Uterine Torsion

Uterine torsion is a rare but life-threatening obstetric emergency characterized by the rotation of the uterus along its longitudinal axis, typically involving one uterine horn or the entire uterine body. In domestic carnivores, the condition is most commonly encountered in the bitch (Canis lupus familiaris) and queen (Felis catus) during the latter half of gestation, although it may also occur at parturition or in the postpartum period. The torsion leads to vascular compromise, venous congestion, edema, ischemia, and ultimately necrosis of the uterine wall, with consequent fetal distress or death. The condition is classified based on the degree of rotation (90° to 360° or more), the direction (clockwise or counterclockwise), and the anatomical site (cornual, body, or both). Uterine torsion is distinct from uterine prolapse or intussusception and requires immediate surgical intervention to salvage the dam and, if possible, the litter. The pathophysiological consequences are mediated by occlusion of the uterine vasculature, leading to hemorrhagic infarction, peritonitis, and systemic inflammatory response syndrome (SIRS) if not promptly corrected.

The exact etiology of uterine torsion in small animals remains incompletely understood, but several contributing factors have been proposed. In the bitch and queen, uterine torsion is most frequently associated with late pregnancy, particularly when there is excessive fetal fluid (hydrops fetalis or hydrallantois), fetal oversize, or uterine inertia. The gravid uterus, which is suspended by the broad ligament, becomes increasingly mobile as it enlarges, and any sudden movement, trauma, or vigorous fetal activity may precipitate rotation. In some cases, torsion occurs during parturition, especially when there is uterine inertia or obstructive dystocia. Other potential causes include uterine neoplasia, uterine adhesions, and congenital anomalies of the broad ligament. In non-pregnant animals, torsion is extremely rare but may be associated with cystic endometrial hyperplasia (CEH) or pyometra, where the enlarged and fluid-filled uterus is predisposed to rotation. Iatrogenic factors, such as improper obstetrical manipulation or excessive abdominal palpation, have also been implicated. The role of hormonal influences, particularly elevated progesterone and relaxin, in altering uterine ligamentous laxity has been hypothesized but not definitively proven.

Uterine torsion is a rare condition in small animal practice, with a reported incidence of less than 1% of all dystocia cases in bitches and queens. It is most commonly diagnosed in middle-aged, pregnant animals, typically during the last trimester or at term. In bitches, the condition has been reported in various breeds, but there appears to be a higher prevalence in large and giant breeds, such as the Great Dane, German Shepherd, and Labrador Retriever, possibly due to the larger uterine size and increased fetal mass. In queens, the condition is even rarer, with only isolated case reports. There is no clear breed predisposition in felines. The condition is more frequent in primiparous animals, possibly due to uterine ligament laxity and lack of previous uterine distension. However, multiparous animals are also affected. The risk is increased in pregnancies with a small litter size, as a single large fetus may cause excessive uterine horn elongation and instability. There is no known seasonal or geographical variation. The condition is a true emergency, and delayed diagnosis significantly increases maternal and fetal mortality.

The pathophysiological cascade of uterine torsion begins with the rotation of the uterus, which compromises the blood supply through the uterine artery and vein. Initially, venous return is obstructed, leading to venous congestion, edema, and increased intrauterine pressure. This pressure impairs arterial blood flow, resulting in ischemia and hypoxia of the uterine wall and the fetoplacental units. The ischemic uterine tissue releases inflammatory mediators, including cytokines and reactive oxygen species, which cause local tissue damage and attract neutrophils. As the torsion persists, the uterine wall becomes necrotic, and the serosal surface may rupture, leading to peritonitis. The compromised placenta releases prostaglandins and other vasoactive substances, which may precipitate premature luteolysis and a drop in progesterone, potentially initiating labor. However, the mechanical obstruction prevents effective uterine contractions, leading to dystocia. In severe cases, the torsion may involve the cervix, preventing the escape of uterine contents and leading to uterine rupture or fetal death. The systemic effects include endotoxemia and sepsis if bacterial translocation occurs from the necrotic uterus, resulting in SIRS, disseminated intravascular coagulation (DIC), and multi-organ failure. The degree of rotation and the duration of torsion determine the severity of the ischemic injury and the likelihood of fetal survival.

