Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 9  |  Issue : 4  |  Page : 623-625

Severe pre-eclampsia masquerading as peripartum cardiomyopathy in an emergency cesarean section: a challenge to the perioperative physician


Department of Anaesthesiology and Critical Care, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India

Date of Submission22-Feb-2016
Date of Acceptance29-Jul-2016
Date of Web Publication12-Jan-2017

Correspondence Address:
Vishal K Pai
Department of Anaesthesiology and Critical Care, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh 221005
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.198263

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  Abstract 

Peripartum cardiomyopathy (PPCM) is a rare and unusual form of cardiac failure of unknown etiology that is observed in late pregnancy or early postpartum. Although the complete pathogenesis of PPCM is not completely understood, the signs and symptoms are similar to those of left-ventricular heart failure. PPCM is diagnosed in a parturient woman only after other causes of cardiac failure have been ruled out. Its management is similar to that of congestive heart failure. This report describes the role of an anesthesiologist in the postoperative management of a parturient woman who was admitted with severe preeclampsia and developed pulmonary edema and heart failure in the postoperative period necessitating management in the ICU. Subsequently, PPCM was diagnosed and managed successfully. The diagnosis of PPCM is challenging and requires a high index of suspicion by the perioperative physician. Routine medical management in the form of digoxin, diuretics, vasodilators, β-blockers, and anticoagulants should be the first step but may also require vasoactive drugs and circulatory support. Future pregnancies are generally avoided in such patients.

Keywords: emergency cesarean section, peripartum cardiomyopathy, pulmonary edema, severe preeclampsia


How to cite this article:
Pai VK, Dhar M, Singh AP, Kumar AA. Severe pre-eclampsia masquerading as peripartum cardiomyopathy in an emergency cesarean section: a challenge to the perioperative physician. Ain-Shams J Anaesthesiol 2016;9:623-5

How to cite this URL:
Pai VK, Dhar M, Singh AP, Kumar AA. Severe pre-eclampsia masquerading as peripartum cardiomyopathy in an emergency cesarean section: a challenge to the perioperative physician. Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2017 Oct 19];9:623-5. Available from: http://www.asja.eg.net/text.asp?2016/9/4/623/198263


  Introduction Top


Peripartum cardiomyopathy (PPCM) is a rare and unusual form of cardiac failure usually presenting in the last month of pregnancy or in the early puerperium [1]. PPCM presents with features similar to congestive heart failure, which includes fatigue, orthopnea, pulmonary edema, pedal edema, and distended neck veins. Symptoms such as fatigue, dyspnea, and pedal edema are common in late pregnancy, making it difficult to identify patients with PPCM. In addition, pre-eclamptic parturients may present with symptoms of respiratory distress because of capillary leak [2]. In the present report, we describe the role of an anesthesiologist in the postoperative management of a parturient who was admitted with pre-eclampsia with ruptured membranes and leaking per-vaginum with fetal distress, and whose health status quickly declined secondary to fulminant pulmonary edema in the immediate postoperative period. Subsequently, PPCM was diagnosed and was managed successfully in the ICU.


  Case report Top


A 27-year gravida2 female weighing 70 kg presented for the first time at 38 weeks of gestation with ruptured membranes, leaking per-vaginum, and fetal distress for an emergency cesarean section. There were complaints suggestive of bilateral pedal edema, occasional headaches, blurred vision, and increased work intolerance for the past 1 week. She was oriented and responding. Initial vital signs included a blood pressure of 164/97 mmHg, heart rate of 129/min, respiratory rate of 22/min, and an oxygen saturation of 94% at conditions of room air. Airway examination revealed Mallampati class II but was otherwise normal. Physical findings included edema in the lower extremities and bilateral crackles at the lung bases. Dipstick urine analysis revealed 3+ protein. On the basis of these findings, the patient was admitted with a diagnosis of severe pre-eclampsia. A bolus of 4 g of magnesium sulfate was given, followed by 2 g/h intravenous infusion.

Initial laboratory results revealed a white blood cell count of 15.4×103/μl; hemoglobin of 11.1 g/dl, hematocrit 34.3%, platelets 150×103/μl, international normalized ratio of 1.0, prothrombin time of 12.5 s, partial thromboplastin time of 25.4 s, sodium 132 mEq/l, potassium 3.6 mEq/l, chloride 102 mEq/l, bicarbonate 23 mEq/l, creatinine 0.7 mg/dl, glucose 89 mg/dl, magnesium 1.9 mg/dl, aspartate aminotransferase 39 U/l, and alanine aminotransferase 32 U/l. The surgery was conducted under spinal anesthesia using 8 mg of 0.5% bupivacaine and 25 μg fentanyl.

