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.

OBJECT:Decision tree analysis highlights patient subgroups and critical values in variables assessed. Importantly, the results are visually informative and often present clear clinical interpretation about risk factors faced by patients in these subgroups. The aim of this prospective study was to compare results of logistic regression with those of decision tree analysis of an observational, head-injury data set, including a wide range of secondary insults and 12-month outcomes.METHODS:One hundred twenty-four adult head-injured patients were studied during their stay in an intensive care unit by using a computerized data collection system. Verified values falling outside threshold limits were analyzed according to insult grade and duration with the aid of logistic regression. A decision tree was automatically produced from root node to target classes (Glasgow Outcome Scale [GOS] score). Among 69 patients, in whom eight insult categories could be assessed, outcome at 12 months was analyzed using logistic regression to determine the relative influence of patient age, admission Glasgow Coma Scale score, Injury Severity Score (ISS), pupillary response on admission, and insult duration. The most significant predictors of mortality in this patient set were duration of hypotensive, pyrexic, and hypoxemic insults. When good and poor outcomes were compared, hypotensive insults and pupillary response on admission were significant. Using decision tree analysis, the authors found that hypotension and low cerebral perfusion pressure (CPP) are the best predictors of death, with a 9.2% improvement in predictive accuracy (PA) over that obtained by simply predicting the largest outcome category as the outcome for each patient. Hypotension was a significant predictor of poor outcome (GOS Score 1-3). Low CPP, patient age, hypocarbia, and pupillary response were also good predictors of outcome (good/poor), with a 5.1% improvement in PA. In certain subgroups of patients pyrexia was a predictor of good outcome.CONCLUSIONS:Decision tree analysis confirmed some of the results of logistic regression and challenged others. This investigation shows that there is knowledge to be gained from analyzing observational data with the aid of decision tree analysis.

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.

Summary. 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.

The objective was to compare secondary insults, particularly decreases in jugular bulb oxyhaemoglobin saturation (SjO(2)), during intensive care in patients with "poor" and "good" outcomes 12 months after traumatic brain injury. A prospective observational study of patients' physiological data collected each minute from multimodality monitoring was carried out. Patients had duration of physiological insults quantified as a percentage of their validated monitoring time (once invalid data due to technical reasons were removed). Treatment protocols were designed to minimise secondary insults by maintaining intracranial pressure (ICP) less than 20 mm Hg, and cerebral perfusion pressure (CPP) greater than 70 mm Hg, with prompt correction of hypoxia and pyrexia. Twelve months after injury patients' neurological function was assessed using the Glasgow outcome scale (GOS). A poor outcome was defined as GOS 1 to 3 (group 1) and a good outcome as GOS 4 and 5 (group 2). Seventy five patients (64 male), median age of 34 years (range 15 to 70), were studied. At 12 months 33 patients had a poor outcome (group 1), and 42 a good outcome (group 2). Group 1 spent proportionately more time with SjO(2) greater than 75% compared with group 2 (p<0.05), and more time with SjO(2) below 54% (p<0.04). Group 1 patients also spent proportionately more time with CPP less than 70 mm Hg than group 2 (p<0.04). Patients in group 1 were older (p<0.04) and had a lower postresuscitation Glasgow coma score (p<0.002). There was no difference between the groups for ICP, injury severity score, peripheral pulse saturation, and pyrexia. This study confirms that secondary insults, including an increased SjO(2), occur significantly more in patients with poor outcomes. More research into strategies to reduce the impact of secondary insults, including management of increased SjO(2), is required.

Teaching and OSCE assessment of core clinical skills requires large resources in time and staff. Therefore, ensuring efficient and effective teaching that produces quantifiably competent students is important. This study compared the content of an 'Advanced Life Support (ALS) Course' with the medical undergraduate curriculum at this institution; it examined the OSCE resuscitation station for medical students to identify common errors where teaching could be improved; and finally it compared the resuscitation station with other skilled task stations. The written curriculum for the 'ALS' course and undergraduates was scrutinized for content and duration. Performance in the resuscitation station was analysed by dividing it into 20 separate skilled tasks marked individually. This station was compared with stations on chest and abdominal examination, and fundoscopy. Undergraduate resuscitation teaching exceeded the 'ALS' course in duration, including theoretical and practical teaching, and in depth of knowledge. During the practical resuscitation OSCE several skilled tasks were identified as deficient. The results of the resuscitation OSCE were better than those from the other skilled task stations. Students perform to a higher standard in OSCE stations that assess ability to deal with stressful situations. Their performance in the simulated environment of the OSCE is of a high standard and may in part be due to the fact that the station is omnipresent, without cross-compensation of marks. Formal 'ALS' courses are expensive and, as this study demonstrates, unnecessary given the high standards attained.

