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  • By Author: Tubbs, R. Shane x
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Ross L. Dawkins, Joseph H. Miller, Omar I. Ramadan, Michael C. Lysek, Elizabeth N. Kuhn, Brandon G. Rocque, Michael J. Conklin, R. Shane Tubbs, Beverly C. Walters, Bonita S. Agee and Curtis J. Rozzelle

OBJECTIVE

There are many classification systems for injuries of the thoracolumbar spine. The recent Thoracolumbar Injury Classification and Severity Score (TLICS) has been shown to be a reliable tool for adult patients. The aim of this study was to assess the reliability of the TLICS system in pediatric patients. The validity of the TLICS system is assessed in a companion paper.

METHODS

The medical records of pediatric patients with acute, traumatic thoracolumbar fractures at a single Level 1 trauma center were retrospectively reviewed. A TLICS was calculated for each patient using CT and MRI, along with the neurological examination recorded in the patient’s medical record. TLICSs were compared with the type of treatment received. Five raters scored all patients separately to assess interrater reliability.

RESULTS

TLICS calculations were completed for 81 patients. The mean patient age was 10.9 years. Girls represented 51.8% of the study population, and 80% of the study patients were white. The most common mechanisms of injury were motor vehicle accidents (60.5%), falls (17.3%), and all-terrain vehicle accidents (8.6%). The mean TLICS was 3.7 ± 2.8. Surgery was the treatment of choice for 33.3% of patients. The agreement between the TLICS-suggested treatment and the actual treatment received was statistically significant (p < 0.0001). The interrater reliability of the TLICS system ranged from moderate to very good, with a Fleiss’ generalized kappa (κ) value of 0.69 for the TLICS treatment suggestion among all patients; however, interrater reliability decreased when MRI was used to contribute to the TLICS. The κ value decreased from 0.73 to 0.57 for patients with CT only vs patients with CT/MRI or MRI only, respectively (p < 0.0001). Furthermore, the agreement between suggested treatment and actual treatment was worse when MRI was used as part of injury assessment.

CONCLUSIONS

The TLICS system demonstrates good interrater reliability among physicians assessing thoracolumbar fracture treatment in pediatric patients. Physicians should be cautious when using MRI to aid in the surgical decision-making process.

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Philipp Hendrix, Paul M. Foreman, Mark R. Harrigan, Winfield S. Fisher III, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Beverly C. Walters, R. Shane Tubbs, Mohammadali M. Shoja, Jean-Francois Pittet, Mali Mathru and Christoph J. Griessenauer

OBJECTIVE

Cystathionine β-synthase (CBS) is involved in homocysteine and hydrogen sulfide (H2S) metabolism. Both products have been implicated in the pathophysiology of cerebrovascular diseases. The impact of CBS polymorphisms on aneurysmal subarachnoid hemorrhage (aSAH) and its clinical sequelae is poorly understood.

METHODS

Blood samples from all patients enrolled in the CARAS (Cerebral Aneurysm Renin Angiotensin System) study were used for genetic evaluation. The CARAS study prospectively enrolled aSAH patients at 2 academic institutions in the United States from 2012 to 2015. Common CBS polymorphisms were detected using 5′exonuclease genotyping assays. Analysis of associations between CBS polymorphisms and aSAH was performed.

RESULTS

Samples from 149 aSAH patients and 50 controls were available for analysis. In multivariate logistic regression analysis, the insertion allele of the 844ins68 CBS insertion polymorphism showed a dominant effect on aSAH. The GG genotype of the CBS G/A single nucleotide polymorphism (rs234706) was independently associated with unfavorable functional outcome (modified Rankin Scale Score 3–6) at discharge and last follow-up, but not clinical vasospasm or delayed cerebral ischemia (DCI).

CONCLUSIONS

The insertion allele of the 844ins68 CBS insertion polymorphism was independently associated with aSAH while the GG genotype of rs234706 was associated with an unfavorable outcome both at discharge and last follow-up. Increased CBS activity may exert its neuroprotective effects through alteration of H2S levels, and independent of clinical vasospasm and DCI.

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Christoph J. Griessenauer, R. Shane Tubbs, Paul M. Foreman, Michelle H. Chua, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Ramaswamy Iyer, Rishikesh Haridas, Beverly C. Walters, Salman Chaudry, Aisana Malieva, Samantha Wilkins, Mark R. Harrigan, Winfield S. Fisher III and Mohammadali M. Shoja

OBJECTIVE

Renin-angiotensin system (RAS) genetic polymorphisms are thought to play a role in cerebral aneurysm formation and rupture. The Cerebral Aneurysm Renin Angiotensin System (CARAS) study prospectively evaluated associations of common RAS polymorphisms and clinical course after aneurysmal subarachnoid hemorrhage (aSAH).

METHODS

The CARAS study prospectively enrolled aSAH patients at 2 academic centers in the United States. A blood sample was obtained from all patients for genetic evaluation and measurement of plasma angiotensin converting enzyme (ACE) concentration. Common RAS polymorphisms were detected using 5′exonuclease genotyping assays and pyrosequencing. Analysis of associations of RAS polymorphisms and clinical course after aSAH were performed.