The intraoperative period was uneventful. A total of 1500 ml Ringer’s lactate was infused and the total intraoperative urine output was 75 ml. The patient delivered a healthy male baby weighing 2.75 kg with no other issues. The patient was shifted to the postoperative recovery room where she was monitored for an hour and then shifted to the inpatient ward.

The patient developed respiratory distress and palpitations 3 h later in the ward and was shifted to the high-dependency unit for management. A reference call was sent to the cardiologist and intensivist. On examination, the patient was found to have extensive bilateral crepitations, dyspnea at rest, and decreased urine output. Her blood pressure was 158/88 mmHg, heart rate of 99/min, and SpO2 was 85%. Symptomatic empirical treatment was initiated in the form of loop diuretics and supplemental oxygen. Nitroglycerin infusion was advised by the cardiologist to control the blood pressure. The patient improved clinically after this initial management. Her urine output increased and chest auscultation revealed minimal basal crepitations.

After 2 h, the patient complained of dizziness, nausea, and palpitations. Cardiac markers and bedside Echo were advised. It showed an elevated Brain Natriuretic Peptide (BNP), whereas two-dimensional (2D) Echo revealed a left-ventricular ejection fraction (LVEF) of 15% and left ventricular fractional shortening of less than 30%. The patient was shifted to the ICU where she was given a trial of noninvasive ventilation for 4 h. Infusions of dobutamine and noradrenaline were started to maintain the mean blood pressure around 75 mmHg. Invasive arterial line and central venous line were inserted to guide fluid therapy. Injectable digoxin was given to improve cardiac contractility. Vasoactive drugs were successfully tapered over 24 h. The patient condition improved and she was subsequently discharged on the third day, from the ICU to the inpatient ward. Repeat Echo subsequently revealed improving contractile function, which was near normal at the time of discharge. The patient was advised Angiotensin-converting-enzyme inhibitor (ACE) inhibitor and oral digoxin under cardiology consultation with 4 weekly routine follow-up visits.


  Discussion Top


PPCM is a type of dilated cardiomyopathy associated with left-ventricular systolic dysfunction resulting in the signs and symptoms of congestive cardiac failure. The patient usually presents in the last trimester and diagnosis is usually made in the peripartum period [3]. According to an Indian study, the incidence of PPCM was one case per 1374 live births [4]. The reported incidence in the and Europe has been reported to be one in 4000 deliveries, out of which 60% present within the first 2 months postpartum and 7% in the last trimester of pregnancy.

The diagnostic criteria for PPCM as described include development of congestive cardiac failure secondary to decreased left-ventricular systolic function in the last month of pregnancy or within 5 months after delivery, absence of any pre-existing cardiac dysfunction, absence of a determinable cause for cardiomyopathy, and left-ventricular systolic dysfunction (ejection fraction less than 45% or M-mode fractional shortening less than 30% or both, and end-diastolic dimension more than 2.7 cm/m2) on 2D Echo [5].

PPCM is considered to be a diagnosis of exclusion. Other types of cardiomyopathy and valvulopathy along with causes like pulmonary embolism, myocardial infarction, infections, and other metabolic causes should be ruled out first. Even though the criteria are defined, the diagnosis of PPCM is confounded by symptoms such as dyspnea, fatigue, and pedal edema, which are normally seen in parturients in the last trimester. Furthermore, concomitant existence of pre-eclampsia with basal pulmonary crackles and increasing intolerance to work in the later pregnancy can be misguiding. Symptoms like paroxysmal nocturnal dyspnea, orthopnea, new regurgitant murmurs, and other signs of heart failure should alert the physician [6].

The etiology of PPCM is not clearly known. Numerous associations and predisposing factors have been described, some of which include maternal immune response to fetal antigen, coronary artery abnormalities, pre-eclampsia, diabetes, gestational hypertension, cesarean delivery, nutritional deficiencies, and family history [1].

Our patient had features like increased intolerance to work, mild breathlessness, frequent headaches, visual disturbances, pedal edema, basal crackles, and proteinuria with a high blood pressure. We managed our patient with considerations mainly focused toward pre-eclampsia and did not consider further investigation of the cardiovascular system in view of the emergency and little time at disposal for further evaluation. The surgery was conducted under low-dose spinal anesthesia and as anticipated the patient had stable hemodynamics throughout the intraoperative period.

The management of PPCM must be a multidisciplinary team approach that includes a cardiologist, an obstetrician, an intensivist, an anesthesiologist, and a neonatologist if diagnosed before delivery. The anesthesiologist plays a vital role in providing adequate perioperative analgesia, early recognition of cardiac decompensation in the postoperative period, adequate fluid therapy, and management as a team member in the ICU.

