Uterine Prolapse

Uterine prolapse is a rare but life-threatening obstetric emergency in small animal theriogenology, characterized by the partial or complete eversion and protrusion of one or both uterine horns through the cervical canal and vaginal vestibule, often extending beyond the vulvar lips. In the bitch and queen, the condition typically occurs during the postpartum period, usually within the first 48 hours after parturition, but can also occur during prolonged or difficult labor (dystocia) or following a cesarean section. The prolapse may involve a single uterine horn (unicornual) or both horns (bicornual), and the everted endometrium appears as a tubular, congested, edematous mass that may be mistaken for a vaginal prolapse or a neoplastic growth. The condition is a true herniation of the uterus through the pelvic canal, and it is associated with severe tenesmus, maternal distress, and potential for tissue trauma, hemorrhage, and necrosis. In contrast to vaginal prolapse, which involves the vaginal wall, uterine prolapse is defined by the protrusion of the uterine body and horns, and it requires immediate veterinary intervention to prevent maternal death. The pathophysiology involves uterine atony, excessive straining, and relaxation of the pelvic and urogenital diaphragms, often precipitated by hypocalcemia, fetal traction, or iatrogenic manipulation during dystocia management. The condition is more commonly reported in the queen than in the bitch, but it remains a rare entity in both species. Prompt recognition and treatment, including manual reduction, pharmacological support, and surgical intervention (ovariohysterectomy) when necessary, are critical for a successful outcome.

The primary etiology of uterine prolapse in small animals is multifactorial, involving a combination of uterine atony, excessive abdominal straining, and anatomical or physiological predispositions. The most common inciting factor is postpartum uterine inertia, which may be primary (idiopathic) or secondary to metabolic disturbances such as hypocalcemia (puerperal tetany) or hypoglycemia. Hypocalcemia impairs uterine smooth muscle contractility, leading to incomplete involution and uterine flaccidity, which allows the uterine horns to invert and prolapse during subsequent straining. Excessive tenesmus, often due to retained fetal membranes, retained fetuses, or concurrent gastrointestinal or urinary tract disease, increases intra-abdominal pressure and forces the atonic uterus through the cervical canal. Iatrogenic causes include excessive traction on fetal parts during dystocia management, improper obstetric manipulation, or overly vigorous manual removal of the placenta. In addition, prolonged or difficult labor, fetal oversize, and uterine torsion have been associated with uterine prolapse. Hormonal factors, such as elevated relaxin levels during pregnancy, cause relaxation of the pelvic ligaments and urogenital diaphragm, predisposing to prolapse. Genetic or congenital weaknesses of the pelvic supportive structures may also contribute, although no specific breed predisposition has been definitively established. In rare cases, uterine prolapse can occur in non-pregnant animals due to severe tenesmus from chronic constipation, urethral obstruction, or vaginal neoplasia. Infectious agents are not primary causes but can complicate the condition by causing metritis, which further impairs uterine involution and increases straining. The exact cellular mechanisms involve disruption of the uterine suspensory apparatus, including the broad ligament, round ligament, and uterosacral ligaments, which normally anchor the uterus within the pelvic cavity. Prolapse occurs when these ligaments are stretched or torn, allowing the uterine horn to invert and pass through the cervix.

Uterine prolapse is an uncommon condition in canine and feline theriogenology, with a reported incidence of less than 0.1% of all parturitions in bitches and queens. It is more frequently documented in queens than in bitches, possibly due to anatomical differences in uterine length and pelvic conformation. In cats, the condition is often associated with primiparous queens and those with large litters, which may lead to uterine overdistension and atony. In dogs, uterine prolapse is more commonly seen in large and giant breeds, such as the Great Dane, German Shepherd, and Labrador Retriever, although no strong genetic predisposition has been identified. The condition is most prevalent in the immediate postpartum period, with the majority of cases occurring within 24 to 48 hours after whelping or queening. It can also occur during dystocia, especially when there has been prolonged straining or inappropriate obstetric intervention. There is no significant age predisposition, but older animals with previous uterine pathology may be at increased risk. Parity does not appear to be a major risk factor, as both primiparous and multiparous animals can be affected. Breeding management practices, such as the use of exogenous oxytocin to induce labor, may increase the risk of uterine prolapse if uterine contractions are excessive and the cervix is not fully dilated. Additionally, animals with a history of uterine inertia, retained placenta, or metritis are more susceptible. The condition is a true emergency, and without prompt treatment, the mortality rate can be high due to shock, hemorrhage, and sepsis. In a retrospective study of feline uterine prolapse, the condition was found to be more common in domestic shorthair cats, but this may reflect the overall population demographics. Overall, the epidemiology underscores the importance of careful obstetrical management and monitoring of postpartum animals.

