Small dead space heat and moisture exchangers do not impede gas exchange during noninvasive ventilation: a comparison with a heated humidifier.

OBJECTIVE: Adverse respiratory and gasometrical effects have been described in patients with acute respiratory failure (ARF) undergoing noninvasive ventilation (NIV) with standard heat and moisture exchangers (HME). We decided to evaluate respiratory parameters and arterial blood gases (ABG) of patients during NIV with small dead space HME compared with heated humidifier (HH). DESIGN: Prospective randomized crossover study. SETTING: A 16-bed medical intensive care unit (ICU). PATIENTS: Fifty patients receiving NIV for ARF. MEASUREMENTS: The effects of HME and HH on respiratory rate, minute ventilation, EtCO(2), oxygen saturation, airway occlusion pressure at 0.1 s, ABG, and comfort perception were compared during two randomly determined NIV periods of 30 min. The relative impact of HME and HH on these parameters was successively compared with or without addition of a flex tube (40 and 10 patients, respectively). MAIN RESULTS: No difference was observed between HME and HH regarding any of the studied parameters, whether or not a flex tube was added. CONCLUSION: If one decides to humidify patients' airways during NIV, one may do so with small dead space HME or HH without altering respiratory parameters.

Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management.

PURPOSE: Surgical treatment is crucial in the management of necrotizing soft tissue infections (NSTIs). The aim of this study was to determine the influence of surgical procedure timing on hospital mortality in severe NSTI. METHODS: A retrospective study including 106 patients was conducted in a medical intensive care unit equipped with a hyperbaric chamber. Data regarding pre-existing conditions, intensive care and surgical management were included in a logistic regression model to determine independent factors associated with hospital mortality. RESULTS: Overall hospital mortality was 40.6%. In multivariate analysis, underlying cardiovascular disease, SAPS II, abdominoperineal compared to limb localization, time from the first signs to diagnosis <72 h, and time from diagnosis to surgical treatment >14 h in patients with septic shock were independently associated with hospital mortality. CONCLUSION: In patients with NSTI and septic shock, hospital mortality is influenced by the timing of surgical treatment.

Influence of cardiac output level on oxygen exchange in chronic obstructive pulmonary disease patients.

STUDY OBJECTIVES: In the course of chronic obstructive pulmonary disease (COPD), pulmonary gas exchange deteriorates as a result of ventilation/perfusion inequalities and hypoxaemia. The aim of the present study was to evaluate the influence of cardiac output (CO) level observed at rest in COPD patients on interaction between central and peripheral O(2) exchange. METHODS: One hundred and nine patients with advanced but stable COPD were analysed in a retrospective study by the multiple inert gas elimination technique. As a function of CO, simulations were conducted to evaluate the respective part of PvO(2) and VA/Q inequalities on the degree of hypoxaemia. MEASUREMENTS AND RESULTS: PaO(2) was linked (i) to cardiac index (CI), (ii) to mean VA/Q ratio of blood flow distribution and (iii) to PvO(2), but PvO(2) was not correlated with CO. By comparing two groups with CI above and below the mean value of the series respectively, a significant difference was identified in PaO(2) (57 +/- 9 mmHg in the high CI group versus 63 +/- 10 mmHg in the low CI group, P<0.05) because of higher VA/Q inequalities in the high CI group. Comparing two other groups with values of PvO(2) above and below the mean value of the series respectively, a significant difference was identified in PaO(2): (mean +/- SD was 65 +/- 8 in high PvO(2) group versus 56 +/- 9 mmHg, P<0.001) but with no difference in either CI or perfusion distribution. Analysis of the cumulated effects of PvO(2) and CI values, indicated that high CI and low PvO(2) gave rise to the lowest PaO(2) (53 +/- 8 mmHg), with the highest PaO(2) (68 +/- 8 mmHg) being found in the low CI and normal PvO(2) group. CONCLUSIONS: We concluded that in COPD patients, PaO(2) appeared to be maintained better when peripheral gas exchange coped with tissue demand without an increase in CO. Conversely, when the physiological increase in CO could not maintain adequate tissue gas exchange, PaO(2) continued to fall due to the cumulative effects of increasing CO on VA/Q inequalities and low PvO(2).

