OBJECTIVE:Subarachnoid haemorrhage (SAH) is associated with sympathetic nervous activation and inflammation. SAH could therefore theoretically be a risk factor for development of cardiovascular disease. The aim of this study was to investigate whether long-term (≥1 year) SAH survivors had an increased risk of death due to cardiovascular causes.MATERIAL & METHODS:SAH patients ≥18 years treated at Umeå University Hospital between 1986 and 2006 were eligible for inclusion. Deceased patients were identified in the Swedish population register. Death certificates from long-term SAH survivors and causes of death in the general population were obtained from the National Board of Health and Welfare, Sweden. The prevalence of comorbidities at the time of SAH was compared with the distribution of cardiovascular risk factors in the northern Sweden MONICA (Multinational Monitoring of Trends and Determinants in Cardiovascular Disease) health survey. Analyses were stratified for age and sex.RESULTS:In the SAH patients, the median year of SAH was 1992 and the median year of death was 2001. The MONICA survey in 1994 and the distribution of deaths in the general population in 2001 were used for comparison. Long-term SAH survivors had, compared to the general population, a significantly increased risk for death due to cerebrovascular disease (P < 0.0001), but not for death due to cardiovascular disease. Hypertension was more common in SAH patients compared to survey participants (P < 0.01).CONCLUSION:Cerebrovascular causes of death were significantly more common in long-term survivors after SAH compared to the general population.

Background Subarachnoid haemorrhage ( SAH ) is a life‐threatening condition that may be aggravated by acute pituitary damage and cortisol insufficiency. Robust diagnostic criteria for critical illness‐related corticosteroid insufficiency ( CIRCI ) are lacking. The aim of this study was to assess the frequency of CIRCI in the acute phase (0–240 h) after SAH and to evaluate associations between cortisol levels and clinical parameters (sedation, circulatory failure, gender, age, severity of disease, treatment). CIRCI was defined as a single morning serum cortisol ( mSC ) < 200 nmol/L. The lower limit for calculated free cortisol ( cFC ) was set at < 22 nmol/L, and for saliva cortisol at < 7.7 nmol/L. Methods Fifty patients were included. Serum/saliva cortisol and corticosteroid‐binding globulin were obtained every second morning. A logistic regression model was used for multivariate analysis comparing cortisol levels with clinical parameters. Results Of the patients, 21/50 (42%) had an mSC < 200 nmol/L and 30/50 (60%) had a cFC < 22 nmol/L. In patients with continuous intravenous sedation, the odds ratio for a mSC to be < 200 nmol/L was 18 times higher (95% confidence interval 4.2–85.0, P < 0.001), and the odds ratio for a cFC to be < 22 nmol/L was 2.4 times higher (95% confidence interval 1.2–4.7, P < 0.05) compared with patients with no continuous intravenous sedation. Conclusions Continuous intravenous sedation was significantly associated with cortisol values under defined limits ( mSC < 200, cFC < 22 nmol/L). The possibility that sedating drugs per se may influence cortisol levels should be taken into consideration before CIRCI is diagnosed.

Background: Several factors associated with an unfavourable outcome after severe traumatic brain injury (TBI) have been described: prolonged pre‐hospital time, secondary referral to a level 1 trauma centre, the occurrence of secondary insults such as hypoxia, hypotension or low end‐tidal carbon dioxide (ETCO2). To determine whether adverse events were linked to outcome, patients with severe TBI were studied before arrival at a level 1 trauma centre. Methods: Prospective, observational study design. Patients with severe TBI (n=48), admitted to Umeå University Hospital between January 2002 to December 2005 were included. All medical records from the site of the accident to arrival at the level 1 trauma centre were collected and evaluated. Results: A pre‐hospital time of >60 min, secondary referral to a level 1 trauma centre, documented hypoxia (oxygen saturation <95%), hypotension (systolic blood pressure <90 mmHg), hyperventilation (ETCO2<4.5 kPa) or tachycardia (heart rate >100 beats/min) at any time before arrival at a level 1 trauma centre were not significantly related to an unfavourable outcome (Glasgow Outcome Scale 1–3). Conclusion: Early adverse events before arrival at a level 1 trauma centre were without significance for outcome after severe TBI in the trauma system studied.

http://jnnp.bmj.com/content/80/11/1241.full.html Updated information and services can be found at: These include: References http://jnnp.bmj.com/content/80/11/1241.full.html#ref-list-1 This article cites 39 articles, 6 of which can be accessed free at: service Email alerting box at the top right corner of the online article. Receive free email alerts when new articles cite this article. Sign up in the Topic collections (11467 articles) Injury • (12250 articles) Trauma • (1911 articles) Trauma CNS / PNS • (1765 articles) Neurological injury • (2639 articles) Coma and raised intracranial pressure • Articles on similar topics can be found in the following collections