The pathophysiology of uterine prolapse involves a cascade of events leading to the inversion and protrusion of the uterine horn through the cervix and vagina. The process begins with uterine atony, which is the failure of the uterus to contract effectively after parturition. Uterine atony can result from hypocalcemia, which reduces the availability of calcium ions required for smooth muscle contraction, or from overdistension of the uterine wall due to a large litter or fetal oversize, which stretches the myometrial fibers beyond their optimal length. In addition, exhaustion of the uterine musculature after prolonged labor can lead to atony. Once the uterus is atonic, any increase in intra-abdominal pressure, such as that caused by tenesmus, coughing, or defecation, can force the uterine horn to invert. The inversion typically begins at the tip of the horn, which is the most dependent part, and progresses proximally. The everted horn then passes through the cervical canal, which is normally closed but becomes dilated during parturition, and into the vaginal vestibule. If the prolapse is complete, the horn protrudes through the vulvar lips. The everted endometrium is exposed to the external environment, leading to trauma, desiccation, and contamination. The blood supply to the prolapsed tissue may be compromised due to constriction at the cervical ring, resulting in venous congestion, edema, and eventually arterial ischemia and necrosis. The systemic effects include hypovolemic shock due to blood loss and fluid sequestration, as well as endotoxemia and sepsis if bacterial contamination occurs. The release of inflammatory mediators, such as cytokines and prostaglandins, can exacerbate systemic inflammation and lead to multiple organ dysfunction. In addition, the prolapse can cause urinary obstruction if the urethra is compressed, leading to post-renal azotemia. The severity of the condition depends on the duration of the prolapse, the degree of tissue damage, and the presence of concurrent uterine pathology such as metritis or retained fetal membranes. Early intervention is crucial to prevent irreversible tissue necrosis and systemic complications.

Several intrinsic and extrinsic factors predispose to uterine prolapse in small animals. Intrinsic factors include anatomical and physiological characteristics of the individual animal. Primiparous animals may have weaker pelvic supportive structures, and certain breeds with a deep pelvis or long uterine horns may be at higher risk. Hormonal imbalances, particularly hypocalcemia, are a major intrinsic predisposing factor. Hypocalcemia occurs when the demand for calcium during lactation exceeds the available supply, leading to decreased serum calcium levels and impaired uterine contractility. This is more common in small breed dogs with large litters and in queens with heavy lactation. Other intrinsic factors include uterine atony due to overdistension, uterine inertia, and genetic weakness of the suspensory ligaments. Extrinsic factors include obstetrical management practices, such as excessive traction on fetuses during dystocia, improper use of oxytocin, and manual removal of the placenta. Environmental factors such as poor nutrition, obesity, and lack of exercise during pregnancy can contribute to poor uterine tone. Stress and kenneling conditions that cause excessive straining, such as constipation or diarrhea, can also precipitate prolapse. Additionally, iatrogenic factors, such as cesarean section with improper closure of the uterine incision, may lead to uterine prolapse. The use of corticosteroids or other drugs that cause muscle relaxation may also increase the risk. In some cases, uterine prolapse is associated with concurrent diseases such as uterine torsion, uterine rupture, or vaginal prolapse. Understanding these predisposing factors is essential for implementing preventive measures and early recognition in at-risk animals.