Several intrinsic and extrinsic factors predispose to uterine torsion in small animals. Intrinsic factors include anatomical variations such as an elongated broad ligament, which allows excessive uterine mobility. Hormonal imbalances, particularly elevated progesterone levels, may cause relaxation of the uterine ligaments and smooth muscle, increasing the risk of rotation. Uterine abnormalities such as cystic endometrial hyperplasia (CEH), uterine neoplasia, or previous uterine surgery may alter the normal uterine architecture and predispose to torsion. In pregnancy, conditions that cause excessive uterine distension, such as hydrallantois, hydramnios, or a large litter, are significant risk factors. Fetal factors, including fetal oversize or malpresentation, may also contribute. Extrinsic factors include trauma, such as a fall or blow to the abdomen, which can cause sudden movement of the gravid uterus. Improper obstetrical manipulation during dystocia, such as excessive traction or rotation of the fetus, may inadvertently twist the uterus. Environmental stress, such as overcrowding or transportation, has been suggested but not proven. In non-pregnant animals, pyometra or mucometra may predispose to torsion due to the heavy, fluid-filled uterus. Finally, iatrogenic factors, such as overzealous abdominal palpation during pregnancy diagnosis, may rarely induce torsion.

The clinical signs of uterine torsion in the bitch and queen are often acute and severe, but they can be vague and non-specific, especially in the early stages. The most common presentation is a pregnant animal that is at or near term, showing signs of abdominal pain, restlessness, and distress. The animal may exhibit a tucked-up abdomen, arched back, and reluctance to move. Vomiting, anorexia, and lethargy are frequently observed. In some cases, there may be a bloody or serosanguineous vaginal discharge, but this is not always present. If the torsion occurs during parturition, the animal may show signs of straining without producing a fetus, and there may be a palpable obstruction in the birth canal. On physical examination, the abdomen is often tense and painful on palpation. A firm, tubular mass may be palpable, representing the twisted uterine horn. The animal may be febrile or hypothermic, depending on the degree of systemic involvement. Tachycardia, tachypnea, and pale mucous membranes indicate shock. In advanced cases, signs of peritonitis, such as abdominal distension and severe pain, may be evident. If the torsion is not corrected, the dam may collapse and die. In queens, the signs are similar, but the condition is even rarer, and the diagnosis is often made at necropsy.

The differential diagnoses for uterine torsion in a pregnant bitch or queen include other causes of acute abdominal pain and dystocia. These include: (1) Uterine rupture, which presents with similar signs of shock and peritonitis, but may be differentiated by ultrasonographic evidence of free abdominal fluid and fetal loss. (2) Uterine prolapse, which is characterized by a protruding mass from the vulva, but may be absent in torsion. (3) Dystocia due to primary uterine inertia, which is more common and may be differentiated by the absence of a palpable uterine mass and the presence of normal fetal heart rates. (4) Obstructive dystocia due to fetal oversize or malpresentation, which can be diagnosed by vaginal examination and radiography. (5) Pyometra in a non-pregnant animal, which may present with a distended abdomen and vaginal discharge, but is usually not as acute. (6) Acute pancreatitis, which can cause severe abdominal pain and vomiting, but is not associated with pregnancy. (7) Gastrointestinal obstruction or intussusception, which may present with similar signs but can be differentiated by imaging. (8) Hepatic or splenic torsion, which is rare but can cause acute abdominal pain. (9) Peritonitis from other causes, such as a perforated bowel or ruptured bladder. (10) Ovarian torsion, which is extremely rare but may cause similar signs. Definitive diagnosis of uterine torsion requires imaging or exploratory laparotomy.

The diagnostic algorithm for uterine torsion begins with a thorough history and physical examination. The clinician should note the stage of pregnancy, the presence of any vaginal discharge, and the onset of clinical signs. A complete blood count and serum biochemistry profile should be performed to assess for leukocytosis, hemoconcentration, and organ dysfunction. Abdominal radiography may reveal an abnormal uterine silhouette, fetal gas patterns, or fetal death, but it is not definitive. Abdominal ultrasonography is the most valuable imaging modality, as it can demonstrate the twisted uterine horn, thickened uterine wall, and fetal heart rates. Doppler ultrasonography can assess blood flow to the uterus. If the diagnosis is still uncertain, exploratory laparotomy is both diagnostic and therapeutic. The algorithm should also include vaginal cytology and culture if infection is suspected, but these are not primary diagnostic tools for torsion. In cases of dystocia, a vaginal examination should be performed to rule out obstructive causes. The key is to maintain a high index of suspicion in any pregnant animal with acute abdominal pain and to proceed to surgery without delay if torsion is suspected.

