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Background Cognitive impairment after traumatic brain injury (TBI) is a main source of morbidity for affected individuals, their family members, and their community. There are numerous serum biomarkers, which are elevated after TBI; one of these is D-dimer. Several studies have related that trauma-related coagulopathy, marked by elevated D-dimer levels, is associated with poor prognosis. Objective The aim of this study was to find if there is a correlation between elevated serum levels of D-dimer and impairment of final cognitive outcome in case suffering of Moderate TBI. Patients and method This is a prospective cohort study with a random sample of 87 patients suffering from moderate TBI. Serum level of D-dimer was requested for all cases after confirming the diagnosis of moderate TBI with post-traumatic GCS 9–12. Head trauma treatment protocols were followed according to each case diagnosis and then at the time of discharge cognitive outcome was assessed for all cases. Neurocognition was assessed by Montreal cognitive assessment-Basic (MoCA-B). Results Eighty-seven cases were included in this trial with a mean age 28 years. 48.3% of cases were treated conservatively while the remaining 51.7% needed surgical interventions for different pathologies. Seventy-five cases had elevated levels of serum D-dimer (86.2%) whereas only 12 cases have within normal levels (13.8%). A twofold increase in the serum D-dimer level was found in 41% of cases, while 34.5% of cases had three- to sixfold increases, and 10% of cases had more than sixfold increase. The mean MoCA-B score was 24 points (range 13–27). Correlating the D-dimer levels statistically with the MoCA scores, age, admission and discharge GCS, and durations of hospital stay did not show any statistical significance with any of these variables. Conclusion The role played by D-dimer in the pathophysiology of cognitive deficits and its correlation with post moderate TBI cognitive outcome was not proven.

BACKGROUND: Myelomeningocele (MMC) is one of the most common developmental anomalies of the CNS. Many of these patients develop hydrocephalus (HCP). The rate of cerebrospinal fluid diversion in these patients varies significantly in literature, from 52% to 92%. MMC repair conventionally occurs in the post-natal period. With the technological advances in surgical practice and fetal surgeries, intra uterine MMC repair IUMR is adopted in some centers. Cerebrospinal fluid shunting has numerous complications, most notably shunt failure and shunt infection. Studies have suggested that patients with greater numbers of shunt revisions have poorer performance on neuropsychological testing. There is also good evidence to suggest that the IQs of patients with MMC who do not undergo shunt placement are higher than that of their shunt treated counterparts. AIM: In this study, we are trying to identify strong clinical and radiological predictors for the need of ventriculoperitoneal (VP) shunt insertion in patients with MMC who underwent surgical repair and closure of the defect initially. This will decrease the overall rate of shunt placement in this group of patients through applying a strict policy adopting only shunt insertion for the desperately needing patient. METHODS: Prospective clinical study conducted on 96 patients with MMC presented to Aboul Reish Pediatric Specialized Hospital, Cairo University. After confirming the diagnosis through clinical and radiological aids, patients are carefully examined, if HCP is evident clinically and radiologically a shunt is inserted together with MMC repair at the same session after excluding sepsis or cerebrospinal fluid (CSF) infection, (GROUP A). If there are no signs of increased ICP, MMC repair shall be done alone (GROUP B). Those patients shall be monitored carefully postoperatively and after discharge and shall be followed up regularly to early detect and promptly manage latent HCP. Multiple clinical and radiological indices were used throughout the follow-up period and statistical significance of each was measured. RESULTS: Shunt placement was required in 45 (46.88%) of the 96 patients. Eighteen patients (18.75%) needed the shunt as soon as they presented to us (GROUP A), because they were having clinically active HCP. Twenty-seven (28.13%) patients were operated on by MMC repair initially without shunt placement because they did not have signs of increased ICP at the time of presentation. Yet, they developed latent HCP requiring shunt placement during the follow-up period (GROUP B2). Fifty-one patients of the study population (53.13%) underwent surgical repair of the MMC without the need of further VP insertion and they were followed up for 6 months period after the repair without developing latent HCP (GROUP B1). Patients of GROUP B were the study population susceptible for the development of latent HCP. Out of 78 patients in GROUP B, only 27 patients (34.62%) needed a VP shunt. CONCLUSION: In our study, we found that the rate of shunt insertion in patients with MMC is lower than the previously reported rate in the literature. A more thorough evaluation of the patient’s post-operative need for a shunt is mandatory. We suggest that we could accept postoperative (after MMC repair) ventriculomegaly provided it does not mean any deterioration in the patient’s clinical or developmental state. We assume that reduction of shunt insertion rate will eventually reduce what has previously been an enormous burden for a significant proportion of children with MMC.