Splenic Torsion

Splenic torsion is a surgical emergency characterized by the rotation of the spleen around its longitudinal axis, leading to vascular occlusion, venous congestion, ischemia, and eventual infarction of the splenic parenchyma. The condition is most commonly observed in large-breed dogs, particularly those with a deep-chested conformation, such as Great Danes, German Shepherds, and Irish Setters. The torsion typically involves the gastrosplenic ligament and the splenic pedicle, which contains the splenic artery and vein. The rotation can be partial (less than 360 degrees) or complete (360 degrees or more), and it may occur in either a clockwise or counterclockwise direction. The resultant venous outflow obstruction leads to rapid splenomegaly, hemorrhage, and systemic inflammatory response syndrome (SIRS), which can progress to hypovolemic shock and death if not promptly treated. In cats, splenic torsion is exceedingly rare and is often associated with concurrent neoplastic or traumatic conditions. The definitive treatment is surgical splenectomy, which is curative in most cases if performed before irreversible systemic complications ensue.

The exact etiology of splenic torsion remains idiopathic in most cases, but several predisposing factors have been identified. Anatomically, the spleen is suspended by the gastrosplenic ligament and the splenocolic ligament, which vary in length and laxity among individuals. In deep-chested breeds, the greater omentum and gastrosplenic ligament are often more lax, allowing excessive mobility of the spleen. Gastric dilatation-volvulus (GDV) is a well-documented concurrent condition, with splenic torsion occurring in approximately 10-20% of GDV cases. The rotation of the stomach can pull the spleen into an abnormal position, predisposing it to torsion. Conversely, isolated splenic torsion can occur without GDV. Trauma, such as blunt abdominal trauma, may cause the spleen to rotate on its pedicle. Additionally, splenic masses (e.g., hemangiosarcoma, hematoma) can increase the weight and size of the spleen, making torsion more likely. In some cases, congenital ligamentous laxity or abnormal development of the suspensory ligaments may be a contributing factor. Iatrogenic causes are rare but may include excessive manipulation of the spleen during abdominal surgery. The exact biomechanical trigger for torsion is unknown, but it is hypothesized that sudden changes in intra-abdominal pressure, vigorous exercise, or gastric filling may initiate the rotation.

Splenic torsion is primarily a disease of large and giant-breed dogs. The most commonly affected breeds include Great Danes, German Shepherds, Irish Setters, Saint Bernards, Weimaraners, and Bloodhounds. These breeds often have a deep, narrow thoracic cavity and a relatively long, mobile spleen. The condition is rare in small-breed dogs and cats. There is no strong sex predilection, although some studies suggest a slight male predominance. The age of onset is typically middle-aged to older dogs, with a mean age of 7-10 years. However, cases have been reported in young adult dogs. The incidence of splenic torsion is significantly higher in dogs with a history of GDV, and it is considered a risk factor for recurrence. In a retrospective study of 100 dogs with splenic torsion, approximately 30% had concurrent GDV. The condition is sporadic and does not appear to have a genetic basis, but the conformational predisposition is clearly breed-related. Working dogs, such as police and military dogs, may be at increased risk due to high levels of physical activity and potential trauma.

The pathophysiology of splenic torsion involves a cascade of vascular, ischemic, and inflammatory events. The spleen is a highly vascular organ with a rich blood supply from the splenic artery and drainage via the splenic vein. When the spleen rotates on its longitudinal axis, the splenic vein, which is more susceptible to compression due to its thinner wall and lower intraluminal pressure, becomes occluded first. This leads to venous congestion and rapid splenomegaly, as blood continues to enter via the artery but cannot exit. The spleen can enlarge to several times its normal size, becoming engorged with blood. The increased intrasplenic pressure eventually compromises arterial inflow, leading to ischemia and infarction of the splenic parenchyma. The ischemic tissue releases inflammatory mediators, including cytokines, reactive oxygen species, and lysosomal enzymes, which enter the systemic circulation. This triggers a systemic inflammatory response syndrome (SIRS), characterized by vasodilation, increased capillary permeability, and activation of the coagulation cascade. The sequestration of blood in the spleen leads to hypovolemia, hypotension, and decreased tissue perfusion. If left untreated, the condition progresses to septic peritonitis (due to bacterial translocation from the ischemic gut or splenic necrosis), disseminated intravascular coagulation (DIC), and multiple organ dysfunction syndrome (MODS). The spleen may also rupture, causing hemoperitoneum and acute anemia. In chronic cases, the torsion may be partial and intermittent, leading to recurrent episodes of splenomegaly and abdominal pain.

