual''' ''Merial''

{{review}}

{{OpenPages}}

[[Category:Gall_Bladder_and_Tract_-_Pathology]]
[[Category:Gall Bladder and Tract Diseases - Dog]][[Category:Gall Bladder and Tract Diseases - Cat]][[Category:Biliary Diseases - Cattle]][[Category:Biliary Diseases - Pig]]
[[Category:Expert_Review]]
[[Category:Liver Diseases - Horse]]

Biliary Tract Rupture

2016-06-25T20:39:39Z

Michuang0720:

{{OpenPagesTop}}
See also: '''[[Biliary Tract Obstruction]]'''

==Introduction==
Rupture of the biliary tract is a severe disease that results in localised or diffuse chemical [[Peritonitis|peritonitis]] as bile leaks into the abdomen. If the biliary tract is infected, the peritonitis will be septic from the outset. If the tract is not infected at the point of rupture, the peritonitis may still become septic as the presence of bile in the peritoneal cavity reduces the integrity of the gut mucosal barrier.

Biliary tract ruptures may occur:
*Secondary to [[Biliary Tract Obstruction|'''obstruction]] of the biliary tract'''.
*After '''blunt abdominal trauma''', with the common bile duct rupturing more frequently than the gall bladder.
*If the tract is eroded by a '''neoplasm'''.
*Secondary to severe inflammatory disease of the gall bladder, including '''cholelithiasis''' and '''ascending [[Cholecystitis|cholecystitis]]'''<ref>Brömel C, Léveillé R, Scrivani PV, Smeak DD, Podell M, Wagner SO. '''Gallbladder perforation associated with cholelithiasis and cholecystitis in a dog''' ''J Small Anim Pract. 1998 Nov;39(11):541-4.''</ref>.
*After '''gall bladder torsion'''<ref>Corfield GS, Read RA, Nicholls PK, Lester N. '''Gall bladder torsion and rupture in a dog.''' ''Aust Vet J. 2007 Jun;85(6):226-31.''</ref>.

==Signalment==
Shetland sheepdogs appear to be predisposed to gall bladder disease<ref>Aguirre AL, Center SA, Randolph JF, Yeager AE, Keegan AM, Harvey HJ, Erb HN. '''Gallbladder disease in Shetland Sheepdogs: 38 cases (1995-2005).''' ''J Am Vet Med Assoc. 2007 Jul 1;231(1):79-88.''</ref>.

==Diagnosis==
It is important that biliary tract rupture is diagnosed promptly as the peritonitis becomes more severe with time.
===Clinical Signs===
The affected animal may show few clinical signs initially besides [[Icterus|icterus]] and evidence of an [[Exudate|ascites]]. As chemical peritonitis develops, the animal may show signs of:
*'''Abdominal pain''' and reluctance to move
*'''Pyrexia''', anorexia and depression
*'''Shock''' and collapse
In cases of septic peritonitis, the animal may suffer from septic or endotoxic [[Shock|shock]].

===Laboratory Tests===
Analysis of blood samples may show evidence of an acute inflammatory response, with a neutrophilic '''leucocytosis''' and elevated fibrinogen. The neutrophilia may have a left shift or, in severe cases, it may have a degenerative right shift. Cases with a very marked inflammatory response may develop a '''leukaemoid response''' with mobilisation of very large numbers of neutrophils from the bone marrow pools.

'''Aspiration and cytological analysis''' of fluid from the abdomen will reveal it to be a form of [[Exudate|exudate]] with an evident green colouration. The fluid may contain mucinous or fibrillar material and it should be expected to have a bilirubin concentration at least twice that of serum<ref>Owens SD, Gossett R, McElhaney MR, Christopher MM, Shelly SM. '''Three cases of canine bile peritonitis with mucinous material in abdominal fluid as the prominent cytologic finding.''' ''Vet Clin Pathol. 2003;32(3):114-20.''</ref>.

===Diagnostic Imaging===
'''Plain radiographs of the abdomen''' may show evidence of an abdominal effusion with loss of serosal detail.

'''Ultrasonography''' may be used to detect the presence of free abdominal fluid and to guide fine needle aspiration. A scan may also reveal the site of the rupture.

===Other Tests===
As with other forms of peritonitis, '''diagnostic peritoneal lavage''' may be employed to reach a diagnosis in cases where free abdominal fluid cannot be easily aspirated. This procedure involves injecting a small volume (20 ml/kg) of warmed isotonic crystalloid solution and then re-aspirating this fluid. Cytological analysis of this fluid may then allow a diagnosis of (bile) peritonitis to be made.

Samples of peritoneal fluid should be submitted for bacterial culture and sensitivity to guide future antibiotic therapy.

==Treatment==
Where possible, urgent surgical intervention is indicated to repair the site of the rupture. Biliary re-routing procedures (such as cholecystojejunostomy) may be indicated in cases where the biliary tract is severely disrupted. The [[Peritonitis - Cats and Dogs#Treatment|bile peritonitis should be managed aggressively]].

==Prognosis==
The prognosis depends on the speed with which the condition is diagnosed and on whether the peritonitis is septic. In one study of cats and dogs, a mortality rate of 54% was reported and this represented those animals that had septic peritonitis<ref>Ludwig LL, McLoughlin MA, Graves TK, Crisp MS. '''Surgical treatment of bile peritonitis in 24 dogs and 2 cats: a retrospective study (1987-1994).''' ''Vet Surg. 1997 Mar-Apr;26(2):90-8.''</ref>.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre60060.asp Gall bladder disease: overview]
|literature search = [http://www.cabdirect.org/search.html?q=%28title%3A%28%22biliary+tract%22%29+AND+ab%3A%28rupture%29%29+ Biliary tract rupture publications]
}}

==References==
<references/>
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine (6th edition, volume 2)''' ''Elsevier Saunders''

{{review}}

{{OpenPages}}

[[Category:Gall_Bladder_and_Tract_-_Pathology]]
[[Category:Gall Bladder and Tract Diseases - Cat]][[Category:Gall Bladder and Tract Diseases - Dog]][[Category:Biliary Diseases - Cattle]][[Category:Biliary Diseases - Pig]]
[[Category:Expert_Review - Small Animal]]
[[Category:Liver Diseases - Horse]]

Biliary Tract Obstruction

2016-06-25T20:39:21Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''Extra-hepatic Biliary Tract Obstruction — EHBO

See also: '''[[Biliary Tract Rupture]]'''

==Introduction==
The biliary tract comprises the [[Gall Bladder - Anatomy & Physiology|gall bladder]], hepatic duct, common bile duct and the duodenal papilla onto which it opens. If any part of this tract is obstructed, the normal flow of [[Bile Formation|bile]] is interrupted resulting in [[Cholestasis, Molecular Pathogenesis|cholestasis]] and [[Icterus#Post-hepatic Jaundice|post-hepatic jaundice]]. If the obstruction is not relieved, the biliary tract may [[Biliary Tract Rupture|rupture]] to produce a chemical [[Peritonitis|bile peritonitis]].

The causes of biliary tract obstruction may be '''intraluminal''' or '''extraluminal''':

Intraluminal obstructions:
*'''[[Cholelithiasis|Choleliths]]''' ('gall stones') are much less common in animals than they are in humans. They are usually composed of bilirubin salts in dogs and calcium carbonate in cats, although they are very rare in the latter species.
*'''Gall bladder mucocoeles''' produce a kiwi sign on radiographs and may be a sequel to cystic mucinous hyperplasia of the gall bladder mucosa.
*'''Biliary neoplasia''', most commonly cholangiocellular cystadenoma (in cats) or carcinoma (in dogs).
*'''Aberrant migration of intestinal helminths''' may cause an obstruction if they enter the common bile duct. This has been reported with ''[[Ascaris suum]]'' in pigs and ''[[Parascaris equorum]]'' in horses and it may occur after these animals have been treated with an anthelmintic that causes spasticity of the parasite muscles.
Extraluminal obstructions:
*[[Pancreatitis|'''Pancreatitis''']] is the most common cause of obstruction in dogs. '''Pancreatic abcesses''' or '''neoplasia''' may also obstruct the flow of bile.
*[[Biliary Tract Rupture|'''Biliary tract rupture''']]
*'''Pyloric''' or '''duodenal mass'''
*'''Diaphragmatic rupture''' with herniation of parts of the liver may result in exertion of pressure on the biliary tract.
*'''Biliary pseudocysts''' are a rare cause of obstruction.

==Diagnosis==
The signs of biliary obstruction relate to the failure of bile to move into the small intestine and to the reduction in function of the hepatic monocyte-phagocyte system.

===Clinical Signs===
'''[[Vomiting]]''' and '''anorexia''' are the most common signs of biliary obstruction.

The failure to excrete [[Bilirubin|bilirubin]] results in an increase in the blood concentration of conjugated bilirubin. Beyond a certain level, this bilirubin stains tissues causing [[Icterus|jaundice]] which may be visible on the mucous membranes or sclera. Since bilirubin has a low renal threshold, high concentrations are found in urine, although bilirubinuria is not necessarily an abnormal finding in healthy animals.

Biliary obstruction results in a reduction in the normal function of the hepatic monocyte-phagocyte system (chiefly composed of Kupffer cells) and the absence of bile salts allows intestinal bacteria to proliferate. Affected animals are not able to remove bacteria from the portal blood with normal efficiency and they may suffer systemic bacterial infection, causing sepsis, polyarthritis, [[Endocarditis|endocarditis]], meningitis or uveitis.

The absence of bile salts in the gut results in fat maldigestion and '''steatorrhoea'''. [[Antibiotic Responsive Diarrhoea|Small intestinal bacterial overgrowth]] (SIBO) may develop over time as bacteria metabolise the additional substrate in the intestinal lumen. Bacteria convert fatty acids to hydroxy fatty acids that irritate the colonic mucosa and may cause diarrhoea. The failure to absorb fat may lead to deficiencies in the fat soluble vitamins (K, E, D and A) and in very severe cases, this may result in a coagulopathy due to poor production of vitamin K-dependent clotting factors.

===Laboratory Tests===
Cholestasis causes damage to the cells of the biliary tract and these may release the biliary tract enzymes '''ALP''' and '''GGT''' which can be measured in serum. Levels of hepatocellular enzymes (such as '''ALT''') may also become elevated if intra-hepatic cholestasis occur. [[Bilirubin|'''Hyperbilirubinaemia''']] and '''hypercholesterolaemia''' may also be detected.

If it can be assayed, '''[[Bilirubin|urobilinogen]]''' will be absent from the urine in cases of complete biliary tract obstruction. Bilirubin may be present in urine but this is not abnormal as it has a low renal threshold.

===Diagnostic Imaging===
'''Plain radiographs of the abdomen''' may show soft tissue masses associated with the region of the biliary tract or pancreas. Signs of pancreatitis (such as a ground glass appearance in the cranial abdomen and a 'hockey stick' duodenum) may also be evident. Choleliths may be visible as radio-opaque structures within the gall bladder and gall bladder mucocoele may resemble kiwi fruit.

'''Ultrasonography''' is a very useful technique in the diagnosis of EHBO as the distention of different parts of the biliary tract can be traced easily. Initially, only the gall bladder is distended (seen as a loss of an evident neck) but the hepatic duct may be seen to dilate after outflow has been obstructed for 3 days and the intrahepatic bile ducts after 7 days. The bile ducts may be dilated in '''[[Caroli Disease]]''' without obstruction but this is extremely rare. Many of the processes that might cause EHBO can also be diagnosed with ultrasound, including mucocoeles which have a striped appearance.

==Treatment==
The appropriate treatment depends on the cause of the obstruction. In cases where biliary obstruction is thought to be secondary to pancreatitis, medical management of this condition is indicated. In advanced cases, fibrosis and abscesses may form and surgical intervention may be warranted to re-establish bile flow. A temporary cholecystostomy tube may be used in cases that are not sufficiently stable to undergo abdominal surgery. The tube may be placed laparoscopically through the right body wall. As with a gastrostomy or cystostomy tube, ten days should elapse before the tube is removed to allow fibrous tissue to form around the tube tract, preventing subsequent leakage of bile.

Intraluminal obstructions such as choleliths can be removed surgically via a '''cholecystotomy''' (incision into the gall bladder) but, if stone is within the common bile duct and this is very dilated, a '''choledochotomy''' can be performed. Alternatively, the duodenal papilla can be catheterised and the cholelith can be flushed back into the gall bladder. If the duct is not dilated, strictures may occur if a choledochotomy is performed and the procedure is associated with higher rates of mortality in humans. The abdomen is entered via a midline coeliotomy and the gall bladder is exposed in its normal position between the quadrate and right medial lobes of the liver. A needle is inserted to aspirate bile (using a syringe or suction) and stay sutures are placed in the infundibulum and fundus of the gall bladder. The incision is made between these sutures and, after removal of any obstruction, it is closed with an inverting suture pattern. In cases of recurrent cholelithiasis, '''cholecystectomy''' is recommended. This involves mobilisation of the gall bladder from its fossa and ligation of the cystic duct and cystic artery with transfixing ligatures.

Palliative surgical intervention may be undertaken in cases with large masses that involve the biliary tract. In these cases, biliary re-routing procedures such as '''cholecystoduodenostomy''' or '''cholcystojejunostomy''' may be considered, where a stoma is created directly between the gall bladder and duodenum or jejunum, respectively. Cholejejunostomy is easier to perform as a loop of jejunum may be brought to the gall bladder but this results in discharge of bile further down the gastro-intestinal tract. It is highly advisable to refer animals to a specialist centre for any biliary tract surgery.

==Prognosis==
The prognosis depends on the cause of the obstruction but affected animals are often very ill.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre60060.asp Gall bladder disease: overview]
|literature search =
[http://www.cabdirect.org/search.html?q=%28title%3A%28%22biliary+tract%22%29+AND+ab%3A%28obstruction%29%29+OR+title%3A%28EHBO%29 Biliary tract obstruction publications]
}}

==References==
* Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''Elsevier Saunders''
* Fossum, T. W. et. al. (2007) '''Small Animal Surgery (Third Edition)''' ''Mosby Elsevier''

{{review}}

{{OpenPages}}

[[Category:Gall_Bladder_and_Tract_-_Pathology]]
[[Category:Gall Bladder and Tract Diseases - Dog]][[Category:Gall Bladder and Tract Diseases - Cat]][[Category:Biliary Diseases - Cattle]][[Category:Biliary Diseases - Pig]]
[[Category:Expert_Review - Small Animal]]
[[Category:Liver Diseases - Horse]]

Hydatid Cyst

2016-06-25T20:36:15Z

Michuang0720:

=== Prevalence in the UK: ===

*human: about 100 new cases of hydatidosis are diagnosed in Britain each year, with 5-10 fatalities occurring. Somw cases are contracted overseas, but endemic “hotspots” occur in Britain, particularly in parts of Wales and some Scottish islands.

*sheep: there is great regional variation. Up to 98% of slaughtered ewes are infected in some localities.

*horses and cattle: up to 10% are infected in some areas.

=== Epidemiology ===
''E. granulosus'' has a wide host range and displays great evolutionary plasticity – that is, strains with different biological properties develop readily, each adapted to a particular ecological niche. Extreme examples include dingo-wallaby, wolf-moose and hyena-human cycles. Two strains are recognised in Britain:

1) Dog-sheep strain: infective for cattle and human (not found in Ireland). Dogs become infected if a) fed infected offal, or b) by scavenging dead sheep in hills or on road-side. Sheep dogs are most likely to defaecate in fields around homestead – eggs deposited in faeces and spread across pasture by rain splash, insect activity etc. = sheep become infected when flock brought down for lambing, dipping etc. Humans are infected when eggs from dogs are accidentally ingested (this is normally the only route of infection for humans.

2) Dog-horse strain: more host-specific (in intermediate host) than sheep strain. The horse strain does occur in Ireland, but no human cases reported there – this provides circumstantial evidence that this strain may not be infective for humans. Hunt kennels have been particularly important in dissemination of the horse strain.

