Association of the time to first epinephrine administration and outcomes in out-of-hospital cardiac arrest: SOS-KANTO 2012 study

Objective

This study assessed the association between the timing of first epinephrine administration (EA) and the neurological outcomes following out-of-hospital cardiac arrests (OHCAs) with both initial shockable and non-shockable rhythms.

A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.     

Malacoplakia of the bladder: Efficacy of enoxacine therapy

Malacoplakia of the urinary bladder was seen in a 69-year-old woman with haematuria. We firstly treated her with distigmine bromide, ascorbic acid and trimethroprim-sulfamethoxazole. Haematuria subsided but the lesion did not change after 6 weeks. Thereafter we tried enoxacine therapy. Eight weeks after the medication the tumorous leson disappeared. Bladder biopsy performed 4 months after the initiation of the treatment revealed predominantly granulation tissue. We can find no previous case treated successfully with long-term enoxacine.     

Relationship between the intestinal permeability to macromolecules and invasion of septicemia-inducing Escherichia coli in neonatal piglets.

The influence of age and diet on the invasion of septicemia-inducing Escherichia coli and the endocytotic activity of the small intestinal epithelium were examined in colostrum-deprived conventional and gnotobiotic piglets orally infected with E. coli 078. The piglets infected at birth and the animals fed glucose-amino acids solution and infected at 3 days after birth soon suffered from septicemia caused by the invasion of E. coli 378. The piglets fed artifical milk and infected at 3 days after birth, however, showed resistance to the invasion of E. coli in the absence of passively acquired serum gamma globulin. The endocytotic activity of the small intestinal epithelium was more intense in the former than in the latter piglets. Some of the ileal epithelial cells of the piglets infected at birth contained organisms, although these cells were morphologically intact and showed intense endocytosis. The present results suggest that the intestinal permeability to macromolecules, which depends on the endocytotic activity of the small intestinal epithelium, might predispose neonatal piglets to colisepticemia.     

Cytotoxic effects of 2,6-di-tert-butyl-4-methylphenyl N-methylcarbamate (terbutol) herbicide on hepatocytes and mitochondria isolated from male rats

The cytotoxic effects of 2,6-di-tert-butyl-4-methylphenyl N-methylcarbamate (terbutol) and its major metabolites were investigated in freshly isolated rat hepatocytes. Terbutol and its metabolite, especially 2,6-di-tert-butyl-4-methylphenyl carbamate (N-demethylterbutol), at a concentration of 1.0 mM resulted in a time dependent cell killing accompanied by losses of intracellular ATP, protein thiols, and glutathione (GSH) and the accumulation of oxidized GSH. Supplementation of the hepatocyte suspension with 5 mM N-acetylcysteine, a precursor of intracellular GSH, inhibited the cytotoxicity of N-demethylterbutol. In mitochondria isolated from rat liver, terbutol and its metabolites impaired respiration related to oxidative phosphorylation and the potency of their toxicity is associated with impairment of mitochondrial respiration. These results indicate that N-demethylterbutol is the most cytotoxic followed by terbutol and other metabolites, and that both the mitochondrial respiratory system and protein thiols are important targets for these compounds.     

Haemodynamic responses to the intubating laryngeal mask and timing of removal

We determined (a) the haemodynamic responses to intubating laryngeal mask (ILM) airway insertion/intubation and removal in anaesthetized patients, and (b) whether the timing of ILM removal influences these responses. One-hundred and twenty patients without cardiovascular disease were studied. ILM airway insertion/intubation was 5 min after induction with propofol 2 mg kg(-1) and maintenance of anaesthesia with sevoflurane 2% in oxygen 33% and nitrous oxide. Patients were randomly assigned for removal of the intubating laryngeal mask airway at 1, 3 and 5 min after successful intubation. Systolic and diastolic arterial pressures and heart rate were recorded preinduction (baseline), before ILM airway insertion/intubation, at 1-min intervals after insertion/intubation, and at 1-min intervals for 5 min after ILM removal. ILM insertion was successful at the first attempt in all patients, but 46 patients required more than one intubation attempt. Compared with baseline values, there were no increases in systolic or diastolic arterial pressure, but there was an increase in heart rate 1 min after ILM insertion/intubation (9%, P<0.001) and 1 min after ILM removal (8%, P<0.01). There was a significant increase in systolic and diastolic pressures and heart rate 1 min after ILM insertion/intubation (30%, 31% and 15%; all: P<0.002) compared with before ILM insertion/intubation values and 1 min after ILM removal (9%, 8% and 7%; all P<0.05) compared with 1 min after ILM insertion/intubation values. Removal of the ILM 1 min after successful intubation resulted in higher arterial pressure compared with removal at 3 min (systolic arterial pressure 10% higher for 1 min, P = 0.01) and 5 min (systolic arterial pressure 10-23% higher for 3 min, P<0.01; diastolic arterial pressure 10-20% higher for 4 min, P>0.02), but there were no differences in heart rate between groups. Systolic and diastolic arterial pressures were greater if more than one intubation attempt was required. Early removal or multiple intubation attempts did not exceed baseline haemodynamic values. We conclude that ILM insertion/intubation and removal in anaesthetized patients produces little or no haemodynamic response, even if multiple intubation attempts are required. The timing of removal exerts a small, but clinically unimportant influence on these responses.     