Several intrinsic and extrinsic factors predispose to splenic torsion. Intrinsic factors include breed conformation, particularly deep-chested breeds with a narrow thoracic inlet and a long, mobile spleen. The length and laxity of the gastrosplenic and splenocolic ligaments are critical; excessive laxity allows the spleen to rotate more freely. Age is a factor, as middle-aged to older dogs have more degenerative changes in connective tissue, potentially increasing ligamentous laxity. Sex may play a minor role, with some studies suggesting a higher incidence in males. Extrinsic factors include a history of gastric dilatation-volvulus (GDV), which is the most significant risk factor. Trauma, such as being hit by a car, can cause the spleen to twist. High-impact exercise or vigorous play may also trigger torsion. The presence of splenic masses, such as hematomas or neoplasms, increases the weight of the spleen and alters its center of gravity, making torsion more likely. Prior abdominal surgery, particularly splenic manipulation, may create adhesions or alter the normal anatomy, predisposing to torsion. Nutritional factors, such as a single large meal per day, may increase the risk of GDV and thus indirectly increase the risk of splenic torsion.

The clinical signs of splenic torsion can be acute or chronic. In acute cases, dogs present with a sudden onset of abdominal pain, distension, and vomiting. The pain is often severe and may be localized to the left cranial abdomen. The dog may assume a 'praying' position (anterior abdomen down, posterior elevated) to relieve pain. Other signs include lethargy, anorexia, pale mucous membranes, tachycardia, tachypnea, and weak femoral pulses, indicating hypovolemic shock. In some cases, the spleen may be palpably enlarged and firm on abdominal palpation, but this is often difficult due to pain and muscle guarding. In chronic or intermittent torsion, the signs may be more subtle, with recurrent episodes of vomiting, diarrhea, and mild abdominal discomfort. The dog may have a history of intermittent anorexia and weight loss. On physical examination, the dog may be dehydrated and have a fever due to systemic inflammation. In advanced cases, signs of peritonitis, such as a 'board-like' abdomen, may be present. If the spleen has ruptured, signs of acute hemorrhage, such as severe pallor, collapse, and a rapid, weak pulse, may dominate. It is important to note that splenic torsion can occur without GDV, and the clinical signs may be indistinguishable from other causes of acute abdomen.

The differential diagnoses for splenic torsion include: 1) Gastric dilatation-volvulus (GDV): GDV presents with similar acute abdominal signs, but the stomach is distended and tympanic on percussion. Radiographs show a 'double bubble' or 'hourglass' stomach. Splenic torsion may be concurrent, so careful evaluation of the spleen is necessary. 2) Splenic neoplasia (e.g., hemangiosarcoma, lymphoma): Splenic masses can cause splenomegaly and abdominal pain, but the onset is usually more gradual. Ultrasonography and fine-needle aspiration can differentiate. 3) Splenic hematoma: A benign hematoma can cause splenomegaly and hemoperitoneum, but it is not typically associated with torsion. Imaging may show a well-defined mass. 4) Acute pancreatitis: Pancreatitis can cause severe abdominal pain and vomiting, but the pain is usually more cranial and midline. Laboratory findings include elevated lipase and amylase. 5) Intestinal obstruction or intussusception: These can cause acute vomiting and abdominal pain, but the pain is often more diffuse. Radiographs may show gas-filled loops of bowel. 6) Peritonitis (septic or sterile): Peritonitis can cause abdominal pain and distension, but it is usually secondary to another condition. Abdominocentesis may reveal septic or inflammatory fluid. 7) Mesenteric torsion: This is a rare condition that causes acute abdominal pain and shock, but it is difficult to differentiate preoperatively. 8) Ureteral obstruction or renal colic: These can cause flank pain and vomiting, but the pain is typically more caudal and lateral. 9) Prostatic disease (in males): Prostatitis or prostatic abscess can cause caudal abdominal pain and systemic signs. 10) Hepatic torsion: Torsion of a liver lobe is extremely rare but can cause similar signs. Imaging and exploratory surgery are often necessary to confirm the diagnosis.

