Jacqueline Urtecho

Association between hyperoxia and mortality after stroke: a multicenter cohort study.

Objective:To test the hypothesis that hyperoxia was associated with higher in-hospital mortality in ventilated stroke patients admitted to the ICU. Design:Retrospective multicenter cohort study. Setting:Primary admissions of ventilated stroke patients with acute ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage who had arterial blood gases within 24 hours of admission to the ICU at 84 U.S. ICUs between 2003 and 2008. Patients were divided into three exposure groups: hyperoxia was defined as PaO2 ≥300 mm Hg (39.99 kPa), hypoxia as any PaO2<60 mm Hg (7.99 kPa) or PaO2/FiO2 ratio ⩽300, and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital mortality. Participants:Two thousand eight hundred ninety-four patients. Methods:Patients were divided into three exposure groups: hyperoxia was defined as PaO2 more than or equal to 300 mm Hg (39.99 kPa), hypoxia as any PaO2 less than 60 mm Hg (7.99 kPa) or PaO2/FIO2 ratio less than or equal to 300, and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital mortality. Interventions:Exposure to hyperoxia. Results:Over the 5-year period, we identified 554 ventilated patients with acute ischemic stroke (19%), 936 ventilated patients with subarachnoid hemorrhage (32%), and 1,404 ventilated patients with intracerebral hemorrhage (49%) of whom 1,084 (38%) were normoxic, 1,316 (46%) were hypoxic, and 450 (16%) were hyperoxic. Mortality was higher in the hyperoxia group as compared with normoxia (crude odds ratio 1.7 [95% CI 1.3-2.1]; p < 0.0001) and hypoxia groups (crude odds ratio, 1.3 [95% CI, 1.1–1.7]; p < 0.01). In a multivariable analysis adjusted for admission diagnosis, other potential confounders, the probability of being exposed to hyperoxia, and hospital-specific effects, exposure to hyperoxia was independently associated with in-hospital mortality (adjusted odds ratio, 1.2 [95% CI, 1.04–1.5]). Conclusion:In ventilated stroke patients admitted to the ICU, arterial hyperoxia was independently associated with in-hospital death as compared with either normoxia or hypoxia. These data underscore the need for studies of controlled reoxygenation in ventilated critically ill stroke populations. In the absence of results from clinical trials, unnecessary oxygen delivery should be avoided in ventilated stroke patients.

Significance of arterial hyperoxia and relationship with case fatality in traumatic brain injury: a multicentre cohort study

Objective In this retrospective multi-centre cohort study, we tested the hypothesis that hyperoxia was not associated with higher in-hospital case fatality in ventilated traumatic brain injury (TBI) patients admitted to the intensive care unit (ICU). Methods Admissions of ventilated TBI patients who had arterial blood gases within 24 h of admission to the ICU at 61 US hospitals between 2003 and 2008 were identified. Hyperoxia was defined as PaO2 ≥300 mm Hg (39.99 kPa), hypoxia as any PaO2 <60 mm Hg (7.99 kPa) or PaO2/FiO2 ratio ≤300 and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital case fatality. Results Over the 5-year period, we identified 1212 ventilated TBI patients, of whom 403 (33%) were normoxic, 553 (46%) were hypoxic and 256 (21%) were hyperoxic. The case-fatality was higher in the hypoxia group (224/553 [41%], crude OR 2.3, 95% CI 1.7-3.0, p<.0001) followed by hyperoxia (80/256 [32%], crude OR 1.5, 95% CI 1.1-2.5, p=.01) as compared to normoxia (87/403 [23%]). In a multivariate analysis adjusted for other potential confounders, the probability of being exposed to hyperoxia and hospital-specific characteristics, exposure to hyperoxia was independently associated with higher in-hospital case fatality adjusted OR 1.5, 95% CI 1.02-2.4, p=0.04. Conclusions In ventilated TBI patients admitted to the ICU, arterial hyperoxia was independently associated with higher in-hospital case fatality. In the absence of results from clinical trials, unnecessary oxygen delivery should be avoided in critically ill ventilated TBI patients.

