2009-08-22T09:27:43Z

RVC2:

{{unfinished}}

{{dog}}
{{cat}}

==Signalment==
*Relatively common in dog, especially small breed dogs
*Purebred dogs are more at risk

==Description==
'''Hepatic encephalopathy''' is characterised by a complex of neurological abnormalities that may occur in the presence of advanced liver disease. By far the most common cause in dog and cat is [[Portosystemic Shunt]] (PSS), although a marked reduction in functional mass of hepatic tissue can also lead to hepatic encephalopathy. In rare cases, when severe acquired shunt due to hepatobiliary disease and congenital PSS have been ruled out, congenital urea enzyme cycle deficiencies and organic acidaemias, where there is lack of ability to degrade ammonia to urea, can be considered.

This is a reversible abnormality of the cerebral metabolism. Its pathogenesis is not yet fully understood. Increased concentration of ammonia level is the most common cause of this disease manifestation, due to its toxicity effect on brain cells. Due to the lack of urea cycle in the brain, ammonia in [[Cerebral Spinal Fluid - Anatomy & Physiology|cerebrospinal fluid (CSF)]] is detoxified into glutamine. Level of glutamine can be shown to correlate with clinical signs. Aromatic amino acids, especially tryptophan and its metabolites, share an antiport transporter with ammonia in CSF. Consequently, dogs with congenital PSS are reported to have increased aromatic amino acid concentrations in CSF. Increased ammonia concentrations also have a number of other effects on the central nervous system, including a reduction in serotonin activity, an increased in NMDA (N-methyl-D-aspartic acid) and peripheral-type benzodiazepine receptors.

The sources responsible for an increase in ammonia levels include:

*the bacterial and intestinal breakdown of urea by urease, which then diffuse into the [[Colon - Anatomy & Physiology|colon]] from the blood.
*the bacterial breakdown of undigested amino acids in the [[Colon - Anatomy & Physiology|colon]].
*the catabolic metabolism of glutamine as an energy source by small intestinal enterocytes.
*endogenous hepatic protein metabolism by excess dietary protein intake, breakdown of lean body mass and gastrointestinal bleeding.

==Diagnosis==
===Clinical Signs===

====Dog====
Typical signs include:
*anorexia, depression and lethargy
*aimless wandering, head pressing, circling and pacing
*central blindness
*poor growth rate
*gastrointestinal signs such as [[Stomach and Abomasum Consequences of Gastric Disease - Pathology|vomiting]]
*coma (uncommon)
*seizures (uncommon)

Other signs include:
*temporary resolution of clinical signs with antimicrobial therapy
*prolonged recovery from sedation or anaesthesia
*polyuria and polydipsia in 33% of cases

====Cat====
Typical signs include:
*well grown and in good body condition which in contrast to dogs
*hypersalivation or ptyalism is the most commonly reported clinical feature, but rarely reported in dogs
*seizures, found in 50% of cases, but uncommon in dogs
*anorexia, vomiting and diarrhoea, polyuria and polydipsia are less common
*compulsive behaviour is less common compared to in dogs

===Laboratory Tests===
====Biochemistry====
*Hypoproteinaemia
*Mild to moderate increase in alanine aminotransferase (ALT) and alkaline phosphatase (ALP)
*Decreased blood urea nitrogen (BUN)
*Hypoglycaemia in a small number of dogs

====Other Tests====
*Fasting hyperammonaemia
*Increased postprandial ± preprandial bile acids

===Diagnostic Imaging===
====Radigraphy====
Abdominal radiography shows microhepatica and often renomegaly. Renomegaly may relate to an altered splanchnic blood flow or to an increased metabolic activity of the kidney due to hyperammonaemia. These findings in a young dog are highly suggestive of [[Portosystemic Shunt]].

Confirmation of a [[Portosystemic Shunt]] requires visualisation of the shunting blood vessel. This may be done with either ultrasonography or contrast portography or at surgery.

==Treatment==
===Surgical management===
*Surgical ligation of shunt is recommended in cases of [[Portosystemic Shunt]].

