Anesthetic management for caesarean section in a case of peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) is a disease of unknown etiology which affects pregnant females during late pregnancy or during the first 5 months post-partum. The clinical presentation of these patients is similar to that of patients with dilated cardiomyopathy. Anesthetic management of such cases poses a challenge; due to the increased risk of various perioperative complications. We report the successful anesthetic management of lower segment caesarean section in a patient with PPCM.

INTRODUCTION

Peripartum cardiomyopathy (PPCM) is a rare life threatening clinical entity of unknown etiology. The definition includes four criteria:[1]

Development of cardiac failure in the last month of pregnancy or within 5months of delivery.

Absence of any identifiable cause for the cardiac failure.

Absence of recognizable heart disease prior to the last month of pregnancy.

Left ventricular systolic dysfunction demonstrated by echocardiography (ejection fraction <45%, reduced fractional shortening).

Potential risk factors include multiparity, advanced maternal age, multifetal pregnancy, pre-eclampsia, gestational hypertension and women of African ethnicity.[2]

Symptoms of PPCM-fatigue, edema and dyspnea are similar to the normal spectrum of peripartum state and pregnancy co morbidities such as pregnancy induced hypertension[3] often leading to delayed diagnosis.

We report a patient with PPCM requiring lower segment caesarean section (LSCS) that was managed with epidural anesthesia.

CASE REPORT

A 32-year-old multigravida with a 36 weeks twin pregnancy was scheduled for an elective LSCS. Her obstetric history regarding previous pregnancies and deliveries was unremarkable. Since past four weeks she complained of progressively worsening fatigue and dyspnea on exertion. A cardiology consultation led to the diagnosis of PPCM. Management was started with digoxin, frusemide and potassium supplementation.

2D echocardiography showed left atrial and left ventricular dilation, global left ventricular hypokinesia and ejection fraction of 16-20% along with trace aortic and mitral regurgitation. ECG tracing showed sinus tachycardia with non-specific ST-T wave abnormalities. Blood investigations were within normal limits.

Pre-operatively the patient required a 15° head up position while supine. She was pale, tachypneic with respiratory rate 20-25 breaths per minute. On auscultation, lungs were clear. Her airway was Mallampati grade II. The patient's baseline blood pressure (BP) and heart rate were 100/70 mmHg and 116/minute, respectively.

Intra operative monitoring included continuous ECG, non-invasive blood pressure (NIBP), blood oxygen saturation (SpO2). In addition to a wide bore peripheral venous cannula, central venous access was secured under local anesthesia in the right internal jugular vein using a double lumen catheter, to monitor central venous pressure (CVP).

Epidural anesthesia was planned in order to avoid sudden hemodynamic variations associated with subarachnoid block. About 200mlof lactated Ringer's solution was infused before epidural catheter insertion.

Epidural catheter was inserted at L2-3 level through an 18 gauge Tuohy needle and fixed at 11 cm. Test dose of 2 ml of 2% lignocaine without adrenaline was administered. This was followed by 12 ml of 0.75% ropivacaine in small increments of 4 ml to avoid hemodynamic instability. After ensuring adequacy of the block up to T6dermatomal level, the surgery was performed. Immediately after epidural drug administration, the patient's BP dropped to 80/50 mmHg. Inj. dopamine infusion was started at the rate of 5 mcg/kg/min. Subsequently BP from 100/60 to 110/70 mmHg was maintained through out the surgery. Heart rate was maintained between 110/minute and 120/minute. The CVP was maintained at 10-12 mmHg.

Ten international units of drug oxytocin to facilitate uterine contraction was infused slowly after delivery of the twin babies. A total of 800mlof lactated Ringer's solution was administered (including the 200 ml administered before anesthesia).

Post-operatively, the patient was monitored in the intensive care unit (ICU). A chest radiograph done in the immediate post-operative period revealed cardiomegaly and increased vascular congestion bilaterally [Figure 1].

Figure 1

X-ray chest P. A. view in post-operative period

Dopamine infusion was continued and gradually tapered and stopped over the next 24 hours. Post-operative analgesia was maintained through continuous epidural infusion of 0.125% ropivacaine with 2 mcg/ml fentanyl at the rate 5 ml/hour. She was discharged a week later after uneventful recovery.

DISCUSSION

PPCM is a diagnosis of exclusion and our case fulfilled all the diagnostic criteria. Treatment of PPCM is similar to other types of congestive heart failure. The mainstay of therapy is a combination of digoxin, diuretics, sodium restriction, anticoagulation and beta blockers.[4] The cardiology consult did not include thromboprophylaxis in the treatment of this patient.

There are different opinions regarding optimal method of anesthesia for LSCS in PPCM. Regardless of the anesthetic technique, hemodynamic goals include avoidance of sudden variation in heart rate and blood pressure.

General anesthesia involves the use of cardio depressant drugs like thiopentone, narcotics and/or inhalational agents. The use of opioid based induction may necessitate post-operative ventilation for both mother and new born. Performing a rapid sequence induction on a patient with compromised cardiac function can be extremely challenging. Thus, a carefully administered regional anesthetic is advantageous. In addition to avoiding the stress of laryngoscopy and intubation, the vasodilatation produced by regional anesthesia is beneficial with isolated left ventricular dysfunction.[5]

We chose epidural anesthesia as it permits gradual and controlled induction with minimal variation in hemodynamic parameters when accompanied by judicious administration of intravenous fluids and inotropes.[6] 0.75% ropivacaine was selected as it is long acting, gives surgical anesthesia of good quality with early recovery from motor blockade.[7] It also has a favorable cardiotoxic and neurotoxic profile compared to bupivacaine.[7] We did not use adrenaline in the test dose as there is increasing evidence that the practice of using high concentration lignocaine and adrenaline as test dose is neither sensitive nor specific to detect intravascular or intrathecal catheter misplacement.[8]

Intra operative monitoring included CVP with double lumen catheter in the right internal jugular vein and NIBP monitoring. Previously, successful outcome using only non-invasive monitoring has been reported.[9] We used dopamine throughout the surgery and gradually tapered and stopped it over twenty four hours post-operatively. Its positive inotropic, chronotropic and vasoconstrictive effects make it suitable for management of adverse cardiovascular effects of anesthesia.[10] Oxytocin after delivery was administered intravenously as a slow infusion to prevent sudden vasodilatation causing hypotension and tachycardia.

Post-operative period is crucial in PPCM as re absorption of third space fluid after 48 hours of LSCS may increase preload causing congestive cardiac failure. Epidural infusion of 0.125% ropivacaine with 2 mcg/ml fentanyl was continued for post-operative analgesia; to avoid post-operative pain associated hemodynamic variations

To conclude, in developing nations, where not all parturients undergo regular antenatal checkups, high degree of clinical suspicion is important for early diagnosis and anesthetic management of PPCM thereby increasing chances of successful patient outcome. Titrated epidural anesthesia with judicious fluid and inotropic support is a prudent choice in such cases.