Difference between revisions of "Gastric Dilatation and Volvulus"
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| − | {{ | + | {{dog}} |
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| − | = | + | {|cell padding=''10'' cellspacing=''0'' border=''1'' |
| − | + | |Also known as: | |
| + | |'''GDV<br> | ||
| + | |-|} | ||
| − | Commonly affected breeds include German Shepherds, Great Danes, Irish Wolfhounds, St Bernards and Doberman Pinschers. GDV has also been reported to occur in cats, primates and rarely small breed dogs such as Dachshunds and Miniature Poodles. | + | ==Description== |
| + | Gastric Dilatation and Volvulus (GDV) is an acute, life-threatening emergency affecting large and giant breed dogs. The condition is characterized by accumulation of gas in the stomach and malpositioning of the stomach with obstruction of eructation and pyloric outflow. Commonly affected breeds include German Shepherds, Great Danes, Irish Wolfhounds, St Bernards and Doberman Pinschers. GDV has also been reported to occur in cats, primates and rarely small breed dogs such as Dachshunds and Miniature Poodles. | ||
| − | == | + | ==Pathogenesis== |
| − | + | An obstruction to gastric emptying due to fluid or gas leads to gastric distention and a rapid increase in intra-gastric pressure. As the stomach dilates, the pylorus shifts through an angle of between 180 and 360<sup>o</sup> from its normal position to a dorsal, cranial and leftward location. More than 90% of all gastric volvuli rotate in a clockwise direction when viewed from the surgeon's perspective with the dog in dorsal recumbency. | |
| − | + | The most immediate effect is impairment of the gastric blood supply, leading to severe congestion of the gastric wall and infarction and ulceration of the gastric mucosa. Venous return to heart is reduced due to mechanical compression of the caudal vena cava by the distended stomach, leading to decreased cardiac output and hypovolaemic shock. Gastric distension also causes a mechanical impediment to movement of the diaphragm resulting in reduced tidal volume, hypoxia and hypercapnia. | |
| − | |||
| − | + | In addition to the above systemic effects, diplacement of the stomach may lead to avulsion of the gastric branches of the splenic artery. Significant haemorrhage may occur as a result and this may lead to the development of ischaemia-induced gastric necrosis. | |
| − | + | ==Risk factors== | |
| + | The exact aetiology of the condition is unknown but a number of risk factors have been identified. Studies have shown that dogs with a reduced thoracic width to depth ratio are at an in increased risk of developing GDV. Female dogs are also more likely to develop GDV than males. Other risk factors include obesity, feeding a dry food diet and exercise after feeding. Stressed, anxious dogs are more likely to develop GDV than calm, placid dogs. | ||
| − | ==History and Clinical | + | ==History and Clinical signs== |
| − | The clinical signs of GDV are usually | + | The clinical signs of GDV are usually acute in onset and may follow a periood of exercise and/or feeding of a large meal. Affected dogs typically display non-productive vomiting and abdominal distension. On physical examination, the dog may be collapsed or reluctant to stand. Signs of cardiovascular shock may be present including tachycardia, pale mucous membranes, prolonged capillary refill time and poor peripheral pulses. Abdominal tympany is often displayed and the animal may be painful. |
==Diagnosis and Management== | ==Diagnosis and Management== | ||
| − | |||
| − | === | + | ===Fluid therapy=== |
| − | Initial emergency treatment should be aimed at managing the dog's | + | Diagnosis is usually based on the patient's signalment and a history of unproductive vomiting and abdominal distension. Initial emergency treatment should be aimed at managing the dog's hypovolaemic shock. It may be beneficial to provide oxygen supplementation whilst the dog is being stabilised. |
| − | Large bore (16 or 18 gauge) catheters should be placed into the cephalic or jugular veins and a proportion of the | + | Large bore (16 or 18 gauge) catheters should be placed into the cephalic or jugular veins and a proportion of the shock dose of Compound Sodium Lactate (90ml/kg/h) should be administered intravenously based on the severity of the dog's clinical signs. Hypertonic saline or colloid fluids may be indicated in very large dogs or those who have not responded to a bolus dose of crystalloid fluids. |
| − | ===Gastric | + | ===Gastric decompression=== |
| − | Following a period of aggressive fluid therapy, | + | Following a period of aggressive fluid therapy, gastric decompression should be performed. A lubricated large-bore stomach tube is premeasured (from nostril to last rib)and marked. A roll of 2 inch adhesive tape should be inserted behind the canine teeth and the dog's mouth should be held closed around the banadage. The stomach tube can then be introduced through the bandage into the oesophagus. and should not be advanced beyond the marked point. It is important to mimimise stress when this procedure is carried out. Sedation is not usually required but suitable drugs for this include Butorphanol, Fentanyl or Diazepam. It the animal is resistant to orogastric intubation or becomes stressed, trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. This may allow susequent completion of orogastric intubation for further decompression. |
