Extracorporeal membrane oxygenation in a patient with stress-induced cardiomyopathy after caesarean section.
We present a case of a young woman who was treated with ECMO for acute heart failure and severe pulmonary oedema that appeared to result from stress-induced cardiomyopathy during the early postpartum period following caesarean delivery.
A 37-year-old Asian female (height 165 cm; weight 72 kg; gravida 4, para 0, miscarriage 3) at 37 weeks gestation underwent caesarean delivery under spinal anaesthesia for failed induction of labour, 34 hours after rupturing her membranes at the primary obstetric clinic. During surgery her vital signs were stable despite requiring intravenous carbetocin 100 [micro]g and sulprostone 500 [micro]g for transient uterine atony. She did not need transfusion of blood components. Approximately two hours after surgery, she suddenly complained of breathlessness and chest heaviness. She developed tachycardia (160 beats/minute), hypotension (74/52 mmHg) and decreased oxygen saturation (84%). She was immediately intubated and transferred to our tertiary referral hospital on an infusion of dopamine (10 [micro]g/kg/minute), dobutamine (20 [micro]g/kg/minute) and noradrenaline (0.3 [micro]g/kg/minute).
The patient's lungs were ventilated with 100% oxygen at a tidal volume of 320 to 340 ml, respiratory rate of 16 to 18 breaths/minute and with positive end-expiratory pressure of 8 cm[H.sub.2]O. An arterial blood gas measurement indicated severe metabolic acidosis and hypoxaemia (pH 7.20, [P.sub.a]C[O.sub.2] 36.1 mmHg, [P.sub.a][O.sub.2] 82.1 mmHg, HC[O.sub.3.sup.-] 4.3 mmol/l, base excess (BE) -12.1, Hb 98 g/l) despite an inspired oxygen fraction (Fi[O.sub.2]) of 1.0. Chest radiography showed diffuse consolidation consistent with pulmonary oedema (Figure 1). ECG revealed T-wave inversion in leads V3-6, II, III, and aVF. Laboratory results were remarkable for elevated cardiac enzymes (troponin T 0.87 ng/ml and creatine phosphokinase MB 7.49 ng/ml). There was no definitive evidence of pulmonary embolism on computed tomography performed three hours after surgery. Echocardiography performed five hours after the surgery showed severe LV systolic dysfunction with apical ballooning, preserved basal function and a LV ejection fraction of 14% (Figure 2). Despite an increasing dose of noradrenaline (0.5 [micro]g/kg/ minute) and increased positive end-expiratory pressure (11 cm[H.sub.2]O), oxygen saturation (84 to 93%), tachycardia (160 to 170 beats/minute) and blood pressure (90/72 to 60/40 mmHg) did not improve.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
At six hours after surgery we decided to use the ECMO device (CAPIOX EBS circuit, Terumo, Japan), based on her uncompensated acute heart failure and inadequate oxygenation. Peripheral femoro-femoral venous-arterial cannulation (Venous Femoral Cannula n 21 and Arterial Femoral Cannula n 17, Medtronic, USA) with distal limb perfusion was performed. To achieve optimal anticoagulation, heparin was initiated immediately after ECMO implantation to reach the target activated clotting time between 150 and 200 seconds. Bypass flow was maintained at 2.5 l/minute for haemodynamic support (cardiac index = 1.6 l/minute/[m.sup.2]) with an Fi[O.sub.2] of 1.0. Following initiation of ECMO her haemodynamic parameters rapidly stabilised and she was gradually weaned from dobutamine and noradrenaline on the first postoperative day. Her oxygenation improved (pH 7.47, [P.sub.a]C[O.sub.2] 26.1 mmHg, [P.sub.a][O.sub.2] 117.1 mmHg, HC[O.sub.3.sup.-] 19.3 mmol/l, BE -2.9, in Fi[O.sub.2] 0.8). There was no active vaginal bleeding and the haematocrit remained above 30% without transfusion. She received conservative medical therapy using an angiotensin-converting enzyme inhibitor, diuretics and beta blockers. She was weaned from ECMO and mechanical ventilation on postoperative days 8 and 10 respectively. She had no respiratory distress or other symptoms of heart failure and the rest of her hospital stay was uneventful.
Heart magnetic resonance imaging and computed tomography coronary angiography performed on postoperative days 17 and 19 showed abnormal wall motion circumferentially to the mid LV, but no significant luminal narrowing in the coronary arteries. She was discharged on postoperative day 22, at which time her ECG showed T-wave inversion in leads V3-4 and a LV ejection fraction of approximately 50%. She remained asymptomatic at six months follow-up, with no regional wall motion abnormalities and an improved LV ejection fraction of 67% without medical therapy.
Stress-induced cardiomyopathy is a reversible cardiomyopathy that mimics acute coronary syndrome and is characterised by chest pain, dyspnoea, ECG changes and minor elevations in serum levels of cardiac enzymes, in the absence of significant coronary artery disease (6). The precise mechanisms are not completely understood, but excessive release of catecholamines, disrupted microcirculation and abnormal myocardial metabolism may contribute to the development of this syndrome (6,7). Generally, the syndrome is more prevalent in postmenopausal women with preceding emotional or physical stress, and forms part of the differential diagnosis in acute coronary syndrome (3,6). However this syndrome has also been reported during uneventful elective surgery performed under regional or general anaesthesia (8,9). In previous cases associated with caesarean delivery (10,11), intravenous ergometrine or treatment of bradycardia and hypotension after spinal anaesthesia with ephedrine and atropine therapy, were considered possible precipitating factors. Caesarean delivery itself is characterised by increased sympathetic tone, so endogenous and exogenous stresses were also considered to be precipitating factors of this cardiomyopathy (10-12). In this case, a previously healthy young woman developed uncompensated acute heart failure and pulmonary oedema in the early postpartum period after caesarean delivery. In a parturient with no history of cardiac disease and no identifiable cause, peripartum cardiomyopathy should also be considered in the differential diagnosis. This is defined as congestive (dilated) heart failure that develops in the last month of pregnancy or the first five months postpartum. Although our case was otherwise consistent with peripartum cardiomyopathy, the patient's echocardiogram showed the typical LV apical ballooning of stress-induced cardiomyopathy, in the presence of normal coronary arteries.
