Difference between revisions of "Gastric Ulceration - Dog"
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− | {{ | + | {{review}} |
− | + | ||
− | + | {{cat}} | |
− | + | {{dog}} | |
− | |||
− | Gastric | + | [[Image:Gastric ulceration.jpg|thumb|right|250px|Gastric Ulceration - Copyright David Walker RVC]] |
+ | ==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: | There are many disease associations including: | ||
Line 17: | Line 21: | ||
|- | |- | ||
|'''Hypotension''' | |'''Hypotension''' | ||
− | |[[Shock|Shock]], Sepsis | + | |[[Shock - Pathology|Shock]], Sepsis |
|- | |- | ||
|'''Drug - induced''' | |'''Drug - induced''' | ||
Line 26: | Line 30: | ||
|- | |- | ||
|'''Inflammatory''' | |'''Inflammatory''' | ||
− | |[[Gastritis, Acute|Gastritis]], [[Pancreatitis - Dog|Pancreatitis]] | + | |[[Gastritis, Acute|Gastritis]], [[Pancreatitis - Dog and Cat|Pancreatitis]] |
|- | |- | ||
|'''Neoplastic''' | |'''Neoplastic''' | ||
− | |Adenocarcinoma, lymphosarcoma, leiomyoma, | + | |Adenocarcinoma, lymphosarcoma, leiomyoma, gastrinoma (Zollinger-Ellison syndrome), |
|- | |- | ||
|'''Metabolic/endocrine''' | |'''Metabolic/endocrine''' | ||
− | |Hypoadrenocorticism, liver disease, | + | |[[Hypoadrenocorticism - Addison's Disease|Hypoadrenocorticism]], liver disease, uraemia, [[Disseminated Intravascular Coagulation - Pathology|Disseminated Intravascular Coagulation (DIC)]], 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|NSAIDs]] directly damage the mucosa and interfere with the prostaglandin synthesis. Gastric ulceration is worsened by the use of [[NSAIDs|NSAIDs]] in combination with [[Steroids|corticosteroids]]. This risk can be minimised by using cyclooxygenase-1 (COX-1) sparing [[NSAIDs|NSAIDs]] (carprofen, meloxicam and deracoxib). |
− | Gastric acid hypersecretion following mast cell degranulation of histamine and gastrin secretion from | + | 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|NSAIDs]] | ||
+ | Clinical Signs: | ||
+ | *Vomiting | ||
+ | *Haematemesis | ||
+ | *Malaena | ||
+ | *Pale mucous membranes | ||
+ | *Abdominal pain | ||
+ | *Weakness | ||
+ | *Inappetance | ||
+ | *Hypersalivation | ||
+ | *Circulatory comprimise | ||
− | |||
− | |||
− | |||
− | |||
− | |||
===Haematology=== | ===Haematology=== | ||
− | [[ | + | *[[Anaemia|Anaemia]] - regenerative initially, may progress to microcytic, hypochromic and minutely regenerative. |
− | + | *Thrombocytosis | |
− | Examination of the buffy coat may detect mastocytosis | + | *Lack of stress leucogram (and lymphocytosis and eosinophilia) supportive of [[Hypoadrenocorticism - Addison's Disease|hypoadrenocorticism]] |
− | + | *Examination of the buffy coat may detect mastocytosis | |
− | + | *[[Changes in Inflammatory Cells Circulating in Blood - Pathology#Neutrophilia|Neutrophilia]] and a left shift - signs of inflammation or gastric perforation | |
+ | *May show abnormalities in [[Haemostasis - Pathology|haemostasis]] | ||
===Biochemistry=== | ===Biochemistry=== | ||
− | + | *Dehydration - azotaemia | |
− | + | *Hepatic disease - increased liver enzymes and bilirubin, decreased urea, albumin and cholesterol | |
− | + | *Renal disease - azotaemia | |
− | + | *[[Hypoadrenocorticism - Addison's Disease|Hypoadrenocorticism]] - Sodium:Potassium ratio of less than 27:1 | |
+ | *Vomiting will lead to electrolyte and acid-base abnormalities - metabolic alkalosis, hypokalaemia and hypochloraemia | ||
===Urinalysis=== | ===Urinalysis=== | ||
− | + | *Dehydration - Hypersthenuria | |
+ | *Renal disease - Isosthenuria | ||
===Plain radiography=== | ===Plain radiography=== | ||
− | [[Image:Gastric ulceration.png|thumb|right|250px|Gastric Ulceration - | + | [[Image:Gastric ulceration.png|thumb|right|250px|Gastric Ulceration - Copyright David Walker RVC]] |
− | Not usually diagnostic but | + | Not usually diagnostic but rules out differentials. |
===Positive contrast radiography=== | ===Positive contrast radiography=== | ||
Line 72: | Line 85: | ||
===Ultrasonography=== | ===Ultrasonography=== | ||
