Severe headache at 36 weeks with platelets of 92,000
A 34-year-old woman, gravida 2 para 1, at 36 weeks and 3 days by a certain first-trimester ultrasound, is admitted with a two-day history of severe frontal headache and blurred vision. Blood pressure is 176/112 mmHg on two readings 15 minutes apart; she has 3+ proteinuria on dipstick, brisk deep tendon reflexes and one beat of clonus at the ankles. She has no seizures and no epigastric pain. Platelets 92,000/mm3, AST 86 U/L, ALT 74 U/L, creatinine 0.9 mg/dL, haemoglobin 12.1 g/dL, uric acid 7.2 mg/dL, urine protein-to-creatinine ratio 1.8. Fetal heart tracing shows a baseline of 140 beats/min with moderate variability and no decelerations; the cervix is 1 cm dilated, 30% effaced, and the fetal head is at -3 station. This is her second admission; a week ago her platelets were 168,000/mm3 and blood pressure was 148/96 mmHg. The delivery unit has magnesium sulfate, intravenous labetalol and hydralazine, and a level-2 neonatal unit.
1. State the diagnosis with the features that make it severe, and explain why expectant management to 37 weeks is wrong here.
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Diagnosis: preeclampsia with severe features at 36 weeks and 3 days. Severe features present: a systolic pressure of 176 mmHg (160 or above), headache and visual disturbance (cerebral symptoms), platelets falling to 92,000/mm3 (under 100,000), and transaminases roughly twice the upper limit of normal. Proteinuria is heavy (protein-to-creatinine ratio 1.8) and the rising uric acid with a platelet fall from 168,000 to 92,000 within a week indicates progressing disease. The brisk reflexes and clonus show neuromuscular irritability and a raised seizure risk.
Why not wait to 37 weeks: delivery is indicated at 34 weeks or later once severe features are present. Expectant management with steroids and close monitoring is reserved for severe preeclampsia before 34 weeks in a tertiary unit, and even then only while mother and fetus remain stable. In this woman the risks of delay are eclampsia, placental abruption, progression to HELLP syndrome, acute kidney injury, pulmonary oedema, intracerebral haemorrhage and fetal demise. At 36 weeks and 3 days the baby is essentially mature, so there is nothing to gain from waiting and much to lose. Antenatal corticosteroids are not required for fetal maturity and must not delay delivery.
Plan: admit to labour ward, start magnesium sulfate for seizure prophylaxis, control blood pressure, take bloods every 6-12 hours, monitor the fetus continuously, and plan delivery after stabilisation, by the safest route for the mother. With a Bishop score this unfavourable, expect induction to be long, so discuss caesarean delivery with the anaesthetist and neonatologist.
2. Write the medication orders: magnesium sulfate regimen with its monitoring and antidote, your antihypertensive choices with doses, and the drugs you must avoid.
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Magnesium sulfate: loading dose 4-6 g intravenously over 15-20 minutes, then 1-2 g per hour as a continuous infusion for at least 24 hours after delivery or after the last seizure. Monitor hourly: deep tendon reflexes present, respiratory rate at least 12-16/min, urine output at least 30 mL/hour (0.5 mL/kg/hour), and oxygen saturation. Reduce the dose in renal impairment and check serum magnesium if there is doubt. Antidote: calcium gluconate 1 g intravenously over 10 minutes for respiratory depression or loss of reflexes.
Antihypertensives to keep blood pressure below 160/110 without dropping it below about 130/80, which would impair placental perfusion: intravenous labetalol 10-20 mg, doubling every 10-20 minutes to a maximum of about 300 mg, or intravenous hydralazine 5-10 mg every 20 minutes, or oral immediate-release nifedipine 10 mg repeated as needed. Avoid ACE inhibitors and angiotensin receptor blockers (fetal renal injury), atenolol, and diuretics except for pulmonary oedema.
Also avoid ergometrine or methylergometrine for the third stage, because of the risk of severe hypertension and stroke; use oxytocin instead. Avoid a fluid bolus beyond about 80 mL/hour of maintenance fluid, since these patients develop pulmonary oedema easily. Document that neuraxial anaesthesia with a platelet count of 92,000 requires individual anaesthetic assessment and a repeat count.
3. She delivers vaginally six hours later. What are her two main postpartum risks, and what do you do in the third stage and over the first 24 hours?
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Risk 1: postpartum haemorrhage. She has a distended uterus from induction, platelet dysfunction, and will receive magnesium, which relaxes the uterus. Third stage: give oxytocin 10 IU intramuscularly (or slowly intravenously) with delivery of the anterior shoulder, use controlled cord traction, massage the uterus, and inspect the perineum. Avoid ergometrine because of her hypertension. If bleeding exceeds 500 mL, escalate to additional uterotonics (carboprost, misoprostol), tranexamic acid 1 g intravenously within 3 hours, bimanual compression and balloon tamponade, and check fibrinogen and platelets early because she has a low platelet count.
Risk 2: eclampsia and HELLP in the postpartum period. Continue magnesium sulfate for 24 hours after delivery, keep blood pressure below 150/100 with labetalol or nifedipine, and repeat platelets, AST, ALT, creatinine and haemoglobin at 24 and 48 hours, since HAEMOLYSIS, elevated liver enzymes and low platelets can worsen in the first two days. Watch for headache, epigastric pain, visual change, falling urine output and breathlessness (pulmonary oedema). Assess venous thromboembolism risk and start prophylactic low-molecular-weight heparin once bleeding risk is acceptable, with the platelet count in mind.
Also: encourage breastfeeding, arrange a postpartum blood pressure review at 7-10 days, and counsel her that preeclampsia raises her long-term risk of hypertension and cardiovascular disease, so she needs lifelong follow-up.