Fractures in the under-3-year-old age cohort.

One hundred twenty-four urban children under 3 years of age admitted for fractures were retrospectively reviewed to determine the frequency of accidental and nonaccidental causes in this population. The fractures were categorized according to their mechanisms: motor-vehicle passenger or pedestrian accident, other accidents, or child abuse. There were no differences in the frequency of fractures by race, date of birth, or season in which the injury occurred. Skull fractures were most frequent (62%), followed by femur fractures (11%). There was a 26% increase in fractures between 1987 and 1989, especially in the non-motor vehicle cohort. Caretaker ignorance and/or carelessness was a common cause of fractures in the infant and toddler age group. Injuries were still occurring in spite of infant care seat use. The American public must be educated in preventive medicine and safety to decrease the senseless morbidity of our greatest resource.

Differential effects of 21-aminosteroids on wound healing.

OBJECTIVE: The aim of this study was to examine the effects of the 21-aminosteroid U74389F on wound healing, compared with corticosteroids using a murine incisional wound model. BACKGROUND DATA: The 21-aminosteroids are extremely potent inhibitors of iron-dependent lipid peroxidation and peroxyl radical formation, and have proven significantly beneficial in reducing neurologic sequelae following head and spinal cord trauma in experimental models. The detrimental effects of currently administered corticosteroids on wound healing are well-documented; however, the effects of the 21-aminosteroids on wound healing are poorly defined to date. METHODS: Male BDF1 mice (n = 28/group) given a left paraspinous wound received daily intraperitoneal injection of vehicle or U74389F (1 to 100 mg/kg/day) for 10 days. Wound disruption strengths (WDSs) in grams were determined on freshly harvested (F) and 36-hour formalin-fixed (FF) wounds. In addition, U74389F (3 mg/kg/day) was compared with equipotent doses of methylprednisolone, dexamethasone, and hydrocortisone (n = 12/group) for alterations in wound healing. RESULTS: The WDSs of the U74389F animals F or following FF were not significantly different from controls. In the comparison study, no significant difference in F or FF WDS was found for U74389F (3 mg/kg/day) or methylprednisolone animals when compared with controls. Dexamethasone-treated and hydrocortisone-treated animals had F and FF WDSs that were 50% of control and U74389F values (p < 0.001; ANOVA). Wounds harvested from both the control and U74389F-treated animals demonstrated the greatest extent of wound cleft contraction, collagen deposition, and neovascularity, with no obvious internal differences detectable under light microscopy. CONCLUSIONS: These results show that the 21-aminosteroid U74389F did not impair wound healing, as determined by WDS and light microscopy. Furthermore, given their greater efficacy in cell membrane stabilization and potent ability to scavenge peroxyl radicals, the 21-aminosteroids may prove beneficial in treating a variety of clinical conditions, wherein ischemia-reperfusion injury plays a major component.

Bone marrow toxicity by silver sulfadiazine.

The effect of silver sulfadiazine (SSD) on the production of granulocytes and macrophages was studied in a murine model of cutaneous injury. Application of SSD daily to mice receiving a 10 percent full-thickness total body surface area burn injury failed to demonstrate consistent suppression of the bone marrow at one, four or seven days postinjury. Mice undergoing a 10 percent full-thickness skin excision (SE) and daily SSD application (SE plus SSD) had a near 50 percent reduction in total peripheral blood leukocyte counts in comparison with a control group and untreated mice that were skin-excised (SE-U) (p < 0.03) to 0.002) on day one postinjury and maintained this reduction compared with SE-U at days four and seven postinjury. The absolute number of granulocytes in SE plus SSD was only 10 percent of control or SE-U (p < 0.04 to 0.002) at day one postinjury and remained less than SE-U at four and seven days postinjury. Femoral bone marrow assay of granulocyte-macrophage progenitor cells (GM-CFC) revealed a marked reduction in nucleated bone marrow cells for SE plus SSD compared with respect to control at days one and seven and SE-U at days four and seven (p < 0.02 to 0.001). GM-CFC were significantly depressed in SE plus SSD on day one compared with C and SE-U and day four compared with SE-U (p < 0.01 to 0.001), but returned to control values by day seven. When SSD (0.5 to 500.0 micrograms per milliliter) was added to culture plates containing maximally stimulated normal murine or human bone marrow cells, the colony count was depressed in a dose-dependent manner. In vitro SSD is directly cytotoxic to myelopoietic tissue, and in vivo, alters the myeloid cell compartment. These observations in combination may explain the transient leukopenia frequently observed in patients receiving topical chemoprophylaxis with SSD.

Systemic administration of interferon-gamma impairs wound healing.

Interferon-gamma (IFN-gamma), a cytokine that has been shown to upregulate macrophage function, has recently been demonstrated to improve outcome when exogenously administered in several animal models of injury. Because the macrophage is also important in the events that govern wound healing, we evaluated the effects of IFN-gamma upon wound healing in a murine model. IFN-gamma was administered in doses of 937.5-22,500 u synchronous with the creation of a left paraspinous wound and then daily. At Day 10, wounds were harvested, evaluated for wound disruption strength (WDS), and subjected to morphometric analysis. Wounds were also subjected to 36-hr formalin fixation to maximally cross-link collagen fibrils and retested for WDS. We found that IFN-gamma impaired wound healing at all doses relative to control, and WDS was impaired in a dose-dependent fashion. Our highest dose of IFN-gamma (22,500 u) produced a WDS only 65% of the control. Morphometric studies demonstrated less collagen deposition and a lower degree of neovascularity in IFN-gamma-treated animals. In addition, formalin fixation studies suggested that IFN-gamma may impair collagen cross-linking. The potential benefits of IFN-gamma in the multiply injured patient must be weighed against the possibility that IFN-gamma might deleteriously effect events fundamental to wound healing.

Interferon-gamma increases mortality following cecal ligation and puncture.

Interferon-gamma (IFN-gamma) has been demonstrated to improve outcome following localized infection and hemorrhagic shock in experimental studies. We sought to determine the effects of IFN-gamma in a clinically relevant murine model of intra-abdominal polymicrobial sepsis. Fifty male BDF1 mice, each weighing 23-28 g, underwent cecal ligation and puncture (CLP) followed by administration of subcutaneous injections of IFN-gamma 100-22,500 U or vehicle control immediately post-CLP and then daily. In a second set of experiments, 60 mice underwent daily injections of vehicle control or 100 U IFN-gamma 24, 48, or 72 hours prior to CLP. Interferon-gamma administered following CLP led to increased mortality and earlier deaths in a dose-dependent fashion (p < 0.05). Interferon-gamma given 24, 48, or 72 hours prior to CLP resulted in no demonstrable benefit when compared with animals that did not receive IFN-gamma (p = 0.14, p = 0.94, and p = 0.97, respectively). While IFN-gamma has been reported to be of value in selected clinical situations by improving resistance to infection, it may not be capable of conferring protection following surgery or trauma with intra-abdominal sepsis, and in fact may be detrimental.