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Case Report

Peripartum cardiomyopathy presenting after Caesarean section

Nishikawa, K.; Sato, H.

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European Journal of Anaesthesiology: February 1999 - Volume 16 - Issue 2 - p 130-132


Peripartum cardiomyopathy (PPCM) is defined as the onset of primary myocardial disease without demonstrable cause during the last month of pregnancy or within the first 5 months after delivery [1-6]. It has also been reported that it occurs in less than one in 4000 pregnancies and represents less than 1% of all cardiovascular disease that occurs during pregnancy [2,4]. We report here two cases of PPCM that were observed immediately after Caesarean section under general anaesthesia and spinal anaesthesia, in patients with no preoperative heart disease and cardiomyopathy associated with pregnancy. Anaesthetic management of these two cases will be discussed with a review of past literature.

Case 1

A healthy, 33-year-old female at 39 weeks gestation, 154 cm in height and 75 kg in weight, underwent elective Caesarean section because of cephalopelvic disproportion (CPD) during her first pregnancy. After the induction of general anaesthesia with i.v. thiopentone 300 mg and i.v. suxamethonium 60 mg for muscle relaxation, the patient was intubated and ventilated manually. Anaesthesia was maintained with a mixture of 33% oxygen and nitrous oxide, and a low concentration of sevoflurane (0.5-1%). After delivery, the patient was maintained with intravenously administered pentazocine, 60 mg, and diazepam, 5 mg, and ventilated mechanically after administration of additional vecuronium for muscle relaxation. Shortly after the end of the operation, as slight hypoxia (pH 7.27, PO2 11.2 KPa, Pco2 6.8 KPa, BE 3.1, Spo2 94.6%) was observed, the inspired oxygen concentration was raised to 50%, and mechanical ventilation was continued. A chest X-ray showed marked cardiomegaly (Fig. 1), and concurrent echocardiography also revealed hypokinesis of the left ventricular wall (ejection fraction 0.40). After the extubation, while oxygen 6 L min−1 was being administrated with a mask, blood gas analysis indicated considerable reduction in the hypoxia (pH 7.34, Po2 38.8 KPa, Pco2 5.4 KPa, BE-3.3). However, an echocardiogram confirmed unchanged hypokinetic responses. The patient was immediately transferred to ICU and treated with diuretics and dopamine (5.0 μg kg−1min−1). Fortunately, she gradually responded to these medications, and her cardiac function was improved after 1 week. Neither cardiomegaly nor hypokinesis was observed after recovery (EF 0.68). During these periods, no ischaemic change was observed on the ECG. Therefore, this patient's pathology was diagnosed as PPCM observed following Caesarean section under general anaesthesia.

Fig. 1
Fig. 1:
Chest X-ray of the patient with marked cardiomegaly.

Case 2

A 33-year-old female at the 33rd week of gestation, who had been seen regularly with a diagnosis of toxaemia, underwent emergency Caesarean section because of premature membrane rupture. Her past history included neurosis for which she received medication at age 22. Preoperative examination immediately before surgery showed a slight cardiomegaly, hypoproteinaemia and a strongly positive urinary protein test. While blood pressure and heart rate were carefully monitored, spinal anaesthesia was performed with 2.0 mL of 0.3% dibucaine in order to minimize cardiac depression. Within 5 min, a T6 level of sensory anaesthesia was detected using the pinprick test. During the operation, she received 2000 mL of crystalloid i.v., lost 1860 mL of blood including amniotic fluids and produced 100 mL of urine. Although the blood pressure fell approximately 10 min after the delivery, this responded to intravenous ephedrine in three 8-mg boluses and an increase in the rate of infusion of crystalloid. The operation was completed uneventfully. After the operation, she complained of shortness of breath. Chest radiography showed severe cardiomegaly with congestive shadow covering the entire lung fields with a decrease in cardiac contractility (EF 0.29, Fig. 2). Although her heart failure was immediately treated with administrations of digoxin, frusemide and albumin in the ICU, the echocardiogram showed global hypokinesis during the first post-operative day, but the ECG and echocardiography did not show any signs of pulmonary embolism. Heart failure improved gradually over the next week and she was discharged 3 weeks after the operation.

Fig. 2
Fig. 2:
Chest X-ray of the patient shows evidence of pulmonary oedema with rounding of the cardiac shadow.