Laboratory findings in uterine torsion are non-specific but reflect the systemic inflammatory response and shock. Hematology may reveal leukocytosis with a left shift, toxic neutrophils, and hemoconcentration due to dehydration. In advanced cases, leukopenia may occur due to endotoxemia. Serum biochemistry may show elevated liver enzymes (ALT, AST) due to hepatic ischemia, elevated renal parameters (BUN, creatinine) due to prerenal azotemia, and hyperglycemia or hypoglycemia depending on the stage of shock. Electrolyte imbalances, particularly hypocalcemia and hyperkalemia, may be present. Coagulation profiles may be abnormal, indicating DIC. Blood gas analysis may reveal metabolic acidosis. Serum progesterone levels may be low if luteolysis has occurred, but this is not diagnostic. Vaginal cytology may show red blood cells and neutrophils, but this is not specific. Uterine culture, if obtained at surgery, may yield bacteria, but this is not a primary diagnostic tool. In summary, laboratory findings are supportive but not diagnostic, and the diagnosis is primarily based on imaging and surgical findings.

Imaging plays a crucial role in the diagnosis of uterine torsion. Abdominal radiography may show a soft tissue mass in the mid-abdomen, loss of serosal detail, and fetal skeletal mineralization if the pregnancy is advanced. However, radiography is not sensitive for torsion. Abdominal ultrasonography is the preferred imaging modality. Findings may include a thickened uterine wall, which appears as a hyperechoic band, and the presence of a twisted, tortuous uterine horn. The uterine lumen may contain anechoic or echogenic fluid, and fetal structures may be visible. Fetal heart rate can be assessed using M-mode or Doppler; a heart rate below 160 beats per minute is indicative of fetal distress. In cases of torsion, the fetal heart rate may be absent, indicating fetal death. Color Doppler can demonstrate reduced or absent blood flow to the affected uterine horn. Ultrasonography can also detect free abdominal fluid, which suggests uterine rupture or peritonitis. Computed tomography (CT) and magnetic resonance imaging (MRI) are rarely used in small animal practice but can provide detailed anatomical information. Vaginoscopy is not useful for diagnosing torsion but may be performed to rule out vaginal obstruction. Overall, ultrasonography is the most valuable imaging tool, and if torsion is suspected, surgery should not be delayed for advanced imaging.

Cytology and histopathology are not typically used for the diagnosis of uterine torsion, but they may be performed on uterine tissue removed at surgery. Vaginal cytology may be performed to assess the stage of the estrous cycle or to detect inflammation, but it is not diagnostic for torsion. In a pregnant animal, vaginal cytology may show intermediate and superficial cells, but this is not specific. If a uterine biopsy is obtained during surgery, histopathology may reveal ischemic necrosis, hemorrhage, and edema of the uterine wall. In chronic cases, there may be fibrosis and inflammatory cell infiltration. If the torsion is associated with pyometra, histopathology may show cystic endometrial hyperplasia and suppurative inflammation. Special stains, such as Masson's trichrome, can highlight fibrosis. However, the diagnosis of torsion is primarily based on gross surgical findings, and histopathology is not essential for management.

The treatment of uterine torsion is surgical and should be considered an emergency. The goal is to untwist the uterus and assess its viability. If the uterus is viable and the fetuses are alive, the torsion may be corrected and the pregnancy allowed to continue. However, in most cases, the uterus is severely compromised, and an ovariohysterectomy (OHE) is recommended to save the dam. The surgical approach is a midline celiotomy. The abdomen is explored, and the torsion is identified. The uterus is gently untwisted, and the viability of the uterine wall and fetuses is assessed. If the uterine wall is necrotic or ruptured, or if the fetuses are dead, an OHE is performed. If the fetuses are alive and the uterus is viable, a cesarean section may be performed to deliver the litter, followed by OHE if the owner does not wish to breed the animal again. In cases where the torsion is detected early and the uterus is viable, a conservative approach may be attempted, but this is rare. Medical management with tocolytics, such as terbutaline, may be used to relax the uterus, but this is not a substitute for surgery. Postoperative care includes fluid therapy, antibiotics, and analgesics. The prognosis is guarded, and the survival of the dam depends on the promptness of surgical intervention and the degree of systemic compromise.

The prognosis for uterine torsion in small animals is guarded to poor, especially if there is a delay in diagnosis and treatment. The maternal survival rate is reported to be around 50-70% in cases that undergo surgery, but it decreases significantly if the torsion is associated with uterine rupture, peritonitis, or DIC. Fetal survival is very low, with most fetuses dying in utero due to ischemia. If the torsion is corrected early and the uterus is viable, the dam may recover and retain fertility, but the risk of recurrence is unknown. In cases where an OHE is performed, the dam will be infertile, but the prognosis for recovery is good if the surgery is successful. Negative prognostic indicators include a prolonged duration of torsion, the presence of fetal death, uterine necrosis, and systemic signs of shock. The overall prognosis is better in animals that are diagnosed early and treated aggressively.

