Quantitative analyses were performed on paediatric HIDA scans (EHIDA a
nd DLSIDA) to measure the flow rates of HIDA into and out of the liver
. Analysis of the tracer outflow rate indicated that HIDA appeared to
leave the liver even when there was complete biliary obstruction, impl
ying 'leakage' from hepatocytes back into the blood. This potentially
explains why a 'hepatogram' does not provide useful information about
hepatic obstruction, whereas a renogram does yield useful information
about renal outflow obstruction. In a small group of patients with no
evidence of either hepatocellular disease or obstruction, the HIDA inf
low rate into the liver was 0.003072 s(-1), which is similar to publis
hed colloid uptake rates in normal livers. This implies that although
the two radiopharmaceuticals are taken up by different mechanisms, bot
h mechanisms have a very similar extraction fraction. Patients with ci
rrhosis had a considerably reduced HIDA uptake rate (0.001072 s(-1)),
and once again this was similar to colloid uptake from the blood in ci
rrhosis. Patients investigated for neonatal jaundice all showed reduce
d KTDA inflow, and this reduction was greatest (mean 0.000477 s(-1)) i
n those neonates whose jaundice was due to hepatocellular impairment.
In biliary atresia, the HIDA rate was reduced to approximately 0.00104
0 s(-1), which was still considerably higher than the rate from patien
ts with neonatal jaundice due to sufficient hepatocellular impairment
to cause complete cholestasis.