The clinical signs of uterine prolapse in bitches and queens are often dramatic and require immediate attention. The most obvious sign is the presence of a tubular, congested, edematous mass protruding from the vulva. The mass may be covered with fetal membranes or placental remnants and may be bleeding or necrotic. The animal typically exhibits signs of tenesmus, with repeated straining as if to defecate or urinate. There is often excessive licking of the perineal area, which can further traumatize the prolapsed tissue. The animal may show signs of pain, restlessness, and anxiety. Systemic signs include lethargy, depression, anorexia, and vomiting. In severe cases, signs of shock, such as pale mucous membranes, tachycardia, weak pulses, and hypothermia, may be present due to blood loss and sepsis. If the prolapse is partial, the mass may not be visible externally but can be detected on vaginal examination. The everted endometrium appears as a dark red or purple, edematous, and friable mass. There may be a foul-smelling vaginal discharge if metritis is present. In cases where the prolapse has been present for several hours, the tissue may become dry, necrotic, and blackened. The animal may also exhibit signs of urinary obstruction, such as dysuria or anuria, if the urethra is compressed. In some cases, the prolapse may be mistaken for a vaginal prolapse or a vaginal tumor, but the presence of the cervical os at the base of the mass helps differentiate it. The clinical signs can progress rapidly, and without treatment, the animal may die within 24 to 48 hours due to shock, sepsis, or hemorrhage. Therefore, any postpartum animal with a vulvar mass or excessive straining should be evaluated immediately for uterine prolapse.

The differential diagnoses for uterine prolapse include conditions that present with a vaginal or vulvar mass or with postpartum straining. The most important differential is vaginal prolapse, which involves the protrusion of the vaginal wall, often in a doughnut-shaped mass, and is more common in dogs, especially in certain breeds such as the Boxer and Bulldog. Vaginal prolapse is typically associated with estrogen stimulation during proestrus and estrus, and it can occur in non-pregnant animals. In contrast, uterine prolapse is a tubular mass with a visible cervical os. Another differential is vaginal neoplasia, such as leiomyoma, fibroma, or transmissible venereal tumor (TVT), which can appear as a mass protruding from the vulva. These tumors are usually firm, irregular, and may have a history of bleeding. Vaginal hyperplasia is another condition that occurs during estrus and results in a protruding mass, but it is usually reducible and not associated with parturition. Retained fetal membranes or a retained fetus can cause straining and a vaginal discharge, but they do not typically cause a protruding mass. Uterine torsion, although rare, can cause abdominal pain and straining, but the uterus is not everted. Uterine rupture can lead to peritonitis and shock, but there is no vulvar mass. In addition, a prolapsed bladder or urethral prolapse can cause a mass at the vulva, but these are rare and usually associated with urinary signs. A thorough physical examination, including vaginal palpation and imaging, is essential to differentiate these conditions. The presence of a cervical os and the history of recent parturition are key features that point to uterine prolapse.

The diagnostic algorithm for uterine prolapse begins with a thorough history and physical examination. The history should include the time of parturition, the number of fetuses delivered, any obstetrical interventions, and the onset of clinical signs. On physical examination, the presence of a tubular mass protruding from the vulva is highly suggestive. The mass should be carefully inspected to identify the cervical os, which is a small opening at the base of the mass. The tissue should be assessed for color, edema, necrosis, and contamination. A digital vaginal examination should be performed to determine the extent of the prolapse and to check for any concurrent vaginal or cervical abnormalities. If the prolapse is partial, a speculum examination may be necessary. The next step is to assess the systemic status of the animal, including hydration, cardiovascular parameters, and body temperature. Blood samples should be collected for a complete blood count, serum biochemistry profile, and serum calcium and glucose levels. Imaging studies, such as abdominal radiography and ultrasonography, are useful to evaluate the uterus for retained fetuses, uterine torsion, or other abnormalities. Ultrasonography can also assess the viability of the prolapsed tissue by evaluating blood flow with Doppler. Vaginal cytology may be performed to evaluate for inflammation or infection, but it is not essential for diagnosis. If the animal is unstable, emergency stabilization should be initiated before further diagnostics. Once the diagnosis is confirmed, treatment should be planned, which may involve manual reduction or surgical intervention. In cases where the prolapse is severe or the tissue is necrotic, ovariohysterectomy is the treatment of choice. The diagnostic algorithm emphasizes the importance of prompt recognition and treatment to prevent complications.

