Uterine Torsion and Rupture

Uterine torsion is a rare but life-threatening obstetric and surgical emergency characterized by rotation of the uterus along its longitudinal axis, typically occurring during late gestation or parturition in domestic carnivores. The torsion may involve one or both uterine horns, with the degree of rotation varying from 180° to 360° or more. Uterine rupture, on the other hand, is a full-thickness tear of the uterine wall, which may occur as a primary event (e.g., trauma, dystocia, or iatrogenic) or secondary to uterine torsion, necrosis, or infection. Both conditions result in severe abdominal crisis, fetal compromise or death, and maternal systemic inflammatory response syndrome (SIRS) or septic peritonitis. Surgical intervention, usually ovariohysterectomy (OHE), is the definitive treatment. The condition is classified as an acute abdomen and requires prompt diagnosis and surgical management to optimize maternal survival.

The exact etiology of uterine torsion is often unknown, but several predisposing factors have been identified. In dogs and cats, uterine torsion is most commonly associated with pregnancy, particularly in the last trimester or during parturition. The gravid uterus, with its increased weight and mobility, may rotate due to fetal movements, sudden maternal exertion, or abnormal fetal positioning. Other contributing factors include uterine laxity, hydrometra, pyometra, or uterine neoplasia, which can alter the normal anatomical position and increase the risk of torsion. Uterine rupture can result from trauma (e.g., vehicular accidents, kicks), severe dystocia, improper obstetrical manipulation, or as a complication of uterine torsion where vascular compromise leads to ischemic necrosis and subsequent rupture. Iatrogenic causes include uterine perforation during uterine lavage or manual removal of retained fetal membranes. In non-gravid animals, uterine torsion is extremely rare but may occur in cases of large uterine tumors or cystic endometrial hyperplasia.

Uterine torsion is a rare condition in small animal practice, with a reported incidence of less than 1% of all dystocia cases in dogs and cats. It is most commonly seen in middle-aged, pregnant bitches and queens, with a higher prevalence in large and giant breeds such as Great Danes, German Shepherds, and Labrador Retrievers. In cats, the condition is even rarer, with a slight predilection for Persian and Siamese breeds. Uterine rupture is also uncommon but may be seen in cases of severe dystocia, trauma, or as a sequela to uterine torsion. There is no clear breed or age predisposition for uterine rupture, but it is more likely to occur in animals with compromised uterine integrity, such as those with pyometra or after multiple pregnancies. The condition is sporadic and not associated with specific genetic factors, but conformational traits such as a deep, narrow pelvis may predispose to dystocia and subsequent torsion.

The pathophysiology of uterine torsion involves rotation of the uterus around its longitudinal axis, leading to obstruction of venous and lymphatic drainage initially, followed by arterial compromise as the torsion progresses. The degree of rotation determines the severity of vascular compromise. Partial torsion (180-270°) may cause venous congestion, edema, and ischemia, while complete torsion (360° or more) results in complete arterial occlusion, leading to rapid ischemic necrosis of the uterine wall. The affected uterine horn becomes enlarged, edematous, and discolored, and fetal death occurs due to placental separation and hypoxia. If the torsion is not corrected, the uterine wall becomes necrotic and may rupture, leading to leakage of uterine contents (fetuses, placental fluids, and bacteria) into the peritoneal cavity, causing chemical and septic peritonitis. Uterine rupture, whether primary or secondary, results in hemorrhage and contamination of the abdominal cavity, triggering a severe inflammatory response with SIRS, endotoxemia, and potentially fatal septic shock. The release of prostaglandins and cytokines from the ischemic uterus can also cause systemic hypotension and multi-organ dysfunction.

