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Journal of Obstrectic Anaesthesia and Critical Care
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LETTER TO THE EDITOR
Year : 2012  |  Volume : 2  |  Issue : 2  |  Page : 113-114

A rare fatal catastrophe during caesarean section: Amniotic fluid embolism


1 LHMC & Associated Hospitals, New Delhi, India
2 VMMC & Safdarjung Hospital, New Delhi, India
3 UCMS & GTB Hospital, New Delhi, India
4 MAMC & Lok Nayak Hospital, New Delhi, India

Date of Web Publication17-Dec-2012

Correspondence Address:
Nishant Kumar
HNo 595, GF Sector 14, Gurgaon
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4472.104740

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How to cite this article:
Kumar N, Saini S, Kumar S, Wadhawan S. A rare fatal catastrophe during caesarean section: Amniotic fluid embolism . J Obstet Anaesth Crit Care 2012;2:113-4

How to cite this URL:
Kumar N, Saini S, Kumar S, Wadhawan S. A rare fatal catastrophe during caesarean section: Amniotic fluid embolism . J Obstet Anaesth Crit Care [serial online] 2012 [cited 2020 Nov 26];2:113-4. Available from: https://www.joacc.com/text.asp?2012/2/2/113/104740

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 5 th 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 (SpO 2 ) decreased suddenly to 60%. Isoflurane and nitrous oxide were switched off; FiO 2 was increased to 100%. EtCO 2 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 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% FiO 2 and a PEEP of 8 cm of H 2 O. 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 H 2 O 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. 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 advocated.

To conclude, early recognition and aggressive resuscitative 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.

 
  References Top

1.Tufnell DJ. United Kingdom amniotic fluid embolism register. Br J Obstet Gynaecol 2005;112:1625-9.  Back to cited text no. 1
    
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.  Back to cited text no. 2
[PUBMED]    
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.  Back to cited text no. 3
[PUBMED]    
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.  Back to cited text no. 4
    
5.Davies S. Amniotic fluid embolus: A review of literature. Can J Anaesth 2001;48:88-98.  Back to cited text no. 5
[PUBMED]    




 

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