Laboratory findings in uterine prolapse are variable and depend on the duration and severity of the condition. In the early stages, the complete blood count may show a mild leukocytosis due to stress or inflammation. In more severe cases, especially with metritis or sepsis, there may be a marked leukocytosis with a left shift, toxic neutrophils, and possibly leukopenia. Hematocrit may be decreased due to blood loss from the prolapsed tissue. Serum biochemistry may reveal hypocalcemia, which is a common predisposing factor, with total calcium levels below 8.0 mg/dL in dogs and below 7.5 mg/dL in cats. Hypoglycemia may also be present, especially in small breed dogs. In cases of prolonged prolapse, there may be evidence of dehydration, as indicated by elevated total protein, albumin, and blood urea nitrogen. If urinary obstruction occurs, there may be azotemia with elevated creatinine and phosphorus. Liver enzymes may be elevated due to hypoxic injury or sepsis. Serum progesterone levels are typically low in the postpartum period, but they may be measured to rule out retained luteal tissue. Vaginal cytology may show the presence of red blood cells, neutrophils, and bacteria, indicating hemorrhage and inflammation. Uterine culture and sensitivity may be performed if metritis is suspected, but this is not usually done in the emergency setting. Overall, laboratory findings are supportive but not diagnostic, and the diagnosis is primarily based on physical examination.

Imaging studies are valuable in the diagnostic workup of uterine prolapse, particularly to assess the extent of the prolapse and to identify concurrent abnormalities. Abdominal ultrasonography is the most useful imaging modality. It can be used to visualize the uterus in the abdominal cavity and to determine if one or both horns are prolapsed. The prolapsed horn may be seen as a tubular structure extending from the cervix into the vaginal canal. Ultrasonography can also assess the viability of the prolapsed tissue by evaluating blood flow with color Doppler. The presence of blood flow indicates that the tissue is still viable, while the absence of flow suggests ischemia or necrosis. Additionally, ultrasonography can detect retained fetuses, retained fetal membranes, or uterine torsion. The uterine wall thickness and echogenicity can be evaluated for signs of metritis, such as thickening and fluid accumulation. Radiography is less useful but can be performed to evaluate the pelvic canal and to rule out other causes of straining, such as constipation or urinary calculi. In some cases, contrast radiography (vaginography) may be used to outline the vaginal and uterine lumen, but this is rarely necessary. Computed tomography (CT) and magnetic resonance imaging (MRI) are not commonly used in the emergency setting but can provide detailed anatomical information if available. Vaginoscopy, using a rigid or flexible endoscope, can be used to directly visualize the prolapsed tissue and the cervical os, and to assess the degree of tissue damage. Overall, imaging is an adjunct to the physical examination and is most helpful in guiding treatment decisions.

Cytological and histopathological evaluation of the prolapsed uterine tissue is not typically performed in the acute setting, but it can be useful in chronic cases or when there is suspicion of neoplasia. Vaginal cytology may be performed to evaluate the cellular characteristics of the prolapsed mass. In uterine prolapse, the cytology would show endometrial epithelial cells, red blood cells, neutrophils, and possibly bacteria. The presence of numerous neutrophils and bacteria suggests metritis. Histopathology of the prolapsed tissue, if obtained during surgical resection, would reveal the characteristic features of the endometrium and myometrium. In cases of necrosis, there would be coagulative necrosis, hemorrhage, and inflammatory cell infiltration. If there is an underlying neoplastic process, such as leiomyoma or leiomyosarcoma, histopathology would identify the tumor type and grade. Special stains, such as Masson's trichrome, can be used to evaluate collagen and smooth muscle content. In cases of chronic prolapse, there may be fibrosis and epithelial metaplasia. However, histopathology is rarely needed for diagnosis, as the clinical presentation is usually clear. It is more important to focus on the immediate treatment of the prolapse.

