Lower Admission Glasgow Coma Scale Research Articles

Clinical Epidemiology of Adults With Moderate Traumatic Brain Injury.

To characterize admission patterns, treatments, and outcomes among patients with moderate traumatic brain injury. Retrospective cohort study. National Trauma Data Bank. Adults (age > 18 yr) with moderate traumatic brain injury (International Classification of Diseases, Ninth revision codes and admission Glasgow Coma Scale score of 9-13) in the National Trauma Data Bank between 2007 and 2014. None. Demographics, mechanism of injury, hospital course, and facility characteristics were examined. Admission characteristics associated with discharge outcomes were analyzed using multivariable Poisson regression models. Of 114,066 patients, most were white (62%), male (69%), and had median admission Glasgow Coma Scale score of 12 (interquartile range, 10-13). Seventy-seven percent had isolated traumatic brain injury. Concussion, which accounted for 25% of moderate traumatic brain injury, was the most frequent traumatic brain injury diagnosis. Fourteen percent received mechanical ventilation, and 66% were admitted to ICU. Over 50% received care at a community hospital. Seven percent died, and 32% had a poor outcome, including those with Glasgow Coma Scale score of 13. Compared with patients 18-44 years, patients 45-64 years were twice as likely (adjusted relative risk, 1.97; 95% CI, 1.92-2.02) and patients over 80 years were five times as likely (adjusted relative risk, 4.66; 95% CI, 4.55-4.76) to have a poor outcome. Patients with a poor discharge outcome were more likely to have had hypotension at admission (adjusted relative risk, 1.10; 95% CI, 1.06-1.14), lower admission Glasgow Coma Scale (adjusted relative risk, 1.37; 95% CI, 1.34-1.40), higher Injury Severity Score (adjusted relative risk, 2.97; 95% CI, 2.86-3.09), and polytrauma (adjusted relative risk, 1.05; 95% CI, 1.02-1.07), compared with those without poor discharge outcomes. Many patients with moderate traumatic brain injury deteriorate, require neurocritical care, and experience poor outcomes. Optimization of care and outcomes for this vulnerable group of patients are urgently needed.

Reversal of antiplatelet therapy in traumatic intracranial hemorrhage: Does timing matter?

Reversal of antiplatelet therapy with platelet transfusion in traumatic intracranial hemorrhage remains controversial. Several studies have examined this topic but few have investigated whether the timing of transfusion affects outcomes. Patients admitted to a level 1 trauma center from 1/1/14 to 3/31/16 with traumatic intracranial hemorrhage taking pre-injury antiplatelet therapy were retrospectively analyzed. Patients on concurrent pre-injury anticoagulant therapy were excluded. Per institutional guideline, patients on pre-injury clopidogrel received 2 doses of platelets while patients on pre-injury aspirin received 1 dose of platelets. Patients with worsening hemorrhage defined by an increase in the Rotterdam score on follow up CT were compared to those without worsening. Mortality, need for neurosurgical intervention, and timing of platelet transfusion were analyzed. A total of 243 patients were included with 23 (9.5%) having worsening hemorrhage. Patients with worsening hematoma had higher injury severity score, head abbreviated injury scale, incidence of subdural hematoma, mortality, and lower Glasgow coma scale. There was no significant difference in the number of minutes to platelet transfusion between groups. After logistic regression analysis the presence of subdural hematoma and lower admission Glasgow coma scale were predictors of worsening hematoma, while there remained no significant difference in minutes to platelet transfusion. The timing of platelet transfusion did not have any impact on rates of worsening hematoma for patients with traumatic intracranial hemorrhage on pre-injury antiplatelet therapy. Potential risk factors for worsening hematoma in this group are the presence of subdural hematoma and lower admission Glasgow coma scale.

Systemic inflammatory response syndrome, infection, and outcome in intracerebral hemorrhage.

