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Wessex
Cardiothoracic Unit and Department of Nuclear Medicine, Southampton
University Hospital NHS Trust, Southampton, UK
Correspondence to: Dr AP Salmon, Wessex Cardiothoracic Centre, Southampton General Hospital, Tremona Road, Southampton SO16 6YD
Accepted 20 October
1999
OBJECTIVE
To evaluate the extent of
intrapulmonary right to left shunting in children after
bidirectional cavopulmonary anastomosis (BCPA).
DESIGNProspective
study of patients who underwent BCPA in a single centre.
PATIENTS17
patients with complex cyanotic congenital cardiac malformations who
underwent BCPA at 1-45 months of age (median 21 months) were evaluated
15-64 months postoperatively (median 32 months). Five children between
1 and 10 years (median 5 years) with normal or surgically corrected
intracardiac anatomy and peripheral pulmonary circulation who required
V/Q scanning for other reasons were used as controls.
INTERVENTIONSAll
patients underwent cardiac catheterisation to exclude angiographically
demonstrable venovenous collaterals followed by pulmonary perfusion
scanning using 99mtechnetium (99mTc) labelled
albumen microspheres to quantify the intrapulmonary right to left shunt.
MAIN OUTCOME
MEASUREPercentage of intrapulmonary right to
left shunt.
RESULTSThe mean
(SD) level of physiological right to left shunting found in the control
group was 5.4 (2.3)%. All patients with BCPA showed the presence of a
significantly higher level of intrapulmonary shunting (26.8 (16.9)%,
p < 0.001). The degree of shunting was significantly increased in
the subgroup of 11 patients with BCPA as the only source of pulmonary
blood flow (34.9 (15.8)%), when compared to the six remaining patients
with an additional source of pulmonary blood supply (12.0 (2.6)%,
p < 0.001). There was a negative correlation between age at BCPA and
the shunt percentage found in the patients with a competitive source of
pulmonary blood flow (r = 
0.63,
p < 0.01).
CONCLUSIONSIntrapulmonary
right to left shunting develops in all patients following BCPA. This
may be caused by a sustained and inappropriate vasodilatation resulting
from absence or decreased levels of a substance that inhibits pulmonary
vasodilatation. Augmenting BCPA with an additional source of blood flow
containing hepatic factor limits the degree of intrapulmonary
arteriovenous shunting and may help provide successful longer term palliation.
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