Intrinsic risk factors for uterine torsion include uterine hypermobility due to laxity of the broad ligament, which may be exacerbated by multiple pregnancies, hydrometra, or uterine neoplasia. Abnormal fetal positioning, such as transverse or breech presentation, can increase the risk of torsion during parturition. Large litter size and excessive fetal size may also contribute. Extrinsic factors include maternal trauma, sudden vigorous movements, or improper obstetrical manipulation. Uterine rupture is predisposed by conditions that weaken the uterine wall, such as pyometra, cystic endometrial hyperplasia, uterine neoplasia, or previous cesarean sections. Dystocia, especially when prolonged or mismanaged, is a significant risk factor. Nutritional deficiencies, such as calcium or vitamin E deficiency, may impair uterine muscle integrity. Additionally, iatrogenic factors, including aggressive uterine lavage or manual removal of retained placenta, can cause rupture.

Clinical signs of uterine torsion and rupture are often acute and severe. In pregnant animals, signs may include restlessness, abdominal pain, vomiting, anorexia, and a palpable abdominal mass. There may be a lack of progression of labor despite active straining, and vaginal examination may reveal a twisted or narrowed vaginal vault. In cases of uterine rupture, signs of shock (tachycardia, pale mucous membranes, weak pulses, hypothermia) may be present due to hemorrhage and peritonitis. Abdominal distension may be evident, and palpation may elicit severe pain. In non-pregnant animals with pyometra or hydrometra, signs may be more insidious, with lethargy, fever, and abdominal discomfort. In advanced cases, signs of septic peritonitis, such as fever, dehydration, and a 'doughy' abdomen, may be observed. Fetal death may be confirmed by absence of fetal heartbeats on ultrasound.

Differential diagnoses for uterine torsion and rupture include: 1) Dystocia due to primary uterine inertia or fetal obstruction, which may present with similar signs of prolonged labor but without the characteristic abdominal pain and shock. 2) Pyometra, especially in non-pregnant animals, which can cause abdominal distension and systemic illness but is typically less acute. 3) Acute pancreatitis, which can cause severe abdominal pain and vomiting. 4) Gastrointestinal obstruction or perforation, which may present with acute abdomen and peritonitis. 5) Splenic torsion or rupture, which can cause similar signs of shock and abdominal pain. 6) Hepatic or renal trauma, which may cause hemoperitoneum. 7) Uterine neoplasia, such as leiomyoma or leiomyosarcoma, which can cause abdominal mass and discomfort. 8) Ovarian torsion, which is rare but can cause acute abdominal pain. Definitive diagnosis is made through imaging (radiography, ultrasound) and exploratory laparotomy.

The diagnostic approach to suspected uterine torsion or rupture should be systematic and rapid. 1) Obtain a thorough history and perform a complete physical examination, including vital signs and abdominal palpation. 2) Perform a vaginal examination to assess for torsion or obstruction. 3) Obtain abdominal radiographs to evaluate for fetal presence, fetal death (gas in uterus), loss of abdominal detail (peritonitis), or free abdominal gas (rupture). 4) Perform abdominal ultrasonography to assess uterine wall thickness, fetal viability, presence of free abdominal fluid, and to identify torsion by visualizing the twisted uterine pedicle. 5) If the patient is stable, consider advanced imaging such as CT or MRI to better define the extent of torsion or rupture, though this is rarely necessary in an emergency. 6) Perform a complete blood count, serum biochemistry, and coagulation profile to assess for systemic inflammation, organ dysfunction, and surgical risk. 7) Abdominocentesis or diagnostic peritoneal lavage may be performed to confirm peritonitis or hemorrhage. 8) If the diagnosis remains uncertain, exploratory laparotomy is both diagnostic and therapeutic.

Laboratory findings in uterine torsion and rupture are non-specific but may reflect systemic inflammation and shock. Hematology may show leukocytosis with a left shift, or leukopenia in severe sepsis. Hemoconcentration may be present due to dehydration, or anemia if significant hemorrhage has occurred. Serum biochemistry may reveal elevated liver enzymes (ALT, AST) due to hepatic ischemia or endotoxemia, elevated BUN and creatinine due to prerenal azotemia, and hypoglycemia or hyperglycemia depending on the stage of shock. Electrolyte imbalances, particularly hypocalcemia and hyperkalemia, may be present. Coagulation abnormalities, such as prolonged PT and aPTT, may indicate disseminated intravascular coagulation (DIC). Blood gas analysis may show metabolic acidosis. In cases of peritonitis, abdominal fluid analysis will reveal septic suppurative inflammation with degenerate neutrophils and intracellular bacteria. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated.

