Difference between revisions of "Gastric Ulceration - Dog"

Revision as of 12:53, 19 August 2009

Signalment

Sled dogs

Description

Is a round or oval punched out lesions ranging from 1-4 cm in diameter caused by damage to the gastric mucosa.

There are many disease associations including:

Disease type	E.g.
Hypotension	Shock, Sepsis
Drug - induced	Non-steroidal anti-inflammatory drugs (NSAIDs)
Idiopathic	Stress, exercise induced
Inflammatory	Gastritis
Neoplastic	Adenocarcinoma, lymphosarcoma, leiomyoma
Metabolic/endocrine	Hypoadrenocorticism, liver disease, uraemia, disseminated intravascular coagulation, mastocytosis and hypergastrinaemia

Gastric ulceration is caused by damage to the gastric mucosa through the above mechanisms. NSAIDs directly damage the mucosa and interfere with the prostaglandin synthesis. Gastric ulceration is worsened by the use of NSAIDs in combination with corticosteroids. This risk can be minimised by using cyclooxygenase-1 (COX-1) sparing NSAIDs (carprofen, meloxicam and deracoxib.

Gastric acid hypersecretion following mast cell degranulation of histamine and gastrin secretion from gastrinomas is a major cause of gastric ulceration. Sled dogs and equine race horses are prone to gastric ulceration.

Diagnosis

History and Clinical Signs

History may involve:

Access to toxins and drugs such as NSAIDs

Clinical Signs:

Vomiting
Haematemesis
Malaena
Pale mucous membranes
Abdominal pain
Weakness
Inappetance
Hypersalivation
Circulatory comprimise

Haematology

Anaemia - regenerative initially, may progress to microcytic, hypochromic and minutely regenerative.
Thrombocytosis
Lack of stress leucogram (and lymphocytosis and eosinophilia) supportive of hypoadrenocorticism
Examination of the buffy coat may detect mastocytosis
Neutrophilia and a left shift - signs of inflammation or gastric perforation
May show abnormalities in haemostasis

Biochemistry

Dehydration - azotaemia
Hepatic disease - increased liver enzymes and bilirubin, decreased urea, albumin and cholesterol
Renal disease - azotaemia
Hypoadrenocorticism - Sodium:Potassium ratio of less than 27:1
Vomiting will lead to electrolyte and acid-base abnormalities - metabolic alkalosis, hypokalaemia and hypochloraemia

Urinalysis

Dehydration - Hypersthenuria
Renal disease - Isosthenuria

Plain radiography

Not usually diagnostic but rules out differentials.

Positive Contrast Radiography

May show filling defects.

Ultrasonography

Shows gastric thickening and rules out differentials.

Endoscopy and Biopsy

Diagnostic test of choice and allows biopsies to be taken. NSAID related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated gastric tumours will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased to avoid further deepening or perforation.

Treatment

The main aim is to treat any primary underlying cause whilst giving general support. This may be hydrating, restoring electrolytes and acid-base and also helping the gastric lining to recover.

Fluid therapy

Acid-base correction

Mucosal protectants

Prophylaxis

Anti-emetics

Analgesia

Antibiotics

Surgery

May be required to investigate or to resect peforating ulcers which may lead to peritonitis.

