Mesenteric Torsion

Mesenteric torsion, also known as mesenteric volvulus, is a rare but life-threatening surgical emergency characterized by the rotation of a segment of the small intestine and its mesentery around the mesenteric root, leading to acute occlusion of the cranial mesenteric artery and vein, rapid intestinal ischemia, necrosis, and systemic inflammatory response syndrome (SIRS). The condition is most commonly reported in large-breed dogs, particularly German Shepherd Dogs, and is associated with a high mortality rate if not promptly diagnosed and surgically corrected. The torsion can involve the entire small intestine (global volvulus) or a segment (segmental volvulus), with the former being more common and more severe. The rotation is typically clockwise when viewed from the cranial aspect, and the degree of rotation can vary from 90° to 360°, with 180° to 270° being most common. The condition is distinct from gastric dilatation-volvulus (GDV), although both can occur concurrently. Mesenteric torsion results in complete or partial obstruction of the cranial mesenteric artery, leading to ischemic necrosis of the intestinal wall, loss of mucosal barrier integrity, translocation of bacteria and endotoxins, and rapid progression to shock and death within hours if untreated.

The exact etiology of mesenteric torsion is often idiopathic, but several predisposing factors have been identified. Anatomical factors include a long, freely movable mesentery, which allows excessive mobility of the small intestine. In dogs, the mesentery is relatively long compared to other species, and certain breeds, such as German Shepherd Dogs, have a deeper chest and a more vertically oriented mesentery, which may predispose to torsion. Dietary factors, such as a single large meal followed by vigorous exercise, have been proposed as triggers, as they may cause intestinal distension and increased motility, leading to abnormal rotation. Trauma, such as blunt abdominal trauma, can also cause mesenteric torsion. Iatrogenic causes include previous abdominal surgery, which may create adhesions or alter the normal anatomical relationships. In some cases, mesenteric torsion is associated with other gastrointestinal diseases, such as intussusception, foreign bodies, or neoplasia, which may alter intestinal motility or create a fulcrum for rotation. Additionally, a genetic predisposition has been suggested due to the high incidence in certain breeds and families. The exact pathophysiological trigger remains unclear, but it is likely a combination of anatomical, dietary, and functional factors that lead to abnormal intestinal rotation.

Mesenteric torsion is a rare condition in dogs and cats, with a reported incidence of less than 1% of all surgical gastrointestinal emergencies. It is most commonly seen in large-breed and giant-breed dogs, with German Shepherd Dogs being overrepresented, accounting for up to 50% of cases in some studies. Other predisposed breeds include Great Danes, Saint Bernards, Weimaraners, and Bloodhounds. The condition is rare in small-breed dogs and cats. There is no clear sex predilection, although some studies suggest a slight male predominance. The age of affected animals ranges from 2 to 10 years, with a median age of 5 to 6 years. The condition is more common in dogs that are fed a single large meal per day and are allowed to exercise vigorously after eating. Working dogs, such as police and military dogs, may be at higher risk due to their activity levels. The mortality rate is high, ranging from 50% to 100%, with most deaths occurring within 24 hours of presentation. Early recognition and aggressive surgical intervention are critical for survival.

The pathophysiology of mesenteric torsion involves a cascade of events that rapidly lead to intestinal ischemia, necrosis, and systemic shock. The torsion causes a mechanical obstruction of the cranial mesenteric artery and vein, leading to both arterial ischemia and venous congestion. The initial venous occlusion causes increased capillary hydrostatic pressure, leading to edema and hemorrhage within the intestinal wall. This is followed by arterial occlusion, which results in severe ischemia and hypoxia of the intestinal tissue. The intestinal mucosa is particularly sensitive to ischemia, and within minutes to hours, the mucosal barrier is compromised, allowing bacteria and endotoxins to translocate into the peritoneal cavity and systemic circulation. This triggers a massive inflammatory response, with release of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukins (IL-1, IL-6), and platelet-activating factor, leading to systemic inflammatory response syndrome (SIRS), sepsis, and multiple organ dysfunction syndrome (MODS). The ischemic intestine also produces reactive oxygen species upon reperfusion, further exacerbating tissue damage. The loss of fluid and electrolytes into the intestinal lumen and peritoneal cavity leads to hypovolemia, hypotension, and shock. Additionally, the torsion can cause obstruction of the intestinal lumen, leading to gaseous distension and further compromise of blood flow. If left untreated, the condition progresses to irreversible intestinal necrosis, perforation, peritonitis, and death.

