Postauthorization safety study of Clottafact® , a triply secured fibrinogen concentrate in acquired fibrinogen deficiency: a prospective observational study.

BACKGROUND AND OBJECTIVES: A postauthorization safety study was performed between 2009 and 2012 to describe the use of Clottafact® in acquired fibrinogen deficiency in real-life medical practice in France. MATERIALS AND METHODS: One hundred and fifty patients were planned for 28 days of prospective follow-up after infusion. The analysis of this observational study was descriptive and performed according to the type of treatment (curative or preventive) and the origin of the bleed. RESULTS: One hundred and fifty-six patients (16-87 years) were included in 13 centres and treated in five different medical bleeding situations: postpartum (59), other gynaecological/obstetrical (6), trauma (34), liver (13), cardiovascular (23) and other various bleeding situations (21). The mean follow-up time was 18·9 ± 12·3 days. Two patients presented adverse drug reactions: one a pulmonary embolism and the other a four-site venous thromboembolic episode. All were serious with a dubious causal relationship with the study treatment. Efficacy data were collected as a secondary objective. In 150 patients receiving curative treatment, 117 of 159 infusions (73·6%) were considered as successful by the investigators, 35 as moderate (22%) and seven as no response (4·4%). CONCLUSION: The Clottafact® safety profile observed during the study matched the known profile of fibrinogen during use.

Severe acute generalized exanthematous pustulosis with blistering mimicking toxic epidermal necrolysis, associated with a primary mumps infection.

Acute generalized exanthematous pustulosis (AGEP) is a severe adverse cutaneous reaction, which is mostly due to drugs, but which has also been described as occurring after infections. We report a case of severe AGEP with extensive blistering mimicking toxic epidermal necrolysis (TEN) in a 47-year-old woman. This was associated with a life-threatening primary mumps infection, complicated by perimyocarditis and encephalitis. The recent increase in the incidence of mumps should lead physicians to be aware of the uncommon clinical features and complications of this disease.

[Myasthenia gravis and pregnancy: clinical course and management of delivery and the postpartum phase]. / Myasthénie auto-immune et grossesse: évolution clinique, accouchement et post-partum.

OBJECTIVES: To study influences of pregnancy on the time-course of myasthenia gravis (MG) and of MG on pregnancy, delivery, postpartum and newborn. METHODS: We retrospectively collected data from 100 women affected with MG, hospitalized between 1994 and 2003 in departments of Neurology of Lille University Hospital. RESULTS: Eighteen patients had a total of 36 pregnancies, occurring 7.2 years on average after MG onset. MG exacerbation occurred in 7 patients (26 percent) during pregnancy and in 4 (14.8 percent) during postpartum. One patient died of acute respiratory failure during postpartum. Delay between the onset of MG and pregnancy was the only variable significantly associated with MG exacerbation: 5.8 years when exacerbation and 9.5 years when no exacerbation (p=0.03). Seven miscarriages, two therapeutic abortions and no death at birth were reported. Levels of anti-acetylcholine receptor antibodies were abnormal in 3 of 27 newborns (11 percent), but only one (3.7 percent) developed seronegative transient neonatal myasthenia gravis. DISCUSSION: During pregnancy, the clinical course of MG is variable but exacerbations were associated with a shorter delay between MG diagnosis and pregnancy. The risk of transient neonatal myasthenia gravis is relatively small but exists even when the parturient has stable MG without elevated levels of anti-acetylcholine receptor antibodies. CONCLUSION: Our study confirms pregnancy is more difficult to manage at the beginning of MG. Given the unpredictable course of MG during pregnancy, we recommend women affected with MG to begin a pregnancy when the disease is stable.

[Hemostasis disorders in severe infections: State of the art]. / Troubles de l'hémostase et états infectieux graves. Mise au point.

