Secondary Logo

Journal Logo

Correspondence

Heart failure after Caesarean section for twin delivery

Crivellari, M.; Bove, T.; Landoni, G.; Zangrillo, A.

Author Information
European Journal of Anaesthesiology: December 2004 - Volume 21 - Issue 12 - p 986-988

EDITOR:

Pulmonary oedema after delivery represents a rare but life-threatening situation. We present the management and outcome of a patient with heart failure following Caesarean section. Amniotic fluid embolism, eclampsia, peripartum cardiomyopathy and idiopathic cardiomyopathy represented the differential diagnoses.

A 34-yr-old primipara was admitted to our hospital with threat of a premature delivery of twins at 25-week gestational age. A premature birth protocol was initiated with tocolytic therapy. The patient had no history of cardiovascular disease and was on propylthiouracil therapy for hyperthyroidism. Laboratory results showed a haemoglobin value of 9.7 g dL−1. Leucocytes, platelets, electrolytes, renal, liver and thyroid function, vitamin B12 and folic acid were all normal. An autoimmune screening (anti-cardiolipin antibody, anti-beta 2-glycoprotein I antibody, Waaler Rose reaction, lupus like anticoagulants, anti-Thyroid stimulating hormone (TSH) receptor antibody, anti-thyroglobulin antibody, anti-thyroid microsomal antibody) proved negative. Only anti-nuclear factor tested positive.

The patient was scheduled for Caesarean section under spinal anaesthesia due to intra-uterine growth retardation of one twin, peripheral oedema and proteinuria (0.4 g 24 h−1). After Caesarean section, the patient presented signs of acute pulmonary oedema with rapid onset of dyspnoea, tachypnoea, hypertension (220/130 mmHg) and fatigue. She was admitted to the intensive care unit (ICU) with suspected diagnosis of amniotic fluid embolism and pre-eclampsia. She required tracheal intubation and ventilatory support.

A thoracic-abdominal computed tomography excluded embolism. A first bedside echocardiographic examination revealed left ventricular failure with an ejection fraction of 40%. Subsequent echocardiography showed worsening of cardiac function with an ejection fraction <20%. A pulmonary artery catheter and an intra-aortic balloon pump (IABP) were inserted. Laboratory investigations revealed a haemoglobin value of 10.8 g dL−1, leucocyte count of 13.4 × 109 L−1 and normal platelet count. Electrolytes, renal and liver functions were normal. Chest X-ray showed an enlarged heart and pulmonary oedema.

Central venous pressure (CVP), pulmonary artery pressure and pulmonary artery wedge pressure were 15, 27 and 16 mmHg, respectively; cardiac output was 9.0 L min−1 (cardiac index 5.4 L min−1 m−2). A diagnosis of postpartum cardiomyopathy was made and an appropriate treatment instituted. The patient was treated with a continuous infusion of dobutamine 5 μg kg−1 min−1, sodium nitroprusside 0.5 μg kg−1 min−1, nitrates, high dose furosemide, corticosteroids, hydralazine, digoxin, angiotensin-converting enzyme (ACE) inhibitors, low molecular weight heparin and continuous positive airway pressure. Her condition gradually improved, and the IABP was removed after 3 days. She was weaned from mechanical ventilation after 4 days, and transferred to the coronary ICU after 8 days. An echocardiograph showed an ejection fraction of 42%, a left ventricular end diastolic volume of 77 mL and a left ventricular end systolic volume of 45 mL. After 14 days, she was discharged on oral therapy with furosemide, carvedilol, spironolactone, an ACEinhibitor and a decreasing prednisone dose. The discharge echocardiography showed a left ventricular ejection fraction of 45-47%.

Since then the patient has been symptom free, with residual slight fatigue only. Echocardiography after 5 months showed a left ventricular ejection fraction of 47% and her two babies were well after a follow-up of 9 months.

Peripartum cardiomyopathy is a rare and life-threatening disease of unknown aetiology that affects previously healthy women. Incidence ranges from 1 in 1300 to 1 in 15 000 pregnancies and it constitutues <1% of all cardiovascular events related to pregnancy. Although the aetiology of the disease remains unclear [1], many causes have been suggested, including myocarditis, abnormal immune response to the haemodynamic stress of pregnancy and prolonged tocolysis. Risk factors include advanced age (>30 yr), multiparity, black racial origin, twin pregnancy, obesity, chronic hypertension, preeclampsia or eclampsia, alcohol and cocaine abuse, malnutrition, familiarity, puerperal infections and postpartum anaemia [2]. Today, no prophylaxis is known apart from recognising and treating the above-mentioned predictive factors.

