Pediatric emergency medicine trisk 2043 2043
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Patients with varices are likely to have portal hypertension, and
therefore are at risk for ascites, spontaneous bacterial peritonitis,
bleeding, and splenomegaly with associated thrombocytopenia and
leukopenia.
Overexpansion of intravascular volume may contribute to
rebleeding.
Patients with portal hypertension are also at risk for bleeding from
congestive gastritis.
Coagulation abnormalities in the setting of active bleeding should be
managed aggressively with IV vitamin K, fresh frozen plasma (FFP),
and platelets. Coagulation abnormalities without active bleeding do
not require FFP or platelets.
Prophylactic antibiotics are part of initial pharmacologic
management. Bleeding varices may be the initial sign of sepsis in
patients with liver disease.
Octreotide is part of initial pharmacologic management with severe
active bleeding due to portal hypertension.
Current Evidence
Upper GI bleeding from EV is a major cause of morbidity and mortality in
patients with underlying liver disease and portal hypertension. Causes of EV
can be seen in Table 91.1 . Varices that develop as a result of portal
hypertension are a type of portal-systemic collateral, which develop secondary
to the abnormally elevated pressure within the portal system and can form in
any area where veins draining the portal venous system are in close
approximation to veins draining into the caval system (i.e., submucosa of the
esophagus, submucosa of the rectum, and anterior abdominal wall). Patients
with EV often have underlying portal hypertension, and their varices may
develop over a few months or after many years. Patients with portal
hypertension are also at risk of GI bleeding from congestive or hemorrhagic
gastritis.
EV are very common in patients with certain types of high-risk underlying
liver disease, particularly biliary atresia (BA) and portal vein thrombosis
where EV have been reported to be present in as many as 70% of patients.
Patients are at increased risk for EV if they have splenomegaly,