Objective:Systemic inflammatory response syndrome (SIRS) may be related to poor outcomes after intracerebral hemorrhage (ICH).Methods:The Ethnic/Racial Variations of Intracerebral Hemorrhage study is an observational study of ICH in whites, blacks, and Hispanics throughout the United Sates. SIRS was defined by standard criteria as 2 or more of the following on admission: (1) body temperature <36°C or >38°C, (2) heart rate >90 beats per minute, (3) respiratory rate >20 breaths per minute, or (4) white blood cell count <4,000/mm3 or >12,000/mm3. The relationship among SIRS, infection, and poor outcome (modified Rankin Scale [mRS] 3–6) at discharge and 3 months was assessed.Results:Of 2,441 patients included, 343 (14%) met SIRS criteria at admission. Patients with SIRS were younger (58.2 vs 62.7 years; p < 0.0001) and more likely to have intraventricular hemorrhage (IVH; 53.6% vs 36.7%; p < 0.0001), higher admission hematoma volume (25.4 vs 17.5 mL; p < 0.0001), and lower admission Glasgow Coma Scale (GCS; 10.7 vs 13.1; p < 0.0001). SIRS on admission was significantly related to infections during hospitalization (adjusted odds ratio [OR] 1.36, 95% confidence interval [CI] 1.04–1.78). In unadjusted analyses, SIRS was associated with poor outcomes at discharge (OR 1.96, 95% CI 1.42–2.70) and 3 months (OR 1.75, 95% CI 1.35–2.33) after ICH. In analyses adjusted for infection, age, IVH, hematoma location, admission GCS, and premorbid mRS, SIRS was no longer associated with poor outcomes.Conclusions:SIRS on admission is associated with ICH score on admission and infection, but it was not an independent predictor of poor functional outcomes after ICH.

Critical Care Resource Utilization and Outcomes of Children With Moderate Traumatic Brain Injury.

To characterize admission patterns, critical care resource utilization, and outcomes in moderate pediatric traumatic brain injury. Retrospective cohort study. National Trauma Data Bank. Children under 18 years old with a diagnosis of moderate traumatic brain injury (admission Glasgow Coma Scale score of 9-13) in the National Trauma Data Bank between 2007 and 2014. We examined clinical characteristics, critical care resource utilization, and discharge outcomes. Poor outcomes were defined as discharge to hospice, skilled nursing facility, long-term acute care, or death. We examined 20,010 patient records. Patients were 9 years old (interquartile range, 2-15 yr), male (64%) with isolated traumatic brain injury (81%), Glasgow Coma Scale score of 12, head Abbreviated Injury Scale score of 3, and Injury Severity Score of 10. Majority (34%) were admitted to nontrauma hospitals. Critical care utilization was 58.7% including 11.5% mechanical ventilation and 3.2% intracranial pressure monitoring. Compared to patients with Glasgow Coma Scale score of 13, admission Glasgow Coma Scale score of 9 was associated with greater critical care resource utilization, such as ICU admission (72% vs 50%), intracranial pressure monitoring (7% vs 1.8%), mechanical ventilation (21% vs 6%), and intracranial surgery (10% vs 5%). Most patients (70%) were discharged to home, but up to one third had poor outcomes. Older age group had a higher risk of poor outcomes (10-14 yr; adjusted relative risk, 1.32; 95% CI, 1.13-1.54; 15-17 yr; adjusted relative risk, 2.39; 95% CI, 2.12-2.70). Poor outcomes occurred with lower Glasgow Coma Scale (Glasgow Coma Scale score of 9 vs Glasgow Coma Scale score of 13: adjusted relative risk, 2.89; 95% CI, 2.47-3.38), higher Injury Severity Score (Injury Severity Score of ≥ 16 vs Injury Severity Score of < 9: adjusted relative risk, 8.10; 95% CI 6.27-10.45), and polytrauma (adjusted relative risk, 1.40; 95% CI, 1.22-1.61). Critical care resources are used in more than half of all moderate pediatric traumatic brain injury, and many receive care at nontrauma hospitals. Up to one third of moderate pediatric traumatic brain injury have poor outcomes, risk factors for which include age greater than 10 years, lower admission Glasgow Coma Scale, higher Injury Severity Score, and polytrauma. There is urgent need to optimize triage, care, and outcomes in this vulnerable population.

Traumatic brain injury and intracranial hemorrhage–induced cerebral vasospasm: a systematic review

OBJECTIVE Little is known regarding the natural history of posttraumatic vasospasm. The authors review the pathophysiology of posttraumatic vasospasm (PTV), its associated risk factors, the efficacy of the technologies used to detect PTV, and the management/treatment options available today. METHODS The authors performed a systematic review in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines using the following databases: PubMed, Google Scholar, and CENTRAL (the Cochrane Central Register of Controlled Trials). Outcome variables extracted from each study included epidemiology, pathophysiology, time course, predictors of PTV and delayed cerebral ischemia (DCI), optimal means of surveillance and evaluation of PTV, application of multimodality monitoring, modern management and treatment options, and patient outcomes after PTV. Study types were limited to retrospective chart reviews, database reviews, and prospective studies. RESULTS A total of 40 articles were included in the systematic review. In many cases of mild or moderate traumatic brain injury (TBI), imaging or ultrasonographic studies are not performed. The lack of widespread assessment makes finding the true overall incidence of PTV a difficult endeavor. The clinical consequences of PTV are important, given the morbidity that can result from it. DCI manifests as new-onset neurological deterioration that occurs beyond the timeframe of initial brain injury. While there are many techniques that attempt to diagnose cerebral vasospasm, digital subtraction angiography is the gold standard. Some predictors of PTV include SAH, intraventricular hemorrhage, low admission Glasgow Coma Scale (GCS) score (< 9), and young age (< 30 years). CONCLUSIONS Given these results, clinicians should suspect PTV in young patients presenting with intracranial hemorrhage (ICH), especially SAH and/or intraventricular hemorrhage, who present with a GCS score less than 9. Monitoring and regulation of CNS metabolism following TBI/ICH-induced vasospasm may play an important adjunct role to the primary prevention of vasospasm.