− | Shows gastric thickening and rules out | + | Shows gastric thickening and rules out differentials. |
===Endoscopy and Biopsy=== | ===Endoscopy and Biopsy=== | ||
− | Diagnostic test of choice and allows biopsies to be taken. NSAID related ulcers are | + | Diagnostic test of choice and allows biopsies to be taken. [[NSAIDs|NSAID]] related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated [[Gastric Neoplasia|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== | ==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. | + | 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. Anti-ulcerative therapy should be continued for up to 6-8 weeks. |
− | ===[[ | + | ===[[Fluid Therapy]]=== |
− | Depends upon | + | Depends upon degree of dehydration, prescence 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 defecits along with a maintenance rate. |
− | + | ||
− | === | + | ===Acid-base correction=== |
− | [[Gastroprotective Drugs#Histamine (H2) Receptor Antagonists|Histamine receptor antagonists]] | + | Imbalances should be corrected after taking a blood gas reading. |
− | + | *If metabolic acidotic: give sodium bicarbonate but do repeated blood gas | |
− | [[Gastroprotective Drugs#Proton Pump Inhibitors| | + | *If metabolic alkalosis: replace volume defecit with intravenous NaCl and KCl. |
+ | *Blocking of acid secretion: | ||
+ | **[[Gastroprotective Drugs#Histamine (H2) Receptor Antagonists|Histamine receptor antagonists]]: | ||
+ | ***cimetidine | ||
+ | ***ranitidine | ||
+ | ***famotidine | ||
+ | **Gastrin antagonists: | ||
+ | ***proglumide | ||
+ | **Acetylcholine receptor antagonists: | ||
+ | ***atropine | ||
+ | ***pirenzepine | ||
+ | **Adenyl cyclase inhibitors: | ||
+ | ***[[Gastroprotective Drugs#Prostaglandin E Analogues|prostaglangin E2 (PGE) analogues]] (misoprostol) | ||
+ | **[[Gastroprotective Drugs#Proton Pump Inhibitors|H<sup>+</sup>:K<sup>+</sup>ATPase inhibitors ]]:- for use when patient is refractory to histamine antagonists | ||
+ | ***omeprazole - good for exercise induced gastric ulceration | ||
===Mucosal protectants=== | ===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. | + | Such as misoprostol can be given alongside [[NSAIDs|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=== | ===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. | + | Prophylactic treatment has been shown not to prevent gastric ulceration. [[Gastroprotective Drugs#Binding Agents|Sucralfate]] is reported to be the best drug in patients receiving high doses of glucocorticoids. |
− | === | + | ===[[Emetics and Anti-Emetic Drugs#Anti-Emetics|Anti-emetics]]=== |
− | [[Emetics and Anti-Emetic Drugs#Anti-Emetics|Anti-emetics]] | + | Indicated if vomiting is severe causing fluid and electrolyte imbalances and discomfort. See [[Emetics and Anti-Emetic Drugs#Anti-Emetics|Anti-emetics]] for drug details. |
===Analgesia=== | ===Analgesia=== | ||
Is best provided by [[Opioids|opiods]] such as buprenorphine, pethidine and fentanyl. | Is best provided by [[Opioids|opiods]] such as buprenorphine, pethidine and fentanyl. | ||
− | ===Antibiotics=== | + | ===[[Antibiotics]]=== |
− | Animals suffering from shock and gastric barrier dysfunction may require prophylactic | + | Animals suffering from shock and gastric barrier dysfunction may require prophylactic antibiotic cover. First line drugs include [[Penicillins|ampicillin]] or a [[Cephalosporins|cephalosporin]] which are effective against Gram-positive, some Gram-negative and some anaerobes. 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 [[Aminoglycosides|aminoglycoside]] in skeletally mature animals |
===Surgery=== | ===Surgery=== | ||
− | May be required to investigate or to resect | + | May be required to investigate or to resect peforating ulcers which may lead to [[Peritonitis - Cats and Dogs|peritonitis]]. |
==Prognosis== | ==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. | 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. | ||
− | |||
− | |||
− | |||
− | |||
− | |||
==References== | ==References== | ||