Mass transfer, clearance and plasma concentration of procalcitonin during continuous venovenous hemofiltration in patients with septic shock and acute oliguric renal failure.

OBJECTIVES: To measure the mass transfer and clearance of procalcitonin (PCT) in patients with septic shock during continuous venovenous hemofiltration (CVVH), and to assess the mechanisms of elimination of PCT. SETTING: The medical department of intensive care. DESIGN: A prospective, observational study. PATIENTS: Thirteen critically ill patients with septic shock and oliguric acute renal failure requiring continuous venovenous postdilution hemofiltration with a high-flux membrane (AN69 or polyamide) and a 'conventional' substitution volume (< 2.5 l/hour). MEASUREMENTS AND MAIN RESULTS: PCT was measured with the Lumitest PCT Brahms(R) in the prefilter and postfilter plasma, in the ultrafiltrate at the beginning of CVVH (T0) and 15 min (T15'), 60 min (T60') and 6 hours (T6h) after setup of CVVH, and in the prefilter every 24 hours during 4 days. Mass transfer was determined and the clearance and the sieving coefficient were calculated according to the mass conservation principle. Plasma and ultrafiltrate clearances, respectively, at T15', T60' and T6h were 37 +/- 8.6 ml/min (not significant) and 1.8 +/- 1.7 ml/min (P < 0.01), 34.7 +/- 4.1 ml/min (not significant) and 2.3 +/- 1.8 ml/min (P < 0.01), and 31.5 +/- 7 ml/min (not significant) and 5 +/- 2.3 ml/min (P < 0.01). The sieving coefficient significantly increased from 0.07 at T15' to 0.19 at T6h, with no difference according to the nature of the membrane. PCT plasma levels were not significantly modified during the course of CCVH. CONCLUSIONS: We conclude that PCT is removed from the plasma of patients with septic shock during CCVH. Most of the mass is eliminated by convective flow, but adsorption also contributes to elimination during the first hours of CVVH. The effect of PCT removal with a conventional CVVH substitution fluid rate (<2.5 l/hour) on PCT plasma concentration seems to be limited, and PCT remains a useful diagnostic marker in these septic patients. The impact of high-volume hemofiltration on the PCT clearance, the mass transfer and the plasma concentration should be evaluated in further studies.

Postvaccinal inflammatory neuropathy: peripheral nerve biopsy in 3 cases.

Autoimmune inflammatory polyneuropathy (PN) can be triggered by vaccination. We report 3 such cases. A 36-year-old female nurse presented 15 days after a hepatitis B vaccination (HBV) with acute sensory disturbances in the lower limbs. She had severe ataxia but no weakness. Cerebrospinal fluid (CSF) protein level was 84 mg/100 mL, with 3 lymphocytes. A 66-year-old man presented 21 days after HBV with severe motor and sensory PN involving all 4 limbs. A 66-year-old man presented 15 days after a yellow fever vaccination with progressive motor and sensory PN involving all 4 limbs and bilateral facial paralysis. CSF protein level was 300 mg/100 mL, with 5 lymphocytes. Six weeks later, a tracheostomy was performed. In these 3 patients, the nerve deficits lasted for months. In each case, peripheral nerve biopsy showed KP1-positive histiocytes but no T-lymphocytes in the endoneurium. On ultrastructural examination, there was axonal degeneration in the first 2 cases; in case 2, a few myelinated fibers exhibited an intra-axonal macrophage but the myelin sheath was preserved. There was only 1 example of macrophage-associated demyelination in case 2, but these were numerous in case 3. It is likely that in the first 2 cases, an autoimmune reaction against some axonal or neuronal components was triggered by HBV. It induced an acute sensory ataxic PN in case 1 and an acute motor and sensory axonal neuropathy (AMSAN) in case 2. The third patient had a chronic inflammatory demyelinating PN, likely triggered by yellow fever vaccination.