Cardiac Arrest after a Cesarean Section

Posted by • December 28th, 2012

In the latest Case Record of the Massachusetts General Hospital, a 43-year-old woman had bradycardia, hypotension, and apnea after cesarean section for placenta previa. Examination revealed pulseless electrical activity. Diagnostic procedures were performed, and management decisions were made.

There are three varieties of emboli to be considered in an obstetrical emergency. A thrombotic pulmonary embolus belongs in the differential diagnosis. Air emboli have been reported at the time of cesarean deliveries. Embolization of amniotic fluid and fetal material is a third type of embolic event.

Clinical Pearls

• What is an amniotic-fluid embolism?    

An amniotic-fluid embolism is thought to result from maternal reaction to fetal material entering the pulmonary circulation and can cause apnea, hypotension, and bradycardia. Amniotic-fluid embolism, although rare, is well known and feared by obstetricians.

Pathophysiologically, amniotic-fluid embolism is thought to be a maternal anaphylactic reaction that unfolds in two phases. A first phase, often lasting less than 30 minutes, is marked by sudden pulmonary vasoconstriction with resulting pulmonary hypertension and right-sided heart failure. This is followed by a second phase, involving left-sided heart failure, endothelial activation and subsequent leakage, and bleeding, all probably caused in part by either the hypoxemia of the first phase or the release of injury-associated agents in the serum.

• What are the risk factors for amniotic-fluid embolism?    

Amniotic-fluid embolisms are described in association with both vaginal and cesarean deliveries and can occur at any time during labor and delivery, as well as during the postpartum period. Risk factors for amniotic-fluid embolism include advanced maternal age, precipitous labor, cesarean delivery, and conditions associated with bleeding in pregnancy.

Morning Report Questions

Q: How is an amniotic-fluid embolism diagnosed? 

A: There is no quick, standard confirmatory test for the diagnosis of amniotic-fluid embolism. It is a clinical diagnosis that is made after ruling out other common causes for a patient’s condition. It has been suggested that transesophageal echocardiography (TEE) may support the diagnosis. Amniotic-fluid embolism causes intense pulmonary vasoconstriction and an acute pressure overload on the right ventricle, leading to dilatation and hypokinesis. Tricuspid regurgitation leads to dilatation of the right atrium and a shift of the intraatrial septum toward the left. Hypotension results from impaired filling of the left ventricle associated with pulmonary vasoconstriction and a shift of the interventricular septum toward the left. The left ventricle initially appears small and underfilled but hyperkinetic. Worsening left ventricular function may be due to hypoxemia and ischemia.

Table 1. Transesophageal Echocardiographic Findings in Acute Amniotic-Fluid Embolism.

Q: What is the appropriate treatment for an amniotic-fluid embolism? 

A: Treatment of an amniotic-fluid embolism is supportive. The airway should be secured and supplemental oxygen delivered. Either crystalloid or blood products are used with pressors as needed to maintain blood pressure. Although volume may be needed acutely, all involved need be mindful of the second phase of amniotic-fluid embolism, in which peripheral and pulmonary edema are prevalent; central monitoring may be vital. Extraordinary measures, including cardiopulmonary bypass, have been used to provide circulatory support and oxygen exchange when such resources are available. A final component of support in cases of amniotic-fluid embolism is treatment of bleeding due to either coagulopathy or atony. Uterine atony should be treated first with uterotonic agents, such as ergot derivatives and prostaglandins, tamponade from an intrauterine balloon, or some combination of these. If these measures are ineffective, hysterectomy may be considered, but performing an operation on women who have this condition and have ongoing coagulopathy is itself fraught with peril.

One Response to “Cardiac Arrest after a Cesarean Section”

  1. Carlos Ramirez Paesano says:

    we recently had a recently case (39 week gestation, IIG,IC, in labor).Gynecologist decided C-Section under spinal anaesthesia.Previous babybirth,patient no invasive arterial presion was 145/90mmHg and cardiac rate 90/min. During manual placent extraction she suddently suffered from cough,very brief gaspping and cardiac arrest (asistolia).We did advanced CPR; external thoracic compression and 1mg endovenous epinephrine was used.Then we canulated a radial artery and trilumen 7.5 Fr catheter into internal yugular vein in just one intents. It was noticed tendecy towards haematoma and bleeding around the yugular punction.Due to uncertain cause of this critical events,it was administrated 5gr Magnesium sulphate in 10 minutes. Hamodynamic situation was stabilized and 30-40 minutes later,TEE was introduced. We saw right chambers no dilatated,mild tricuspidea insuficience with calculated sistolic pulmonary pression about 4ommHg,main and right side pulmonary arteries no dilatated without mass, dilatated left ventricular chamber with global sistolic function,FE 30-35% and anterior-septal akinesia,no permable oval foramen. We gave transfusional and inotropic-vasopresor and undergone a hysterectomy was decided owing to atony.Then patient developed a DIC suscceful treated in critical care. Do you think this cardiac arrest could have been caused for a Amniotic Liquid embolism eventhougt TEE didn`t show right side chambers dilatation. Could we have seem by TEE the second haemodynamic stage of a Amniotic Liquid Embolism?.Could the Magnesium Sulphated help to reduce acute pulmonary hypertension and improve her outcome?. Patient survived