Any patient having features of acute cardiac decompensation in the peripartum period should be evaluated with a chest radiograph, cardiac markers, ECG, 2D echocardiogram, and arterial blood gas analysis [7]. Immediate emphasis should be placed on the management of acute cardiac failure, which includes strict monitoring in the high-dependency unit, propped up position, and supplemental oxygen. Restriction of oral salt and fluid intake and monitoring of input and output should be carried out on hourly basis. Loop diuretics can be used for symptomatic relief and to decrease preload provided there is no hypotension [7].

Most patients do better with this conservative approach; however, patients requiring inotropic support and those with refractory to regular measures should be considered to be shifted to the ICU where they may require intubation or positive pressure ventilation, invasive arterial blood pressure monitoring, vasoactive drugs, and circulatory support. Strict goal-directed fluid therapy should be carried out next. In case of hypertension with cardiac failure, Systemic Vascular Resistance (SVR) can be controlled using nitroglycerin, hydralazine, or nitruprusside. In case of cardiac failure with hypotension, drugs like dopamine, dobutamine, or noradrenaline can be considered. Digoxin can be used for both inotropic and chronotropic effects [7].

Clinical recovery can be considered at relief of symptoms, when all circulatory support drugs have been tapered off. In PPCM patients, recovery of ventricular dysfunction has been defined as an LVEF greater than or equal to 50% or more than 20% improvement, and left ventricular fractional shortening greater than or equal to 30% [7].

PPCM is also associated with a risk for venous thromboembolism and mural thrombus, and therefore prophylactic low molecular weight heparin therapy is indicated in patients with LVEF less than 35% and for bedridden patients with atrial fibrillation, mural thrombi, and obesity. If thromboembolic sequelae or mural thrombus have been identified, full anticoagulation is indicated. Other complications include arrhythmias and myocardial infarction [7]. Recovery usually takes up to 2 months. However, it can take 6–12 months for complete recovery [7]. A 5-year survival rate of 94% of patients with complete recovery of ventricular function has been reported [8]. Therefore, in any suspected case of heart failure, bedside echocardiography has to be performed as soon as possible [9]. Such patients should receive preconception counseling for future pregnancies.


  Conclusion Top


PPCM is a rare and unusual cardiac failure of unknown etiology occurring in late pregnancy or early puerperium. It is a diagnosis of exclusion that requires a high index of suspicion by the anesthesiologist. It should be based on clinical suspicion initially and confirmed with echocardiographic evidence of left-ventricular dysfunction. Routine medical management should be in the form of digoxin, diuretics, vasodilators, and anticoagulants like in case of any other cause of heart failure. Patients with persistent cardiac failure are generally advised against planning future pregnancies.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA 2000; 283:1183–1188.  Back to cited text no. 1
    
2.
Sibai BM, Stella CL. Diagnosis and management of atypical pre-eclampsia-eclampsia. Am J Obstet Gynecol 2009; 200:481.  Back to cited text no. 2
    
3.
Sharma V. Peripartum cardiomyopathy. Cardiol Today 2004; 8:127–129.  Back to cited text no. 3
    
4.
Pandit V, Shetty S, Kumar A, Sagir A. Incidence and outcome of peripartum cardiomyopathy from a tertiary hospital in South India. Trop Doct 2009; 39:168–169.  Back to cited text no. 4
    
5.
Hibbard JU, Lindheimer M, Lang RM. A modified definition for peripartum cardiomyopathy and prognosis based on echocardiography. Obstet Gynecol 1999; 94:311–316.  Back to cited text no. 5
    
6.
Indira K, Sanjeev K, Sunanda G. Sequential combined spinal epidural anaesthesia for caesarean section in peripartum cardiomyopathy. Indian J Anaesth 2007; 51:137.  Back to cited text no. 6
  Medknow Journal  
7.
Bhakta P, Biswas BK, Banerjee B. Peripartum cardiomyopathy: review of the literature. Yonsei Med J 2007 48:731–737.  Back to cited text no. 7
    
8.
Felkar GM, Thompson RE, Hare JM, Hruban RH, Clemetson DE, Howard DL et al. Underlying cause and long term survival in patients with initially unexplained cardiomyopathy. N Engl J Med 2000; 342:1077–1084.  Back to cited text no. 8
    
9.
Dennis AT, Castro JM. Echocardiographic differences between preeclampsia and peripartum cardiomyopathy. Int J Obstet Anesth 2014; 23:260–266  Back to cited text no. 9
    




 

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