Objective: To prospectively study S-100B and neuron specific enolase (NSE) levels in subjects treated for severe head injury (sTBI), and investigate the prognostic value of these biomarkers.Methods: Subjects included in a prospective double blind randomised study for sTBI. Inclusion criteria: Glasgow Coma Score (GCS) <= 8, age 15-70 years, first recorded cerebral perfusion pressure of >10 mm Hg and arrival, 24 h after trauma. Subjects were treated with an intracranial pressure (ICP) targeted therapy. Blood samples for S-100B and NSE were drawn immediately after arrival and every 12 h for 5 days. Outcome was evaluated as Glasgow Outcome Scale (GOS) by independent staff at 3 and 12 months.Results: 48 subjects, mean age 35.5 years, and median GCS 6 were included. The first blood sample was drawn at 15.6 (1.4) h after injury. Initial concentration of S-100B was 1.04 (0.21) mu g/l and for NSE 18.94 (2.32) mu g/l. The biomarkers were significantly higher in subjects with GCS 3 and in those who died compared with those with GCS 4-8 and GOS 2-5, respectively. Receiver operated characteristic curve analyses of the initial S-100B and NSE levels to GOS dichotomised as unfavourable (GOS 1-3) and favourable (GOS 4-5) showed a weak correlation: AUC 0.585 and 0.555, respectively. Using the dichotomisation dead (GOS 1)/alive (GOS 2-5), the AUC values were 0.687 and 0.734, respectively. Furthermore, a correlation was found between the biomarkers themselves and the biomarkers and ICP.Conclusion: At 3 and 12 months after trauma, no differences in prognostic values between the markers were apparent nor was there any clinical significant value of the markers as predictors of clinical outcome.

Koskinen, L. O. D.; Olivecrona, M.; Rodling-Wahlström, M.; Naredi, S. Author Information

Background: Evidence‐based guidelines for severe traumatic brain injury (TBI) do not include strategies for fluid administration. The protocol used in this study includes albumin administration to maintain normal colloid osmotic pressure and advocates a neutral to slightly negative fluid balance. The aim of this study was to analyze the occurrence of organ failure and the mortality in patients with severe TBI treated by a protocol that includes defined strategies for fluid therapy.Methods: Ninety‐three patients with severe TBI and Glasgow Coma Score≤8 were included during 1998–2001. Medical records of the first 10 days were retrieved. Organ dysfunction was evaluated with the Sequential Organ Failure Assessment (SOFA) score. Mortality was assessed after 10 and 28 days, 6 and 18 months.Results: The total fluid balance was positive on days 1–3, and negative on days 4–10. The crystalloid balance was negative from day 2. The mean serum albumin was 38±6 g/l. Colloids constituted 40–60% of the total fluids given per day. Furosemide was administered to 94% of all patients. Severe organ failure defined as SOFA≥3 was evident only for respiratory failure, which was observed in 29%. None developed renal failure. After 28 days, mortality was 11% and, after 18 months, it was 14%.Conclusions: A protocol including albumin administration in combination with a neutral to a slightly negative fluid balance was associated with low mortality in patients with severe TBI in spite of a relatively high frequency (29%) of respiratory failure, assessed with the SOFA score.

Acta Anaesthesiologica ScandinavicaVolume 51, Issue 10 p. 1294-1296 Conventional treatments for severe head injury: are they effective, ineffective, or even harmful? P.-O. Grände, Corresponding Author P.-O. Grände 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkPer-Olof Grände Department of Anaesthesiology and Intensive CareUniversity Hospital of LundSwedene-mail: [email protected]Search for more papers by this author 1 L.-O. Koskinen, L.-O. Koskinen 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 2 S. Naredi, S. Naredi 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 3 P. Reinstrup, P. Reinstrup 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 1 B. Romner, B. Romner 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 4 P.-O. Grände, Corresponding Author P.-O. Grände 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkPer-Olof Grände Department of Anaesthesiology and Intensive CareUniversity Hospital of LundSwedene-mail: [email protected]Search for more papers by this author 1 L.-O. Koskinen, L.-O. Koskinen 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 2 S. Naredi, S. Naredi 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 3 P. Reinstrup, P. Reinstrup 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 1 B. Romner, B. Romner 1Department of Anaesthesiology and Intensive Care, Lund University Hospital, Sweden, 2Department of Neurosurgery, Umeå University Hospital, Sweden, 3Department of Anaesthesiology and Intensive Care, Umeå University Hospital, Sweden, 4Clinic of Neurosurgery, Neuroscience Centre, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author 4 First published: 18 October 2007 https://doi.org/10.1111/j.1399-6576.2007.01475.xCitations: 1Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume51, Issue10November 2007Pages 1294-1296 RelatedInformation

