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 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.

Skilled task teaching and assessment.

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.