Anaesthetic management of a patient with isolated pulmonary stenosis posted for caesarean section.

Cardio circulatory changes associated with pregnancy result in a significant haemodynamic burden and lead to morbidity and even mortality in women with cardiac disease. We report a rare case of severe pulmonary stenosis who underwent elective caesarean section under general anaesthesia with satisfactory maternal and neonatal outcome.

INTRODUCTION

Pulmonary stenosis refers to a dynamic or fixed anatomic obstruction to flow from the right ventricle to the pulmonary arterial vasculature.[1] Although most commonly diagnosed and treated in the paediatric population, individuals with complex congenital heart disease and more severe forms of isolated pulmonary stenosis are surviving into adulthood and require ongoing assessment and cardiovascular care.[23] Considering the rarity, the optimal anaesthetic management is either controversial or inconclusive.

CASE REPORT

A 28 year-old, 55-kg female, 3rd gravida with 38 weeks 3 days of pregnancy was admitted for safe confinement. She had history of breathlessness on mild exertion, otherwise well adjusted to normal course of life. There was no evidence of right heart failure.

On pre-anaesthetic examination, she was found to be comfortable lying on the bed with a heart rate of 80/min, baseline pressure 120/80 mmHg, respiratory rate 14/min and New York Heart Association class 1. On inspection, precordial heave was present; on auscultation, chest was clear with normal S1 and a widely split S2, with a soft and delayed P2 and a systolic crescendo–decrescendo ejection murmur in the left upper sternal border.

Her investigations revealed Hb of 11.4 g% and serum creatinine 0.7 mg. The electrocardiogram (ECG) showed sinus rhythm with right axis deviation, a dominant R wave in aVR and a prominent R wave (20 mm) in V1. An echocardiography demonstrated congenital heart disease, severe valvular pulmonary stenosis gradient of 68 mmHg, right atrium and right ventricle dilated, normal biventricular function, no Patent Ductus Arteriosus and no coarctation of aorta. Plain chest radiograph showed prominence of pulmonary artery, with right atrial and ventricular dilatation.

She received prophylactic antibiotics, ranitidine, ondansetron and metoclopramide intravenously (IV) in the pre-induction room. In the operating room, routine monitors (ECG, pulse oxymeter) were attached. Invasive blood pressure and central venous line were secured. A 15° wedge was given for left uterine displacement. She was premedicated with glycopyrrolate 0.005 mg/kg body weight IV and pre-oxygenated with 100% O2 for 3 min. Lignocaine 2% 1.5 mg/kg body weight IV was administered. Rapid sequence induction was performed with thiopentone 5 mg/kg body weight IV and succinylcholine 1.5 mg/kg body weight IV. The patient was intubated with a 7.5 mm-sized oral cuffed endotracheal tube and ventilated on volume control mode with a tidal volume of 10 mL/kg. The respiratory rate was adjusted according to EtCO2 of 30 cmH2O. Anaesthesia was maintained with oxygen/air mixture at 50:50, isoflurane in concentrations of 0.4–0.6% and vecuronium 0.1 mg/kg body weight IV loading dose, with top-ups accordingly. After delivery of the baby, syntocinon 10 units in infusion was started. Fentanyl 2 μg/kg body weight IV and midazolam 0.05 mg/kg body weight IV was given. Before reversal, a 20 G epidural catheter was inserted at the L3–L4 space using a 18 G Tuohy needle by loss of resistance to air technique. One hundred and fifty micrograms of inj buprenorphine in 10 mL of normal saline was injected via an epidural catheter. She was reversed with glycopyrrolate 0.01 mg/kg body weight IV and neostigmine 0.05 mg/kg body weight IV and extubated after thorough suctioning. She was shifted to the post-anesthesia care unit and observed for 3 h. Intra-operatively, a total of 1 L of crystalloids was infused. Urine output at the end of surgery was 300 mL. The estimated blood loss was 500 mL. Pulse rate ranged between 90 and 110/min and blood pressure between 120/80 and 140/90 mmHg. A male baby weighing 2.8 kg was delivered with APGAR score of 6 and 10 at 1 and 5 min. Post-operatively, she was continued on supplemental oxygen at 4 L/min through a venti-mask. Dextrose Normal Saline was started at a rate of 70 mL/h. Inj buprenorphine 150 μg in 8–10 mL of normal saline was administered via an epidural catheter every 8th hourly for analgesia. Her further course in the hospital was uneventful.

DISCUSSION

Pulmonary stenosis is a common form of congenital heart disease that occasionally is diagnosed for the first time in adulthood. Isolated valvular pulmonary stenosis comprises approximately 10% of all congenital heart diseases.[4] Many of these patients remain asymptomatic to adult life.[56] Except for critical stenosis in neonates, survival is the rule in congenital pulmonary stenosis. A slight female predominance exists.[1]

Anaesthetic management of patients with severe pulmonary stenosis requires understanding of its physiological adaptations and also the events and drugs that can alter the magnitude of right ventricular outflow.

Pulmonary stenosis increases right ventricular work and dramatically impairs left ventricular output. It is important to maintain right ventricular filling pressure to optimize myocardial contractility. Also, excessive fluid can precipitate acute right heart failure and atrial arrhythmias.[7] During pregnancy, preload may decrease due to aortocaval compression, also by reduced forward flow, which can be further precipitated by neuraxial sympathetic blockade. Hence, avoiding activation of epidural intra-operatively and also by using buprenorphine, local anaesthetics were avoided, which can decrease the preload excessively.

The goals of haemodynamic management are maintenance of right ventricular preload, left ventricular afterload and right ventricular contractility[7] and also avoiding further increase in pulmonary vascular resistance. The goals of anaesthetic management are to reduce pulmonary vascular resistance and systemic vascular resistance. In general, hypothermia, hypercarbia, acidosis, hypoxia and high ventilator pressures should be avoided.[7] Our parturient did not have any signs of right heart failure and no other associated medical illness. The goals of anaesthetic management were met by giving intravenous induction drugs in titrated doses and slowly. Invasive monitoring could be avoided.

The cardiovascular changes associated with labour and vaginal delivery, including a further increase in cardiac output and oxygen consumption and Valsalva manoeuvres, were thought to be too hazardous to attempt induction of labour. Considering these factors, general anaesthesia was chosen. Both the inhalational and the narcotic-based induction were avoided in view of slow induction, neonatal depression and maternal myocardial depression. Nitrous oxide may increase pulmonary vascular resistance; hence, it was avoided. Stress response to induction was decreased by giving xylocard 2% 1.5 mg/kg body weight IV. Systemic vascular resistance was kept low by fentanyl. Normocarbia was maintained by adjusting the respiratory rate according to EtCO2 levels.

CONCLUSION

Pulmonary stenosis can worsen during labour and delivery, resulting in high maternal mortality. Spinal anaesthesia may be associated with an uncontrolled reduction in right ventricular preload and should therefore be avoided in severe cases. Epidural anaesthesia again can result in episodes of hypotension, which is not acceptable. General anaesthesia offers a safe approach for fluid management. Although no conclusions can be drawn from this single case report, it is demonstrated that in selected cases, caesarean section can be performed safely under general anaesthesia.