Intracranial Hemorrhage in a Cirrhotic Patient: Does Hyponatremia Correction Plays a Role?

Abstract

Purpose: A 58-year-old male with decompensated Laennec's cirrhosis presented with lethargy and fatigue. His liver disease was complicated by ascites, prior spontaneous bacterial peritonitis; esophageal varices; and hepatic encephalopathy. No other medical comorbidities. His last alcohol consumption was 2 years prior to admission. His home medications included spironolactone, ciprofloxacin and rifaximin. Physical exam revealed normal vital signs, jaundice, ascites, lower extremity edema, asterixis and otherwise normal neurologic evaluation. Laboratory data upon presentation revealed platelet count of 68,000, sodium of 113, creatinine 0.6, bilirubin 8.8 and INR 2.12, MELD score 23, Child-Pugh class C. Hyponatremia was medically managed, and sodium rose to 119 within first 24 hours. 48 hours after admission, he developed right side weakness and global aphasia. GCS decreased from 15 to 9. Vital signs had remained normal. Sodium level 48 hours after admission was 129, INR 2.7, PTT 200, fibrinogen 72 and platelet count 43,000. Liver biochemistries remained unchanged, but hemoglobin dropped from 11.7 to 7.5. CT of the head showed a 4.5 × 4.0 × 6.5 cm left temporo-parietal intraparenchymal hemorrhage, with surrounding edema and midline shift. Multiple units of platelets, cryoprecipitate, fresh frozen plasma, recombinant factor VII and red blood cells were administered. However, GCS rapidly deteriorated and intracranial bleeding worsened. No neurosurgical intervention was performed and patient died 48 hours after the initial bleed. Intracerebral hemorrhage (ICH) is a catastrophic and potentially deadly disease. Heavy alcohol intake has also been identified as a major risk factor for ICH. The risk of ICH is increased in cirrhosis from both alcoholic and non-alcoholic etiology. Degree of liver dysfunction appears to correlate with patient outcomes but not with an increased incidence of ICH. This is the first report of an association of hyponatremia correction with ICH. Correction of hyponatremia has been linked to the development of central pontine myelinolysis (CPM). CPM usually occurs in association with alcoholism, malnutrition and liver disease. The temporal association of the hyponatremia correction with the development of ICH suggests a potential causative role for the first one.