RESULTS

A total of 166 patients were screened, and 149 aSAH patients were included for analysis. A recessive effect of allele I (insertion) of the ACE I/D (insertion/deletion) polymorphism was identified for Hunt and Hess grade in all patients (OR 2.76, 95% CI 1.17–6.50; p = 0.0206) with subsequent poor functional outcome. There was a similar effect on delayed cerebral ischemia (DCI) in patients 55 years or younger (OR 3.63, 95% CI 1.04–12.7; p = 0.0439). In patients older than 55 years, there was a recessive effect of allele A of the angiotensin II receptor Type 2 (AT2) A/C single nucleotide polymorphism (SNP) on DCI (OR 4.70, 95% CI 1.43–15.4; p = 0.0111).

CONCLUSIONS

Both the ACE I/D polymorphism and the AT2 A/C single nucleotide polymorphism were associated with an age-dependent risk of delayed cerebral ischemia, whereas only the ACE I/D polymorphism was associated with poor clinical grade at presentation. Further studies are required to elucidate the relevant pathophysiology and its potential implication in the treatment of patients with aSAH.

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Christoph J. Griessenauer, R. Shane Tubbs, Paul M. Foreman, Michelle H. Chua, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Ramaswamy Iyer, Rishikesh Haridas, Beverly C. Walters, Salman Chaudry, Aisana Malieva, Samantha Wilkins, Mark R. Harrigan, Winfield S. Fisher III and Mohammadali M. Shoja

OBJECTIVE

Renin-angiotensin system (RAS) genetic polymorphisms are thought to play a role in cerebral aneurysm formation and rupture. The Cerebral Aneurysm Renin-Angiotensin System (CARAS) study prospectively evaluated common RAS polymorphisms and their relation to aneurysmal subarachnoid hemorrhage (aSAH).

METHODS

The CARAS study prospectively enrolled aSAH patients and controls at 2 academic centers in the United States. A blood sample was obtained from all patients for genetic evaluation and measurement of plasma angiotensin-converting enzyme (ACE) concentration. Common RAS polymorphisms were detected using 5′ exonuclease (TaqMan) genotyping assays and restriction fragment length polymorphism analysis.

RESULTS

Two hundred forty-eight patients were screened, and 149 aSAH patients and 50 controls were available for analysis. There was a recessive effect of the C allele of the angiotensinogen (AGT) C/T single-nucleotide polymorphism (SNP) (OR 1.94, 95% CI 0.912–4.12, p = 0.0853) and a dominant effect of the G allele of the angiotensin II receptor Type 2 (AT2) G/A SNP (OR 2.11, 95% CI 0.972–4.57, p = 0.0590) on aSAH that did not reach statistical significance after adjustment for potential confounders. The ACE level was significantly lower in aSAH patients with the II genotype (17.6 ± 8.0 U/L) as compared with the ID (22.5 ± 12.1 U/L) and DD genotypes (26.6 ± 14.2 U/L) (p = 0.0195).

CONCLUSIONS

The AGT C/T and AT2 G/A polymorphisms were not significantly associated with aSAH after controlling for potential confounders. However, a strong trend was identified for a dominant effect of the G allele of the AT2 G/A SNP. Downregulation of the local RAS may contribute to the formation of cerebral aneurysms and subsequent presentation with aSAH. Further studies are required to elucidate the relevant pathophysiology and its potential implication in treatment of patients with aSAH.

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Paul M. Foreman, Michelle Chua, Mark R. Harrigan, Winfield S. Fisher III, Nilesh A. Vyas, Robert H. Lipsky, Beverly C. Walters, R. Shane Tubbs, Mohammadali M. Shoja and Christoph J. Griessenauer

OBJECTIVE

Delayed cerebral ischemia (DCI) is a recognized complication of aneurysmal subarachnoid hemorrhage (aSAH) that contributes to poor outcome. This study seeks to determine the effect of nosocomial infection on the incidence of DCI and patient outcome.

METHODS

An exploratory analysis was performed on 156 patients with aSAH enrolled in the Cerebral Aneurysm Renin Angiotensin System study. Clinical and radiographic data were analyzed with univariate analysis to detect risk factors for the development of DCI and poor outcome. Multivariate logistic regression was performed to identify independent predictors of DCI.

RESULTS

One hundred fifty-three patients with aSAH were included. DCI was identified in 32 patients (20.9%). Nosocomial infection (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.09–11.2, p = 0.04), ventriculitis (OR 25.3, 95% CI 1.39–458.7, p = 0.03), aneurysm re-rupture (OR 7.55, 95% CI 1.02–55.7, p = 0.05), and clinical vasospasm (OR 43.4, 95% CI 13.1–143.4, p < 0.01) were independently associated with the development of DCI. Diagnosis of nosocomial infection preceded the diagnosis of DCI in 15 (71.4%) of 21 patients. Patients diagnosed with nosocomial infection experienced significantly worse outcomes as measured by the modified Rankin Scale score at discharge and 1 year (p < 0.01 and p = 0.03, respectively).

CONCLUSIONS

Nosocomial infection is independently associated with DCI. This association is hypothesized to be partly causative through the exacerbation of systemic inflammation leading to thrombosis and subsequent ischemia.