Targeted temperature management in patients with intracerebral haemorrhage, subarachnoid haemorrhage, or acute ischaemic stroke: consensus recommendations.

BACKGROUND: A modified Delphi approach was used to identify a consensus on practical recommendations for the use of non-pharmacological targeted temperature management in patients with intracerebral haemorrhage, subarachnoid haemorrhage, or acute ischaemic stroke with non-infectious fever (assumed neurogenic fever). METHODS: Nine experts in the management of neurogenic fever participated in the process, involving the completion of online questionnaires, face-to-face discussions, and summary reviews, to consolidate a consensus on targeted temperature management. RESULTS: The panel's recommendations are based on a balance of existing evidence and practical considerations. With this in mind, they highlight the importance of managing neurogenic fever using a single protocol for targeted temperature management. Targeted temperature management should be initiated if the patient temperature increases above 37.5°C, once an appropriate workup for infection has been undertaken. This helps prevent prophylactic targeted temperature management use and ensures infection is addressed appropriately. When neurogenic fever is detected, targeted temperature management should be initiated rapidly if antipyretic agents fail to control the temperature within 1 h, and should then be maintained for as long as there is potential for secondary brain damage. The recommended target temperature for targeted temperature management is 36.5-37.5°C. The use of advanced targeted temperature management methods that enable continuous, or near continuous, temperature measurement and precise temperature control is recommended. CONCLUSIONS: Given the limited heterogeneous evidence currently available on targeted temperature management use in patients with neurogenic fever and intracerebral haemorrhage, subarachnoid haemorrhage, or acute ischaemic stroke, a Delphi approach was appropriate to gather an expert consensus. To aid in the development of future investigations, the panel provides recommendations for data gathering.

Systematic review of head cooling in adults after traumatic brain injury and stroke.

BACKGROUND: Brain injuries resulting from trauma and stroke are common and costly. Cooling therapy may reduce damage and potentially improve outcome. Head cooling targets the site of injury and may have fewer side effects than systemic cooling, but there has been no systematic review and the evidence base is unclear. OBJECTIVE: To assess the effect of non-invasive head cooling after traumatic brain injury (TBI) and stroke on intracranial and/or core body temperature, functional outcome and mortality, determine adverse effects and evaluate cost-effectiveness. REVIEW METHODS: Search strategy Major international databases [including MEDLINE, EMBASE, Cumulative Index to Nursing and Allied Health Literature, Web of Science, the British Library's Electronic Table of Contents (Zetoc)], The Cochrane Library, trial registers, country-specific databases (including China, Japan), Google Scholar, hypothermia conference reports and reference lists of papers were searched with no publication or language restrictions. The searches were conducted from March 2010 to April 2011, with no back date restriction. Selection criteria For formal analysis of effect of head cooling on functional outcome and mortality: randomised controlled trials (RCTs) of non-invasive head cooling in TBI or stroke in adults (aged ≥ 18 years). RCT prespecified in protocol to include adequate randomisation and blinded outcome assessment. For assessment of effect on temperature and adverse effects of cooling methods/devices: studies of any type in TBI, stroke, cardiac arrest and neonatal hypoxic-ischaemic encephalopathy (adverse effects only). Data collection and analysis A study assessment and data collection form was developed and piloted. Data on functional outcome, mortality, temperature change and adverse effects of devices were sought and extracted. Two authors independently assessed RCTs for quality using the Cochrane Renal Group checklist. RESULTS: Out of 46 head-cooling studies in TBI and stroke, there were no RCTs of suitable quality for formal outcome analysis. Twelve studies had useable data on intracranial and core body temperature. These included 99 patients who were cooled after TBI or stroke and 198 patients cooled after cardiac arrest. The data were too heterogeneous for a single summary measure of effect (many studies had no measure of spread) and are therefore presented descriptively. The most effective techniques for which there were adequate data (nasal coolant and liquid cooling helmets) could reduce intracranial temperature by ≥ 1 °C in 1 hour. The main device-related adverse effects were localised skin problems, which were generally mild and self-limiting. There were no suitable data for economic modelling, but an exploratory model of possible treatment effects and cost-effectiveness of head cooling in TBI was created using local patient data. LIMITATIONS: We conducted extensive and sensitive searches but found no good-quality RCTs of the effect of head cooling on functional outcome that met the review inclusion criteria. Most trials were small and/or of low methodological quality. However, if the trial reports did not reflect the true quality of the research, there may be some excluded trials that should have been included. Temperature data were often poorly reported which made it difficult to assess the effect of head cooling on temperature. CONCLUSIONS: Whether head cooling improves functional outcome or has benefits and fewer side effects compared with systemic cooling or no cooling could not be established. Some methods of head cooling can reduce intracranial temperature, which is an important first step in determining effectiveness, but there is insufficient evidence to recommend its use outside of research trials. The principal recommendations for research are that active cooling devices show the most promise for further investigation and more robust proof of concept of intracranial and core body temperature reduction with head cooling is required, clearly showing whether temperature has changed and by how much. FUNDING: The National Institute for Health Research Health Technology Assessment programme.

