Gastric Dilatation and Volvulus

Gastric dilatation and volvulus (GDV) is a rapidly progressive, life-threatening gastrointestinal emergency characterized by abnormal accumulation of gas and/or fluid within the stomach (gastric dilatation) followed by rotation of the stomach along its mesenteric axis (volvulus). In rabbits, the condition is often referred to as gastric dilatation with or without torsion, and it is distinct from the more common gastrointestinal stasis syndrome. The stomach of the rabbit is a large, thin-walled, J-shaped organ located in the cranial abdomen, and its relatively loose attachment to the diaphragm and liver predisposes it to rotation. GDV results in complete or partial obstruction of the cardia and pylorus, leading to severe gastric distension, ischemia, necrosis, and rapid cardiovascular collapse. The condition is a true emergency requiring immediate medical and surgical intervention. In rabbits, GDV is less common than in dogs but carries a high mortality rate if untreated. The disease is classified based on the degree of rotation (90° to 360°) and the direction (clockwise or counterclockwise), with clockwise rotation being most frequent. Systemic consequences include hypovolemic shock, endotoxemia, reperfusion injury, and multi-organ failure.

The exact etiology of GDV in rabbits is multifactorial and not fully understood. Primary causative factors include dietary indiscretion, such as ingestion of large amounts of fermentable carbohydrates (e.g., grains, bread, or sugary treats) that lead to rapid gas production. Sudden changes in diet, especially from high-fiber to low-fiber, high-starch diets, can disrupt normal gastrointestinal motility. Gastric outflow obstruction due to trichobezoars (hairballs) or foreign bodies may predispose to dilatation. Anatomical factors, such as the relatively mobile nature of the rabbit stomach and the presence of a weak gastrohepatic ligament, increase the risk of torsion. Other contributing factors include excessive aerophagia (air swallowing) during stress or pain, and conditions that cause gastric atony, such as ileus secondary to pain, anesthesia, or systemic illness. In some cases, GDV occurs spontaneously without an identifiable trigger. Bacterial overgrowth, particularly with gas-producing organisms like Clostridium spp., can exacerbate dilatation. Additionally, a history of gastrointestinal stasis or previous abdominal surgery may increase the risk. Environmental stressors, such as overcrowding, transport, or changes in routine, have been implicated as precipitating events.

GDV is a relatively rare but severe condition in domestic rabbits (Oryctolagus cuniculus). It is more commonly reported in larger breeds, such as the Flemish Giant and the French Lop, possibly due to their deeper chest conformation and larger stomach size. However, any breed can be affected. The condition is seen in both sexes, with no clear sex predilection. Age distribution ranges from young adults to geriatric rabbits, with a median age of 3-5 years. There is no known seasonal variation, but cases may be more frequent during periods of dietary indiscretion, such as holidays when rabbits are fed inappropriate treats. In captive rabbits, the incidence is lower than in dogs, but the mortality rate is high, approaching 100% without intervention. Wild rabbits are rarely affected, likely due to their natural high-fiber diet and active lifestyle. Husbandry factors that increase risk include feeding a diet low in hay and high in pellets or concentrates, lack of exercise, and obesity. Stressful environments, such as those with inadequate hiding spaces or high noise levels, may also contribute. The condition is more commonly diagnosed in rabbits presented to emergency veterinary clinics, and early recognition is critical for survival.

The pathophysiology of GDV in rabbits involves a cascade of events leading to rapid clinical deterioration. Initially, gastric dilatation occurs due to accumulation of gas and fluid, often from fermentation of ingested carbohydrates or aerophagia. As intraluminal pressure rises, the stomach expands, compressing the caudal vena cava and abdominal aorta, leading to decreased venous return and cardiac output. This results in hypovolemic shock and tissue hypoxia. If the stomach rotates, the blood supply to the gastric wall is compromised, causing ischemia, venous congestion, and eventually necrosis. The spleen may also become engorged and displaced. Ischemia and reperfusion injury release reactive oxygen species and inflammatory mediators, leading to systemic inflammatory response syndrome (SIRS) and endotoxemia. Bacterial translocation across the damaged gastric mucosa can cause sepsis. The distended stomach also impairs diaphragmatic movement, leading to respiratory compromise. In rabbits, the thin-walled stomach is particularly prone to rupture if the pressure becomes excessive. Metabolic derangements include metabolic acidosis, electrolyte imbalances (e.g., hypokalemia, hyponatremia), and prerenal azotemia. Without prompt decompression and surgical correction, the condition is fatal.