=== Principles of Control ===
''E. granulosus'' has been eradicated from New Zealand, but this took greater than 20years of intensive effort. Schemes are well advanced in several other countries, but not the UK. To make progress, the following steps must be implemented:

1) Define local epidemiology and collect base-line statistics

2) Registration of all dogs

3) Regular treatment of all dogs (initially at 6week intervals; praziquantel is currently the only suitable drug available – because it is the only drug that kills both adult and immature Echinococcus)

4) Intensive educational programme aimed at farmer and dog owner

5) Regular testing of all dogs to monitor progress and identify non-compliance (the old arecoline purge technique is being replaced by serology or copro-antigen detection)

6) Ensure dogs do not get access to raw offal: meat inspection; burial of carcasses

7) Boiling or freezing offal used for dog food

8) Legislation to enforce compliance

==Hepatitis==

*Hydatid Disease
*final host
**dog, fox, and other canids
*intermediate host
**sheep most commonly affected
**ox and horses
NB: can also affect man - zoonosis
*'''hydatids''' - the cyst form
**develops from the ova
**occur in the lung and [[Liver - Anatomy & Physiology|liver]]
**cysts are usually multiple
**5-10cm in diameter
**contain a clear fluid with numerous scolices or '''"hydatid sand"'''
**the small calcified lesions that are sometimes present in the [[Liver - Anatomy & Physiology|liver]] of sheep may represent degenerate hydatid cysts
**can be very prevalent in some geographical areas

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Bug/bug00007.asp Echinococcus granulosus]
}}

[[Image:Echinococcus cysts.jpg|right|thumb|100px|<center>Echinococcus cysts (Image sourced from Bristol Biomed Image Archive with permission)</center>]]

*The intermediate stage of ''Echinococcus granulosus'' can be found in the lungs of many species, most commonly in lungs of cattle and sheep
*They range in size up to 5-10 cm diameter and although of little clinical significance, are important as a zoonosis (can be upto football size in man) and because of carcass condemnation

==Learning Resources==
[[Hydatid Cysts in the Liver of a Horse video|View a video potcast]] about hydatid cysts in the equine liver
[[Category:Liver - Pathology]]
[[Category:To Do - Medium]]
[[Category:To Do - Alimentary]]

Amyloidosis

2016-06-25T20:33:53Z

Michuang0720:

==Introduction==
Amyloid infiltration occurs in all species - amyloid is an inert substance that becomes deposited under the endothelium and basement membranes of a variety of tissues, notably the renal glomeruli,
[[Pancreas - Anatomy & Physiology#Endocrine|Islets of Langerhans]] in the [[Pancreas - Anatomy & Physiology|pancreas]] and the [[Liver - Anatomy & Physiology|liver]] (between the sinusoidal reticulum and the hepatic cords).

==Causes==
May be a primary condition or appear secondary to some chronic tissue destructive process such as:
*an infectious process elsewhere in the body
*sustained antigenic stimulation, eg repeated injections with an antigenic substance or production of excessive antibody by leukocytes

==Gross Pathology==
Affected organs will apear:
*pale (greyish waxy appearance)
*enlarged with rounded edges
*firm
*very prone to rupture

====Microscopically====
*deposition of amyloid in the space of Disse (or perisinusoidal space) which is in the liver between the hepatocytes and a sinusoid.
*shows 'apple-green' fluorescence under polarised light after staining with Congo Red

==Arterial Dissemination==
Amyloid is an eosinophilic, homogenous, hyaline material. Due to its beta-pleated-sheet structure it is almost insoluble. Amyloid may be present in one of two forms:
*'''AA''': Serum amyloid A, alpha-2 globulin.
*'''AL''': Derived from immunoglobulin light chains.

Disease may be truly idiopathic (dogs and cats) or may be secondary to another disease process, often chronic inflammation or neoplasia. Chronic antigenic stimulation induces the overproduction of AA protein which may become deposited throughout the body.

Deposits can be found in:
*Renal vessels and glomeruli.
*Splenic white pulp.
*Space of Disse.
*Coronary arteries.
*Meningeal arteries.

Affected organs are non-functional and appear waxy and pale.

*Amyloid is an insoluble protein that can accumulate in the kidney and compress the glomerulus, interfering with its normal function.
*Hypoproteinaemia and nephrotic syndrome can result due to substantial protein loss in the urine.
*Causes can be idiopathic or associated with underlying chronic inflammatory conditions.
'''Gross pathology'''
*Kidneys are firm, enlarged, and pale. Affected glomeruli may be seen as yellowish spots in the cortex.
*Amyloid can be visualised by treating the freshly cut surface of the kidneys with iodine.

'''Histopathology'''
*Amyloid stains pink with congo red.
*Presence of a pink, homogenous material replacing the epithelium and endothelium of the glomerulus.
<center><gallery>
Image:Congo red.jpg|'''Amyloidosis Stained with Congo Red''' Susan Rhind, University of Edinburgh
Image:Amyloidosis_histology.jpg|'''Amyloidosis Histology''' Susan Rhind University of Edinburgh

</gallery></center>

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=amyloidosis Amyloidosis]
|flashcards=[[Vascular Pathology Flashcards|Vascular Pathology]]
}}

[[Category:Liver_-_Storage_Diseases]]

[[Category:Cardiovascular_System_-_Degenerative_Pathology]][[Category:Cardiovascular_System_-_Vascular_Pathology]][[Category:Arterial_Pathology]]
[[Category:Glomerular Disease]]
[[Category:To Do - Urinary]][[Category:Cardiology Section]]

Hepatic Neoplasia

2016-06-25T20:32:47Z

Michuang0720:

==Description==
Primary hepatic tumours are rare, accounting for less than 1.5% of all canine tumours and 1.0-2.9% of all feline tumours. However, the liver is a common site for the establishment of metastatic tumours due to its rich blood supply from the hepatic portal vein and hepatic artery. In dogs, hepatic neoplasia are 2.5 times more likely to be metastases than primary neoplasia whereas primary hepatobillary tumours are more frequent than metastatic tumours in cats.

Malignant tumours are more common in dogs but benign neoplasia are more common in cats. Primary tumours found in the liver include:
* [[Carcinoma#Hepatocytic|Hepatocellular carcinoma]] or [[Adenoma#Hepatocytic|adenoma]] (hepatoma)
* [[Carcinoma#Cholangiocellular|Cholangiocellular carcinoma]] or [[Adenoma #Cholangiocellular|cystadenoma]]
* Gall bladder carcinoma or adenoma
* [[Haemangiosarcoma|Haemangiosarcoma]]
* Mast cell tumour
* Hepatic carcinoids (neuroendocrine)
* Lymphoma

Care must be taken to distinguish between all hepatic tumours and [[Liver - Nodular Hyperplasia|'''benign nodular hyperplasia''']] which is frequently observed in older dogs. The most significant primary tumours in the dog are hepatomas, [[Carcinoma #Hepatocytic|hepatocellular]] and [[Carcinoma#Cholangiocellular|cholangiocellular]] carcinomas and hepatic carcinoids. [[Carcinoma#Hepatocytic|Hepatocellular carcinomas]] and [[Carcinoma#Cholangiocellular|cholangiocellular carcinomas]] are the most significant tumours to occur in cats.

==Signalment==
===Hepatocellular Tumours===
Hepatocellular tumours include [[Carcinoma#Hepatocytic|hepatocellular '''carcinomas''']] (HCC) and [[Adenoma#Hepatocytic|'''hepatomas''']]. HCC occurs more frequently in dogs but hepatomas are more common in cats. These are the most common primary liver tumour in dogs and the second most common in cats.

Male dogs over 10 years old are most frequently affected by HCC and the Miniature schnauzer breed may be predisposed to the disease. The metastatic rate of hepatocellular tumours depends on the nature of the mass, with massive tumours spreading at a rate of 0-37% and nodular or diffuse tumours metastasising in 93-100% of cases. The most common sites of metastasis are the regional lymph nodes (the hepatic and diaphragmatic nodes), the peritoneum and lungs. [[Adenoma#Hepatocytic|Hepatomas]]) are usually incidental findings but they may cause hypoglycaemia as a paraneoplastic syndrome.

===Cholangiocellular Tumours ===
Cholangiocellular tumours include bile duct '''carcinomas''' and '''adenomas'''. Bile duct carcinomas are the most common malignant hepatobillary tumours in cats and the second most frequent in dogs, with female animals possibly being predisposed. Intra-hepatic carcinomas are more frequent in dogs but in cats, it is unclear whether extra-hepatic masses occur more frequently or whether intra- and extra-hepatic masses occur with equal frequency.

Bile duct carcinomas are aggressive and they often metastasise to distant sites. In dogs, these metastases are most common in the regional lymph nodes and lungs but diffuse intra-peritoneal metastasis and carcinomatosis are more common in cats. Bile duct adenomas (also known as biliary or hepatobiliary cystadenomas) are common in cats, particularly in males. These tumours are generally insignificant unless they of sufficient size to compress surrounding soft tissue structures and cause [[Biliary Tract Obstruction|biliary tract obstruction]].

===Carcinoids===
Carcinoids are neuroendocrine tumours that usually occur in younger animals than do the other primary hepatobiliary tumours. Primary tumours are aggressive and often affect more than one liver lobe with frequent metastasis to the regional lymph nodes, lungs and peritoneum.

===Sarcomas===
The most common sarcomas encountered are [[Haemangiosarcoma|'''haemangiosarcomas''']] (HSA), '''leiomyosarcomas''' and '''fibrosarcomas'''. HSA is the most common hepatic sarcoma in cats whereas leiomyosarcomas are more common in dogs. These tumours are aggressive and metastasis to the spleen and lungs is frequently observed.

==Diagnosis==
Tumours are symptomatic in approximately 75% of dogs and 50% of cats and this is more likely to be the case with malignant neoplasia.
===Clinical signs===
Signs are usually non-specific or they may indicate a disease of the liver:
*'''Weight loss''', inappetance and lethargy.
*'''Polyuria''' and '''polydipsia'''.
*'''[[Vomiting]]'''
*'''[[Modified Transudate|Ascites]]''' due to the development of portal hypertension.
*'''Neurological signs''', including seizures, ataxia and weakness are not as common as the signs described above. They may be due to metastasis to the central nervous system, [[Hepatic Encephalopathy|hepatic encephalopathy]] or hypoglycaemia which can occur as a paraneoplastic syndrome.
*'''[[Icterus]]''' occurs particularly in dogs with extrahepatic cholangiocellular carcinomas and diffuse carcinoids.
*A '''cranial abdominal mass''' will be palpable in up to 75% of cats and dogs

===Laboratory Tests===
The results of blood samples are usually unremarkable but the following findings may be documented in affected animals:
*Mild '''non-regenerative anaemia''' of unknown cause. The anaemia may be caused by anaemia of chronic disease, inflammation, red blood cell sequestration and iron deficiency may play roles
*'''Leucocytosis''' resulting from the associated inflammation and necrosis that can occur with large liver masses.
*'''Thrombocytosis''', of which potential causes include production of thrombopoietin as a paraneoplastic syndrome, iron deficiency, production of inflammatory cytokines and presence of concurrent anaemia.
*Elevation in the blood levels of '''hepatic enzymes''' probably occurs due to hepatocellular damage or biliary stasis. The extent of the elevation is not proportional to severity of liver damage.
*'''[[Hypoalbuminaemia]]''' due to reduced hepatic synthesis of albumin.
*'''Hyperglobulinaemia''' due to a chronic inflammatory process.
*'''Hypoglycaemia''' can occur as a paraneoplastic syndrome where there is increased utilisation of glucose or increased production of hormones with insulin-like activity (such as the somatomedins or insulin-like growth factors).
*Elevated pre- and post-prandial '''[[Bile acids|bile acids]]'''
*[[Bilirubin|'''Hyperbilirubinaemia]]''' which may be sufficiently severe to cause [[Icterus|icterus]].

===Diagnostic Imaging===
====Radiography====
'''Plain radiographs of the abdomen''' may show hepatomegaly and rounding of the margins of the liver. With massive hepatic neoplasia, a cranial abdominal mass may be visible with displacement of the stomach caudally and laterally. Mineralisation of the biliary tree is occasionally observed in dogs with cholangiocellular carcinoma. Ideally, all three thoracic views should also be taken to assess for the presence of pulmonary metastases, although this finding is uncommon at the time of diagnosis.

====Ultrasonography====
An abdominal ultrasound scan is advised to evaluate the condition of structures surrounding the liver. It also allows classification of the mass as massive, nodular or diffuse. Doppler techniques can be utilised to assess the vascular structure of tumours and guided fine-needle aspirates or core biopsies can be taken at this time, although it is desirable to await the results of a coagulation profile before undertaking this procedure. It is traditionally stated that hepatic lymphoma produces a hyperechoic texture on an ultrasound scan.

====Advanced Imaging====
CT and MRI are more sensitive in detecting small lesions and confirming the relationship of the mass with surrounding tissues and vasculature. They may also be used to detect early metastases.

===Other Tests===
Cytological examination of ascitic fluid may reveal the presence of neoplastic cells. Effusions are usually [[Modified Transudate|modified transudates]] but [[Haemorrhagic Effusion|haemorrhage]] may indicate that the tumour has ruptured.

==Treatment==
===Surgery===
Surgical excision is advised for hepatic adenomas, bile duct adenomas and massive [[Carcinoma#Hepatocytic|hepatocellular carcinomas]]. Nodulectomy or lobectomy can be used for focal tumours involving only one or a small number of lobes. Diffuse tumours and widespread nodular disease carry a poorer prognosis and they have frequently metastasised by the time they are diagnosed.

===Chemotherapy===
This treatment modality is not recommended for primary hepatic neoplasia. Some metastatic sarcomas, such as [[Haemangiosarcoma|haemangiosarcomas]], may show some response.

===Radiotherapy===
This procedure is not undertaken as it involves irradiating the entire abdomen and some surrounding organs may show poor tolerance.

==Prognosis==
The median survival time for massive [[Carcinoma#Hepatocytic|hepatocellular carcinomas]] following surgery is approximately 1 year. Otherwise the prognosis is poor for other types of malignant and metastatic tumours. If successfully excised the prognosis for benign tumours is good.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis01101.asp Liver: neoplasia in canines] [https://www.vetstream.com/felis/Content/Disease/dis01101.asp Primary hepatic neoplasia in felines]
}}

==References==
* Morris J, Dobson J (2001) Gastrointestinal Tract, in Small Animal Oncology, Blackwell Science, pp 137-140

* Liptak J. M, Withrow S.J, (2007), Cancer of the Gastrointestinal Tract, in Withrow and MacEwen's Small Animal Clinical Oncology, fourth edition, Eds Withrow S.J, Vail D.M, Missouri, Saunders Elsevier, pp 483-489

{{Unfinished}}
[[Category:Liver_-_Proliferative_Pathology]]
[[Category:Neoplasia]]
[[Category:To_Do_-_Alimentary]][[Category:To Do - Major]]
[[Category:Liver Diseases - Dog]][[Category:Liver Diseases - Cat]]

Melanoma

2016-06-25T20:30:31Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
In the past, melanoma has been used to describe both the benign and malignant neoplasms. In general, '''melanocytoma''' is used to describe the benign neoplasm arising from melanocytes and '''melanoma''' is used synonymously with '''malignant melanoma'''.

Melanocytes are '''neuroectodermal cells''' and proliferations may arise from the '''epidermis, the dermis or the adnexa'''.

The link between UV-light radiation and the development of melanocytic tumours, which is seen in humans, has not been seen in domestic animals.

These tumours are most common in '''dogs, gray horses and miniature pigs'''. They are uncommon in goats and cattle and rare in cats and sheep.

==Melanomas in Dogs==
Melanocytomas are more frequent than malignant melanomas.

===Clinical Signs===
Melanocytomas are frequently found on the '''head and forelimbs''' of middle-aged and older dogs. There may be a predilection for males.

They appear as macules or patches, papules or plaques, or as elevated, occasionally pedunculated masses. Most have a pigmented surface.

Malignant melanomas are found in older dogs. The '''mucocutaneous junction''' of the lips, the '''oral cavity''' and the '''nail bed''' are the most common sites affected. They appear as raised, ulcerated nodules that are variably pigmented.

When present on the lip, the tumour may be pedunculated. When present in the nail bed, they appear as swelling of the digit, often with loss of the nail and destruction of bone.

===Diagnosis===
'''Cytology''' of the mass will help identify cells containing melanin granules or blue-green material consistent with melanin. It may be difficult to identify whether the cells are of epithelial or mesenchymal origin, and depending on the grade, the cells may appear poorly-differentiated.

Digit lesions may require '''radiography and a deep punch biopsy''' for diagnosis.

'''Staging''' of the tumour should be performed, and the regional lymph node sampled, as well as further abdominal and thoracic imaging to determine any metastatic spread, which is very common with malignant melanomas.

===Treatment===
Treatment of melanocytomas involves '''complete excision'''. The tumours are benign and this is curative.

Malignant melanomas are '''aggressive and have considerable metastatic potential'''. '''Complete excision''' is generally indicated, however this may be difficult if the tumour is very infiltrated into the tissue. Digit tumours require '''amputation''' and oral tumours may be treated by '''hemimandibulectomy'''.

Radiotherapy and chemotherapy have not been shown to be effective.

A '''vaccine''' has been developed which encourages the development of antigen and a T-cell response and has shown potential in treating the disease in some cases.

===Prognosis===
Lesions at the '''rostral end''' of the oral cavity show the best survival times.

Prognosis is generally '''poor''', with an overall survival time of less than a year.

==Melanomas in Horses==
They are mostly found in '''gray horses''', especially in Lipizzaners, Arabs and Percherons.

