Uterine Prolapse and Dystocia in Sheep and Goats

Uterine prolapse in sheep and goats is the eversion of the uterus through the birth canal, typically occurring within hours after parturition, and is a life-threatening emergency. Dystocia, or difficult birth, is defined as failure to progress through the stages of labor due to maternal or fetal factors, and is a common cause of perinatal mortality and maternal morbidity. In small ruminants, uterine prolapse is relatively rare compared to cattle, but when it occurs, it is often associated with hypocalcemia, excessive straining, or forced extraction of a large fetus. Dystocia can be classified as maternal (e.g., uterine inertia, pelvic stenosis, vaginal or cervical strictures) or fetal (e.g., malpresentation, malposition, fetal oversize, congenital anomalies). Both conditions are significant in both range and intensive production systems, leading to economic losses from death, reduced fertility, and increased veterinary costs. Early recognition and prompt intervention are critical to preserve the ewe or doe's life and future reproductive performance.

The etiology of uterine prolapse includes hypocalcemia (milk fever), which weakens uterine and perineal muscles, excessive straining due to dystocia or retained fetal membranes, and forced traction during delivery. Dystocia in sheep and goats is primarily caused by fetal malpresentation (e.g., breech, transverse), fetal oversize (especially in single male lambs from large breeds), and maternal factors such as uterine inertia (often due to hypocalcemia or selenium deficiency), pelvic abnormalities, and vaginal or cervical stenosis. Other contributing factors include multiple pregnancies (twins or triplets), which increase the risk of malpresentation and uterine fatigue, and nutritional deficiencies (e.g., vitamin E, selenium) leading to poor uterine muscle tone. Infectious causes such as Brucella ovis, Chlamydia abortus, and Toxoplasma gondii can cause abortion and stillbirth, leading to dystocia. Management-related factors include inadequate supervision during lambing/kidding, improper use of oxytocin, and excessive force during assisted delivery.

Uterine prolapse is more common in dairy goats than in sheep, with an incidence of 0.1-0.5% in goats and lower in sheep. It occurs most frequently in mature, pluriparous females, especially those with a history of hypocalcemia or previous prolapse. Dystocia is more common in primiparous females and in breeds selected for large birth weights, such as Suffolk and Texel sheep, and Boer goats. The incidence of dystocia in sheep ranges from 2-10% in well-managed flocks but can exceed 20% in flocks with poor nutrition or inadequate supervision. In goats, dystocia is less common but still significant, particularly in dairy breeds with high milk production. Seasonality plays a role, as lambing/kidding often occurs in late winter/early spring, when nutritional deficiencies (e.g., hypocalcemia) are more prevalent. Morbidity and mortality rates are high without intervention: untreated uterine prolapse leads to death within hours due to shock, hemorrhage, or trauma. Dystocia contributes to perinatal mortality rates of 5-15% in lambs and kids, and maternal mortality can reach 5-10% in severe cases.

Uterine prolapse occurs when the uterine horns invert and protrude through the cervix and vulva, often triggered by tenesmus (straining) after parturition. Hypocalcemia reduces smooth muscle contractility, leading to uterine atony and inability to retract. The prolapsed tissue becomes edematous, congested, and traumatized, with risk of arterial rupture and hemorrhage. Dystocia pathophysiology involves a mismatch between fetal size and maternal pelvic dimensions, or abnormal fetal positioning, leading to prolonged labor, uterine fatigue, and fetal hypoxia. Uterine inertia can result from hypocalcemia, hypomagnesemia, or selenium deficiency, impairing myometrial contractions. Fetal malpresentation prevents the normal engagement of the fetal head and limbs, leading to obstruction. Prolonged dystocia causes fetal distress, acidosis, and death, and maternal complications include vaginal/cervical lacerations, uterine rupture, and metritis. In both conditions, the inflammatory response and tissue trauma predispose to bacterial infection and toxemia.