Predisposing factors for GDV in rabbits can be divided into intrinsic and extrinsic categories. Intrinsic factors include anatomical features such as the relatively mobile stomach and weak gastrohepatic ligament, which allow torsion. Large breed size and deep chest conformation increase the risk. Age may play a role, as older rabbits may have decreased gastrointestinal motility. Sex does not appear to be a significant factor. Extrinsic factors are primarily husbandry-related. Inappropriate diet, particularly one low in long-stem fiber (hay) and high in carbohydrates or pellets, is a major risk factor. Sudden dietary changes can disrupt the normal gut flora and motility. Lack of exercise and obesity contribute to poor gastrointestinal tone. Stress, whether from environmental changes, transport, or pain, can lead to ileus and aerophagia. Ingestion of foreign bodies or excessive hair (trichobezoars) can cause gastric outflow obstruction. Previous abdominal surgery or gastrointestinal disease may predispose to adhesions or motility disorders. Additionally, certain medications, such as opioids, can decrease gastrointestinal motility. In some cases, no specific predisposing factor is identified, and the condition appears idiopathic.

Clinical signs of GDV in rabbits are acute and rapidly progressive. Early signs include anorexia, lethargy, and a hunched posture. As the stomach distends, the rabbit may show signs of abdominal pain, such as teeth grinding (bruxism), restlessness, and reluctance to move. The abdomen becomes visibly distended and tympanic on percussion. The rabbit may exhibit dyspnea due to diaphragmatic compression. Vomiting is not possible in rabbits due to their anatomical and physiological limitations, so regurgitation or drooling may occur. As shock develops, the rabbit becomes weak, pale, and tachycardic, with weak peripheral pulses. Hypothermia may be present. In severe cases, collapse and death can occur within hours. On physical examination, the stomach may be palpable as a large, firm, gas-filled mass in the cranial abdomen. Mucous membranes may be pale or cyanotic. Capillary refill time is prolonged. The rabbit may show signs of dehydration, such as sunken eyes and reduced skin turgor. If gastric rupture occurs, the rabbit may suddenly deteriorate with signs of septic shock. It is crucial to recognize these signs early and initiate emergency treatment.

Differential diagnoses for GDV in rabbits include: 1) Gastrointestinal stasis (ileus) - a common condition characterized by reduced motility and accumulation of gas and ingesta, but without torsion; radiography may show gas-filled stomach but no malposition. 2) Trichobezoar (hairball) - a mass of hair in the stomach causing partial obstruction; may be visible on radiography or ultrasound. 3) Gastric foreign body - ingestion of indigestible material causing obstruction; history and imaging can differentiate. 4) Cecal impaction - a large, firm cecum due to dehydration or low-fiber diet; palpation and ultrasound can help. 5) Enteritis - inflammation of the intestines due to bacterial, viral, or parasitic infection; diarrhea and fever may be present. 6) Uterine adenocarcinoma (in intact females) - can cause abdominal distension and pain; imaging and history of intact status. 7) Hepatobiliary disease - such as hepatic lipidosis or cholangiohepatitis, which can cause anorexia and abdominal discomfort; liver enzymes and ultrasound are useful. 8) Renal disease - such as hydronephrosis or renal failure, which can cause lethargy and abdominal pain; blood work and ultrasound. 9) Peritonitis - due to infection or rupture of an organ; may present with acute abdomen. 10) Neoplasia - such as lymphoma or gastric carcinoma, which can cause obstruction or abdominal mass. Definitive diagnosis of GDV requires imaging showing a distended, malpositioned stomach.