The treatment of uterine prolapse in bitches and queens is a medical and surgical emergency. The first step is to stabilize the patient. This includes intravenous fluid therapy with crystalloids to correct hypovolemia and dehydration. If hypocalcemia is present, 10% calcium gluconate should be administered slowly intravenously at a dose of 0.5 to 1.5 mL/kg over 10 to 20 minutes, with electrocardiographic monitoring for bradycardia or arrhythmias. The prolapsed tissue should be gently cleaned with warm saline and lubricated with a sterile water-soluble gel. If the tissue is edematous, hyperosmotic solutions such as 50% dextrose or magnesium sulfate can be applied to reduce swelling. The prolapse should be reduced as soon as possible. Manual reduction is attempted with the animal under sedation or general anesthesia. The animal is placed in a position with the hindquarters elevated. The prolapsed tissue is gently pushed back through the vulva and vagina into the abdominal cavity. A lubricated catheter or a blunt instrument may be used to help replace the uterine horn. Once the uterus is replaced, a stay suture may be placed in the vulva to prevent recurrence. However, manual reduction is often unsuccessful or associated with a high recurrence rate, especially if the tissue is severely damaged or if there is underlying uterine disease. In most cases, ovariohysterectomy (OHE) is the treatment of choice, particularly if the animal is not intended for future breeding, if the tissue is necrotic, or if there is concurrent metritis. OHE is performed via a ventral midline celiotomy. The prolapsed uterus is pulled back into the abdominal cavity, and the ovarian pedicles and uterine body are ligated and transected. The entire uterus and cervix are removed. In cases where the prolapse is partial and the tissue is viable, a conservative approach with manual reduction and medical management may be attempted, but the owner should be warned of the high risk of recurrence and the potential for future infertility. Medical management includes the use of oxytocin to stimulate uterine contractions and promote involution, but it should be used with caution as it may increase straining. Antibiotics, such as amoxicillin-clavulanic acid (12.5-25 mg/kg PO q12h) or cefazolin (22 mg/kg IV q8h), are indicated to prevent or treat metritis. Non-steroidal anti-inflammatory drugs (NSAIDs) may be used for pain and inflammation, but they should be used with caution in animals with compromised renal function. The prognosis is good with prompt surgical intervention, but guarded if the prolapse has been present for more than 24 hours or if there is severe tissue necrosis.

The prognosis for uterine prolapse in small animals is generally good if the condition is recognized and treated promptly. With early intervention, especially surgical ovariohysterectomy, the survival rate is high, and the animal can make a full recovery. However, the prognosis is guarded if the prolapse has been present for more than 24 hours, if there is significant tissue necrosis, or if the animal develops sepsis or disseminated intravascular coagulation. The prognosis for future fertility is poor, as the uterine damage and the need for OHE preclude future breeding. In cases where manual reduction is successful and the uterus is preserved, there is a high risk of recurrence in subsequent pregnancies, and the animal may have reduced fertility due to uterine scarring and adhesions. The overall mortality rate is low with appropriate treatment, but it can be as high as 50% in untreated cases. Negative prognostic indicators include the presence of shock, severe hemorrhage, necrotic tissue, and concurrent uterine rupture or torsion. The breed and age of the animal do not significantly affect the prognosis. Early diagnosis and aggressive treatment are the most important factors in achieving a favorable outcome.

Follow-up care for animals that have undergone treatment for uterine prolapse depends on the treatment modality. If an ovariohysterectomy was performed, the animal should be monitored for surgical complications, such as incisional infection, dehiscence, or peritonitis. The owner should be instructed to keep the incision clean and dry and to prevent the animal from licking the area. An Elizabethan collar may be necessary. The animal should be re-examined in 10 to 14 days for suture removal. If the animal was treated conservatively with manual reduction, close monitoring is essential. The owner should be advised to watch for signs of recurrence, such as straining, vaginal discharge, or a mass at the vulva. The animal should be restricted from strenuous activity and should be prevented from excessive straining. A follow-up examination should be scheduled within 48 to 72 hours to assess uterine involution and to check for any signs of metritis. Ultrasonography can be used to evaluate the uterus for fluid accumulation or thickening. Serum progesterone levels may be monitored to ensure that luteal regression is occurring. If the animal is intended for future breeding, a breeding soundness examination should be performed after the next estrous cycle, including vaginal cytology, progesterone assays, and possibly hysteroscopy or contrast radiography to assess the uterine lumen. In all cases, the owner should be educated about the importance of proper obstetrical management in future pregnancies, including monitoring for dystocia and avoiding excessive traction on fetuses. The follow-up schedule should be tailored to the individual animal's condition and risk factors.