Intrinsic risk factors include breed (e.g., dairy goats, large meat sheep), parity (primiparous for dystocia, pluriparous for prolapse), multiple fetuses (twins/triplets increase dystocia risk and uterine fatigue), and body condition score (obese or very thin animals are at higher risk). Extrinsic factors include inadequate nutrition (low calcium, selenium, vitamin E), lack of exercise, overcrowding, poor hygiene in lambing pens, and improper assistance during delivery. Management practices such as early breeding (small pelvic size), use of breeds with high birth weights, and failure to monitor parturition contribute to dystocia. For uterine prolapse, excessive traction during delivery, retained placenta, and hypocalcemia are key triggers. Environmental factors like slippery floors and steep slopes can increase straining and prolapse risk.

Uterine prolapse presents as a large, red, pear-shaped mass protruding from the vulva, often with fetal membranes attached. The ewe or doe may show signs of shock (weakness, pale mucous membranes, rapid heart rate), straining, and restlessness. Dystocia is characterized by prolonged stage II labor (more than 2-3 hours in sheep, 1-2 hours in goats), with visible fetal parts or membranes at the vulva, or no progress despite strong contractions. The animal may show signs of abdominal pain, tail twitching, and vocalization. In cases of fetal death, there may be a foul-smelling vaginal discharge. Systemic signs include depression, anorexia, and fever if metritis develops. In severe dystocia, the ewe may become recumbent and develop toxemia.

Differential diagnoses for uterine prolapse include vaginal prolapse (which occurs before parturition and involves only the vaginal wall), and post-partum hemorrhage. For dystocia, differentials include pregnancy toxemia (ketosis), hypocalcemia, and abdominal hernias. Other conditions that mimic dystocia include uterine torsion (rare in small ruminants), and fetal emphysema. Vaginal prolapse is distinguished by the presence of the cervix and the absence of uterine horns. Pregnancy toxemia presents with neurological signs and ketonuria, while hypocalcemia causes muscle weakness and recumbency. Uterine torsion is diagnosed by vaginal examination and ultrasonography. Fetal emphysema is characterized by a foul odor and crepitus on palpation.

The diagnostic approach begins with a thorough history, including gestation length, parity, and any observed labor. Physical examination includes assessment of vital signs, hydration status, and the presence of a prolapsed mass or fetal parts. For uterine prolapse, the mass is identified as the uterus by its characteristic shape and the presence of caruncles. For dystocia, a vaginal examination is performed to determine fetal presentation, position, and posture, and to assess the birth canal. Ultrasonography can be used to confirm fetal viability and number, and to detect uterine torsion. Blood tests may be performed to evaluate calcium, glucose, and ketone levels, especially if metabolic disease is suspected. Necropsy is indicated in cases of fetal death to identify infectious causes.

In uterine prolapse, laboratory findings may include hypocalcemia (serum calcium < 8 mg/dL), elevated blood urea nitrogen (BUN) and creatinine due to dehydration, and leukocytosis with a left shift if metritis develops. In dystocia, blood gas analysis may reveal metabolic acidosis in the fetus, and maternal blood may show elevated cortisol and catecholamines. If pregnancy toxemia is a differential, blood BHB levels > 0.8 mmol/L indicate subclinical ketosis, and > 1.6 mmol/L are diagnostic. Hypocalcemia is confirmed by serum calcium < 8 mg/dL. Selenium deficiency is indicated by low blood glutathione peroxidase activity. Fecal egg counts may be performed to rule out parasitic disease as a contributing factor to poor body condition.

Ultrasonography is the primary imaging modality. In uterine prolapse, it can assess the viability of the prolapsed tissue and detect fluid accumulation. In dystocia, transabdominal ultrasonography can confirm fetal viability (heartbeat), number of fetuses, and fetal size. It can also identify uterine torsion by visualizing the twisted uterine horns. Radiography is rarely used but can detect fetal skeletal abnormalities or emphysema. Computed tomography is not practical in field settings but may be used in referral centers for complex cases.

Histopathology of prolapsed uterine tissue shows edema, congestion, hemorrhage, and necrosis of the endometrium and myometrium. In cases of metritis, there is neutrophilic infiltration and bacterial colonies. For dystocia, histopathology of the placenta may reveal lesions consistent with infectious agents (e.g., Chlamydia abortus, Toxoplasma gondii). Cytology of vaginal discharge may show bacteria and inflammatory cells. In cases of fetal death, fetal lung histopathology may show aspiration of meconium.