The diagnostic algorithm for GDV in rabbits should be rapid and systematic. 1) Triage: Assess the rabbit's stability; if in shock, begin emergency stabilization (oxygen, IV/IO fluid therapy) before extensive diagnostics. 2) Physical examination: Perform a thorough exam, noting abdominal distension, tympany, pain, and vital signs. 3) Immediate radiography: Obtain right lateral and ventrodorsal (or dorsoventral) radiographs of the abdomen. In GDV, the stomach appears as a large, gas-filled structure with a compartmentalized appearance (double bubble) and may be displaced cranially or dorsally. The pylorus may be seen craniodorsal to the fundus. 4) If radiography is inconclusive, perform abdominal ultrasound to assess stomach position, wall thickness, and presence of free fluid. 5) Blood sampling: Collect blood for hematology and biochemistry, including lactate, to assess shock and organ function. 6) Electrocardiography: Monitor for arrhythmias. 7) If the rabbit is stable, consider advanced imaging (CT) for surgical planning, but this is often not feasible in an emergency. 8) Once GDV is confirmed, proceed with emergency decompression (gastric trocarization or orogastric intubation) and surgical correction. 9) During surgery, assess gastric viability and perform gastropexy to prevent recurrence. 10) Postoperatively, provide intensive care and monitoring.

Laboratory findings in rabbits with GDV reflect shock, ischemia, and organ dysfunction. Hematology may show hemoconcentration (elevated PCV) due to dehydration, but later may show anemia from blood loss or hemodilution. White blood cell count may be elevated due to stress or inflammation, with a heterophilia and lymphopenia. Serum biochemistry often reveals elevated blood urea nitrogen (BUN) and creatinine due to prerenal azotemia. Liver enzymes (ALT, AST) may be elevated due to hepatic ischemia. Alkaline phosphatase may be increased. Electrolyte imbalances are common, including hypokalemia, hyponatremia, and hypochloremia. Blood lactate is typically elevated (>4 mmol/L) indicating tissue hypoxia and poor perfusion. Blood gas analysis may show metabolic acidosis with a decreased pH and bicarbonate. In rabbits, uric acid is not a significant parameter, but bile acids may be elevated if hepatic dysfunction is present. Fecal analysis is not typically helpful in the acute setting. Serology and PCR are not indicated for GDV. Urinalysis may show casts and proteinuria due to renal ischemia. These findings are nonspecific but support the diagnosis and help guide fluid therapy and monitoring.

Imaging is essential for the diagnosis of GDV in rabbits. Radiography: On a right lateral view, the stomach appears as a large, gas-filled, compartmentalized structure with a characteristic 'double bubble' or 'twin bubble' appearance, representing the fundus and pylorus separated by a soft tissue band. The stomach may be displaced cranially, and the pylorus may be seen craniodorsal to the fundus. On the ventrodorsal view, the stomach is often displaced to the left or right, and the gas-filled stomach may be seen crossing the midline. The spleen may be enlarged and displaced. Free abdominal gas may be present if gastric rupture has occurred. Ultrasonography: Ultrasound can be used to confirm the diagnosis by visualizing the stomach in an abnormal position, with a thickened wall and lack of peristalsis. The pylorus may be seen in an abnormal location. Color Doppler can assess blood flow to the gastric wall. CT: Computed tomography provides detailed cross-sectional images and can accurately assess the degree of rotation and gastric wall viability, but is rarely used in emergency settings due to time constraints. Endoscopy: Rigid or flexible endoscopy can be used to visualize the stomach and potentially decompress it, but is not commonly performed in rabbits due to the risk of perforation and the need for general anesthesia. In practice, radiography is the primary imaging modality for GDV in rabbits.