The haemostatic system is greatly modified during severe infections. The early activation of coagulation is triggered by tissue factor expression and secondary fibrinolysis impaired by the upregulation of fibrinolysis inhibitors. This imbalance is a major cause of subsequent organ dysfunction. Natural anticoagulants (Tissue factor pathway inhibitor (TFPI), Antithrombin (AT), and Protein C (PC) are consumed or inhibited in this pathological process justifying a therapeutic supplementation with these inhibitors to improve sepsis-induced organ failure and mortality. No effect on the mortality rate could be documented in controlled studies using recombinant TFPI or AT concentrates but a biological interaction with heparin therapy could have biased the results. Treatment with recombinant activated PC was associated with a significant reduction in the mortality rate of severely ill patients. An increase in the rate of hemorrhagic adverse effects was observed with these compounds, justifying a strict observance of contraindications and of patient selection.

[Hemostasis disorders in severe infections: state of the art]. / Troubles de l'hémostase et états infectieux graves. Mise au point.

The haemostatic system is greatly modified during severe infections. The early activation of coagulation is triggered by tissue factor expression and secondary fibrinolysis impaired by the upregulation of fibrinolysis inhibitors. This imbalance is a major cause of subsequent organ dysfunction. Natural anticoagulants (Tissue factor pathway inhibitor (TFPI), Antithrombin (AT), and Protein C (PC) are consumed or inhibited in this pathological process justifying a therapeutic supplementation with these inhibitors to improve sepsis-induced organ failure and mortality. No effect on the mortality rate could be documented in controlled studies using recombinant TFPI or AT concentrates but a biological interaction with heparin therapy could have biased the results. Treatment with recombinant activated PC was associated with a significant reduction in the mortality rate of severely ill patients. An increase in the rate of hemorrhagic adverse effects was observed with these compounds, justifying a strict observance of contraindications and of patient selection.

Fulminant Epstein-Barr virus (EBV) hepatitis in a young immunocompetent subject.

We report a case of fulminant hepatitis related to a primary Epstein-Barr virus (EBV) infection in an immunocompetent 15-year-old male patient. The main causes of fulminant hepatitis are viral infections, drugs, and autoimmune diseases. Primary Epstein-Barr virus infection is usually a benign, self-limited disease in pediatrics but can exceptionally be fatal.

Are there any additional mechanisms for haemolysis in HELLP syndrome?

HELLP syndrome is a microangiopathy that leads to severe maternal complications. The objective of this study was to identify any additional mechanisms that could have contributed to HELLP syndrome-induced haemolysis. This is a pilot, prospective and observational study that lasted 9months. All patients with HELLP syndrome treated at academic tertiary care women hospital accepted to participate. Sixteen patients were included. In ten patients (63%), schizocytes were detected following a blood smear test. Six patients (38%) were diagnosed with a partial expression deficiency of proteins regulating the complement system (CD 55 or CD 59). In nine patients (56%), an activation of the complement classical pathway was detected. In two patients (13%), an ADAMTS 13 activity below 30% was detected. Three patients (19%) were diagnosed with a folate deficiency and one (6%) with an antiphospholipid syndrome. All patients developed maternal or fetal morbidity including nine (56%) an acute kidney injury. All patients but one had at least one additional mechanism that could contribute to haemolysis, besides a simple physical injury. Larger studies should be promoted to understand haemolysis in HELLP syndrome.

[Severe blunt liver injury: reappraisal of criteria for nonoperative management decision. Experience with 88 cases]. / Traumatismes graves fermés du foie: à la recherche de critères décisionnels pour le choix du traitement non-opératoire. A propos d'une série de 88 cas.