Early Systolic Dysfunction Following Traumatic Brain Injury: A Cohort Study

Prior studies have suggested that traumatic brain injury may affect cardiac function. Our study aims were to determine the frequency, longitudinal course, and admission risk factors for systolic dysfunction in patients with moderate-severe traumatic brain injury. Prospective cohort study. Level 1 trauma center. Transthoracic echocardiogram within 1 day and over the first week after moderate-severe traumatic brain injury; transthoracic echocardiogram within 1 day after mild traumatic brain injury (comparison group). Systolic function was assessed by transthoracic echocardiogram, and systolic dysfunction was defined as fractional shortening less than 25%. Multivariable Poisson regression models examined admission risk factors for systolic dysfunction. Systolic function in 32 patients with isolated moderate-severe traumatic brain injury and 32 patients with isolated mild traumatic brain injury (comparison group) was assessed with transthoracic echocardiogram. Seven (22%) moderate-severe traumatic brain injury and 0 (0%) mild traumatic brain injury patients had systolic dysfunction within the first day after injury (p < 0.01). All patients with early systolic dysfunction recovered in 1 week. Younger age (relative risk, 0.87; 95% CI, 0.79-0.94; for 1 yr increase in age) and lower admission Glasgow Coma Scale score (relative risk, 0.34; 95% CI, 0.20-0.58; for one unit increase in Glasgow Coma Scale) were independently associated with the development of systolic dysfunction among moderate-severe traumatic brain injury patients. Early systolic dysfunction can occur in previously healthy patients with moderate-severe traumatic brain injury, and it is reversible over the first week of hospitalization. Younger age and lower admission Glasgow Coma Scale score are independently associated with the development of systolic dysfunction after moderate-severe traumatic brain injury.

Significance of admission hypoalbuminemia in acute intracerebral hemorrhage.

Low levels of serum albumin may increase the risk of infections and mortality in critically ill patients. We tested the hypothesis that admission hypoalbuminemia predicted infectious complications and poor outcome in subjects with acute intracerebral hemorrhage (ICH). We analyzed a single center cohort of ICH patients collected between 1994 and 2015. Pneumonia, urinary tract infection and sepsis were retrospectively identified, according to validated criteria. Serum albumin was measured on admission and hypoalbuminemia was defined as total albumin≤3.5g/dL. The association between albumin levels, infections, and mortality at 90days was tested with multivariable logistic regression analyses. A total of 2010 patients were included (median age 74years, 54.5% males) of whom 444 (22.1%) had hypoalbuminemia on admission and 763 (38%) died within 90days. The frequency of pneumonia, urinary tract infection, and sepsis was 19.9, 15.1, and 2.7%, respectively. Hypoalbuminemic patients had lower admission Glasgow coma scale, higher frequency of intraventricular hemorrhage and were more likely to have a history of chronic kidney or liver disease. After adjustment for potential confounders, hypoalbuminemia was an independent predictor of pneumonia [odds ratio (OR) 1.76, 95% confidence interval (CI) 1.34-2.33, p<0.001] and sepsis (OR 2.29, 95% CI 1.22-4.30, p=0.010). Low levels of albumin were also independently associated with higher mortality at 90days (OR 1.78, 95% CI 1.30-2.44, p<0.001). In conclusion, early hypoalbuminemia is common and predicts poor outcome in ICH patients. Increased susceptibility to pneumonia and sepsis may be the pathophysiological mechanism underlying this association.

Clinical Features and Outcomes of Bilateral Decompression Surgery for Immediate Contralateral Hematoma after Craniectomy Following Acute Subdural Hematoma.

