Bacteriology of aspiration pneumonia in patients with acute coma.

Loss of protective airway reflexes in patients with acute coma puts these patients at risk of aspiration pneumonia complicating the course of the primary disease. Available data vary considerably with regard to bacteriology, role of anaerobic bacteria, and antibiotic treatment. Our objective was to research the bacteriology of aspiration pneumonia in acute coma patients who were not pre-treated with antibiotics or hospitalized within 30 days prior to the event. We prospectively analyzed 127 patient records from adult patients admitted, intubated and ventilated to a tertiary medical intensive care unit with acute coma. Bacteriology and antibiotic resistance testing from tracheal aspirate sampled within 24 h after admission, blood cultures, ICU scores (APACHE II, SOFA), hematology, and clinical chemistry were assessed. Patients were followed up until death or hospital discharge. The majority of patients with acute coma suffered from acute cardiovascular disorders, predominantly myocardial infarction, followed by poisonings, and coma of unknown cause. In a majority of our patients, microaspiration resulted in overt infection. Most frequently S. aureus, H. influenzae, and S. pneumoniae were isolated. Anaerobic bacteria (Bacteroides spec., Fusobacteria, Prevotella spec.) were isolated from tracheal aspirate in a minority of patients, and predominantly as part of a mixed infection. Antibiotic monotherapy with a 2nd generation cephalosporin, or a 3rd generation gyrase inhibitor, was most effective in our patients regardless of the presence of anaerobic bacteria.

Toxicity of antihypertensives in unintentional poisoning of young children.

BACKGROUND: Knowledge is limited about the toxicity of unintentional exposure to antihypertensives in young children (0-6 years of age). OBJECTIVE: Our aim was to research symptoms and poisoning severity in unintentional poisonings in this group of age and determine adequate poisoning management. METHODS: We performed a 10-year retrospective, explorative analysis of the Mainz Poison Center/Germany database with regard to circumstances of poison exposure, dosage, symptoms, and treatment. To be able to relate drug exposure with reported symptoms, analyses were restricted to single drug exposures. Written follow-up information was obtained in about 50% of all cases. RESULTS: A total of 1489 cases were analyzed, of which 957 were single drug exposures with 421 exposures to beta-blocking agents, 364 to inhibitors of the renin-angiotensin system, 122 to calcium channel blockers, and 50 to antiadrenergic drugs. No severe (Poisoning Severity Score [PSS]=3) or fatal poisonings (PSS=4) were reported and, with the exception of atenolol, propranolol, irbesartan, isradipin, clonidine, and moxonidine, no poisonings with a PSS>1. We did not find a significant relationship between dosage, release formulation and symptoms, or PSS. All patients fully recovered without specific treatment. CONCLUSIONS: In young children with unintentional, single drug exposure to the most popular antihypertensive medication (i.e., metoprolol, bisoprolol, ramipril, enalapril, lisinopril, captopril, candesartan, valsartan, amlodipine, and verapamil), only mild symptoms occurred, and hospital evaluation is not a must. However, children with recent exposure to clonidine or moxonidine should be evaluated at a hospital due to an increased likelihood of poisonings of at least moderate severity.

C1-esterase inhibitor reverses functional consequences of superior mesenteric artery ischemia/reperfusion by limiting reperfusion injury and restoring microcirculatory perfusion.

Activated complement contributes significantly to reperfusion injury after ischemia. This study explores functional consequences of C1-esterase inhibitor (C1-INH) treatment after superior mesenteric artery occlusion (SMAO)/reperfusion using intravital microscopy. Thirty anesthetized, spontaneously breathing, male Sprague-Dawley rats underwent SMAO for 60 min followed by reperfusion (4 h). C1-esterase inhibitor (100 and 200 IU/kg body weight) or saline (0.9%) was given as a single bolus before reperfusion. Sham-operated animals (n = 10) without SMAO served as controls. Systemic hemodynamics were monitored continuously, arterial blood gases analyzed intermittently, and leukocyte/endothelial interactions in the mesenteric microcirculation quantified at intervals using intravital microscopy. Ileal lipid-binding protein (I-LBP) levels were determined from serum samples with an enzyme-linked immunosorbent assay at the end of the experiments. C1-esterase inhibitor restored microcirculatory perfusion to baseline levels in a dose-dependent manner and reduced adherent leukocytes after SMAO/reperfusion to similar levels in both C1-INH-treated groups during reperfusion. Furthermore, C1-INH treatment efficiently prevented metabolic acidosis, reduced the need for intravenous fluids to support blood pressure, and decreased I-LBP levels in a dose-dependent manner. Survival rates were 100% in controls and after 200 IU/kg C1-INH, 90% after 100 IU/kg C1-INH, and 30% in saline-treated animals. C1-esterase inhibitor bolus infusion efficiently blunted functional consequences of mesenteric ischemia/reperfusion with I-LBP, proving to be a valuable serum marker mirroring the effect of ischemia/reperfusion and treatment at the end of the experiments.