Cytology and histopathology are not typically used for the antemortem diagnosis of GDV, but they may be performed during surgery or postmortem. During surgery, a biopsy of the gastric wall may be taken to assess viability. Histopathology of the gastric wall in GDV shows ischemic necrosis, hemorrhage, edema, and inflammatory cell infiltration. If the stomach has ruptured, cytology of abdominal fluid may reveal septic suppurative inflammation with bacteria. Postmortem examination may reveal a rotated stomach, with the greater curvature displaced, and evidence of ischemia or necrosis. Histopathology can also identify underlying conditions such as trichobezoars or neoplasia. In chronic cases, fibrosis and atrophy of the gastric muscularis may be seen. These findings are not specific to GDV but confirm the diagnosis and help rule out other causes of gastric dilatation.

Treatment of GDV in rabbits is a medical and surgical emergency. The goals are to stabilize the patient, decompress the stomach, correct the torsion, and prevent recurrence. 1) Emergency stabilization: Administer oxygen via face mask or flow-by. Place an intravenous (IV) or intraosseous (IO) catheter for fluid therapy. Use crystalloids (e.g., Lactated Ringer's solution) at a shock dose of 10-20 mL/kg IV over 15-30 minutes, then reassess. Colloids (e.g., hetastarch) may be used if hypoproteinemia is present. 2) Gastric decompression: Attempt orogastric intubation with a well-lubricated tube to release gas. If this fails, perform percutaneous trocarization with a large-bore needle or catheter in the right flank to relieve pressure. 3) Analgesia: Administer opioids such as buprenorphine (0.01-0.05 mg/kg IV or IM q8-12h) or butorphanol (0.1-0.5 mg/kg IV or IM q4-6h). Avoid NSAIDs due to risk of renal and gastrointestinal toxicity. 4) Surgical correction: Once the rabbit is stable, perform exploratory laparotomy. The stomach is derotated, and any necrotic tissue is resected. A gastropexy is recommended to prevent recurrence. 5) Postoperative care: Continue fluid therapy, provide nutritional support (syringe feeding with a high-fiber diet), and administer prokinetics (e.g., metoclopramide 0.2-0.5 mg/kg SC or PO q8-12h) once the stomach is decompressed. 6) Antibiotics: If there is evidence of peritonitis or necrosis, administer broad-spectrum antibiotics such as enrofloxacin (5-15 mg/kg PO or SC q12h) and metronidazole (20 mg/kg PO q12h). 7) Monitor for complications: Reperfusion injury, arrhythmias, and sepsis. 8) Husbandry: Correct dietary and environmental factors to prevent recurrence.

The prognosis for GDV in rabbits is guarded to poor, especially if treatment is delayed. Without intervention, the condition is fatal. With prompt medical and surgical treatment, the survival rate is approximately 50-70%, but this depends on the degree of gastric ischemia, the presence of necrosis, and the speed of decompression. Negative prognostic indicators include severe shock, gastric necrosis requiring resection, peritonitis, and elevated lactate levels (>6 mmol/L). Rabbits that survive surgery and the immediate postoperative period have a good chance of recovery, but they may have long-term gastrointestinal motility issues. Recurrence is possible if gastropexy is not performed. The overall prognosis is better in rabbits that are diagnosed early and treated aggressively. Owners should be counseled about the high risk of mortality and the need for intensive postoperative care.

Follow-up care for rabbits after GDV is critical. Immediately postoperatively, monitor vital signs, hydration, and urine output every 2-4 hours for the first 24 hours. Check blood work (PCV, total protein, electrolytes, lactate) every 12-24 hours until stable. Provide nutritional support with syringe feeding of a high-fiber recovery diet (e.g., Critical Care) at 10-15 mL/kg q6-8h until the rabbit is eating voluntarily. Administer analgesics and prokinetics as prescribed. Recheck with the veterinarian at 3-5 days post-surgery for suture removal and assessment of wound healing. At 2 weeks, perform a full physical examination and repeat blood work to assess organ function. At 4-6 weeks, evaluate the rabbit's weight and body condition, and discuss long-term dietary management. Long-term follow-up should include regular weight checks, dental examinations, and monitoring for signs of gastrointestinal stasis. Owners should be educated on the importance of a high-fiber diet (unlimited grass hay), limited pellets, and daily exercise. Any recurrence of abdominal distension or anorexia should be treated as an emergency.

