Abstract A 39-year-old male with known alcohol cirrhosis and previous withdrawal seizures presented to the ED for acute renal failure found on outpatient labs, and was found to have ascites. Labs showed neutrophil predominant leukocytosis of 28.3 k/uL, aspartate aminostransferase of 92 U/L, alanine aminostransferase of 28 U/L, and total bilirubin 23.7 mg/dL. Paracentesis resulted in an iatrogenic inferior epigastric artery injury requiring angioembolization. Admission chest x ray (CXR) was grossly normal. He developed hepatic encephalopathy and worsening renal failure resulting in hemodialysis. Overnight on day 3, he developed significant left naris epistaxis and melena, along with worsening dyspnea and hypoxia. Chest computed tomography (CT) showed diffuse bilateral ground glass opacities and consolidations suggesting multifocal pneumonia. On day 5, he was intubated and esophagogastroduodenoscopy was done showing hematin in the stomach and no varices. Bronchoscopy was performed with lavage fluid showing increasingly bloody aliquots indicative of diffuse alveolar hemorrhage (DAH). Fluid characterization revealed 44,000 red blood cells, 725 white blood cells with 77% neutrophils, 6% lymphocytes, and 17% macrophages. Further fluid workup and cultures showed no fungal, bacterial, or acid-fast bacilli growth. Fungitell was normal. Coccidiomycosis, pneumocystis jirovecii, legionella, aspergillus, and cytomegalovirus testing were negative. Anti-neutrophil cytoplasmic antibodies, anti-myeloperoxidase, specificity protein 3, rheumatoid factor, and antinuclear antibody were negative. IgG, IgM, and IgA levels were normal. Serum C3 and C4 complement levels were low. CXR on day 6 showed improvement, which was corroborated by chest CT on day 9. He was treated with 7 days of broad-spectrum antibiotics and anti-fungals and was given intermittent stress dose steroids for shock. He was discharged 16 days after admission to hospice care, where he passed 11 days later. DAH is a severe, life-threatening complication of severe systemic disease, most commonly of autoimmune or infectious origin, and has been rarely reported in alcoholic hepatitis. The etiology of DAH in liver dysfunction has not been formally studied, however a combination of bland hemorrhage with prolonged INR and thrombocytopenia versus capillaritis resulting from overall systemic inflammation is reasonable. It is possible that DAH development in alcoholic hepatitis is avoided by treatment with high dose corticosteroids also acting as prevention for capillaritis mediated DAH. Investigation into etiologies, risk factors, and therapies for DAH in cirrhosis is needed, especially in cases where there is concurrent infection and steroids are to be avoided. DAH should be considered in decompensated cirrhosis with worsening hypoxia and chest imaging findings. This abstract is funded by: None
Tishkoff et al. (Fri,) studied this question.