They begin their development when horses are 3-4 years old, but are usually recognised in '''older horses'''.

Most are '''benign''' but some invasive variants with metastatic potential exist.

===Clinical Signs===
Predilection sites include: the '''perineum and the base of the tail''', but they can also occur in other areas including the '''parotid gland'''.

The tumours are often multiple and appear as coalescent, pedunculated nodules. They increase in size and number over time.

===Diagnosis===
Most tumours are '''black''' on cross-section.

'''Cytology''' is helpful in identifying the tumour cells.

'''Regional lymph node involvement''' should be checked for, but there is a debate as to whether involvement represents metastasis or whether the intranodal melanocytes and melanophages represent a stimulation of extracutaneous melanocytes that are normally present in the lymph node.

===Treatment===
This consists of '''surgical or cryosurgical removal'''. Animals are predisposed to developing additional tumours over time.

'''Intra-lesional chemotherapy''' with cisplatin or carboplatin has been used after surgical debulking if the mass cannot be entirely removed.

==Melanomas in Pigs==
Melanocytic neoplasms of pigs are seen as '''congenital lesions and sporadically in adults''' of the Sinclair (Hormel) miniature pigs and Duroc and Duroc crosses.

===Clinical Signs===
These tumours can be found anywhere on the body. Generally multiple, they can appear as pigmented macules or patches with smooth borders, ulcerated pigmented lesions, or as deeper, slightly raised, blue masses. Deeply invasive melanomas are often associated with metastatic disease.

The lymph nodes and lungs are the most common sites of metastasis.

===Treatment and Prevention===
Not all of these tumors become invasive, and many undergo '''spontaneous regression''' associated with an intense lymphocytic infiltrate.

Melanocytic lesions in pigs are '''not treated'''. Prevention by '''selective breeding''' is recommended if lesions are frequently recognised in a herd.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=Melanoma Melanoma]
}}

==References==
Merck and co (2008) '''Merck veterinary manual''' ''Merial''

Meuten, D. (2002) '''Tumors in domestic animals''' ''Wiley-Blackwell''

Withrow, S. (2007) '''Withrow and MacEwen's small animal clinical oncology''' ''Elsevier Health Sciences''

{{review}}

{{OpenPages}}

[[Category:Expert Review]]
[[Category:Oropharynx_-_Pathology]]
[[Category:Liver, Secondary Tumours]]
[[Category:Dermatological Diseases - Dog]]
[[Category:Dermatological Diseases - Horse]]
[[Category:Dermatological Diseases - Pig]]
[[Category:Neoplasia]]

Sarcoma

2016-06-25T20:29:48Z

Michuang0720:

==Secondary Liver Tumours==

[[Image:sarcoma metastasis.jpg|right|thumb|125px|<center>'''Sarcoma metastasis'''. Courtesy of T. Scase</center>]]

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=sarcoma Sarcoma]
}}

[[Category:Liver,_Secondary_Tumours]]
[[Category:Neoplasia]]

Mast Cell Tumour

2016-06-25T20:28:45Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''Mastocytosis'''''

==Introduction==
[[Mast Cells|Mast cells]] are a cell population that '''originate in the bone marrow''' and mature in connective tissue.

Mast cell tumours are '''ubiquitous''' in domestic animal species. The tumours can be '''focal or multicentric in the skin''' and may occasionally involve '''internal viscera such as the spleen, liver and intestine'''.

==Canine mast cell tumours==
Mast cell tumours are the '''most common cutaneous tumour in the dog''', primarily a disease of older dogs. Boxers, Labrador Retrievers, Beagles and Schnauzers are reported to be predisposed.

'''Boxers are more predisposed''', but generally develop the low or intermediate grade forms of the disease which have a more favourable prognosis.

There is no gender predilection.

All tumours should be '''considered malignant''' as each tumour has metastatic potential.

===Clinical signs===
Mast cell tumours '''vary widely in appearance'''.

The most common gross appearance is a '''small, raised, well circumscribed mass''' that may be hyperaemic, alopecic, ulcerated or look like normal skin. They may also appear as a '''poorly-defined, soft, fluctuant lesion'''. The tumours may become quite large, up to 30 cm, or may occur as a '''diffuse, inflamed, dermal thickening'''.

They are more commonly found on the '''caudal half of the body'''.

'''Regional lymph node involvement''' is common, up to 75%, but widely disseminated metastasis is less common.

'''Clinical signs''' reflect the extent of systemic involvement and the presence or absence of paraneoplastic disorders. Signs vary from: pruritus and excoriation to nausea, vomiting, diarrhoea, melena, abdominal pain and microcytic, hypochromic anaemia.

More than 50% of patients with systemic mastocytosis have systemic signs, but it is rare for patients with cutaneous MCTs to have systemic signs.

The release of mast cell granule contents lead to: '''gastric ulceration, peritumour inflammation, cardiopulmonary abnormalities, prolonged bleeding and delayed wound healing'''.

Aggressive palpation of masses can lead to histamine release and '''immediate peritumour erythema, pruritus, oedema and swelling'''.

The '''metastatic pattern''' typically includes lymphatic spread to regional lymph nodes, spleen, liver and bone marrow.

===Diagnosis===
'''Cytological examination''' of the mass is usually sufficient to diagnose a mast cell tumour and should be performed before surgery in all cases.

Mast cell tumours have '''blue to purple granules''' which differentiate them from other round cell tumours.

'''Histology''' is necessary to confirm the diagnosis, to '''grade''' the tumour, and to determine that the surgical margins are free of mast cells.

There are three '''histological grades''' for mast cell tumours:
:Grade I: well-differentiated, mature cells
:Grade II: moderate or intermediate differentiation
:Grade III: poorly-differentiated, anaplastic cells

'''Clinical staging''' of the disease should also be performed as it is strongly associated with prognosis:

Modified World Health Organisation clinical staging format:
:Stage 0: one tumour incompletely excised from the dermis, identified histologically, without regional lymph node involvement
:Stage 1: one dermal tumour without regional lymph node involvement
:Stage 2: one dermal tumour with regional lymph node involvement
:Stage 3: multiple dermal tumours or large, infiltrating tumours with or without regional lymph node involvement
:Stage 4: any tumour with distant metastasis (including bone marrow) or recurrence with metastasis.
:a: no clinical signs
:b: clinical signs

All palpable lymph nodes should be sampled regardless of their size.

'''Abdominal palpation, radiographs and ultrasound''' will help determine the presence of an enlarged spleen or liver. Fine needle aspirates should be obtained from any enlarged organ.

'''Bone marrow aspiration cytology''' is also useful if bone marrow involvement is suspected.

'''Complete haematology and biochemistry''', urinalysis and faecal occult blood test should be performed to check for paraneoplastic syndromes and the animal's ability to withstand treatment.

===Treatment and prognosis===
The behaviour and response to treatment of mast cell tumours is often '''unpredictable'''.

'''Surgical excision''' is the treatment of choice where possible, usually Stage 1 tumours. Well localised tumours may be completely resected. '''Wide excision''' is necessary, with 3cm laterally and one fascial plane deep to the tumour.

All margins should be examined for residual tumour.

All incomplete surgical resections need additional local treatment. Either re-excision or radiotherapy should be performed.

The '''grade of the tumour is important''' in predicting post-surgical survival, and dogs with well-differentiated tumours are more likely to survive longer than dogs with poorly-differentiated tumours, which are more likely to metastasise and cause early death.

'''Radiation therapy''' is also an effective mode of treatment.

Treatment for Stage 2-4 mast cell tumours varies. For stage 2 tumours, options include excision of the mass and of the regional lymph node, prednisolone and radiotherapy, either singly or in combination.

Treatment of stage 3 or 4 is generally palliative and may involve '''chemotherapy''' agents such as L-asparaginase, prednisolone, chlorambucil, cyclophosphamide, vincristine and doxorubicin, alone or in combination.

'''Supportive therapy''' should be given, with '''histamine receptor antagonists''' such as cimetidine or ranitidine, to treat the systemic effects of histamine release.

==Feline mast cell tumours==
Mast cell tumours are less common in cats than in dogs, but they are '''more commonly multicentric'''.

'''Siamese cats''' are most are risk, and also develop a '''histiocytic variant''' of the disease.

Mast cell tumours occur in different forms in the cat. In one form, one or more tumours '''originate in the skin''' and may metastasise to regional nodes and other viscera. In the other, more common form, the neoplasm '''arises in internal organs''' without obvious cutaneous involvement. There is also a '''systemic''' and a '''leukaemic''' form.

===Clinical features===
Most mast cell tumours are of the 'mast cell form' and are similar to the cutaneous mast cell tumours of dogs. They usually appear on the head and neck of cats over the age of 4. Most are '''benign''' and appear as well-differentiated dermal tumours.

Cats that develop '''histiocytic variants''' are usually Siamese cats under the age of 4, but they can be of other breeds and older. Lesions are usually multiple, small subcutaneous papulonodules. The overall histological appearance is that of granulomatous inflammation with eosinophilic and lymphoid aggregates.

Special stains may be required to diagnose the uncommon variants of the disease.

For the visceral and systemic form, signs will include: '''vomiting''', enlarged lymph nodes, depression, anorexia and possibly ascites.

===Treatment===
Complete excision of the cutaneous mast cell tumours is curative, unless there are multiple tumours which may metastasise or recur.

For the histiocytic variant, the lesions often '''regress spontaneously''' and no treatment is usually necessary. The prognosis is good.

==Mast cell tumours in other species==
===Horses===
Most cases are in '''male horses''' and occur as focal masses on the head or legs. They respond to complete excision and are '''invariably benign'''.

In younger horses the tumours may '''spontaneously regress'''.

===Cattle===
The majority of bovine mast cell tumours are '''malignant and have high metastatic potential'''.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=mastcell Mast cell tumour]
|flashcards = [[Small Animal Dermatology Q&A 10]]
}}

==References==
Morrison, W. (2002) '''Cancer in dogs and cats''' ''Teton NewMedia''

Meuten, D. (2002) '''Tumors in domestic animals''' ''Wiley-Blackwell''

Withrow, S. (2007) '''Withrow and MacEwen's small animal clinical oncology''' ''Elsevier Health Sciences''

Merck and Co (2008) '''Merck Veterinary Manual''' ''Merial''

{{review}}

{{OpenPages}}

[[Category:Dermatological Diseases - Cat]][[Category:Dermatological Diseases - Dog]]
[[Category:Expert Review]]
[[Category:Liver,_Secondary_Tumours]]
[[Category:Neoplasia]]

Haemangiosarcoma

2016-06-25T20:26:48Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
A highly malignant tumour of vascular endothelial origin. Commonly affect dogs and the most frequently affected areas are the spleen, pericardium, right atrium, liver and muscle. The cat is affected less frequently and the most common sites are the liver, spleen and mesentry. Metastasis occurs via the haematogenous route or via rupture and transabdominal spread. Metastatic sites include, lungs, liver, omentum, diaphragm and less commonly brain. Surgery is the treatment of choice but even with this survival time remains very short.

==Signalment==
Often found in German Shepherd Dogs and Golden Retrievers over 9 years of age. Domestic Short haired cats are the most commonly affected cat breed.

==History and Clinical Signs==
Can vary depending on the anatomic site that the mass is affecting.
Signs such as anorexia, lethargy, weakness, [[vomiting]] and [[Regenerative and Non-Regenerative Anaemias|anaemia]] are common.
Animals may have history of multiple episodes of collapse following repeated rupture of an abdominal mass, leading to non-fatal haemoabdomen. Occasionally can be found dead following catastrophic rupture and fatal haemoabdmen.

In instances where the heart (right auricle) is involved, animals may die suddenly or present in [[:Category:heart Failure|heart failure]]. Rupture of the mass and haemorrhage into the pericardial sac leads to compression of the heart, which can no longer fill with blood during diastole ([[Cardiac Tamponade|cardiac tamponade]]).

If the nervous system is involved a range of neurological abnormalities will also be present.

==Laboratory Tests==
====Haematology====
Anaemia will be evident which may be [[Regenerative and Non-Regenerative Anaemias|regenerative]] if due to blood loss, or microangiopathic due to the passage of [[erythrocytes|red blood cells]] through the microvascular network of the tumour.
This results in the presence of schistocytes in dogs but not cats.
A [[Neutrophilia|neutrophilia]] and [[Platelet Abnormalities#Thrombocytopaenia|thrombocytopenia]] may also be present.

==Diagnostic Imaging==
===Radiography===
Useful to look for evidence of metastasis.

===Ultrasonography===
This is sensitive in identifying liver and splenic masses where the spleen will show a mixed or non-homogenoeous pattern and the liver will look hypoechoic or anechoic. It can also be useful to detect metastatic spread.

==Biopsy==
The only way to to form a definitive diagnosis is following a biopsy and histopathology. This is needed to differentiate haemangiosarcoma from splenic haematoma, haemangioma and accessory splenic tissue.

==Treatment==
===Surgery===
Surgery is the treatment of choice for haemangiosarcoma in the dog and cat. All diseased tissue should be removed and splenic haemangiosarcoma should be treated via splenectomy. Local removal is difficult if the pericardium and right atrium is involved. A pericardectomy can be undertaken but the prognosis with tumours at this location is grave.

===Chemotherapy===
This will provide a palliative treatment for animals with multiple masses or as an adjuvant therapy post-operatively.
Doxorubicin based products are the most commonly used drugs for haemangiosarcomas.

==Prognosis==
Poor due to high risk of metastasis in the early course of the disease.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis01993.asp Haemangiosarcoma]
|flashcards = [[Liver_Flashcards_-_Pathology|Liver Pathology Flashcards]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=Haemangiosarcoma&occuring1=title&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&x=55&y=10&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Haemangiosarcoma]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103181324.pdf ''' A review and what's new in canine hemangiosarcoma.''' Garrett, L. D.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 16-20 January 2010, 2010, pp 956-959]
}}

==References==
Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition) ''W.B. Saunders Company''.

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.

{{review}}

{{OpenPages}}
[[Category:Liver,_Primary_Tumours]][[Category:Cardiac Diseases - Dog]][[Category:Lymphoreticular and Haematopoietic Diseases - Dog]][[Category:Peritoneal Cavity Diseases - Dog]][[Category:Cardiac Diseases - Cat]][[Category:Lymphoreticular and Haematopoietic Diseases - Cat]][[Category:Peritoneal Cavity Diseases - Cat]]
[[Category:Peritoneal_Cavity_-_Neoplastic_Pathology]]
[[Category:Neoplasia]][[Category:Splenic Neoplasia]]

[[Category:Expert_Review]]
[[Category:Cardiology Section]]

Carcinoma

2016-06-25T20:25:35Z

Michuang0720:

==Primary Liver Tumours==
===Hepatocytic===
*more in dogs and cats
=====Gross=====
*can be difficult to distinguish grossly from adenomas
*usually one single large mass and additional smaller masses (intrahepatic metastases)
*may have features of malignancy such as internal necrosis and haemorrhage
=====Microscopically=====
*can be very variable appearing as sheets or cords of neoplastic cells
*cells generally smaller with a higher nucleus to cytoplasmic ratio

===Cholangiocellular - bile duct===
*more common than adenoma
*reported in all species (mostly dogs and cats)
=====Gross=====
*usually multiple whitish umbilicated nodules that are present diffusely throughout the [[Liver - Anatomy & Physiology|liver]]
**actually look as though they were secondary tumours
*firm on cut surface
**due to fibrosis
=====Microscopically=====
*distinctly adenocarcinomatous
*ductal and acinar proliferation in abundant fibrous tissue
*sometimes papillary formations

==Secondary Liver Tumours==
*from a variety of origins

==Pancreatic==

[[Image:Pancreatic carcinoma.jpg|right|thumb|100px|<center>Pancreatic carcinoma (Image sourced from Bristol Biomed Image Archive with permission)</center>]]

[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=11616 Image of haemorrhage and pancreatic carcinoma in a cat from Cornell Veterinary Medicine]

*In older dogs, more common in Airedale terriers, rare in cats, other species too
*Tend to arise centrally in the gland
*Highly invasive and infiltrative
*Metastases to the [[Liver - Anatomy & Physiology|liver]], visceral serosa, abdominal [[Lymph Nodes - Anatomy & Physiology|lymph nodes]], [[Spleen - Anatomy & Physiology|spleen]], [[Adrenal Glands - Anatomy & Physiology|adrenals]] etc.
*Similar to malignant ovarian tumours - implant on the [[Peritoneal Cavity - Anatomy & Physiology|peritoneum]]

===Gross appearance===
[[Image:Pancreatic carcinoma histo.jpg|right|thumb|100px|<center>Pancreatic carcinoma (Image sourced from Bristol Biomed Image Archive with permission)</center>]]

*Usually spherical nodules with adhesions to nearby structures
*Single or multiple, variable size
*Greyish or yellow fibrous tissue - firm on cutting
*May show internal necrosis and haemorrhage
*Some tumours may contain cysts wih mucinous content
*Adhesions may occur

===Microscopic appearance===
*May be well differentiated with normal acini and ducts
*Or diffuse sheet of undifferentiated cells

==Endocrine Pancreatic==

*Larger than adenomas
*Multilobular
*Invasive into parenchyma and surrounding tissue
*Metastasis into [[Lymph Nodes - Anatomy & Physiology|lymph nodes]], [[Liver - Anatomy & Physiology|liver]] mesentery, omentum
*Few mitotic figures

==Peritoneal==

*'''Carcinomas'''
**[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=11314 Image of carcinoma in a cow's peritoneum from Cornell Veterinary Medicine]
**Must be differentiated from mesotheliomas
**More common than sarcomas
**Sometimes very scirrhous
**May resemble chronic [[Peritonitis|peritonitis]] when present with ascites
**Absence of adhesions

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=carcinoma carcinoma]
}}

[[Category:Liver,_Primary_Tumours]]
[[Category:Liver,_Secondary_Tumours]]
[[Category:Pancreas_-_Hyperplastic_and_Neoplastic_Pathology]]
[[Category:Endocrine_System_-_Pathology]]
[[Category:Peritoneal_Cavity_-_Neoplastic_Pathology]]

[[Category:Neoplasia]]

Hepatitis, Chronic

2016-06-25T19:57:27Z

Michuang0720:

==Introduction==
'''Chronic hepatitis''' is an inflammatory-necrotising disease of at least 6 months duration. It is characterised by hepatocellular [[Adaptive Immunity to Viruses|apoptosis]] or [[Necrosis - Pathology|necrosis]], a variable mononuclear or mixed inflammatory cell infiltrate, [[Liver Regeneration|regeneration]] and [[Liver Fibrosis|fibrosis]] (1). It predominantly consists of lymphocytic-plasmacytic inflammatory infiltration, and the disease process typically involves a slowly progressive inflammation which leads to fibrosis and posibly cirrhosis.