AIM OF THE STUDY: To analyze the predictive value of computed tomography (CT) and initial physiologic and laboratory data findings in the immediate operative (OP) or non-operative (NOP) management of blunt liver injury (BL). METHODS: Eighty-eight BL, grade III (51), grade IV (28) and nine grade V (9), aged 26.2 years (16-75) were identified. Hemoperitoneum on CT, hemodynamic status, physiologic and laboratory data <24 hours or preoperative (transfusion, vascular filling) and follow-up >48 hours were analyzed. RESULTS: Data of 71/88 (80%) NOP and 17/88 (20%) OP patients were reviewed. A secondary laparotomy or laparoscopy was necessary in 11/71 TNO. Six OP (35%) and 1 NOP patients died. Blood units transfused were 1.33 (0-10) vs 5.9 (0-22) and vascular filling 1.45 (0.5-5.5) vs 3.6L (2-12) (P<10(-6), P<4.10(-3) respectively). NOP patients had less severe hemoperitoneum (31 vs 94%, P<10(-5)) and hemodynamic instability (8.5 vs 94%, P<10(-4)). But, there was an overlap of values of blood units transfused, amount of vascular filling and initial haemoglobin levels between NOP and OP patients and among CT grades of liver injury. No cut-off values could be determined: 33% NOP received >4 blood units and >3 L vascular filling; 30% had severe hemoperitoneum. In OP group 23.5% patients had lower values and no severe hemoperitoneum. CONCLUSION: In the management of BL, vascular filling and blood transfusion increased with the grade of CT liver injury and were globally more elevated in the operative group but did not individually correlate with hemodynamic stability and did not authorize, by themselves, to decide between operative versus non-operative management.

Pig I alpha I appears unmodified in plasma in case of endotoxin-induced disseminated intravascular coagulation.

The unrestricted activity of leukocyte proteinases is thought to contribute to the degradation of plasma proteins and thus amplify the coagulation disorders occurring in septic shock. Inter-alpha-inhibitor (I alpha I) is a plasma protein particularly susceptible to their action. Therefore we investigated its behavior in a porcine model of endotoxin shock which reproduces the coagulation changes observed in human sepsis. We did not detect any qualitative or quantitative modification of porcine I alpha I in plasmas collected from pigs after endotoxin infusion. To explain these data, I alpha I was incubated with polymorphonuclear neutrophils (PMN) stimulated by FMLP in the presence of cytochalasin B. We found that, unlike human PMN, porcine cells were unable to proteolyze I alpha I. Moreover, in the incubation medium of pig PMN, triggered either by FMLP or PMA, no measurable elastase activity was evidenced. Therefore, we urge to better take into account species differences in functional responses of PMN, to explain the experimental results obtained in animal models of septic shock.

Effects of a combined antithrombin III and protein C supplementation in porcine acute endotoxic shock.

Antithrombin III (ATIII) and protein C (PC) are major inhibitors of the coagulation cascade and might regulate the cytokine network. We tested the possibility that a combined supplementation using these two inhibitors might have synergistic effects on sepsis-induced disseminated intravascular coagulation and shock. Hemodynamics, coagulation parameters, tumor necrosis factor (TNF) alpha, and interleukin 6 levels were measured in pigs submitted to a bolus infusion of Escherichia coli endotoxin (lipopolysaccharide). Four groups were studied: control lipopolysaccharide, ATIII (100 IU/kg), PC (50 IU/kg), and ATIII-PC (same doses). The endotoxin infusion resulted in a typical hypokinetic shock with disseminated intravascular coagulation in all animals. Compared with the control group, a significant improvement in mean arterial pressure and systemic vascular resistance was observed in the PC and ATIII-PC groups. The increase in lactate levels was almost completely blunted in the PC group. A significant lesser increase in TNFalpha levels was observed in the ATIII-PC group. No effects were seen on interleukin 6 levels. Coagulation and fibrinolysis parameters were not improved by ATIII and/or PC, except for a lesser decrease in prothrombin time in the ATIII-PC group. We conclude that in this acute endotoxic model, a combined supplementation using PC and ATIII concentrates has favorable effects on hemodynamic parameters and TNFalpha levels, independently from the anticoagulant actions of these inhibitors.

Antithrombin reduces mesenteric venular leukocyte interactions and small intestine injury in endotoxemic rats.

