Acute CMV infection in the immunocompetent host is usually asymptomatic or produces only mild symptoms. CMV infection in immunocompromized patients, especially transplant recipients and those infected with HIV, is a result of profound lymphopenia or dysfunction of CD4+/CD8+ cells and can cause substantial rates of complication and death. We present a case of CMV infection in a previously healthy man who just had splenectomy for blunt trauma: a short incubation of the CMV disease, a strongly positive CMV antigenemia, severity of the disease including prominent lymphocytosis, massive hepatic sinusoidal infiltration, and retinitis. Splenectomy changed the immunological defense against the virus and brought the infection to nearly fulminant scale.

Case reportFulminant hepatic failure (FHF) is a multisystemic disorder associated with high mortality rates [1]. The causes can be categorized broadly as viral, toxin-mediated, metabolic, autoimmune, ischemic, neoplastic, and idiopathic [2]. Because many FHF deaths result from impaired hepatic regeneration [3] and increased hepatocyte apoptosis [4], an appropriate treatment strategy would consist of medical intervention that either directly promotes hepatic regeneration or negates the effects of circulating inhibitors and prevents apoptosis [3][4][5].Ischemic hepatitis refers to the development of centrilobular hepatic necrosis after a reduction in hepatic blood flow and is associated with a poor prognosis [6]. The high mortality rate of this disorder (about 60%) is related mainly to the underlying disease rather than the hepatitis itself [7]. In the absence of hypoxemia and prolonged shock, congestive heart failure (CHF) alone as a cause of FHF has been reported only in a very few patients [8]. The precise pathogenesis is uncer-N. Assy ( ) Liver Clinic, tain, and it is doubtful whether circulatory hepatic failure is the only cause of fulminant hepatitis, because the alteration in hepatic structure and function is minimal in most cases of CHF [9]. This suggests that other additional factors like increase oxidative stress and endotoxemia are also involved [10,11]. The present case documents the promising role of N-acetylcysteine and ciprofloxacin combination in the treatment of FHF due to ischemic hepatitis.A 56-year-old male in severe respiratory distress with clinical signs of left and right heart failure was admitted to the hospital. The patient reported a history of ischemic heart disease and CHF (EF, 35%) 2 years earlier. He also had diabetes and long-standing hypertension. Two weeks prior to admission he gradually decreased his activity because of severe dyspnea and orthopnea for about 2 weeks. On the second day after admission, acute pulmonary edema had subsided, but jaundice and encephalopathy developed. Physical examination revealed atrial fibrillation ±120/min and blood pressure of 130/90. The sclera was icteric, and the jugular venous pressure was markedly increased (12 cm). Crepitant rales were present in the bases of both lungs. There was a grade 3/6 systolic murmur along the left sternal border. The abdomen was tender in the right upper quadrant, with a 15-cm vertical span of the liver. Hepatojugular reflex was positive (2-cm increase above baseline). Edema of 3 + was noted in both pretibial regions. There were no other stigmata of chronic liver disease. A rectal examination was normal. On neurologic examination, the patient was confused, combative, and unable to communicate or cooperate with the examiners; muscle strength and deep tendon reflexes were normal. An electrocardiogram showed chronic atrial fibrillation. A radiograph of the chest disclosed enlarged heart size with signs of venous congestion and pleural effusion. An abdominal ultrasonogram showed an enlarged Springer

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