No abstract

A recent, frequently quoted study has suggested that for bloodstream infections (BSIs) due to extended-spectrum β-lactamase-producing Enterobacteriaceae (ESBL) Escherichia coli, treatment with β-lactam/β-lactamase inhibitors (BLBLIs) might be equivalent to treatment with carbapenems. However, the majority of BSIs originate from the urinary tract. A multicenter, multinational efficacy analysis was conducted from 2010 to 2012 to compare outcomes of patients with non-urinary ESBL BSIs who received a carbapenem (69 patients) vs those treated with piperacillin-tazobactam (10 patients). In multivariate analysis, therapy with piperacillin-tazobactam was associated with increased 90-day mortality (adjusted odds ratio, 7.9, P=.03). For ESBL BSIs of a non-urinary origin, carbapenems should be considered a superior treatment to BLBLIs.

Objectives: To determine the prevalence of hypomagnesaemia and hypermagnesaemia, to discern various factors associated with abnormal serum magnesium, and to estimate prognostic significance of serum magnesium aberrations in patients with congestive heart failure. Design: Observational study. Setting: Medical department of a university hospital (tertiary referral centre). Patients: 404 consecutive patients admitted with congestive heart failure as one of the diagnoses and previously treated with furosemide (frusemide) for at least three months. Main outcome measures: Clinical, biochemical, and electrocardiographic variables were analysed with respect to serum magnesium aberrations. Following discharge, mortality rates, including sudden death, were registered. Results: Hypomagnesaemia was found in 50 patients (12.3%) and 20 (4.9%) were hypermagnesaemic. Female sex (p < 0.04), diabetes mellitus (p < 0.006), hypocalcaemia (p = 0.03), hyponatraemia (p < 0.05), malignant disease (p = 0.05), and high fever (p = 0.05) were statistically associated with hypomagnesaemia. Renal failure, severe congestive heart failure, and high dose furosemide treatment (> 80 mg/day) were associated with hypermagnesaemia (p < 0.001, p = 0.05, and p < 0.03, respectively). Hypermagnesaemic patients were older and weighed less. On follow up (median duration 43 months), 169 (41.8%) died, with 22 (13%) sudden deaths. Mortality was highest with hypermagnesaemia, lowest with normomagnesaemia, and intermediate with hypomagnesaemia. After adjustment for renal failure, old age, and severity of congestive heart failure, hypomagnesaemia but not hypermagnesaemia emerged as being significantly associated with shorter survival (p = 0.009). No statistical association was found between sudden death and magnesium concentrations. Conclusions: While hypermagnesaemia seems to represent a prognostic marker only, hypomagnesaemia appears to have an adverse pathophysiological effect. The subgroup of patients at risk for hypomagnesaemia requires frequent serum magnesium determinations and magnesium replacement for as long as hypomagnesaemia persists. M agnesium is the second most abundant intracellular cation after potassium. Ninety nine per cent of total body magnesium is located intracellularly, so that less than 1% is restricted to the serum. Magnesium plays a key role in a variety of enzymatic reactions. Thus more than 300 enzyme systems, including all ATPases, are magnesium dependent. In addition to energy-requiring metabolic processes and anaerobic phosphorylation, magnesium is involved in protein and DNA synthesis as well as in transmembrane transport mechanisms.

Combined low-dose intravenous dopamine and oral furosemide have similar efficacy but induce less renal impairment and hypokalemia than higher doses of intravenous furosemide taken either alone or with low-dose dopamine. The renal impairment induced by intravenous furosemide is probably related to its hypotensive effect in patients with refractory congestive heart failure.