Traumatic brain injury is associated with the development of deep vein thrombosis independent of pharmacological prophylaxis.

INTRODUCTION: Deep venous thrombosis (DVT) is common among trauma patients. If left untreated it may result in lethal pulmonary thromboembolism. Previous studies have suggested that intracranial hemorrhage serves as an independent risk factor for the development of DVT. These studies were not able to exclude anticoagulation therapy as a confounding variable in their analysis. Our objective was to determine the association of traumatic brain injury (TBI) to the formation of DVT irrespective of the use of anticoagulation therapy. METHODS: All patients admitted to an academic level I Trauma Center between 2000 and 2007 with blunt or penetrating injuries were selected for inclusion in this study. Patients who died or who were discharged within 24 hours of admission were excluded in the analysis. TBI was defined as any intraparenchymal hemorrhage or extra-axial intracranial bleeding identified on radiographic imaging or both. Anticoagulation therapy was defined as the uninterrupted use of either subcutaneous lovenox or heparin. Risk ratios and 95% confidence intervals compared the risk of DVT among patients with and without TBI according to the initiation of anticoagulation therapy (no therapy, <24 hours, 24-48 hours, and >48 hours) adjusted for age, gender, race, injury severity, mechanism of injury, spinal injury, and lower extremity fracture. RESULTS: Irrespective of the time of initiation of pharmacologic prophylaxis, TBI is independently associated with the formation of DVT. A threefold to fourfold increased risk of DVT formation is consistent across all prophylaxis groups among patients with TBI. CONCLUSION: The incidence of DVT among injured patients with TBI is significantly higher than those patients without head injury independent of anticoagulation therapy. Rigorous surveillance to detect DVT among trauma patients with TBI should be undertaken and where appropriate alternate means for pulmonary thromboembolism prevention used.

Left ventricular hypertrophy in pediatric kidney transplant recipients: long-term follow-up study.

Cross-sectional studies indicate that LVH, known cardiovascular risk factor, is frequent in pediatric patients post-kidney transplant. We performed a retrospective longitudinal analysis of echocardiographic data collected in children and adolescents who received kidney transplant from 1998 to 2003. The first echo was performed at a median time post-transplant of 14 months in 47 children; a second echo (echo 2) was carried out at a median time of 33 months in 31 and a third echo (echo 3) was performed at a median time of 49 months in 14 children. LVH was defined as LV mass index >/=95th percentile for children. LVH was present in echo 1 in 25 (54%) subjects. Systolic blood pressure (p = 0.02) and BMI (p = 0.02) independently predicted the LVH seen in echo1 in multivariate logistic regression. In 14 subjects with three consecutive echocardiograms LVM index significantly decreased from echo 1 to echo 2 and from echo 1 to echo3 (p < 0.05), but no significant changes were observed between echo 2 and echo 3. The overall prevalence of LVH remained unchanged but its severity significantly decreased during the follow-up. The results of the study suggest that despite regression of LVM index overtime-pediatric patients post-kidney transplant are at continuous risk for developing cardiovascular disease.

Urinary neutrophil gelatinase-associated lipocalcin in D+HUS: a novel marker of renal injury.

BACKGROUND: Diarrhea-associated hemolytic uremic syndrome (D+HUS) causes acute renal failure. Neutrophil gelatinase-associated lipocalcin (NGAL) is an early indicator of kidney injury. OBJECTIVE: To determine if urinary NGAL excretion is a biomarker of severe renal injury and predicts the need for dialysis in D+HUS. METHODS: Patients were randomly selected from among participants in the SYNSORB Pk trial. Urine samples were collected daily if available during the first week of hospitalization. NGAL levels were determined by ELISA. RESULTS: 34 children, age 5.9+/-3.9 yr, were studied; ten (29%) required dialysis. Patients were categorized based on urinary NGAL concentration within five days of hospitalization - <200 ng/ml and >or=200 ng/ml. Twenty patients (58%) had increased urinary NGAL excretion. The severity of D+HUS at enrollment was similar in the two groups. However, children with increased urinary NGAL levels had higher peak BUN and creatinine concentrations (P<0.01) and required dialysis more often, 9/20 versus 1/14 (P=0.024) compared to children with normal excretion. CONCLUSION: The majority of patients with D+HUS have renal tubular epithelial injury, as evidenced by elevated urinary NGAL excretion. Urinary NGAL levels below 200 ng/ml within five days of hospitalization may be an adjunctive marker that defines less severe renal involvement.