==Signalment==
*Common in dogs, especially young to middle-aged dogs.
*Mixed and purebred dogs are affected but there is a familial predisposition in the following breeds:
<gallery>
Image:Dobermann.jpg|'''Dobermann'''John Adams (2007) WikiMedia Commons
Image:Bedlington.jpg|'''Bedlington Terrier''' Pleple2000 (2006) WikiMedia Commons
Image:Cocker_spaniel.jpg‎|'''Cocker Spaniel''' Ellen Levy Finch (2004) WikiMedia Commons
Image:Dalmatian.jpg|'''Dalmatian''' Miroslav Cacik (2006) WikiMedia Commons
Image:Skye_terrier.jpg|'''Skye Terrier''' Pleple2000 (2007) WikiMedia Commons
Image:Standard_poodle.jpg|'''Standard Poodle''' John Leslie (2007) WikiMedia Commons
Image:labrador.jpg|'''Labrador Retriever''' Ellen Levy Finch (2004) WikiMedia Commons
Image:GermanShep.jpg|'''German Shepherd (Alsatian)''' Ellen Levy Finch (2004) WikiMedia Commons
Image:Scottish_terrier.jpg|'''Scottish Terrier''' Svencb (2003) WikiMedia Commons
Image:Beagle.jpg|'''Beagle''' sannse (2003) WikiMedia Commons
</gallery>
==Aetiology==
A number of aetiologies include:
*Familial predisposition
*Copper accumulation (copper storage disease)
**This may be a cause or consequence of chronic hepatitis. Copper is normally excreted in bile, therefore it can occur with any cholestatic hepatobiliary disorder.
*Chronic drug therapy
*Infectious, for example [[Infectious Canine Hepatitis|infectious canine hepatitis]]
*Autoimmune or steroid responsive disorder

===Clinical Signs===
These include:
*anorexia, lethargy and depression
*weight loss
*[[Vomiting|vomiting]] and [[Diarrhoea|diarrhoea]]
*polyuria and polydipsia
*ascites - most consistent in dogs with [[Cirrhosis|cirrhosis]]
*and rarely [[Icterus|icterus]], seizures, fever and bleeding diathesis

===Laboratory tests===
Haematology:
*Mild non-regenerative anaemia and microcytosis

Biochemistry:
*Increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP). However these may not be increased if end-stage [[Cirrhosis|cirrhosis]] is reached.
*Hyperbilirubinaemia
*Hypoalbuminaemia
*Hyperglobulinaemia
*Decreased blood urea nitrogen (BUN)
*Hypoglycaemia

====Further tests====
*Increased bile acids
*Abnormal ammonia tolerance test
*Increased prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT) indicates severe liver dysfunction or [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]

==Imaging==
Abdominal radiographs will only reveal microhepatica or ascites when advanced stages of disease are reached.

Ultrasonographically, liver may be normal or non specific changes in echogenecity may be seen in early stages of the disease. In cases of [[Cirrhosis|cirrhosis]], microhepatica, irregularity in hepatic margin, focal lesions corresponding to regenerative nodules, hyperechogenicity of liver parenchyma associated with increased fibrous tissue and ascites may be seen.

==Histopathology==
This is required for definitive diagnosis and to differentiate chronic hepatitis from other hepatopathies. Chronic hepatitis is characterised by moderate to severe lymphoplasmacellular [[Inflammation - Pathology|inflammation]] and [[Liver Necrosis|necrosis]] of the hepatocytes adjacent to the portal tracts.

==Treatment==
*[[Steroids|Glucocorticoids]]
**Taper down with improved clinical signs and normal liver enzymes values.
**This is not indicated for chronic hepatitis caused by drug therapy, primary copper accumulation or infectious agents.
**Response to treatment should be followed up by liver biopsy 3-6 months later as glucocorticoid causes steroid induced ALP
*Ursodeoxycholic acid at 15mg/kg PO SID
**It is a synthetic hydrophilic bile acid that has hepatoprotective (anti-inflammatory, immunomodulatory and antifibrotic effects) properties and choleretic effect. It expands the bile acid pool and displaces potentially hepatotoxic hydrophobic bile acids that accumulate in cholestasis.
*Vitamin E
**An antioxidant to scavenge free radicals which may contribute to oxidative hepatocellular injury.
*Copper chelation if copper exceeds 2000ppm
**Penicillamine
**Zinc

==Prognosis==
Response to treatment is variable. Dogs with [[Liver Fibrosis|fibrosis]] and [[Cirrhosis |cirrhosis]] carry a poorer prognosis.

{{Learning
|Vetstream = [https://www.vetstream.com/felis/Content/Disease/dis01088.asp Liver: chronic disease in feline] [https://www.vetstream.com/canis/Content/Disease/dis01089.asp Chronic heptatitis in canines]
}}

==References==
*(1) Van den Ingh, TSGAM et. al. (2006). Morphological classification of parenchymal disorders of the canine and feline liver. In Rothuizen J et. al., editors: WSAVA standards for clinical and histological diagnosis of canine and feline liver disease, Oxford, England, Saunders.
*Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition) ''W.B. Saunders Company''.
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.

[[Category:Liver_-_Inflammatory_Pathology]]
[[Category:Liver Diseases - Dog]][[Category:To Do - Clinical]]

Hepatitis, Acute

2016-06-25T19:55:18Z

Michuang0720:

*main lesion is necrosis of the parenchyma and a later inflammatory cell reaction
*sequelae
**complete resolution by regeneration
**repair by fibrosis - scarring
**abscessation
**granuloma

{{Learning
|Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00061.asps Acute hepatitis in equine] [https://www.vetstream.com/felis/Content/Disease/dis01079.asp Liver: acute disease in feline]
}}

[[Category:Liver - Inflammatory Pathology]]
[[Category:To_Do_-_Clinical]]

Hepatitis, Acute

2016-06-25T19:54:58Z

Michuang0720:

*main lesion is necrosis of the parenchyma and a later inflammatory cell reaction
*sequelae
**complete resolution by regeneration
**repair by fibrosis - scarring
**abscessation
**granuloma

{{Learning
|Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00061.asps Acute hepatitis in equine] [https://www.vetstream.com/felis/Content/Disease/dis01079.asp Liver: acute disease in feline
}}

[[Category:Liver - Inflammatory Pathology]]
[[Category:To_Do_-_Clinical]]

Equine Serum Hepatitis

2016-06-25T19:50:28Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''Theiler's disease — ESH

==Introduction==

Equine Serum Hepatitis (ESH) is the most common cause of acute hepatitis in horses. It is often associated with prior administration of an equine biologic product, most commonly tetanus antitoxin (TAT). In some cases, the affected horse may not have received the antitoxin but may have been in contact with another horse that received TAT. Other biologic products that have been implicated include encephalitis vaccines and equine serum. Other aetiologies such as alkaloid toxicity and mycotoxins have been reported. Several cases have been reported occurring in groups of horses in which no biologic product had been administered, indicating that there may be an infectious or viral component to the disease. A [[Type III Hypersensitivity|Type III (immune-complex mediated) hypersensitivity]] reaction has also been proposed.

==Signalment==

ESH occurs predominantly in older horses. Cases (both individual cases and outbreaks) occur relatively frequently during the autumn months in north western USA, however some parts of the world have no reported cases. Some reports suggest that lactating broodmares given tetanus antitoxin after parturition are particularly prone to ESH.

==Clinical Signs==

The affected animal's history often includes administration of an equine-derived biologic product approximately four to six weeks prior to the onset of clinical signs. Clinical signs are generally sudden in onset and rapidly progressive.

Signs may range from mild non-specific signs of lethargy, weight loss or inappetance to signs of acute or chronic hepatic failure. Affected horses are often severely icteric and pass dark urine due to the presence of bilirubin. Signs relating to [[Hepatic Encephalopathy - Horse|hepatic encephalopathy]] may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as [[Photosensitisation|photosensitisation]] or pruritus may also be seen. The course of the disease is usually around five days, with death usually occurring within ten days.

Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.

==Diagnosis==

Diagnosis of ESH and evaluation of hepatic function may be achieved using a combination of clinical history, abrupt onset of clinical signs and diagnostic tests indicative of hepatic insufficiency.

'''Serum biochemistry''' may indicate the following abnormalities:
* Increased conjugated and unconjugated bilirubin
* Increased liver enzymes- SDH, AST, GGT and ALP
* Hypoglycaemia
* Increased urea

'''Ultrasound''' may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts. In several studies, biopsy is considered as the ‘gold standard’ technique for definitive diagnosis of hepatic disease. Biopsy is usually performed on the right hand side between the twelth and fourteenth intercostal spaces. A coagulation profile is often performed prior to performing the procedure due to the possibility of a clotting defect.

==Pathology==

''Post mortem'' examination often shows generalised [[Icterus|icterus]] and ascites, with an enlarged and pale liver. Histologically there may be signs of acute hepatocellular degeneration including centrilobular to midzonal necrosis, with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.

==Treatment==

The aims of treatment are mainly to support liver function and minimise any neurological signs. Affected horses should be housed in a quiet, darkened stable in order to reduce stimulation. Sedation may be required if signs of hepatic encephalopathy are present. Stressful situations such as moving the horse or separation from field mates should be avoided.

If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. In order to reduce the severity of neurological signs, the protein should be high in branched-chain amino acids; corn and molasses are often used to achieve this. If the horse is anorexic, a [[Nasogastric intubation in the horse|naso-gastric tube]] can be passed and high energy foods given directly into the stomach.

==Prognosis==

The prognosis for horses with signs of hepatic encephalopathy is extremely poor with a mortality rate approaching 88%. Horses that survive for a week after the onset of clinical signs may recover. A fall in SDH is associated with a better prognosis.

==Prevention==

Use of tetanus antitoxin in pregnant mares should be avoided. TAT should only be adminstered to horses with an unknown or absent tetanus toxoid vaccination history.

{{Learning
|Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00061.asps Acute hepatitis in equine]
|literature search = [http://www.cabdirect.org/search.html?q=%28%28title%3A%28%22serum+hepatitis%22%29+AND+od%3A%28horses%29%29%29+OR+%28%28title%3A%28%22Theiler%27s+disease%22%29%29%29 Equine Serum Hepatitis publications]
}}

==References==

* Edward Robinson, N and Sprayberry, K. A. (2009) '''Current Therapy In Equine Medicine Sixth edition''' ''Saunders Elsevier''

* Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''' ''University of Liverpool''

* Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''Wiley-Blackwell''

* Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial''

* Smith, H. L., Chalmers, G. A., Wedel, R. (1991) '''Acute hepatic failure (Theiler's disease) in a horse''' ''Canadian Veterinary Journal 32, 362-364.

{{review}}

{{OpenPages}}

[[Category:Liver_-_Inflammatory_Pathology]]

[[Category:Expert_Review]]
[[Category:Liver Diseases - Horse]]

Cholecystitis

2016-06-25T19:31:10Z

Michuang0720:

*inflammation of the [[Gall Bladder - Anatomy & Physiology|gall bladder]]

Gall Bladder
*can become inflamed
**eg [[Salmonellosis]]
**[[Infectious Canine Hepatitis]]
*hyperplasia of the mucosa
**common reaction to any irritation of this area

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre60060.asp Gall bladder disease: overview]
}}

[[Category:Liver_-_Inflammatory_Pathology]]
[[Category:Gall_Bladder_and_Tract_-_Pathology]]
[[Category:To_Do_-_Clinical]]

Liver Fibrosis

2016-06-25T19:28:14Z

Michuang0720:

== Introduction ==
Fibrosis is one way in which the liver responds to injury. It commonly occurs in association with chronic hepatic injury, and represents a repair stage in response to diseases that lead to [[Liver Necrosis|necrosis]] and inflammation. The process is complex and involves increased deposition of extracellular matrix in the liver, following injury-induced activation of [[Hepatic Stellate Cells|stellate cells]].

The distribution pattern of fibrosis is a reflection of the pathogenesis of the condition, and can indicate the type of underlying pathology.

==Patterns of Fibrosis ==
===Centrilobular (periacinar) Fibrosis===
This involves fibrosis around the hepatic venule (centrilobular vein). It is associated with chronic toxic injury since hepatocytes in this region are involved in drug metabolism. It is also associated with chronic passive congestion due to long-term [[Heart Failure, Right-Sided|right sided congestive heart failure]].

===Periportal (biliary) Fibrosis===
This involves fibrosis that is mostly confined to the portal region, and is associated with chronic inflammatory conditions that lead to inflammation in the portal triads.

===Post-Necrotic Scarring===
This occurs following massive hepatic necrosis where large areas of parenchyma are lost and replaced by fibrosis.

===Bridging (diffuse) Fibrosis===
This is the sequel to chronic parenchymal injury, such as prolonged inflammation or numerous episodes of zonal necrosis. Fibrosis occurs throughout lobules and leads to bridging between portal areas, or between portal regions and central veins, causing pseudolobulation.

Although all types of fibrosis can lead to hepatic dysfunction if severe enough, bridging fibrosis is more likely to impair hepatic function than any of the other types.

Hepatic fibrosis is now known to be potentially reversible, provided the source of injury is removed. If the insult persists, however, fibrosis can be self-perpetuating, resulting in a small scarred liver with functional failure.

<big>Also see: [[Cirrhosis]]</big>

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=cirrhosis Cirrhosis] [https://www.vetstream.com/canis/Content/Disease/dis01098.asp Idiopathic fibrosis in dogs]
}}

== References ==
Blood, D.C. and Studdert, V. P. (1999) '''Saunders Comprehensive Veterinary Dictionary''' (2nd Edition), ''Elsevier Science''.

Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat''' Volume 2 (Fifth Edition),'' W.B. Saunders Company.''

Maxie, M.G. (2007) '''Pathology of Domestic Animals Volume''' 2 (Fifth Edition), ''Elsevier Saunders''.

McGavin, M.D. and Zachary, J.F. (2007) '''Pathologic Basis of Veterinary Disease''' (Fourth Edition), ''Elsevier Mosby''.

Smyth, B (2008) ''' Alimentary System Study Guide, ''''' Royal Veterinary College.''

{{Nicky Parry
|date = 22 August 2011
}}
[[Category:Liver_-_General_Pathology]]
[[Category:Nicola Parry reviewed]]

Cirrhosis

2016-06-25T19:25:29Z

Michuang0720:

==Introduction==
Cirrhosis represents an “end-stage liver” - the final, irreversible result of diffuse hepatic disease, involving architectural disruption of the entire liver. Underlying chronic injury leads to loss of hepatic tissue with replacement [[Liver Fibrosis|fibrosis]]. Nodular regeneration occurs within regions of hepatic tissue in between fibrous tissue bands, giving rise to the characteristic multinodular gross appearance of this condition. Overall, the liver is smaller than normal and firm to cut, firmness is due to the presence of fibrous tissue. It is pale, sometimes yellow in colour.

