Abstract
Hepatic encephalopathy (HE) is a frequent complication in cirrhotic patients undergoing transjugular intrahepatic portosystemic shunt (TIPS). Hyponatremia (HN) is a known contributing risk factor for the development of HE. Predictive factors, especially the effect of HN, for the development of overt HE within one week of TIPS placement were assessed. A single-center, retrospective chart review of 71 patients with cirrhosis who underwent TIPS creation from 2006–2011 for non-variceal bleeding indications was conducted. Baseline clinical and laboratory characteristics were collected. Factors associated with overt HE within one week were identified, and a multivariate model was constructed. Seventy one patients who underwent 81 TIPS procedures were evaluated. Fifteen patients developed overt HE within one week. Factors predictive of overt HE within one week included pre-TIPS Na, total bilirubin and Model for End-stage Liver Disease (MELD)-Na. The odds ratio for developing HE with pre-TIPS Na <135 mEq/L was 8.6. Among patients with pre-TIPS Na <125 mEq/L, 125–129.9 mEq/L, 130–134.9 mEq/L and ≥135 mEq/L, the incidence of HE within one week was 37.5%, 25%, 25% and 3.4%, respectively. Lower pre-TIPS Na, higher total bilirubin and higher MELD-Na values were associated with the development of overt HE post-TIPS within one week. TIPS in hyponatremic patients should be undertaken with caution.
Highlights
Hepatic encephalopathy (HE) is a frequent complication of liver disease affecting 50%–70% of patients with cirrhosis [1]
The Vascular and Interventional Radiology database of patients undergoing the placement of a transjugular intrahepatic portosystemic shunt (TIPS) between January 2006 and December 2011, at the New York University Langone Medical Center was retrospectively reviewed for patients undergoing the procedure electively for non-variceal bleeding indications
We deliberately excluded variceal bleeding in this study to limit factors outside the TIPS creation influencing the development of early overt hepatic encephalopathy
Summary
Hepatic encephalopathy (HE) is a frequent complication of liver disease affecting 50%–70% of patients with cirrhosis [1]. Defined by the West Haven criteria, HE represents a range of neuropsychiatric abnormalities, from mildly abnormal psychometric testing, to severe neurologic dysfunction, in which asterixis, impaired cognition, lethargy and coma are present [2]. These latter grades have been termed overt HE. The most important contributor is the presence of an elevated serum ammonia level due to impaired hepatic function and portosystemic shunting. Hyperammonemia leads to HE by altering the osmotic gradient within astrocytes, changing intracellular glutamine-glutamate metabolism, decreasing cerebral blood flow and cerebral oxygen metabolism [3,4,5]. Elevated serum ammonia leads to the conversion and accumulation of glutamine from glutamate. An active organic osmolyte, leads to astrocytic edema and impairs neurotransmission [6,7]
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