Outcome after severe head injury: focal surgical lesions do not imply a better Glasgow Outcome Score than diffuse injuries at 3 months.

BACKGROUND: Historically neurosurgeons have accepted head injured patients only in the presence of a mass lesion requiring surgical decompression. Underpinning this is an assumption that these patients have a better outcome than patients without a surgical lesion. This has meant that many patients without a surgical lesion have been managed locally in the referring hospital. However, there is now evidence that treatment of all head injured patients in a specialist centre leads to improved outcomes. Therefore, we have asked the question: does the presence of a surgical lesion imply better outcome from severe head injury? RESULTS: We prospectively recorded the Glasgow Outcome score (GOS), at 3 months, of all the severely head injured patients treated at our institution over a two and a half year period. Of 116 patients admitted with an initial Glasgow Coma Score (GCS) of 8 or less, 58 had surgical lesions and 58 non-surgical head injuries. The two groups were well matched for presenting GCS and age. Overall our favourable outcome rate (GOS 4 and 5) at 3-months for the patients with a surgical lesion and for the non-surgical group were 47.3% and 46.6% respectively, with no significant difference between the two (P = 0.54). CONCLUSION: The assumption in the past has always been that patients presenting in coma from traumatic diffuse brain injury will do worse than those that have a mass lesion amenable to surgical decompression. Our series would suggest that this is not the case and all severely head injured patients should expect similar outcome when cared for in a neuroscience centre.

Brain temperature and outcome after severe traumatic brain injury.

INTRODUCTION: In humans, raised body temperature is linked to poor outcome after brain injury. Because deviations between brain and body temperature have been reported after severe traumatic brain injury (TBI), the aim of this study was to explore the relationship between initial and mean brain temperature and survival at 3 months. METHODS: Intraparenchymal temperature was measured 3 - 4 cm within white matter. Logistic regression was used to explore linear and quadratic relationships between initial and average brain temperature and survival at 3 months. RESULTS: In 36 patients, initial brain temperatures ranged from 33.5 to 39.2 degrees C (median 37.4 degrees C). There was no evidence of an association between initial brain temperature and risk of death, either linear (odds ratio [OR] 95% confidence interval [CI] = 1.3 [0.68 to 2.5], p = 0.42) or quadratic ( p = 0.26). Assuming a linear relationship, patients with higher mean brain temperatures were less likely to die: OR (95% CI) for death per 1 degrees C was 0.31 (0.09 to 1.1), p = 0.06. However, by fitting the quadratic relationship, there was a suggestion that both high and low temperatures were associated with increased risk of death: p = 0.06. CONCLUSION: Initial brain temperature measured shortly after admission did not predict outcome. There is a suggestion that patients with "middle range" temperatures were less likely to die.

Body temperature management after severe traumatic brain injury: methods and protocols used in the United Kingdom and Ireland.

OBJECTIVE: To establish whether there is consensus in the management of body temperature in patients with severe traumatic brain injury (TBI) admitted to hospitals in the United Kingdom and Ireland for neurosurgical intensive care. METHODS: Permission was granted from the Society of British Neurosurgeons (SBNS) and the Local Research Ethics Committee to undertake the survey. A senior member of nursing staff from all adult neurosurgical units, excluding our own, was contacted by telephone. RESULTS: All 33 adult neurosurgical centres participated. Six units had a formal written protocol for the management of body temperature. For the remainder (27 units), interest was expressed in a protocol for temperature management particularly for those patients with intractable hyperthermia/fever. Administration of the antipyretic paracetamol was the most common 'first-line' treatment (13 units). Other 'first-line' methods were: circulating air-cooling blankets (9 units), water-filled cooling blankets (6 units), tepid sponging or wet soaks (2 units), convection fans (2 units) and administration of cold fluids via the gut or circulation (1 unit). When 'first-line' methods failed to bring about a fall in temperature, different combinations of these methods were used. CONCLUSIONS: From this survey, it is evident that there is no consensus in the approach to temperature management in neurosurgical intensive care patients with severe TBI. Review and rationalisation of systems of care may be required in an effort to develop evidence-based nationwide guidelines.

Mechanisms of gastroesophageal reflux in critically ill mechanically ventilated patients.

BACKGROUND & AIMS: Gastroesophageal reflux is a major problem in mechanically ventilated patients and may lead to pulmonary aspiration and erosive esophagitis. Transient lower esophageal sphincter relaxations are the most common mechanism underlying reflux in nonventilated patients. The mechanisms that underlie reflux in critically ill ventilated patients have not been studied. The aim of this study was to determine the mechanisms underlying gastroesophageal reflux in mechanically ventilated patients in the intensive care unit. METHODS: In 15 mechanically ventilated intensive care unit patients, esophageal motility, pH, and intraluminal impedance (11/15 patients) were recorded for 1 hour before and 5 hours during continuous nasogastric feeding. RESULTS: Basal lower esophageal sphincter pressure was uniformly low (2.2 +/- 0.4 mmHg). The median (interquartile range) acid exposure (pH <4) was 39.4% (0%-100%) fasting and 32% (7.5%-94.2%) fed. Acid reflux occurred in 10 patients, but slow drifts in esophageal pH were also an important contributor to acid exposure. If esophageal pH decreased to pH <4, it tended to remain so for prolonged periods. A total of 46 acid reflux events were identified. Most (55%) occurred because of absent lower esophageal sphincter pressure alone; 45% occurred during straining or coughing. CONCLUSIONS: Gastroesophageal reflux in mechanically ventilated patients is predominantly due to very low or absent lower esophageal sphincter pressure, often with a superimposed cough or strain. These data suggest that measures that increase basal LES pressure may be useful to prevent reflux in ventilated patients.