Equine Retained Placenta and Placentitis – NAVLE Study Guide
Overview and Clinical Importance
Retained fetal membranes (RFM) and placentitis represent two of the most clinically significant reproductive conditions in equine practice. Retained placenta occurs when the fetal membranes fail to be expelled within 3 hours postpartum, and is considered a veterinary emergency due to the potential for life-threatening complications including metritis, laminitis, septicemia, and death. Placentitis, inflammation of the placenta typically due to ascending bacterial infection, is responsible for up to 30% of late-term pregnancy losses in mares. Understanding the pathophysiology, diagnosis, and treatment of these conditions is essential for NAVLE success and clinical practice.
Normal Equine Placental Anatomy
The equine placenta is classified as diffuse, microcotyledonary, and epitheliochorial. This means the entire surface of the chorioallantois attaches to the endometrium through millions of microscopic finger-like projections called microcotyledons, and six tissue layers separate maternal and fetal circulations. This placental arrangement has critical clinical implications.
Key Anatomical Features and Clinical Significance
Placental Examination: The F-Shape Method
Every placenta should be examined immediately after expulsion. Lay the membranes out in an "F" shape with the chorionic (red, velvety) surface exposed. The bottom leg represents the cervical end with the cervical star rupture site. The vertical portion corresponds to the uterine body. The upper arm (longer, thicker) represents the gravid horn, and the lower arm (thinner, wrinkled) represents the nongravid horn. Normal placental weight should be approximately 11% of foal body weight.
Retained Fetal Membranes (RFM)
Definition and Incidence
Retained fetal membranes are defined as failure to expel the chorioallantois within 3 hours postpartum. Normal expulsion typically occurs within 30 minutes to 1 hour, with 95% of mares expelling membranes within 4 hours. The overall incidence ranges from 2-10% in light horse breeds, but is significantly higher in Friesian and heavy draft breeds where incidence may reach up to 50%.
Pathophysiology
The exact cause of RFM is not fully understood, but involves failure of the microcotyledonary attachments to release from endometrial crypts. Normally, postpartum uterine contractions stimulated by oxytocin facilitate separation of the microvilli. Proposed contributing factors include uterine inertia from hormonal imbalances (particularly low oxytocin), calcium and phosphorus imbalances, dysregulation of extracellular matrix remodeling, and placental edema or inflammation.
Risk Factors
Clinical Signs and Diagnosis
Diagnosis of complete retention is straightforward when membranes are visible protruding from the vulva. However, partial retention may not be obvious and is equally dangerous. Clinical signs develop as bacterial growth and toxin absorption progress.
Early Signs (less than 12 hours)
- Visible membranes hanging from vulva (may be absent with partial retention)
- Mare may appear normal initially
- Mild discomfort or straining
Progressive Signs (12-24 hours)
- Fever (greater than 38.5C / 101.5F)
- Depression and anorexia
- Fetid vulvar discharge
- Congested or muddy mucous membranes
- Signs of endotoxemia
Severe Complications
- Laminitis: May develop as early as 8 hours; secondary to endotoxemia affecting laminar blood flow
- Toxic metritis: Gram-negative bacterial overgrowth with massive endotoxin release
- Septicemia: Systemic bacterial infection from uterine absorption
- Death: Without treatment, mortality significantly increases after 12-24 hours
Treatment of Retained Fetal Membranes
Treatment goals are threefold: (1) facilitate placental expulsion, (2) prevent systemic complications including endotoxemia and laminitis, and (3) preserve future fertility.
Manual Removal: Controversy and Risks
Manual removal of retained placenta is controversial and generally NOT recommended unless the membranes are almost completely detached. Complications include uterine hemorrhage, endometrial damage, uterine horn invagination/intussusception, uterine prolapse, pulmonary emboli, placental tearing leaving retained tags, and delayed uterine involution. If attempted, use gentle twisting motion while applying minimal traction - never pull forcefully downward.
Placentitis
Definition and Types
Placentitis is inflammation of the placenta, most commonly due to bacterial infection, responsible for 9.8-33.5% of abortions, stillbirths, and neonatal deaths in horses. Three main types exist based on pathogenesis and lesion distribution.
Clinical Signs of Placentitis
Clinical signs typically appear in late gestation (last trimester). The two hallmark signs are premature mammary gland development and vulvar discharge. Normal udder development begins 2-6 weeks before foaling, with pronounced development in the week immediately preceding parturition. Premature lactation months before expected foaling strongly suggests placental pathology.
- Premature udder development: Most common presenting sign; may be subtle
- Vulvar discharge: May be purulent, bloody, or mucopurulent; often missed as mare swishes tail
- Premature lactation: Streaming of mammary secretions
- Poor vulvar conformation: Predisposes to ascending infection; assess vulvar seal
Diagnosis
Combined Thickness of Uterus and Placenta (CTUP)
Transrectal ultrasonography measuring CTUP at the cervical star region is the primary diagnostic tool for ascending placentitis. The probe is positioned cranial and lateral to the cervix, measuring from the middle branch of the uterine artery to allantoic fluid at the ventral aspect of the uterine body.
Normal CTUP Values and Abnormal Thresholds
Additional Diagnostic Tools
- Transabdominal ultrasound: Essential for nocardioform placentitis (lesions at horn base); assess fetal viability, detect twins
- Speculum examination: Assess cervical integrity and discharge; controversial due to infection risk
- Serum amyloid A (SAA): Acute phase protein; elevated in placentitis; promising biomarker
- Mammary secretion electrolytes: Calcium and potassium rise before parturition
- Progesterone/progestagen levels: May be elevated with placental stress; serial monitoring useful
Treatment of Placentitis
Treatment goals include eliminating infection, reducing inflammation, maintaining uterine quiescence, and supporting pregnancy to term. Multimodal therapy is standard.
Prognosis
Retained Fetal Membranes
With prompt, appropriate treatment, prognosis is excellent for survival and future fertility. Mares that recover from uncomplicated RFM do not generally have lower fertility. However, mares that develop metritis, endotoxemia, and/or laminitis have poor to moderate long-term survival prognosis. Foal heat breeding is typically avoided; breed on subsequent cycle.
Placentitis
Prognosis depends on extent of infection, timing of diagnosis, and response to treatment. Early detection and aggressive treatment can result in live foals, though they may be premature, septicemic, or dysmature. Foals born from mares with placentitis should be considered high-risk for neonatal complications. Nocardioform placentitis has the poorest prognosis.
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