Dr Peter McLaren
Aboriginal Health
Women's Health
Amniotic Fluid Embolism
Antenatal Diagnosis of Congenital Abnormality
Emotional aspects of menopause
Endoscopic Surgery in Gynaecology
Obstetric Emergencies - Antepartum
Obstetric Emergencies - Intrapartum
Obstetric Emergenies - Postpartum
Preventable Causes of Congenital Abnormalities
The Principles of Antenatal Care
Table of Contents |
It has been described as "the most dangerous and untreatable condition in obstetrics".
Incidence:
The incidence of clinically detectable AFE is low and is estimated to be 1 in 20,000 to 1 in 80,000 live births. Mortality may be as high as 86%. In Australia from 1970 - 1990, AFE contributed to 7.5% of direct maternal mortality. This accounted for 34 out of 427 direct maternal deaths and 0.67 deaths per 100,000 pregnancies. It is important to note that these figures are quite rubbery. Definitive diagnosis is at present by post-mortem examination which makes the diagnosis difficult in the milder cases.
Presentation
:The clinical presentation of AFE is generally dramatic, with the abrupt onset of dyspnoea and hypotension with rapid progression to cardiopulmonary arrest. In 40% of cases, this is followed by some degree of consumptive coagulopathy, which may be the presenting manifestation in 10-15% of cases. Evidence of CNS hypoxia is present, with alterations in mental status progressing to coma. In 10-20% of cases, the patient my present with seizure activity. These dramatic features may be heralded by patient's non-specific symptoms of shivering, anxiety, cough, vomiting and the sensation of a bad taste in their mouths. Foetal distress is often present. Up to 50% of patients die withing the first hour after the onset of their symptoms. Of the survivors, pulmonary oedema has been observed in anywhere from 24% to 70% of cases.
However, this is one disease where I thought that the more I read about it the less I knew. Although the classic presentation has always been an elderly, in obstetric terms, multiparous woman with a large baby experiencing a short tumultuous labour associated with the use of uterine stimulants, this is hardly common. Some of the following cases may demonstrate the unpredictable nature of this condition.
In keeping with the concept of creating a deficit in both membranes and blood vessels, links have been shown on some studies with following conditions:
- closed abdominal injury
- IUD present at full term
- amniocentesis
- caesarian section
- placenta accreta
- ruptured uterus
- retained placenta
The concept of increased pressure gradient has been shown to be a problem with the injection of saline to induce abortion when the foetus is dead. However, AFE can occur before, during and after delivery. It has occurred 90 minutes after caesarian section for breech presentation. It was suggested that in this patient an amniotic fluid collection in dilated uterine veins was mobilised as venous tone returned following the offset of spinal anaesthesia and sympathetic blockade. The most inexplicable of all, is the case of a woman, 20 weeks pregnant who collapsed with all the features of AFE, namely respiratory distress, cyanosis, hypotension and incoagulable blood. The pregnancy was terminated 82 hours later by hysterectomy when the foetus was dead. There was no retro-placental bleeding and no liquor present.
Pathogenesis:
It is mostly agreed that this condition results from amniotic fluid entering the uterine veins. In order for this to occur, there are three pre-requisites:
- ruptured membranes
- ruptured uterine or cervical veins
- a pressure gradient from uterus to vein
Dr Peter McLaren, FANZCA, amprak@nor.com.au
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