Line 118: | Line 140: | ||
Hall, J.E., Simpson, J.W. and Williams, D.A., (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA'' | Hall, J.E., Simpson, J.W. and Williams, D.A., (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA'' | ||
− | + | Merck & Co (2008) '''The Merck Veterinary Manual''' | |
+ | ==From Pathology Section== | ||
+ | [[Gastric Ulceration - all species]] | ||
+ | * Although ulcers are often secondary to other diseases, primary idiopathic peptic ulcers do occur, due to | ||
+ | ** Hyperacidity | ||
+ | ** Gastric carcinoma in older dog | ||
− | |||
− | + | * Secondary ulcers are often associated with systemic diseases particularly '''uraemia''' and '''mast cell tumours'''. Gastric ulcer may be the cause of death but is not the primary disease. | |
+ | *# '''Mast cell tumours''' | ||
+ | *#*Boxers and Labradors are predisposed to these. | ||
+ | *#* Vomit continually together with abdominal pain. | ||
+ | *#* Ulcers are usually near the duodenum. | ||
+ | *#** Frequently secondarily infected. | ||
+ | *#** Often penetrate deeply. | ||
+ | *#* Actively secreting mast cell tumours produce histame, leasing to gastric hyperacidity and therefore secondary peptic ulcers. | ||
+ | *# '''Uraemia''' | ||
+ | *#* Gastric lesions usually occur with chronic renal disease. | ||
+ | *#** Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion . | ||
+ | *#*** Acts on H2 receptors on parietal cells to increase production of HCl. | ||
+ | *#*** Increases release of histamine from gastric mucosal mast cells to increase HCl release. | ||
+ | *#** Serum levels of gastrin are increased in chronic renal disease in dogs and cats. | ||
+ | *#* In acute renal failure death ensues before gastric ulceration develops. | ||
+ | *#* '''Pathogenesis''' | ||
+ | *#** Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid. | ||
+ | *#*** A common cause of interstitial nephritis in the dog was leptospirosis. | ||
+ | *#** Consequently, the animal drinks and urinates in enormous quantities, and urea is washed out with large quantities of fluid ("compensated renal failure"). | ||
+ | *#** If fluid is restricted, urea cannot be washed out and the animal becomes uraemic. | ||
+ | *#*** Urea is excreted into [[Forestomach - Anatomy & Physiology|stomach]], giving it a horrible ammoniacal smell and filling it with brown smelly liquid. | ||
+ | *#*** Urea is also excreted into the [[Colon - Anatomy & Physiology|colon]]. | ||
+ | *#** Urea in the stomach breaks down to ammonia, irritating the mucosa and contributing to gastric ulcer. | ||
+ | *#** Uraemia also causes arteriolar degeneration in the submucosa, leading to hypoxic damage to the mucosa. This is another contributing factor to gastric ulcer. | ||
+ | *#** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] causes dehydration and further raises blood urea. | ||
+ | *#*** A vicious circle is produced- ends in death by [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]], dehydration and shock. | ||
+ | *#** '''Note:''' If an animal in compensated renal failure is given anaesthetic, it will not drink much. It then may start to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomit]] and die due to uraemia. | ||
+ | |||
− | [[Category:Gastric_Ulceration]][[Category: | + | * NSAIDs, Zollinger-Ellison syndrome (due to pancreatic gastrin-secreting tumour), cirrhosis and bile reflux can all also cause gastric ulcers in the dog. |
− | [[Category: | + | [[Category:Gastric_Ulceration]][[Category:Dog]] |
+ | [[Category:To_Do_-_Clinical]] |
Revision as of 13:47, 28 June 2010
This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
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, Pancreatitis |
Neoplastic | Adenocarcinoma, lymphosarcoma, leiomyoma, gastrinoma (Zollinger-Ellison syndrome), |
Metabolic/endocrine | Hypoadrenocorticism, liver disease, uraemia, Disseminated Intravascular Coagulation (DIC), 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. Anti-ulcerative therapy should be continued for up to 6-8 weeks.
