Anesthetic management for laparoscopic surgery in a patient with Ebstein's anomaly
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0975-2870.197918
Sir, Ebstein's anomaly (EA) is a rare congenital heart disease, affecting 1/200,000 live births and accounts for <1% of congenital heart diseases.[1] The anomaly consists of downward displacement of the septal and posterior leaflet of tricuspid valve resulting in atrialization of the right ventricle and tricuspid regurgitation. Displacement of septal leaflet creates substrate for accessory conduction pathways resulting in tachyarrythmias. A 25-year-old female, a known case of EA was posted for laparoscopic cholecystectomy. She was hemodynamically stable with no signs of heart failure pansystolic murmur was audible in the tricuspid area. Electrocardiogram (ECG) revealed first-degree heart block. Echocardiogram revealed posterior leaflet displacement by 49 mm and septal leaflet displacement by 18 mm [Figure 1]. There was severe tricuspid regurgitation with small right ventricular (RV) functional cavity and left ventricular ejection fraction was 65%. The right atrium was moderately enlarged with size 4.9 cm. There was no interatrial communication.
She was premedicated with alprazolam 0.25 mg p.o. and intravenous (IV) pantoprazole 40 mg on the night before surgery. Anesthesia monitoring was done with ECG, invasive blood pressure and pulse oximetry. She was sedated with 1 mg midazolam and 100 µg IV fentanyl. Anesthesia was induced with inhalational agent sevoflurane 4% and intubation was facilitated with atracurium. Anesthesia was maintained with oxygen, air and isoflurane on pressure controlled ventilation. Following anesthesia induction, she had one episode of hypotension which was treated with IV 50 µg phenylephrine. Ventilation was adjusted so as to avoid hypercapnia. Carbon dioxide (CO2) was insufflated at the rate of 2 L/min and intrabdominal pressure (IAP) was kept at 10 mmHg. She remained hemodynamically stable throughout the procedure. Total 1.2 L of crystalloid was given. Her postoperative course was uneventful. Pooling of drugs in an enlarged right atrium can result in slow IV induction and delayed response to inotropes.[2] The risk of paradoxical air embolism is high as interatrial communications are invariably present in EA. Insertion of central venous catheter carries the risk of serious arrhythmias and bacterial endocarditis. Hypoxia and hypotension worsen the right to left shunting. Treatment of hypotension with conventional fluid and vasopressors may result in further instability in these patients.[3] Ephedrine a potent beta-agonist can precipitate supraventricular tachycardia. Phenylephrine is preferable as it is a selective alpha agonist. There is 20% incidence of supraventricular tachycardia during general anesthesia induction. Tachycardia is poorly tolerated as it impairs the filling of functionally small volume RV. Esmolol is a short-acting agent and achieves rapid control of heart rate. Pneumoperitonium results in reduction in preload and increase in afterload. The combined effect of anesthesia, head up tilt and pneumoperitonium produces 50% reduction in cardiac index. Exogenous CO2 can provoke dysrhythmias. These hemodynamic fluctuations can be minimized by keeping IAP around 8–10 mmHg and slow insufflation of CO2.[4] Kumar et al. reported a case of prone position induced a reduction in cardiac output and sudden cardiac arrest in a child with EA who had well-preserved cardiac function.[5] We preferred inhalational induction over IV as inhalational route provide more stable hemodynamics and faster recovery.[6] Hence, we conclude irrespective of the severity of the lesion, meticulous monitoring is essential in such patients. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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