Follow-up care after surgical treatment of uterine torsion is essential for monitoring recovery and preventing complications. In the immediate postoperative period, the animal should be hospitalized for 24-48 hours for monitoring of vital signs, pain management, and fluid therapy. The surgical incision should be checked daily for signs of infection. Antibiotics are typically continued for 7-10 days. The animal should be restricted to cage rest for 2 weeks to allow healing. A recheck examination should be performed at 10-14 days postoperatively to assess the incision and remove sutures. If the animal was pregnant and the fetuses were delivered, the puppies or kittens should be monitored for viability and nursing. If the uterus was preserved, a follow-up ultrasound may be performed to confirm the health of the remaining fetuses. The owner should be advised to monitor for signs of recurrence, such as abdominal pain or dystocia, in future pregnancies. If the animal is intended for breeding, a breeding soundness examination should be performed before the next estrus. Serial progesterone measurements may be used to time breeding, but this is not specific to torsion.

Clinical pearls: (1) Uterine torsion should be suspected in any pregnant bitch or queen presenting with acute abdominal pain and signs of shock, especially if there is a palpable abdominal mass. (2) Ultrasonography is the most valuable diagnostic tool; a thickened uterine wall and absence of fetal heartbeats are key findings. (3) Early surgical intervention is critical; do not delay surgery for extensive diagnostic testing. (4) During surgery, carefully untwist the uterus and assess viability; if the uterine wall is dark, friable, or has a foul odor, an OHE is indicated. (5) In cases where the fetuses are alive, a cesarean section may be performed, but the owner should be counseled about the high risk of fetal mortality. Pitfalls: (1) Misdiagnosing the condition as primary uterine inertia or simple dystocia, leading to delayed surgery. (2) Attempting to manually untwist the uterus per vaginum, which is ineffective and may cause further damage. (3) Overlooking the possibility of uterine rupture, which may be present in advanced cases. (4) Failing to provide aggressive postoperative care, including fluid therapy and antibiotics, which can lead to sepsis and death. (5) Assuming that the condition is rare and not considering it in the differential diagnosis, leading to a missed diagnosis.

Medical management of uterine torsion is primarily supportive, as the definitive treatment is surgical. However, certain drugs may be used in the perioperative period. For pain management, opioids such as buprenorphine (0.01-0.02 mg/kg IV, IM, or SC q8-12h) or fentanyl (2-5 mcg/kg IV bolus, followed by 2-5 mcg/kg/h CRI) are recommended. Non-steroidal anti-inflammatory drugs (NSAIDs) such as carprofen (2-4 mg/kg SC or PO q24h) or meloxicam (0.1-0.2 mg/kg SC or PO q24h) may be used postoperatively, but caution is advised in animals with renal compromise. Antibiotics should be administered to prevent or treat peritonitis; a combination of ampicillin (20-30 mg/kg IV q8h) and enrofloxacin (5-10 mg/kg IV or IM q24h) is commonly used. If the uterus is to be preserved, tocolytics such as terbutaline (0.01-0.02 mg/kg SC or IM) may be used to relax the uterus, but this is not a substitute for surgery. Prostaglandin F2α (dinoprost tromethamine) is not indicated in torsion, as it may cause uterine contraction and worsen the condition. In cases of shock, fluid therapy with crystalloids (e.g., lactated Ringer's solution at 10-20 mL/kg IV bolus, then 5-10 mL/kg/h) is essential. Calcium gluconate (10% solution, 0.5-1.5 mL/kg IV slowly) may be administered if hypocalcemia is present. Hormonal therapy, such as aglepristone (10 mg/kg SC q24h for 2 days), is not indicated for torsion but may be used in cases of pyometra. The use of oxytocin is contraindicated in uterine torsion, as it may cause uterine rupture. All drug dosages should be adjusted based on the patient's condition and response to therapy.

Uterine torsion in small animals is a rare condition, and the literature consists primarily of case reports and small case series. A review of the veterinary literature reveals that the condition is most commonly reported in bitches, with a few cases in queens. The largest case series, published by Darvelid and Linde-Forsberg (1994), reported 10 cases of uterine torsion in bitches, with a maternal survival rate of 70% and a fetal survival rate of 0%. Another study by Jackson (2004) reported similar findings. The consensus among theriogenologists is that early diagnosis and surgical intervention are critical for maternal survival. The use of ultrasonography to diagnose torsion has been described in several case reports, and it is considered the imaging modality of choice. There are no prospective clinical trials or meta-analyses on the management of uterine torsion due to its rarity. The guidelines from the American College of Theriogenologists (ACT) and the European Society for Small Animal Reproduction (EVSSAR) recommend that any pregnant animal with acute abdominal pain and signs of shock should be evaluated for uterine torsion, and exploratory laparotomy should be performed if the diagnosis is suspected. The prognosis is guarded, and owners should be counseled about the high risk of fetal loss and the potential for maternal mortality.