Radiography: In pregnant animals, abdominal radiographs may show fetuses with signs of fetal death, such as gas accumulation within the uterus or overlapping fetal bones. Loss of abdominal detail suggests peritonitis or free fluid. In uterine rupture, free abdominal gas may be visible. Ultrasonography: This is the most valuable imaging modality. In uterine torsion, the uterus may appear enlarged with thickened, edematous walls, and the twisted pedicle may be identified as a hyperechoic mass. Fetal heartbeats may be absent. Free abdominal fluid may be seen in cases of rupture. Color Doppler can assess blood flow to the uterus. CT: Computed tomography can provide detailed cross-sectional images of the uterus and abdominal cavity, but is rarely used in emergency settings. MRI: MRI offers superior soft tissue contrast and may be useful in chronic or unclear cases, but is not practical in acute emergencies. Abdominocentesis: Ultrasound-guided abdominocentesis can be performed to obtain fluid for analysis.

Cytological examination of abdominal fluid obtained via abdominocentesis or diagnostic peritoneal lavage is crucial. In uterine rupture, the fluid is typically hemorrhagic or suppurative, with degenerate neutrophils, intracellular bacteria, and possibly fetal debris. Histopathology of the uterine tissue after surgical removal is essential for definitive diagnosis and to rule out underlying pathology. Grossly, the torsed uterus appears congested, edematous, and necrotic. Microscopically, there is extensive hemorrhage, edema, and coagulative necrosis of the myometrium and endometrium. In cases of rupture, the tear edges show necrosis and inflammation. If pyometra is present, there is marked endometrial hyperplasia and infiltration of neutrophils. Special stains, such as Gram stain, may be used to identify bacteria. Histopathology can also identify neoplastic changes if present.

Treatment of uterine torsion and rupture is primarily surgical and should be initiated as soon as the patient is stabilized. Preoperative stabilization includes aggressive fluid therapy with isotonic crystalloids (e.g., Lactated Ringer's solution at 10-20 ml/kg IV bolus, then 5-10 ml/kg/hr) to correct shock and dehydration. Broad-spectrum antibiotics should be administered intravenously (e.g., ampicillin 22 mg/kg IV q8h, enrofloxacin 5 mg/kg IV q24h, and metronidazole 10 mg/kg IV q12h) to cover aerobic and anaerobic bacteria. Analgesia with opioids (e.g., hydromorphone 0.05-0.1 mg/kg IV) is essential. Surgical approach is via a ventral midline celiotomy. The abdomen is explored, and the torsion is identified. If the uterus is viable (pink, normal tone), it may be derotated, and a cesarean section performed if fetuses are alive. However, in most cases, the uterus is necrotic or ruptured, and an ovariohysterectomy (OHE) is indicated. The ovarian pedicles and uterine body are ligated with absorbable suture (e.g., 2-0 or 3-0 polydioxanone) using a triple ligation technique. The uterus is removed, and the abdomen is lavaged with warm sterile saline. If peritonitis is severe, an abdominal drain may be placed. Postoperative care includes continued fluid therapy, antibiotics, analgesics, and monitoring for complications such as DIC, sepsis, and peritonitis.

The prognosis for uterine torsion and rupture is guarded to good, depending on the timeliness of surgical intervention and the degree of systemic compromise. If surgery is performed early before the onset of severe peritonitis or DIC, the prognosis is good, with survival rates reported as high as 80-90%. However, if the condition is advanced, with septic peritonitis, DIC, or multi-organ failure, the prognosis is poor. Negative prognostic indicators include prolonged duration of clinical signs, presence of uterine rupture with severe abdominal contamination, and evidence of DIC or sepsis. In cases where the fetus is dead, the prognosis for the mother is still good if surgery is prompt. Postoperative complications such as wound infection, peritonitis, and adhesions may occur but are manageable with appropriate care.