Predisposing factors for mesenteric torsion can be divided into intrinsic and extrinsic factors. Intrinsic factors include anatomical variations such as a long, redundant mesentery, which allows excessive mobility of the small intestine. Certain breeds, such as German Shepherd Dogs, have a deeper chest and a more vertically oriented mesentery, which may increase the risk of torsion. A genetic predisposition is suspected due to the breed predilection. Age may also be a factor, as the condition is more common in middle-aged dogs. Extrinsic factors include dietary habits, such as feeding a single large meal per day, which can cause gastric and intestinal distension, and vigorous exercise immediately after eating, which may increase intestinal motility and predispose to rotation. Trauma, such as blunt abdominal trauma, can also cause mesenteric torsion. Previous abdominal surgery may create adhesions or alter the normal anatomical relationships, increasing the risk. Additionally, concurrent gastrointestinal diseases, such as intussusception, foreign bodies, or neoplasia, may alter intestinal motility or create a fulcrum for rotation. Stress and anxiety may also play a role, as they can affect gastrointestinal motility.

Clinical signs of mesenteric torsion are acute and rapidly progressive. The most common presenting signs include sudden onset of severe abdominal pain, which may be manifested as restlessness, panting, pacing, or assuming a prayer position (anterior abdomen down, posterior abdomen up). Vomiting is common and may be projectile, often non-productive or producing frothy fluid. Abdominal distension may be present, but it is often less pronounced than in gastric dilatation-volvulus. The animal may show signs of shock, including pale mucous membranes, prolonged capillary refill time, tachycardia, weak pulses, and hypothermia. As the condition progresses, the animal may become depressed, recumbent, and eventually comatose. In some cases, there may be diarrhea, which may be bloody. On physical examination, the abdomen may be painful on palpation, and a fluid wave or gas-filled loops of intestine may be felt. In advanced cases, signs of peritonitis, such as abdominal rigidity and pain, may be present. The clinical signs can progress rapidly, with death occurring within hours of onset if not treated.

Differential diagnoses for mesenteric torsion include other causes of acute abdominal pain and gastrointestinal obstruction. Gastric dilatation-volvulus (GDV) is a common differential, especially in large-breed dogs, and can occur concurrently with mesenteric torsion. GDV is characterized by severe abdominal distension, non-productive vomiting, and rapid progression to shock. Intestinal obstruction due to foreign bodies, intussusception, or neoplasia can also cause similar signs, but the onset is usually less acute. Acute pancreatitis can cause severe abdominal pain and vomiting, but is typically associated with a history of dietary indiscretion and may have characteristic laboratory findings. Peritonitis, whether septic or sterile, can cause similar signs, but is often secondary to other conditions. Mesenteric volvulus can also mimic other causes of acute abdomen, such as splenic torsion, hepatic torsion, or renal torsion. In cats, mesenteric torsion is extremely rare, and other causes of acute abdomen, such as feline infectious peritonitis or pancreatitis, should be considered. Diagnostic imaging, particularly abdominal radiography and ultrasonography, can help differentiate these conditions. In mesenteric torsion, radiographs may show a gas-filled, distended small intestine with a 'whirl' pattern, and ultrasonography may reveal a 'whirlpool' sign of the mesenteric vessels. However, definitive diagnosis often requires exploratory surgery.

