Modified Blalock-Taussig Shunt (MBTS), immediate post-operative management

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  • To allow standardised management of anticoagulation in patients with a Blalock-Taussig Shunt in PICU
  • Provide evidence base for management of a suspected blocked BT shunt.
  • Provide educational material to assist staff managing a child with a BT shunt in the PICU.


This guideline applies to the immediate post-operative management of any patient with a Blalock-Taussig Shunt in PICU.


All healthcare professionals involved in caring for a post-operative cardiac patient in the PICU should be aware of this guideline.

History & Epidemiology

The Blalock- Taussig shunt (BTS) was first described by Alfred Blalock & Helen Taussig in Baltimore in the 1940s (JAMA 1945; 128:189-202). The Classical BTS was a direct anastomosis of the subclavian artery to the pulmonary artery (PA). This developed into the Modified BT shunt in the 1970’s - Right or Left subclavian artery to branch PA with a Gore-Tex shunt, this is the type of shunt that will be found on the unit today [1-3].

The annual number of BT shunts being performed has fallen over the last 20 years. This is largely due to advancing surgical technique. BT shunts were originally used predominately in the management of Tetralogy of Fallot (TOF), now most TOF go straight to a full repair. BTS however remains an option for infants; particularly those that are unstable at presentation or who have anatomical considerations that prevent early total correction [1-3]. 

Although the overall numbers of BT shunts being inserted has fallen, increasing proportions are being used in the management of the single ventricle patient. This has coincided with an increased length of stay of shunt babies in the ICU. The mean length of stay for an uncomplicated shunt is 3 days [4].

Rationale for use

A BT shunt may be placed in isolation or increasingly may be part of a more complex operation such as the Stage 1 Norwood for the hypoplastic left heart [2,3].

The BT shunt is usually inserted to increase blood to flow to the lungs. The size and length of the shunt in part determine the amount of blood flow to the lungs. If the shunt is too big this may lead to relatively excessive pulmonary blood flow and high saturations described as pulmonary overcirculation. This may reveal itself with oedematous lungs, heart failure and poor systemic perfusion. The current trend would be to place as big a shunt as possible and allow the baby to grow into it, meanwhile managing the circulation with diuretics.

Pitfalls and emergencies

If a shunt is too big this may lead to difficulties when ventilation is weaned. The shunt may occasionally be clipped or taken-down. This may need to be done quickly if low diastolic pressure is compromising the coronary circulation. Pulmonary overcirculation may also present with systemic hypoperfusion. This may be revealed with low blood pressure, low mixed venous saturations and a rising base excess and lactate [1-3, 5-7].

If the shunt is too small the baby will be desaturated and inadequate pulmonary perfusion will lead to hypoxia and poor oxygen delivery to tissues [5-7]. Obviously there needs to be a careful balancing act between pulmonary and systemic perfusion. When a BT shunt is inserted there occurs a dramatic change in physiology from the pre-operative state. The phrase “It’s just a shunt” should be completely banned from the Intensive Care Unit. In the postoperative period attention to detail is required as there can be frequent haemodynamic shifts as the cardiovascular system readjusts [5].

The immediate post operative period is the time where the incidence of shunt failure is highest. This can present acutely with precipitously dropping saturations. Acute shunt failure is usually secondary to the shunt becoming obstructed by a blood clot or kinking. This is an emergency and the management is discussed below [1,5,8]. It is good practice to always auscultate for the presence of a shunt murmur when the patient returns to PICU from theatre

The incidence of shunt thrombosis is reported at 12%.[9] Prevention of clot formation within shunts is controversial. Some studies have suggested that aspirin may reduce rate of shunt thrombosis while others have failed to prove this [9-12]. The use of heparin post-operatively is also controversial, some believe it is unnecessary and may be linked to causation of seromas [10,13]. Shunts done on cardiopulmonary bypass as part of a combined procedure are potentially higher risk of clot following reversal of heparinisation at the end of bypass. 

All shunts have an attrition rate; a study looking at the histopathology of shunts electively taken down found 21% had a 50% stenosis at a median age of 8 months. Smaller shunts were more likely to stenose [3,7]. Many centres anticoagulate. Our current anticoagulation guideline is displayed in the following section.

Post-op Handover & Anticoagulation management

Ongoing anti-coagulant therapy with intravenous heparin should be instituted as soon as is safely possible after theatre. 

The status of the PDA should be detailed in handover (still open, tied off, or already completely closed). Confirm with the Consultant Surgeon at handover that there are no specific reasons to avoid the following standard anticoagulation approach.

Anticoagulation therapy should be managed as noted in the Cardiac Anticoagulation guideline.

Arterial and central lines should be kept in place or replaced if not functioning, for at least the immediate 24 hours post-operatively to aid clinical management. 

Management of a suspected blocked BT Shunt

This is an EMERGENCY


Consider in any patient who has a significant sustained desaturation with a systemic to pulmonary cardiac shunt, or whose saturations drop and whose shunt murmur is no longer audible.

This can be differentiated from Pulmonary over-circulation where you will see a rise in the oxygen saturations and evidence of reduced systemic cardiac output (poor capillary refill, reduced blood pressure, especially diastolic). For help on managing pulmonary overcirculation see section below.