Esophageal temperature after out-of-hospital cardiac arrest: an observational study.

INTRODUCTION: Out-of-hospital cardiac arrest (OHCA) is a significant cause of death and severe neurological disability. The only post-return of spontaneous circulation (ROSC) therapy shown to increase survival is mild therapeutic hypothermia (MTH). The relationship between esophageal temperature post OHCA and outcome is still poorly defined. METHODS: Prospective observational study of all OHCA patients admitted to a single centre for a 14-month period (1/08/2008 to 31/09/2009). Esophageal temperature was measured in the Emergency Department and Intensive Care Unit (ICU). Selected patients had pre-hospital temperature monitoring. Time taken to reach target temperature after ROSC was recorded, together with time to admission to the Emergency Department and ICU. RESULTS: 164 OHCA patients were included in the study. 105 (64.0%) were pronounced dead in the Emergency Department. 59 (36.0%) were admitted to ICU for cooling; 40 (24.4%) died in ICU and 19 (11.6%) survived to hospital discharge. Patients who achieved ROSC and had esophageal temperature measured pre-hospital (n=29) had a mean pre-hospital temperature of 33.9 degrees C (95% CI 33.2-34.5). All patients arriving in the ED post OHCA had a relatively low esophageal temperature (34.3 degrees C, 95% CI 34.1-34.6). Patients surviving to hospital discharge were warmer on admission to ICU than patients who died in hospital (35.7 degrees C vs 34.3 degrees C, p<0.05). Patients surviving to hospital discharge also took longer to reach T(targ) than non-survivors (2h 48min vs 1h 32min, p<0.05). CONCLUSIONS: Following OHCA all patients have esophageal temperatures below normal in the pre-hospital phase and on arrival in the Emergency Department. Patients who achieve ROSC following OHCA and survive to hospital discharge are warmer on arrival in ICU and take longer to reach target MTH temperatures compared to patients who die in hospital. The mechanisms of action underlying esophageal temperature and survival from OHCA remain unclear and further research is warranted to clarify this relationship.

Forced convective head cooling device reduces human cross-sectional brain temperature measured by magnetic resonance: a non-randomized healthy volunteer pilot study.