===Medical management===
*Enemas to decrease the amount of bacteria in the [[Colon - Anatomy & Physiology|colon]].
*Oral antibiotics such as [[Penicillins|ampicillin]], [[Aminoglycosides|neomycin]] or [[Nitroimidazoles|metronidazole]] can be given initially reduce the amount of bacteria in intestines and hence decrease the production of ammonia.
*[[Drugs Acting on the Intestines#Osmotic Laxatives|Lactulose]] PO
**This is a synthetic disaccharide which is metabolised by the acidifying colonic bacteria. Ammonia is converted into ammonium ions, which cannot be absorbed and hence trapped in the colon and excreted in the faeces. [[Drugs Acting on the Intestines#Osmotic Laxatives|Lactulose]] also acts as an osmotic laxative, allowing more faeces and bacteria to be washed out.
*A high carbohydrate, low protein (2g/kg/day) and low fat diet is recommended.
**The aim is to provide adequate nutrients and energy to support hepatic tissue [[Liver General Pathology - Pathology#Fibrosis - Repair|repair]], reduce the metabolic load on the liver and minimise the development of hepatic encephalopathy

==Prognosis==
In cases of PSS, the prognosis in dogs for resolution of clinical signs after total surgical ligation is excellent. However, the response of cat to surgical intervention in cats is less promising than in dogs.

==References==
*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''.
*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''.

2009-08-22T08:46:06Z

RVC2:

Short Bowel Syndrome

2009-08-22T08:44:39Z

RVC2: /* Description */

{{review}}

{{dog}}
{{cat}}

==Description==
'''Short bowel syndrome''' occurs when greater than 75-90% of [[Small Intestine - Anatomy & Physiology|small intestine]] is absent. It is most commonly caused by iatrogenic surgical resection, although congenital anomaly can occur in rare cases. The remaining [[Small Intestine - Anatomy & Physiology|small intestine]] cannot adequately absorb nutrients and electrolytes, resulting in [[Intestine Diarrhoea - Pathology|diarrhoea]]. If the [[Colon - Anatomy & Physiology|ileocolic valve]] has been removed, large number of bacteria is more likely to reach the small intestine. Changes in gastrointestinal hormone regulation such as hypergastrinaemia and increased acid secretion may occur.

This syndrome may only be transient until the remaining intestine can undergo adaptive [[Patología - Alteraciones del Crecimiento Celular #Hyperplasia|hyperplasia]]. However, it does not necessary occur in all cases of massive intestinal resection. Large resection of intestine should ideally be avoided in the first instance. If needed, it may be better to perform a second surgery 24-48 hours after the first surgery.

==Diagnosis==
===Clinical Signs===
*Small intestinal [[Intestine Diarrhoea - Pathology|diarrhoea]], often with undigested food particles in the faeces
*Severe weight loss

In cases which occur after surgical bowel resection, the presenting clinical signs are sufficient to make a diagnosis. In cases of congenital origin, a plain or contrast radiography is required.

==Treatment==
===Nutritional support===
*Total or partial parenteral nutrition may be required to provide adequate nutrition until adaptive hyperplasia takes place.
*At the same time, it is important to continue oral feeding to stimulate mucosal [[Patología - Alteraciones del Crecimiento Celular #Hypertrophy|hypertrophy]].

===Dietary modification===
*Small, frequent meals of highly digestible, low fat diet is recommended.
*Vitamin supplementation may be required.

===Antimicrobials===
*A secondary [[Small Intestinal Bacterial Overgrowth and Antibiotic Responsive Diarrhoea - WikiClinical|antibiotic responsive diarrhoea]] may result if the ileocaecal valve is removed.
*[[Nitroimidazoles|Metronidazole]] or [[Macrolides and Lincosamides|tylosin]] can be given in these cases.

===Antisecretory agents & antacids===
*These may be needed in cases which are poorly responsive diet and antimicrobials alone. Its aim is to lessen diarrhoea and gastric hypersecretion.
*Antisecretory agents such as [[Drugs Acting on the Intestines #Opioid Receptor Agonists|loperamide]], [[Drugs Acting on the Intestines #Opioid Receptor Agonists|diphenoxylate]].
*Antacids such as [[Gastroprotective Drugs #Histamine (H2) Receptor Antagonists|ranitidine]], [[Gastroprotective Drugs #Histamine (H2) Receptor Antagonists|famotidine]].

==Prognosis==
This is dependent on the length of the small intestine left and response to therapy. If adequate adaption occurs, the patient may respond well and eventually be able to consume a near-normal diet. However, there will always be a limitation in the absorptive capacity of these animals. Some cases may respond poorly and can never be fed on a normal diet and others may die. Malnourished animals have a poorer prognosis.

==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''.

