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This trial showed no significant difference in the percentage of patients who died or had severe disability or coma when higher or lower blood-pressure targets were used after an out-of-hospital cardiac arrest.

A trial involving comatose survivors of cardiac arrest tested whether aggressively treating rhythmic and periodic EEG activity would improve neurologic outcomes. Despite suppression of abnormal EEG activity, the incidence of a poor neurologic outcome did not differ significantly from that with standard care, and mortality was high.

In a trial involving patients with coma after out-of-hospital cardiac arrest, a strategy targeting mild hypercapnia for 24 hours did not improve neurologic outcomes at 6 months as compared with targeted normocapnia.

Background/Objective For patients with disorders of consciousness (DoC) and their families, the search for new therapies has been a source of hope and frustration. Almost all clinical trials in patients with DoC have been limited by small sample sizes, lack of placebo groups, and use of heterogeneous outcome measures. As a result, few therapies have strong evidence to support their use; amantadine is the only therapy recommended by current clinical guidelines, specifically for patients with DoC caused by severe traumatic brain injury. To foster and advance development of consciousness-promoting therapies for patients with DoC, the Curing Coma Campaign convened a Coma Science Work Group to perform a gap analysis. Methods We consider five classes of therapies: (1) pharmacologic; (2) electromagnetic; (3) mechanical; (4) sensory; and (5) regenerative. For each class of therapy, we summarize the state of the science, identify gaps in knowledge, and suggest future directions for therapy development. Results Knowledge gaps in all five therapeutic classes can be attributed to the lack of: (1) a unifying conceptual framework for evaluating therapeutic mechanisms of action; (2) large-scale randomized controlled trials; and (3) pharmacodynamic biomarkers that measure subclinical therapeutic effects in early-phase trials. To address these gaps, we propose a precision medicine approach in which clinical trials selectively enroll patients based upon their physiological receptivity to targeted therapies, and therapeutic effects are measured by complementary behavioral, neuroimaging, and electrophysiologic endpoints. Conclusions This personalized approach can be realized through rigorous clinical trial design and international collaboration, both of which will be essential for advancing the development of new therapies and ultimately improving the lives of patients with DoC.

In this trial involving patients after out-of-hospital cardiac arrest, fever prevention for 36 or 72 hours did not result in different percentages of patients dying or having severe disability or coma.

PurposeThe effect of renal replacement therapy (RRT) in comatose patients with acute kidney injury (AKI) remains unclear. We compared two RRT initiation strategies on the probability of awakening in comatose patients with severe AKI.MethodsWe conducted a post hoc analysis of a trial comparing two delayed RRT initiation strategies in patients with severe AKI. Patients were monitored until they had oliguria for more than 72 h and/or blood urea nitrogen higher than 112 mg/dL and then randomized to a delayed strategy (RRT initiated after randomization) or a more-delayed one (RRT initiated if complication occurred or when blood urea nitrogen exceeded 140 mg/dL). We included only comatose patients (Richmond Agitation-Sedation scale [RASS] < − 3), irrespective of sedation, at randomization. A multi-state model was built, defining five mutually exclusive states: death, coma (RASS < − 3), incomplete awakening (RASS [− 3; − 2]), awakening (RASS [− 1; + 1] two consecutive days), and agitation (RASS >  + 1). Primary outcome was the transition from coma to awakening during 28 days after randomization.ResultsA total of 168 comatose patients (90 delayed and 78 more-delayed) underwent randomization. The transition intensity from coma to awakening was lower in the more-delayed group (hazard ratio [HR] = 0.36 [0.17–0.78]; p = 0.010). Time spent awake was 10.11 days [8.11–12.15] and 7.63 days [5.57–9.64] in the delayed and the more-delayed groups, respectively. Two sensitivity analyses were performed based on sedation status and sedation practices across centers, yielding comparable results.ConclusionIn comatose patients with severe AKI, a more-delayed RRT initiation strategy resulted in a lower chance of transitioning from coma to awakening.

Background. The reported case-fatality rate associated with severe malaria varies widely. Whether age is an independent risk factor is uncertain. Methods. In a large, multicenter treatment trial conducted in Asia, the presenting manifestations and outcome of severe malaria were analyzed in relation to age. Results. Among 1050 patients with severe malaria, the mortality increased stepwise, from 6.1% in children (age, <10 years) to 36.5% in patients aged >50 years (P < .001). Compared with adults aged 21–50 years, the decreased risk of death among children (adjusted odds ratio, 0.06; 95% confidence interval, 0.01–0.23; P < .001) and the increased risk of death among patients aged 150 years (adjusted odds ratio, 1.88; 95% confidence interval, 1.01–3.52; P = .046) was independent of the variation in presenting manifestations. The incidence of anemia and convulsions decreased with age, whereas the incidence of hyperparasitemia, jaundice, and renal insufficiency increased with age. Coma and metabolic acidosis did not vary with age and were the strongest predictors of a fatal outcome. The number of severity signs at hospital admission also had a strong prognostic value. Conclusion. Presenting syndromes in severe malaria depend on age, although the incidence and the strong prognostic significance of coma and acidosis are similar at all ages. Age is an independent risk factor for a fatal outcome of the disease.

Improved glycemic control reduces complications in type 1 diabetes, but tight control of glucose is associated with more hypoglycemic episodes. The long-term effect of recurrent hypoglycemic events on cognitive function is not known. In this 18-year follow-up of patients enrolled in the Diabetes Control and Complications Trial, relatively high rates of severe hypoglycemic events were not associated with worse cognitive outcomes. In this 18-year follow-up of patients with type 1 diabetes, relatively high rates of severe hypoglycemic events were not associated with worse cognitive outcomes. Over time, improving glycemic control decreases the risk of microvascular, peripheral neuropathic, and macrovascular complications of type 1 diabetes. 1 – 4 However, it is unclear whether type 1 diabetes and its treatment have substantial effects on the structure and function of the central nervous system. 5 – 8 The widespread use of intensive therapies designed to achieve glycemic control near the nondiabetic range and the attendant increased risk of severe hypoglycemia 9 have elevated concern about the effects of hypoglycemia on the central nervous system. The Diabetes Control and Complications Trial (DCCT) incorporated a comprehensive battery of cognitive tests to evaluate the effect of . . .

Summary points The vegetative state is a complex neurological condition in which patients appear to be awake but show no sign of awareness of themselves or their environment Current clinical methods of diagnosis are limited in scope, evidenced by a high rate (about 40%) of misdiagnosis (that is, patients who are aware are considered to be unconscious) The main causes of misdiagnosis are associated with a patient's disability (such as blindness), confusion in terminology, and lack of experience of this relatively rare condition Furthermore, standard behavioural assessments cannot distinguish an aware (that is, minimally conscious) but completely immobile patient from a non-aware patient (one with vegetative state) In such behaviourally non-responsive patients, functional neuroimaging methods (such as magnetic resonance imaging or electroencephalography) can detect residual cognition and awareness and can even establish two way communication, without requiring any behavioural output from patients Current guidelines should therefore be modified to include functional neuroimaging as an independent source of diagnostically relevant information The vegetative state may develop suddenly (as a consequence of traumatic or non-traumatic brain injury, such as hypoxia or anoxia; infection; or haemorrhage) or gradually (in the course of a neurodegenerative disorder, such as Alzheimer's disease). Misdiagnosis has many implications for a patient's care-such as day to day management, access to early interventions, and quality of life-and has ethical and legal ramifications pertaining to decisions on the discontinuation of life supporting therapies. 2 w2-w4 Overall, our understanding of the vegetative state is incomplete. The 2003 guidance from the UK's Royal...