Amniotic fluid embolism is a clinician’s nightmare any day. First, the event could be so dramatic and the progression to death so fast that you begin to wonder what happened. Secondly there is no way of predicting this fatal condition in a pregnant woman and the index of suspicion in a woman in labor is almost zero.
First, what is embolism? It is a process where the product of an activity in one part of the body is transferred to another leading to catastrophic events in that part and the whole body. The commonest described is PULMONARY EMBOLISM, in which blood clots in the deep veins are dislodged and are carried to the lungs where they cause infarction which could be fatal if intervention slow.
Amniotic fluid is that water near white in color that is contained in amniotic sac of a pregnant world. The fluid serves
as a protective medium for the unborn child and helps in buoyancy during foetal movements. The fluid comes from various sources, the mother and the baby. Shortly after fertilization, there are rapid multiplication of cells in a geometrical order i.e. 2 – 4 – 8 – 16 – 32 – 64….until a solid mass of cells is formed. At about the 5th week of life, this cell mass develops an extracoelom cavity, named extra because potentially it is going to be outside and covering the baby. The old terminology used to be a blastocyst. Blast cell means primitive or new cells while cyst means water bag. The source of this fluid at this age is from non-cellular component of the mother’s blood known as PLASMA. This fluid passes through the foetal membranes through hydrostatic forces and osmosis.
As the embryo matures, with the development of the placenta and the foetal circulation, the amniotic fluid now is produced by the foetus flowing from the foetal skin. By the third month of life the amniotic fluid contains proteins, carbohydrates, fats, electrolytes or rather salts and wait for it, STEM cells. These cells are said to be pluripotent, which means that they have the ability to differentiate into different cell types like skin, liver, bone, brain etc.
The baby drinks, breaths and urinates into the amniotic. This makes the amniotic fluid a complex fluid. It reaches its maximum volume of about one liter about the seventh month of life and decreases to about half its volume before the child is delivered.
So when we talk of amniotic fluid embolism we are referring to a situation where this complex fluid gains entry into the mother’s blood circulation through the placental bed or any vein in the reproductive system and triggers off allergic reaction in the lungs of the mother. This reaction is so severe that it causes the collapse of the lungs and the heart, often described as CARDIORESPIRATORY failure. It also causes severe clothing problems for the mother leading to bleeding which may be the final pathway of the event if the facilities available are able to cope with the lungs onslaught.
The diagnosis of amniotic fluid embolism is usually post mortem which is useless to the clinician whose mission is to save the life of the mother and baby. However there are tell-tale clinical signs that may be suggestive if the obstetrician has a high index suspicion. But he/she hardly does because the condition is RARE.
In the first phase of this condition, there is a sudden shortness of breath with drop in blood pressure. This leads to low oxygen delivery to the heart and lungs with loss of consciousness and possible death. A kind of picture you get in serious allergic reaction known as ANAPHYLACTIC SHOCK.
Those who survive this phases would progress to the next in which there is severe shivering – which may be confused with malaria in this environment except that there is No FEVER. There is bad taste in the mouth; yet another common compliant with those who have malaria, then vomiting; coughing with severe bleeding that may lead to the death of the baby if not delivered immediately and of course the mother. It is no longer rigidly considered to be a phasic event but a progression depending on the severity of the maternal reaction at a point in time and the buildup of the antigens in the maternal system.
For amniotic fluid embolism to occur there has to be an entrance of the fluid into the veins of the woman’s womb. And for this to happen, the amniotic sac must be ruptured to express the fluid and also a rupture of the uterine (womb) or cervical (neck of the womb) veins. This is now facilitated by a pressure gradient created by the contractions of the uterus that propels the amniotic fluid onward to the lungs for this catastrophic event.
It must be stated here that finding amniotic fluid content and foetal tissue within maternal circulation is common and most of the time not significant, but why does it cause this phenomenon in some? This is what makes amniotic fluid embolism a complex situation to understand.
Having said that, what the risk factors are. It is agreed that trauma to the abdomen of a pregnant world is highly associated with this event. Lately it is becoming commonplace to use MISOPROSTOL, a synthetic, prostaglandin to induce labor. This increases uterine contraction and it is has been shown that this double the risk of the patient ending up with amniotic fluid embolism. Yet this is used on daily basis and maternal mortality rate has not skyrocketed.
Artificial ruptures of membranes known as amniocentesis has also been associated with amniotic fluid embolism. Others include caesarian section, instrumental delivery like using vacuum extractor or obstetric forceps to bring out the baby if the baby or mother is in distress; which on their own are risk factors. One thing that is common above these factors listed is that they are associated with trauma to the birth canal. They are normal standard operating procedures. Other associated risk factors include excessive amniotic fluid known as POLYHDRAMNIOUS; tear in the cervix or uterus, low lying placenta known as PLANCENTA PRAEVIA, premature separation of the placenta from its bed, known as ABRUPTIO and pregnancy induced hypertension with ECLAMPSIA. You may want ask, what is then left?
The frustrating thing is that there is no way of predicting during antenatal period the likelihood of your patient developing amniotic fluid embolism. There is no biological and chemical marker for the condition. Perchance, a very high index of suspicion especially when a woman is in labor might be of help.
The only intervention known so far in case of amniotic fluid embolism is an emergency caesarean section to at least salvage or better put save a lifer. In our environment where prayers had to be said first and consent for surgery reluctant to give, this could be very frustrating and the outcome very distressing.