Critical pulmonary valve stenosis in neonates is characterised by severe obstruction to right ventricular outflow, resulting in elevated right ventricular pressures and duct-dependent pulmonary circulation(1). Balloon pulmonary valvotomy has become the preferred treatment, offering effective relief of obstruction while avoiding surgical valvotomy.(2) Although procedural techniques are well established, peri-procedural physiological disturbances can significantly influence valve opening, residual gradients, and early right ventricular adaptation.(3)Anaesthetic management during neonatal valvotomy plays a pivotal role in maintaining favourable valve haemodynamic. Alterations in intrathoracic pressure, oxygenation, and systemic vascular resistance may directly affect pulmonary valve excursion and right ventricular output.(4) Despite this, reports focusing on anaesthetic–valve interactions during neonatal pulmonary valvotomy remain limited. We describe a case that underscores how targeted anaesthetic strategies supported optimal pulmonary valve relief and right ventricular recovery.(5)

CASE REPORT

A 3-day-old term male neonate, born at 37 weeks + 5 days gestation via elective lower segment caesarean section (LSCS) for a previous LSCS and foetal distress history, presented with central cyanosis noted at 69 hours of life. The birth weight was 2.71 kg, with Apgar scores of 8/10 at 1 minute and 9/10 at 5 minutes. Maternal history included a 22-year-old primipara with no consanguinity, O-positive blood group, and negative viral markers. Her obstetric profile was G5 P1 A3 L1, with prior abortions and one healthy child. The antenatal scans were unremarkable, showing normal growth and low-risk screening.

On postnatal day 3, the neonate weighed 2.5 kg and exhibited saturations of 65-70% without pre-post ductal disparity, unresponsive to oxygen trial. Echocardiography revealed a thickened pulmonary valve with an 80 mmHg gradient, trivial pulmonary regurgitation, moderate tricuspid regurgitation, right ventricular systolic pressure of 80 mmHg, mild right ventricular dysfunction, adequate left ventricular function, a small muscular VSD with bidirectional shunt, stretched PFO with right-to-left shunt, stretched patent ductus arteriosus (PDA) with left-to-right shunt, and no coarctation. Prostaglandin E1 (PGE1) infusion at 60 ng/kg/min was initiated, improving saturations to 80%, Baby developed apnoea after infusion and requiring intermittent positive pressure ventilation (IPPV) with a fractional inspired oxygen concentration of (Fio2) 21%, respiratory rate 60 bpm, preductal SpO2 70-77%, and post ductal 65-71%. Intravenous fluids (N/10 with 10% dextrose at 6.7 ml/hr) were administered via a 26G venflon in the left hand.

The plan was to take up the child for urgent balloon pulmonary valvotomy in the catheterization laboratory. Preoperative assessment vitals were heart rate 150/min, respiratory rate 60/min, temperature 36.5°C; with normal physical examination including patent anus/oesophagus, bilateral red reflex, and intact reflexes. The neonate was on intermittent positive pressure ventilation, and we counselled the parents on risks such as arrhythmia, vessel injury, and anaesthetic complications.

The neonate was transported to the catheterization laboratory in a portable IPPV ventilator, maintaining a saturation of 80% with FiO2 of 30% along with a warming blanket, maintaining PGE1, and fluids. In the Cath lab, induction was tailored to avoid further desaturation and it involved the use of ketamine (2mg/kg) and vecuronium (0.1 mg/kg) for muscle relaxation, titrated cautiously given the neonate's immature metabolism, and oral intubation using a 3mm uncuffed endotracheal tube was done maintained with 60% Fio2 (air and oxygen). After intubation the saturation was maintained at 85-88%. Vascular access was challenging in this case; we secured an additional 22 g peripheral line and the femoral vein was cannulated under ultrasound guidance.

The balloon dilatation catheter was passed through the femoral vein, Inferior vena cava, right atrium and right ventricle and pulmonary artery. Prior to procedure and after the procedure right ventricle pressure trace was obtained (Figure 1 a ,1b). Balloon dilatation was done using a 6 x 2 Tyshak balloon (Figure 2 a). During the procedure once the catheter reached the pulmonary artery, and oxygen saturation decreased to 60%, following which the FiO2 was increased to 80% for a brief period until the catheter was disengaged from the pulmonary artery. Post-dilation, gradients reduced markedly, with improved saturation up to 88-90% requiring an FiO2 of 60% (Figure 2 b). The neonate was extubated to CPAP at 10 h postoperatively in NICU, transitioning to room air without distress. Monitoring showed stable urine output, blood pressure, and SpO2; Post procedure echocardiography demonstrated a thickened dysplastic pulmonary valve with mild residual pulmonary stenosis (peak gradient 24 mmHg), mild pulmonary regurgitation, mild to moderate tricuspid regurgitation (tricuspid regurgitation pressure gradient, 35 mmHg), patent foramen ovale with bidirectional but predominantly right-to-left shunt, small muscular ventricular septal defect, good biventricular function, and normal left aortic arch. The patient was discharged on day 5, with stable hemodynamics.