We examined the hypothesis that recombinant human antithrombin would reduce mesenteric venule leukocyte adhesion and small intestine injury in endotoxemic rats. Endotoxemic (endotoxin 10 mg/kg, intravenously) rats were treated either with saline or recombinant human antithrombin (250 and 500 U/kg). In some rats, indomethacin (100 mg/kg, intraperitoneally) was injected 60 min prior to endotoxin and recominant human antithrombin (500 U/kg) treatment. Compared to controls, intravital videomicroscopy of the mesentric venule showed an increase of leukocyte rolling (55+/-17 versus 70+/-19 leukocytes/min; P < 0.05) and firm adhesion (1.1+/-0.3 versus 5.8+/-0.8 leukocytes/100 microm; P < 0.05) in endotoxemic rats. Recombinant human antithrombin attenuated endotoxin-induced venular endothelium leukocyte adhesive cascade. The beneficial effects of recombinant human antithrombin on leukocyte adhesion were inhibited by indomethacin (100 mg/kg, intraperitoneally) in endotoxemic rats. Endotoxin treatment increased fluorescein isothiocyanate (FITC)-labeled dextran 4,000 (FD4) gut lumen to plasma ratio and wet weight/dry weight ratio. Recombinant human antithrombin (500 U/kg) attenuated endotoxin-induced gut injury. These observations suggest that recombinant human antithrombin reduces endothelium-leukocyte interactions in endotoxemic rats by interacting with local prostacyclin production.

Double-blind, placebo-controlled trial of antithrombin III concentrates in septic shock with disseminated intravascular coagulation.

BACKGROUND: Septic shock is frequently complicated by a syndrome of disseminated intravascular coagulation (DIC). Numerous uncontrolled clinical studies have reported that antithrombin III (ATIII) substitution might prevent DIC and death in septic shock. METHODS: We conducted a randomized double-blind placebo-controlled trial in patients with a documented septic shock and DIC. The patients received either a placebo or ATIII (90 to 120 IU/kg in loading dose, then 90 to 120 IU/kg/d during 4 days). Administration of fresh frozen plasma, platelets, and fibrinogen concentrates was restricted to patients with hemorrhages and severe decreases in prothrombin time, platelet count, and fibrinogen levels. RESULTS: Thirty-five patients entered the study (18 placebo, 17 ATIII). Both groups were well balanced for all demographic, hemodynamic, and biologic data. Three patients were excluded before the treatment allocation code was broken. In the ATIII group, ATIII levels were rapidly corrected and remained over normal levels until day 10; sequential protein C and protein S levels were not modified. The duration of DIC was significantly reduced: in the ATIII group, 64 percent of patients were cured of DIC at day 2, and 71 percent were cured at the end of treatment vs in the placebo group, 11 percent (p < 0.01) and 33 percent (p < 0.05), respectively. In the 32 included patients, the mortality in ICU was reduced by 44 percent in the ATIII group (p = 0.22, NS). Care loads and transfusion requirements were not different. No side effect was observed. CONCLUSIONS: Mortality was reduced by 44 percent in this trial, but the difference did not reach the statistical significance. Circulating protein C and protein S levels were not modified by ATIII supplementation. High doses of ATIII concentrates significantly improved sepsis-induced DIC during septic shock. The trend toward improved survival suggests further randomized studies.

Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies.

STUDY OBJECTIVE: Our aim was to document the following in patients with septic shock and disseminated intravascular coagulation (DIC): (1) the influence of DIC in the mortality rate and the occurrence of organ failure; (2) the comparative prognostic value of initial antithrombin III (ATIII), protein C (PC), and protein S (PS) levels; and (3) the compared pattern of sequential ATIII, PC, and PS levels according to clinical outcome. DESIGN: Demographic data, criteria of severity, mortality in ICU, frequency of organ failure, hemodynamic and oxygenation parameters, and laboratory findings were compared in patients with septic shock according to the occurrence of DIC. Initial and sequential levels of ATIII (activity), PC (antigen and activity), PS (total and free), and C4b binding protein (C4bBP) were compared according to the outcome in patients with DIC. PATIENTS: Sixty patients with septic shock were studied. Forty-four entered the group DIC+; 16 entered the group DIC-. RESULTS: Simplified acute physiologic score (SAPS), frequency of acquired organ failure, blood lactate, and transaminase values were significantly higher in the group DIC+. The mortality rate reached 77 percent in group DIC+ vs 32 percent in DIC- (p less than 0.001). In patients with DIC, a fatal outcome was associated with higher bilirubin and transaminase levels, lower PaO2/FIo2 ratio, Vo2, Do2 and O2 extraction. In the group DIC+, all patients but two had severe deficiencies in ATIII and PC levels. Significant correlations were found between initial ATIII and PC levels, PC and free PS levels, and free PS and C4bBP levels. Initial ATIII levels had the best prognostic value for prediction of subsequent death. Serial measurements were consistent with a prolonged ATIII and PC deficiency with significantly different levels between survivors and nonsurvivors. CONCLUSIONS: DIC is a strong predictor of death and multiple organ failure in patients with septic shock. Sequential ATIII, PC, and PS measurements were consistent with prolonged consumption or inhibition that might account for a sustained procoagulant state and inhibition of fibrinolysis. The initial ATIII level was the best laboratory predictor of death in these patients.

