What is the Melbourne shunt, when is it indicated in neonates or infants with cyanotic congenital heart disease, and how is it placed and managed?

Melbourne Shunt in Cardiac Surgery

The Melbourne shunt is a central end-to-side aortopulmonary shunt used primarily in neonates and infants with pulmonary atresia, ventricular septal defect (VSD), and major systemic-to-pulmonary collateral arteries (MAPCAs) when central pulmonary arteries are diminutive or hypoplastic.

What is the Melbourne Shunt?

The Melbourne shunt is a surgical palliative procedure that creates a direct connection from the ascending aorta to the main or central pulmonary artery in an end-to-side fashion, specifically designed to promote growth of diminutive central pulmonary arteries as a bridge to eventual complete repair 1.

Key Distinguishing Features:

• Central location: Unlike the modified Blalock-Taussig shunt (which connects a systemic artery to a branch pulmonary artery), the Melbourne shunt connects directly to the central pulmonary arteries
• Growth promotion: Specifically intended to stimulate development and enlargement of hypoplastic central pulmonary arteries
• Staged approach: First step in a multi-stage surgical strategy toward complete repair

Indications

The Melbourne shunt is indicated for:

• Pulmonary atresia with VSD and MAPCAs when central pulmonary arteries are severely diminutive (typically ≤2-3 mm diameter)
• Inadequate native pulmonary artery size that would preclude immediate complete repair or unifocalization procedures
• Goal of pulmonary artery growth to achieve adequate size for eventual complete repair

Surgical Placement

The procedure involves:

• Median sternotomy approach
• Direct anastomosis from the ascending aorta to the main or central pulmonary artery
• End-to-side configuration to maximize flow and growth stimulus
• Typically performed without cardiopulmonary bypass

Expected Outcomes and Growth

Based on the largest reported series 1:

Pulmonary Artery Growth:

• Baseline: Median PA diameter of 2 mm at surgery
• First assessment (median 6.4 months): Median PA diameter increased to 5.5 mm
• Final assessment (median 19.7 months): Median PA diameter reached 7 mm
• Modified Nakata index: Increased from 27 mm²/m² at surgery to 138 mm²/m² at first assessment and 176 mm²/m² at final assessment

Clinical Outcomes:

• Complete repair achieved: 62.5% of patients (25/40)
• Acute shunt failure: 2.5% (1/40 from anastomotic stenosis)
• Need for interventions: 32.5% required percutaneous interventions (21 total procedures in 13 patients)
• Mortality: 10% (4/40) during median follow-up of 68 months

Postoperative Management

Anticoagulation Strategy:

Initiate low-dose aspirin for long-term thromboprophylaxis once bleeding risk has resolved 2. This is a Class I recommendation with Level of Evidence B for polytetrafluoroethylene systemic-to-pulmonary shunts.

Early Postoperative Period:

• Start continuous low-dose heparin infusion when surgical bleeding concerns have resolved (Class IIa, Level of Evidence C) 2
• For high-risk patients (infection, known thrombus, hypercoagulable state): systemic heparinization is recommended (Class IIa, Level of Evidence C) 2

Long-term Management:

• Low-dose aspirin is the recommended therapy for prevention of long-term shunt thrombosis 2
• For sustained high thrombosis risk: consider combined LMWH plus aspirin or clopidogrel (Class IIb, Level of Evidence C) 2

Monitoring Requirements:

• Serial echocardiography to assess pulmonary artery growth
• Cardiac catheterization at approximately 6-month intervals to measure PA dimensions and assess for need for additional interventions
• Monitor for signs of shunt dysfunction: increasing cyanosis, inability to correct hypoxemia with supplemental oxygen

Management of Acute Shunt Thrombosis

If acute shunt thrombosis is suspected, immediate aggressive intervention is life-saving and must include 2:

1. Systemic anticoagulation: IV heparin bolus 50-100 U/kg with ongoing infusion
2. Increase systemic blood pressure: IV phenylephrine or epinephrine to maximize shunt perfusion pressure
3. Optimize oxygen delivery: Intubation, mechanical ventilation, and neuromuscular blockade to minimize oxygen consumption
4. Prepare for rescue interventions: Interventional catheterization, surgical shunt revision, or ECMO should be immediately available

Critical Pitfall:

Avoid tPA for shunt thrombosis outside the catheterization suite—bleeding complications occur in 39% of cases, which is unacceptably high when preparing for potential catheterization, surgery, or ECMO 2.

Subsequent Interventions

Common Requirements:

• All patients in the reported series required pulmonary artery augmentation at time of complete repair 1
• 32.5% required percutaneous interventions for branch PA stenosis or shunt-related issues 1
• Timing of complete repair typically occurs when PA size is adequate (modified Nakata index >150 mm²/m²)

Outcomes After Complete Repair:

• Some patients remain in staged palliation
• Small percentage develop irreversible pulmonary hypertension (10% in reported series) 1
• Occasional need for VSD fenestration after complete repair

Key Clinical Pearls

• The Melbourne shunt is not the same as a modified Blalock-Taussig shunt—it has a central location and different growth-promoting characteristics
• Expect modest but clinically significant PA growth over 6-24 months
• Plan for multiple staged interventions—this is a palliative procedure, not definitive repair
• Maintain high index of suspicion for shunt thrombosis in any infant with increasing cyanosis
• The majority of patients will eventually achieve complete repair, but all require PA augmentation at that time