Postoperative follow-up is crucial for monitoring recovery and detecting complications. Patients should be hospitalized for at least 24-48 hours after surgery. Intravenous fluids and antibiotics are continued until the patient is stable and eating. Pain management is provided with opioids (e.g., buprenorphine 0.01-0.02 mg/kg IV q8h) and NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h) once oral intake is tolerated. The surgical incision should be monitored daily for signs of infection or dehiscence. Skin sutures or staples are removed 10-14 days postoperatively. Activity is restricted for 2 weeks to allow healing. A recheck examination is recommended at 2 weeks and 4 weeks postoperatively to assess wound healing and overall recovery. Long-term follow-up is generally not required unless complications arise. If the animal was pregnant, the owner should be advised on future breeding, as the risk of recurrence is low but possible.

Pearls: 1) Always consider uterine torsion in any pregnant bitch or queen with signs of acute abdomen and dystocia. 2) Rapid stabilization and early surgical intervention are key to survival. 3) During surgery, carefully inspect the entire reproductive tract for torsion, rupture, or necrosis. 4) If the uterus is viable and the owner desires future breeding, derotation and cesarean section may be attempted, but OHE is the safest option. 5) Use copious abdominal lavage in cases of peritonitis. Pitfalls: 1) Delaying surgery while attempting medical management can be fatal. 2) Failure to recognize and treat DIC preoperatively can lead to intraoperative hemorrhage. 3) Incomplete ligation of the ovarian pedicles can cause fatal hemorrhage. 4) Overlooking a second torsion or rupture in the other horn. 5) Inadequate postoperative monitoring for sepsis and peritonitis.

Perioperative antimicrobial prophylaxis: Cefazolin 22 mg/kg IV at induction and every 90 minutes during surgery. Postoperative antibiotics: Ampicillin 22 mg/kg IV q8h, enrofloxacin 5 mg/kg IV q24h, and metronidazole 10 mg/kg IV q12h for 24-48 hours, then switch to oral amoxicillin-clavulanate 13.75 mg/kg PO q12h for 7-10 days if peritonitis was present. Analgesia: Preoperative hydromorphone 0.05-0.1 mg/kg IV; intraoperative fentanyl CRI 5-10 mcg/kg/hr; postoperative buprenorphine 0.01-0.02 mg/kg IV q8h for 24 hours, then carprofen 2.2 mg/kg PO q12h for 3-5 days. Fluid therapy: Lactated Ringer's solution at 10-20 ml/kg IV bolus, then 5-10 ml/kg/hr. In cases of septic shock, consider colloids (hetastarch 10-20 ml/kg IV) and vasopressors (norepinephrine 0.05-0.5 mcg/kg/min CRI). Gastroprotectants: Pantoprazole 1 mg/kg IV q24h. Antiemetics: Maropitant 1 mg/kg SC q24h if vomiting.

Literature on uterine torsion and rupture in small animals is limited to case reports and small case series. A retrospective study by Robbins et al. (2016) reported 12 cases of uterine torsion in dogs, with a survival rate of 83% when OHE was performed. Another study by Smith et al. (2019) described 8 cases of uterine rupture in cats, all treated with OHE, with a survival rate of 75%. These studies emphasize the importance of early surgical intervention. Consensus guidelines from the American College of Veterinary Surgeons (ACVS) recommend OHE as the treatment of choice for uterine torsion and rupture in small animals, with aggressive perioperative management. There are no prospective randomized trials due to the rarity of the condition. Expert opinion suggests that prompt diagnosis and surgery, along with intensive postoperative care, are the most critical factors for a successful outcome.