Compared evolution of plasma fibronectin and angiotensin-converting enzyme levels in septic ARDS.

Serum angiotensin converting enzyme (serum ACE) levels and plasma fibronectin levels were measured daily in 46 septic patients during a ten day period. Thirty-eight patients developed ARDS; 28 survived (group 1), ten died (group 2), eight patients had no features of ARDS and survived (group 3). Sequential measurements of ACE and fibronectin levels were compared and plotted against indexes of respiratory impairment: PaO2 max Qs/Qt, static compliance and VD/VA ratio. These indexes were taken as criteria of weaning from controlled ventilation. During ARDS (groups 1 and 2), serum ACE levels decreased and were closely correlated with the severity of lung injury. Persistently decreased levels after eight days were consistent with continuing injury or lack of endothelial repair. On the other hand, plasma fibronectin levels increased throughout the study in survivors (group 1 and 3) and decreased in the group with fatal ARDS only (group 2). These results indicate that serum ACE levels might be a good index of endothelial injury and repair during ARDS and fibronectin a better index for evolution of sepsis and vital prognosis.

Angiotensin-converting enzyme in human adult respiratory distress syndrome.

Angiotensin-converting enzyme (ACE) levels, complement activation, and intravascular coagulation were studied in 36 patients with adult respiratory distress syndrome (ARDS) (17 aseptic, 19 septic), in order to investigate the possible interrelations among ACE, immunologic data, and hematologic findings. The severity of respiratory impairment was assessed with measurements of mechanical and gas exchange functional qualities of the lung. Serial measurements of ACE could be done in 14 patients during an eight-day period. During the first 24 hours, ACE levels were always normal (38 percent) or decreased (62 percent). No difference could be found between patients with septic and aseptic ARDS. Complement activation occurred in 78 percent (28/36) and used, in most cases, the classic pathway with presence of circulating immune complexes. Criteria for intravascular coagulation were present in 58 percent (21/36). No relation between coagulation, complement, and ACE could be found except for the patients with a greater respiratory impairment, who had complement activation, intravascular coagulation, and significantly lower ACE levels. In all patients together, ACE levels had no diagnostic value for aseptic cause of ARDS and a poor prognostic value. Only intravascular coagulation was linked with a higher significant mortality and a greater functional impairment. Serial measurements showed a diphasic evolution of ACE levels, with a maximum decrease between the 72nd and 96th hours and a further normalization (seventh day). The persistence of low levels seemed to be associated with evolutive sepsis or secondary aggravation and fibrosis.

Myasthenia gravis and steroid-induced myopathy of the respiratory muscles.

OBJECTIVE: We report a case of corticosteroid-induced myopathy with involvement of respiratory muscles observed in a myasthenic patient. PATIENT: A 37-years-old woman, under corticosteroid treatment for two years for typical myasthenia gravis was admitted to ICU for acute myasthenic respiratory failure. Weaning from mechanical ventilation remained impossible despite 4 plasma exchanges and azathioprine. The patient exhibited a progressive 12 kg weight loss with muscular weakness and atrophy. MEASUREMENTS AND RESULTS: Peripheral and diaphragmatic electromyography as well as histological study were consistent with a steroid-induced myopathy. Discontinuation of corticosteroid treatment was followed by a rapid weight gain with general improvement and allowed weaning from mechanical ventilation with a complete recovery. CONCLUSION: This case provides evidence that corticosteroid-induced myopathy may be observed in myasthenia gravis and may involve the respiratory muscles as well as the peripheral musculature.