Hospital mortality in primary admissions of septic patients with status epilepticus in the United States

Objective:To determine the prevalence of status epilepticus, associated factors, and relationship with in-hospital mortality in primary admissions of septic patients in the United States. Design:Cross-sectional study. Setting:Primary admissions of adult patients more than 18 years old with a diagnosis of sepsis and status epilepticus from 1988 to 2008 identified through the Nationwide Inpatient Sample. Participants:A total of 7,669,125 primary admissions of patients with sepsis. Interventions:None. Results:During the 21-year study period, the prevalence of status epilepticus in primary admissions of septic patients increased from 0.1% in 1988 to 0.2% in 2008 (p < 0.001). Status epilepticus was also more common among later years, younger admissions, female gender, Black race, rural hospital admissions, and in those patients with organ dysfunctions. Mortality of primary sepsis admissions decreased from 20% in 1988 to 18% in 2008 (p < 0.001). Mortality in status epilepticus during sepsis decreased from 43% in 1988 to 28% in 2008. In-hospital mortality after admissions for sepsis was associated with status epilepticus, older age, and Black and Native American/Eskimo race; patients admitted to a rural or urban private hospitals; and patients with organ dysfunctions. Conclusion:Our analysis demonstrates that status epilepticus after admission for sepsis in the United States was rare. Despite an overall significant reduction in mortality after admission for sepsis, status epilepticus carried a higher risk of death. More aggressive electrophysiological monitoring and a high level of suspicion for the diagnosis of status epilepticus may be indicated in those patients with central nervous system organ dysfunction after sepsis.

Severe human parechovirus type 3 myocarditis and encephalitis in an adolescent with hypogammaglobulinemia

Human parechovirus (HPeV) belongs to the Picornaviridae family of RNA viruses. HPeV infections can be asymptomatic, lead to mild respiratory and/or gastrointestinal symptoms, or less frequently cause severe diseases such as sepsis, meningitis, encephalitis, and myocarditis. Severe neurological HPeV infections occur most commonly in infants and neonates. There are currently 16 recognized types of HPeV. HPeV type 3 (HPeV3) has been the predominant type associated with severe central nervous system disease in neonates and newborns since its discovery in 1999. Although HPeV-related infections have been reported in adults, symptomatic HPeV3 infections in adolescents and adults are uncommon. A case of severe HPeV3 myocarditis and encephalitis in an adolescent is described.

Ethics in Critical Care

Know the four fundamental principles of medical ethics. Understand the importance of obtaining informed consent. Know when an order for no resuscitation is appropriate. Understand the issues regarding withholding and withdrawing life-sustaining therapy, organ donation, and the concept of medical futility. Understand the role of ethics consultation in the critical care setting.

758: CAN PROCALCITONIN DIFFERENTIATE BETWEEN CENTRAL AND INFECTIOUS FEVER IN PATIENTS WITH ICH

Crit Care Med 2016 • Volume 44 • Number 12 (Suppl.) median dose of 4FPCC in the SD and HD groups was 25 units/kg and 50 units/ kg, respectively. The repeat INR post 4FPCC in the SD was 1.2 [1.2–1.3] and 1.1 [1.1–1.2] in the HD 4FPCC group (p=0.19). No difference was observed in achieving an INR of 1.3 or less when comparing the HD and SD 4FPCC groups (77 vs 82%, p=0.72). Hematoma expansion occurred equally in both groups at 13% (p=0.96). Lastly, in the HD group, there was one thrombotic event reported vs none in the SD group. Conclusions: Administering SD or HD 4FPCC to patients with WICH effectively lowered the INR to 1.3 or less in most patients. HD 4FPCC was not associated with a significant increase in thrombotic events. Further studies are warranted to evaluate the impact of HD 4FPCC on functional outcomes and mortality.

Critical Care Neurology

After studying this chapter, you should be able to: Recognize the signs and symptoms of selected neurologic conditions, and the approach to diagnosis. Discuss treatments used in selected neurologic conditions. Appreciate the diverse array of neurologic diseases that may be encountered in the intensive care unit. Recognize ethical aspects of selected neurologic disorders.