An outbreak of Legionella longbeachae infection in an intensive care unit?

During a nine-day period, five patients in a 14-bed intensive care unit (ICU) were shown to have seroconverted with a four-fold or greater rise in serum antibody titre to Legionella longbeachae serogroup 1. A further two patients were observed to have high titres consistent with previous exposure but earlier serum samples were not available for comparison. No patients had antibody responses to Legionella pneumophila serogroups 1 and 2. L. longbeachae was not cultured from respiratory secretions from patients or from the environment within the unit. Legionella anisa was recovered from one cooling tower on the ninth floor of the tower block. The ICU is located on the first floor of the same tower and receives external air from two vents, one on the eastern and the other on the western aspect. All patients with serological evidence of L. longbeachae infection were concomitantly infected with multiresistant Staphylococcus aureus, and were located in bays on the eastern side of the unit. A large pigeon nest was discovered within 1-2 m of the eastern vent. Following removal of the birds' nest, no further cases were seen on routine screening of all patients within the unit over the next eight weeks. Alternatively, seroconversion may have been related to demolition of the adjacent nine-storey nurses home. This was begun one month before the first case was diagnosed and was completed four months later. The periodic northerly winds could have carried legionellae from the demolition site directly over the block housing the ICU and may have concentrated them near the eastern air vent. All patients had pneumonia, which was probably multifactorial in origin. There is some uncertainty whether the serological responses seen were an epiphenomenon or were truly indicative of infection with L. longbeachae.

Hypocortisolaemia and adrenocortical responsiveness at onset of septic shock.

OBJECTIVE: To characterise the plasma cortisol profile and adreno-cortial responsiveness (short Synacthen test) of patients in septic shock. DESIGN: Retrospective assessment using case-notes and ICU charts. SETTING: University teaching hospital ICU. PATIENTS: 68 septic shock patients with plasma cortisol and/or short Synacthen test measured at ICU-admission or onset of shock post ICU-admission. Patients were identified from a total population of 155 patients who had PCL and/or SST measured over a 4.5 year period. INTERVENTION: None. MEASUREMENTS AND RESULTS: Patients with septic shock had a plasma cortisol ranging from 210-8900 nmol/l and mortality of 56%. There were 22 (32%) below (low) and 46 (68%) above (high) a 'critical' plasma cortisol of 500 nmol/l. Using stepwise logistic regression, mortality was adequately predicted by and increased with, increasing plasma cortisol and onset of shock remote from ICU-admission. Short Synacthen tests were available in 33 patients: 11 responders (cortisol increment > 200 nmol/l above baseline 30 min after 0.25 mg intravenous Synacthen) and 22 hypo-responders. Mortality in patients was adequately predicted by and increased with a decrease in cortisol increment post-Synacthen. Thirteen patients (plasma cortisol 606 +/- [SD] 297 nmol/l) had complete haemodynamic profiles before inotropic therapy; no relationship was demonstrated between plasma cortisol and circulatory variables. Follow-up revealed no cases of Addison's disease. CONCLUSIONS: In septic shock, 'hypocortisolaemia' is not uncommon and does not predict a high mortality; adrenocortical hypo-responsiveness may be associated with poor outcome.

Epinephrine as an inotropic agent in septic shock: a dose-profile analysis.

OBJECTIVE: To characterize the acute actions and physiologic dose profile of epinephrine, as a single inotrope, in patients with septic shock. DESIGN: Prospective clinical study. The relationship between epinephrine dose and cardiovascular variables was analyzed using repeated-measures analysis of variance. SETTING: ICU in a university teaching hospital. PATIENTS: Eighteen patients with septic shock, mean age 64 +/- 8 (SD) yrs, and with a mean admission Acute Physiology and Chronic Health Evaluation (APACHE II) score of 23 (range 14 to 35). INTERVENTIONS: Initial volume loading and the measurement of a baseline hemodynamic profile were followed by the administration of an epinephrine infusion at 3 microgram/min with subsequent increments of 3 micrograms/min and the determination of a hemodynamic profile after each dose increment. Therapy was titrated to clinical goals of perfusion and restoration of premorbid systolic arterial BP. MEASUREMENTS AND MAIN RESULTS: After volume loading, mean hemodynamic indices were as follows: mean arterial pressure (MAP) 62 +/- 7 mm Hg; cardiac index 3.8 +/- 1.1 L/min/m2; left ventricular stroke work index 25 +/- 11 g.m/m2; oxygen delivery (Do2) index 460 +/- 168 mL/min/m2; and oxygen consumption (VO2) index 165 +/- 64 mL/min/m2. In the dose range of 3 to 18 microgram/min, epinephrine produced linear increases in average heart rate, MAP, cardiac index, left ventricular stroke work index, stroke volume index, VO2, and DO2. No effect was noted on pulmonary artery occlusion pressure (PAOP), mean pulmonary arterial pressure, or systemic vascular resistance index. CONCLUSIONS: Epinephrine increases DO2 in septic shock by increasing cardiac index without an effect on systemic vascular resistance index or PAOP.

Management of atrial tachyarrhythmias in the critically ill: a comparison of intravenous procainamide and amiodarone.

OBJECTIVE: To compare the efficacy and safety of intravenous (IV) amiodarone and procainamide for the treatment of atrial tachyarrhythmias (AT) in the critically ill. DESIGN: In this prospective study, patients were allocated to drug treatment on the basis of hospital identification number, even for procainamide and odd for amiodarone. SETTING: Patients were recruited from a teaching hospital ICU and did not include postoperative cardiac patients. PATIENTS AND PARTICIPANTS: 26 patients with AT sustained for at least 1 h and failure to respond to correction of possible precipitating factors were entered in the study. Exclusion criteria were systolic blood pressure (SBP) < 80 mmHg, and known hypersensitivity to either drug. Two patients with chronic atrial fibrillation (who received amiodarone) were later excluded from the analysis. In the final analysis, 14 patients received procainamide and 10 amiodarone. INTERVENTIONS: IV amiodarone (3 mg/kg followed by 10 mg/kg/24 h, with repeat dose of 3 mg/kg at 1 h if no response) or i.v. procainamide (10 mg/kg at 1 mg/kg/min followed by infusion of 2-4 mg/min for 24 h, with repeat dose of 5 mg/kg at 1 h if no response). MEASUREMENTS AND RESULTS: In the procainamide group 10/14 (71%) and in the amiodarone group 7/10 (70%) had converted to sinus rhythm by 12 h. There was no significant difference in response between the groups. SBP was not significantly different from baseline after administration of either drug. CONCLUSIONS: Procainamide and amiodarone appear to be safe and equally effective in the treatment of AT in the critically ill.

A high flow turbine CPAP system.

A continuous high flow CPAP system incorporating a turbine blower is described. The system achieves inspiratory flow rates of 150 l/min or more by means of reticulated gas flow and inspired oxygen fractions of 0.21-0.95. Positive airway pressure is provided by weighted disc valves and a modified aviation-type CPAP face mask provides electronic communication with the patient. The mobility of the system also enables its use as an intermittent physiotherapy aid. Work of breathing of the system, as assessed by total pressure fluctuations is at a minimum.