The three characteristic microscopic features of cirrhosis are:
*Nodular regeneration
*[[Liver Fibrosis|Fibrosis]]
*Bile duct hyperplasia

'''Bile duct hyperplasia''' around portal regions is a non-specific response to a variety of long-standing hepatic insults, but occurs especially in association with diseases that [[Biliary Tract Obstruction|obstruct bile drainage]].

'''Vascular abnormalities''' are also associated with cirrhosis. Anastomoses occur between the hepatic portal vein and systemic vasculature due to increased portal pressure. Additionally, [[Portosystemic Shunt|vascular shunts]] can result within regenerative nodules, either between central and portal veins, or between hepatic arteries and central veins.

==Causes of Cirrhosis==
Some of the many possible causes of cirrhosis in animals include:
*Chronic [[Heart Failure, Right-Sided|right sided heart failure]]
*[[Hepatitis, Chronic|Chronic hepatitis]]
**[[Hepatitis, Lobular Dissecting|Lobular dissecting hepatitis in dogs]]
**Hepatitis due to [[Infectious Canine Hepatitis|infectious canine hepatitis virus]]
*Chronic [[cholangitis]] or [[Biliary Tract Obstruction|bile duct obstruction]]
*Chronic toxicity
**[[Ragwort Toxicity|Pyrrolizidine alkaloid plants]] in herbivores
**[[Primidone]] anticonvulsants in dogs
*Inherited diseases of metal metabolism
**[[Copper]] (Dalmatians, Bedlington terriers, West Highland white terriers)
**[[Iron]] metabolism

Cirrhosis is usually the end result of multiple pathological processes, in particular cell death and active inflammation with fibrosis. Regardless of the original underlying aetiology, however, the end-stage liver can no longer perform its functions, and is therefore associated with clinical manifestations of [[Liver Failure|hepatic failure]].

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=cirrhosis Cirrhosis]
}}

==References ==
Blood, D.C. and Studdert, V.P. (1999)''' Saunders Comprehensive Veterinary Dictionary''' (2nd Edition), ''Elsevier Science''.

Ettinger, S.J. and Feldman, E.C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat''' Volume 2 (Fifth Edition), ''W.B. Saunders Company''.

Maxie, M.G. (2007) '''Pathology of Domestic Animals Volume''' 2 (Fifth Edition), ''Elsevier Saunders''.

McGavin, M.D. and Zachary, J.F. (2007) '''Pathologic Basis of Veterinary Disease''' (Fourth Edition),'' Elsevier Mosby.''

Smyth, B (2008) '''Alimentary System Study Guide''''', Royal Veterinary College''.

{{Nicky Parry
|date = 22 August 2011
}}

[[Category:Liver_-_General_Pathology]]
[[Category:Nicola Parry reviewed]]

Cholestasis, Molecular Pathogenesis

2016-06-25T19:24:33Z

Michuang0720:

[Trauner M, Meier PJ, Boyer JL. NEJM (1998) 339 1217-26]

== [[Bile Formation]] ==

== Animal models of cholestasis: ==

*Endotoxin treated rats – sepsis-induced cholestasis
*Oral-contraceptive treated animals
*Ethinyl estradiol-treated rats – cholestasis of pregnancy
*Extrahepatic – ligation of common bile duct
*Many drugs cause cholestasis e.g.: cyclosporine A, chlorpromazine

== Molecular mechanisms of cholestasis ==

'''Hepatocellular transporters'''

*Various inherited disorders of hepatocellular transport seen in humans that can result in reduction in bile flow and therefore cholestasis.

*Phospholipids within normal bile protect the bile ductule epithelial cells from the toxicity of bile salts by forming mixed micelles – there is a mutation in the MDR3 gene that causes marked decrease in PL transport into the bile  hence bile ductule damage and inflammation. Patients with primary biliary cirrhosis have normal MDR3 expression though…

*Dubin-Johnson disease – mutation in a MRP2  hyperbiliruninaemia but not cholestasis due to inappropriate excretion of endogenous conjugates (bilirubin digluconuride and coproporphyrin I). Seen in South Down sheep and Corridale sheep.

*Acquired forms of cholestasis may have effects on the basolateral or canalicular transport mechanisms e.g.: altered expression of the transport proteins. Molecular alterations in basolateral transport may contribute to the functional impairment of bile formation by diminishing the hepatocellular uptake of biliary constituents. Also may reduce build up of toxic substances (bile salts, etc) within hepatocytes. Promotors to these transporters have signal sequences transcription regulating factors that are responsive to bile salts, cytokines, etc. Indeed, endotoxin-induced cholestasis in rats is caused by inhibition of activity of hepatocyte nuclear factor 1 (and other cytokines) that decreases expression of transport proteins.
Organic-anion transporting polypeptide is upregulated in cholestatic disease – possibly helping to export toxic substances out of hepatocytes and into the bile canaliculi.
*As the transport across the canalicular membrane is the rate limiting step, it is one of the major causes of cholestasis – expression of the transport proteins across this membrane are downregulated in experimental cholestasis models (e.g. decreased expression of bile-salt export pump, multispecific organic-anion transporter).
*Bicarbonate exchangers also play a role in the decrease in canalicular and ductular bile flow (some patients have generalized syndromes that also affect saliva secretion as well).

'''Cholangiocyte transporters'''

*CFTR – on cholangiocytes and not on hepatocytes – mutations impair ductular secretion of chloride and water.

*Other defects:
*Most cholestatic liver disease causes profound hepatocyte cytoskeletal changes – disruption of microtubules, increases in intermediate filaments, accumulations of disorganized actin microfilaments in the pericanalicular domain. Result in loss of apical microvilli, decreased contractility of the canalicular membrane, increased permeability of intercellular tight junctions (latter results in regurgitation of bile into plasma, reduction of osmotic gradients in the bile canaliculi (the driving force for bile secretion)).
*Changes in the tight junction permeability is affected by the altered location and accumulation of the tight junction proteins (occludin and zonula occludens I).
*Also membrane components, transcytosis and canalicular exocytosis are also altered during cholestasis. Results in retention of apical transporters on the basolateral surface of hepatocytes and a delay in vesicle transport to the bile canaliculi. Accumulations of vesicles within the pericanalicular region of hepatocytes is characteristic of choleostatic liver injury.
*High concentrations of bile salts inhibit function of molecular motors (dynein and kinesin) that move the vesicles.
*Calcium signaling within and between hepatocytes decreases with choleostasis – changes in gap junctions so may change microperistalsis down the terminal canaliculi to the bile ducts in the portal triads (counter to direction of blood flow).
*cAMP mediated signaling in the hepatocyte is impaired due changes in G protein expression and localization. This together with changes in membrane composition and the detergent effects of the bile salts – contribute to decreased adenylate cyclase activity. Also therefore decrease effects of glucagons and VIP that normal stimulate bile secretion.
[[Category:Liver_-_General_Pathology]]

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02688.asp Cholestatic disease]
}}

[[Category:To_Do_-_Clinical]]

Liver Rupture

2016-06-25T19:17:31Z

Michuang0720:

*common result of '''trauma'''
*often clinically occult (small capsular ruptures may clot and heal) unless larger, severe ruptures cause rapid exsanguination or the biliary tract is involved
*rupture of major bile ducts leads to yellow-stained bile peritonitis
**may remain sterile and become chronic
**may be infected by enterohepatic circulation of bacteria such as clostridia followed by rapid death
NB: fatal ruptures can occur in foals during parturition, sometimes concurrent with costal fractures
*'''predisposition to rupture'''
**diffuse hepatic disease causes enlargement and friability of the [[Liver - Anatomy & Physiology|liver]]
**may occur spontaneously
*predisposing lesions include:
1. [[Infectious Canine Hepatitis|infectious canine hepatitis]]

2. amyloidosis

3. severe congestion

4. fatty degeneration

5. secondary neoplasms

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis00663.asp Liver trauma in dogs]
}}

[[Category:Liver_-_Developmental_Pathology]]
[[Category:To_Do_-_Clinical]]

Liver Fibrosis, Capsular

2016-06-25T19:16:27Z

Michuang0720:

*commonly found in older horses
*many fibrous tags or plaques present on the diaphragmatic surface of the [[Liver - Anatomy & Physiology|liver]] as well as the adjacent diaphragm
*cause
**most considered due to migrating parasites
**some may be focal areas of non-septic peritonitis that have resolved

{{Learning
|Vetstream = [https://www.vetstream.com/equis/search?s=liver Liver disease]
}}

[[Category:Liver_-_Developmental_Pathology]]
[[Category:To_Do_-_Clinical]]

Ketosis

2016-06-25T19:04:20Z

Michuang0720:

==Introduction==
Ketosis occurs in starvation and also in [[Diabetes Mellitus|diabetes mellitus]], [[Ketosis of Cattle|ketosis of cattle]] and [[Pregnancy Toxaemia|pregnancy toxaemia of sheep]]. Basically, no carbohydrates are metabolised, in starvation none are available and in diabetes mellitus because there is no insulin present to allow glucose transport into cells.
When carbohydrates are not available the body produces energy via the metabolism of fat. Fatty changes can be seen in the liver and kidney following deposition of the mobilised fat.
This results in an accumulation of ketone bodies (B-hydroxybutyric acid, acetoacetic acid and acetone) in the blood and other tissues. Two of the ketone bodies are acids resulting in a metabolic acidosis hence the name ketoacidosis.

==Signalment==
Affects cattle, ewes and deer, diabetic dogs
More frequently affecting animals who have a high body condition store.

==Diagnosis==
This condition can often be diagnsis on clinical signs combined with simple tests. It is possible to test milk or urine on the farm for the presence of ketone bodies. This can be carried out using dipsticks which change colour in the presence of ketone bodies. False positives can occur with these tests and they should be used in conjunction with clinical signs suggestive of ketosis.

Additionally, serum concentrations of NEFAs will be high and glucose levels will be low.

The acetone that is formed during ketosis is a volatile agent which can be blown off and this accounts for the 'pear drop' like smell on affected animals breath.

==Clinical signs==
Include, depression, lethargy, dehydration, anorexia and decreased rumenal activity.

==Laboratory Tests==
==Treatment==
==Prognosis==
==References==

See also: '''[[Ketosis of Cattle|Ketosis of cattle]] — [[Pregnancy Toxaemia|Pregnancy toxaemia of sheep]]'''

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=ketosis Ketosis]
}}

[[Category:Liver_-_Degenerative_Pathology]]
[[Category:To Do - Clinical]]

Ketosis

2016-06-25T19:03:37Z

Michuang0720:

==Introduction==
Ketosis occurs in starvation and also in [[Diabetes Mellitus|diabetes mellitus]], [[Ketosis of Cattle|ketosis of cattle]] and [[Pregnancy Toxaemia|pregnancy toxaemia of sheep]]. Basically, no carbohydrates are metabolised, in starvation none are available and in diabetes mellitus because there is no insulin present to allow glucose transport into cells.
When carbohydrates are not available the body produces energy via the metabolism of fat. Fatty changes can be seen in the liver and kidney following deposition of the mobilised fat.
This results in an accumulation of ketone bodies (B-hydroxybutyric acid, acetoacetic acid and acetone) in the blood and other tissues. Two of the ketone bodies are acids resulting in a metabolic acidosis hence the name ketoacidosis.

==Signalment==
Affects cattle, ewes and deer, diabetic dogs
More frequently affecting animals who have a high body condition store.

==Diagnosis==
This condition can often be diagnsis on clinical signs combined with simple tests. It is possible to test milk or urine on the farm for the presence of ketone bodies. This can be carried out using dipsticks which change colour in the presence of ketone bodies. False positives can occur with these tests and they should be used in conjunction with clinical signs suggestive of ketosis.

Additionally, serum concentrations of NEFAs will be high and glucose levels will be low.

The acetone that is formed during ketosis is a volatile agent which can be blown off and this accounts for the 'pear drop' like smell on affected animals breath.

==Clinical signs==
Include, depression, lethargy, dehydration, anorexia and decreased rumenal activity.

==Laboratory Tests==
==Treatment==
==Prognosis==
==References==

See also: '''[[Ketosis of Cattle|Ketosis of cattle]] — [[Pregnancy Toxaemia|Pregnancy toxaemia of sheep]]'''

{{Learning
[https://www.vetstream.com/canis/search?s=ketosis Ketosis]
}}

[[Category:Liver_-_Degenerative_Pathology]]
[[Category:To Do - Clinical]]

Hyperlipaemia - Horse

2016-06-25T19:02:21Z

Michuang0720:

{{OpenPagesTop}}
Also known as/ see also: '''[[Fatty Liver Syndrome|Fatty liver syndrome]]''' (intended to refer to cattle disease) — [[Hyperlipaemia - Donkey|Hypelipaemia in donkeys]] — [[White Liver Disease - Sheep|White liver disease in sheep]] — [[Pregnancy Toxaemia|Preganacy toxaemia in sheep]] — [[Hepatic Lipidosis|Hepatic lipidosis in cats and dogs]]

Do not confuse with: [[Hyperlipidaemia - Horse|'''Hyperlipidaemia ]]

==Introduction==
'''Hyperlipaemia''' is a severe metabolic disorder which occurs in response to a negative energy balance, the end result is multi-organ failure as lipid is deposited in the liver and kidneys. Fatty acids are mobilised from adipose tissue, some are used peripherally but most are taken up by the liver. Here they are oxidized to provide energy or re-esterified to triglycerides and phospholipids, and deposited in hepatocytes or released into the blood as very low density lipoproteins. These very low density lipoproteins are the cause of lipaemic plasma in hyperlipaemic ponies. Hypoglycaemia reduces insulin response, compounding the problem by increasing peripheral lipid mobilisation and decreasing removal of triglyercides from the circulating blood. Insulin resistance has been reported to be a factor in many cases of hyperlipaemia but affected animals may aslo have a normal insulin response.

Metabolic acidosis can occur in the terminal stages of the disease and is a poor prognostic indicator. Secondary laminitis is a common complicating factor.

==Signalment==
Occurs most commonly in '''Shetland''' and '''miniture ponies''' but has also been reported in horses; it is also relatively common in [[Hyperlipaemia - Donkey|donkeys]] and follows the same pathogenesis.

Affected animals are usually but not consistently obese and the condition occurs in animals which are in a negative energy balance, most frequently due to pregnancy, lactation, [[Colic in Horses|colic]] or chronic disease.

==Diagnosis==
Visual inspection of plasma is usually sufficient to diagnose the condition, in affected animals the serum will be turbid and cloudy with elevated triglyceride concertrations (5.7mmol/L). Liver enzymes, bilirubin and bile acid concentrations are often elevated and there may be a concurrent azotaemia.

===Clinical Signs===
*Depression
*Anorexia
*Ataxia
*Diarrhoea
*Peripheral oedema

===Biochemistry===
*Elevated liver enzymes, AST AP GGT
*Elevated bile acids
*Hypoglycaemia
*Hypoalbuminaemia
*Azoteamia

==Pathology==
Liver biopsy shows fatty infiltration of hepatocytes.

Post mortem exam reveals lipaemic serum, and a pale enlarged friable liver with a greasy surface when cut.

==Treatment==
Treatment must be prompt and aggressive.
Nutritional support is the most important part of treatment. Constant slow infusion of glucose IV (dextrose 5%) should be given initially. Followed by protamine zinc insulin and glucose or high energy gruel based on barley or oats given by stomach tube and supportive amino acids. Heparin may be given in an attempt to reduce plasma triglycerides but will not correct the underlying cause and may alter haemostasis.

==Prognosis==
Prognosis is poor.

{{Learning
|Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00329.asp Hyperlipemia syndrome]
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28Hyperlipaemia%29+AND+od%3A%28horses%29 Hyperlipaemia in horses publications]
}}

==References==
* Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''' ''University of Liverpool''
*Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Saunders.

{{review}}

{{OpenPages}}

[[Category:Liver_-_Degenerative_Pathology]][[Category:Alimentary Diseases - Horse]]
[[Category:Expert_Review]]

Liver Congestion, Passive

2016-06-25T18:53:08Z

Michuang0720:

Usually associated with right-sided heart failure because when the right side of the heart fails to function properly, blood will back up through the veins into the [[Liver - Anatomy & Physiology|liver]].

The appearances and changes in the [[Liver - Anatomy & Physiology|liver]] will depend on whether the conggestion is of short or long duration.