The diagnostic algorithm for splenic torsion begins with a thorough history and physical examination. Any large-breed dog with acute abdominal pain, vomiting, and signs of shock should be suspected of having splenic torsion or GDV. Immediate stabilization with intravenous fluids and pain management is essential. The next step is imaging. Abdominal radiographs may show a large, soft-tissue opacity in the left cranial abdomen, loss of the normal splenic silhouette, and possibly a gas-filled stomach if GDV is present. However, radiographs are not definitive for splenic torsion. Abdominal ultrasonography is the preferred imaging modality. It can reveal an enlarged spleen with a hypoechoic or heterogeneous parenchyma, and Doppler ultrasound can demonstrate absent or reversed blood flow in the splenic vein. The 'whirl sign' or 'target sign' may be seen at the splenic hilus, indicating torsion of the pedicle. If ultrasonography is inconclusive, computed tomography (CT) with contrast can provide a definitive diagnosis by showing the twisted pedicle and lack of contrast enhancement of the spleen. In unstable patients, a focused assessment with sonography for trauma (FAST) can be performed quickly. If the diagnosis is still uncertain, an exploratory laparotomy is indicated, as it is both diagnostic and therapeutic. Preoperative laboratory tests, including a complete blood count, serum biochemistry, coagulation panel, and blood gas analysis, are essential to assess the severity of systemic involvement and to guide treatment.

Laboratory findings in splenic torsion are nonspecific but reflect the systemic inflammatory response and hypovolemia. A complete blood count may show hemoconcentration (elevated hematocrit) due to dehydration, or anemia if there is hemorrhage. Leukocytosis with a left shift is common due to inflammation. Thrombocytopenia may be present due to platelet consumption or DIC. Serum biochemistry may reveal elevated liver enzymes (ALT, AST) due to hepatic ischemia, elevated bilirubin due to hemolysis or biliary stasis, and elevated blood urea nitrogen (BUN) and creatinine due to prerenal azotemia. Electrolyte imbalances, such as hyponatremia and hyperkalemia, may occur due to vomiting and shock. Coagulation abnormalities, including prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), and elevated D-dimer levels, indicate DIC. Blood gas analysis may show metabolic acidosis with a compensatory respiratory alkalosis. Inflammatory biomarkers, such as C-reactive protein (CRP) and serum amyloid A (SAA), are elevated. Abdominocentesis or peritoneal lavage may yield sanguineous or serosanguineous fluid with a high protein content and nucleated cell count, consistent with nonseptic inflammation. If the spleen has ruptured, the fluid may be frankly hemorrhagic. Cytology of the fluid may show reactive mesothelial cells and neutrophils, but bacteria are typically absent unless there is concurrent peritonitis.

Imaging plays a crucial role in the diagnosis of splenic torsion. Abdominal radiographs (lateral and ventrodorsal views) may show a large, soft-tissue opacity in the left cranial abdomen, displacing the stomach and intestines. The splenic silhouette may be absent or abnormally positioned. In cases with concurrent GDV, the stomach is distended with gas and has a characteristic 'double bubble' appearance. However, radiographs are not sensitive or specific for splenic torsion. Abdominal ultrasonography is the most useful imaging modality. On B-mode ultrasound, the spleen appears enlarged, with a rounded, hypoechoic or heterogeneous parenchyma. The echotexture may be mottled due to hemorrhage and infarction. The splenic hilus may show a 'whirl sign' or 'target sign', which is a cross-sectional view of the twisted pedicle. Color Doppler and pulsed-wave Doppler can demonstrate absent or reversed blood flow in the splenic vein, and reduced or absent arterial flow. Contrast-enhanced ultrasound (CEUS) can further characterize perfusion defects. Computed tomography (CT) with intravenous contrast is highly sensitive and specific. It can show the twisted pedicle, lack of contrast enhancement of the spleen, and the presence of free abdominal fluid. CT is particularly useful in stable patients or when the diagnosis is uncertain. Magnetic resonance imaging (MRI) is rarely used due to the need for general anesthesia and the availability of other modalities. In some cases, diagnostic laparoscopy may be used to directly visualize the spleen and confirm the diagnosis, but this is not commonly performed in emergency settings.