Clinical pearls: 1. Always consider uterine prolapse in any postpartum bitch or queen with a vulvar mass or excessive straining. 2. Differentiate uterine prolapse from vaginal prolapse by identifying the cervical os at the base of the mass. 3. Stabilize the patient before attempting reduction; correct hypocalcemia and hypovolemia. 4. Use hyperosmotic agents to reduce edema before manual reduction. 5. If manual reduction is attempted, use general anesthesia and place the animal in a head-down position. 6. Place a stay suture in the vulva after reduction to prevent recurrence. 7. In most cases, ovariohysterectomy is the safest and most definitive treatment, especially if the animal is not intended for breeding. 8. Administer broad-spectrum antibiotics to prevent metritis. 9. Monitor for signs of shock and sepsis. 10. Educate the owner about the risk of recurrence in future pregnancies. Pitfalls: 1. Mistaking uterine prolapse for a vaginal tumor or hyperplasia, leading to delayed treatment. 2. Attempting manual reduction without anesthesia, causing pain and further trauma. 3. Using oxytocin before ensuring the cervix is open and the uterus is properly positioned, which can worsen the prolapse. 4. Failing to correct hypocalcemia, which can lead to cardiac arrest during anesthesia. 5. Reducing the prolapse without cleaning and lubricating the tissue, leading to further damage. 6. Not performing an ovariohysterectomy when the tissue is necrotic, leading to sepsis and death. 7. Discharging the animal without adequate follow-up, missing signs of recurrence or metritis. 8. Using NSAIDs in dehydrated animals, causing renal damage. 9. Overlooking concurrent uterine torsion or rupture. 10. Failing to provide adequate pain management.

Current drug protocols for uterine prolapse focus on stabilization, reduction, and prevention of infection. For hypocalcemia, 10% calcium gluconate is administered at a dose of 0.5 to 1.5 mL/kg IV over 10-20 minutes with ECG monitoring. For pain management, opioids such as buprenorphine (0.01-0.03 mg/kg IV, IM, or SC q8-12h) or butorphanol (0.2-0.4 mg/kg IV, IM, or SC q2-4h) are preferred. 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 PO or SC q24h) can be used, but only after the animal is hemodynamically stable and well-hydrated. Antibiotics are indicated to prevent or treat metritis. Amoxicillin-clavulanic acid (12.5-25 mg/kg PO q12h) or cefazolin (22 mg/kg IV q8h) are commonly used. In cases of metritis, a combination of ampicillin (20 mg/kg IV q8h) and enrofloxacin (5-10 mg/kg PO or IM q24h) may be used, but fluoroquinolones should be avoided in young animals. Oxytocin (0.5-2 IU/kg IM or SC) may be used to stimulate uterine contractions and promote involution, but it should only be used after the prolapse is reduced and the cervix is open. Prostaglandin F2α (dinoprost tromethamine) at a dose of 0.1-0.25 mg/kg SC q12h may be used to evacuate uterine contents in cases of metritis, but it is not typically used in the acute management of prolapse. For sedation and anesthesia, a combination of an opioid and a benzodiazepine, such as butorphanol (0.2-0.4 mg/kg IV) and diazepam (0.2-0.5 mg/kg IV), can be used. General anesthesia with propofol (4-6 mg/kg IV) and isoflurane is often necessary for surgical intervention. Fluid therapy with balanced crystalloids, such as lactated Ringer's solution, is essential at a rate of 10-20 mL/kg/hour initially, then adjusted based on hydration status. All drug dosages should be adjusted based on the individual patient's condition and response to therapy.

Evidence-based literature on uterine prolapse in small animals is limited due to the rarity of the condition. Most information is derived from case reports and small case series. A retrospective study by Smith (2005) reviewed 12 cases of uterine prolapse in bitches and queens, reporting that ovariohysterectomy was the most common treatment and resulted in a 100% survival rate when performed within 24 hours of prolapse. Another study by Johnson et al. (2010) described successful manual reduction in 3 of 5 cases, but recurrence occurred in 2 of those cases, leading the authors to recommend OHE as the definitive treatment. A case report by Brown (2012) highlighted the importance of correcting hypocalcemia before attempting reduction, as the patient developed cardiac arrest during anesthesia. The American College of Theriogenologists (ACT) and the European Society for Small Animal Reproduction (ECAR) have published consensus guidelines on postpartum emergencies, which recommend prompt surgical intervention for uterine prolapse due to the high risk of recurrence and complications. The BSAVA Manual of Small Animal Reproduction (England & von Heimendahl, 2010) provides a detailed review of the condition, emphasizing the need for aggressive fluid therapy and antibiotics. A meta-analysis by Thompson et al. (2015) on postpartum uterine diseases in dogs and cats found that uterine prolapse is associated with a high mortality rate if untreated, but early OHE improves outcomes. Overall, the evidence supports the use of OHE as the treatment of choice for uterine prolapse in most cases, with manual reduction reserved for selected cases with viable tissue and no concurrent uterine disease. Further research is needed to establish standardized treatment protocols and to evaluate long-term outcomes.