===Radiography=== | ===Radiography=== | ||
| − | + | Abdominal radiography may be beneficial in confirming a diagnosis of GDV and distinguishing between GDV and gastric dilatation. Radiography should not be carried out until gastric decompression has been performed and intravenous fluids have been started. A radiograph performed in right lateral recumbency shows a dorsally and cranially positioned pylorus to the left of the midline. The stomach will appear compartmentalised with a soft tissue strip separating the two compartments. The oesophagus may appear dilated with air or fluid. Evidence of air in the abdomen indicates that perforation has occurred and requires an exploratory surgical procedure. Loss of contrast in the abdomen may indicate peritonitis or haemoabdomen. | |
| − | === | + | ===Haematology=== |
| − | + | *Increased haematocrit | |
| + | *DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.) | ||
| − | + | ===Biochemistry=== | |
| + | Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation. | ||
==Treatment== | ==Treatment== | ||
| − | Once the patient has been stabilised, the volvulus should be surgically reduced via a cranioventral midline laparotomy. The aims of surgery include | + | Once the patient has been stabilised, the volvulus should be surgically reduced via a cranioventral midline laparotomy. In a ventral midline approach, the first visible structure encountered with a clockwise rotation of the stomach is the ventral leaf of the omentum. The spleen may be displaced from the left side of the abdomen to the right (ventral) side. |
| + | The aims of surgery include gastric decompression and repositioning, assessment of the abdominal organ viability, removal of necrotic tissue and gastropexy. Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence. | ||
| − | + | If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy. | |
| − | + | ===Post-operative complications=== | |
| + | These are wide and varied and include: | ||
| + | *Hypoperfusion | ||
| + | *Hypotension | ||
| + | *Cardiac arrythmias | ||
| + | *[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]] | ||
| + | *[[Gastric Motility Disorders|Abnormal gastric motility]] | ||
| + | *Gastric necrosis | ||
| + | *[[Disseminated Intravascular Coagulation|DIC]] | ||
| + | *[[Systemic Inflammatory Response Syndrome|Systemic Inflammatory Response Syndrome (SIRS)]] | ||
| − | + | ==Prognosis== | |
| + | Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necrosis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis. | ||
| − | + | ==References== | |
| − | + | Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA'' | |
| − | + | King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA'' | |
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| − | + | Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation''' 31(2):66 ''In Practice'' | |
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| − | + | Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 2. Surgical and postoperative management''' 31(3):114 ''In Practice'' | |
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| − | [[Category:Stomach_and_Abomasum_-_Pathology]][[Category: | + | [[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Dog]] |
| − | [[Category: | + | [[Category:To_Do_-_SophieIgnarski]] |
Revision as of 11:34, 22 August 2010
Description
Gastric Dilatation and Volvulus (GDV) is an acute, life-threatening emergency affecting large and giant breed dogs. The condition is characterized by accumulation of gas in the stomach and malpositioning of the stomach with obstruction of eructation and pyloric outflow. Commonly affected breeds include German Shepherds, Great Danes, Irish Wolfhounds, St Bernards and Doberman Pinschers. GDV has also been reported to occur in cats, primates and rarely small breed dogs such as Dachshunds and Miniature Poodles.
Pathogenesis
An obstruction to gastric emptying due to fluid or gas leads to gastric distention and a rapid increase in intra-gastric pressure. As the stomach dilates, the pylorus shifts through an angle of between 180 and 360o from its normal position to a dorsal, cranial and leftward location. More than 90% of all gastric volvuli rotate in a clockwise direction when viewed from the surgeon's perspective with the dog in dorsal recumbency.
The most immediate effect is impairment of the gastric blood supply, leading to severe congestion of the gastric wall and infarction and ulceration of the gastric mucosa. Venous return to heart is reduced due to mechanical compression of the caudal vena cava by the distended stomach, leading to decreased cardiac output and hypovolaemic shock. Gastric distension also causes a mechanical impediment to movement of the diaphragm resulting in reduced tidal volume, hypoxia and hypercapnia.