ObjectiveImmediate contralateral epidural hematoma (EDH) and traumatic intracerebral hematoma (T-ICH) after craniectomy for traumatic subdural hematoma (SDH) are rare but devastating post-operative complications. Their clinical features and outcomes are not well studied. In this report, we present the clinical features and outcomes of immediate contralateral acute hematoma cases requiring a second operation.MethodsThis study includes 10 cases of immediate contralateral EDH and T-ICH following bilateral craniectomy for the evacuation of traumatic SDH and contralateral hematoma between 2004 and 2015. Their medical records and radiographic findings were reviewed and analyzed retrospectively.ResultsTen of the 528 patients (1.89%) who underwent craniectomy for the evacuation of traumatic SDH developed post-operative EDH (n=5), T-ICH (n=5). The trauma was caused by a fall in 5 patients and by a traffic accident in 5 patients. The patients who suffered trauma due to pedestrian accidents died. Seven patients had a low admission Glasgow Coma Scale (GCS; GCS≤8) score in the preoperative state (average admission GCS, 7.7; average discharge GCS, 3.4; and average discharge Glasgow Outcome Scale, 2.0). Severe intra-operative brain swelling was noted in all patients, while skull fracture was observed in 8. Multiple associated injuries and medication for heart disease were characteristic of patients who died.ConclusionThe prognosis of delayed contralateral hematoma was very poor. Multiple associated injuries, past medical history and traffic accidents, especially pedestrians were seemed to be associated with higher mortality rates. Finally, contralateral skull fractures can indicate high risk of delayed contralateral acute intracranial hematoma.

Hydrocephalus associated with childhood nonaccidental head trauma.

OBJECTIVE The incidence of posttraumatic ventriculomegaly (PTV) and shunt-dependent hydrocephalus after nonaccidental head trauma (NAHT) is unknown. In the present study, the authors assessed the timing of PTV development, the relationship between PTV and decompressive craniectomy (DC), and whether PTV necessitated placement of a permanent shunt. Also, NAHT/PTV cases were categorized into a temporal profile of delay in admission and evaluated for association with outcomes at discharge. METHODS The authors retrospectively reviewed the cases of patients diagnosed with NAHT throughout a 10-year period. Cases in which sequential CT scans had been obtained (n = 28) were evaluated for Evans' index to determine the earliest time ventricular dilation was observed. Discharge outcomes were assessed using the King's Outcome Scale for Childhood Head Injury score. RESULTS Thirty-nine percent (11 of 28) of the patients developed PTV. A low admission Glasgow Coma Scale (GCS) score predicted early PTV presentation (within < 3 days) versus a high GCS score (> 1 week). A majority of PTV/NAHT patients presented with a subdural hematoma (both convexity and interhemispheric) and ischemic stroke, but subarachnoid hemorrhage was significantly associated with PTV/NAHT (p = 0.011). Of 6 patients undergoing a DC for intractable intracranial pressure, 4 (67%) developed PTV (p = 0.0366). These patients tended to present with lower GCS scores and develop ventriculomegaly early. Only 2 patients developed hydrocephalus requiring shunt placement. CONCLUSIONS PTV presents early after NAHT, particularly after a DC has been performed. However, the authors found that only a few PTV/NAHT patients developed shunt-dependent hydrocephalus.

Abstract 94: Mortality Review For The First 400 Patients Enrolled In The Clot Lysis: Evaluation Of Accelerated Resolution Of Intraventricular Hemorrhage Trial (CLEAR III)

Objective: CLEAR III is a Phase III, 500-subject, multicenter, double-blind, randomized study comparing extraventricular drainage (EVD) plus intraventricular recombinant tissue plasminogen activator (rtPA) vs. EVD plus placebo for treatment of intraventricular hemorrhage (IVH) in patients with intracerebral hemorrhage (ICH) volume &lt;30cc. We compared proximate causes of death in the acute and post-hospitalization phase of the first 400 subjects enrolled. Methods: We reviewed serious adverse event (SAE) reports for 106 events that resulted in death within 1 year follow-up. We recorded clinical and volumetric data including ICH and IVH volumes on diagnostic, stability, and end-of-treatment (EOT) computed tomography (CT) scans. EOT was defined as the CT at 72 hours post administration of last dose of test article. Results: Of the first 400 subjects enrolled, 27% (106) died, 12% (47) within 30 days of symptom onset. Median [iqr] time to death was 41.5 [71] days. Mean age (±SEM) was 64.0(±1.0) years. Proximate cause of death was neurologic in 52.8% (56), followed by respiratory (14.1%; 15), cardiac (10.4%; 11), multi-organ failure (5.7%; 6), infection (3.8%; 4) and unknown (11.3%; 12). Withdrawal of care (WOC) occurred in 46.2% (49); the majority of deaths were neurologic. Median time to death depended on proximate cause (p=0.0005): Neurologic deaths occurred at 25.5 [36] days vs. 67 [102] days for non-neurologic deaths (p=0.0002). WOC led to death 22 [53] days after ICH and cardiac arrest at 27 [25] days. Patients with no WOC and non-neurologic death died at 76 [106.5] days after ICH. After adjusting for diagnostic IVH volume, age and WOC, factors independently associated with early (≤30d) vs. later (&gt;30-365d) death were male gender (p=0.01), lower admission Glasgow coma scale (p=0.02), no pneumonia (p=0.02) and higher EOT IVH volume (trend p=0.06). Conclusion: The CLEAR III mortality rate for the first 400 subjects enrolled remains below literature estimates for severe IVH and is below the pre-specified recruitment suspension threshold of 40%. Approximately half of known causes of death are directly due to neurologic events and occur significantly earlier than non-neurologic causes. Reduction in IVH volume may lower early mortality risk.

