Relationship between guideline adherence and outcomes in severe traumatic brain injury.

INTRODUCTION: Traumatic brain injury (TBI) is a leading cause of death and morbidity worldwide. Evidence-based guidelines for managing severe TBI have been available for over 25 years. However, adherence to guidelines remains variable despite evidence highlighting improvement in outcomes with individual recommendations. There is limited evidence to support a superior outcome with compliance to whole sets of recommendations. The aim of this review was to determine whether adherence to TBI guidelines as a package improves outcomes in adults and paediatric patients with severe TBI. METHODS: A structured literature search was conducted using the MEDLINE®, Embase™, PubMed and CINAHL® (Cumulative Index to Nursing and Allied Health Literature) databases. Studies were considered eligible for inclusion in this review if they were quantitative studies investigating the use of TBI guidelines in relation to one or more of the following outcomes: mortality, functional outcome and length of hospital stay. RESULTS: Nine cohort studies were identified that fulfilled the inclusion criteria and answered the clinical question. A review of these papers was conducted. CONCLUSIONS: Mortality after severe TBI improves with increasing adherence to evidence-based guidelines in both adults and children. The evidence also suggests that compliance with guideline recommendations results in improved functional outcomes and reduced length of hospital stay.

In vitro models of neurotrauma.

Traumatic brain injury (TBI) continues to be an important cause of mortality and morbidity, but its pathophysiology is no longer considered an instantaneous irreversible event occurring at the time of injury. Therein, neuroprotection is the attempt to salvage sublethally injured neurons which subsequently die in post-primary sequelae. Key to the discovery of neuroprotective strategies is the development of reliable models of brain injury--both in vivo and in vitro. While numerous studies on in vivo animal models have yielded encouraging results, these have largely failed to translate effectively in humans. One approach out of this impasse may be to re-explore in vitro models to dissect out specific pathophysiological mechanisms and only then test clearer hypotheses on in vivo models, which are more likely to subsequently translate into neuroprotective therapies of the future. Moreover, milder forms of TBI are a more realistic target for therapeutic intervention as more is understood about the vulnerability of surviving neurons and the capacity to salvage them. Several types of injury models are described including transection, compression, barotrauma, acceleration, hydrodynamic and cell stretch models with their advantages and disadvantages discussed in turn, as well as a survey of the cell cultures used, namely immortalized cell lines, primary cultures and organotypic (explant) cultures. We emphasize advances in three-dimensional strain simulation and a recent interest in modelling milder injuries, and argue that in vitro models may be a useful complement to in vivo models in studying TBI.

Cerebral abscess associated with a pulmonary arteriovenous malformation in a patient suffering from alpha thalassaemia.

We report the case of a young girl suffering from alpha thalassaemia and presenting with a brain abscess caused by a silent pulmonary arteriovenous malformation. To our knowledge this is the first such case associated with alpha thalassaemia. Diagnostic investigations and treatment options are discussed.

Astrocytes rather than neurones mediate interleukin-1beta dependent nitric oxide and superoxide radical release in primary hypothalamic rat cell cultures.

The cellular sources of nitric oxide in the hypothalamus are thought to be 'NOergic' neurones. Using free radical electrochemical sensors we investigated nitric oxide and superoxide radical release in primary hypothalamic cell cultures. We present evidence that under interleukin-1beta (IL-1beta) stimulation hypothalamic astrocytes rather than neurones release nitric oxide. Under L-arginine deprivation and IL-1beta stimulation a concentration-dependent release of superoxide was also observed, which was inhibited in the presence of nitric oxide synthase inhibitor nitro-L-argininemethyl-ester. These findings support the hypothesis that the balance between nitric oxide and superoxide may be of vital importance in hypothalamic pathophysiology.

Superoxide generation from constitutive nitric oxide synthase in astrocytes in vitro regulates extracellular nitric oxide availability.

Oxygen-derived free radicals play an important role in the physiology and pathophysiology of brain cell function. Because of their labile nature, however, it has been difficult to investigate their actions directly. This problem has been addressed, in primary rat brain cell cultures, in this study by utilization of two novel electrochemical sensors. It has been demonstrated that extracellular superoxide originates from the astrocytic subpopulation in a calcium/calmodulin dependent manner and responds to constitutive nitric oxide synthase inhibition. The results indicate a novel function for the astrocytic constitutive nitric oxide synthase in regulating extracellular superoxide release and, therefore, controlling neuronal nitric oxide availability.

Giant lumbar meningioma: a common tumour in an unusual location.

We report a 27-year-old woman with atypical sciatica due to a giant, rapidly growing, lumbar (T12-S1) meningioma. The unique features of this case are discussed and the importance of early investigation by MRI of patients with atypical low back pain and sciatica is highlighted.

Will increased awareness among physicians of the significance of sudden agonizing headache affect the outcome of subarachnoid hemorrhage? Coventry and Warwickshire Study: audit of subarachnoid hemorrhage (establishing historical controls), hypothesis, campaign layout, and cost estimation.

BACKGROUND AND PURPOSE: The most common symptom associated with aneurysmal minor bleed ("warning leak") is a sudden agonizing headache. Early screening of these patients may improve the outcome of subarachnoid hemorrhage and may be highly cost-effective. METHODS: We conducted an extensive retrospective audit of subarachnoid hemorrhage over the last 10 years in the region of Coventry and Warwickshire, England, and initiated a continuous campaign among all physicians in the region for early neurosurgical referral of patients with sudden agonizing headache. RESULTS: Over the last 10 years the incidence of subarachnoid hemorrhage in the region was 8.7/100 000 per year. Surgical activity was 34% and early mortality 45.2%. Functional outcome, both overall and by grade on admission, was within internationally accepted levels. Warning leak symptoms before admission were experienced by 20% of patients. These patients sought medical advice but were not referred immediately to the neurosurgical unit. CONCLUSIONS: We have established our population as valid historical controls and outlined our campaign strategy. Lowering the clinical threshold at which patients with sudden agonizing headache are screened for aneurysms or arteriovenous malformations will undoubtedly increase diagnostic costs. However, for reasons given in the text, we estimated the cost per quality-adjusted life year gain to be 1000 pounds ($1500).

Severe hyponatraemia in elderly patients: cause for concern.

An increased incidence of severe hyponatraemia in an orthopaedic unit led to an investigation into the possible causes. Routine perioperative administration of 'hypotonic' intravenous fluid to an elderly population emerged as the most important aggravating factor. Care is necessary in prescribing intravenous fluid regimens in order to avoid potentially serious complications.