BACKGROUND: This pilot study in five healthy adult humans forms the pre-clinical assessment of the effect of a forced convective head cooling device on intracranial temperature, measured non-invasively by magnetic resonance spectroscopy (MRS). METHODS: After a 10 min baseline with no cooling, subjects received 30 min of head cooling followed by 30 min of head and neck cooling via a hood and neck collar delivering 14.5 degrees C air at 42.5 litre s(-1). Over baseline and at the end of both cooling periods, MRS was performed, using chemical shift imaging, to measure brain temperature simultaneously across a single slice of brain at the level of the basal ganglia. Oesophageal temperature was measured continuously using a fluoroptic thermometer. RESULTS: MRS brain temperature was calculated for baseline and the last 10 min of each cooling period. The net brain temperature reduction with head cooling was 0.45 degrees C (SD 0.23 degrees C, P=0.01, 95% CI 0.17-0.74 degrees C) and with head and neck cooling was 0.37 degrees C (SD 0.30 degrees C, P=0.049, 95% CI 0.00-0.74 degrees C). The equivalent net reductions in oesophageal temperature were 0.16 degrees C (SD 0.04 degrees C) and 0.36 degrees C (SD 0.12 degrees C). Baseline-corrected brain temperature gradients from outer through intermediate to core voxels were not significant for either head cooling (P=0.43) or head and neck cooling (P=0.07), indicating that there was not a significant reduction in cooling with progressive depth into the brain. CONCLUSIONS: Convective head cooling reduced MRS brain temperature and core brain was cooled.

Similarity between the suprasystolic wideband external pulse wave and the first derivative of the intra-arterial pulse wave.

BACKGROUND: Wideband external pulse (WEP) monitoring, using a broad bandwidth piezoelectric sensor located over the brachial artery under the distal edge of a sphygmomanometer cuff, can be used for evaluating the contour of the arterial pressure pulse wave. The pulse contour contains valuable information relating to cardiovascular function which may be of clinical use in addition to blood pressure measurements. The aim of this study was to compare the shape of the WEP signal during inflation of the cuff to suprasystolic pressure, with intra-arterial pressure waves, after the administration of vasoactive drugs. METHODS: Radial intra-arterial and suprasystolic WEP waveforms were recorded in 11 healthy men (mean 23 yr) before and at the end of infusion of glyceryl trinitrate, angiotensin II, norepinephrine, and salbutamol. Waveform similarity was assessed by comparing the timing and pressure of incident and reflected waves and by root mean square error (RMSE). RESULTS: The WEP signal was found to closely resemble the first derivative of intra-arterial pressure. The WEP signal could be used to derive an arterial pressure wave with minimal bias in the timing of incident [- 8 (18) ms, mean (SD)] and reflected [- 1 (24) ms] waves. Augmentation index was underestimated by WEP [- 7 (18)%]. WEP also provided a measure of compliance which correlated with pulse wave velocity (r = - 0.44). RMSE values after the administration of each of the four drugs mentioned earlier were 12.4 (3.8), 17.7 (5.0), 22.1 (11.7), and 28.9 (22.4) mm Hg, respectively. Changes in derived WEP signals were similar to those measured by arterial line with all drugs. CONCLUSIONS: The suprasystolic WEP signals can be used to derive arterial pressure waves which, although not identical, track changes in the intra-arterial pulse wave induced by vasoactive drugs.

Enhanced upper respiratory tract airflow and head fanning reduce brain temperature in brain-injured, mechanically ventilated patients: a randomized, crossover, factorial trial.

BACKGROUND: Heat loss from the upper airways and through the skull are physiological mechanisms of brain cooling which have not been fully explored clinically. METHODS: This randomized, crossover, factorial trial in 12 brain-injured, orally intubated patients investigated the effect of enhanced nasal airflow (high flow unhumidified air with 20 p.p.m. nitric oxide gas) and bilateral head fanning on frontal lobe brain temperature and selective brain cooling. After a 30 min baseline, each patient received the four possible combinations of the interventions--airflow, fanning, both together, no intervention--in randomized order. Each combination was delivered for 30 min and followed by a 30 min washout, the last 5 min of which provided the baseline for the next intervention. RESULTS: The difference in mean brain temperature over the last 5 min of the preceding washout minus the mean over the last 5 min of intervention, was 0.15 degrees C with nasal airflow (P=0.001, 95% CI 0.06-0.23 degrees C) and 0.26 degrees C with head fanning (P<0.001, 95% CI 0.17-0.34 degrees C). The estimate of the combined effect of airflow and fanning on brain temperature was 0.41 degrees C. Selective brain cooling did not occur. CONCLUSION: Physiologically, this study demonstrates that heat loss through the upper airways and through the skull can reduce parenchymal brain temperature in brain-injured humans and the onset of temperature reduction is rapid. Clinically, in ischaemic stroke, a temperature decrease of 0.27 degrees C may reduce the relative risk of poor outcome by 10-20%. Head fanning may have the potential to achieve a temperature decrease of this order.