===Acute congestion===
*occurs in acute right-sided heart failure and in shock
====Gross====
*[[Liver - Anatomy & Physiology|liver]] is swollen and engorged with rounded edges to the lobes
*fibrin may be present on the surface, coming from the dilated subcapsular lymphatics
*blood oozes freely from the cut surface
*the sinusoids are dilated and packed with red blood cells
====Microscopically====
*hepatic venules and sinusoids engorged with blood

===Chronic congestion===
*occurs in chronic right-sided heart following on from left-sided heart failure eg endocardiosis in dogs, cardiomyopathy in cats [need link in future]
====Gross====
*slightly swollen with rounded edges
*capsular surface may be paler and thicker than normal
*alternating red and yellow areas on the cut surface: accentuates the acinar pattern
**this contrasting red and yellow mottled gross appearance (especially that of the formalin-fixed specimen) resembles the cut surface of a nutmeg, and is referred to as ''''nutmeg'''' [[Liver - Anatomy & Physiology|liver]]
**at this stage the [[Liver - Anatomy & Physiology|liver]] may have returned to normal size or be slightly smaller than normal
*fibrosis can develop in the congested centrilobular zones and the liver becomes firm to section, ie cardiac fibrosis

====Microscopically====
*the red areas are engorged and dilated hepatic venules which may show a substantial increase in perivenular fibrous tissue due to atrophy and loss of adjacent hepatocytes
*the yellowish areas are the midzonal and perhaps periportal hepatocytes in very long standing cases which have undegone fatty change due to hypoxia and malnutrition
*the Kuppfer cells may contain considerable haemosiderin pigment
**golden brown in H&E sections
**blue with Perls' Prussian blue stain (specific for haemosiderin)

==Test yourself with the Liver Pathology Flashcards==

[[Liver_Flashcards_-_Pathology|Liver Pathology Flashcards]]

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Illustration/ill01391.asp CHF: Liver congestion - pathology]
}}

[[Category:Liver_-_Circulatory_Disturbances]]
[[Category:To_Do_-_Clinical]]

Atresia

2016-06-25T18:51:08Z

Michuang0720:

===== Atresia ani =====
[[Image:atresia ani PM.jpg|right|thumb|125px|<center>Pig - atresia ani (Courtesy of Elspeth Milne)</center>]]
*A common congenital defect of the lower gastrointestinal tract.
*Both the [[Anus - Anatomy & Physiology|anus]] and [[Rectum - Anatomy & Physiology|rectum]] can be affected.
*Occurs in all species but is most often seen in calves and pigs.

===== Atresia coli =====
*Considered the most common segmental anomaly of the intestine in domestic animals.
*Can affect in particular the spiral [[Colon - Anatomy & Physiology|colon]] of Holstein calves and the small [[Colon - Anatomy & Physiology|colon]] of foals.

===== Atresia ilei =====
*It is less common to see atresia in the [[Small Intestine Overview - Anatomy & Physiology|small intestine]].
*Mostly seen in calves.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis00658.asp Anus: atresia]
}}

[[Category:Recto-Anal - Pathology]][[Category:Intestinal Diseases - Pig]][[Category:Intestinal Diseases - Cattle]]
[[Category:To_Do_-_Alimentary]][[Category:To Do - Minor]]

[[Category:Large Intestinal Diseases - Horse]][[Category:Small Intestinal Diseases - Horse]]

Anal Sac Abscessation

2016-06-25T18:49:36Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
Infection of the anal sac to form an abscess, may occur following [[Anal Sacculitis|Anal Sacculitis]] or [[Anal Sac Impaction|Anal Sac Impaction]]. Fistulous tracts may arise from the abscess and rupture to the skin.

==Signalment==
Can occur in any age, breed or gender of dog however small breed overweight dogs are most commonly infected. Cats can also be affected.

==Diagnosis==
Anal sac abscessation is diagnosed when there is noticeable swelling of the anal sac with a purulent exudate, inflammation of the surrounding perianal region, pain and fever. Rupture of the anal sac can occur with this condition producing a draining tract.

===History and Clinical Signs===
See [[Anal Sac Disease - General|Anal Sac Disease - General]]

===Microscopic Examination===
On microscopic examination of the fluid following anal sac expression, polymorphonuclear [[Leukocytes|leukocytes]] and bacteria will be seen.

==Treatment==
Incision of the sacs and drainage plus lavage with an isotonic solution or 0.05% chlorhexidine. Hot compresses can be useful when applied twice daily for 15 minutes prior to surgery. The incisions should be left open and broad spectrum systemic antibiotics given until results of culture and sensitivity are back. Common organisms are ''[[Escherichia coli]]'', ''[[:Category:Streptococcus species|Streptococcus]] faecalis'' and ''[[Proteus]]'' species. If the condition becomes chronic, it is best managed by an anal sacculectomy.

==Prognosis==
Good

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Illustration/ill34083.asp Anal sac abscess rupture - picture]
|flashcards = [[Small Animal Dermatology Q&A 21]]
}}

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

Foster, A. Foil, C. (2003) '''BSAVA Manual of Small Animal Dermatology (2nd Edition)''' ''BSAVA''

Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' Merial

{{review}}

{{OpenPages}}

[[Category:Recto-Anal_-_Pathology]][[Category:Expert_Review]]
[[Category:Rectal and Anal Diseases - Cat]][[Category:Rectal and Anal Diseases - Dog]]

Diarrhoea

2016-06-25T18:47:15Z

Michuang0720:

==Introduction==

* Defined as "'''an increase in volume and fluidity of faeces, and increased frequency of defaecation'''".
** Associated with malabsorption of fluid and electroyles in the intestines.
* The precise pathogenesis of diarrhoea in many individual diseases is not well defined.
** Four major mechanisms are known to exist.
*** One or more of these may operate in many diseases.

==Interference with normal mucosal cell transport processes==

===Normal intestinal absorption and secretion===

* Normal intestinal water absorption and secretion is mainly due to passive osmotic forces created by active solute transport.
** The sodium ion (Na+) is the most important solute.
*** Is actively absorbed from the intestine.
*** Is largely responsible for the passive absorption of water.
* Active Na+ absorption from the intestine results from a combination of processes.
*# Na+ is secreted from intestinal epithelial cells into the underlying interstitium
*#* This is ATPase dependent
*#* Creates a gradient for uptake of Na+ from the intestinal lumen.
*# There is coupled Na+ and Cl- absorption.
*#* Na+ and Cl- are activily absorbed at the luminal surface of the cell.
*#** The mechanism for this is dependent on adenyl cyclase activity.
*# Na+ is also absorbed in association with glucose and some amino acids (i.e. coupled).
*#* This is also energy dependent.
* Once absorbed into the intestinal epithelial cells by these coupled mechanisms, Na+ is pumped out by the basal and lateral primary pumps.
** This increases the gradient for water absorption.
* These overall absorption mechanisms operate primarily on mature villus absorptive cells and [[Colon - Anatomy & Physiology|colon]]ic surface cells.
** The small intestinal crypts are lined by rapidly dividing and relatively immature cells.
*** Although there is primary active Na+ absorption there is also active secretion of Na+, Cl-, HCO3-, and therefore H2O.
**** Consequently there is an overall balance of secretion into the crypt - normal intestinal secretions.
*** The same potential secretory mechanisms probably exist in the villus cells.
**** These are grossly outweighed by absorptive mechanisms.
*** Considering both villus and crypt mechanisms, there is '''net absorption''' of Na+ and H2O.

===Secretory Diarrhoeas===

* The overall balance of the absorptive and secretory mechanisms above is shifted in a number of diseases.
** There is net secretion of Na+ and H2O into the lumen of the intestine.
*** '''“Secretory” diarrhoeas'''.
* The best known secretory diarrhoeas are those caused by the '''enterotoxin producing strains of bacteria'''.

====Enterotoxin Producing Strains of Bacteria====

* E.g. ''Vibrio cholerae'', [[Escherichia coli|''E. coli'']].
* Organisms adhere to the surface of intestinal epithelial cells and secrete their enterotoxins.
** Enterotoxins are absorbed into cells and interfere with intracellular enzymes and metabolism.
* The heat labile enterotoxin of [[Escherichia coli|''E. coli'']] and cholera toxin interfere with adenyl cyclase activity.
** Result in increased intracellular levels of cAMP.
** Increased cAMP interferes with chloride coupled sodium transport
*** Promotes Na+, Cl- and hence H2O secretion from the epithelial cells.
*** The overall balance is shifted and the intestine becomes a '''net secretor''' of fluid.
** The increased cAMP levels probably act via a number of other intracellular processes including:
*** Activation of protein kinases.
*** Increased intracellular Ca++ levels.
*** Calmodulin stimulation.
* Other enterotoxins may act by other mechanisms.
** E.g. the heat stable toxin of E. coli acts by guanyl cyclase and increased cGMP.

====Other types of disease processes====

* Other types of disease processes may also interfere with mucosal transport.
* Prostaglandins, released during inflammation, and intestinal polypeptides (e.g. VIP) act via adenyl cyclase and increased cAMP.
* Acetylcholine stimulation from the parasympathetic nervous system promotes secretion via increased intracellular Ca++ levels.

====Treatment====

* Chloride coupled mechanisms of Na<sup+ (and H2 are affected as described above.
** However, other mechanisms remain intact provided the epithelial cells are not destroyed.
*** E.g. glucose and primary active transport.
* It is therefore possible to “drive” the surviving absorptive processes.
** Forms the basis for oral fluid and electrolyte replacement therapy.
*** A mixture of salt, sugar and water is used to treat diarrhoea.

==Alterations in structure/permeability==

===Inflammation/ Infiltration===

* The absorptive capacity of the intestine is dependent on intestinal surface area.
* Many diseases cause massive cellular infiltration into the small intestinal lamina propria, resulting in:
** Stunting and fusion of villi.
** Loss of surface area.
** Overall decreased absorptive capacity.
* The cellular infiltrate may result from:
** Chronic inflammation (e.g. [[Johne's Disease|Johnes disease]]).
** Immunologically mediated reactions (e.g. [[Inflammatory Bowel Disease#Eosinophilic Enteritis|eosinophilic enteropathy]]).
** Neoplasia (e.g. [[Lymphoma|intestinal lymphoma]]).
* Inflammatory or reactive processes immediately below the epithelium may provoke interference with epithelial transport processes and increase the tendency to diarrhoea.

===Acute Destructive Enteropathies===

* Invasive bacterial infections such as [[Salmonellosis|Salmonellosis]] result in epithelial destruction and loss of surface area.
* There is also active exudation of extracellular fluids from the eroded/ ulcerated mucosal surface.
** Exacerbated by the increased vascular permeability associated with inflammation.
** Prostaglandin release associated with inflammation may also provoke secretion from surviving epithelial cells.
* The presence of blood and mucosal shreds in watery faeces is known as '''dysentery rather than diarrhoea'''.

==Osmotic diarrhoea==

* If non-absorbable solutes accumulate in the gut lumen, there will be retardation of water and electrolyte absorption and diarrhoea will occur.
** Large amounts of osmotically active solutes will cause net movement of water from the plasma into the lumen.
* Seen in animals deficient in specific brush border enzymes.
** E.g. lactase deficiency.
*** Feeding lactase deficient animals on milk means that lactose will remain in the lumen as an osmotically active solute rather than being broken down to glucose and galactose.
**** Provokes diarrhoea.
** The presence of immature epithelial cells on villi will also cause an osmotic type of diarrhoea.
*** Lack their normal brush border enzymes.
* Many laxatives act in this way.
** E.g. those containing magnesium.

==Derangement of intestinal mobility==

* In some cases diarrhoea is related to intestinal mobility.
* Some pharmacologically active substances stimulate intestinal motility.
** E.g prostaglandins.
** Decreases the transit time for intestinal contents.
*** Less absorption occurs.
** May cause diarrhoea.
* Intestinal stasis may also stimulate diarrhoea.
** Appears to be due to excessive bacterial multiplication in the intestinal contents.
*** "Small intestinal bacterial overgrowth" (S.I.B.O.) .
*** Results in the production of large amounts of osmotically active substances in the intestinal lumen.

==An Example of the Mechanisms of Diarrhoea==

* In any individual disease associated with diarrhoea, a combination of two or more of the mechanisms above may be involved in the disease pathogenesis.
* For example, transmissible gastroenteritis (TGE).

===Transmissable Gastro-Enteritis (TGE)===

* Affects pigs, cattle and dogs.
** For more information on the pig, see [[Transmissible Gastroenteritis Virus|transmissable gastro-enteritis in the pig]].
* Caused by a coronavirus, which attacks mature absorptive cells of the intestinal villi.
* Gives excessive loss of surface epithelial cells.
** Results in villus stunting and fusion in an attempt to maintain epithelial continuity.
*** Surface area is decreased.
**** '''Loss of absorptive capacity'''.
* The intestinal crypts become hyperplastic to increase the replacement of lost epithelial cells.
** Crypt cells are normally net secretors- there is therefore '''increased secretion''' from this source.
* New cells move up from the crypts onto the villus more rapidly than usual.
** Cells are immature and lack their normal brush border enzymes.
*** There is therefore an '''osmotic component''' to the diarrhoea.
* There may be inflammation in the underlying lamina propria.
** Prostaglandin is released, and
*** '''Increases intestinal motility'''.
*** Provokes '''increased secretory activity''' from remaining epithelial cells.

==Diarrhoea in Small Intestinal Disease Only==

* When disease is present only in the [[Small Intestine Overview - Anatomy & Physiology|small intestine]], diarrhoea occurs only when the reserve capacity of the [[Colon - Anatomy & Physiology|colon]] to resorb water is exceeded.
** The [[Colon - Anatomy & Physiology|colon]] is able to resorb up to 3-4 times the volume normally presented from the [[Small Intestine Overview - Anatomy & Physiology|small intestine]].
* Therefore, for diarrhoea to occur, small intestinal disease must either:
** Be severe, or
** Occur in conjunction with large intestinal problems.
* Some small intestinal diseases cause only weight loss.
** May see hypoalbuminaemia and oedema in very severe cases.
** Weight loss is due to:
*** Maldigestion.
*** Malabsorption of nutrients
**** Cannot be retrieved by [[Colon - Anatomy & Physiology|colon]]ic resorption (except in horses).

==Diarrhoea in the [[Large Intestine - Anatomy & Physiology|Large Intestine]]==

* Diarrhoea may occur because of failure of large intestine function, e.g.
** Colitis due to ''Treponema hyodysenteriae'' in pigs.
** Large intestinal parasitism in the horse.
* Mechanisms are similar to those described above.
** Interference with mucosal transport processes.
** Destruction or loss of surface area.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre00889.asp Diarrhea: overview]
}}

[[Category:Intestines,_Small_and_Large_-_Pathology]]
[[Category:To_Do_-_Clinical]]

Adenoma

2016-06-25T18:44:14Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
[[Image:dogpap1.gif|right|thumb|100px|<center>Oral Papilloma Neoplasia in Dog (Courtesy of Alun Williams (RVC))</center>]]
An adenoma is a '''benign epithelial tumour''' arising in the epithelium of the '''mucosa''' (stomach and intestines), '''glands''' (endocrine and exocrine) and '''ducts'''.

Adenomas observed in veterinary species include:

==Perianal Adenoma==
[[Image:normal perianal gland.jpg|thumb|right|200px|Perianal gland - normal (Courtesy of Bristol BioMed Image Archive)]]
[[Image:perianal gland adenoma histopath.jpg|thumb|200px|Perianal gland - adenoma (Courtesy of Bristol BioMed Image Archive)]]
[[Image:perianal gland adenoma.jpg|thumb|right|200px|Perianal adenoma - gross appearance (Courtesy of Bristol BioMed Image Archive)]]
These tumours, also called hepatoid gland tumours, arise from the solid, '''modified sebaceous circumanal glands'''. They are the third most common tumour in '''intact male dogs''', and arise more frequently in '''older dogs'''.

The tumour is '''under hormonal control'''. Hepatoid glands are also found at the tail head, prepuce and other skin sites, and tumours can also arise from there.

====Clinical features====
Adenomas occur alone or in number, as round, well-differentiated, freely-movable masses. Tumours can become ulcerated and secondarily infected. There can be signs of perianal pain and tenesmus.

====Diagnosis====
'''Cytology''' of the mass will reveal large hepatoid cells with a round, central nuclei, multiple nucleoli, and an abundant cytoplasm. There may be concurrent inflammation or haemorrhage. Cytology cannot distinguish adenomas from [[Adenocarcinoma#Perianal gland adenocarcinoma|adenocarcinomas]], and further investigations should be carried out if malignancy is suspected.

====Treatment====
'''Castration''' is the treatment of choice and 95% of tumours will regress. Administration of oestrogens or anti-androgens can also be considered, but side-effects of those hormones should not be forgotten. Surgical removal of the tumour may be necessary if it is large, or in females.

==Sweat Gland Adenoma==
This is a tumour of the '''apocrine sweat gland''' and is rare in dogs and cats. It can be difficult to differentiate from an adenocarcinoma, and '''immunohistochemistry''' has been used for this purpose.

Adenomas rarely ulcerate, are associated with '''little local inflammation''' and have a cystic feel on palpation.

They occur most commonly in '''older dogs and cats''', and are usually restricted to the head.

Wide surgical excision usually carries a good prognosis.