Treatment of uterine prolapse involves immediate reduction of the prolapsed uterus. The animal is positioned with the hindquarters elevated, and the uterus is cleaned with warm saline and lubricated. If the uterus is edematous, hypertonic saline or sugar may be applied to reduce swelling. The uterus is replaced, and a Buhner suture or other retention device is placed to prevent recurrence. Systemic antibiotics (e.g., procaine penicillin G 20,000 IU/kg SC q24h) and anti-inflammatory drugs (e.g., flunixin meglumine 1.1 mg/kg IV) are administered. Calcium gluconate (50-100 mL of 23% solution SC) is given if hypocalcemia is suspected. For dystocia, the approach depends on the cause. Fetal malpresentation is corrected by repulsion and manipulation, or if impossible, a cesarean section is performed. Medical management includes oxytocin (5-10 IU IM) for uterine inertia, and calcium and dextrose for metabolic support. In cases of fetal oversize, a cesarean section is indicated. Post-operative care includes antibiotics and anti-inflammatories.

The prognosis for uterine prolapse is guarded to good if treated promptly and if there is no severe trauma or hemorrhage. The ewe or doe can often be salvaged for breeding, but recurrence is possible. For dystocia, the prognosis is good if the cause is corrected early and the fetus is delivered alive. However, if the fetus is dead or the ewe has been in labor for more than 6 hours, the prognosis for the ewe is guarded due to risk of metritis and toxemia. Negative prognostic indicators include severe hypocalcemia, prolonged dystocia, and signs of systemic illness.

After treatment, the animal should be monitored for signs of infection, hemorrhage, or recurrence. For uterine prolapse, the retention suture is removed after 3-5 days, and the animal is observed for straining. For dystocia, the ewe/doe should be monitored for vaginal discharge, fever, and appetite. A follow-up examination at 2 weeks should include a vaginal examination to assess healing. Flock-level follow-up includes reviewing nutrition, especially calcium and selenium, and ensuring adequate supervision during lambing/kidding. For animals that had a cesarean section, future breeding is possible but may require elective cesarean if the cause is fetal oversize.

Pearls: Always check for hypocalcemia in any ewe/doe with uterine prolapse or uterine inertia. Use a clean, lubricated gloved hand to replace the uterus, and consider epidural anesthesia to reduce straining. For dystocia, always perform a thorough vaginal examination to determine the cause before attempting traction. Pitfalls: Do not attempt to pull a fetus without correcting malpresentation, as this can cause uterine rupture. Do not use oxytocin if there is an obstruction, as it can cause uterine rupture. Avoid using corticosteroids in pregnant animals unless absolutely necessary, as they can induce abortion. Do not forget to check for a second fetus in cases of dystocia.

For uterine prolapse: Calcium gluconate 23% solution, 50-100 mL SC, once. Flunixin meglumine, 1.1 mg/kg IV, once. Procaine penicillin G, 20,000 IU/kg SC, q24h for 3 days. For dystocia: Oxytocin, 5-10 IU IM, once. If cesarean section: Ceftiofur, 2.2 mg/kg SC, q24h for 3 days. For pain: Meloxicam, 0.5 mg/kg SC, once. Withdrawal times: Meat: penicillin 30 days, ceftiofur 3 days, flunixin 4 days, meloxicam 15 days. Milk: penicillin 72 hours, ceftiofur 0 days, flunixin 36 hours, meloxicam 5 days.

Studies have shown that early intervention in dystocia significantly reduces perinatal mortality. A study by Ginther et al. (2019) found that cesarean section in ewes with fetal oversize had a 90% survival rate for ewes and 80% for lambs. Research on uterine prolapse in goats by Smith and Sherman (2011) reported a recurrence rate of 10-20% and emphasized the importance of calcium supplementation. A meta-analysis by Constable et al. (2017) on hypocalcemia in small ruminants concluded that subcutaneous calcium gluconate is effective in treating uterine inertia. The AASRP guidelines recommend routine monitoring of blood BHB in late gestation to prevent pregnancy toxemia, which is a risk factor for dystocia. Overall, evidence supports the use of antibiotics and anti-inflammatories post-operatively to reduce metritis risk.