Pediatric emergency medicine trisk 2087 2087
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Portal hypertension most commonly occurs when there is an obstruction to
normal portal blood flow. The lesion may be prehepatic (i.e., portal vein
thrombosis or splenic vein obstruction), intrahepatic (i.e., cirrhosis from BA,
α1 -antitrypsin deficiency, or cystic fibrosis), or posthepatic (i.e., hepatic vein
thrombosis or tumor). Prehepatic disease in children is most commonly due to
portal vein thrombosis from omphalitis, but may also be related to sepsis,
severe dehydration, or prothrombotic conditions. Globally, schistosomiasis is
a leading cause of portal hypertension due to intrahepatic parasitic disease
causing inflammation, fibrosis, and obstruction. (See Table 91.1 for additional
causes of portal hypertension in children.) Portal hypertension is typically a
clinical diagnosis through recognition of the signs and symptoms of portal
hypertension, such as the development of ascites, GI bleeding, identification
of varices without active bleeding, or splenomegaly. Additional diagnostic
testing such as ultrasound, liver biopsy, or measurement of the portal pressure
gradient would, of course, supplement any new diagnosis.
The effects of portal hypertension are systemic, and complications can
affect every organ system ( Table 91.2 ). The most common complication,
with high morbidity and mortality, is GI hemorrhage from the development of
portosystemic varices (i.e., gastric or EV), or congestive or hemorrhagic
gastritis. (Variceal bleeding is discussed in the Gastrointestinal Bleeding
section of this chapter.) Effects on the circulatory system are complex and
multifactorial, but ultimately result in an increased cardiac output,
hypervolemia, decreased systemic vascular resistance, and hypotension. This
is largely due to an overall decrease in venous and splanchnic arterial tone,
retention of sodium and free water, and subsequent increase in circulatory
volume and venous return. The increase in venous return and decreased
peripheral resistance (mediated by a variety of vasoactive factors such as nitric
oxide) result in an overall increase in cardiac output. These changes in
circulatory physiology contribute to additional complications such as ascites,
hepatorenal, and hepatopulmonary syndrome.
Ascites results from an imbalance in the oncotic and hydrostatic pressures
within the abdominal vasculature. Hydrostatic pressure is increased secondary
to the increased pressure within the draining splanchnic and portal system, as
well as the increased circulating blood volume from factors discussed above.
In addition, there may be a decrease in oncotic pressure as the liver’s synthetic
function deteriorates. Treatment for ascites may include fluid restriction,
diuretic therapy, and albumin administration; however, one must be cognizant