Independent risk factors for a complicated hospital course in intensive care unit overdose patients.

The purpose of the present study was to identify risk factors associated with a complicated hospital course in overdose patients admitted to the intensive care unit. A total of 335 overdose patients were retrospectively studied in the surgical and medical intensive care unit of an academic tertiary hospital. Factors possibly associated with a complicated hospital course were evaluated. Complicated hospital course was defined as the occurrence of pneumonia, rhabdomyolysis, decubitus ulcer, nerve palsy, prolonged intubation, prolonged hospitalization, or death. Of the 335 overdose patients, 93 (27.8%) had a complicated hospital course. Complicated hospital course was found to be associated with a high number of ingested pills (median, 135 [interquartile range, 78-240] versus 84 [53-134] tablets, P < 0.0001), low Glasgow Coma Scale score on admission (7 [3-11] versus 13 [8-15], P < 0.0001), and a high serum lactate level on admission (1.8 [1.0-3.0] versus 1.4 [0.9-2.0] mg/dL, P < 0.01) on univariate analysis of these factors in patients with and without a complicated hospital course. The independent risk factors for a complicated hospital course identified on multivariate analysis were a high number of ingested pills (≥100 tablets), low admission Glasgow Coma Scale score (<9), and high serum lactate on admission (≥2.0 mg/dL). The probability of a complicated hospital course for patients with 0, 1, 2, or all 3 independent risk factors were 7%, 22%, 40%, and 81%, respectively. The total number of ingested pills, admission Glasgow Coma Scale score, and serum lactate level on admission are predictive of a complicated hospital course in overdose patients admitted to the intensive care unit.

Nonconvulsive Electrographic Seizures are Common in Children With Abusive Head Trauma*

To determine the prevalence of nonconvulsive seizures in children with abusive head trauma. Retrospective study of children with abusive head trauma undergoing clinically indicated continuous electroencephalographic monitoring. PICU of a tertiary care hospital. Children less than or equal to 2 years old with evidence of abusive head trauma determined by neuroimaging, physical examination, and determination of abuse by the Child Protection Team. None. Thirty-two children with abusive head trauma were identified with a median age of 4 months (interquartile range 3, 5.5 months). Twenty-one of 32 children (66%) underwent electroencephalographic monitoring. Those monitored were more likely to have a lower admission Glasgow Coma Scale (8 vs 15, p = 0.05) and be intubated (16 vs 2, p = 0.002). Electrographic seizures occurred in 12 of 21 children (57%) and constituted electrographic status epilepticus in 8 of 12 children (67%). Electrographic seizures were entirely nonconvulsive in 8 of 12 children (67%). Electroencephalographic background category (discontinuous and slow-disorganized) (p = 0.02) and neuroimaging evidence of ischemia were associated with the presence of electrographic seizures (p = 0.05). Subjects who had electrographic seizures were no more likely to have clinical seizures at admission (67% electrographic seizures vs 33% none, p = 0.6), parenchymal imaging abnormalities (61% electrographic seizures vs 39% none, p = 0.40), or extra-axial imaging abnormalities (56% electrographic seizures vs 44% none, p = 0.72). Four of 21 (19%) children died prior to discharge; none had electrographic seizures, but all had attenuated-featureless electroencephalographic backgrounds. Follow-up outcome data were available for 16 of 17 survivors at a median duration of 9.5 months following PICU admission, and the presence of electrographic seizures or electrographic status epilepticus was not associated with the Glasgow Outcome Scale score (p = 0.10). Electrographic seizures and electrographic status epilepticus are common in children with abusive head trauma. Most seizures have no clinical correlate. Further study is needed to determine whether seizure identification and management improves outcome.

