Traumatic brain injury related hospitalization and mortality in california

Authors: Lagbas C, Bazargan-Hejazi S, Shaheen M, Kermah D, Pan D.

Objective. The aim of this study is to describe the traumatic brain injury (TBI) population and causes and identify factors associated with TBI hospitalizations and mortality in California. Methods. This is a cross-sectional study of 61,188 patients with TBI from the California Hospital Discharge Data 2001 to 2009. We used descriptive, bivariate, and multivariate analyses in SAS version 9.3. Results. TBI-related hospitalizations decreased by 14% and mortality increased by 19% from 2001 to 2009. The highest percentages of TBI hospitalizations were due to other causes (38.4%), falls (31.2%), being of age ≥75 years old (37.2%), being a males (58.9%), and being of Medicare patients (44%). TBIs due to falls were found in those age ≤4 years old (53.5%), ≥75 years old (44.0%), and females (37.2%). TBIs due to assaults were more frequent in Blacks (29.0%). TBIs due to motor vehicle accidents were more frequent in 15-19 and 20-24 age groups (48.7% and 48.6%, resp.) and among Hispanics (27.8%). Higher odds of mortality were found among motor vehicle accident category (adjusted odds ratio (AOR): 1.27, 95% CI: 1.14-1.41); males (AOR: 1.36, 95% CI: 1.27-1.46); and the ≥75-year-old group (AOR: 6.4, 95% CI: 4.9-8.4). Conclusions. Our findings suggest a decrease in TBI-related hospitalizations but an increase in TBI-related mortality during the study period. The majority of TBI-related hospitalizations was due to other causes and falls and was more frequent in the older, male, and Medicare populations. The higher likelihood of TBI-related mortalities was found among elderly male ≥75 years old who had motor vehicle accidents. Our data can inform practitioners, prevention planners, educators, service sectors, and policy makers who aim to reduce the burden of TBI in the community. Implications for interventions are discussed.

A patient with low pressure idiopathic intracranial hypertension and multiple cranial neuropathies

Authors: Arora A, Sreenivasan S, Naeem Raza M.

Idiopathic intracranial hypertension is a disorder of increased intracranial pressure of unknown cause. Idiopathic intracranial hypertension can present with a wide spectrum of neurological signs, especially cranial nerve palsies, which are mostly thought to be caused by a pressure-dependent stretching mechanism. Treatment is guided by aetiology whenever possible; otherwise drainage of CSF by ventriculostomy or shunt is needed.

Managing children with raised intracranial pressure: part one (introduction and meningitis)

Authors: Paul S, Smith J, Green J, Smith-Collins A, Chinthapalli R.

Intracranial pathologies in children need urgent identification and management. This article is presented in two parts, with part one describing intracranial pressure and outlining the features and management of meningitis. Part two, to be published in February 2014, outlines the features and management of brain tumours and intracranial bleeds. Each condition is accompanied by an illustrative case study to give an idea of what nurses might encounter in a child presenting with raised intracranial pressure.

Successful treatment of suprasellar tumors associated with poor brain blood perfusion by severe intracranial arterial stenosis: two case reports

Authors: Ogawa Y, Tominaga T.

BACKGROUND: Treatment strategy to prevent perioperative cerebral infarction in patients with asymptomatic severe stenosis of the internal carotid artery is not fully established.
CASE PRESENTATION: Two patients were treated for skull base tumor in the presence of severe stenosis of the internal carotid artery, unilateral in one patient and bilateral in the other patient. Both patients were asymptomatic but had reduced vascular reserve capacity. The extended transsphenoidal approach was planned avoiding the low perfusion pressure region, with only conventional methods of maintaining blood pressure and PaCO2 rather than performing prophylactic vascular reconstruction surgery, and successful tumor removals were achieved without causing further neurological or radiological deficits.
CONCLUSION: If the surgical route is planned to avoid the distribution of stenotic vessels and low perfusion pressure, prophylactic vascular reconstruction surgery would be unnecessary. Although more experiences based on sub-classified etiology for internal carotid artery stenosis are required, various types of operations including intracranial-extracranial vascular surgery might be justified based on this principle.

A case of Bardet-Biedl syndrome complicated with intracranial hypertension in a Japanese child

Authors: Saida K, Inaba Y, Hirano M, Satake W, Toda T, Suzuki Y, Sudo A, Noda S, Hidaka Y, Hirabayashi K, Imai H, Kurokawa T, Koike K.

Bardet-Biedl syndrome (BBS) is a rare heterogeneous autosomal recessive disorder characterized by rod-cone dystrophy, postaxial polydactyly, truncal obesity, hypogonadism, learning disability, and renal anomaly that are caused by ciliary dysfunction. 16 genes have been associated with the BBS phenotype. Although recent pathophysiological studies using animal models have shown that ciliary dysfunction may induce hydrocephalus, there have been no reports of BBS with intracranial hypertension. We here describe a 9-year-old Japanese girl who was diagnosed as having BBS and later received renal transplantation due to chronic renal failure. She also exhibited intracranial hypertension, including papilledema and increased intrathecal pressure (260-300mmH2O), but her brain magnetic resonance imaging was normal. No genetic abnormalities were detected by DNA chip analysis or exome sequencing. Her papilledema improved following administration of acetazolamide. This is the first report of a case of BBS complicated with intracranial hypertension and its treatment.

Intracranial pressure monitoring, cerebral perfusion pressure estimation, and ICP/CPP-guided therapy: a standard of care or optional extra after brain injury?

Authors: Kirkman MA, Smith M.

Measurement of intracranial pressure (ICP) and mean arterial pressure (MAP) is used to derive cerebral perfusion pressure (CPP) and to guide targeted therapy of acute brain injury (ABI) during neurointensive care. Here we provide a narrative review of the evidence for ICP monitoring, CPP estimation, and ICP/CPP-guided therapy after ABI. Despite its widespread use, there is currently no class I evidence that ICP/CPP-guided therapy for any cerebral pathology improves outcomes; indeed some evidence suggests that it makes no difference, and some that it may worsen outcomes. Similarly, no class I evidence can currently advise the ideal CPP for any form of ABI. 'Optimal' CPP is likely patient-, time-, and pathology-specific. Further, CPP estimation requires correct referencing (at the level of the foramen of Monro as opposed to the level of the heart) for MAP measurement to avoid CPP over-estimation and adverse patient outcomes. Evidence is emerging for the role of other monitors of cerebral well-being that enable the clinician to employ an individualized multimodality monitoring approach in patients with ABI, and these are briefly reviewed. While acknowledging difficulties in conducting robust prospective randomized studies in this area, such high-quality evidence for the utility of ICP/CPP-directed therapy in ABI is urgently required. So, too, is the wider adoption of multimodality neuromonitoring to guide optimal management of ICP and CPP, and a greater understanding of the underlying pathophysiology of the different forms of ABI and what exactly the different monitoring tools used actually represent.


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