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Letters to the Editor
2. Schachner SM, Reynolds AC. Horner syndrome during lumbar epidural
analgesia for obstetrics. Obstet Gynecol 1982;59(6 Suppl):31S-2.
3. Paw HG. Horner’s syndrome following low-dose epidural infusion for
labour: A cautionary tale. Eur J Anaesthesiol 1998;15:110-1.
4. Wong SY, Lin CF, Lo LM, Peng TC, Chuah EC. Postpartum unilateral
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delivery. Chang Gung Med J 2004;27:624-8.
5. Merrison AF, Lhatoo SD. Horner’s syndrome postpartum. BJOG
2004;111:86-8.
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DOI:
10.4103/2249-4472.104739
A rare fatal catastrophe
during caesarean
section: Amniotic fluid
embolism
Sir,
A 22-year-old third gravida weighing 50 kg, booked patient
presented at 36 weeks of gestation with pre-eclampsia. Patient
was receiving tab. methyldopa 500 mg TDS and tab. labetalol
100  mg BD. On 5th day of admission, artificial rupture of
membranes was done and labor was induced in view of a
presumptive diagnosis of HELPP syndrome and worsening
liver functioning tests. Fetal distress was noted and hence
a decision for urgent caesarean section was taken. General
anesthesia was planned.
A rapid sequence induction of anesthesia and intubation was
performed and balanced general anesthesia maintained. A
male Baby weighing 2 200 g was delivered with an APGAR
score of 8 and 9 at 1 and 5 min, respectively. Oxytocin 20 IU
iv infusion at the rate of 0.3 IU/min and morphine 5 mg were
given after delivery of the baby. As the rectus sheath was being
sutured, patient’s oxygen saturation (SpO2) decreased suddenly
to 60%. Isoflurane and nitrous oxide were switched off; FiO2
was increased to 100%. EtCO2 also decreased to 10 mm of Hg.
Heart rate decreased to 30 beats/min, carotid pulse was not
palpable. Isoflurane and nitrous oxide were switched off. The
ECG complexes were normal and sinus in rhythm, pulseless
electrical activity was suspected, and chest compressions were
Journal of Obstetric Anaesthesia and Critical Care / Jul-Dec 2012 / Vol 2 | Issue 2
started. After 4 min of cardiopulmonary resuscitation and iv
adrenaline 1 mg twice, sinus rhythm with rate of 146 beats/
min with a palpable carotid pulse was achieved. Causes of
decrease in saturation due to circuit failure, air embolism, and
acute myocardial ischemia were ruled out. Vasopressors in the
form of dopamine @ 5 μg/kg/min followed by noradrenaline @
2 μg/min were started, which were later increased to maintain
a mean blood pressure of 65  mmHg. There was no undue
bleeding or ooze from the surgical site during closure. Over the
next 15 minutes, patient developed bilateral crepitations and
pink frothy secretions through the endotracheal tube. IPPV
was continued with 100% FiO2 and a PEEP of 8 cm of H2O.
Furosemide 10 mg and morphine 4.5 mg iv were administered.
Repeat arterial blood gas showed a worsening hypoxia and
metabolic acidosis soda bicarbonate 50 mEq was administered.
On auscultation, there were no crepitations and the chest was
clear. However, after patient had been shifted to the intensive
care unit, she developed florid pulmonary edema and the ETT
was again filled with pink frothy secretions. The patient was
connected to the ventilator set to volume control mode with
a PEEP of 8  cm H2O in the ICU. One hour later, she again
sustained bradycardia (HR, 30 beats/min) and hypotension
(BP, 50 mmHg systolic) leading to asystole. Resuscitation was
attempted for 30 minutes, but the patient could not be revived.
Criteria for the diagnosis of amniotic fluid embolism (AFE)
consist of the presence of acute hypotension or cardiac arrest,
acute hypoxia, coagulopathy, and all of these occurring during
labor, caesarean section, or dilatation and evacuation or within
30 minutes postpartum with no other explanations for the
findings. The United Kingdom AFE register reports of two cases
under anesthesia without coagulopathy.[1] Thus, this patient
most probably had AFE.
A tear in the fetal membranes is a factor consistently related to
the occurrence of AFE. Artificial rupture of membranes may
permit exposure of fetal tissues to the maternal vasculature
and may increase the risk for AFE. Other risk factors include
turbulent labor, trauma, multiparity, increased maternal age,
use of oxytocin, male fetus, and LSCS.[2] All factors except
turbulent labor, trauma, and increased maternal age were
present in our patient.
The diagnosis of AFE remains clinical and that of exclusion.
Additional diagnostic tools include chest radiograph, lung
scan, CVP monitoring, and coagulation profile. Conditions
that may mimic AFE include thrombotic pulmonary embolism,
air embolism, eclamptic convulsions, toxic reaction to local
anesthetic drugs, acute left heart failure, aspiration of gastric
contents, and hemorrhagic shock. There was no history of
venous thrombosis in lower limbs; air embolism was ruled
out since the characteristic mill wheel murmur was absent.
113
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Letters to the Editor