Extracellular histone release in response to traumatic injury

Tissue injury leads to the release of DAMPs (damage-associated molecular patterns) that may drive a sterile inflammatory response; however, the role of extracellular histone levels after traumatic injury remains unexplored. We hypothesized that extracellular histone levels would be increased and associated with poor outcomes after traumatic injury. In this prognostic study, plasma was prospectively collected from 132 critically injured trauma patients on arrival and 6 hours after admission to an urban Level I trauma intensive care unit. Circulating extracellular histone levels and plasma clotting factors were assayed and linked to resuscitation and outcome data. Of 132 patients, histone levels were elevated to a median of 14.0 absorbance units (AU) on arrival, declining to 6.4 AU by 6 hours. Patients with elevated admission histone levels had higher ISS (Injury Severity Score), lower admission GCS (Glasgow Coma Scale) score, more days of mechanical ventilation, and higher incidences of multiorgan failure, acute lung injury, and mortality (all p ≤ 0.05). Histone levels correlated with prolonged international normalized ratio and partial thromboplastin time, fibrinolytic markers D-dimer and tissue-type plasminogen activator, and anticoagulants tissue factor pathway inhibitor and activated protein C (aPC; all p < 0.03). Increasing histone level from admission to 6 hours was a multivariate predictor of mortality (hazard ratio, 1.005; p = 0.013). When aPC level trends were included, the impact of histone level increase on mortality was abrogated (p = 0.206) by a protective effect of increasing aPC levels (hazard ratio, 0.900; p = 0.020). Extracellular histone levels are elevated in response to traumatic injury and correlate with fibrinolysis and activation of anticoagulants. An increase in histone levels from admission to 6 hours is predictive of mortality, representing evidence of ongoing release of intracellular antigens similar to that seen in sepsis. Concomitant elevation of aPC abrogates this effect, suggesting a possible role for aPC in mitigating the sterile inflammatory response after trauma through the proteolysis of circulating histones. Prognostic study, level III.

Incidence and Risk Factors for Post-Traumatic Hydrocephalus following Decompressive Craniectomy for Intractable Intracranial Hypertension and Evacuation of Mass Lesions

There continues to be a considerable interest in decompressive craniectomy in the management of severe traumatic brain injury (TBI). Though technically straightforward, the procedure is not without significant complications. In this study we assessed the incidence and risk factors for the development of subdural hygroma and hydrocephalus after decompressive craniectomy. A total of 195 patients who had had a decompressive craniectomy for severe TBI between 2004 and 2010 at the two major trauma centers in Western Australia were considered. Of the 166 patients who survived after the acute hospital stay, 93 (56%; 95% confidence interval [CI] 48,63%) developed subdural hygroma; 45 patients (48%) had unilateral and 48 patients (52%) had bilateral subdural hygromas. Of the 159 patients who survived more than 6 months after surgery, 72 (45%; 95% CI 38,53%) developed radiological evidence of ventriculomegaly, and 26 of these 72 patients (36%; 95% CI 26,48%) developed clinical evidence of hydrocephalus and required a ventriculoperitoneal (VP) shunt. Maximum intracranial pressure prior to decompression (p=0.005), subdural hygroma (p=0.012), and a lower admission Glasgow Coma Scale score (p=0.009), were significant risk factors for hydrocephalus after decompressive craniectomy. Hydrocephalus requiring a VP shunt was associated with a higher risk of unfavorable neurological outcomes at 18 months (odds ratio 7.46; 95%CI 1.17,47.4; p=0.033), after adjusting for other factors. Our results showed a clear association between injury severity, subdural hygroma, and hydrocephalus, suggesting that damage to the cerebrospinal fluid drainage pathways contributes to the primary brain injury rather than the margin of the craniectomy as the factor responsible for these complications.

The Etiology And Outcome Of Adult Patients Presenting With Sepsis To The University Teaching Hospital, Lusaka, Zambia.

Sepsis accounts for a significant burden of morbidity and mortality.In developed world, it is implicated as the second leading cause of non-cardiac death. Mortality from sepsis is on the increase with a mortality rate of 33-61%. In spite of the high burden of sepsis in sub Saharan Africa, data regarding the etiology and outcome of septic patients is limited. We conducted a prospective cohort study to describe the etiology, characteristic and outcome of patients presenting with sepsis to the University Teaching Hospital in Lusaka, Zambia. Patients who met the inclusion criteria were enrolled into the study and after a thorough examination, bloods were drawn for full blood count, urea and electrolytes, liver function tests and for culture. Samples for culture were collected under aseptic techniques and cultured for aerobic organisms. Biochemical and bacteriological methods were used to identify the isolates and antibiotic sensitivity patterns were determined using agar diffusion methods. Patients were then followed up until they either demised or were discharge. A total of 161 patients were enrolled of which 110(68%) were HIV positive and 23(14%) had unknown HIV status. Bacteremia was found in 39 (24%) with the most isolated organism being staphylococcus aureus. Mortality in our cohort of septic patients was determinedat 40%. Identified predictors for in patient mortality were low admission Glasgow coma scale[OR 11.2(CI 3.5-36.4)], positive blood culture[OR 2.38(CI 1.14-4.95)] and HIV status, those with unknown HIV status were more likely to die than those who were HIV negative[OR 8.38(CI2.36-29.7)]. Most of the septic patients presenting to UTH had advanced immunosuppression (WHO stage 3 and 4) and had a high mortality rate. Staphylococcus aureus and streptococcus pneumoniae were the highest isolates. Identified predictors for in patient mortality could be used to try and improve outcome in septic patients at UTH.

