As of 20 May 2016 there have been 28,646 cases and 11,323 deaths resulting from the West African Ebola virus disease (EVD) outbreak reported to the World Health Organization. There continue to be sporadic flare-ups of EVD cases in West Africa.EVD presentation is nonspecific and characterized initially by onset of fatigue, myalgias, arthralgias, headache, and fever; this is followed several days later by anorexia, nausea, vomiting, diarrhea, and abdominal pain. Anorexia and gastrointestinal losses lead to dehydration, electrolyte abnormalities, and metabolic acidosis, and, in some patients, acute kidney injury. Hypoxia and ventilation failure occurs most often with severe illness and may be exacerbated by substantial fluid requirements for intravascular volume repletion and some degree of systemic capillary leak. Although minor bleeding manifestations are common, hypovolemic and septic shock complicated by multisystem organ dysfunction appear the most frequent causes of death.Males and females have been equally affected, with children (0–14 years of age) accounting for 19 %, young adults (15–44 years) 58 %, and older adults (≥45 years) 23 % of reported cases. While the current case fatality proportion in West Africa is approximately 40 %, it has varied substantially over time (highest near the outbreak onset) according to available resources (40–90 % mortality in West Africa compared to under 20 % in Western Europe and the USA), by age (near universal among neonates and high among older adults), and by Ebola viral load at admission.While there is no Ebola virus-specific therapy proven to be effective in clinical trials, mortality has been dramatically lower among EVD patients managed with supportive intensive care in highly resourced settings, allowing for the avoidance of hypovolemia, correction of electrolyte and metabolic abnormalities, and the provision of oxygen, ventilation, vasopressors, and dialysis when indicated. This experience emphasizes that, in addition to evaluating specific medical treatments, improving the global capacity to provide supportive critical care to patients with EVD may be the greatest opportunity to improve patient outcomes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1325-2) contains supplementary material, which is available to authorized users.

BACKGROUND: Protective ventilation implementation requires the calculation of predicted body weight (PBW), determined by a formula based on gender and height. Consequently, height inaccuracy may be a limiting factor to correctly set tidal volumes. The objective of this study was to evaluate the accuracy of different methods in measuring heights in mechanically ventilated patients. METHODS: Before cardiac surgery, actual height was measured with a height gauge while subjects were standing upright (reference method); the height was also estimated by alternative methods based on lower leg and forearm measurements. After cardiac surgery, upon ICU admission, a subject's height was visually estimated by a clinician and then measured with a tape measure while the subject was supine and undergoing mechanical ventilation. RESULTS: One hundred subjects (75 men, 25 women) were prospectively included. Mean PBW was 61.0 ؎ 9.7 kg, and mean actual weight was 30.3% higher. In comparison with the reference method, estimating the height visually and using the tape measure were less accurate than both lower leg and forearm measurements. Errors above 10% in calculating the PBW were present in 25 and 40 subjects when the tape measure or visual estimation of height was used in the formula, respectively. With lower leg and forearm measurements, 15 subjects had errors above 10% (P < .001). CONCLUSIONS: Our results demonstrate that significant variability exists between the different methods used to measure height in bedridden patients on mechanical ventilation. Alternative methods based on lower leg and forearm measurements are potentially interesting solutions to facilitate the accurate application of protective ventilation.

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The authors describe the clinical course of a 50-year-old woman who presented with life-threatening cardiac dysfunction after aneurysmal subarachnoid hemorrhage (Fisher Grade 4). The pathophysiology of cardiac injury in this setting is not fully understood, but excess sympathetic activation can lead to neurogenic stressed myocardium. A metabolic intervention using the continuous intravenous infusion of high doses of insulin with euglycemia resulted in a rapid improvement of cardiac contractility. The observed benefit could be due to better myocardial glucose utilization that could not have been achieved by catecholamine administration.

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