Prognosis

Depends upon the cause

References

@@ Line 1: / Line 1: @@
-{{OpenPagesTop}}
+{{unfinished}}
-Also known as: '''''Gastrointestinal ulceration
-==Introduction==
-See also:'''[[Gastric Ulceration - all species]]'''
+See also [[Stomach and Abomasum Inflammation - Pathology#Erosive and Ulcerative Gastritis|Pathology in WikiPath]]
-Gastric ulcer is a round or oval punched out lesion of the gastric mucosa ranging from 1-4 cm in diameter.
+==Signalment==
+*Sled dogs
+==Description==
+Is a round or oval punched out lesions ranging from 1-4 cm in diameter caused by damage to the gastric mucosa.
 There are many disease associations including:
@@ Line 17: / Line 18: @@
 |-
 |'''Hypotension'''
-|[[Shock|Shock]], Sepsis
+|Shock, Sepsis
 |-
 |'''Drug - induced'''
-|[[NSAIDs|Non-steroidal anti-inflammatory drugs (NSAIDs)]]
+|Non-steroidal anti-inflammatory drugs (NSAIDs)
 |-
 |'''Idiopathic'''
@@ Line 26: / Line 27: @@
 |-
 |'''Inflammatory'''
-|[[Gastritis, Acute|Gastritis]], [[Pancreatitis - Dog|Pancreatitis]]
+|Gastritis
 |-
 |'''Neoplastic'''
-|Adenocarcinoma, lymphosarcoma, leiomyoma, [[Gastrinoma|gastrinoma]], (Zollinger-Ellison syndrome), Mast cell Tumours.
+|Adenocarcinoma, lymphosarcoma, leiomyoma
 |-
 |'''Metabolic/endocrine'''
-|Hypoadrenocorticism, liver disease, [[Uraemia|uraemia]], [[Disseminated Intravascular Coagulation|Disseminated Intravascular Coagulation (DIC)]], mastocytosis and hypergastrinaemia
+|Hypoadrenocorticism, liver disease, uraemia, disseminated intravascular coagulation, mastocytosis and hypergastrinaemia
 |}
-Gastric ulceration is caused by damage to the gastric mucosa through the above mechanisms. [[NSAIDs|NSAIDs]] directly damage the mucosa and interfere with prostaglandin synthesis. Gastric ulceration is worsened by the use of NSAIDs in combination with [[Steroids|corticosteroids]]. This risk can be minimised by using cyclooxygenase-1 (COX-1) sparing NSAIDs.
+Gastric ulceration is caused by damage to the gastric mucosa through the above mechanisms. NSAIDs directly damage the mucosa and interfere with the prostaglandin synthesis. Gastric ulceration is worsened by the use of NSAIDs in combination with corticosteroids. This risk can be minimised by using cyclooxygenase-1 (COX-1) sparing NSAIDs (carprofen, meloxicam and deracoxib.
-Gastric acid hypersecretion following mast cell degranulation of histamine and gastrin secretion from [[Gastrinoma|gastrinomas]] is a major cause of gastric ulceration.
+Gastric acid hypersecretion following mast cell degranulation of histamine and gastrin secretion from gastrinomas is a major cause of gastric ulceration. Sled dogs and equine race horses are prone to gastric ulceration.
-==Signalment==
+==Diagnosis==
-[[Image:Gastric ulceration.jpg|thumb|right|250px|Gastric Ulceration - by David Walker RVC]]
+===History and Clinical Signs===
-Sled dogs are prone to gastric ulceration.
+History may involve:
+*Access to toxins and drugs such as NSAIDs
+Clinical Signs:
+*Vomiting
+*Haematemesis
+*Malaena
+*Pale mucous membranes
+*Abdominal pain
+*Weakness
+*Inappetance
+*Hypersalivation
+*Circulatory comprimise
-==Clinical Signs==
-History may involve access to toxins and drugs such as [[NSAIDs|NSAIDs]].
-Clinical Signs can include vomiting, haematemesis, malaena, pale mucous membranes, abdominal pain, weakness, inappetance and hypersalivation which can progress to circulatory compromise.
-==Laboratory Tests==
 ===Haematology===
-[[Regenerative and Non-Regenerative Anaemias|Anaemia]] which may be regenerative initially, and can progress to microcytic, hypochromic and minutely regenerative anaemia.
+*Anaemia - regenerative initially, may progress to microcytic, hypochromic and minutely regenerative.
-A thrombocytosis may also be present. If a [[Stress Leucogram|stress leucogram]] (lymphopenia and neutrophilia) is not present this is supportive of hypoadrenocorticism.
+*Thrombocytosis
-Examination of the buffy coat may detect mastocytosis.
+*Lack of stress leucogram (and lymphocytosis and eosinophilia) supportive of hypoadrenocorticism
-A [[Neutrophilia|Neutrophilia]] and a left shift are indicative of inflammation or gastric perforation.
+*Examination of the buffy coat may detect mastocytosis
-There may also be abnormalities in [[:Category:Haemostasis and Bleeding Disorders|haemostasis]].
+*Neutrophilia and a left shift - signs of inflammation or gastric perforation
+*May show abnormalities in haemostasis
 ===Biochemistry===
-Increased liver enzymes and bilirubin, decreased urea, albumin and cholesterol will indicate hepatic disease as an underlying problem.
+*Dehydration - azotaemia
-If renal disease is present, an azotaemia will be present on biochemistry.
+*Hepatic disease - increased liver enzymes and bilirubin, decreased urea, albumin and cholesterol
-If Hypoadrenocorticism is the cause of the ulceration, it is likely biochemistry will show a Sodium:Potassium ratio of less than 27:1.
+*Renal disease - azotaemia
-If the animal is vomiting this will lead to electrolyte and acid-base abnormalities, a metabolic alkalosis, hypokalaemia and hypochloraemia.
+*Hypoadrenocorticism - Sodium:Potassium ratio of less than 27:1
+*Vomiting will lead to electrolyte and acid-base abnormalities - metabolic alkalosis, hypokalaemia and hypochloraemia
