A 33-year-old female, G4 P1 L1 A1 E1 36 weeks + 5 days, approached our hospital with mild pain. She had been planned for normal vaginal delivery and later decided for emergency LSCS in view of slow progression and maternal exhaustion. Patient had history of hypothyroidism and gestational diabetes mellitus which was under control. Preoperatively, patient was hemodynamically stable and proceeded with sub arachnoid block. Baby was delivered; to follow, placenta with membranes were removed. Immediately after removal of placenta, patient developed cough followed by breathlessness, hypoxia, hypotension and tachycardia. She was resuscitated with crystalloids and colloids to optimize hemodynamics and airway was also secured in view of breathlessness and hypoxia. Surgery proceeded after stabilization. After 20 minutes, patient showed profuse fresh vaginal bleeding, which was not controlled with regular uterotonic drugs. Invasive monitoring was placed and Hb, coagulation profile, D-dimer and fibrinogen were done; in the meantime, we alerted the cardiologist and interventional radiologist too. Fresh bleeding continued but not with much hemodynamic alteration. Two units of FFP and 1 unit of PRBC were transfused. In all these events uterine contractility checked periodically, it was well contracted. Emergency echo showed normal chambers and function, but labs showed a classical picture of disseminated intravascular coagulation, Hb – 8.1 g/dl, fibrinogen – 90 mg/dl, FDP – positive and D-dimer – 92000 ng/ml. With these parameters, 4 units of cryoprecipitate were transfused at the time. After this blood products transfusion, the vaginal bleeding was controlled. Then the patient was shifted to the ICU and electively ventilated for the next 2 hours and extubated. Repeat Hb was 7.7 g/dl; 1 more unit of PRBC was transfused. On subsequent days, repeat blood investigations showed gradual improvements in Hb, coagulation values and other parameters, D-dimer – 18900 ng/ml, fibrinogen – 247 mg/dl and FDP – positive. Serial lab tests over days noted improvement in the levels of fibrinogen and reduction in D-dimer levels. Patient recovered well and was later discharged.
Amniotic fluid embolism is a rare and extremely life-threatening obstetrics emergency associated with amniotic fluid, fetal cells, hair, or other debris entering the maternal circulation resulting in cardiovascular collapse. It usually presents as sudden, profound and unexpected maternal collapse associated with hypotension, hypoxemia and disseminated intravascular coagulation (DIC). Maternal risk factors associated with AFE include:
Amniotic fluid embolism pathophysiology has two phases. In phase 1, maternal circulation is exposed to amniotic fluid. There is release of biochemical mediators that results in pulmonary artery vasospasm leading to pulmonary hypertension. This results in hypoxemia and hypotension. In phase 2, patients who survived phase 1, proceeded to have biochemically mediated disseminated intravascular coagulation (DIC) and also uterine atony. This results in massive haemorrhage. DIC will be noted in more than 80% of AFE cases. The diagnosis of amniotic fluid embolism is mainly clinical and is essentially a diagnosis of exclusion. The above-mentioned phases were noted in our patient, early intervention like hemodynamic stability and coagulation correction were the main key factors behind this successful management.
V.Karthickraja, MD, DA, FIPM Senior Consultant, Anaesthesiologist and Pain Physician Kauvery Hospital, Chennai
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