Pregnancy toxemia ranks as the top “can’t-miss” metabolic condition in late gestation for small ruminants. The syndrome combines ketosis with hepatic lipidosis and develops when fetal glucose demand exceeds maternal supply. As blood glucose drops, the dam experiences hypoglycemic encephalopathy, progressive depression, and, without timely intervention, death.
Why Late Gestation is the Danger Zone
Most fetal growth happens in the final trimester. The dam ramps up gluconeogenesis and mobilizes fat reserves to meet rising glucose demands of the enlarging fetus. When this overwhelms hepatic capacity, triglycerides accumulate, impairing hepatic function and triggering ketosis. Multiple fetuses, poor body conditioning (too thin or obese), and any cause of inappetence increase the risk for pregnancy toxemia during this period.
The Classic Case Pattern You Can’t Miss
Typical early signs include going off grain, separation from the flock, and bruxism in late gestation. As the disease progresses, the dam may pace, show facial tremors, develop opisthotonos or central blindness, and become recumbent. Most affected animals are either over- or under-conditioned (BCS 1/5 or 5/5, ideal is 3/5). The presence of multiple fetuses greatly increases glucose demand and therefore risk.
Field-Testing: What to Test First
In the field, clinical signs are diagnostic clues. Confirm the diagnosis by checking urine ketones or measuring blood BHBA with a stall-side meter.
- Urine ketones are the quickest and most accurate diagnostic tool, as they provide a more sensitive and specific result than blood alone
- BHBA > ~1.0 mmol/L supports ketosis; many clinical cases run higher
- Blood chemistry may reveal hypoglycemia, low calcium, magnesium, and potassium; and elevated liver enzymes
Treatment Priorities (And What to Avoid)
Focus on three goals: restore energy, reduce pain, and correct deficits
- Administer propylene glycol PO and limit duration/frequency to protect rumen flora and avoid worsening anorexia
- Offer highly palatable feed away from flockmates to encourage intake
- Provide calcium (SQ or PO) if levels are borderline or low
- Use NSAIDs (e.g., flunixin) to manage pain and improve both dam and fetal outcomes
- Deliver oral or IV fluids as needed to correct dehydration and potassium imbalances
When to Induce Parturition vs. Wait
Getting the fetuses out is not always the answer. Consider induction when:
- The dam is valuable
- The fetuses are alive and within ~3 days of due date
If the fetuses are dead or far from term, induction with steroids and dexamethasone may still protect the dam. Evaluate the need for a C-section on a case-by-case basis.
Herd-Level Prevention
- Maintain a BCS of 2.5–3.5/5; avoid thin or obese dams
- Implement good feeding management: provide enough space at feeders and group animals by gestation size, age, or BCS
- Ensure adequate bunk space, minimize social stress, address parasitism, and correct dental issues that reduce intake
- In large herds, consider performing late-gestation BHBA screening to identify subclinical disease early
When you detect disease early and the dam remains ambulatory, the prognosis is favorable with prompt supportive care. Recumbent or comatose animals face much poorer outcomes, and fatalities can approach ~40% in severe presentations. Rapid field testing and decisive intervention make all the difference.
More from Zuku Learning:
- Master NAVLE® concepts
- Subscribe to the Question of the Day to receive a NAVLE® question delivered to your inbox daily
- Review the LDA vs. RDA in Dairy Cows: Key Differences Every Vet Student Must Know blog
- Review the Ketosis in Fresh Dairy Cows: Causes, Diagnosis, and How to Treat It blog