Extracorporeal life support with ECMO was introduced in the early 1950s and was pioneered in the late 1960s outside the operating room, as a bridge to recovery therapy for patients with acute heart failure. Its application has been extended to several other areas, such as for patients with postoperative cardiogenic shock or cardiogenic shock related to acute myocardical infarction, acute myocarditis, and severe, reversible cardiomyopathy. The first successful use of ECMO was reported in 1972 (13). In the present case, we selected ECMO as the treatment of choice because the patient had both uncompensated acute heart failure and respiratory failure, despite inotropic and ventilatory support. Although extracorporeal life support for severe cardiogenic pulmonary oedema induced by stress-induced cardiomyopathy following caesarean delivery has not been previously reported, we found this therapeutic option was effective for ventricular recovery. However, a delicate balance between haemostasis and thrombosis is needed by means of frequent clinical and laboratory monitoring of anticoagulation, especially during the immediate post-caesarean period, because excessive bleeding is the most common reason for premature separation from ECMO (14). In a recent retrospective review of 604 consecutive paediatric ECMO patients, higher heparin dosing was associated with improved survival, even in the case of previous surgery, although larger heparin doses and no previous surgery were associated with increased survival (15).
This case illustrates that extracorporeal life support may be a useful treatment modality in patients with severe stress-induced cardiomyopathy, who need prompt cardiopulmonary support due to a refractory response to inotropic and ventilatory support, even in the early postpartum period.
(1.) Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004; 141:858-865.
(2.) Grawe H, Katoh M, Kuhl HP. Stress cardiomyopathy mimicking acute coronary syndrome: case presentation and review of the literature. Clin Res Cardiol 2006; 95:179-185.
(3.) Wittstein IS, Thiemann DR, Lima JAC, Baughman KL, Schulman SP, Gerstenblith G et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005; 352:539-548.
(4.) Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy--a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008; 5:22-29.
(5.) Bonacchi M, Valente S, Harmelin G, Gensini GF, Sani G. Extracorporeal life support as ultimate strategy for refractory severe cardiogenic shock induced by tako-tsubo cardiomyopathy: a new effective therapeutic option. Artif Organs 2009; 33:866-870.
(6.) Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006; 27:1523-1529.
(7.) Pilgrim TM, Wyss TR. Takotsobo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systemic review. Int J Cardiol 2008; 124:283-292.
(8.) Daly MJ, Dixon LJ. Takotsubo cardiomyopathy in two preoperative patients with pain. Anesth Analg 2010; 110:708-711.
(9.) Littlejohn FC, Syed O, Ornstein E, Connolly ES, Heyer EJ. Takotsubo cardiomyopathy associated with anesthesia: three case reports. Cases J 2008; 1:227.
(10.) Citro R, Pascotto M, Provenza G, Gregorio G, Bossone E. Transient left ventricular ballooning (tako-tsubo cardiomyopathy) soon after intravenous ergonovine injection following caesarean delivery. Int J Cardiol 2010; 138:e31-34.
(11.) Crimi E, Baggish A, Leffert L, Pian-Smith MC, Januzzi JL, Jiang Y. Images in cardiovascular medicine. Acute reversible stress-induced cardiomyopathy associated with cesarean delivery under spinal anesthesia. Circulation 2008; 117:3052-3053.
(12.) Kim SY, Yoon JH, Lee SH. Takotsubo-like severe left ventricular dysfunction after cesarean delivery in a 28-year old woman. Korean Circ J 2011; 41:101-104.
(13.) Bartlett RH. Extracorporeal life support: history and new directions. ASAIO J 2005; 51:487-489.
(14.) Oliver WC. Anticoagulation and coagulation management for ECMO. Semin Cardiothorac Vasc Anesth 2009; 13:154-175.
(15.) Baird CW, Zurakowski D, Robinson B, Gandhi S, Burdis-Koch L, Tamblyn J et al. Anticoagulation and pediatric extracorporeal membrane oxygenation: impact of activated clotting time and heparin dose on survival. Ann Thorac Surg 2007; 83:912-919.
Y. Y. JO *, S. PARK ([dagger]), Y. S. CHOI ([double dagger])
Department of Anaesthesiology and Pain Medicine, Yonsei University College of Medicine, Seodaemun-gu, Seoul, Korea
* M.D., Ph.D., Assistant Professor, Department of Anaesthesiology and Pain Medicine, Gachon University of Medicine and Science Gil Medical Center, Incheon.
([dagger]) M.D., Ph.D., Assiociate Professor, Cardiology Division.
([double dagger]) M.D., Assistant Professor.
Address for correspondence: Dr Y. S. Choi, Department of Anaesthesiology and Pain Medicine, Yonsei University College of Medicine, 134 Shinchondong, Seodaemun-gu, Seoul, 120-752, Korea.
Accepted for publication on April 18, 2011.
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|Author:||Jo, Y.Y.; Park, S.; Choi, Y.S.|
|Publication:||Anaesthesia and Intensive Care|
|Date:||Sep 1, 2011|
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