 ===Urinalysis===
-Animals will be dehydrated resulting in hypersthenuria. If renal disease is the underlying cause, urine may be isosthenuric.
+*Dehydration - Hypersthenuria
+*Renal disease - Isosthenuria
 ===Plain radiography===
-[[Image:Gastric ulceration.png|thumb|right|250px|Gastric Ulceration - by David Walker RVC]]
+Not usually diagnostic but rules out differentials.
-Not usually diagnostic but can rule out differentials such as [[Gastric Foreign Objects|foreign bodies]] and [[Peritonitis|peritonitis]].
-===Positive contrast radiography===
+===Positive Contrast Radiography===
 May show filling defects.
 ===Ultrasonography===
-Shows gastric thickening and rules out other differential diagnoses.
+Shows gastric thickening and rules out differentials.
 ===Endoscopy and Biopsy===
-Diagnostic test of choice and allows biopsies to be taken. NSAID related ulcers are regularly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated [[Gastric Neoplasia - Dog and Cat|gastric tumours]] will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased tissue to avoid further deepening or perforation.
+Diagnostic test of choice and allows biopsies to be taken. NSAID related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated [[Gastric Neoplasia - WikiClinical|gastric tumours]] will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased to avoid further deepening or perforation.
 ==Treatment==
-The main aim is to treat any primary underlying cause whilst giving general support. This may be hydrating, restoring electrolytes and acid-base and also helping the gastric lining to recover. [[Gastroprotective Drugs|Anti-ulcerative]] therapy should be continued for up to 6-8 weeks.
+The main aim is to treat any primary underlying cause whilst giving general support. This may be hydrating, restoring electrolytes and acid-base and also helping the gastric lining to recover.
-===[[Principles of Fluid Therapy|Fluid Therapy]]===
-Depends upon the degree of dehydration, presence of shock and any other diseases that are affected by volume. Prolonged vomiting or anorexia may lead to hypokalaemia so KCl may need adding to any fluids given. Normal rates for treatment of shock apply with dehydration being overcome by a fluid rate over 24 hours to replace the deficits along with a maintenance rate.
-===Reducing acid secretion===
+===Fluid therapy===
-[[Gastroprotective Drugs#Histamine (H2) Receptor Antagonists|Histamine receptor antagonists]] inhibit acid secretion and include cimetidine, ranitidine and famotidine.
-[[Gastroprotective Drugs#Proton Pump Inhibitors|Omeprazole]] is the drug of choice to treat ulceration associated with mass cell tumours and gastrinomas. It inhibits the hydrogen-potassium ATPase which prevents hydrogen ion production by the parietal cells.
+===Acid-base correction===
 ===Mucosal protectants===
-Such as misoprostol can be given alongside NSAIDs to decrease the risk of ulceration. [[Gastroprotective Drugs#Binding Agents|Sucralfate]] which is polyaluminium sucrose sulphate, binds to damaged mucosa and assists in the treatment of gastric ulceration. It is best given 2 hours after acid inhibitors to prevent interference.
 ===Prophylaxis===
-Prophylactic treatment has been shown not to prevent gastric ulceration. Sucralfate is reported to be the best drug in patients receiving high doses of glucocorticoids.
 ===Anti-emetics===
-[[Emetics and Anti-Emetic Drugs#Anti-Emetics|Anti-emetics]] are indicated if vomiting is severe causing fluid and electrolyte imbalances and discomfort.
 ===Analgesia===
-Is best provided by [[Opioids|opiods]] such as buprenorphine, pethidine and fentanyl.
 ===Antibiotics===
-Animals suffering from shock and gastric barrier dysfunction may require prophylactic [[Antibiotics|antibiotic]] cover. First line drugs include [[Penicillins|ampicillin]] or a [[Cephalosporins|cephalosporin]] which are effective against Gram-positive, some Gram-negative and some anaerobic bacteria. These can be combined with an [[Aminoglycosides|aminoglycoside]] which are effective against Gram-negative aerobes if sepsis is present. [[Fluoroquinolones|Enrofloxacin]] can also be used instead of an aminoglycoside in skeletally mature animals.
 ===Surgery===
-May be required to investigate or to resect perforating ulcers which may lead to [[Peritonitis - Cats and Dogs|peritonitis]].
+May be required to investigate or to resect peforating ulcers which may lead to [[Peritonitis - WikiClinical|peritonitis]].
 ==Prognosis==
-For animals with peptic ulcers is good. Prognosis is poorer for patients with renal or hepatic failure related ulcers. It is also poor for animals with gastric carcinoma and gastrinoma.
+Depends upon the cause
-{{Learning
-|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis01152.asp, Gastric ulceration]
-|literatures search = [http://www.cabdirect.org/search.html?q=%28title%3A%28gastr*%29+OR+title%3A%28stomach%29%29+AND+title%3A%28ulcer*%29+AND+od%3A%28dogs%29 Gastric Ulceration in Dogs publications]
-}}
 ==References==
-Hall, J.E., 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) ''W.B. Saunders Company''
-{{review}}
-{{OpenPages}}
-[[Category:Gastric_Ulceration]][[Category:Gastric Diseases - Dog]]
-[[Category:Expert_Review - Small Animal]]