The diagnostic algorithm for mesenteric torsion begins with a thorough history and physical examination. The presence of acute, severe abdominal pain, vomiting, and signs of shock in a large-breed dog should raise suspicion. Immediate stabilization with intravenous fluids, oxygen, and analgesia is essential before diagnostic tests. Abdominal radiographs (right lateral and ventrodorsal views) are the first imaging modality and may show a gas-filled, distended small intestine, with a 'whirl' pattern or 'coffee bean' sign. However, radiographs are not always diagnostic. Abdominal ultrasonography is more sensitive and may reveal a 'whirlpool' sign of the mesenteric vessels, which is pathognomonic for mesenteric torsion. Doppler ultrasonography can assess blood flow to the intestine. If the patient is stable, a computed tomography (CT) scan can provide detailed images of the mesenteric vasculature and intestinal rotation, but this is often not feasible in an emergency setting. Laboratory tests, including a complete blood count, serum biochemistry, and blood gas analysis, are useful for assessing the severity of shock and organ dysfunction. However, surgery should not be delayed for diagnostic tests if the clinical suspicion is high. Exploratory laparotomy is both diagnostic and therapeutic, and is the definitive method for confirming mesenteric torsion. The surgical approach is a ventral midline celiotomy, and the torsion is identified by the twisted mesentery and congested, dark-colored intestine.

Laboratory findings in mesenteric torsion are consistent with severe shock, ischemia, and systemic inflammation. A complete blood count may show hemoconcentration (elevated packed cell volume) due to dehydration, or leukopenia due to endotoxemia and sequestration of white blood cells. A left shift may be present. Serum biochemistry may reveal elevated liver enzymes (ALT, AST) due to hepatic ischemia, elevated renal parameters (BUN, creatinine) due to prerenal azotemia, and hypoglycemia due to decreased gluconeogenesis and increased glucose consumption. Electrolyte imbalances, such as hyponatremia, hypokalemia, and metabolic acidosis, are common. Blood gas analysis may show metabolic acidosis with elevated lactate levels, indicating tissue hypoxia. Coagulation abnormalities, such as prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), may be present due to disseminated intravascular coagulation (DIC). Inflammatory biomarkers, such as C-reactive protein (CRP) and serum amyloid A (SAA), may be elevated. However, these findings are non-specific and should not delay surgical intervention. In cases where peritonitis is suspected, abdominocentesis or diagnostic peritoneal lavage may be performed, and the fluid may show suppurative inflammation with intracellular bacteria.

Imaging plays a crucial role in the diagnosis of mesenteric torsion. Abdominal radiographs (right lateral and ventrodorsal views) are the first-line imaging modality. In mesenteric torsion, radiographs may show a gas-filled, distended small intestine, with a 'whirl' pattern or 'coffee bean' sign. The 'whirl' pattern is caused by the twisted mesentery and is characterized by a circular arrangement of gas-filled loops of intestine. However, this finding is not always present, and radiographs may be non-specific. Abdominal ultrasonography is more sensitive and can reveal a 'whirlpool' sign of the mesenteric vessels, which is pathognomonic for mesenteric torsion. The 'whirlpool' sign is seen as a swirling pattern of the mesenteric vessels and is best visualized with color Doppler. Ultrasonography can also assess the thickness and echogenicity of the intestinal wall, which may be thickened and hypoechoic due to edema and ischemia. In addition, free abdominal fluid may be detected. Computed tomography (CT) is the most sensitive imaging modality and can provide detailed images of the mesenteric vasculature, intestinal rotation, and the extent of ischemia. CT angiography can demonstrate the 'whirl' sign of the mesenteric vessels and the lack of contrast enhancement in the affected intestine. However, CT is often not feasible in an emergency setting due to the time required and the need for general anesthesia. In some cases, diagnostic laparoscopy may be used to confirm the diagnosis, but this is rarely performed in an emergency setting.

Cytology and histopathology are not typically performed in the acute management of mesenteric torsion, as the diagnosis is made surgically. However, if abdominal fluid is collected, cytology may show suppurative inflammation with degenerate neutrophils and intracellular bacteria, indicating septic peritonitis. Histopathology of the resected intestine may show hemorrhagic necrosis of the intestinal wall, with loss of the mucosal epithelium, congestion of the submucosal vessels, and infiltration of inflammatory cells. The mesentery may show thrombosis of the blood vessels. In chronic cases, fibrosis and adhesions may be present. Histopathology is useful for confirming the extent of necrosis and for ruling out underlying diseases, such as neoplasia or inflammatory bowel disease. However, the primary goal of surgery is to resect non-viable intestine and restore blood flow, and histopathology is not necessary for the immediate management.

