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of the patient’s functional intravascular volume status. Patients with portal
hypertension are at high risk of infectious complications, such as spontaneous
bacterial peritonitis in patients with ascites. Indeed, an underlying infection is
often the cause for a sudden clinical deterioration.
Hematologic complications are generally, but not completely, related to
splenomegaly, and patients may present with thrombocytopenia, leukopenia,
and anemia. Coagulopathies are often present, but are secondary to the
underlying liver disease and liver failure, as opposed to the portal
hypertension itself. When the patient is not actively bleeding, these
hematologic abnormalities should not be treated aggressively as treatment
may result in hypervolemia and place a patient at higher risk for GI bleeding.
A provider should not attempt to correct thrombocytopenia and anemia to
normal levels. Active and life-threatening bleeding should be treated
aggressively with blood products. The management of GI bleeding and
transfusion parameters are discussed in the GI bleeding section of this chapter.
Pulmonary complications include hepatopulmonary syndrome and
portopulmonary hypertension. Hepatopulmonary syndrome occurs when there
is an increase in the levels of vasoactive agents, causing pulmonary
vasodilation and subsequent ventilation–perfusion mismatch. There is also
likely a degree of venous–arterial shunting within the pulmonary vasculature.
Both can result in hypoxemia. Portopulmonary hypertension may also occur
and likely results from vascular remodeling and endothelial cell dysfunction.
Ultimately, significant pulmonary hypertension may result in right-sided heart
failure.
Renal complications are secondary to the changes in circulatory physiology
described above and may result in hepatorenal syndrome.
Ultimately, portal hypertension is a chronic and complex problem that
requires a multidisciplinary team to manage. Emergency management is
directly related to the presenting complications. The emergency provider must
be familiar with the complex pathophysiology in patients with advanced portal
hypertension as it directly affects the emergency management of conditions