==Ceruminous Gland Adenoma==
This occurs with some frequency in dogs and cats, and is thought to be linked to the '''presence of long-standing [[Otitis Externa - Cat and Dog|otitis externa]]''', leading to increased glandular dysplasia.

These tumours usually occur in older animals, and conservative local resection is usually sufficient to manage them.

==Sebaceous Gland Adenoma==
These are common in older dogs and cats and are usually distinctly '''wart-like or cauliflower-like''' in appearance.

Histopathology shows large mature sebaceous lobules with increased numbers of basaloid epithelial cells and a low mitotic activity.

The prognosis is good with surgical resection.

==Salivary Gland Adenoma==
This tumour is rare in animals, and the malignant adenocarcinoma is much more common.

==Mammary Gland Adenoma==
This is a benign tumour which is quite common in cats and dogs.

Find out more information on [[Mammary Neoplasia|mammary tumours]].

==Intestinal Adenoma==
[[Image:brunner gland adenoma.jpg|thumb|right|200px|Adenoma of brunners glands (duodenum) (Courtesy of Bristol BioMed Image Archive)]]
Intestinal adenomas are found in both the [[Small Intestine Overview - Anatomy & Physiology|small]] and [[Large Intestine - Anatomy & Physiology|large intestines]]. Intestinal adenomas usually grow into the lumen and can be called '''adenomatous polyps'''.

Depending on the type of the insertion base, the adenoma may be '''pedunculated''' with a long stalk, or '''sessile''' with a broad base. This influences the method of resection and the rate of recurrence, as pedunculated tumours are much more easily removed.

==Hepatic Adenoma==
It is seen mostly in '''sheep and cattle''' and usually presents as a single, pale, soft, often large nodule, which is well demarcated from adjacent tissue, often with a noticeable capsule. The tissue has a '''normal hepatocytic appearance'''. No portal tracts can be seen within the mass and a capsule surrounds the growth.

==Cholangiocellular Adenoma==
Also called '''biliary adenoma''', it is very rare but has been reported in dogs and cats. It shows an expansive growth and consists of slightly dilated, occasionally cystic structures, lined with cuboidal or flattened, well differentiated biliary epithelium.

==Pancreatic Adenoma==
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=7754 Image of multifocal pancreatic adenoma in a dog from Cornell Veterinary Medicine]
Adenoma of the '''exocrine (zymogen) cells of the pancreas''' is known in several species and is recognised by its ductal or acinar pattern of cells, with an expanding growth pattern and '''complete encapsulation'''. Cystic spaces may be created by the tumour cells, which may also project in a papillary pattern into the lumen of the cysts.

'''Hyperplastic nodules''' may be present in the pancreas of older animals. They are usually less well encapsulated than adenomas, but may be difficult to distinguish with certainty. They are usually multiple.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis01994.asp Adenoma and adenocarcinoma] [https://www.vetstream.com/equis/search?s=adenoma Search: adenoma]
|flashcards = [[Cytology Q&A 07]]
}}

==References==
Withrow, S. (2001) '''Small animal clinical oncology''' ''Elsevier Health Sciences''

Morrison, W. (2002) '''Cancer in dogs and cats: medical and surgical management''' ''Teton NewMedia''

Carlyle Jones, T. (1997) '''Veterinary pathology''' ''Wiley-Blackwell''

Cheville, N. (1999) '''Introduction to veterinary pathology''' ''Wiley-Blackwell''

{{review}}

{{OpenPages}}
[[Category:Expert Review]]
[[Category:Oropharynx - Pathology]]
[[Category:Intestines - Proliferative Pathology]]
[[Category:Liver, Primary Tumours]]
[[Category:Pancreas_-_Hyperplastic_and_Neoplastic_Pathology]]
[[Category:Neoplasia]]

Hernia

2016-06-25T18:39:51Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
[[Image:hernial sac.jpg|thumb|right|150px|Diagram of a hernial sac (Copyright Elspeth Milne 2007)]]
A hernia is defined as the displacement of an organ through a normal aperture (a '''true hernia''') or pathological aperture ('''false hernia''' or '''rupture'''). The mobile organs of the abdomen are most commonly displaced through apertures in the abdominal wall, diaphragm, inguinal canal or femoral canal.

In a true abdominal hernia, the displaced organs are contained within a '''hernial sac''' which consists of the parietal peritoneum together with any overlying soft tissues. In an '''external hernia''', the skin forms the outermost layer and the hernial sac and its contents are palpable. '''Internal hernias''' involve an aperture within the abdominal cavity. Since the parietal peritoneum is torn when ruptures occur, these do not have defined hernial sacs.

Hernias may be '''congenital''' or '''acquired'''. Congenital hernias usually result from a failure of physiological apertures (such as the umbilical canal) to close fully during embryonic or neonatal development whereas acquired hernias may be related to trauma, wounds or to physiological weakening of tissues with age, pregnancy or chronic straining.

==Pathogenesis==
The sequelae of a hernia depend on whether the hernia is reducible and if the herniated organs are incarcerated or strangulated.

===Reducible hernia===
The contents of the hernial sac can be moved back to their original position. These hernias tend not to cause clinical disease.

===Incarceration===
If the hernial ring narrows or if the displaced organs expand, the contents of the hernial sac may be trapped or 'incarcerated'. These structures cannot be moved back to their original position and surgical intervention is usually required to increase the size of the hernial ring. Incarcerated hernias also carry a greater risk of strangulation.

===Strangulation===
The contents of the hernial sac are trapped and their blood supply is impaired. Initially, only venous drainage is reduced leading to oedema and congestion but infarction may occur if the arterial blood supply is also affected. Strangulated loops of small intestine are unable to maintain an effective barrier against gastro-intestinal bacteria and bacterial endotoxin, leading to peritonitis, sepsis and endotoxic shock. The intestine may also rupture causing acute septic peritonitis.

==Types of hernia==
*'''[[Umbilical Hernia|Umbilical hernias]]''' are congenital and result from a failure of closure of the foetal umbilical canal. They occur in all of the major domestic species.
*'''Diaphragmatic hernias''' may be congenital or, much more commonly, [[Diaphragmatic Rupture|diaphragmatic ruptures]] may occur following blunt abdominal trauma in small animals. Congenital diaphragmatic hernias are an unusual cause of small intestinal incarceration and strangulation in horses, manifesting as severe colic. If the septum transversum (the embryonic structure that forms the diaphragm) fails to develop fully, congenital [[Hernia, Peritoneopericardial Diaphragmatic|Peritoneal-Pericardial-Diaphragmatic hernias]] (PPDH) or [[Hernia, Pleuroperitoneal Diaphragmatic|Pleuroperitoneal hernias]] may occur.
*'''[[Inguinal Hernia|Inguinal/scrotal hernias]]''' may be congenital or acquired. Congenital hernias are rare and usually occur in young male dogs with late testicular descent. It is suggested that this process holds the inguinal canal open for longer than normal, allowing abdominal organs to displace into them. Acquired hernias occur in obese animals (in which the canal is held open by the local accumulation of fat) and in older entire bitches (in which the gravid uterus may be herniated). Inguinal hernias also occur in stallions after castration and may cause severe colic.
*'''[[Perineal Hernia| Perineal hernias]]''' are true hernias where abdominal organs move into space created by the weakening or rupture of muscles forming the pelvic diapragm and anus. Older male entire dogs are particularly affected and these often have concurrent enlargement of the prostate gland.
*'''Ventral abdominal ruptures''' occur at sites of wound breakdown (after ventral midline coeliotomy) and in older pregnant mares and cows, particularly those suffering from hydrops uteri.
*'''Traumatic abdominal ruptures''' may occur at various locations in the abdomen resulting in prepubic ruptures, femoral hernias and paracostal ruptures in cats.
*'''Omental/mesenteric rents''' may result in internal hernias causing partial or complete intestinal obstruction.
*'''Epiploic foramen entrapment''' is a form of internal hernia affecting horses. Loops of small intestine may become trapped within the epiploic foramen and omental bursa causing complete intestinal obstruction and severe colic. Anecdotally, horses which 'windsuck' are at particular risk of this form of colic and it requires urgent surgical correction.
*'''[[Richter's Hernia|Richter's hernia]]''' is a rare form of hernia in which only one wall of the small intestine is trapped in the hernial sac, resulting in a partial intestinal obstruction.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/search?s=hernia Hernia]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=hernia&occuring1=title&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&publishedstart=2000&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all&x=43&y=15 Hernia publications since 2000]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103304730.pdf '''Biomaterials in the reconstruction of abdominal wall defects in animals: a review.''' Sharma, A. K.; Naveen Kumar; Gangwar, A. K.; Maiti, S. K.; SAARC Agricultural Information Centre (SAIC), Dhaka, Bangladesh, SAARC Journal of Agriculture, 2003, 1, pp 85-98, many ref.]
}}

==References==
Fossum, T. W. et. al. (2007) '''Small Animal Surgery (Third Edition)''' ''Mosby Elsevier''

[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=22114 Image of congenital umbilical hernia in a pig from Cornell Veterinary Medicine]

{{review}}

{{OpenPages}}

[[Category:Intestine_-_Physical_Disturbances]]
[[Category:Peritoneal_Cavity_-_Developmental_Pathology]][[Category:Peritoneal Cavity Diseases - Dog]][[Category:Peritoneal Cavity Diseases - Cat]][[Category:Donkey]][[Category:Peritoneal Diseases - Cattle]][[Category:Peritoneal Diseases - Sheep]]
[[Category:Expert_Review]]

[[Category:Peritoneal Cavity Diseases - Horse]]

Stomach Rupture

2016-06-25T18:31:16Z

Michuang0720:

* Occurs in:
** '''Dogs'''
*** Seen in animals that develop [[Gastric Dilatation and Volvulus|torsion of the stomach]]; however, they usually die first.
** '''Horses'''
***See [[Gastric Dilation and Rupture - Horse|Gastric dilatation and rupture]]
*** The equine [[Monogastric Stomach - Anatomy & Physiology|stomach]] may rupture if the animal eats too much, as the horse cannot [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomit]].

===Pathogenesis===

* Rupture usually occurs along greater curvature.
* While the muscle ruptures, the mucosa does not as it is much more flexible.
** Occasionally [[Monogastric Stomach - Anatomy & Physiology|stomach]] ruptures completely.
* Bacteria invade the abdomen, producting peritonitis.
** Horses are acutely sensitive to peritonitis (ruminants are much less so).
** This makes rupture acutely fatal, but animals usually die first from shock.

===Note===

* Post- mortem rupture of the [[Monogastric Stomach - Anatomy & Physiology|stomach]] may be seen in horses that have been dead for a few days.
** This is due to gas accumulation
* Ante-mortem rupture usually has haemorrhage associated with edges of lesion.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Illustration/ill03194.asp GDV: Gastric rupture picture 1] [https://www.vetstream.com/canis/Content/Illustration/ill03195.asp GDV: gastric rupture picture 2]
}}

[[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Gastric Diseases - Dog]]

[[Category:To_Do_-_Alimentary]][[Category:To Do - Major]]

Diaphragmatic Rupture

2016-06-25T18:26:17Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''Acquired Diaphragmatic Hernia — Displacement of Stomach into Thorax

Do not confuse with: [[Hiatal Hernia]], [[Hernia, Peritoneopericardial Diaphragmatic|Peritoneopericardial Hernia]], [[Hernia, Pleuroperitoneal Diaphragmatic|Pleuroperitoneal Hernia]], Congenital Diaphragmatic Hernia

==Description==
[[Image:stomach diaphragmatic hernia.jpg|thumb|right|150px|Post-mortem image of displacement of the stomach into the thorax through a diaphragmatic rupture (Sourced from BioMed Image Archive)]]
Rupture of the diaphragm is an acquired condition that often has a traumatic origin in small animals. The rupture is not a true [[Hernia|hernia]] as the parietal peritoneum is disrupted and displaced organs are not contained within a defined hernial sac. Most cases occur in animals which have suffered blunt abdominal trauma with an open glottis, most commonly during a road traffic accident (RTA). If the animal has a closed glottis at the moment of impact, the lung parenchyma is more likely to rupture. Any of the peritoneal abdominal organs may move into the thorax, of which the most commonly herniated are the liver and small intestine. In some cases, the stomach may be displaced into the thorax and, as its outflow is disrupted, it may become dilated and filled with gas. This situation requires urgent surgical intervention. Affected animals often have other injuries associated with the traumatic event, including:
*'''Thoracic injuries'''
**Pulmonary contusion
**Rib fracture or flail chest
**Haemothorax or chylothorax
**Pneumothorax with or without pneumomediastinum
**Tension pneumothorax
**Traumatic myocarditis
**Ruptured trachea
*'''Abdominal injuries'''
**Ruptured liver or spleen with haemabdomen
**Ruptured kidney, ureter or bladder with uroabdomen
**Traumatic abdominal wall rupture
**Pancreatitis
*'''Broken claws'''
*'''Fractured mandibular symphysis'''
*'''Pelvic, spinal or appendicular fractures'''
*'''Tail pull injuries'''
*'''Wounds'''

==Diagnosis==
===Clinical Signs===
*The animal may have a '''history consistent with blunt trauma''' (such as a road traffic accident, kick or blow to the abdomen) and broken claws are a common finding after an RTA.
*'''Respiratory distress''' as displaced abdominal organs in the thorax prevent the lungs from expanding fully and because the damaged diaphragm is incapable of contracting normally. Affected animals may also develop pleural effusion if abdominal organs become incarcerated or strangulated in the thorax or if they have concurrent thoracic pathology.
*'''Heart sounds may be muffled''' on auscultation and borborygmi may be heard.
*'''Percussion''' of the chest wall may reveal hyporesonance (due to a displaced gas-filled stomach) or hyperresonance (due to the presence of pleural fluid or solid organs, such as the liver, in the chest).
*'''The apex beat''' of the heart can usually be palpated and this may be displaced from the normal position on the left cranial ventral chest wall.
*In chronically affected animals, '''gastro-intestinal signs''' may be observed due to partial intestinal obstruction or pancreatitis.

===Radiography===
'''Plain chest radiographs''' will show that the margin of the diaphragm is no longer evident and abdominal organs, particularly gas-filled loops of small intestine, may be observed within the chest. This appearance should be distinguished from that of [[Hernia, Peritoneopericardial Diaphragmatic|peritoneopericardial diaphragmatic hernia]] in which abdominal organs only overly the cardiac silhouette. If the diagnosis is not certain, a barium swallow series could be performed or contrast medium could be instilled directly into the peritoneal cavity but these procedures have largely been superseded by the use of ultrasound.

===Ultrasonography===
This technique has been shown to be much more accurate than radiography for the diagnosis of diaphragmatic ruptures but care should be taken not to confuse the appearance of displaced abdominal organs with a reverberation artefact generated by the intact diaphragm.

===Pathology===
Displaced organs begin to form fibrinous adhesions within the chest almost immediately and these organise into fibrous structures over the following seven days. The rent in the diaphragm usually occurs in the muscular portion in small animals, often at different locations depending on the species affected:
*'''Dog''': Either radial or circumferential.
*'''Cat''': Circumferential tears are much more common than radial.
*'''Horse''': Tears usually occur through the tendinous portion.
The edges of the tear are gradually replaced by fibrous tissue and these may need to be resected if a surgical repair is subsequently attempted.

==Treatment==
===Stabilisation===
In most acute cases, animals must be stabilised before the tear in the diaphragm can be repaired surgically. This may involve the following steps:
*Provision of '''oxygen''' to dyspnoeic animals, using a mask, flow-by or intra-nasal catheter.
*'''[[Pleurocentesis]]''' if pleural effusion or pneumothorax are suspected.
*Keeping the animal in '''sternal recumbency''' to allow more efficient thoracic excursion.
*'''Gastric decompression''' by orogastric tube or percutaneously if the stomach is though to be dilated.
*Provision of '''analgesia'''.
*Other measures to treat other traumatic injuries.

===Surgical Repair===
Traditionally, it was recommended that at least 24 hours elapse from the traumatic event until the rupture was repaired to reduce perioperative mortality but newer evidence suggests that, if animals are adequately stabilised before this, surgical repair may still be successful <ref> Gibson TW, Brisson A and Sears W (2005): '''Perioperative survival rates after surgery for diaphragmatic hernia in dogs and cats: 92 cases''' J of the Am Vet Med Assoc '''227''' 105-109.</ref>. If possible, the repair should be conducted in the first week after rupture as fibrous adhesions begin to form after this time. Post-operative mortality is also higher if the rupture is repaired after a very long interval (more than 1 year) due to the formation of extensive fibrous adhesions.