Figure 2A :This fluoroscopic image from the cardiac catheterization laboratory depicts the intra-procedural phase of balloon pulmonary valvotomy. The centrally positioned, curved structure represents the inflated 6x2 Tyshak balloon traversing and dilating the stenotic pulmonary valve, with visible guidewires providing stabilization and access through the right ventricular outflow tract.

Figure 2B : Echocardiogram - A representative echocardiographic image showing the post-procedure assessment of the pulmonary valve, highlighting the thickened dysplastic valve with residual stenosis and associated tricuspid regurgitation. The Doppler waveform illustrates the reduced pressure gradient post-valvotomy, correlating with the reported 24 mmHg peak gradient.

Pulmonary valve stenosis in the neonate represents a dynamic interaction between valve morphology, right ventricular compliance, and transitional circulation.(5) While balloon valvotomy effectively relieves anatomical obstruction, physiological factors surrounding the intervention can significantly influence immediate valve performance and right ventricular recovery(2). Anaesthetic management directly affects pulmonary valve opening through modulation of right ventricular preload and afterload. Positive pressure ventilation and excessive oxygen administration can reduce pulmonary vascular resistance, altering right ventricular–pulmonary artery coupling and transvalvular flow(4). In this case, controlled ventilation and cautious oxygen titration were essential to maintain stable transvalvular flow before and after dilation. Airway management poses another hurdle in the confined space. The intubated neonate on IPPV required seamless transitions during balloon inflation, which transiently worsened hypoxia by obstructing flow. Desaturations up to 60% were anticipated and witnessed which were managed by controlled hand ventilatory bursts and 100% Fi02 pre-emptively; however the cathlab’s remote location from the NICU meant no immediate back up ventilators, forcing reliance on portable units. To obtain ideal view for manoeuvring the catheter, C-arm angulation was constantly mobilized, which threatened the dislodgement of the airway and the intravenous access.(6) The presence of intracardiac shunts further complicates interpretation of oxygenation changes during valvotomy. Transient hypoxaemia during balloon inflation reflected predictable interruption of pulmonary flow rather than procedural failure(1). Anticipating these events allowed avoidance of aggressive ventilatory manoeuvres that could have destabilised right ventricular function. Residual pulmonary regurgitation following valvotomy is common and often reflects improved valve mobility rather than pathological incompetence. Mild residual stenosis with preserved right ventricular function, as observed here, is generally associated with favourable medium-term outcomes(1). Anticipated mechanical complications are important to acknowledge even when the index procedure is uncomplicated.(4,1,7) During catheter and balloon manipulation, transient mechanical obstruction of the right ventricular outflow tract or main pulmonary artery can occur, producing predictable desaturation that typically resolves with prompt balloon deflation/withdrawal and supportive ventilation.(7) Rhythm disturbances (sinus bradycardia, atrial/ventricular ectopy, and rarely sustained arrhythmias) are also described during wire and balloon passage and can acutely worsen systemic output in small neonates.(2,7) More serious but infrequent complications include pulmonary annulus rupture, right ventricular outflow tract or pulmonary artery perforation, pulmonary artery dissection, and subsequent pericardial effusion/tamponade; these events are described in infant series and outcome cohorts of balloon pulmonary valvotomy.(8) Procedures performed in the cardiac catheterisation laboratory also introduce additional considerations, including radiation exposure to neonates and staff, supporting adherence to dose-minimisation principles during fluoroscopic procedures(9). This case reinforces that successful neonatal pulmonary valvotomy depends not only on procedural execution but also on anaesthetic strategies that respect valve physiology and right ventricular adaptation during the transitional neonatal period.

Even when technically uneventful, neonatal balloon pulmonary valvotomy requires anaesthetic management tailored to pulmonary valve physiology. Careful control of ventilation, oxygenation, and preload supports optimal valve opening and right ventricular recovery. Recognition of these anaesthetic–valve interactions may improve consistency of outcomes following neonatal pulmonary valve intervention.

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