Elevated Admission Blood Pressure and Acute Ischemic Lesions in Spontaneous Intracerebral Hemorrhage

Concomitant acute ischemic lesions are detected in a subset of patients with intracerebral hemorrhage (ICH). In this study, our aim was to analyze the pattern of acute ischemic lesions detected by diffusion-weighted imaging (DWI) in patients with ICH, and to use this information, in combination with clinical characteristics of patients, to understand the underlying mechanisms of these lesions. We retrospectively analyzed patients with a diagnosis of ICH who underwent DWI within 14 days of symptom onset. We compared demographic, clinical, and imaging characteristics in patients with and without acute ischemic lesions. We also assessed the number, location, and topographic distribution of DWI bright lesions. Acute ischemic lesions were detected in 15 of 86 patients (17.4%); the lesions had a small, dot-like appearance in 13 patients (87%) and were located in an arterial territory separate from the incident ICH in 12 patients (80%). Patients with acute ischemic lesions had higher admission systolic, diastolic, and mean arterial blood pressure levels; greater periventricular leukoaraiosis burden; more microbleeds, and lower admission Glasgow Coma Scale score. In multivariate analyses, admission mean arterial blood pressure (P < .01) and Glasgow Coma Scale score (P =.03) remained as the only significant variables associated with DWI lesion positivity. Our findings highlight the role of elevated admission blood pressure in the development of concomitant acute ischemic lesions in patients with ICH. The pattern of DWI bright lesions, together with a trend toward an increased burden of leukoaraiosis and microbleeds in patients with acute ischemic lesions, suggest an underlying dysfunctional cerebral microvasculature in the etiology of these lesions.

The prognostic value of thrombelastography in identifying neurosurgical patients with worse prognosis

Coagulopathy in patients with intracranial haemorrhage or traumatic brain injury (TBI) is associated with clinical deterioration and worse outcome. Whole blood viscoelastic haemostatic assays, like thrombelastography (TEG), might aid conventional coagulation assays in identification of patients with worse prognosis. We performed a review of patients (totalling 78 patients) with primary acute intracranial haemorrhage or isolated TBI admitted to a neurointensive care unit (NICU) for more than 24 h during a period of 9 months, who had TEG analysis performed at admission. Primary outcome was all-cause 30-day mortality, whereas decline in Glasgow Coma Scale (GCS) score at 24 h after admission or death due to cerebral incarceration were secondary outcomes. Patients were defined as hypocoaguable if TEG reaction time was more than 8 min, angle less than 55° and/or maximal amplitude less than 51 mm. Patients were defined hypocoaguable according to conventional coagulation assays if international normalized ratio was more than 1.3, platelet counts less than 100×10/l and/or activated partial thromboplastine time more than 35 s. Eight patients were hypocoaguable by TEG on admission to NICU and had higher 30-day mortality (63% vs. 16%, P=0.008), more often declined in GCS (57% vs. 16%, P=0.02) and expired due to cerebral incarceration (50% vs. 6%, P=0.02). Hypocoagulability by TEG, lower admission GCS and subarachnoid haemorrhage were independently associated with higher 30-day mortality [TEG: odds ratio (OR) 14.8 (2.2-100.1), P=0.006; GCS: OR 1.3 (1.1-1.5), P=0.006; subarachnoid haemorrhage: OR: 5.3 (1.3-22.3), P=0.02]. Only two patients were hypocoaguable by both conventional coagulation assays and TEG. The current data indicate that hypocoagulability by TEG at admission to NICU predicts worse prognosis. Low concordance with conventional coagulation assays indicates that TEG might be valuable in identifying patients with clinically relevant coagulopathy.