The defect is approached by a ventral midline coeliotomy (which may be extended cranially beside the xiphisternum or into a median sternotomy) and the abdominal organs are retracted. Fibrinous adhesions can be easily separated but strangulated organs (such as torsed liver lobes or loops of small intestine) should be sacrificed and resected. If the rupture has been present for a long period, its fibrous edges may be debrided before suturing using polydioxanone in a continuous pattern. If there is a large defect that cannot be closed without tension, the following approaches may be used:
*Use of the muscle transversus abdominis as a flap to fill the defect.
*Use of porcine intestinal submucosa or synthetic mesh to fill the defect.
*Graft of omentum over sutures placed in the diaphragm.

===Post-operative Care===
Animals that have been treated for diaphragmatic rupture often require intensive care in a dedicated unit. The following aspects of care should be considered:
*'''Thoracostomy tube''': This can be placed through the diaphragm during surgery or a conventional tube can be passed through the chest wall. Negative pressure should restore to the pleural cavity after the rupture is repaired and the diaphragm should be seen to return to its concave shape when viewed from the abdomen. The chest should be drained (of air or fluid) regularly until no more can be aspirated than is expected due to the presence of the tube (~2 ml/kg/hour). Bupivacaine or another local anaesthetic agent can be instilled through the tube to provide topical analgesia.
*'''Pulmonary oedema''' may develop as the lungs re-expand due to physical forces acting on the alveoli and due to reperfusion injury to the alveolar capillaries. This condition should be suspected if the patient remains hypoxaemic even with oxygen therapy and it can be avoided by removing air from the pleural space slowly so that the lungs reinflate in a controlled manner. Animals can also be pre-treated with intra-venous corticosteroids to try to prevent the formation of reactive species in reperfusion injury.
*'''Incomplete repair''' or presence of a '''second rupture''': The whole diaphragm should be assessed before closure to ensure that a second tear is not present.
*Provision of '''analgesia'''.

==Prognosis==
Patients that undergo surgical repair of a rupture have a favourable prognosis, with around 90% being discharged after treatment. Animals that survive the first 24 hours after surgical repair are generally considered to do well subsequently.

{{Learning

|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre00521.asp Anesthesia: for ruptured diaphram] [https://www.vetstream.com/canis/Content/Illustration/ill06111.asp Intraoperative picture 1] [https://www.vetstream.com/canis/Content/Illustration/ill06112.asp Intraoperative picture 2] [https://www.vetstream.com/canis/Content/Illustration/ill00333.asp Radiograph DV] [https://www.vetstream.com/canis/Content/Illustration/ill00334.asp Radiograph lateral]
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22Diaphragmatic+rupture%22%29+OR+title%3A%28%22acquired+Diaphragmatic+hernia%22%29+OR+%28ab%3A%28diaphragm%29+AND+ab%3A%28rupture%29%29 Diaphragmatic rupture publications]
}}

==References==
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=11491 Image of traumatic diaphragmatic hernia with displaced intestine in a dog by Cornell Veterinary Medicine]
Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier
<references/>

{{review}}

{{OpenPages}}

[[Category:Stomach_and_Abomasum_-_Pathology]]

[[Category:Musculoskeletal Diseases - Cat]][[Category:Respiratory Diseases - Cat]][[Category:Peritoneal Cavity Diseases - Cat]][[Category:Peritoneal Cavity Diseases - Dog]][[Category:Musculoskeletal Diseases - Dog]][[Category:Respiratory Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Peritoneal Cavity Diseases - Horse]]

Diaphragmatic Rupture

2016-06-25T18:25:22Z

Michuang0720:

{{OpenPagesTop}}
Also known as: '''''Acquired Diaphragmatic Hernia — Displacement of Stomach into Thorax

Do not confuse with: [[Hiatal Hernia]], [[Hernia, Peritoneopericardial Diaphragmatic|Peritoneopericardial Hernia]], [[Hernia, Pleuroperitoneal Diaphragmatic|Pleuroperitoneal Hernia]], Congenital Diaphragmatic Hernia

==Description==
[[Image:stomach diaphragmatic hernia.jpg|thumb|right|150px|Post-mortem image of displacement of the stomach into the thorax through a diaphragmatic rupture (Sourced from BioMed Image Archive)]]
Rupture of the diaphragm is an acquired condition that often has a traumatic origin in small animals. The rupture is not a true [[Hernia|hernia]] as the parietal peritoneum is disrupted and displaced organs are not contained within a defined hernial sac. Most cases occur in animals which have suffered blunt abdominal trauma with an open glottis, most commonly during a road traffic accident (RTA). If the animal has a closed glottis at the moment of impact, the lung parenchyma is more likely to rupture. Any of the peritoneal abdominal organs may move into the thorax, of which the most commonly herniated are the liver and small intestine. In some cases, the stomach may be displaced into the thorax and, as its outflow is disrupted, it may become dilated and filled with gas. This situation requires urgent surgical intervention. Affected animals often have other injuries associated with the traumatic event, including:
*'''Thoracic injuries'''
**Pulmonary contusion
**Rib fracture or flail chest
**Haemothorax or chylothorax
**Pneumothorax with or without pneumomediastinum
**Tension pneumothorax
**Traumatic myocarditis
**Ruptured trachea
*'''Abdominal injuries'''
**Ruptured liver or spleen with haemabdomen
**Ruptured kidney, ureter or bladder with uroabdomen
**Traumatic abdominal wall rupture
**Pancreatitis
*'''Broken claws'''
*'''Fractured mandibular symphysis'''
*'''Pelvic, spinal or appendicular fractures'''
*'''Tail pull injuries'''
*'''Wounds'''

==Diagnosis==
===Clinical Signs===
*The animal may have a '''history consistent with blunt trauma''' (such as a road traffic accident, kick or blow to the abdomen) and broken claws are a common finding after an RTA.
*'''Respiratory distress''' as displaced abdominal organs in the thorax prevent the lungs from expanding fully and because the damaged diaphragm is incapable of contracting normally. Affected animals may also develop pleural effusion if abdominal organs become incarcerated or strangulated in the thorax or if they have concurrent thoracic pathology.
*'''Heart sounds may be muffled''' on auscultation and borborygmi may be heard.
*'''Percussion''' of the chest wall may reveal hyporesonance (due to a displaced gas-filled stomach) or hyperresonance (due to the presence of pleural fluid or solid organs, such as the liver, in the chest).
*'''The apex beat''' of the heart can usually be palpated and this may be displaced from the normal position on the left cranial ventral chest wall.
*In chronically affected animals, '''gastro-intestinal signs''' may be observed due to partial intestinal obstruction or pancreatitis.

===Radiography===
'''Plain chest radiographs''' will show that the margin of the diaphragm is no longer evident and abdominal organs, particularly gas-filled loops of small intestine, may be observed within the chest. This appearance should be distinguished from that of [[Hernia, Peritoneopericardial Diaphragmatic|peritoneopericardial diaphragmatic hernia]] in which abdominal organs only overly the cardiac silhouette. If the diagnosis is not certain, a barium swallow series could be performed or contrast medium could be instilled directly into the peritoneal cavity but these procedures have largely been superseded by the use of ultrasound.

===Ultrasonography===
This technique has been shown to be much more accurate than radiography for the diagnosis of diaphragmatic ruptures but care should be taken not to confuse the appearance of displaced abdominal organs with a reverberation artefact generated by the intact diaphragm.

===Pathology===
Displaced organs begin to form fibrinous adhesions within the chest almost immediately and these organise into fibrous structures over the following seven days. The rent in the diaphragm usually occurs in the muscular portion in small animals, often at different locations depending on the species affected:
*'''Dog''': Either radial or circumferential.
*'''Cat''': Circumferential tears are much more common than radial.
*'''Horse''': Tears usually occur through the tendinous portion.
The edges of the tear are gradually replaced by fibrous tissue and these may need to be resected if a surgical repair is subsequently attempted.

==Treatment==
===Stabilisation===
In most acute cases, animals must be stabilised before the tear in the diaphragm can be repaired surgically. This may involve the following steps:
*Provision of '''oxygen''' to dyspnoeic animals, using a mask, flow-by or intra-nasal catheter.
*'''[[Pleurocentesis]]''' if pleural effusion or pneumothorax are suspected.
*Keeping the animal in '''sternal recumbency''' to allow more efficient thoracic excursion.
*'''Gastric decompression''' by orogastric tube or percutaneously if the stomach is though to be dilated.
*Provision of '''analgesia'''.
*Other measures to treat other traumatic injuries.

===Surgical Repair===
Traditionally, it was recommended that at least 24 hours elapse from the traumatic event until the rupture was repaired to reduce perioperative mortality but newer evidence suggests that, if animals are adequately stabilised before this, surgical repair may still be successful <ref> Gibson TW, Brisson A and Sears W (2005): '''Perioperative survival rates after surgery for diaphragmatic hernia in dogs and cats: 92 cases''' J of the Am Vet Med Assoc '''227''' 105-109.</ref>. If possible, the repair should be conducted in the first week after rupture as fibrous adhesions begin to form after this time. Post-operative mortality is also higher if the rupture is repaired after a very long interval (more than 1 year) due to the formation of extensive fibrous adhesions.

The defect is approached by a ventral midline coeliotomy (which may be extended cranially beside the xiphisternum or into a median sternotomy) and the abdominal organs are retracted. Fibrinous adhesions can be easily separated but strangulated organs (such as torsed liver lobes or loops of small intestine) should be sacrificed and resected. If the rupture has been present for a long period, its fibrous edges may be debrided before suturing using polydioxanone in a continuous pattern. If there is a large defect that cannot be closed without tension, the following approaches may be used:
*Use of the muscle transversus abdominis as a flap to fill the defect.
*Use of porcine intestinal submucosa or synthetic mesh to fill the defect.
*Graft of omentum over sutures placed in the diaphragm.

===Post-operative Care===
Animals that have been treated for diaphragmatic rupture often require intensive care in a dedicated unit. The following aspects of care should be considered:
*'''Thoracostomy tube''': This can be placed through the diaphragm during surgery or a conventional tube can be passed through the chest wall. Negative pressure should restore to the pleural cavity after the rupture is repaired and the diaphragm should be seen to return to its concave shape when viewed from the abdomen. The chest should be drained (of air or fluid) regularly until no more can be aspirated than is expected due to the presence of the tube (~2 ml/kg/hour). Bupivacaine or another local anaesthetic agent can be instilled through the tube to provide topical analgesia.
*'''Pulmonary oedema''' may develop as the lungs re-expand due to physical forces acting on the alveoli and due to reperfusion injury to the alveolar capillaries. This condition should be suspected if the patient remains hypoxaemic even with oxygen therapy and it can be avoided by removing air from the pleural space slowly so that the lungs reinflate in a controlled manner. Animals can also be pre-treated with intra-venous corticosteroids to try to prevent the formation of reactive species in reperfusion injury.
*'''Incomplete repair''' or presence of a '''second rupture''': The whole diaphragm should be assessed before closure to ensure that a second tear is not present.
*Provision of '''analgesia'''.

==Prognosis==
Patients that undergo surgical repair of a rupture have a favourable prognosis, with around 90% being discharged after treatment. Animals that survive the first 24 hours after surgical repair are generally considered to do well subsequently.

{{Learning

|Vetstream = [https://www.vetstream.com/canis/Content/Freeform/fre00521.asp Regurgitation] [https://www.vetstream.com/canis/Content/Freeform/fre00521.asp Anesthesia: for ruptured diaphram] [https://www.vetstream.com/canis/Content/Illustration/ill06111.asp Intraoperative picture 1] [https://www.vetstream.com/canis/Content/Illustration/ill06112.asp Intraoperative picture 2] [https://www.vetstream.com/canis/Content/Illustration/ill00333.asp Radiograph DV] [https://www.vetstream.com/canis/Content/Illustration/ill00334.asp Radiograph lateral]
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22Diaphragmatic+rupture%22%29+OR+title%3A%28%22acquired+Diaphragmatic+hernia%22%29+OR+%28ab%3A%28diaphragm%29+AND+ab%3A%28rupture%29%29 Diaphragmatic rupture publications]
}}

==References==
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=11491 Image of traumatic diaphragmatic hernia with displaced intestine in a dog by Cornell Veterinary Medicine]
Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier
<references/>

{{review}}

{{OpenPages}}

[[Category:Stomach_and_Abomasum_-_Pathology]]

[[Category:Musculoskeletal Diseases - Cat]][[Category:Respiratory Diseases - Cat]][[Category:Peritoneal Cavity Diseases - Cat]][[Category:Peritoneal Cavity Diseases - Dog]][[Category:Musculoskeletal Diseases - Dog]][[Category:Respiratory Diseases - Dog]]
[[Category:Expert_Review]]
[[Category:Peritoneal Cavity Diseases - Horse]]

Regurgitation

2016-06-25T18:15:21Z

Michuang0720:

{{OpenPagesTop}}
==Introduction==
Regurgitation describes the '''passive, retrograde movement of food and water''' from the mouth or the oesophagus.

It is important to differentiate regurgitation from [[Vomiting|vomiting]] as they represent very different disease aetiologies.

Regurgitation is the '''hallmark sign of oesophageal disorders'''.

Causes include:

'''Oesophageal obstruction''':
:Congenital [[Vascular Ring Anomalies|vascular ring anomaly]]
:[[Oesophageal Foreign Body|Foreign body]]
:[[Oesophageal Stricture|Stricture]]
:Neoplasia
:Extraoesophageal compression: thyroid carcinoma, pulmonary alveolar cell carcinoma
:Rare miscellaneous causes: cricopharyngeal achalasia, oesophageal diverticulum, oesophageal atresia

'''[[Oesophagitis]]''':
:Gastrooesophageal reflux
:Persistent vomiting
:[[Hiatal Hernia|Hiatal hernia]]
:Caustic agents

'''[[Megaoesophagus]]''':
:Congenital megaoesophagus: idiopathic or [[Myasthenia Gravis|myasthenia gravis]]
:Acquired megaoesophagus
:Neuropathy: polyradioculoneuropathy
:Immune-mediated: polyneuritis, polymyositis, [[SLE]], myasthenia gravis, [[Canine Dermatomyositis|dermatomyositis]]
:Myopathy
:Metabolic: [[Hypothyroidism|hypothyroidism]], [[Hypoadrenocorticism|hypoadrenocorticism]]
:[[Lead Poisoning|Lead toxicity]]
:[[Canine Distemper Virus|Canine distemper]]
:[[Key-Gaskell Syndrome|Dysautonomia]]

'''Pharyngeal disorders''':
:[[Rabies|Rabies]]
:Foreign body
:Other obstructions

==Clinical Signs==
{| class="wikitable collapsible"
|'''Regurgitation'''
|'''Vomiting'''
|-
|Passive event
|Abdominal effort
|-
|No prodromal nausea
|Prodromal nausea
|-
|Undigested tubular food
|Usually digested food
|-
|Possibly painful
|No swallowing pain
|-
|Usually alkaline pH
|Alkaline or acidic pH
|-
|}

There may be additional signs such as '''coughing and dyspnoea''' secondary to [[Aspiration Pneumonia|aspiration pneumonia]].

Weakness may be present due to a '''systemic disorder''' such as myasthenia gravis, [[Addison's disease]], polymyositis.

Animals usually have a '''ravenous appetite'''.

'''Dysphagia''' may be present if the pharynx is involved.

==Diagnosis==
Diagnosis should take into account the signalment and history.

'''Physical examination''' may involve oesophageal palpation, lung auscultation to check for aspiration pneumonia, checking for underlying or concurrent diseases.

'''Plain radiography''': may detect a radioopaque foreign body.

'''Contrast radiography''': for radiolucent foreign bodies, obstructions, megaoesophagus.

'''Endoscopy''' may also be indicated to visualise the problem.

==Treatment==
'''The initiating cause should be treated''', which may involve removal of a foreign body or resection of a persistent right aortic arch.

Minimising the chances of '''aspiration pneumonia''' is important, and includes: feeding solid large pieces of food from a height.

General '''medical management''' may include: sucralfate liquid to act as a chemical bandage for the oesophagus, ranitidine and omeprazole to inhibit gastric acid secretion which may contribute to oesophagitis.

'''Complications''' following oesophageal disease include: [[Aspiration Pneumonia|aspiration pneumonia]] which should be treated aggressively, [[Oesophageal Stricture|oesophageal strictures]], continued [[oesophagitis]], perforation, [[Oesophageal Fistula|fistula]], diverticulum formation, motility disorders.

The prognosis is usually '''guarded'''.

{{Learning
|Vetstream = [https://www.vetstream.com/felis/Content/Disease/dis02654.asp Regurgitation]
|flashcards = [[Feline Medicine Q&A 07]]
}}

==References==
Allenspach, K. (2009) '''Dysphagia and regurgitation in small animals''' ''RVC student notes''

Pasquini, C. (1999) '''Tschauner's guide to small animal clinics''' ''Sudz Publishing''

{{review}}

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[[Category:Oesophagus - Pathology]]
[[Category:Expert Review]]