OBJECTIVES:Hemicraniectomy in patients with malignant middle cerebral artery (mMCA) infarct may be life-saving. The long-term prognosis is unknown.METHODS:Patients with mMCA infarct treated with hemicraniectomy between 1998 and 2002 at three hospitals were included. The criterion for surgical intervention was if the patients deteriorated from awake to being responding to painful stimuli only. All patients were followed for at least 1 year. Outcome was defined as alive/dead, walkers/non-walkers or modified Rankin Scale (mRS) score <or=2.RESULTS:Thirty patients were included (median age at stroke onset 49 years, range 17-67 years). Fourteen patients had mMCA infarct on the left side and 16 patients on the right side. Fourteen patients had pupil dilatation before surgery. Hemicraniectomy was performed at a median of 52 h (range 13-235 h) after stroke onset. Nine patients died within 1 month after surgery because of cerebral herniation (n = 6), myocardial infarction (n = 1) or intensive care complications (n = 2). No further deaths occurred during follow-up, which was at median 3.4 years after surgery. Status for the 21 survivors at the last follow-up was: mRS 2 or less (n = 6) and mRS 3-5 (n = 15). The oldest patient with mRS 2 or less was 53 years at stroke onset. Thirteen patients (43%) could walk without substantial aid.CONCLUSION:The long-term survival after mMCA infarction treated with hemicraniectomy seems to be favourable if the patient survives the acute phase. The outcome as measured with mRS may be better among younger patients.

Koskinen, L.-O. D.1; Olivecrona, M.1; Rodling-Wahlström, M.2; Naredi, S.2 Author Information

Olivecrona, M.1; Rodling-Wahlström, M.2; Naredi, S.2; Koskinen, L.-O. D.1 Author Information

We reported findings concerning continuous intracranial pressure (ICP) and cerebral perfusion pressure (CPP) measurements and mortality in patients with severe bacterial meningitis treated on the basis of an ICP-targeted approach. Eighteen patients with severe bacterial meningitis were admitted for neurointensive care at Umeå University Hospital (Umeå, Sweden). In 15 patients, ICP was measured continuously through an ICP measuring device. During care, all patients but one developed intracranial hypertension with an ICP of >or=15 mm Hg (14 [93%] of 15 patients). Ten (67%) of 15 patients survived and were discharged, and 5 patients (33%) died. Mean ICP was significantly higher and CPP was markedly decreased in nonsurvivors, compared with survivors. Among the survivors, ICP was gradually reduced. Treatment of patients with severe bacterial meningitis should include neurointensive care and continuous ICP measurement. Increased ICP may be reduced by using the ICP-targeted therapy that closely resembles the "Lund concept."

Naredi, Silvana; Koskinen, Lars-Ove; Grände, P-O; Nordström, Carl-Henrik; Nellgård, Bengt; Rydenhag, Bertil; Vegfors, Magnus Author Information

Subarachnoid haemorrhage is a serious condition, often accompanied by cerebral vasospasm and hydrocephalus, which may result in delayed cerebral ischaemia and neurological deterioration. While the mechanisms responsible remain unknown, activation of the sympathetic nervous system, leading to elevated levels of circulating catecholamines is, at least in part, implicated. In this study, we sought to examine the importance of sympathetic nervous activation and its relation to brain monoaminergic neurotransmission in 25 patients following subarachnoid haemorrhage by examining plasma and cerebrospinal fluid levels of the catecholamines noradrenaline, adrenaline and dopamine, and their metabolites. Total body sympathetic activity was concurrently assessed using isotope dilution methodology. In the early phase following subarachnoid haemorrhage patients exhibited markedly elevated rates of spillover of noradrenaline to plasma (9.11±1.12 vs. 3.39±0.26nmol/min, p<0.01), with rates being higher in those patients in whom hydrocephalus developed (11.15±1.40 vs. 7.90±1.41nmol/min, p=0.05). The degree of sympathetic nervous activation tended to be higher in females compared with males. Lower cerebral perfusion pressures were observed in those patients in whom cerebrospinal fluid concentrations of noradrenaline and dopamine metabolites were high. A marked sympathetic nervous activation, more pronounced in women and in those with hydrocephalus, occurs following subarachnoid haemorrhage. The diminished cerebral perfusion seen following subarachnoid bleeding may occur as a result of activation of central catecholaminergic neurones.