Monitoring the injured brain: ICP and CBF.

Raised intracranial pressure (ICP) and low cerebral blood flow (CBF) are associated with ischaemia and poor outcome after brain injury. Therefore, many management protocols target these parameters. This overview summarizes the technical aspects of ICP and CBF monitoring, and their role in the clinical management of brain-injured patients. Furthermore, some applications of these methods in current research are highlighted. ICP is typically measured using probes that are inserted into one of the lateral ventricles or the brain parenchyma. Therapeutic measures used to control ICP have relevant side-effects and continuous monitoring is essential to guide such therapies. ICP is also required to calculate cerebral perfusion pressure which is one of the most important therapeutic targets in brain-injured patients. Several bedside CBF monitoring devices are available. However, most do not measure CBF but rather a parameter that is thought to be proportional to CBF. Frequently used methods include transcranial Doppler which measures blood flow velocity and may be helpful for the diagnosis and monitoring of cerebral vasospasm after subarachnoid haemorrhage or jugular bulb oximetry which gives information on adequacy of CBF in relation to the metabolic demand of the brain. However, there is no clear evidence that incorporating data from CBF monitors into our management strategies improves outcome in brain-injured patients.

A comparison of bispectral index and entropy monitoring, in patients undergoing embolization of cerebral artery aneurysms after subarachnoid haemorrhage.

BACKGROUND: Processed EEG monitoring of anaesthetic depth could be useful in patients receiving general anaesthesia following subarachnoid haemorrhage. We conducted an observational study comparing performance characteristics of bispectral index (BIS) and entropy monitoring systems in these patients. METHODS: Thirty-one patients of the World Federation of Neurosurgeons grades 1 and 2, undergoing embolization of cerebral artery aneurysms following acute subarachnoid haemorrhage, were recruited to have both BIS and entropy monitoring during general anaesthesia. BIS and entropy indices were matched to clinical indicators of anaesthetic depth. Anaesthetists were blinded to the anaesthetic depth monitoring indices. Analysis of data from monitoring devices allowed calculation of prediction probability (P(K)) constants, and receiver operating characteristic (ROC) analysis to be performed. RESULTS: BIS and entropy [response entropy (RE), state entropy (SE)] performed well in their ability to show concordance with clinically observed anaesthetic depth. P(K) values were generally high (BIS 0.966-0.784, RE 0.934-0.663, SE 0.857-0.701) for both forms of monitoring. ROC curve analysis shows a high sensitivity and specificity for all monitoring indices when used to detect the presence or absence of eyelash reflex. Area under curve for BIS, RE and SE to detect the absence or presence of eyelash reflex was 0.932, 0.888 and 0.887, respectively. RE provides earlier warning of return of eyelash reflex than BIS. CONCLUSION: BIS and entropy monitoring perform well in patients who receive general anaesthesia after good grade subarachnoid haemorrhage.

Critical thresholds of intracranial pressure and cerebral perfusion pressure related to age in paediatric head injury.