Principles of managment

  • Think shunt!
  • Think could shunt have blocked? Act quickly! 
    • Most likely to occur in a new shunt or in a dehydrated patient known to have a shunt.
    • It is more likely if flow is competing with an open duct (PDA).
  • Check & exclude the respiratory reasons:
    • Displaced ETT position 
    • Obstructed ETT 
    • Pneumothorax
    • Equipment failure
  • Auscultate: – has previous obvious shunt murmur disappeared?
  • Check arterial blood gas: - ?low PaO2, rising lactate, correct acidosis
  • Review most recent APTT.

Management 5,6,15

CALL FOR HELP & call Surgeon, Cardiac Theatre team and Cardiologist

Resuscitate – A,B,C

Request Urgent Echo but do not wait for Echo & surgical team to initiate treatment   


  1. Hand ventilate in appropriate oxygen concentration
  2. Bolus sedation
  3. Bring chest reopening trolley, suction and diathermy units to bedside
  4. Increase SVR – Stepwise
    1. 5ml/kg aliquots of 4% human albumin
    2. Phenylephrine(The dose is 3-10microgram/kg. Dilute 10mg in 50ml 5% glucose and give 0.02-0.05ml/kg as a slow IV injection)
    3. Start or increase adrenaline infusion
    4. Start noradrenaline infusion 0.1mcg/kg/min
  5. Reduce PVR
    1. Sedate and consider paralysis
    2. Hand-ventilate with aim to decrease pCO2 – aim alkalosis.
    3. Oxygenate
    4. Consider bolus magnesium sulphate (0.4mmoll/kg magnesium sulphate 50%)
  6. Anti-coagulate: 
    1. Bolus heparin 50 units/kg IV
    2. Start heparin infusion at 20 units/kg/hr or increase rate by 10% if infusion is running.
  7. Restart prostaglandin in neonate if duct has not been surgically ligated
  8. Consider second bolus of heparin 50 units/kg
  9. Decide for ECMO vs cardiac catheter vs surgical intervention.**

**Cardiac catheter may be useful from a diagnostic and interventional  viewpoint. Echocardiography does not always demonstrate clot, angiography may help if there is doubt regarding diagnosis. Clot destruction via catheter has been demonstrated and may be an option in some specific circumstances.16,19,22 -25

However, if there is any concern regarding surgical repair or a deteriorating child despite above interventions – return to theatre or chest reopening in PICU should not be delayed. Emergent ECMO may be needed to stabilise prior to re-intervention.

Management of pulmonary over-circulation

Think of pulmonary over-circulation in any collapsed BT shunt patient (see section 4) – they will have high oxygen saturations in the lead up to the collapse poor systemic perfusion, rising lactate and falling SvO2 

The management of pulmonary over-circulation can be complex and is dependent on the anatomy and physiology of the underlying lesion. The following is only a beginners’ guide to recognising and managing this difficult problem. Consultant input is essential

If the BT shunt is too big this may lead to relatively excessive pulmonary blood flow and high saturations described as pulmonary over-circulation. This is more common if the ductus arteriosus or other aortopulmonary collateral shunts are still open. It may resolve as the duct closes.

Pulmonary over-circulation may reveal itself in the early post-operative period or become more problematic when ventilation is weaned. Depending on shunt size, small babies less than 3kg are particularly at risk and will need careful monitoring and timely management of pulmonary over-circulation

Diagnostic clues:

  • Relatively high saturations (>88%)
  • CXR- oedematous lungs
  • Low central venous saturations
  • Review NIRS – decreased splanchnic and then cerebral saturations
  • Rising lactate
  • Increase in base deficit
  • Often tachycardic
  • May have relatively low mean blood pressure
  • Widening toe-core temperature gap
  • Signs of right heart failure e.g large liver, ascites (late sign)

Important to review diastolic pressure – if low this may compromise coronary flow: look for signs of ischaemia on ECG - ST depression


Mild form may be treated simply with fluid restriction and diuretics. As this becomes more problematic, manipulation of pulmonary and systemic vascular resistance(PVR and SVR) is required.

If high lactate (>2.5mmol/l) or ECG changes are present then this is an EMERGENCY. Inform PICU Consultant & Consultant Cardiac Surgeon & Consultant Cardiologist.
Repeat Echo and 12-lead ECG. 

  1. Increase PVR
    1. Reduce inspired oxygen concentration
    2. Increase PEEP
    3. Allow pCO2 to rise gently (reduce minute ventilation)

  2. Reduce SVR
    1. Consider reducing vasopressor therapy slowly
    2. Consider vasodilation – eg. Milrinone or SNP (discuss with intensive care consultant)
    3. Overcirculation may also be present in conjunction with a low cardiac output state therefore inotropy may be required.
    4. Avoid inadvertent cooling as will increase SVR - aim to keep the patient warm

  3. Optimise oxygen delivery
    1. Target haematocrit 35 - 45%

It may be important to surgically ligate the PDA if not already undertaken in theatre. One should avoid relying on iv paracetomol for PDA closure in these situations.

The shunt may occasionally need to be clipped or taken-down. This may need to be done quickly if low diastolic pressure is compromising the coronary circulation. 1 2,3,5,5-7

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Editorial Information

Last reviewed: 04 July 2018

Next review: 02 February 2021

Author(s): Mark Davidson

Version: 3.1

Co-Author(s): C Begg, E Peng, A McLean

Approved By: Paediatric & Neonatal Clinical Risk & Effectiveness Committee