ABOUT THROMBOEMBOLISM IN PREGNANCY
It was the month of September 1959; I was still a junior resident and only qualified two
months ago. I was escorting the lovely Tara and her eight day old new baby, to
her parents at the time of her discharge from hospital. This was the rule in
our hospital that a resident doctor had to escort the mother and the baby to
her relatives. We were happily going down the stairs, suddenly I heard a loud thud,
and Tara was falling down. In the blink of an eye she was on the floor, after the
last step. The professors, room was next to the staircase, she came out, looked
at Tara. It was too late for Tara she was already dead. What could it be except
for a Pulmonary Embolism? Pulmonary embolism has only been recently recognized
(1990) as a part of, Thromboembolic disorders, after the nineties. In America
more than one million people die of thromboembolic diseases each year which is
more than, all the deaths put together from breast cancer, prostate cancer and road
trauma. In the developed world maternal deaths from thromboembolic disorders are
still among the top four causes although with current management it is
declining. In the United Kingdom there are 14 deaths per million maternities.
In the developing world the percentage to maternal deaths from thrombosis
related disorders is 2.2%. To make the public aware of this problem The ISTH(
The International Society on Thrombosis and Haemostasis) has announced a
thrombosis day, which commenced in 2014 and will be held annually on the “13th
of October.” 150 years ago Virchows, triangle was described as hypercoagubility,
vascular damage, and venous stasis. This still holds good as a cause of blood clotting.
Many developments in the past two decades have improved our understanding of
why blood clots. This can be both in our arteries or veins. These risk factors
can be both inherited or acquired. We had known about the acquired factors for
a long time , but a recent understanding of genetic factors has improved our
management in preventing thrombosis. In
the western world it is suggested that we look for these factors in pre
pregnancy and use anticoagulant treatment during pregnancy in women who have
high risk factors , and use Anticoagulants in special circumstances for example
after a caesarean section. This has been added to obstetric management since
1990.Tara had arrived at our hospital from a village after a five hour journey
on a bullock cart. This was her third birth. The other two had been totally
normal, four and two years ago. The only contraception they had used was coitus
interruptus There were no significant findings in her history or clinical examination.
She was a slim fit woman, the B.P., was normal. She had seen the village dula(
the village midwife) a few times. She had told her that all was going well. The
labour progressed nicely; she had a normal healthy male child. All went well, everybody
was happy. At this time India was going through an intense family planning
programme. Every couple who had a tubal ligation or a vasectomy got a
transistor radio from the government. The main reason for Tara to come to the hospital
was to have a tubal ligation. This was done the following day. At the time we
did not have a qualified anesthetist, we did our own spinal anesthesia, and
tubal ligation was done by mini laparatomy. A small longitudinal cut was made
just above the bladder, both tubes were tied cut and diathermy of cut the ends
was done. The abdominal cavity was closed. This was called modified Pomeroy’s
method. This was usually done by a resident doctor and usually took about
twenty five to thirty minutes. All this was progressing well. The women where
usually discharged on the seventh day. I still have tears when I think of Tara she
had three risk factors for thrombosis as we know today and these were as
follows, 1) She came to hospital sitting in a bullock cart for five hours. 2) She
had an operation which took about half an hour. 3) She was not mobilized quickly
as we do now. We had not known about thrombosis associated with pregnancy. Hospitals
where not as well equipped as they are today, as India was still very new and
it had only been 12 years since independence.
The other sad day I had was when Gita left us. It was august
1961 She was also a young, first mother, nineteen years of age. Like a lot of
the women she came from a village. She had not seen a care giver during
pregnancy however when she went into labour they had doctor, a new young doctor.
Her husband called him. When, the doctor
came over ,he found her blood pressure to be high 150/90, luckily he advised
them to take her to the medical college. It was not very far from her village. He
brought her to the hospital, sitting on the back of his scooter. She was not
over weight. She was in good labour. The scooter ride did not put her blood
pressure up; there was some protein in her urine. I started the treatment for
toxaemia of pregnancy. Her membranes were ruptured. There was a touch of
muconium (baby’s poo) in the liquor that came out suggesting, that the baby was
distressed. In those days we did not have CTG (foetal heart recording) machines. We depended
on our hearing using a foetascope. Soon after (3hours) she was ready for
delivery. In view of raised blood pressure and mild foetal distress I lifted
the baby out easily with forceps. All was well, her urine was clearing, the blood
pressure was stable. I left her room for some lunch, a midwife was with her. When
I came back in 20 minutes the midwife was trying to suck her secretions from
her mouth, but she was dead. I tried a cardiac massage, but no luck. My chief
resident and professor came over, a diagnosis of amniotic fluid embolism (AFE)
was made. AFE means some amniotic fluid goes in the circulation. It is
suggested that, amniotic fluid enters through, endocervical veins, placental site
and uterine trauma. It is believed that substances in amniotic fluid set up vasodilatation,
interfere with coagulation, and set up an immune mediated response. Decades ago
the mortality from AFE was as high as 85 %. Now with better understanding multi-specialist, resuscitators things have improved. AFE cannot be predicted or prevented. It
has a higher risk with advanced maternal age, placenta praevia, induction of labour
and operative delivery. I wonder if I can apply the last two to this case after
having done thousands of inductions, and operative deliveries and never seen
another AFE.
My third case after 15years of peace and quiet, happened in
another country, the United Kingdom. It was in July 1975. I had done a repeat
number 2 caesarean section on a slim healthy young woman very active. Rita who was 28 years old and her first child
was three years old with no history of any thrombosis. By now it was not routine to use prophylactic
anticoagulants after cesarean section, although the patients were mobilised earlier.
Prophylactic anticoagulant routines were only started in 1990. When Rita was
getting ready to go home on day 7, very early in the morning she collapsed in
the bath room, a colleague of mine happened to be in the hospital, he attended
to her but with no luck. She had already died. Things have changed in 50 years,
we know a lot about thrombosis, do prophylactic testing and use prophylactic anticoagulants,
and there is multidisciplinary help, Interventionists and resuscitators. I
have never experienced a maternal death after Rita. I must add after 1971 I
have always practiced in the western world.