BACKGROUND: The principal strategy for managing head injury is to reduce the frequency and severity of secondary brain insults from intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and hence improve outcome. Precise critical threshold levels have not been determined in head injured children. OBJECTIVE: To create a novel pressure-time index (PTI) measuring both duration and amplitude of insult, and then employ it to determine critical insult thresholds of ICP and CPP in children. METHODS: Prospective, observational, physiologically based study from Edinburgh and Newcastle, using patient monitored blood pressure, ICP, and CPP time series data. The PTI for ICP and CPP for 81 children, using theoretical values derived from physiological norms, was varied systematically to derive critical insult thresholds which delineate Glasgow outcome scale categories. RESULTS: The PTI for CPP had a very high predictive value for outcome (receiver operating characteristic analyses: area under curve = 0.957 and 0.890 for mortality and favourable outcome, respectively) and was more predictive than for ICP. Initial physiological values most accurately predicted favourable outcome. The CPP critical threshold values determined for children aged 2-6, 7-10, and 11-15 years were 48, 54, and 58 mm Hg. respectively. CONCLUSIONS: The PTI is the first substantive paediatric index of total ICP and CPP following head injury. The insult thresholds generated are identical to age related physiological values. Management guidelines for paediatric head injuries should take account of these CPP thresholds to titrate appropriate pressor therapy.

Quantification of secondary CPP insult severity in paediatric head injured patients using a pressure-time index.

This paper describes and validates a new Cumulative Pressure-Time Index (CPT) which takes into account both duration and degree of cerebral perfusion pressure (CPP) derangement and determines critical thresholds for CPP, in a paediatric head injury dataset. Sixty-six head-injured children, with invasive minute-to-minute intracranial pressure (ICP) and blood pressure monitoring, had their pre-set CPP derangement episodes (outside the normal range) identified in three childhood age-bands (2-6, 7-10, and 11-16 years) and global outcome assessed at six months post injury. The new cumulative pressure-time index more accurately predicted outcome than previously used summary measures and by varying the threshold CPP values, it was found that these physiological threshold values (< or = 48, < or = 52 and < or = 56 mmHg for 2-6, 7-10, and 11-16 years respectively) best predicted brain insult in terms of subsequent mortality and morbidity.

Randomized controlled trial of effects of the airflow through the upper respiratory tract of intubated brain-injured patients on brain temperature and selective brain cooling.

BACKGROUND: Pyrexia is common after brain injury; it is generally believed to affect outcome adversely and the usual clinical methods of reducing temperature are not effective. The normal physiological mechanisms of brain cooling are heat loss from the upper airways and through the skull, and these can produce selective brain cooling. METHODS: Air at room temperature and humidity was continuously administered to 15 brain-injured, intubated and mechanically ventilated patients via a sponge-tipped oxygen catheter in each nostril at a combined rate of 115 ml kg(-1) min(-1). Brain temperature was measured using a pressure-temperature Camino catheter which is designed to site the thermistor 1 cm into the parenchyma in the frontal lobe. Oesophageal temperature was measured using an oesophageal stethoscope with a thermistor. After establishing baseline for 30 min, patients were randomized to receive airflow or no airflow for 6 h and then crossed over for a further 6 h. RESULTS: Airflow replicating normal resting minute volume did not produce clinically relevant or statistically significant reductions in brain temperature [0.13 (SD 0.55) degrees C; 95% CI, 0.43-0.17 degrees C]. However, we serendipitously found some evidence of selective brain cooling via the skull, but this needs further substantiation. CONCLUSIONS: A flow of humidified air at room temperature through the upper respiratory tracts of intubated brain-injured patients did not produce clinically relevant or statistically significant reductions in brain temperature measured in the frontal lobe.

QTc dispersion as a marker for medical complications after severe subarachnoid haemorrhage.

