Inflammatory cells, particularly neutrophil granulocytes, have been implicated in the pathogenesis of the adult respiratory distress syndrome (ARDS). In this study, we investigated whether a relationship exists between neutrophil elastase in the plasma of multiple-trauma patients on initial hospital presentation and the subsequent development of lung injury and ARDS. Sixty-one multiple-trauma patients were enrolled prospectively. Neutrophil elastase was measured by a specific radioimmunoassay, and analysis was performed by nonparametric statistical methods. A highly significantly elevated plasma elastase level was found in patients who progressed to ARDS (median 217 ng/ml, range 127 to 480) (n = 8) compared with those who did not (median 117 ng/ml, range 21.4 to 685) (n = 53) (p = 0.009). Significant correlation was found between initial elastase values and subsequent requirement for mechanical ventilation (p = 0.01), lowest arterial oxygen saturation/oxygen supplementation recorded (p = 0.003), and organ failure score (p = 0.006). This study shows that within minutes of the initiating trauma event, there is evidence of enhanced neutrophil degranulation as manifested by elevated levels of immunoreactive neutrophil elastase in the peripheral blood. The level of this enzyme correlates with the degree of subsequent lung injury and ARDS. These findings reinforce the importance of neutrophils and their secretory products in early ARDS disease pathogenesis.
Hypoglycemia is a serious problem in insulin-treated diabetic patients. In this study the efficacy of intravenous glucagon (1 mg) was compared with that of intravenous dextrose (25 g) in the treatment of hypoglycemia in insulin-treated patients attending an accident and emergency department. In addition, the prevailing glycemic control of these patients was compared with patients routinely attending a diabetic outpatient clinic. Both intravenous glucagon and dextrose were effective in the treatment of hypoglycemic coma. There was a difference in the glycemic profile after intravenous glucagon compared with intravenous dextrose, and recovery of a normal level of consciousness after glucagon was slower than after dextrose (6.5 vs. 4.0 min, respectively; P less than .001), although the average duration of hypoglycemic coma was 1.4 h. The glucagon- and dextrose-treated groups had significantly lower HbA1 than comparable patients routinely attending the clinic (9.5 +/- 0.8 vs. 12.0 +/- 3.8%, respectively; P less than .001). In view of the ease of administration and the small risk of vascular and extravascular complications, intravenous glucagon appears to be a useful alternative to intravenous dextrose in the treatment of severe hypoglycemia.
SUMMARYHypoglycaemia remains a serious and much feared complication of insulin therapy. In this study, patients attending an accident and emergency department in hypoglycaemic coma were randomized to treatment with either intravenous dextrose (25g) or intramuscular glucagon (lmg), administered into the right thigh. Restoration of normal conscious level was slower after glucagon than dextrose (90 vs 30 min, P<0-01), although the average duration of hypoglycaemic coma was 120 min. Two patients in the glucagon-treated group, who failed to show satisfactory recovery after 15 min, required additional treatment with intravenous dextrose. On questioning following recovery, all except two patients reported loss of awareness of the onset of hypoglycaemia.Intramuscular glucagon is valuable in the treatment of severe hypoglycaemia outwith hospital and, although the slightly slower and less predictable recovery may appear to make it a less attractive option than intravenous dextrose in the accident and emergency department, this must be balanced against the advantages of ease of administration and a lower incidence of serious adverse effects.
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