Treatment of mesenteric torsion is a surgical emergency. The initial management involves aggressive stabilization of the patient, including intravenous fluid resuscitation with isotonic crystalloids (e.g., lactated Ringer's solution) at a rate of 20-40 ml/kg/hour, oxygen supplementation, and analgesia with opioids (e.g., hydromorphone 0.05-0.1 mg/kg IV, or fentanyl 2-5 µg/kg IV bolus followed by a constant rate infusion of 2-5 µg/kg/hour). Broad-spectrum antibiotics should be administered intravenously, such as ampicillin (20 mg/kg IV q8h) and enrofloxacin (5-10 mg/kg IV q24h), or cefazolin (22 mg/kg IV q8h) and metronidazole (10 mg/kg IV q12h). Once the patient is stabilized, emergency exploratory laparotomy is performed. The surgical approach is a ventral midline celiotomy from the xiphoid to the pubis. Upon entering the abdomen, the torsion is identified and the intestine is carefully untwisted. The viability of the intestine is assessed by evaluating the color, pulsation of the mesenteric vessels, and peristalsis. Non-viable intestine should be resected and an end-to-end anastomosis performed. The anastomosis is performed using a simple interrupted or continuous pattern with absorbable monofilament suture (e.g., polydioxanone, 3-0 or 4-0). In cases of extensive necrosis, a large portion of the small intestine may need to be resected, which can lead to short bowel syndrome. After resection, the abdomen is lavaged with warm sterile saline and closed routinely. Postoperative management includes continued fluid therapy, antibiotics, analgesics, and nutritional support. Early enteral nutrition is recommended if the intestine is functional. The prognosis is guarded, and the mortality rate is high, especially if the torsion is severe or if surgery is delayed.

The prognosis for mesenteric torsion is guarded to poor. The mortality rate ranges from 50% to 100%, with most deaths occurring within 24 hours of presentation. Factors that negatively affect the prognosis include a delay in surgical intervention, the extent of intestinal necrosis, the presence of septic peritonitis, and the development of systemic inflammatory response syndrome (SIRS) or disseminated intravascular coagulation (DIC). The survival rate is higher in animals that are stabilized aggressively and undergo surgery within a few hours of the onset of signs. In one study, the survival rate was 50% for dogs that underwent surgery, but it dropped to 10% if the torsion was associated with gastric dilatation-volvulus. Short-term complications include postoperative ileus, peritonitis, and wound dehiscence. Long-term complications may include short bowel syndrome if a large portion of the intestine is resected, leading to chronic diarrhea and malnutrition. However, some animals can have a good quality of life if the resection is limited and the remaining intestine adapts. The prognosis is also influenced by the underlying cause, if any, and the presence of concurrent diseases.

Follow-up care for animals that survive mesenteric torsion is crucial for monitoring recovery and detecting complications. Immediately postoperatively, the animal should be monitored closely for signs of shock, sepsis, and ileus. Intravenous fluids, antibiotics, and analgesics should be continued as needed. The surgical incision should be monitored for signs of infection or dehiscence. Suture removal is typically performed 10-14 days after surgery. The animal should be fed a bland, easily digestible diet in small, frequent meals. If a large portion of the intestine was resected, a low-residue diet may be recommended. The animal should be gradually returned to normal activity over 2-4 weeks. Follow-up examinations should be scheduled at 1, 2, 4, and 8 weeks postoperatively. At each visit, the animal's weight, appetite, and fecal consistency should be assessed. Blood work, including a complete blood count and serum biochemistry, may be repeated to monitor for nutritional deficiencies or ongoing inflammation. If short bowel syndrome is present, long-term management may include nutritional supplementation, such as vitamin B12 and fat-soluble vitamins, and antidiarrheal medications. The owner should be educated on the signs of recurrence, which are rare but possible, and the importance of seeking immediate veterinary care if they occur.