BACKGROUND AND OBJECTIVE: Morbidity from subarachnoid haemorrhage is common and results from complications including myocardial dysfunction and neurogenic pulmonary oedema causing hypotension and hypoxia--both major causes of secondary brain injury. Predicting patients at risk of developing these complications may facilitate early intervention. METHODS: Using QTc dispersion to assess repolarization inhomogeneity, patients who had suffered severe acute subarachnoid haemorrhage were studied in an intensive care unit. Electrocardiograms were recorded within 24 h of ictus. Subsequent development of myocardial dysfunction was defined as a requirement for inotropes, and neurogenic pulmonary oedema as a PaO2 (kPa)/FiO2 ratio < 40. Together they constituted cardiorespiratory compromise. RESULTS: Twenty-seven patients were recruited. QTc dispersion was greater in patients (74.1 ms, SD +/- 26.1) than in controls (48.3 ms, 12.0) P < 0.0001, 95% CI 14.6, 37.0. Thirteen patients developed cardiorespiratory compromise and had greater QTc dispersion (84.5 ms, 26.2) than patients who did not develop cardiorespiratory compromise (64.5 ms, 22.7) P = 0.046, 95% CI 0.3, 39.6. There was no difference in QTc dispersion between patients who did and those who did not develop myocardial dysfunction alone. Similarly, there was no difference in QTc dispersion between patients who did and those who did not develop neurogenic pulmonary oedema alone. CONCLUSIONS: Increased QTc dispersion is associated with the later development of cardiorespiratory compromise in poor-grade subarachnoid haemorrhage patients. QTc dispersion may be used as a marker to predict impending clinical deterioration, providing an opportunity for early intervention.

Traumatic brain injury in childhood: intensive care time series data and outcome.

Age-specific norms are necessary to determine potential secondary brain insult after head injury in children. We describe and quantify the secondary physiological derangement recorded in children of different ages following traumatic brain injury, and relate it to outcome at 12 months post-injury. Prospective time-series data (including intracranial pressure, arterial blood pressure, cerebral perfusion pressure, oxygen saturation, temperature and heart rate) downloaded from ICU monitors, were examined to identify abnormal (i.e. outside normal age-specific limits) recordings lasting more than 5 min. Cumulated total duration of derangement was calculated for each parameter and as a percentage of the time that the ICP monitor was in situ. Univariate and multivariate logistic regression modelling was used to evaluate predictors of outcome. Age-specificity allows realistic comparisons of physiological data among children. Duration of age-specific derangement of CPP was found to predict outcome (dead v. alive: p = 0.003 and Glasgow Outcome Score 1-3 v. 4-5, i.e. poor v. independent outcome p = 0.004).

Graphical display of variability and inter-relationships of pressure signals in children with traumatic brain injury.

A prospective observational study was undertaken to examine time series ICU data of pressure variables (mean arterial pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP)) and relate their variability (SD) to outcome, together with simple graphical displays which could be useful at the ICU bedspace. Forty-three children (aged < 1-15 years) were admitted to the intensive care unit for Regional Neurosurgical Service, Edinburgh, following traumatic brain injury (TBI). The standard deviations from 221,291 validated pressure data measurements (representing three variables) were calculated for the duration of ICP monitoring (and in 48 h epochs from the time of injury). Data were displayed on polygraphs, and several well-defined 'patterns' were described. The standard deviations of MAP, ICP and CPP for the total duration of monitoring were found to be significantly related to survival (p = 0.003, <0.001 and 0.005, respectively), while the SD of ICP alone was strongly related to global recovery (p = 0.008) in the first 48 h post-injury. Patterns in 104 epochs (each of 48 h) were identified. Ninety-two were of the type I (MAP > CPP > ICP) pattern and 12 were of the non-type I pattern. Glasgow Outcome Scale scores at 12 months were significantly related to the dichotomized pattern type (Fisher's exact test p < 0.001 for both alive versus dead and independent versus dependent outcomes). Only one patient with type I pattern died in this series. While variability of ICP during the first 48 h post-injury is predictive of the outcome, the pattern behaviour of three pressure signals gives useful outcome prediction information throughout monitoring. These displays may help interpret some of the plethora of data produced at the bedside.

Effect of deprivation and gender on the incidence and management of acute brain disorders.

