Korak Sarkar, Krista Keachie, UyenThao Nguyen, J. Paul Muizelaar, Marike Zwienenberg-Lee and Kiarash Shahlaie
Traumatic brain injury (TBI) is a leading cause of injury, hospitalization, and death among pediatric patients. Admission CT scans play an important role in classifying TBI and directing clinical care, but little is known about the differences in CT findings between pediatric and adult patients. The aim of this study was to determine if radiographic differences exist between adult and pediatric TBI.
The authors retrospectively analyzed TBI registry data from 1206 consecutive patients with nonpenetrating TBI treated at a Level 1 adult and pediatric trauma center over a 30-month period.
The distribution of sex, race, and Glasgow Coma Scale (GCS) score was not significantly different between the adult and pediatric populations; however, the distribution of CT findings was significantly different. Pediatric patients with TBI were more likely to have skull fractures (OR 3.21, p < 0.01) and epidural hematomas (OR 1.96, p < 0.01). Pediatric TBI was less likely to be associated with contusion, subdural hematoma, subarachnoid hemorrhage, or compression of the basal cisterns (p < 0.05). Rotterdam CT scores were significantly lower in the pediatric population (2.3 vs 2.6, p < 0.001).
There are significant differences in the CT findings in pediatric versus adult TBI, despite statistical similarities with regard to clinical severity of injury as measured by the GCS. These differences may be due to anatomical characteristics, the biomechanics of injury, and/or differences in injury mechanisms between pediatric and adult patients. The unique characteristics of pediatric TBI warrant consideration when formulating a clinical trial design or predicting functional outcome using prognostic models developed from adult TBI data.
Krista Greenan, Sandra L. Taylor, Daniel Fulkerson, Kiarash Shahlaie, Clayton Gerndt, Evan M. Krueger and Marike Zwienenberg
A recent retrospective study of severe traumatic brain injury (TBI) in pediatric patients showed similar outcomes in those with a Glasgow Coma Scale (GCS) score of 3 and those with a score of 4 and reported a favorable long-term outcome in 11.9% of patients. Using decision tree analysis, authors of that study provided criteria to identify patients with a potentially favorable outcome. The authors of the present study sought to validate the previously described decision tree and further inform understanding of the outcomes of children with a GCS score 3 or 4 by using data from multiple institutions and machine learning methods to identify important predictors of outcome.
Clinical, radiographic, and outcome data on pediatric TBI patients (age < 18 years) were prospectively collected as part of an institutional TBI registry. Patients with a GCS score of 3 or 4 were selected, and the previously published prediction model was evaluated using this data set. Next, a combined data set that included data from two institutions was used to create a new, more statistically robust model using binomial recursive partitioning to create a decision tree.
Forty-five patients from the institutional TBI registry were included in the present study, as were 67 patients from the previously published data set, for a total of 112 patients in the combined analysis. The previously published prediction model for survival was externally validated and performed only modestly (AUC 0.68, 95% CI 0.47, 0.89). In the combined data set, pupillary response and age were the only predictors retained in the decision tree. Ninety-six percent of patients with bilaterally nonreactive pupils had a poor outcome. If the pupillary response was normal in at least one eye, the outcome subsequently depended on age: 72% of children between 5 months and 6 years old had a favorable outcome, whereas 100% of children younger than 5 months old and 77% of those older than 6 years had poor outcomes. The overall accuracy of the combined prediction model was 90.2% with a sensitivity of 68.4% and specificity of 93.6%.
A previously published survival model for severe TBI in children with a low GCS score was externally validated. With a larger data set, however, a simplified and more robust model was developed, and the variables most predictive of outcome were age and pupillary response.
Nancy McLaughlin, Alexander Vandergrift, Leo F. Ditzel Filho, Kiarash Shahlaie, Amalia A. Eisenberg, Ricardo L. Carrau, Pejman Cohan and Daniel F. Kelly
Symptomatic sellar arachnoid cysts (ACs) have typically been treated via the transsphenoidal route. After sellar cyst wall fenestration, some authors have advocated cyst wall resection and increasing communication between the AC and suprasellar subarachnoid space (SAS). This study is a report of the authors' experience using a simplified approach to reinforce a defective diaphragma sellae or unseen arachnoid diverticulum by deliberately not enlarging the AC-SAS communication and obliterating the cyst cavity with adipose tissue followed by skull base reconstruction.
A retrospective analysis was conducted of patients who underwent an endonasal transsphenoidal obliteration of symptomatic ACs with a fat graft and skull base repair.
Between July 1998 and September 2010, 8 patients with a sellar AC were identified (6 women and 2 men, mean age 57 years). Clinical presentation included headache, pituitary dysfunction, and visual dysfunction (4 patients each group). Maximal cyst diameter averaged 22 mm (range 15–32 mm). In all cases the sellar communication to the SAS was deliberately not enlarged. The endoscope was used for visualization in 8 of 9 procedures. Postoperatively, headache improved in all 4 patients, vision in all 4 patients, and partial resolution of endocrine dysfunction (hyperprolactinemia and/or recurrent hyponatremia) occurred in 3 (75%) of 4 patients. No new endocrinopathy, CSF leak, meningitis, or neurological deficits occurred. Two patients experienced cyst reaccumulation: 1 symptomatic recurrence was treated with reoperation at 43 months postsurgery, and 1 asymptomatic partial recurrence continued to be monitored at 29 months postsurgery.
Sellar ACs can be effectively treated using endonasal fenestration and obliteration with fat with resultant reversal of presenting symptoms in the majority of patients. This simplified technique of AC cavity obliteration without enlarging communication to the SAS has a low risk of CSF leakage, and in most cases appears to effectively disrupt cyst progression, although longer follow-up is required to monitor for cyst recurrence.
Kiarash Shahlaie, Krista Keachie, Irene M. Hutchins, Nancy Rudisill, Lori K. Madden, Karen A. Smith, Karen A. Ko, Richard E. Latchaw and J. Paul Muizelaar
Posttraumatic vasospasm (PTV) is an underrecognized cause of ischemic damage after severe traumatic brain injury (TBI) that independently predicts poor outcome. There are, however, no guidelines for PTV screening and management, partly due to limited understanding of its pathogenesis and risk factors.
A database review of 46 consecutive cases of severe TBI in pediatric and adult patients was conducted to identify risk factors for the development of PTV. Univariate analysis was performed to identify potential risk factors for PTV, which were subsequently analyzed using a multivariate logistic regression model to calculate odds ratios (ORs) and 95% confidence intervals (CIs).
Fever on admission was an independent risk factor for development of PTV (OR 22.2, 95% CI 1.9–256.8), and patients with hypothermia on admission did not develop clinically significant vasospasm during their hospital stay. The presence of small parenchymal contusions was also an independent risk factor for PTV (OR 7.8, 95% CI 0.9–69.5), whereas the presence of subarachnoid hemorrhage or other patterns of intracranial injury were not. Other variables, such as age, sex, ethnicity, degree of TBI severity, or admission laboratory values, were not independent predictors for the development of clinically significant PTV.
Independent risk factors for PTV include parenchymal contusions and fever. These results suggest that diffuse mechanical injury and activation of inflammatory pathways may be underlying mechanisms for the development of PTV, and that a subset of patients with these risk factors may be an appropriate population for aggressive screening. Further studies are needed to determine if treatments targeting fever and inflammation may be effective in reducing the incidence of vasospasm following severe TBI.