Clinical pearls for mesenteric torsion include: 1) Always consider mesenteric torsion in any large-breed dog with acute, severe abdominal pain and signs of shock, even if abdominal distension is not pronounced. 2) Rapid stabilization and early surgical intervention are critical for survival; do not delay surgery for extensive diagnostic testing. 3) During surgery, carefully assess the viability of the intestine before deciding to resect. Use fluorescein dye or Doppler ultrasound if available to assess blood flow. 4) When performing an anastomosis, ensure a tension-free closure and adequate blood supply. 5) Consider the use of a jejunostomy tube for early enteral nutrition in cases of extensive resection. Pitfalls to avoid include: 1) Delaying surgery due to diagnostic tests, which can be fatal. 2) Failing to recognize the torsion during surgery, especially if the intestine is twisted in a way that is not obvious. 3) Resecting too much intestine, leading to short bowel syndrome, or too little, leaving non-viable tissue. 4) Inadequate postoperative monitoring for complications such as peritonitis and sepsis. 5) Not providing adequate analgesia, which can lead to postoperative ileus and increased stress.

Perioperative pharmacological protocols for mesenteric torsion are based on Plumb's Veterinary Drug Handbook and include: 1) Preoperative stabilization: Intravenous fluids (lactated Ringer's solution or Normosol-R) at a shock rate of 20-40 ml/kg/hour, with colloids (e.g., hetastarch 10-20 ml/kg IV) if hypoproteinemia is present. Oxygen supplementation via mask or nasal cannula. Analgesia: Opioids such as hydromorphone (0.05-0.1 mg/kg IV) or fentanyl (2-5 µg/kg IV bolus, then 2-5 µg/kg/hour CRI). 2) Antibiotics: Broad-spectrum coverage with ampicillin (20 mg/kg IV q8h) and enrofloxacin (5-10 mg/kg IV q24h), or cefazolin (22 mg/kg IV q8h) and metronidazole (10 mg/kg IV q12h). Continue for 24-48 hours postoperatively or longer if peritonitis is present. 3) Postoperative analgesia: Continue opioids (e.g., fentanyl CRI at 2-5 µg/kg/hour) for 24-48 hours, then transition to oral opioids (e.g., tramadol 2-5 mg/kg PO q8-12h) and NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h) once the animal is hemodynamically stable and renal function is normal. 4) Gastroprotectants: Sucralfate (0.5-1 g PO q8h) and omeprazole (0.7-1 mg/kg PO q24h) to prevent gastric ulceration. 5) Antiemetics: Maropitant (1 mg/kg SC q24h) or metoclopramide (1-2 mg/kg/day CRI) if vomiting is present. 6) Nutritional support: Early enteral nutrition via a jejunostomy tube or nasoesophageal tube with a liquid diet (e.g., Clinicare Canine/Feline) at a rate of 25-50% of resting energy requirement, gradually increasing over 24-48 hours. 7) Monitoring: Serial blood gas analysis, lactate, and coagulation parameters to guide therapy.

Evidence-based literature on mesenteric torsion is limited due to the rarity of the condition. Most studies are retrospective case series. A landmark study by Nemzek et al. (1993) reported a survival rate of 50% in dogs with mesenteric volvulus that underwent surgery, with a higher mortality in dogs with concurrent GDV. Another study by Junius et al. (2004) found that German Shepherd Dogs were overrepresented and that the survival rate was 33%. A more recent study by Schwartz et al. (2018) reported a survival rate of 40% and identified factors such as duration of clinical signs, heart rate, and lactate levels as prognostic indicators. There are no prospective randomized controlled trials due to the emergency nature of the condition. Consensus guidelines from the American College of Veterinary Surgeons (ACVS) recommend aggressive fluid resuscitation, early surgical intervention, and resection of non-viable intestine. The use of postoperative enteral nutrition has been shown to improve outcomes in other gastrointestinal surgeries and is recommended. Overall, the evidence supports the need for rapid diagnosis and surgical treatment, but the prognosis remains guarded.