OBJECTIVE: To determine the impact of deprivation and gender on the incidence and emergency management of acute brain disorders. DESIGN: Retrospective database review of mortality, hospital discharge, and ICU discharge data. SETTING: Lothian Health Board area, 1995-1999. PATIENTS AND PARTICIPANTS: All persons over the age of 15 dying or being discharged from hospital with a primary diagnosis of stroke, epilepsy, subarachnoid haemorrhage (SAH) or traumatic brain injury; patients registered in the Scottish Intensive Care Society Audit Database as having been discharged from the supraregional neurosciences intensive care unit with one of these as a primary diagnoses and a home postcode within the Lothian Health Board area. MEASUREMENTS AND RESULTS: Standardised ratios were calculated for hospital admission, mortality, and ICU admission by deprivation category and gender. Data were available for 29,205 hospital admissions, 5,227 deaths, and 360 ICU admissions. For all diagnoses, deprivation was associated with higher rates of hospital admission and death. Deprivation was associated with lower rates of ICU admission for traumatic brain injury and stroke. There was a U-shaped relationship between deprivation and ICU admission with epilepsy. There were no gender differences in rates of ICU admission. Males had higher rates of hospital admission for all conditions and of death from epilepsy and SAH, and lower rates of death from stroke. CONCLUSIONS: We have demonstrated deprivation- and gender- differences in the incidence and emergency management of four acute brain disorders. The identification of the source(s) of these differences is an important subject for further research.

Traumatic brain injury and subarachnoid hemorrhage: in vivo occult pathology demonstrated by magnetic resonance spectroscopy may not be "ischaemic". A primary study and review of the literature.

OBJECTIVES: To look for evidence of early ischaemic neurochemical changes in patients suffering severe traumatic brain injury (TBI) and severe subarachnoid haemorrhage (SAH). Proton metabolite concentrations were measured in normal and abnormal areas of brain on T2 MR imaging, in regions considered particularly vulnerable to ischaemic injury. METHODS: Intensive care patients underwent T2 weighted imaging in a 1.5 Tesla MR scanner and proton magnetic resonance spectroscopy (single voxel or chemical shift imaging). Metabolite values in areas that appeared 'normal' and 'abnormal' on T2 MR imaging were compared with those obtained from normal controls. RESULTS: 18 TBI and 6 SAH patients were imaged at 1 to 26 days. N-acetyl aspartate (NAA) was lower in TBI and SAH patients compared to controls in both T2 normal and T2 abnormal areas (p<0.0005). SAH, but not TBI patients also had increased choline and creatine compared to controls in the T2 normal (p<0.02, p<0.02 respectively) and T2 abnormal (p=0.0003, p=0.003) areas. No lactate was found in TBI or SAH patients. CONCLUSIONS: Significant loss of normal functioning neurones was present in TBI and SAH, but no evidence of anaerobic metabolism using lactate as a surrogate marker, questioning the role of 'ischemia' as a major mechanism of damage. Increased choline and creatine were found in SAH patients suggestive of increased cell-wall turnover. Current theories of brain injury after TBI or SAH do not explain these observed neurochemical changes and further research is required.

Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management?

Cardiac injury and pulmonary oedema occurring after acute neurological injury have been recognised for more than a century. Catecholamines, released in massive quantities due to hypothalamic stress from subarachnoid haemorrhage (SAH), result in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). The acute, reversible cardiac injury ranges from hypokinesis with a normal cardiac index, to low output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPO, while others exhibit signs of either one or other, or have subclinical evidence of the same. Hypoxia and hypotension are two of the most important insults which influence outcome after acute brain injury. However, despite this, little attention has hitherto been devoted to prevention and reversal of these potentially catastrophic medical complications which occur in patients with SAH. It is not clear which patients with SAH will develop important cardiac and respiratory complications. An active approach to investigation and organ support could provide a window of opportunity to intervene before significant hypoxia and hypotension develop, potentially reducing adverse consequences for the long-term neurological status of the patient. Indeed, there is an argument for all SAH patients to have echocardiography and continuous monitoring of respiratory rate, pulse oximetry, blood pressure and electrocardiogram. In the event of cardio-respiratory compromise developing i.e. cardiogenic shock and/or NPO, full investigation, attentive monitoring and appropriate intervention are required immediately to optimise cardiorespiratory function and allow subsequent definitive management of the SAH.