Neurosurgical injuries resulting from the 2011 tornados in Alabama: the experience at the University of Alabama at Birmingham Medical Center.

OBJECT: The April 27, 2011, tornados that affected the southeastern US resulted in 248 deaths in the state of Alabama. The University of Alabama at Birmingham (UAB) Medical Center, the largest Level I trauma center in the state, triaged and treated a large number of individuals who suffered traumatic injuries during these events, including those requiring neurosurgical assessment and treatment. METHODS: A retrospective review of all adult patients triaged at UAB Medical Center during the April 27, 2011, tornados was conducted. Those patients who were diagnosed with and treated for neurosurgical injuries were included in this cohort. RESULTS: The Division of Neurosurgery at UAB Medical Center received 37 consultations in the 36 hours following the tornado disaster. An additional patient presented 6 days later, having suffered a lumbar spine fracture that ultimately required operative intervention. Twenty-seven patients (73%) suffered injuries as a direct result of the tornados. Twenty-three (85%) of these 27 patients experienced spine and spinal cord injuries. Four patients (15%) suffered intracranial injuries and 2 patients (7%) suffered combined intracranial and spinal injuries. The spinal fractures that were evaluated and treated were predominantly thoracic (43.5%) and lumbar (43.5%). The neurosurgery service performed 14 spinal fusions, 1 ventriculostomy, 2 halo placements, 1 diagnostic angiogram, 1 endovascular embolectomy, and 1 wound debridement and lavage. Twenty-two patients (81.5%) were neurologically intact at discharge and all but 4 had 1 year of follow-up. Three patients had persistent deficits from spinal cord injuries and there was 1 death in a patient with multisystem injuries in whom no procedures were performed. Two patients experienced postoperative complications in the form of 1 wound infection and 1 stroke. CONCLUSIONS: The April 27, 2011, tornados in Alabama produced significant neurosurgical injuries that primarily involved the spine. There were a disproportionate number of patients with thoracolumbar fractures, a finding possibly due to the county medical examiner's postmortem findings that demonstrated a high prevalence of fatal cervical spine and traumatic brain injuries. The UAB experience can be used to aid other institutions in preparing for the appropriate allotment of resources in the event of a similar natural disaster.

Heparin-binding EGF-like growth factor down regulates proinflammatory cytokine-induced nitric oxide and inducible nitric oxide synthase production in intestinal epithelial cells.

We have previously shown that heparin-binding EGF-like growth factor (HB-EGF) protects intestinal epithelial cells (IEC) from necrosis and apoptosis in vitro and from intestinal ischemia/reperfusion injury in vivo; however, the mechanisms of HB-EGF cytoprotection are unclear. Overproduction of iNOS and NO have been implicated in the pathogenesis of several forms of ischemia/reperfusion injury. We therefore studied whether HB-EGF could down-regulate proinflammatory cytokine-induced iNOS and NO production in intestinal epithelial cells in vitro. DLD-1 human intestinal epithelial cells were exposed to the proinflammatory cytokines interleukin-1beta (IL-1beta) (20 ng/ml) and interferon-gamma (IFN-gamma) (10 ng/ml) to stimulate iNOS induction and NO production. Cells were treated with HB-EGF (0-100 ng/ml) either before or with cytokine exposure, and cells and supernatants were harvested 24 and 48 h later. Accumulated NO was measured in supernatants by chemiluminescence. Total RNA was extracted from cell lysates for iNOS mRNA quantification using real-time reverse transcription-polymerase chain reaction (RT-PCR), and total protein was extracted from cell lysates for detection of iNOS protein. HB-EGF significantly decreased cytokine-induced NO production in a dose dependent manner, and NO reduction was associated with iNOS suppression at both the mRNA and protein levels. While cytokine exposure resulted in a significant increase in iNOS mRNA expression in these cells (109 plus minus 9 fold), HB-EGF reduced iNOS expression by 5.7-fold (P < 0.05). These results suggest that HB-EGF may exert its cytoprotective effects, in part, by down-regulating iNOS and NO production, and provides further rationale for additional testing of the effects of HB-EGF in the treatment of intestinal ischemia/reperfusion injury in vivo.