Amniotic fluid embolism, first described in 1926 , is a rare complication of pregnancy and labour, but one that is responsible for approximately 10% of all maternal deaths, and has been described as 'the most dangerous and untreatable condition in obstetrics'. The incidence of amniotic fluid embolism has been reported to be between 1 per 8000 and 1 per 80 000 deliveries.
A 36-year-old primigravida woman was admitted in spontaneous labour at term, following a noncomplicated pregnancy. A few minutes after delivery of a normal healthy child, she became suddenly cyanosed whilst the episiotomy was being repaired. The patient had an attack of tightness in the chest associated with cyanosis, tachycardia, visual disturbance, confusion, irritability, convulsions, coma, cardiovascular and respiratory collapse. The systolic arterial pressure was 40 mmHg and pulse rate 160 beats min−1. Blood gases drawn from the right radial artery demonstrated severe metabolic acidosis (pH 6.528, PaCO2 5.95 kPa, PaO2 72.75 kPa while breathing 100% oxygen).
Respiratory distress with cyanosis was the initial indicator of the condition. During resuscitation the patient started to bleed, and a clinical diagnosis of disseminated intravascular coagulation (DIC) was made . The diagnosis of DIC was confirmed by laboratory investigation of the coagulation studies, which revealed an international normalized ratio (INR) of 4.2, an activated partial thromboplastin time (APTT) of 6.8 s, a platelet concentration of 68 × 109 L−1 and a fibrinogen concentration of 2.2 mg L−1.
Resuscitation was performed immediately in the labour ward, which consisted of endotracheal intubation, intermittent positive pressure ventilation of the lungs with 100% oxygen and external cardiac massage. Volume resuscitation with appropriate blood products, packed red cells to correct the haemoglobin deficiency, fresh frozen plasma to correct the INR, and cryoprecipatate to correct the hypofibrinogenemia was given. Seven units of packed red cells, six units of fresh frozen plasma and six units of cryoprecipitate were used. The haemoglobin concentration increased from 3.7 to 8.2 g dL−1, the INR decreased from 4.2 to 1.8, and the fibrinogen concentration increased from 0.8 to 2.3 g dL−1. Also three litres of 0.9% saline and one litre of Gelofusine® was given during resuscitation. Four hours later blood gases improved: pH 7.43, PaCO2 3.4 kPa, HCO−3 16.6 mmol L−1, PaO2 12.71 kPa breathing 40% oxygen.
The patient's condition remained critical: she was transferred to the intensive care unit. After a few hours she developed a clinical picture of acute renal failure . Rhabdomyalysis was suspected, confirmed by significant myoglobinuria, elevated creatinine kinase (CK) of 22 755 IU and rising creatinine concentration of 153 μg L−1. The urine output remained about 100 mL h−1 with fluid therapy. The patient remained ventilated and sedated overnight. The next day the endotracheal tube was removed and she gradually recovered and she was discharged from the intensive care unit after two days, then discharged a few days later with no medical problems.
Amniotic fluid embolism remains a frustrating challenge and only general recommendations can be made. Rapid diagnosis and resuscitation could reduce the death rate from amniotic fluid embolism. The diagnosis of amniotic fluid embolism is based on the clinical picture of acute hypotension or cardiac arrest, acute hypoxia (dyspnoea, cyanosis or respiratory arrest), coagulopathy (laboratory evidence of intravascular coagulation or severe haemorrhage), onset of all of the above during labour, Caesarean section, or within 30 min of delivery, and no other condition or potential explanation for the symptoms and signs .
E. S. AZIZ
28 Primrose Lane, Croydon, Surrey, CR0 8YR, UK
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London, UK: HMSO, 1998.