Increased QT dispersion is a marker for cardiac morbidity and mortality. Carbon monoxide (CO) is a potent myocardial toxin and this report describes the change in QT dispersion during intensive care therapy for severe CO poisoning.

Measurement of the saturation of brain effluent blood gives a global estimate of cerebral oxygenation. It may provide clinicians with information to assist in reducing secondary insults to the brain with potential benefits to a range of patients with actual or potential acute brain injury such as trauma and cardiac bypass procedures. The technology to continuously measure this variable is simple to use but requires attention to detail; it is limited in its ability to detect discrete regions of ischaemia or hyperaemia unless these are of sufficient magnitude to influence the saturation of brain effluent blood. There are few complications that result from this invasive technique and they are usually of a minor nature. The technique also enables research opportunities from the ability to sample blood as it leaves the cranium. Poor outcomes are seen in patients with traumatic brain injury who exhibit either reduced or increased cerebrovenous oxygen saturation and it remains to be seen if detection and correction of these anomalies will produce patient benefits.

A postal survey of NHS hospital-based anaesthetists providing out-patient anaesthesia for dental procedures in children under 10 years of age was conducted in February 1999. Information was sought about quality of care and common practice in Scotland. The experience of the anaesthetists involved in such work was substantial, but the monitoring used did not meet current standards, with only 16% of respondents indicating use of a full range of standard devices. Separate recovery facilities were available to 99%, and all had access to a defibrillator, but the qualifications of dedicated assistant and recovery staff were lacking in 14 and 30%, respectively. Intravenous access was not obtained routinely after inhalational induction of anaesthesia by up to 71% (49%, never; 22%, sometimes). Systemic analgesia or local anaesthesia was used by 88%. Discharge times ranged from 10 min to 6 h.

Objective: To quantify central neuronal damage in patients with acute traumatic brain injury (TBI), to determine if brain tissue ischaemia was present using lactate as a marker, and to describe methods of delivering intensive anaesthetic care within a magnetic resonance scanner. Design: Patients underwent T2 weighted magnetic resonance and spectroscopic imaging (SI) early after TBI. Setting: A tertiary referral centre for neurosurgery and neurointensive care in Scotland. Subjects: Eight adults with TBI imaged 4-26 days (mean 13) after injury. Findings were compared to six healthy volunteer control subjects. Measurements and results: A significant reduction of N-acetyl aspartate (NAA- a neurone specific amino acid) was found in areas of brain with obvious lesions on T2 weighted imaging (p<0.001), and in areas where there were no obvious T2 lesions (p<0.02) compared with volunteer control spectra. We found no evidence of lactate. Conclusions: SI may be useful in assessing the extent of neuronal injury which compliments CT and MRI information. Traumatic brain injury affects all age groups and the associated morbidity has devastating consequences, SI may therefore assist clinicians in the management of these patients in the future. As demand for MR imaging of intensive care patients increases, clinicians will require to continue to develop safe working practices and maintain intensive care monitoring and therapies during these investigations.

Magnetic resonance imaging (MRI) of patients with acute brain injury has never been straightforward due to the duration of the scan, the need for the patient to remain motionless and because patients are often unable to co-operate due to their injury. The investigation of choice at the present time for these brain injured patients is computed tomography (CT) scans [1] which can be performed in minutes but involve large doses of radiation (2μSv per scan) and have lower resolution for brain tissue lesions. Patients who are confused or comatose require a general anesthetic during the CT scan for their own safety, and to reduce movement artifact so that the results are interpretable. The need for the same precautions, anesthesiology staff, support staff, and equipment, also apply to intensive care unit (ICU) patients. Anesthesiologists involved in ICU patient transfers will appreciate the organization and training required to carry this out safely, especially if the patients are unstable but require urgent imaging, e.g., for suspected intracranial hematoma. The safe organization of (MRI) for these patients takes time and, additionally, the imaging sequences often take up to an hour. This explains the scarcity of research into acute brain injury utilizing MRI techniques: in principle, with the right patient selection, this is a safe procedure [2].

Using single slice two-dimensional spectroscopic imaging (SI), nine acute head injury patients and six controls have been successfully scanned. The problems presented by the need for ITU monitoring of these patients during MR scanning was overcome using MR compatible monitoring equipment. In previous studies of head injury which used proton spectroscopy, single voxel localisation procedures have meant that the spatial extent of the spectral data has been limited. With spectral data from a whole axial slice, we have been able to identify NAA abnormalities in regions remote to any T2 visible lesions. This suggests that SI (of NAA in particular) will be useful for the diagnosis of diffuse axonal injury.