Improvement of quality of life (QOL) between 1 and 3-4 years after traumatic brain injury (TBI) in ICU patients.

BACKGROUND: Evaluation of changes in quality of life (QOL) in ICU patients several years after traumatic brain injury (TBI) is not well documented. METHODS: A prospective cohort study was conducted in all patients with TBI admitted between 2004 and 2008 to the ICU of Regional Hospital of Malaga (Spain). Functional status was evaluated by Glasgow Outcome Scale (GOS) and QOL by PAECC (Project for the Epidemiologic Analysis of Critical Care patients) questionnaire between 0 (normal QOL) to 29 points (worst QOL). RESULTS: A total of 531 patients. Median(Quartile1,Quartile 3) age: 35 (22, 56) years. After 3-4 years, 175 died (33%). Survivor QOL was deteriorated (median total PAECC score: 5 (0, 11) points) although 75.76% of patients who survived showed good functional situation (GOS normal or mild dysfunction). An improvement in QOL scores between 1 and 3-4 years was observed (median PAECC score differences between 3-4 years and 1 year: - 1(- 4, 0) points). QOL score improved during this interval of time: 62.6% of patients. Change in QOL was related by multivariate analysis to admission cranial-computed tomography scan (Marshall's classification), age, and Injury Severity Score (ISS), with the biggest improvement seen in younger patients and with more severe ISS. Basic physiological activities were maintained in the majority of patients. Subjective aspects and working activities improved between 1 and 3-4 years but with a high proportion still impaired in these items after 3-4 years. CONCLUSIONS: ICU patients with TBI after 1 year show improvement in QOL between 1 and 3-4 years, with the biggest improvement in QOL seen in younger patients and in those with more severe ISS.

Relationship between quality-of-life after 1-year follow-up and severity of traumatic brain injury assessed by computerized tomography.

PURPOSE: This paper studies the relationship between computed tomography (CT) scan on admission, according to Marshall's tomographic classification, and quality-of-life (QoL) after 1 year in patients admitted to the Intensive Care Unit (ICU) with traumatic brain injury (TBI). METHODS: This study used validated scales including the Glasgow Outcome Scale and the PAECC (Project for the Epidemiologic Analysis of Critical Care Patients) QoL questionnaire. RESULTS: We enrolled 531 patients. After 1 year, 171 patients (32.2%) had died (missing data = 6.6%). Good recovery was seen in 22.7% of the patients, while 20% presented moderate disability. The PAECC score after 1 year was 9.43 ± 8.72 points (high deterioration). Patients with diffuse injury I had a mean of 5.08 points vs 7.82 in those with diffuse injury II, 11.76 in those with diffuse injury III and 19.29 in those with diffuse injury IV (p < 0.001). Multivariate analysis found that QoL after 1 year was associated with CT Marshall classification, depth of coma, age, length of stay, spinal injury and tracheostomy. CONCLUSIONS: Patients with TBI had a high mortality rate 1 year after admission, deterioration in QoL and significant impairment of functional status, although more than 40% were normal or self-sufficient. QoL after 1 year was strongly related to cranial CT findings on admission.

Seafood intoxication by tetrodotoxin: first case in Europe.

BACKGROUND: Tetrodotoxin is considered the most lethal toxin in the marine environment. Prior cases of intoxication previously described correspond to consumption of tetrodotoxin in tropical or subtropical regions of Asia or the Pacific Islands. OBJECTIVES: We present the first European case of tetrodotoxin intoxication in a patient who ingested part of a trumpet shellfish (Charonia sauliae) from the Atlantic Ocean in Southern Europe. CASE REPORT: Our patient suffered general paralysis, including the respiratory muscles, a few minutes after the consumption of a few grams of C. sauliae. Intubation and mechanical ventilation were necessary for 52 h after the intoxication. The corresponding electrophysiologic studies showed complete non-excitability, with no recordable sensory or motor nerve conduction. We detected the presence of tetrodotoxin in the mollusk and the patient's blood and urine by means of high-performance liquid chromatography-mass spectrometry analysis technique. A previous bioassay showed extremely high quantities of the toxin in the mollusk. CONCLUSIONS: This case alerts us to the possibility of a very harmful biotoxin in European coastal waters. This now should be included in the differential diagnosis of similar cases in Europe, and we must be vigilant for its possible presence in Europe.

Paroxysmal sympathetic hyperactivity after acquired brain injury: consensus on conceptual definition, nomenclature, and diagnostic criteria.

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.

Paroxysmal sympathetic hyperactivity after traumatic brain injury: clinical and prognostic implications.

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.

Prognostic influence and computed tomography findings in dysautonomic crises after traumatic brain injury.

BACKGROUND: Dysautonomic crises represent a relatively unknown complication in patients with severe traumatic brain injury (TBI). Few studies have been undertaken of their pathophysiology and prognostic repercussions. We studied the prevalence of dysautonomic crises after TBI, their radiologic substrate, influence on the clinical course in the intensive care unit (ICU), and effect on neurologic recovery. METHODS: A case-control study involving 11 patients with dysautonomic crises admitted with TBI during a span of 1 year and 26 patients admitted with TBI but no crises during the first 3 months of the same year. The initial severity was assessed from Apache II, Glasgow Coma Scale (GCS) scores, and computed tomography (CT) during the first 24 hours. Complications were assessed by the duration of ICU stay, days on mechanical ventilation, need for tracheotomy, and number of infectious complications. Neurologic recovery was assessed with the GCS at discharge from the ICU and with the Glasgow Outcome Scale 12 months later. RESULTS: Both groups were similar at admission. The prevalence of dysautonomic crises was 9.3%. Patients with dysautonomic crises had more focal lesions on cranial CT than patients without crises, a significantly longer ICU stay, and a tendency to have a worse level of consciousness at discharge from the ICU but not 12 months later. CONCLUSIONS: Almost 10% of patients with severe TBI have dysautonomic crises during their ICU stay. Patients with dysautonomia were more likely to have focal intraparenchymal lesions, and crises were associated with greater morbidity and a longer ICU stay. Dysautonomic crises determined a worse short-term neurologic recovery.