The evaluation of casualties from Operation Iraqi Freedom on return to the continental United States from March to June 2003.

BACKGROUND: Most seriously wounded US Army casualties from the Iraqi theater of operations come through Walter Reed Army Medical Center on their return to the United States. General surgery and orthopaedic surgery services have developed a multidisciplinary team approach to triage and treatment of incoming casualties. STUDY DESIGN: Prospective database of returning casualties to Walter Reed Army Medical Center from Operation Iraqi Freedom (OIF) from March 1 to July 1, 2003. RESULTS: Of 294 casualties seen, 119 were triaged to inpatient status and treated within 1 hour of arrival; mean age 26.6 +/- 6.2 years (range 23 to 37). Time from original battlefield injury was a mean of 8 days (range 3 to 28 days). Forty-six (39%) sustained gunshot wounds, 37 (31%) sustained blast and shrapnel injuries, and 41 (34%) had blunt/motor vehicle collision mechanisms. There were a total of 184 wounded locations in these 119 casualties; of these, there were 29 head and neck, 25 chest, 20 abdomen, 74 lower extremity, and 36 upper extremity. Twenty-eight casualties (23%) required emergent surgical procedures on the night of arrival. Another 30 (25%) required an urgent surgical procedure within 48 hours of arrival. CONCLUSIONS: Followup surgical procedures were urgently or emergently required in 43% of admitted battlefield casualties from OIF on transfer to Level V care in the continental United States. The injury pattern of wounds from this engagement is described. The Walter Reed Army Medical Center system of incoming battlefield casualty evaluation using multidisciplinary teams is successful in expediting care and ensuring evaluation of the full range of potential injuries.

Effect of hyperglycemia and nitric oxide synthase inhibition on heat tolerance and induction of heat shock protein 72 kDa in vivo.

Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/ reperfusion injury. Heat shock protein 72 (HSP-72) protects against KDa ischemia/reperfusion damage in vivo. The effect of diabetes on HSP-72 expression in vivo is unknown. The aim of this study was to determine the effects of diabetes and NOS inhibition on HSP-72 induction in vivo. Rats were assigned to four groups: control (C), streptozotocin-induced diabetic (D), acute hyperglycemia (A), and L-N(omega)-nitro-L-arginine treated (L). Rats were subjected to hyperthermia and allowed to recover for 4 hours. Intestine and liver samples from heated (H) and nonheated (NH) rats were analyzed for HSP-72 by Western blot. HSP-72 levels were increased significantly in CH compared to CNH rats. No deaths occurred in CH rats; however, death rates were significant in AH, DH, and LH rats. DH rats died earlier than LH and AH rats. HSP-72 in liver and intestine was reduced significantly in LH rats. When compared with CH rats the surviving AH and DH rats exhibited similar HSP-72 levels in the liver. Diabetes, acute hyperglycemia, and L-N(omega)-nitro-L-arginine treatment lower heat stress tolerance. NOS is required for HSP-72 expression, but not survival. Diabetics who survive heat stress moderately express HSP-72. Characterization of altered thermotolerance and HSP-72 may provide mechanisms for the deranged diabetic stress response.