Iatrogenic Pseudoaneurysm-Associated Cerebral Hemorrhage: A Rare Complication of Burr Hole Drainage - A Case Report.

BACKGROUND: Nontraumatic intracranial hemorrhage occurs most commonly due to hypertension and is treated nonoperatively. Iatrogenic pseudoaneurysm from prior neurosurgical therapy represents a rarely described etiology for intracranial hemorrhage that may require emergent surgical therapy. CASE REPORT: An elderly female patient was brought to the emergency department with fatigue but no recent trauma. Subsequent computed tomography of the brain revealed a right-sided intraparenchymal hematoma. Her history included burr hole drainage of a subdural hematoma near the site, so additional imaging was performed and revealed an arteriovenous malformation, later discovered on operative findings to be a pseudoaneurysm, as the cause of the current bleeding episode. Why Should an Emergency Physician Be Aware of This? Awareness of prior neurosurgical treatment, even including minor procedures, in patients with apparent spontaneous intracranial bleeding should prompt angiographic evaluation for arteriovenous malformation. If found, these lesions are more likely to benefit from surgical treatment.

The role of extracorporeal membrane oxygenation in severe pulmonary coccidioidomycosis.

BACKGROUND: Severe coccidioidal pneumonia with acute respiratory distress syndrome (ARDS) is associated with high mortality. Extracorporeal membrane oxygenation (ECMO) has been applied successfully to other severe fungal pneumonia associated with ARDS. We review our experience with the use of ECMO in severe coccidioidal ARDS. OBJECTIVES: To review indications and outcome of ECMO in severe pulmonary coccidioidomycosis. METHODS: Three cases of severe ARDS caused by coccidioidomycosis are presented. All were managed with ECMO. Clinical course, complications, antifungal therapy and outcome are reviewed. RESULTS: Three cases of severe coccidioidal ARDS survived after treatment with ECMO. Common complications included bacterial pneumonia, encephalopathy and critical illness myopathy. They received liposomal amphotericin during ECMO, and transitioned to azole therapy. All required prolonged hospitalization and rehabilitation. CONCLUSIONS: ECMO was life-saving in cases of coccidioidal ARDS. Common complications included pneumonia, encephalopathy and critical illness myopathy. All cases were successfully managed with liposomal amphotericin followed by azole therapy. They required prolonged hospitalization and rehabilitation.

Natural history of compensated and decompensated HCV-related cirrhosis in HIV-infected patients: a prospective multicentre study.

OBJECTIVE: To define the course of HIV-HCV-coinfected patients with compensated and decompensated liver cirrhosis and to investigate the survival and the risk factors for death. PATIENTS AND METHODS: Ninety-two HIV-infected patients with HCV-related cirrhosis (50 of them without and 42 with previous decompensations) were prospectively followed up during a median period of 20 months. Clinical, biochemical, virological and immunological factors were analysed. Multivariate analyses were performed of those factors associated with decompensations and mortality. RESULTS: There were 168 readmissions due to liver-disease-related causes. A Child-Pugh index > or =6 in those without previous decompensations (hazard ratio [HR] 7.94, 95% confidence interval [CI] 1.59-39.58; P = 0.014), and Child-Pugh index > or =9 (HR 2.68, 95% CI 1.13-6.33; P = 0.003) and absence of HAART (HR 0.44, 95% CI 0.19-0.98; P = 0.048) in those with previous decompensations were independently associated with decompensation during the follow up. There were 27 deaths, 22 of them attributable to liver disease. Independent factors associated with liver-related mortality were a Child-Pugh index > or =9 (HR 6.24, 95% CI 2.31-16.85; P < 0.001), progression of Child-Pugh index during the follow up (HR 4.27, 95% CI 1.54-11.80; P = 0.008), more than one decompensation (HR 24.25, 95% CI 7.27-40.45; P < 0.001) and absence of HAART (HR 0.35, 95% CI 0.12-0.98; P = 0.002). CONCLUSIONS: Evolution from compensated to decompensated cirrhosis and death is influenced by markers of liver function and the absence of HAART. The importance of this last element must be adequately stressed.