Short Bowel Syndrome

2009-08-22T08:44:25Z

RVC2:

{{review}}

{{dog}}
{{cat}}

==Description==
'''Short bowel syndrome''' occurs when greater than 75-90% of [[Small Intestine - Anatomy & Physiology|small intestine]] is absent. It is most commonly caused by iatrogenic surgical resection, although congenital anomaly can occur in rare cases. The remaining [[small intestine]] cannot adequately absorb nutrients and electrolytes, resulting in [[Intestine Diarrhoea - Pathology|diarrhoea]]. If the [[Colon - Anatomy & Physiology|ileocolic valve]] has been removed, large number of bacteria is more likely to reach the small intestine. Changes in gastrointestinal hormone regulation such as hypergastrinaemia and increased acid secretion may occur.

This syndrome may only be transient until the remaining intestine can undergo adaptive [[Patología - Alteraciones del Crecimiento Celular #Hyperplasia|hyperplasia]]. However, it does not necessary occur in all cases of massive intestinal resection. Large resection of intestine should ideally be avoided in the first instance. If needed, it may be better to perform a second surgery 24-48 hours after the first surgery.

==Diagnosis==
===Clinical Signs===
*Small intestinal [[Intestine Diarrhoea - Pathology|diarrhoea]], often with undigested food particles in the faeces
*Severe weight loss

In cases which occur after surgical bowel resection, the presenting clinical signs are sufficient to make a diagnosis. In cases of congenital origin, a plain or contrast radiography is required.

==Treatment==
===Nutritional support===
*Total or partial parenteral nutrition may be required to provide adequate nutrition until adaptive hyperplasia takes place.
*At the same time, it is important to continue oral feeding to stimulate mucosal [[Patología - Alteraciones del Crecimiento Celular #Hypertrophy|hypertrophy]].

===Dietary modification===
*Small, frequent meals of highly digestible, low fat diet is recommended.
*Vitamin supplementation may be required.

===Antimicrobials===
*A secondary [[Small Intestinal Bacterial Overgrowth and Antibiotic Responsive Diarrhoea - WikiClinical|antibiotic responsive diarrhoea]] may result if the ileocaecal valve is removed.
*[[Nitroimidazoles|Metronidazole]] or [[Macrolides and Lincosamides|tylosin]] can be given in these cases.

===Antisecretory agents & antacids===
*These may be needed in cases which are poorly responsive diet and antimicrobials alone. Its aim is to lessen diarrhoea and gastric hypersecretion.
*Antisecretory agents such as [[Drugs Acting on the Intestines #Opioid Receptor Agonists|loperamide]], [[Drugs Acting on the Intestines #Opioid Receptor Agonists|diphenoxylate]].
*Antacids such as [[Gastroprotective Drugs #Histamine (H2) Receptor Antagonists|ranitidine]], [[Gastroprotective Drugs #Histamine (H2) Receptor Antagonists|famotidine]].

==Prognosis==
This is dependent on the length of the small intestine left and response to therapy. If adequate adaption occurs, the patient may respond well and eventually be able to consume a near-normal diet. However, there will always be a limitation in the absorptive capacity of these animals. Some cases may respond poorly and can never be fed on a normal diet and others may die. Malnourished animals have a poorer prognosis.

==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''.

Protein Losing Enteropathy

2009-08-22T08:43:08Z

RVC2:

{{review}}

{{dog}}
{{cat}}

==Signalment==
Breed predisposition:
*[[Canine Breeds - WikiNormals #Hound Group|Basenji]]
*Lundehund
*[[Canine Breeds - WikiNormals #Terrier Group|Soft-Coated Wheaten Terrier]]
*[[Canine Breeds - WikiNormals #Toy Group|Yorkshire Terrier]]
*[[Canine Breeds - WikiNormals #Utility Group|Shar Pei]]

==Description==
'''Protein-losing enteropathy (PLE)''' can result from any intestinal disease which produces sufficient [[Inflammation - Pathology|inflammation]], congestion or bleeding. This causes protein to leak into the intestines, which exceeds capacity of the gut lumen protein synthesis. Hence, there are numerous causes of PLE, including [[Lymphangiectasia - WikiClinical|lymphangiectasia]], infectious causes, structural causes, neoplasia, [[Inflammation - Pathology|inflammation]], endoparasites and gastrointestinal [[Haemorrhage - Pathology|haemorrhage]].

