Carta Acesso aberto Revisado por pares

Anaesthetic management of the parturient with massive peripartum haemorrhage and fetal demise

2003; Wiley; Volume: 58; Issue: 9 Linguagem: Inglês

10.1046/j.1365-2044.2003.03362_30.x

ISSN

1365-2044

Autores

A. Chulu, Krzysztof M. Kuczkowski,

Tópico(s)

Neonatal Respiratory Health Research

Resumo

Obstetric haemorrhage is still a significant cause of maternal morbidity and mortality – worldwide [1]. In many developing countries, not all pregnant women who seek care at a medical facility arrive in time to be treated. Some die while trying to get there [2, 3]. We herein report a case of a parturient who presented to rural health care facility in Zambia with placenta praevia-related severe peripartum haemorrhage, hypovolaemic shock and fetal demise, and required emergency Caesarean section under general anaesthesia. Complete maternal recovery was accomplished, despite a greatly delayed diagnosis and treatment (over 48 h). A 20-year-old, 153-cm, 52-kg, gravida 3, para 2, otherwise healthy female at term with undiagnosed placenta praevia had been in labour for 2 days prior to admission to the rural hospital in Mporokoso, Zambia. The patient presented to the medical facility with severe peripartum haemorrhage, hypovolaemic shock and intra-uterine fetal demise, and required emergency evacuation of retained fetus and placenta under general anaesthesia. She had no known drug allergies and no prior anaesthesia. The course of her pregnancy had been uneventful, specifically no spotting or bleeding in the third trimester, indicative of placental pathology, had been reported. On admission, she was pale, diaphoretic and lethargic. Her admission blood pressure was 60/40 mmHg, heart rate 130 beats.min−1 and respiratory rate 30 breath.min−1. Fetal heart rate was not detectable upon auscultation. Laboratory studies revealed haemoglobin concentration of 4.3 g.dl−1. In the presence of ongoing haemorrhage from placenta praevia, hypovolaemic shock and intra-uterine fetal demise, prompt evacuation of the uterus via an abdominal route was necessary. Pre-anaesthetic evaluation of the airway was normal. The chest was clear to auscultation. An intravenous access was established and aggressive intravenous fluid resuscitation with lactated Ringer's solution was initiated. The patient was taken to the operating room and standard anaesthesia monitoring was applied. Pre-oxygenation was accomplished with 3 min of normal tidal volume ventilation with 100% oxygen. Rapid sequence induction of general anaesthesia consisted of intravenous ketamine 75 mg, atropine 0.3 mg and succinylcholine 50 mg while cricoid pressure was continuously applied, and the trachea was intubated with a 7.0 internal diameter cuffed tracheal tube. Anaesthesia was maintained with halothane 0.5% in oxygen and intravenous fentanyl. Extraction of the dead fetus was accomplished via the Caesarean incision. The placenta was removed and uterine bleeding was controlled with surgical repair and parenteral administration of ergonovine. Intra-operative haemoglobin concentration was 3.5 g.dl−1, and blood transfusion was initiated. Postoperatively, the patient received three more blood transfusions and accomplished full recovery. The physiological changes during pregnancy are designed to protect the mother from blood loss at parturition [4]. When this protective reserve is exceeded, hypovolaemia and shock ensue. Placenta praevia occurs when part of the placenta implants within the lower uterine segment. It complicates 4.8 per 1000 deliveries with an associated mortality rate of 0.03%[5]. Massive haemorrhage is a recognised complication of placenta praevia and a major cause of maternal and fetal morbidity and mortality. Rapid sequence induction of general anaesthesia is the preferred technique for actively bleeding, hypovolaemic parturients. The choice of intravenous induction agents depends on the degree of hypotension and maternal haemodynamic stability [6]. Etomidate and ketamine are the preferred induction agents for actively bleeding obstetric patients. Ketamine causes central nervous system-mediated catecholamine release. In most hypovolaemic parturients, this effect supports heart rate and blood pressure. All uterine relaxants including volatile halogenated agents should be used with caution if bleeding continues peri-operatively. Small doses of opioids can be given without causing significant cardiovascular depression. In the severely compromised parturient, muscle relaxants alone may be the only safe choice [6]. Central venous access may be helpful to guide volume states; however, blood loss, urine output and maternal haemodynamics usually provide enough information. Although hypotension usually accompanies hypovolaemic shock, the blood pressure can be normal. The clinical manifestations of hypovolaemic shock include pallor, sweating, disorientation, tachycardia, cardiac arrhythmia, tachypnoea, hypotension, low cardiac output, oliguria, disseminated intravascular coagulation (DIC) and acidosis. The key to treatment of hypovolaemic shock is aggressive intravenous fluid therapy. In cases of acute blood loss where haemoglobin is < 6 g.dl−1, transfusion of red blood cells is indicated. Ideally, typed and cross-matched blood should be transfused. However, if the blood type is unknown, type O-negative packed red blood cells should be used [6]. Coagulopathy rarely occurs with placenta praevia; the most common deficit is dilutional thrombocytopaenia. Once fetal demise is suspected, confirmation usually is obtained by sonographic evaluation. The absence of fetal cardiac activity confirms the diagnosis. The parturient should be evaluated for a consumptive coagulopathy, which can result from the release of fetal thromboplastic substances into the maternal circulation. However, coagulopathy typically does not appear until several days after the death of the fetus. We are not aware of any reports concerning anaesthetic management of a parturient with placenta praevia, massive peripartum haemorrhage, hypovolaemic shock and fetal demise. We consider this clinical scenario to be a near miss of the 'cannot resuscitate' situation. Aggressive resuscitation of the haemorrhaging mother and expeditious extraction of the dead fetus and haemorrhaging placenta is the key to optimal outcome. This was presented in part at the Second All Africa Anaesthesia Congress in Durban, South Africa, 25 September 2001.

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