BACKGROUND: Despite rapid diagnosis and aggressive neurosurgical intervention, acute subdural hematoma (ASDH) is a severe type of head injury that can result in high morbidity and mortality. Although surgical procedures, such as craniotomy and decompressive craniectomy (DC), can be effective, the preferred approach for treating an ASDH remains controversial. The aim of this report was to evaluate factors associated with mortality in patients with ASDH and determinants of outcome in those with ASDH who underwent DC. METHODS: The demographic details and clinical and radiological characteristics of a total of 93 patients with ASDH who underwent DC during a 60-month period from 2012 to 2017 were evaluated to determine the effect on mortality and any association with the Glasgow Coma Scale (GCS) score recorded on arrival. RESULTS: Sixty-five male and 28 female subjects with a mean age of 59.82±19.49 years (range: 16-88 years) were included in the study. Sixteen patients (17.2%) died following the surgery. Older age (p=0.007) and lower GCS scores (p=0.022) were statistically significantly associated with the mortality rate. The mean hematoma thickness was 15.46±5.73 mm, and the mean midline shift was 9.90±4.84 mm. The mortality rate was positively correlated with an excessive midline shift (p=0.011; r=0.262) and age (p=0.022; r=0.237) in patients with ADSH. A midline shift of ≥10 mm and a hematoma thickness of ≥15 mm was significantly associated with mortality (p=0.014; p=0.039). The etiology of the trauma; comorbidities of subarachnoid, epidural, or intracranial hemorrhage; compression fractures; or contusions were not significantly correlated. CONCLUSION: The results indicated that there was a higher mortality rate among older patients and those with a GCS score of <6 on arrival. A midline shift of ≥10 mm and a hematoma thickness of ≥15 mm were significantly related to mortality. Our study supports the conclusion that DC may help prevent further midline shift and be associated with a lower mortality rate compared with a craniotomy.
AIM: To examine ischemic neurodegeneration of the ciliospinal center on permanent miosis following subarachnoid hemorrhage (SAH). MATERIAL and METHODS: Nineteen rabbits were examined in this study. The animals were divided into three groups, as control (GI, n=5), sham (GII, n=5) and study group (GIII, n=9). Pupil diameters were measured after giving 0.5 mL physiological saline for sham and autologous arterial blood for the study group into the cervico-thoracic subarachnoid space. After three weeks of follow up, the cervico-thoracic cord and bilateral superior cervical sympathetic ganglia were removed. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia and degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods. RESULTS: The mean pupil diameter was 5180 ± 370 µm and the mean degenerated neuron density of the ciliospinal center was 4 ± 1/mm 3 in animals of the control group (GI). These values were 9850 ± 610 µm, 10 ± 3/mm 3 in sham (GII), and 7.010 ± 440 µm and 98 ± 21/mm 3 in the study (GIII) groups. There was an inverse relationship between degenerated neuron density of the ciliospinal nuclei and pupil diameters. CONCLUSION: We showed and reported for the first time that ciliospinal sympathetic center ischemia-induced neurodegeneration may have been responsible for permanent miosis following SAH.
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