[Early lumbar puncture and cutaneous rash: a clear CSF is not always a normal CSF]. / Ponction lombaire précoce et rash cutané: un liquide céphalorachidien normal peut en cacher un autre.

The clinical and biological characteristics of adult bacterial meningitis are usually unequivocal, but more subtle clinical presentations can be observed. A 24-year-old woman was admitted with fever and abdominal discomfort, which had been developing for 24 hours. There were no meningeal signs, but a transient cutaneous rash was observed on admission. A clear CSF was obtained showing no cytological or biochemical abnormality. Ceftriaxone 2 g was administrated intravenously. In the following hours of admission, a frank meningeal syndrome with purpura appeared, leading to a second lumbar puncture, which revealed purulent CSF. The culture of the first CSF yielded Neisseria meningitidis, while the second CSF remained sterile. This case showed a probable meningococcal rash. This is a reminder that a normal CSF can be obtained early in the course of a proved bacterial meningitis, and that CSF bacterial eradication can occur very rapidly after a single dose of third-generation cephalosporin.

How to identify patients with no risk for postextubation stridor?

The aim of this study was first, to evaluate the value of cough following tracheal tube cuff deflation, and second, to reassess the value of the cuff-leak test to predict postextubation stridor (PES). In spontaneously breathing patients, immediately before extubation, the tracheal tube was deflated and the absence of cough was monitored. The tube was then obstructed with a finger, and the absence of leak was monitored. Extubation was then performed. Four PESs were observed after 115 extubations (incidence: 3.5%). The absence of cough was more frequently observed when PES occurred than when it did not (75% v 21%, P =.04). The absence of leak was observed in 100% of PES and in 20% of PES free extubations (P =.01). The absence of both leak and cough was more frequently observed in PES (75% v 7%, P <.0001). In the absence of leak, the likelihood ratio of developing PES was 5.04 and rose to 10.4 when cough was also absent. The likelihood ratio of not developing PES in the absence of leak alone was 0. We conclude that in a population of medical intensive care unit spontaneously breathing patients, just before extubation, the presence of leaking around the endotracheal tube rules out PES, whereas the absence of cough and of leak are good predictors of PES.

Circulating endotoxin and antiendotoxin antibodies during severe sepsis and septic shock.

The presence of circulating endotoxin is common during sepsis but its prognostic value is poor. We hypothesized that this lack of correlation with outcome could be related in part to the presence of circulating antiendotoxin antibodies. In a 14-bed medical intensive care unit, in an 821-bed tertiary teaching hospital, we prospectively assessed endotoxin and antiendotoxin antibodies in patients with severe sepsis or septic shock. Blood samples for the determination of circulating endotoxin and antiendotoxin antibodies were drawn when severe sepsis or septic shock were diagnosed (day 0) and then on day 1, day 2, and day 4. Daily measurements of antiendotoxin antibodies did not discriminate survivors from nonsurvivors. No antibody depletion was observed. However, during follow-up, the antiendotoxin immunoglobulin (Ig)M antibody level increased among survivors but decreased among nonsurvivors (51.2 vs -44.8 MU/mL, P=007). Circulating endotoxin was detectable among 9 of 17 patients on inclusion but neither the basal value nor sequential measurements correlated with outcome. These results suggest that during severe sepsis and septic shock, circulating endotoxin is a poor prognostic marker whereas the detection of an increase in IgM antiendotoxin antibody levels could identify survivors. This increase in IgM antibody levels could be attributed to a reactivation of the immune system.

Osmolar gap hyponatremia in critically ill patients: evidence for the sick cell syndrome?

OBJECTIVE: Accumulation of nondiffusible solutes in plasma leads to redistribution hyponatremia with an increased osmolar gap (i.e., the difference between measured and calculated osmolality). In critically ill patients, intracellular solutes may leak out of the cell because of an increased membrane permeability and may lead to redistribution hyponatremia with increased osmolar gap, a concept called the "sick cell syndrome." The aims of this prospective study were to determine whether an increased osmolar gap related to endogenous solutes accumulation was present in intensive care patients with true hyponatremia and to identify the solutes accounting for this increased osmolar gap. SETTING: A 14-bed medical intensive care unit in an 821-bed university hospital. DESIGN: A 20-wk prospective observational study. PATIENTS: Fifty-five consecutive patients with a measured plasma sodium concentration 10 mosm/kg. Total plasma amino acid concentration also was measured. Organ dysfunctions were assessed with the Sequential Organ Failure Assessment. Thirty of the 55 patients (54%) had an osmolar gap >10 mosm/kg (17.2 +/- 7.1 mosm/kg). Sequential Organ Failure Assessment score was significantly higher in the osmolar gap patients (6.4 +/- 3.2 vs. 4.5 +/- 2.0; p =.015). No difference of amino acids concentration was observed between osmolar gap and non-osmolar gap patients, and no correlation was observed between osmolar gap and amino acid concentration. Accumulation of ketone bodies and lactic acid was also unlikely. During correction of hyponatremia in osmolar gap patients, a significant decrease of plasma osmolar gap was observed and a statistically significant inverse relationship was demonstrated between osmolar gap decrease and plasma sodium concentration increase. CONCLUSION: Hyponatremia with increased osmolar gap related to endogenous solutes accumulation is observed frequently in hyponatremic intensive care patients, especially in patients with the most severe organ dysfunctions. The nature of the endogenous solutes accounting for the increased osmolar gap remains to be determined. Simultaneous correction of sodium and osmolar gap suggests a causal link between increased osmolar gap and hyponatremia and may support the concept of sick cell syndrome.