Fluid Therapy
Depends upon degree of dehydration, prescence 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 defecits along with a maintenance rate.
Acid-base correction
Imbalances should be corrected after taking a blood gas reading.
- If metabolic acidotic: give sodium bicarbonate but do repeated blood gas
- If metabolic alkalosis: replace volume defecit with intravenous NaCl and KCl.
- Blocking of acid secretion:
- Histamine receptor antagonists:
- cimetidine
- ranitidine
- famotidine
- Gastrin antagonists:
- proglumide
- Acetylcholine receptor antagonists:
- atropine
- pirenzepine
- Adenyl cyclase inhibitors:
- prostaglangin E2 (PGE) analogues (misoprostol)
- H+:K+ATPase inhibitors :- for use when patient is refractory to histamine antagonists
- omeprazole - good for exercise induced gastric ulceration
- Histamine receptor antagonists:
Mucosal protectants
Such as misoprostol can be given alongside NSAIDs to decrease the risk of ulceration. 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
Indicated if vomiting is severe causing fluid and electrolyte imbalances and discomfort. See Anti-emetics for drug details.
Analgesia
Is best provided by opiods such as buprenorphine, pethidine and fentanyl.
Antibiotics
Animals suffering from shock and gastric barrier dysfunction may require prophylactic antibiotic cover. First line drugs include ampicillin or a cephalosporin which are effective against Gram-positive, some Gram-negative and some anaerobes. These can be combined with an aminoglycoside which are effective against Gram-negative aerobes if sepsis is present. Enrofloxacin can also be used instead of an aminoglycoside in skeletally mature animals
Surgery
May be required to investigate or to resect peforating ulcers which may lead to 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.
References
Hall, J.E., Simpson, J.W. and Williams, D.A., (2005) BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition) BSAVA
Merck & Co (2008) The Merck Veterinary Manual
From Pathology Section
Gastric Ulceration - all species
- Although ulcers are often secondary to other diseases, primary idiopathic peptic ulcers do occur, due to
- Hyperacidity
- Gastric carcinoma in older dog
- Secondary ulcers are often associated with systemic diseases particularly uraemia and mast cell tumours. Gastric ulcer may be the cause of death but is not the primary disease.
- Mast cell tumours
- Boxers and Labradors are predisposed to these.
- Vomit continually together with abdominal pain.
- Ulcers are usually near the duodenum.
- Frequently secondarily infected.
- Often penetrate deeply.
- Actively secreting mast cell tumours produce histame, leasing to gastric hyperacidity and therefore secondary peptic ulcers.
- Uraemia
- Gastric lesions usually occur with chronic renal disease.
- Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion .
- Acts on H2 receptors on parietal cells to increase production of HCl.
- Increases release of histamine from gastric mucosal mast cells to increase HCl release.
- Serum levels of gastrin are increased in chronic renal disease in dogs and cats.
- Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion .
- In acute renal failure death ensues before gastric ulceration develops.
- Pathogenesis
- Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid.
- A common cause of interstitial nephritis in the dog was leptospirosis.
- Consequently, the animal drinks and urinates in enormous quantities, and urea is washed out with large quantities of fluid ("compensated renal failure").
- If fluid is restricted, urea cannot be washed out and the animal becomes uraemic.
- Urea in the stomach breaks down to ammonia, irritating the mucosa and contributing to gastric ulcer.
- Uraemia also causes arteriolar degeneration in the submucosa, leading to hypoxic damage to the mucosa. This is another contributing factor to gastric ulcer.
- Vomiting causes dehydration and further raises blood urea.
- A vicious circle is produced- ends in death by vomiting, dehydration and shock.
- Note: If an animal in compensated renal failure is given anaesthetic, it will not drink much. It then may start to vomit and die due to uraemia.
- Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid.
- Gastric lesions usually occur with chronic renal disease.
- Mast cell tumours
- NSAIDs, Zollinger-Ellison syndrome (due to pancreatic gastrin-secreting tumour), cirrhosis and bile reflux can all also cause gastric ulcers in the dog.