A syndrome of paroxysmal, episodic sympathetic hyperactivity after acquired brain injury has been recognized for almost 60 years. This project sought to simplify the confused nomenclature for the condition (>31 eponyms) and simplify the nine overlapping sets of diagnostic criteria. A consensus-developed questionnaire based on a systematic review of the literature was circulated to a widely representative, international expert group utilizing a Delphi approach. Diagnostic criteria were dropped if group consensus failed to agree on their relative importance, with a goal of reaching a Cronbach α of 0.8 (suitable for research purposes). The resulting criteria were combined into an assessment measure for clinical and research settings. The consensus group recommend that the term "paroxysmal sympathetic hyperactivity" replace previous terms to describe the "syndrome, recognised in a subgroup of survivors of severe acquired brain injury, of simultaneous, paroxysmal transient increases in sympathetic [elevated heart rate, blood pressure, respiratory rate, temperature, sweating] and motor [posturing] activity." An 11 point probabilistic diagnostic scale was developed with reference to published criteria, yielding an acceptable Cronbach α of 0.8. These 11 items were proceduralized and combined with a symptom severity index to produce a diagnostic tool for use with adults (the paroxysmal sympathetic hyperactivity assessment measure [PSH-AM]). Development of a pediatric version of the scale and further research into the validity of the PSH-AM is recommended. The consensus position builds on previous literature to establish diagnostic definitions and criteria, an important move to standardize research and management of this condition.

Diet volume ratio of mechanically ventilated patients treated with enteral nutrition is not affected by increasing the limit in GRV. A limit of 500 ml is not associated with adverse effects in gastrointestinal complications or in outcome variables. A value of 500 ml can be equally recommended as a normal limit for GRV.

A proportion of patients surviving severe traumatic brain injury (TBI) have symptoms suggestive of excessive sympathetic discharge, here termed paroxysmal sympathetic hyperactivity (PSH). The goals of this study were: (1) to describe the clinical associations and radiological findings of PSH, its incidence, and features in subjects with severe TBI in the intensive care unit (ICU); (2) to investigate the potential role of increased intracranial pressure in the pathogenesis of PSH; and (3) to determine the prognostic influence of PSH during the ICU stay, on discharge from the ICU, and at 12 months post-injury. A prospective cohort study was undertaken of all ICU admissions with severe TBI older than 14 years over an 18-month period. The PSH symptoms consisted of paroxysmal increases in blood pressure, respiratory rate, and heart rate; worsening level of consciousness; muscle rigidity; and hyperhidrosis. Subjects demonstrating PSH episodes were compared with a group of non-PSH consecutive subjects studied over the first 6 months of the study period. Data were recorded on the clinical variables associated with PSH episodes, early post-injury cerebral CT findings, and neurological status at 1 year. Of 179 severe TBI patients admitted over the study period, 18 (10.1%) experienced PSH. Injury severity-related variables (e.g., initial APACHE II score, admission coma level, and proportion with intracranial hypertension) were similar between the two groups. The PSH group had a longer ICU stay and a greater incidence of infectious complications. At 1 year post-injury, 20% of this group demonstrated ongoing PSH episodes. Over 18 months, 10.1% of admissions following severe TBI demonstrated PSH features in ICU. Subjects with PSH had a longer ICU stay and higher rate of complications, although this did not appear to compromise their long-term neurological recovery.

In intensive care patients, 24-h CrCl results in a large proportion of non-valid determinations, even under conditions of close monitoring. Two-hour CrCl is an adequate substitute, even in patients who are unstable or who have irregular diuresis where a 24-h collection is impossible. The Cockroft-Gault equation seems less useful in this setting.