Septic shock due to candidemia: outcomes and predictors of shock development.

BACKGROUND: The present report describes the outcomes of a cohort of patients with Candida induced septic shock. METHODS: Retrospective analysis of individuals who had at least one positive blood culture for Candida species ≥ 48 h after ICU admission. Data from patients that developed septic shock within 48 hr of the positive blood culture were compared to non-shock candidemic patients. Patients with a concomitant bacteremia and/or endocarditis were excluded. RESULTS: Fifteen patients with Candida induced septic shock were studied and compared to 35 candidemic patients without shock. Overall mortality was 76% (87 % among those who had shock). A high proportion of non-albicans Candida species causing fungemia (74%) was observed. All patients with shock were receiving antibiotics but not antifungal treatment at the time of shock development, eight were on parenteral nutrition, six on steroids and nine had a cancer history. High dose fluconazole was the most common initial treatment provided. Four patients died before receiving any antifungal treatment. Time in ICU before the development of candidemia was identified as a predictor of shock development (higher chance if fungemia developed < 7 days after ICU admission). CONCLUSIONS: Septic shock due to invasive candidiasis is a near fatal condition. No conventional risk factors were identified to predict shock development other than time (shorter) spent in ICU before the development of candidemia. We encourage clinicians to consider the initiation of appropriate empiric antifungal treatment in high-risk patients who develop septic shock while on antimicrobial treatment. KEYWORDS: Septic shock; Candidemia; Outcome; Predictor.

Unique case of presumed lisinopril-induced hepatotoxicity.

PURPOSE: A case of presumed lisinopril-induced hepatotoxicity is reported. SUMMARY: A 30-year-old woman had complained of fatigue and yellow eyes for two days. Her medical history included hypertension and nephrotic syndrome. Her medications included furosemide 20 mg daily (for almost 6.5 years) and lisinopril 10 mg daily (for eight months). She had been treated with quinapril, enalapril, and lisinopril in the past by different primary care physicians without any adverse effects. She did not abuse alcohol and denied any liver-related problems in the past. Her physical examination revealed icterus and right-upper-quadrant abdominal tenderness. Initial laboratory tests revealed elevated liver enzyme values. Ultrasonography and computed tomography (CT) scans of the patient's abdomen suggested hepatocellular disease with mild hepatomegaly and a normal biliary tract. Due to worsening bilirubin and liver enzyme values, lisinopril was stopped. In the absence of a probable cause of the patient's hepatotoxicity, a CT-guided liver biopsy was performed. Histological examination of the liver tissue showed moderate chronic inflammatory cell infiltrates in the portal area, predominantly composed of lymphocytes with mild-to-moderate interface hepatitis. No centrolobular necrosis or steatosis was seen. After lisinopril was discontinued, there was a rapid improvement in the patient's clinical and biochemical pictures. On her follow-up clinic visit approximately two months later, all of her liver enzyme values had normalized. CONCLUSION: A woman who had received quinapril, enalapril, and lisinopril in the past without apparent adverse effects developed hepatocellular disease that became evident eight months after lisinopril therapy was reinstituted. The presumed hepatotoxicity resolved after discontinuation of lisinopril.

Acute pulmonary edema following pericardiocentesis for cardiac tamponade.

Pericardiocentesis for therapeutic drainage of pericardial fluid may be associated with a variety of complications, including laceration of the right ventricle or coronary artery, arrhythmias, viscus perforation, hypotension, pneumothorax, adult respiratory distress syndrome and death. Hemodynamic derangements such as acute left ventricular failure, pulmonary edema and cardiogenic shock are infrequent and, hence, less well recognized. The present report describes a patient with pericardial effusion and tamponade who developed cardiogenic shock requiring inotropic support shortly following uncomplicated ultrasound-guided pericardial drainage.