Unique pattern of complications in elderly trauma patients at a Level I trauma center.

BACKGROUND: Trauma centers are caring for increased proportions of elderly patients. Although age and Injury Severity Score are independently associated with mortality, trauma centers were originally designed to care for seriously injured patients without age-specific guidelines. We hypothesized that elderly patients would have different complication patterns than their younger counterparts. METHODS: The trauma registry of an American College of Surgeons -verified Level I trauma center was queried for all patients older than 14 years admitted between January 2005 and December 2008. Mechanism, mortality, and complications were evaluated after dividing patients into eight age groups. RESULTS: Of the 15,223 patients, 13% were elderly (≥65), and 86% were injured via a blunt mechanism. Increasing age correlated with fatality (all Injury Severity Scores), end-organ failure, and thromboembolic complications (deep venous thrombosis and coagulopathy). Analysis revealed a significant breakpoint at 45 years of age for mortality, decubitus ulcer, and renal failure (all p values <0.05). Infectious complications (sepsis, wound infection, and abscess) all peaked between 45 years and 65 years and then declined with increasing age. CONCLUSIONS: We document that elderly trauma patients suffer the same complications as their younger counterparts, albeit at a different rate. More importantly, we identified a "breakpoint" of increased risk of complications and mortality at greater than 45 years. Although the mechanisms behind these observations remain unknown, understanding their unique patterns may allow appropriate allocation of resources and focus research efforts on interventions that should improve outcomes.

Effect of an oral iron chelator or iron-deficient diets on uroporphyria in a murine model of porphyria cutanea tarda.

UNLABELLED: Porphyria cutanea tarda is a liver disease characterized by elevated hepatic iron and excessive production of uroporphyrin (URO). Phlebotomy is an effective treatment that probably acts by reducing hepatic iron. Here we used Hfe(-/-) mice to compare the effects on hepatic URO accumulation of two different methods of hepatic iron depletion: iron chelation using deferiprone (L1) versus iron-deficient diets. Hfe(-/-) mice in a 129S6/SvEvTac background were fed 5-aminolevulinic acid (ALA), which results in hepatic URO accumulation, and increasing doses of L1 in the drinking water. Hepatic URO accumulation was completely prevented at low L1 doses, which partially depleted hepatic nonheme iron. By histological assessment, the decrease in hepatic URO accumulation was associated with greater depletion of iron from hepatocytes than from Kupffer cells. The L1 treatment had no effect on levels of hepatic cytochrome P4501A2 (CYP1A2). L1 also effectively decreased hepatic URO accumulation in C57BL/6 Hfe(-/-) mice treated with ALA and a CYP1A2 inducer. ALA-treated mice maintained on defined iron-deficient diets, rather than chow diets, did not develop uroporphyria, even when the animals were iron-supplemented either directly in the diet or by iron dextran injection. CONCLUSION: The results suggest that dietary factors other than iron are involved in the development of uroporphyria and that a modest depletion of hepatocyte iron by L1 is sufficient to prevent URO accumulation.

Effect of iron and ascorbate on uroporphyria in ascorbate-requiring mice as a model for porphyria cutanea tarda.

UNLABELLED: Excess hepatic iron is known to enhance both porphyria cutanea tarda (PCT) and experimental uroporphyria. Since previous studies have suggested a role for ascorbate (AA) in suppressing uroporphyria in AA-requiring rats (in the absence of excess iron), the present study investigated whether AA could suppress uroporphyria produced by excess hepatic iron. Hepatic URO accumulation was produced in AA-requiring Gulo(-/-) mice by treatment with 3,3',4,4',5-pentachlorbiphenyl, an inducer of CYP1A2, and 5-aminolevulinic acid. Mice were administered either sufficient AA (1000 ppm) in the drinking water to maintain near normal hepatic AA levels or a lower intake (75 ppm) that resulted in 70 % lower hepatic AA levels. The higher AA intake suppressed hepatic URO accumulation in the absence of administered iron, but not when iron dextran (300-500 mg Fe/kg) was administered. This effect of iron was not due to hepatic AA depletion since hepatic AA content was not decreased. The effect of iron to prevent AA suppression of hepatic URO accumulation was not observed until a high hepatic iron threshold was exceeded. At both low and high AA intakes, hepatic malondialdehyde (MDA), an indicator of oxidative stress, was increased three-fold by high doses of iron dextran. MDA was considerably increased even at low iron dextran doses, but without any increase in URO accumulation. The level of hepatic CYP1A2 was unaffected by either AA intake. CONCLUSION: In this mouse model of PCT, AA suppresses hepatic URO accumulation at low, but not high hepatic iron levels. These results may have implications for the management of PCT.