Heart failure during the peripartum period was first described in 1849. The first reports, in the last century, are attributed to Ritchie, Virchow and Porak [2]. In 1971, Demakis and colleagues described criteria for its diagnosis, namely the development of heart failure during the last month of pregnancy or within 5 months after delivery, lack of an aetiology for the cardiac failure and absence of heart disease prior to the last month of pregnancy. More recently, echocardiographic evidence of diminished left ventricular systolic function was suggested as a further criterion. Some authors use very strict echocardiographic criteria; for instance, ejection fraction <45%, or M-mode fractional shortening <30%, or both and end-diastolic dimension >2.7 cm m−2[3].

Most patients (78%) present with symptoms during the first 4 months postpartum. Only 9% present in the last month before delivery, and 13% either >1 month antepartum or >4 months postpartum. Clinical signs are those of heart failure, i.e. dyspnoea, cough and orthopnoea. Other common symptoms are haemoptysis, chest pain and abdominal pain. Cardiomegaly, tachycardia and a third heart sound (85%) can be found on physical examination. Frequently, an elevated blood pressure (BP), increased jugular venous pressure, hepato-splenomegaly, peripheral oedema, crackles on lung auscultation, a mitral regurgitation murmur and dysrhythmia are also present [4]. Rarely, a lower extremity arterial thromboembolism may be the initial manifestation of peripartum cardiomyopathy. More frequently this is a later complication. The tendency towards formation of thrombi is probably caused by the hypercoagulation state of late pregnancy, in combination with stasis and turbulent flow in the dilated heart.

Medical treatment of peripartum cardiomyopathy does not differ from that for other forms of congestive heart failure. During pregnancy, it includes digoxin, loop diuretics, sodium restriction, afterload reducing agents, hydralazine and nitrates. After delivery, ACE inhibitors are used. High-dose ACE inhibitor treatment has been associated with a significant decrease in interleukin-6 levels, one of the pro-inflammatory cytokines that may play a role in the genesis of peripartum cardiomyopathy. Due to a high risk for venous and arterial thrombosis, anti-coagulation with heparin should be instituted [1]. The role of immunosuppressive therapy remains ambiguous [2].

Patients who fail to recover may require intensive care, pulmonary artery catheterization, intra-aortic balloon counter-pulsation, and, as an extreme measure, a left ventricular assistance device. Cardiac transplantation should be considered for patients who fail therapy.

Strict bed rest that was advised in early studies may have contributed to the development of deep venous thrombosis and subsequent pulmonary embolism and may in part be an explanation for the high mortality rates in older studies. Since normal pregnancy can cause symptoms similar to heart failure, the New York Heart Association classification may not adequately estimate the severity of the heart failure. Mortality from peripartum cardiomyopathy remains high, about 25-50% [3]. However, compared with patients with idiopathic cardiomyopathy, patients with peripartum cardiomyopathy have a better survival [5]. About half of the patients recover without any complication. Persistence of the disease after 6 months indicates irreversible cardiomyopathy and a worse survival [4]. Causes of death include chronic progressive congestive heart failure, fatal dysrhythmias and thromboembolic complications [2].

In case of persisting left ventricular dysfunction, subsequent pregnancy can be very dangerous and should be discouraged although successful pregnancies, or changes in left ventricular diameter of fractional shortening have been reported [6]. However, recurrence of peripartum cardiomyopathy despite a rapid normalization of heart size and heart function after a previous pregnancy is possible [7]. Women should be informed of that the risk is high.

M. Crivellari

T. Bove

G. Landoni

A. Zangrillo

Department of Cardiovascular Anaesthesia; Vita-Salute University of Milano; IRCCS San Raffaele Hospital; Milano, Italy

Acknowledgements

We are indebted to Tabino Alessandra and Sana Fabiola for their support.

References

1. Ferrero S, Colombo BM, Fenini F, Abbamonte LH, Arena E. Peripartum cardiomyopathy. A review. Minerva Ginecol 2003; 55: 139-158.
2. Ruiz Bailèn M, Lòpez Martinez A, Fierro Rosòn LJ. Miocardiopatia periparto. Med Clin (Barc) 2000; 114: 551-557.
3. Hibbard JU, Lindheimer M, Lang RM. A modified definition for peripartum cardiomyopathy and prognosis based on echocardiography. Obstet Gynecol 1999; 94: 311-316.
4. de Beus E, van Mook WNKA, Ramsay G, Stappers JLM, van der Putten HWHM. Peripartum cardiomyopathy: a condition intensivists should be aware of. Intensive Care Med 2003; 29: 167-174.
5. Felker GM, Thompson RE, Hare JM, et al. Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy. New Engl J Med 2000; 342: 1077-1084.
6. Brown CS, Bertolet BD. Peripartum cardiomyopathy: a comprehensive review. Am J Obstet Gynecol 1998; 178: 409-414.
7. Ceci O, Berardesca C, Caradonna F, Corsano P, Guglielmi R, Nappi L. Recurrent peripartum cardiomyopathy. Eur J Obstet Gynecol Reprod Biol 1998; 76: 29-30.
© 2004 European Academy of Anaesthesiology