Eclamptic convulsions could have been masked since the
patient was anesthetized and no local anesthetics were
administered. Patient had no history of heart disease and
though anemia can lead to pulmonary edema and shock,
this had been previously corrected. Aspiration of gastric
contents was not a possibility since trachea was intubated and
a nasogastric tube was in situ. The blood loss was only 400 ml
and there was no undue bleeding or ooze from the surgical site
thus ruling out hemorrhagic shock.
Early recognition of AFE is critical to a successful outcome.
Transesophageal echocardiography has emerged as an invaluable
tool for the diagnosis of AFE. Newer strategies like intra-
aortic balloon counterpulsation for hemodynamic support,
extra corporeal membrane oxygenator and cardiopulmonary
bypass[3] exchange transfusion, uterine artery embolization,
continuous hemofiltration, cell salvage,[4] and serum protease
inhibitors, inhaled nitric oxide and prostacyclin[5] have been
LHMC & Associated Hospitals, New Delhi, 1VMMC & Safdarjung
Hospital, 2UCMS & GTB Hospital, 3MAMC &
Lok Nayak Hospital, New Delhi, India
Address for correspondence: Dr. Nishant Kumar,
HNo 595, GF Sector 14, Gurgaon, India.
E-mail: kumarnishant@yahoo.co.uk
REFERENCES
1. Tufnell DJ. United Kingdom amniotic fluid embolism register. Br J Obstet
Gynaecol 2005;112:1625-9.
2. Stein PD, Matta F, Yaekoub AY. Incidence of amniotic fluid embolism:
Relation to cesarean section and to age. J Womens Health 2009;18:327-9.
3. Ho CH, Chen KB, Liu SK, Liu YF, Cheng HC, Wu RS. Early application
of extracoeporeal membrane oxygenation in a patient with amniotic fluid
embolism. Acta Anaesthesiol Taiwan 2009;47:99-102.
4. Goldszmidt E, Davies S. Two cases of hemorrhage secondary to amniotic
fluid embolism managed with uterine artery embolisation. Can J Anaesth
2004;50:917-21.
5. Davies S. Amniotic fluid embolus: A review of literature. Can J Anaesth
2001;48:88-98.

advocated.
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To conclude, early recognition and aggressive resuscitative Quick Response Code: www.joacc.com
measures form the backbone of management of such cases.
Despite the best efforts, mortality remains high in the absence
of newer modalities to diagnose and manage cases of AFE.

Nishant Kumar, Suman Saini1, Sunny Kumar2, DOI:

Sonia Wadhawan3 10.4103/2249-4472.104740

114 Journal of Obstetric Anaesthesia and Critical Care / Jul-Dec 2012 / Vol 2 | Issue 2