List the causes of postoperative hepatic dysfunction.
Numerous etiologies of hepatic dysfunction
occur post-operatively. It is important to establish the cause quickly and to
initiate therapy as soon as possible. Three major concerns are bilirubin
overload, hepatocellular injury, and cholestasis. A common cause of
postoperative jaundice is a relative overproduction of bilirubin from
hemoglobin. This commonly results from blood transfusion reactions, hematoma
resorption, and hemolysis. Old and damaged stored erythrocytes will break down
and release hemoglo-bin. The liver easily handles small increases in bilirubin;
however, if there is significant pre-existing hepatic disease or large amounts
of blood are transfused, significant increases in unconjugated and conjugated
bilirubin may result even with mild liver impairment secondary to anes-thesia.
Similarly, hematoma resorption may also contribute to postoperative jaundice in
a patient who has significantly bled into a limb, e.g., hip or femur fractures.
Significant hemolysis from blood transfusion reactions can also result in
jaundice. An increase in unconjugated bilirubin without increases in conjugated
bilirubin suggests the presence of Gilbert syndrome, which is present in 7–10%
of otherwise normal patients.
Persistent jaundice following surgery of the
hepatobil-iary tree is usually an indication of retained common bile duct
stones. Trauma to the bile duct during surgery may result in spasm and/or
stenosis. High-dose fentanyl can, on rare occasions, result in sphincter spasm.
The most common abnormalities found on liver
function tests performed postoperatively suggest that parenchymal liver cell
damage is not a dominant feature. The mild degree of liver dysfunction probably
reflects a nonspecific perioperative change in hepatic blood flow. Transient
hepatic oxygen deprivation is common and usu-ally resolves without specific
treatment. Some authorities believe that the minor transient alterations in
liver func-tion tests are in fact manifestations of mild hepatotoxicity of a
potent inhaled agent. Indeed, following exposure to halogenate anesthetics,
transient elevations in liver transaminase levels are common. There are many
reports of minor alterations in liver function tests even when intra-venous
anesthetic techniques are used, and probably reflect the nonspecific
perioperative changes in hepatic blood flow. It should be noted that a “shock
liver” syndrome secondary to prolonged marked hypotension can occur.
In some patients postoperative liver
dysfunction is the result of having pre-existing liver disease that only
becomes evident after surgery. The manifestations of overt disease, which both
the patient and the clinician may have been unaware of preoperatively, may be
precipitated by the detrimental effects of decreased hepatic blood flow on
liver function. Additionally, patients may be in a latent phase of an illness
and postoperative liver dysfunction may be the result of the natural
progression of the pre-existing liver disease.
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