Cytology and histopathology are important for confirming the diagnosis and ruling out underlying neoplasia. Fine-needle aspiration (FNA) of the spleen can be performed under ultrasound guidance, but it is often avoided in cases of suspected torsion due to the risk of hemorrhage and the need for emergency surgery. If FNA is performed, cytology may show necrotic debris, red blood cells, and inflammatory cells, but it is not diagnostic for torsion. Histopathology of the spleen after splenectomy is the gold standard. Grossly, the spleen is enlarged, dark red to black, and congested. The parenchyma may be friable and infarcted. Microscopically, there is extensive hemorrhage, congestion, and necrosis of the red pulp. The white pulp may be depleted. There may be evidence of thrombosis in the splenic vessels. If a mass is present, histopathology can identify the underlying cause, such as hemangiosarcoma, lymphoma, or hematoma. Immunohistochemistry may be used to differentiate between benign and malignant lesions. In cases of chronic torsion, there may be fibrosis and hemosiderin deposition. It is important to submit the entire spleen for histopathology to rule out neoplasia, as the incidence of splenic tumors in dogs with torsion is not negligible.

The treatment of splenic torsion is surgical splenectomy. Preoperative stabilization is critical. Intravenous fluid therapy with isotonic crystalloids (e.g., lactated Ringer's solution) at a rate of 10-20 ml/kg bolus, followed by a maintenance rate of 5-10 ml/kg/hr, is initiated to correct hypovolemia. Colloids (e.g., hetastarch) may be used if hypoproteinemia is present. Pain management with opioids (e.g., hydromorphone 0.05-0.1 mg/kg IV, or fentanyl 2-5 mcg/kg IV) is essential. Broad-spectrum antibiotics (e.g., cefazolin 22 mg/kg IV) are administered preoperatively. Once the patient is stabilized, exploratory laparotomy is performed. A midline incision is made from the xiphoid to the pubis. The spleen is exteriorized, and the torsion is identified. The splenic pedicle is ligated and transected. The splenic artery and vein are individually ligated with absorbable suture (e.g., polydioxanone or polyglactin 910, size 2-0 or 3-0) using a triple ligation technique. The spleen is then removed. The abdomen is thoroughly lavaged with warm sterile saline, and the abdomen is closed in a routine manner. If GDV is present, the stomach is derotated and a gastropexy is performed to prevent recurrence. Postoperative care includes continued fluid therapy, pain management, and monitoring for complications such as DIC, peritonitis, and cardiac arrhythmias. The prognosis is good if surgery is performed early, but the mortality rate can be as high as 30-40% in cases with severe systemic involvement.

The prognosis for splenic torsion is generally good if surgical intervention is performed promptly. The survival rate for dogs with isolated splenic torsion is approximately 80-90%. However, the prognosis is worse if there is concurrent GDV, splenic rupture, or DIC. In a retrospective study of 100 dogs with splenic torsion, the overall survival rate was 78%. Dogs that survived to discharge had a median survival time of 3 years. The most common postoperative complications were cardiac arrhythmias (especially ventricular arrhythmias), DIC, and peritonitis. The presence of a splenic mass, particularly hemangiosarcoma, significantly worsens the prognosis, with a median survival time of less than 6 months. Negative prognostic indicators include a prolonged duration of clinical signs, severe hypovolemic shock, elevated lactate levels, and the presence of DIC. Early diagnosis and aggressive surgical management are the most important factors for a successful outcome. Long-term, most dogs that recover from splenic torsion have a good quality of life, but they may be at increased risk for other splenic diseases, so regular monitoring is recommended.

Postoperative follow-up is essential to monitor for complications and ensure a full recovery. The dog should be hospitalized for at least 24-48 hours after surgery. Intravenous fluids are continued until the dog is hemodynamically stable and eating and drinking normally. Pain management is continued with opioids (e.g., buprenorphine 0.01-0.02 mg/kg IV q8-12h) and NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h) once oral medications are tolerated. The incision should be monitored daily for signs of infection, such as redness, swelling, or discharge. Skin sutures or staples are removed 10-14 days after surgery. The dog should be restricted to leash walks and minimal activity for 2 weeks to allow for proper healing. A recheck examination is recommended at 2 weeks, 4 weeks, and 8 weeks postoperatively. At each recheck, a physical examination and abdominal ultrasound may be performed to assess for any abnormalities. Blood work, including a complete blood count and serum biochemistry, should be repeated at 2 weeks to ensure that organ function has returned to normal. If the spleen was removed due to a neoplastic process, additional staging (e.g., thoracic radiographs, abdominal ultrasound) and chemotherapy may be recommended. Long-term, the dog should be monitored for signs of recurrence of splenic disease, although this is rare. Regular veterinary check-ups every 6-12 months are advised.

