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[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]
Insights
Hemorrhage in cirrhosis stems from neglected coagulation disorders, not just portal hypertension. Addressing platelet issues and hypercoagulability is crucial for effective treatment.
Area of Science:
- Hepatology and Coagulation Science
- Gastroenterology and Internal Medicine
Context:
- Current cirrhotic hemorrhage management overlooks critical coagulation disorders.
- Portal hypertension is often the sole focus, neglecting underlying hemostatic abnormalities.
Purpose:
- To highlight the central role of coagulation disorders in cirrhotic hemorrhage.
- To propose a shift in management strategies focusing on hemostasis.
Summary:
- Cirrhosis induces chronic hypercoagulability and platelet dysfunction, leading to hemorrhage.
- Lesions like varices or gastritis are triggers, but primary issues lie in coagulation pathways and splenic effects on platelets.
- Acetylsalicylic acid and alcohol exacerbate platelet problems.
Impact:
- Revising treatment protocols to include comprehensive coagulation assessment and management.
- Improving patient outcomes by addressing the root causes of bleeding in liver disease.
- Potential for splenectomy in select cases to restore platelet function.
Abstract:
Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.