Mona Haj1, Don C Rockey1. 1. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Abstract
INTRODUCTION: Ammonia appears to play a major role in the pathophysiology of hepatic encephalopathy (HE), but its role in guiding management is unclear. We aimed to understand the impact of ammonia levels on inpatient HE management, hypothesizing that patients with elevated ammonia levels would receive more aggressive lactulose therapy than patients with normal ammonia or no ammonia level drawn. METHODS: We examined patients with cirrhosis older than 18 years admitted for management of HE from 2005 to 2015. We additionally used propensity matching to control for confounding by the severity of underlying disease. Patients with an ammonia level taken at time of HE diagnosis were further separated into those with normal or elevated ammonia levels. The primary endpoint was the total lactulose (mL) amount (or dose) given in the first 48 hours of HE management. RESULTS: One thousand two hundred two admissions with HE were identified. Ammonia levels were drawn in 551 (46%) patients; 328 patients (60%) had an abnormal ammonia level (>72 μmol/L). There were no significant differences in the Child-Pugh score, MELD, or Charlson Comorbidity Index in those with and without ammonia levels drawn. The average total lactulose dose over 48 hours was 167 and 171 mL in the no ammonia vs ammonia groups, respectively (P = 0.42). The average lactulose dose in patients with an elevated ammonia level was 161 mL, identical to the lactulose dose in patients with a normal ammonia level. There was no correlation between lactulose dose and ammonia level (R = 0.0026). DISCUSSION: Inpatient management of HE with lactulose was not influenced by either the presence or level of ammonia level, suggesting that ammonia levels do not guide therapy in clinical practice.
INTRODUCTION:Ammonia appears to play a major role in the pathophysiology of hepatic encephalopathy (HE), but its role in guiding management is unclear. We aimed to understand the impact of ammonia levels on inpatient HE management, hypothesizing that patients with elevated ammonia levels would receive more aggressive lactulose therapy than patients with normal ammonia or no ammonia level drawn. METHODS: We examined patients with cirrhosis older than 18 years admitted for management of HE from 2005 to 2015. We additionally used propensity matching to control for confounding by the severity of underlying disease. Patients with an ammonia level taken at time of HE diagnosis were further separated into those with normal or elevated ammonia levels. The primary endpoint was the total lactulose (mL) amount (or dose) given in the first 48 hours of HE management. RESULTS: One thousand two hundred two admissions with HE were identified. Ammonia levels were drawn in 551 (46%) patients; 328 patients (60%) had an abnormal ammonia level (>72 μmol/L). There were no significant differences in the Child-Pugh score, MELD, or Charlson Comorbidity Index in those with and without ammonia levels drawn. The average total lactulose dose over 48 hours was 167 and 171 mL in the no ammonia vs ammonia groups, respectively (P = 0.42). The average lactulose dose in patients with an elevated ammonia level was 161 mL, identical to the lactulose dose in patients with a normal ammonia level. There was no correlation between lactulose dose and ammonia level (R = 0.0026). DISCUSSION: Inpatient management of HE with lactulose was not influenced by either the presence or level of ammonia level, suggesting that ammonia levels do not guide therapy in clinical practice.