A diagnosis of peripartum cardiomyopathy (PPCM) can be made only after excluding other causes of acute heart failure, although it is still controversial whether PPCM does represent a distinct clinical entity [1-5,7] or a subset of dilated cardiomyopathy with initial manifestation during pregnancy [6]. For the following reasons, we strongly suspected that our two cases were PPCM. First, no ischaemic changes were observed on the ECG or changes in enzyme activity. Secondly, chest radiography and blood gas analysis in the ICU did not show any signs of pulmonary embolism. In addition, perioperative echocardiographic findings showed no evidence of amniotic fluid embolism in either case. Thirdly, acute cardiomyopathy was observed shortly after Caesarean section under general anaesthesia and spinal anaesthesia in patients not having heart disease. As has been pointed out [8], a previous paper suggests that anaesthesia may trigger this disease. However, the time courses of recovery in our cases are slower than in the case of congestive heart failure.

It is strongly suggested that pregnancy itself plays an important aetiological role in its occurrence. Pregnancy or delivery itself trigger heart failure. Impaired cardiac function recovers in 50% of patients [1], and it recurs when the patient becomes pregnant again [1,4]. In addition, cross-immunity between uterine and cardiac muscles, the myocardial disorders caused by the production of anti-myocardial antibodies from substances delivered from the fetus may be the mechanism by which peripartum cardiomyopathy is caused [7].

The incidence of peripartum cardiomyopathy is between 1:1300 and 1:4000 live births in the USA, representing less than 1% of cardiovascular problems associated with pregnancy [2,4,5], and has an overall mortality rate of 25-50%. Predisposing factors for this disease include maternal age greater than 30 years, multiparous or eclamptic patients, twinning, racial origin, hypertension and nutritional deficiencies. In the majority of cases, there is no family history.

The differential diagnosis includes non-cardiac causes such as toxaemia (pre-eclampsia), beta2-adrenergic tocolysis, pulmonary embolism, amniotic fluid embolism and aspiration pneumonitis [2-4]. In addition, cardiac causes include valvular disease, myocardial infarction and fluid overload. Clinical examination of this disease may reveal evidence of a raised CVP, cardiomegaly with a gallop rhythm, mitral regurgitation, pulmonary rales and peripheral oedema. Chest radiography may show cardiomegaly with pulmonary oedema and pulmonary venous congestion [9]. The electrocardiogram may show nonspecific ST-T wave changes, atrial or ventricular arrhythmia and conduction defects.

It is possible that cardiodepressant effects of general anaesthesia and excessive fluid infusion can give rise to heart failure in patients without any evident manifestation of heart disease before surgery. At late stages in pregnancy, the circulating blood volume is increased by about 20-30% [3]. Because of this relative volume overload, there are many factors that may cause pregnant patients to develop heart failure. A decision to use regional anaesthesia for surgery in our second patient was made in order to avoid potentially cardio-depressant general anaesthetic agents, and because it was thought that we could then diagnose cardiovascular compromise in the awake patient at an earlier stage. Blood gas analysis and chest radiography could be performed during surgery in an attempt to detect heart failure and other relevant abnormalities. However, it is not unlikely that such heart failure as was observed in our cases might frequently be missed if the patient's condition was not evaluated carefully.

The recommended treatment of this condition follows that of other forms of congestive cardiac failure [2,7]. This includes bed rest, low sodium diet, diuretics, vasodilators, ACE inhibitors and anti-coagulation to counter the risk of endocardial clot formation [2,3]. Digoxin is often added to the above regimen. Prognosis largely depends on the duration and degree of cardiomegaly at presentation and in the following 6 months [10]. Patients with persistent cardiomegaly at 6 months have a reported mortality of 85% at 5 years [1,4].

Choice of monitors will depend on the severity of the pre-existing myocardial disease and degree of symptomatology [11]. If the patient is asymptomatic, non-invasive haemodynamic monitoring can provide a safe, reliable means of following the cardiopulmonary status of the patient. However, it has been reported that an unusual case of peripartum cardiomyopathy presented as a cardiac arrest at induction of anaesthesia for emergency Caesarian section [12]. Therefore, it should be noticed that peripartum cardiomyopathy associated with pregnancy may have lethal complications. Particular care is required by anesthesiologists to prevent complications such as peripartum cardiomyopathy in patients undergoing Caesarean section.


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© 1999 European Academy of Anaesthesiology