Pearls: 1) Always consider GDV in any rabbit presenting with acute abdominal distension and shock. 2) Rapid decompression is life-saving; do not delay trocarization if the rabbit is deteriorating. 3) Use intraosseous catheterization if IV access is difficult, especially in small or dehydrated rabbits. 4) Administer oxygen and fluids immediately. 5) In rabbits, the stomach is thin-walled; use caution during trocarization to avoid gastric rupture. 6) Perform a gastropexy during surgery to prevent recurrence. 7) Monitor lactate levels as a prognostic indicator. 8) Provide aggressive postoperative analgesia and nutritional support. Pitfalls: 1) Do not administer oral medications or feed before decompression, as this can worsen distension. 2) Avoid NSAIDs in shock or renal compromise. 3) Do not use corticosteroids, as they can cause immunosuppression and worsen outcome. 4) Do not delay surgery; medical management alone is rarely successful. 5) Be cautious with orogastric intubation; improper technique can cause esophageal or gastric perforation. 6) Do not overlook concurrent conditions such as trichobezoars or dental disease. 7) Avoid using fipronil or other toxic agents in rabbits. 8) Do not assume that a rabbit with a distended abdomen has simple stasis; always rule out GDV.

Current drug protocols for GDV in rabbits are based on Carpenter's Exotic Animal Formulary and include: 1) Fluid therapy: Lactated Ringer's solution (LRS) or Normosol-R at 10-20 mL/kg IV or IO bolus, then 4-10 mL/kg/h for maintenance. Colloids (e.g., hetastarch 6% at 5-10 mL/kg IV over 30-60 minutes) may be used for hypoproteinemia. 2) Analgesics: Buprenorphine (0.01-0.05 mg/kg IV or IM q8-12h) or butorphanol (0.1-0.5 mg/kg IV or IM q4-6h). 3) Prokinetics: Metoclopramide (0.2-0.5 mg/kg SC or PO q8-12h) or cisapride (0.5 mg/kg PO q8-12h, if available). 4) Antibiotics: Enrofloxacin (5-15 mg/kg PO or SC q12h) and metronidazole (20 mg/kg PO q12h) for peritonitis or necrosis. 5) Gastroprotectants: Famotidine (0.5 mg/kg IV or PO q12-24h) or omeprazole (0.7 mg/kg PO q24h) to reduce gastric acidity. 6) Anti-arrhythmics: Lidocaine (1-2 mg/kg IV slow bolus) if ventricular arrhythmias occur. 7) Nutritional support: Oxbow Critical Care or equivalent, 10-15 mL/kg PO q6-8h. 8) Electrolyte supplementation: Potassium chloride (0.5-1 mEq/kg/h IV) if hypokalemic. 9) Oxygen therapy: 40-60% oxygen via mask or cage. 10) Emergency drugs: Atropine (0.05 mg/kg IV or IM) for bradycardia, and epinephrine (0.01-0.02 mg/kg IV) for cardiac arrest. All dosages should be adjusted based on patient response and monitoring.

Evidence-based literature on GDV in rabbits is limited, but several key studies and case reports provide guidance. A retrospective study by DeCubellis and Graham (2013) reviewed 12 cases of gastric dilatation and volvulus in rabbits, reporting a survival rate of 50% with surgical intervention. They identified that rabbits with gastric necrosis had a poorer prognosis. Another study by Harcourt-Brown (2007) highlighted the importance of early diagnosis and aggressive fluid therapy. A case series by Varga (2014) described successful management of GDV in two rabbits using gastropexy. Consensus guidelines from the Association of Exotic Mammal Veterinarians (AEMV) recommend immediate decompression and surgery for GDV. The BSAVA Manual of Rabbit Medicine (2014) provides detailed protocols for emergency management. A review by Jenkins (2010) emphasized the role of dietary factors in the pathogenesis of GDV. While there are no randomized controlled trials due to the rarity and emergency nature of the condition, the available evidence supports a combination of medical stabilization and surgical correction. Future research should focus on identifying risk factors and improving surgical techniques to reduce mortality.