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A clinicopathologic study of hepatic dysfunction following shock.
Surgery, Gynecology & Obstetrics
|May 1, 1976
Summary
Profound hypotensive shock causes liver damage, leading to jaundice. Liver repair and regeneration occur, but subsequent bilirubin peaks indicate ongoing hepatic dysfunction, highlighting the need for liver support.
Area of Science:
- Hepatology
- Pathology
- Critical Care Medicine
Background:
- Profound hypotensive shock can lead to multi-organ dysfunction, including the liver.
- Hepatic dysfunction in shock is complex, with various contributing etiologies and patterns of injury.
Purpose of the Study:
- To correlate liver morphology (light and electron microscopy) with clinical and biochemical markers of hepatic dysfunction in patients with hypotensive shock.
- To understand the temporal relationship between shock, hepatocellular damage, jaundice, and liver recovery.
Main Methods:
- Studied nineteen patients with profound hypotensive shock.
- Correlated light and electron microscopic liver findings with clinical and biochemical data.
- Monitored bilirubin levels and liver enzyme patterns over time.
Main Results:
- Hepatocellular damage and jaundice peaked 8-10 days post-shock, correlating with initial shock insult.
- Evidence of liver repair and regeneration was observed, with increased cholestatic enzymes.
- Subsequent bilirubin peaks indicated further hepatocellular dysfunction or overload, influenced by intercurrent conditions like infection.
Conclusions:
- Hypotensive shock induces significant hepatic injury with a characteristic pattern of dysfunction and recovery.
- Intercurrent diseases, especially systemic infections, can delay or impede liver recovery.
- Future development of hepatic support systems may improve patient prognosis, analogous to pulmonary and renal support.