Increased chromatid-type chromosomal aberrations in mouse m5S cells exposed to power-line frequency magnetic fields

PURPOSE: To investigate the induction of chromosomal aberrations in mouse m5S cells after exposure to power-line frequency magnetic fields (extremely low frequency magnetic fields; ELFMF) at high-flux densities. MATERIAL AND METHOD: m5S cells were either untreated or pretreated during the G1 phase with mitomycin C (MMC, 1 microM) for 1 h or 3 Gy X-rays, and then exposed to ELFMF at three different flux densities (5 and 50 mT at 60 Hz, 400 mT at 50 Hz) for 40 h. Unexposed control cells were incubated for the same period in a conventional CO2 incubator. Chromosomal aberrations were analysed in the first post-treatment metaphases. Cell kinetics were assessed by DNA flow cytometry and the mitotic index. RESULTS AND CONCLUSIONS: ELFMF enhanced the formation of spontaneous and MMC- or X-ray-induced chromosomal aberrations, in a flux-density-dependent manner. Statistically significant increases in the frequency of chromosomal aberrations were observed in cells exposed to 400 mT ELFMF with respect to unexposed controls. The aberrations induced by ELFMF were mostly chromatid-type, not chromosome-type. The cells exposed to 400 mT ELFMF exhibited a three-fold higher level of chromatid-type aberrations than did the unexposed cells. Flow cytometric and mitotic index analyses revealed that the S or G2 arrest following MMC or X-irradiation was more profound in ELFMF-exposed cells than in unexposed cells. Our results suggest that ELFMF can interfere with post-replication repair, resulting in increased levels of chromatid-type chromosomal aberrations induced spontaneously and by DNA damaging agents.     

Combining intermediate levels of the Endotoxin Activity Assay (EAA) with other biomarkers in the assessment of patients with sepsis: results of an observational study

ABSTRACT: INTRODUCTION: The Endotoxin Activity Assay (EAA) is a useful test to risk stratify patients with severe sepsis and assess for Gram negative infection. However, the significance of intermediate levels of EAA (0.4-0.59) at the bedside has not been well elucidated. The purpose of this study was to interpret intermediate EAA levels in clinical practice. METHODS: This retrospective observational study included all adult patients with suspected sepsis admitted to our medico-surgical intensive care unit (ICU) in whom EAA was measured from July 2008 to September 2011. Data collected included EAA, white blood cell (WBC) count and differential, C-reactive protein (CRP), procalcitonin (PCT) and bacterial cultures. Data were analyzed by comparative statistics. RESULTS: Two hundred and ten patients were studied. Ninety two (43%) patients had culture documented gram negative infection. Patients with Gram-negative organisms in cultures had significantly higher EAA levels (0.47, IQR 0.27) than those without any Gram-negative organisms in cultures (0.34, IQR 0.22) (p < 0.0001). For patients with intermediate EAA levels (0.40 to 0.59), PCT levels and presence of left shift of WBC significantly differed between patients with Gram negative organisms in their blood or other cultures and those who had no organisms in any of the cultures (4.9 versus 1.7 ng/mL, p < 0.05; 57.9 versus 18.9%, p < 0.0004, respectively). CONCLUSIONS: We confirm that high levels of EAA in our cohort of patients with suspected sepsis are strongly associated with gram negative infection. In those patients with intermediate elevation in EAA levels, use of PCT and WBC differential can provide additional diagnostic value to clinicians at the bedside.     

A new thrombolytic agent,monteplase, is independent of the plasminogen activator inhibitor in patients with acute myocardial infarction: initial results of the COmbining Monteplase with Angioplasty (COMA) trial

Background Both thrombolytic therapy and coronary angioplasty have been inconsistent together for primary acute myocardial infarction (AMI) therapy, because conventional thrombolytic agents accelerate plasminogen activator inhibitor-1 (PAI-1) activity. However, combining newly developed mutant tissue-type plasminogen activators with coronary angioplasty should be reconsidered. Methods This study was designed to investigate clinical usefulness of such an agent, monteplase, for treatment of AMI in light of PAI-1 kinetics. One hundred fifty-four consecutive patients with AMI were randomly assigned to receive direct coronary angioplasty (Group I) or coronary angioplasty after pretreatment with intravenous monteplase (Group II). In 90 of these patients, total PAI-1 antigen levels were serially measured. Results Baseline PAI-1 levels at admission were higher in patients with occluded infarct-related arteries than in patients with patent arteries in Group I (39 ± 4 vs 20 ± 2 ng/mL, P < .01) and in Group II (36 ± 3 vs 27 ± 2 ng/mL, P < .05). In the high PAI-1 level subgroup (≥27 ng/mL, n = 53), Group II showed a higher patency rate than Group I (56 vs 18%, P < .01). Multiple logistic regression analysis indicated that patency could be predicted by the PAI-1 level in Group I (Wald χ²= 3.94, P = .02, odds ratio 0.924, 95% CI 0.855-0.999), but not in Group II. Serial change patterns in the PAI-1 level were identical in Group I and Group II. Conclusion Because monteplase can be used independently of PAI-1 kinetics, a combination of monteplase administration at a community hospital with prompt transfer to a tertiary center for coronary intervention may be a powerful strategy for AMI. (Am Heart J 2002;144:e5.)