Pius Ochieng

Obstructive sleep apnea and acute respiratory failure: An analysis of mortality risk in patients with pneumonia requiring invasive mechanical ventilation.

PURPOSE Although obstructive sleep apnea (OSA) is common and pneumonia is a frequent cause of acute respiratory failure requiring admission to the intensive care unit, little is known about the effect of OSA on this patient population. This study examined outcomes associated with OSA in patients with pneumonia requiring invasive mechanical ventilation. MATERIALS AND METHODS The Nationwide Inpatient Sample was investigated for discharges with a primary diagnosis of pneumonia requiring invasive mechanical ventilation between 2009 and 2011. Persons aged 18 to 75 years with OSA were compared with patients without OSA. Outcomes included in-hospital mortality and nonroutine discharges. RESULTS Among 74032 hospitalizations, 13.8% (10227) were obese, and 10.3% (7610) had OSA. Obstructive sleep apnea patients had decreased in-hospital mortality (17.0% vs 25.8%; P < .01) and nonroutine discharge (74.4% vs 79.4%; P < .01) when compared with non-OSA patients. In adjusted logistic models, OSA was associated with a 27% decreased risk of in-hospital mortality (odds ratio, 0.73; 95% confidence interval, 0.68-0.79; P < .01) and a 21% decreased risk of nonroutine discharge (odds ratio, 0.79; 95% confidence interval, 0.74-0.84; P < .01). CONCLUSIONS In mechanically ventilated patients with pneumonia, OSA was associated decreased in-hospital mortality and nonroutine discharge. It is possible that differences in treatment pattern may partially explain improved survival.

Rare coexistence of sarcoidosis and lung adenocarcinoma.

Case An eighty year old African-American female was evaluated for cough, chest pain, asymptomatic anemia and 21 pound weight loss over a six month period. Computerized tomography (CT) revealed a spiculated 2.8 cm right upper lobe lung nodule, other smaller nodules and lymphadenopathy. Gallium scan revealed abnormal uptake of radiotracer in lacrimal, hilar and mediastinal glands. Broncho-alveolar lavage showed CD4/CD8 ratio of 2:1 with 15% lymphocytes. Biopsy of right upper lobe lesion and mediastinoscopic lymph node biopsy showed numerous matured uniform non-caseating granulomatous inflammation, however stains and culture for Acid fast bacilli (AFB)/fungal organisms were negative. Patient improved on oral steroids. Six months later she returned with worsening dyspnea and chest X-ray showed bilateral pleural effusions. Thoracocentesis revealed Thyroid transcription factor 1 (TTF1) positive adenocarcinoma cells and Video assisted thoracic surgery (VATS) procedure revealed numerous pleural, pericardial, diaphragmatic metastasis. Biopsy also was positive for TTF1 adenocarcinoma and positive for Epidermal Growth Factor receptor (EGFR) mutation, however negative for Anaplastic Lymphoma Kinase (ALK). Talc pleurodesis was performed. She was treated with erlotinib while steroid was kept on hold. Initial tumor burden decreased but follow-up PET scan six months later showed progression of tumor with lymphadenopathy. After discussion with patient and family, patient opted for hospice care. Discussion Oncocentric theory postulates sarcoidosis as an immunological reaction to dispersal of tumor antigen. Sarcocentric theory postulates that cell-mediated immune abnormalities induced by sarcoidosis in CD4 and CD8 cells is involved in the onset of lung cancer. Thus considerable controversy exists regarding sarcoidosis and malignancy. In our case, TTF1 adenocarcinoma cells from thoracocentesis suggest peripheral nodules in right upper lobe and lingula were likely metastatic, presenting as malignant pleural effusions. However if noncaseating granulomatous inflammation is expected as an immunological reaction to tumor antigen, it is very interesting to observe that initial tissue biopsy of primary right upper lobe mass and mediastinal lymph nodes showed matured uniform non-caseating granulomatous inflammation and no evidence of adenocarcinoma. This being said, it would be highly unlikely for sarcoidosis to progress to lung adenocarcinoma within six months. This adds further controversy to whether granulomatous inflammation is a precursor to future malignancy or whether this elderly African-American female was predisposed to develop granulomatous inflammation in presence of a tumor antigen. One can also speculate whether repeat tissue sampling from right upper lobe mass would have shown granulomatous inflammation or TTF1 adenocarcinoma. Conclusion While evidence is still lacking regarding association between sarcoidosis and lung adenocarcinoma, it is important for clinicians to exclude metastatic malignancy in patients exhibiting clinical and radiographic findings consistent with sarcoidosis.

485: SLEEP IN THE ICU

Crit Care Med 2015 • Volume 43 • Number 12 (Suppl.) early after TBI paralleling increased expression of inflammatory cytokines. Methods: Sprague-Dawley rats (Post Natal Day-17,N=72) were randomized 2:1 to controlled cortical impact vs sham, sacrificed at 3, 12, 24, 72, 168, and 336 hr post TBI, and mRNA was isolated from the ipsilateral hippocampus of each rat. Following a review of the literature, a panel of 36 transporters, biomarkers, and transcription regulators was developed for absolute quantification on the nCounter® Analysis System. Transcript counts over time for TBI rats were compared with sham for fold change with the False Discovery Rate (FDR) to correct for multiple comparisons. Results: At 3, 12, and 24 hr post TBI, 9 transporters showed a decrease in expression and 3 showed increased expression (FDR<0.05). At 72, 168, and 336 hr only 1 transporter had reduced expression, while 6 transporter showed increased expression (FDR<0.05). Slc22a6 had a >10 fold decrease in expression at 12 h (FDR=0.01) and 24 hr (FDR=0.04). Abcb1b had >2 fold decrease in expression at 12 (FDR=0) and 24 hr (FDR=0) post TBI. These were met with changes in transcription factors, including IL-6 with a 93.9 fold increase in expression at 3 hr (FDR=0) and a 7.6 fold increase at 12 h (FDR=0.04). Conclusions: Transporter expression generally decreases early after TBI, and increases in the weeks following. Slc22a6 and Abcb1b showed large changes, suggesting that TBI impairs the ability of the brain to remove xenobiotics and toxic solutes. Brain detoxification and transporter-mediated drug pharmacokinetics may be altered in time dependent manner.