The major causes of PLE in adult dogs are [[Inflammatory Bowel Disease - WikiClinical|inflammatory bowel disease (IBD)]], alimentary tract lymphoma, fungal infections (e.g. [[Systemic Mycoses #Histoplasmosis|histoplasmosis]]). Other causes include ulcerations or erosions, severe disease of intestinal crypts and parasites. The most common causes in very young dogs are [[Small Animals #Nematodes of Dogs - the HOOKWORMS|hookworms]] and chronic intussusception. Chronic intussusception results from acute enteritis which has not resolved completely. The animal shows some clinical improvement but diarrhoea still continues. PLE is less common in cats than dogs, and most often caused by alimentary tract lymphoma and IBD. Cats almost never suffer from [[Lymphangiectasia - WikiClinical|lymphangiectasia]], and rarely have severe parasitic infection severe enough to cause PLE. Non-intestinal diseases can be associated with PLE include ][[Pathophysiology of Heart Failure - Pathology|congestive heart failure]], caval obstruction and portal hypertension. However, these animals usually present with ascites rather than [[Intestine Diarrhoea - Pathology|diarrhoea]].

==Diagnosis==
===Clinical Signs===
*Weight loss (predominant feature)
*Vomiting and diarrhoea ± melena
*[[Oedema - Pathology|Oedema]], ascites and pleural effusion
*Thickened intestines
*[[Thrombosis - Pathology #Thromboembolism|Thromboembolic]] disease if procoagulants predominant due to loss of anticoagulant

===Laboratory Tests===
====Haematology====
*Panhypoproteinaemia
**Hepatic insufficiency and protein-losing nephropathy should also be pursued with hypoalbuminaemia.
*[[Changes in Inflammatory Cells Circulating in Blood - Pathology #Lymphopenia|Lymphopaenia]]

====Biochemistry====
*Hypocholesterolaemia
*[[Hypocalcaemia - Small Animal|Hypocalcaemia]]

====Other Tests====
*Measurement of faecal loss alpha1-protease inhibitor

===Diagnostic Imaging===
====Radiography====
*Abdominal radiographs are usually unremarkable.
*Thoracic radiographs may show [[Peritoneal Cavity Effusions - Pathology|pleural effusion]], metastatic neoplasia or eveidence of [[Systemic Mycoses #Histoplasmosis|histoplasmosis]]).

====Ultrasonography====
*This may reveal thickening of intestines, mesenteric lymphadenopathy or abdominal effusion.

===Histopathology===
*Endoscopically-guided multiple biopsies are useful. Surgical biopsy may be required for a definitive diagnosis of lymphoma and [[Lymphangiectasia - WikiClinical #Description|secondary lymphangiectasia]]. A small fatty meal could be given the night before biopsy to increase the chance of diagnosing [[Lymphangiectasia - WikiClinical|lymphangiectasia]].

==Treatment==
===Plasma transfusion===
*This may be used to increase plasma volume. However, much of the albumin is lost in the gut and a substantial amount fails to remain in the intravascular compartment. Therefore, the extent of increase in serum albumin level is not great.
*Administration of [[Colloids|colloid]] may be more suitable if it is essential to increase the plasma oncotic pressure.

===Diuretics===
*This can be used to reduce ascites.
*[[Treatment of Heart Failure - WikiClinical #C. Pharmacological |Spironolactone]] 1-2 mg/kg PO BID may be more effective than [[Treatment of Heart Failure - WikiClinical #C. Pharmacological|frusemide]].

==Prognosis==
This depends on the underlying cause.

==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''.
*Willard, M. (2005) '''Protein-Losing Enteropathy in Dogs and Cats''' ''30th World Congress of the WSAVA''.

Lymphangiectasia

2009-08-22T08:42:23Z

RVC2: /* Immunosuppressive */

{{review}}

{{dog}}
{{cat}}

==Signalment==
*Breed predisposition:
**[[Canine Breeds - WikiNormals #Toy Group|Yorkshire Terrier]]
**Lundehund
**[[Canine Breeds - WikiNormals #Working Group|Rottweiler]]
**[[Canine Breeds - WikiNormals #Terrier Group|Soft Coated Wheaten Terriers]]

==Description==
'''Lymphangiectasia''' is characterised by dilation and dysfunction of the [[Lymphatic Vessels - Anatomy & Physiology|lymphatic vessels]] of the intestines. Consequently, protein rich [[Lymph - Anatomy & Physiology|lymph]] leaks into the intestinal lumen, causing a [[Intestines Protein-Losing Diseases - Pathology|
protein-losing enteropathy]] and severe lipid malabsorption. It is relatively common in dogs but rare in cats.