In addition to the above systemic effects, diplacement of the stomach may lead to avulsion of the gastric branches of the splenic artery. Significant haemorrhage may occur as a result and this may lead to the development of ischaemia-induced gastric necrosis.
Risk factors
The exact aetiology of the condition is unknown but a number of risk factors have been identified. Studies have shown that dogs with a reduced thoracic width to depth ratio are at an in increased risk of developing GDV. Female dogs are also more likely to develop GDV than males. Other risk factors include obesity, feeding a dry food diet and exercise after feeding. Stressed, anxious dogs are more likely to develop GDV than calm, placid dogs.
History and Clinical signs
The clinical signs of GDV are usually acute in onset and may follow a periood of exercise and/or feeding of a large meal. Affected dogs typically display non-productive vomiting and abdominal distension. On physical examination, the dog may be collapsed or reluctant to stand. Signs of cardiovascular shock may be present including tachycardia, pale mucous membranes, prolonged capillary refill time and poor peripheral pulses. Abdominal tympany is often displayed and the animal may be painful.
Diagnosis and Management
Fluid therapy
Diagnosis is usually based on the patient's signalment and a history of unproductive vomiting and abdominal distension. Initial emergency treatment should be aimed at managing the dog's hypovolaemic shock. It may be beneficial to provide oxygen supplementation whilst the dog is being stabilised. Large bore (16 or 18 gauge) catheters should be placed into the cephalic or jugular veins and a proportion of the shock dose of Compound Sodium Lactate (90ml/kg/h) should be administered intravenously based on the severity of the dog's clinical signs. Hypertonic saline or colloid fluids may be indicated in very large dogs or those who have not responded to a bolus dose of crystalloid fluids.
Gastric decompression
Following a period of aggressive fluid therapy, gastric decompression should be performed. A lubricated large-bore stomach tube is premeasured (from nostril to last rib)and marked. A roll of 2 inch adhesive tape should be inserted behind the canine teeth and the dog's mouth should be held closed around the banadage. The stomach tube can then be introduced through the bandage into the oesophagus. and should not be advanced beyond the marked point. It is important to mimimise stress when this procedure is carried out. Sedation is not usually required but suitable drugs for this include Butorphanol, Fentanyl or Diazepam. It the animal is resistant to orogastric intubation or becomes stressed, trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. This may allow susequent completion of orogastric intubation for further decompression.
Radiography
Abdominal radiography may be beneficial in confirming a diagnosis of GDV and distinguishing between GDV and gastric dilatation. Radiography should not be carried out until gastric decompression has been performed and intravenous fluids have been started. A radiograph performed in right lateral recumbency shows a dorsally and cranially positioned pylorus to the left of the midline. The stomach will appear compartmentalised with a soft tissue strip separating the two compartments. The oesophagus may appear dilated with air or fluid. Evidence of air in the abdomen indicates that perforation has occurred and requires an exploratory surgical procedure. Loss of contrast in the abdomen may indicate peritonitis or haemoabdomen.
Haematology
- Increased haematocrit
- DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)
Biochemistry
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.
Treatment
Once the patient has been stabilised, the volvulus should be surgically reduced via a cranioventral midline laparotomy. In a ventral midline approach, the first visible structure encountered with a clockwise rotation of the stomach is the ventral leaf of the omentum. The spleen may be displaced from the left side of the abdomen to the right (ventral) side. The aims of surgery include gastric decompression and repositioning, assessment of the abdominal organ viability, removal of necrotic tissue and gastropexy. Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence.
If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.
Post-operative complications
These are wide and varied and include:
- Hypoperfusion
- Hypotension
- Cardiac arrythmias
- Aspiration pneumonia
- Abnormal gastric motility
- Gastric necrosis
- DIC
- Systemic Inflammatory Response Syndrome (SIRS)
Prognosis
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necrosis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis.
References
Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition) BSAVA
King, L. and Hammond, R. (1999) BSAVA Manual of Canine and Feline Emergency and Critical Care BSAVA
Tivers, M. and Brockman, D. (2009) Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation 31(2):66 In Practice
Tivers, M. and Brockman, D. (2009) Gastric dilation–volvulus syndrome in dogs 2. Surgical and postoperative management 31(3):114 In Practice
| Also known as: | GDV |