Determinants of mortality in trauma patients following massive blood transfusion

Aim:This study was designed to find out the factors influencing mortality in trauma patients receiving massive blood transfusion (MBT).Materials and Methods:Records of all patients admitted during December 2007 to November 2008 at a Level I Trauma Center emergency and who underwent massive transfusion (≥10 units of packed red cells in 24 h) were retrospectively analyzed. Death during the hospital stay was considered as the study outcome and various demographic, laboratory, and clinical parameters were included as its potential determinants.Statistical Analysis:Bivariate and multivariate logistic regression analyses were done to identify the risk factors associated with mortality.Results:Of the 4054 transfused patients who were admitted to the trauma center during the study period, 71 (1.8%) patients underwent massive transfusion. Of this, there were 37 survivors and 34 nonsurvivors (48%). The median overall ISS was 27 (22–34). The patients who died had shorter mean length of hospital stay, shorter mean duration of intensive care unit (ICU) stay, and low admission Glasgow Coma Scale (GCS) compared to the survivors (P < 0.01). The mean prothrombin time (PT) and the mean activated partial thromboplastin time was significantly high (P < 0.01) among nonsurvivors. Total leukocyte count (TLC ≥ 10,000 cells/cubic mm), GCS ≤ 8, the presence of coagulopathy and major vascular surgery were the four independent determinants of mortality in multivariate logistic regression analysis. The FFP:PRBC (fresh frozen plasma:packed red cells) ratio and PC:PRBC (platelet concentrate:packed red cells) ratio calculated in our study was not statistically significant in correlation to the in hospital mortality.Conclusions:Overall mortality among the MBT patients was comparable with the studies in the literature. Mortality is not affected by the amount of packed red cells given in the first 12 h and the total number of packed red cells transfused. Prospective studies are required to further validate the determinants of mortality and establish guidelines for MBT.

Characteristics and correlates of rehabilitation charges during inpatient traumatic brain injury rehabilitation in Singapore

A prospective study of 91 consecutive traumatic brain injury admissions to rehabilitation over a 2-year period to determine factors impacting on rehabilitation charges. Discharge records of 91 adult traumatic brain injury patients comprising total unsubsidized billings for each completed inpatient rehabilitation episode were used to derive total charges. Co-variates analysed included demographic, acute traumatic brain injury and rehabilitation variables including the Modified Barthel Index score. The total median rehabilitation charge per episode was S$7845.50 (range: S$970.55-$44,817.20) [1 Euro=S$2.10]. The top 3 contributory median total charges/episode included bed, board and nursing (S$5616.00), occupational therapy (S$606.00), and physical therapy (S$526.00). Patients with lower admission Glasgow Coma Scale scores, longer post-traumatic amnesia duration, dysphagia and medical complications during rehabilitation, lower admission Modified Barthel Index scores, longer acute and rehabilitation length of stay had significantly higher rehabilitation charges (p<0.001). Using multiple regression analyses, only rehabilitation length of stay and change in Modified Barthel Index were significantly correlated with total rehabilitation charges (p<0.001). Measures to reduce rehabilitation length of stay, to prevent medical complications, to facilitate transfers to rehabilitation, and expedient discharge planning may help to reduce rehabilitation charges. This study has potential implications for healthcare resource planning for traumatic brain injury rehabilitation.

Significance of Troponin Elevation After Severe Traumatic Brain Injury

Elevation of serum troponin (cTnI) after nontraumatic cerebral insult has been associated with an adverse prognosis. This association has not been well documented in traumatic brain injury (TBI). To evaluate the association and prognostic significance of cTnI elevation in severe TBI. To evaluate the role of beta-blocker (BB) therapy in TBI patients with elevated cTnI. Retrospective review of all blunt trauma patients with severe TBI (head Abbreviated Injury Scale score [AIS] >/=3) admitted to the intensive care unit (ICU) with serial TnI measurements at a Level I trauma center from January 1998 to December 2005. Patients with AIS score >/=3 to other body regions were excluded. Univariate and multivariate logistic regression was performed to determine prognostic significance of TnI elevation. There were 420 severe blunt TBI patients who had serial cTnI measurements during the study period. One hundred twenty-five (29.8%) had an elevated admission cTnI. TBI patients with an elevated cTnI had a lower admission Glasgow Coma Scale (GCS) score (7.5 vs. 8.7, p < 0.05), higher Injury Severity Score (27.4 vs. 24.8, p < 0.01), and increased hospital mortality (44% vs. 29%, p < 0.05), compared with TBI patients with a normal cTnI. Increasing severity of head injury was associated with an increasing cTnI (TnI level 0.8 mug/L for head AIS score = 3 vs. TnI Level I 0.3 mug/L for head AIS score = 4, 5, p = 0.09). After adjusting for injury severity, elevated cTnI was an independent predictor for mortality (Odds ratio [OR[: 8.5; 95% confidence interval [CI]: 3.46, 22.15, p < 0.0001). BB therapy was associated with a significant survival advantage (OR: 0.38; 95% CI: 0.15, 0.87, p = 0.03) in TBI patients with any elevation of cTnI. Elevated TnI is frequently observed after severe TBI. The level of TnI correlates with the severity of head injury and is an independent predictor of adverse outcomes. BB therapy is associated with a survival advantage in TBI patients with elevated cTnI.