Lymphangiectasia can be classified into a primary or a secondary lymphangiectasia. '''Primary lymphangiectasia''' may form part of a localised or a more widespread lymphatic abnormality. '''Secondary lymphangiectasia''' results from lymphatic obstruction, which may be caused by:
*[[Inflammation - Pathology|inflammation]],[[Neoplasia - Pathology|neoplastic]] infiltration or fibrosis
*thoracic duct obstruction
*[[Right-Sided Heart Failure - WikiClinical|right sided cardiac failure]]
*caval obstruction
*hepatic disease

Lymphangiectasia often accompanies a lipogranulomatous [[Inflammation - Pathology|inflammation]], but it is not clear which is the primary event. [[Oedema - Pathology#Lymphatic oedema|Lymphangitis]] can cause lymphatic obstruction but the leakage of [[Lymph - Anatomy & Physiology|lymph]] can also cause a [[Chronic Inflammation - Pathology#Granulomatous Inflammation|granuloma]] to form.

==Diagnosis==
===Clinical Signs===
*Weight loss
*Chronic [[Intestine Diarrhoea - Pathology|diarrhoea]]; steatorrhoea
*Ascites, oedema or chylothorax may result if there is severe hypoproteinaemia or lymphatic obstruction
*Increased appetite
*[[Stomach and Abomasum Consequences of Gastric Disease - Pathology|Vomiting]], lethargy and anorexia (less common)

===Laboratory Tests===
====Haematology====
*'''Panhypoproteinaemia'''
*'''[[Changes in Inflammatory Cells Circulating in Blood - Pathology #Lymphopenia|Lymphopaenia]]'''

====Biochemistry====
*'''Hypocholesterolaemia'''
*[[Hypocalcaemia - Small Animal|Hypocalcaemia]] due to hypoproteinaemia, vitamin D and calcium malabsorption
*Hypomagnesaemia

[[Image:Lymphangiectasia.jpg|thumb|right|300px|Lymphangiectasia Endoscopy- Copyright Karin Allenspach's lecture RVC]]

====Other Tests====
*Faecal α1-proteinase inhibitor concentrations or chromium 51-labelled albumin may be used to confirm [[Intestines Protein-Losing Diseases - Pathology|protein-losing enteropathy]].

===Diagnostic Imaging===
====Ultrasound====
Abdominal ultrasonography may reveal pleural fluid or ascites as well as helping to narrow down other differential diagnoses. Mucosa of intestinal loops may appear thickened due to oedema.

====Endoscopy====
Grossly, multiple white lipid droplets with prominent mucosal blebs can be seen.

===Histopathology===
Preferably, a full thickness biopsy is needed for a definitive diagnosis.

Refer to [[Intestines Inflammatory Bowel Disease And Related Conditions - Pathology #Lymphangiectasia|Lymphangiectasia]] for pathology

It is essential to distinguish a true lymphangiectasia from a secondary lacteal dilation due to [[Inflammatory Bowel Disease - WikiClinical|Inflammatory Bowel Disease ]] (IBD). In the case of IBD, inflammatory infiltrate will be seen in the lamina propria, but the degree of infiltration may be underestimated if [[Oedema - Pathology|oedema]] is present.

==Treatment==
*Identify and treat the underlying cause if it is a secondary lymphangiectasia
===Dietary modification===
*Fat-restricted diet
*The diet needs to be calorific and highly digestible
*Supplementation of fat soluble vitamins
*Anecdotal report of glutamine supplementation

===Immunosuppressive===
*[[Steroids|Prednisolone]]
*[[Anti-Inflammatory Drugs|Anti-inflammatory]] and immunosuppressive effect may be beneficial.
*This is particularly true if there is associated lymphangitis, lipogranulomas or a [[Lymphocytic - Plasmacytic Enteritis - WikiClinical|lymphocytic-plasmacytic]] infiltration of the lamina propria.
*Azathioprine or Ciclosporin can also be considered

===Antimicrobials===
*[[Nitroimidazoles|Metronidazole]] or [[Macrolides and Lincosamides|tylosin]] can be given
*This may be beneficial due to their potential immunomodulatory effect and modulation of the enteric flora
*Diuretics such as [[Treatment of Heart Failure - WikiClinical #C. Pharmacological|frusemide]] and [[Treatment of Heart Failure - WikiClinical #C. Pharmacological|spironolactone]] are used to manage effusions.

===Fluid therapy===
*Short term treatment with [[Plasma - WikiBlood|plasma]] or [[Colloids|colloids]] can be given for plasma expansion.

==Prognosis==
Guarded. The response to treatment is generally poor although some dogs may do well. Dogs may be in remission for several years but the disease eventually progress to fulminant hypoproteinaemia.

==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''.