Factors Affecting the Intensive Care Stay of Patients with Spinal Neural Tube Defects.

AIM: To evaluate the duration of hospitalization and the factors that increase this duration in cases treated in the neonatal intensive care unit with the diagnosis of a spinal neural tube defect (NTD). MATERIAL AND METHODS: The demographic characteristics, NTD type and level, ventriculoperitoneal (V-P) shunt needs, accompanying spinal deformity, antibiotherapy applied during treatment, and intensive care stay periods of 73 patients treated in our clinic between July 2017 and 2020 were retrospectively evaluated. RESULTS: The intensive care stay of NTD cases was 7?109 (mean=23) days. Fifty-one cases (69.9%) had myeloschisis, and 22 cases (30.1%) had myelomeningocele (MMC) sac. A V-P shunt was applied to 24 cases (32.9%) during hospitalization, and additional antibiotherapy was given to 32 (43.8%) cases. CONCLUSION: In myeloschisis cases compared with MMC marsupial cases, incidences of ventricular dilatation, kyphotic/scoliotic spine pathology, V-P shunt requirement, and longer hospital stay were observed. No difference in the duration of hospitalization was found in patients who underwent defect repair between the first day and 48 h after birth. However, the length of stay in hospital increased in patients operated on after 48 h. The period was longer in cases operated after seven days postnatally. Therefore, by performing NTD surgical treatment within the first 48 hours, the need for additional antibiotherapy and hospital stay can be shortened.

Serum neuron-specific enolase as a predictor of short-term outcome and its correlation with Glasgow Coma Scale in traumatic brain injury.

Elevated serum neuron-specific enolase levels are correlated with brain cell damage. Low scores according to Glasgow Coma Scale are also considered as serious poor prognostic factor. The aims of the study were to investigate whether there is a correlation between the two measurements in patients with traumatic brain injury and whether serum neuron-specific enolase levels have potential as a screening test to predict outcome. A total of 169 consecutive patients with traumatic brain injury admitted to our clinic between 2002 and 2005 are included in this study. Those patients, who had any major health problem before trauma, were excluded from the study. However, patients with isolated head injury were included in the study. Serial serum neuron-specific enolase concentrations taken at the first 2, 24, and 48 h after traumatic brain injury were analyzed. A computed tomography was performed on each patient on admission. Their Glasgow Coma Scale scores were recorded serially. The relationship between Glasgow Coma Scale scores and the serum neuron-specific enolase levels were assessed by statistical methods. There was a significant negative correlation between the serum neuron-specific enolase levels and Glasgow Coma Scale scores. The levels of neuron-specific enolase were significantly higher in the patients who died in 30 days after trauma and whose scores were lower than or equal to 8 points in Glasgow Coma Scale. Although there are several serious limitations of the use of neuron-specific enolase as a biomarker in traumatic brain injury (i.e., hypoperfusion, extracranial trauma, bleeding, liver, or kidney damage also increase the level of neuron-specific enolase), its concentrations may be useful as a practical and helpful screening test to identify neurotrauma patients who are at increased risk and may provide supplementary estimation with radiological and clinical findings.