Clinical pearls: 1) Always consider splenic torsion in any large-breed dog with acute abdominal pain and shock, even in the absence of GDV. 2) Ultrasonography is the most valuable diagnostic tool; look for the 'whirl sign' at the splenic hilus. 3) Preoperative stabilization is crucial; do not rush to surgery until the dog is hemodynamically stable. 4) During surgery, exteriorize the spleen carefully to avoid rupture. 5) Ligate the splenic artery and vein individually to prevent hemorrhage. 6) Perform a gastropexy if GDV is present to prevent recurrence. 7) Monitor for cardiac arrhythmias postoperatively, as they are common and can be fatal. Pitfalls: 1) Delaying surgery due to diagnostic uncertainty can be fatal. 2) Failing to recognize concurrent GDV. 3) Inadequate fluid resuscitation before surgery. 4) Rough handling of the spleen, leading to rupture and hemorrhage. 5) Incomplete ligation of the splenic vessels, causing postoperative bleeding. 6) Overlooking the possibility of splenic neoplasia, which requires additional treatment. 7) Discharging the dog too early, before arrhythmias and DIC have resolved.

Perioperative drug protocols are based on Plumb's Veterinary Drug Handbook. Preoperative: Cefazolin (22 mg/kg IV) or cefoxitin (30 mg/kg IV) administered 30 minutes before incision, repeated every 90 minutes during surgery. Analgesia: Hydromorphone (0.05-0.1 mg/kg IV) or fentanyl (2-5 mcg/kg IV bolus, then 2-5 mcg/kg/hr CRI) for intraoperative and immediate postoperative pain. Postoperative: Buprenorphine (0.01-0.02 mg/kg IV or IM q8-12h) or fentanyl patch (2-5 mcg/kg/hr transdermal) for 72 hours. NSAIDs: Carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) after the dog is eating and hydrated. Antiemetics: Maropitant (1 mg/kg IV or PO q24h) or metoclopramide (1-2 mg/kg/day CRI) if vomiting. Gastroprotectants: Omeprazole (0.7-1 mg/kg PO q24h) or famotidine (0.5 mg/kg IV or PO q12h) to prevent gastric ulceration. Fluid therapy: Lactated Ringer's solution or Normosol-R at a rate of 10-20 ml/kg bolus, then 5-10 ml/kg/hr. Colloids: Hetastarch (10-20 ml/kg/day) if hypoalbuminemia. Inotropic support: Dobutamine (2-10 mcg/kg/min CRI) if hypotension persists despite fluids. Antiarrhythmics: Lidocaine (2 mg/kg IV bolus, then 50-80 mcg/kg/min CRI) or amiodarone (5 mg/kg IV over 15 minutes) for ventricular arrhythmias. Coagulation support: Fresh frozen plasma (10-20 ml/kg IV) if DIC is present. Antibiotics: Continue cefazolin (22 mg/kg IV q8h) for 24 hours postoperatively, then switch to amoxicillin-clavulanate (13.75 mg/kg PO q12h) for 5-7 days if needed.

The veterinary literature on splenic torsion is limited but informative. A landmark retrospective study by Neath et al. (2002) evaluated 100 dogs with splenic torsion and found that 30% had concurrent GDV. The survival rate was 78%, and the most common complications were cardiac arrhythmias and DIC. Another study by Goldhammer et al. (2010) compared dogs with splenic torsion to those with splenic masses and found that torsion was more likely in deep-chested breeds and was associated with a better prognosis if treated surgically. A study by Spangler and Culbertson (1992) examined the histopathologic features of splenic torsion and found that infarction and necrosis were common, and that the presence of neoplasia was a negative prognostic indicator. In terms of surgical technique, a study by Glickman et al. (2000) on GDV recommended routine gastropexy to prevent recurrence, which is also applicable to splenic torsion cases with concurrent GDV. There are no prospective randomized controlled trials on splenic torsion due to the emergency nature of the condition. However, consensus guidelines from the American College of Veterinary Surgeons (ACVS) recommend prompt surgical intervention and aggressive postoperative monitoring for arrhythmias and DIC. The use of ultrasonography for diagnosis is well-supported by case series, and CT is increasingly used for definitive diagnosis. Overall, the evidence supports early splenectomy as the treatment of choice, with a favorable prognosis in the absence of concurrent disease.