Background A subdural hematoma (SDH) following a traumatic brain injury (TBI) in children can lead to unexpected death or disability. The nomogram is a clinical prediction tool used by physicians to provide prognosis advice to parents for making decisions regarding treatment. In the present study, a nomogram for predicting outcomes was developed and validated. In addition, the predictors associated with outcomes in children with traumatic SDH were determined.
Methods In this retrospective study, 103 children with SDH after TBI were evaluated. According to the King’s Outcome Scale for Childhood Head Injury classification, the functional outcomes were assessed at hospital discharge and categorized into favorable and unfavorable. The predictors associated with the unfavorable outcomes were analyzed using binary logistic regression. Subsequently, a two-dimensional nomogram was developed for presentation of the predictive model.
Results The predictive model with the lowest level of Akaike information criterion consisted of hypotension (odds ratio [OR], 9.4; 95% confidence interval [CI], 2.0–42.9), Glasgow coma scale scores of 3–8 (OR, 8.2; 95% CI, 1.7–38.9), fixed pupil in one eye (OR, 4.8; 95% CI, 2.6–8.8), and fixed pupils in both eyes (OR, 3.5; 95% CI, 1.6–7.1). A midline shift ≥5 mm (OR, 1.1; 95% CI, 0.62–10.73) and co-existing intraventricular hemorrhage (OR, 6.5; 95% CI, 0.003–26.1) were also included.
Conclusions SDH in pediatric TBI can lead to mortality and disability. The predictability level of the nomogram in the present study was excellent, and external validation should be conducted to confirm the performance of the clinical prediction tool.
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A 49-year-old man with end-stage renal disease was admitted to the hospital with a severe headache and vomiting. On neurological examination the Glasgow Coma Scale (GCS) score was 15 and his brain CT showed acute subdural hematoma over the right cerebral convexity with approximately 11-mm thickness and 9-mm midline shift. We chose a conservative treatment of scheduled neurological examination, anticonvulsant medication, serial brain CT scanning, and scheduled hemodialysis (three times per week) without using heparin. Ten days after admission, he complained of severe headache and a brain CT showed an increased amount of hemorrhage and midline shift. Emergency burr hole trephination and removal of the hematoma were performed, after which symptoms improved. However, nine days after the operation a sudden onset of general tonic-clonic seizure developed and a brain CT demonstrated an increased amount of subdural hematoma. Under the impression of persistent increased intracranial pressure, the patient was transferred to the intensive care unit (ICU) in order to control intracranial pressure. Management at the ICU consisted of regular intravenous mannitol infusion assisted with continuous renal replacement therapy. He stayed in the ICU for four days. Twenty days after the operation he was discharged without specific neurological deficits.
A case of "spontaneous" acute subdural hematoma caused by aspirin and plavix therapy has not been described previously. As an isolated cerebrovascular event related to aspirin and plavix therapy, this is the first report described in the literature. It also represents a new differential diagnosis for nontraumatic acute subdural hematomas.