Intravenous nitroglycerin in acute respiratory failure of patients with chronic obstructive lung disease, secondary pulmonary hypertension and cor pulmonale.

We have studied the hemodynamic effects of an intravenous single dose of nitroglycerin in 13 patients with secondary pulmonary hypertension and Cor Pulmonale, during the acute course of respiratory failure and under assisted ventilation. We observed a significant decrease in systolic, diastolic and mean pulmonary arterial pressures, and in pulmonary resistance and systolic right ventricular work index, without any change in right or left pre-loads. The systolic arterial pressure decreased slightly, without any change in cardiac index or diastolic pressure. The arterial and mixed venous oxygen contents, and the pulmonary shunting ( Qs/Qt) were unchanged. These results suggest that nitroglycerin may be a useful therapy in patients in the acute stages of pulmonary hypertension resulting from chronic lung disease and under assisted ventilation. In addition, the lack of change in cardiac index, intrapulmonary shunting and oxygen content suggests that this decrease in pulmonary resistance is not linked with any deleterious effect in oxygen transfer.

Coagulation inhibitor substitution during sepsis.

This review presents the rationale for and main results of coagulation inhibitor substitution during experimental and human sepsis. Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kinins pathway and of fibrinolysis. Physiologic inhibition depends on the C1-inhibitor (C1-Inh.). Septic patients exhibit a relative deficiency of biologically active C1-Inh. Substitution with concentrations of C1-Inh has been safely performed and preliminary results are consistent with a possible beneficial effect on hypotension and vasopressor requirement in septic shock. The extrinsic pathway is the main initial coagulation process involved in sepsis-induced DIC. Endothelial and monocyte generation of tissue factor (TF) is activated by bacterial products and endotoxin. Activation of TF is counteracted by a specific tissue factor pathway inhibitor (TFPI). The potential for TFPI substitution to inhibit the activation of the coagulation cascade in sepsis requires further study. Thrombin generation is inhibited by antithrombin III (AT III) and the protein C-protein S system. During sepsis, AT III is consumed and degraded by elastase. Animal studies have shown that DIC and death were prevented by high doses of AT III concentrates. Although a significant reduction in the duration of biological symptoms of DIC has been reported in most human studies, the usefulness of AT III substitution in human sepsis is still debated. None of the studies was able to document a statistically significant reduction in mortality. Protein C is activated by thrombomodulin and, with its cofactor protein S, inhibits factors Va and VIIIa. The free level of protein S depends on the level of the C4b binding protein (C4bBP), an acute-phase complement regulatory protein. During sepsis, protein C activity is significantly reduced, either by acute consumption or by thrombomodulin down-regulation, and increased levels of plasma C4bBP inhibit protein S. Infusion of activated protein C and protein S substitution both protect animals from the lethal effects of bacteria. Combining these different coagulation inhibitors should be carefully studied before its use in septic patients is recommended.

Cefepime-induced neurotoxicity: an underestimated complication of antibiotherapy in patients with acute renal failure.

OBJECTIVES: To describe five new cases of life-threatening cefepime-induced neurotoxicity observed in a 2-year period. SETTING: A university intensive care unit. PATIENTS: Five patients recently treated with cefepime, admitted for seizures and coma. All suffered from acute renal failure, induced by sepsis and combined aminoside therapy, or by cefepime itself in one case. INTERVENTIONS: All patients underwent hemodialysis, which led to complete neurological improvement in four of them. One patient remained comatose and subsequently died. MEASUREMENTS: Blood and CSF cefepime levels were measured by high performance liquid chromatography before and after hemodialysis. CONCLUSION: The frequency of cefepime-induced neurotoxicity is probably underestimated. Monitoring of renal function and close neurological survey in treated patients should allow an early diagnosis of this complication. Urgent hemodialysis seems the best therapeutic method to obtain a rapid neurological improvement.

Effects of dental plaque antiseptic decontamination on bacterial colonization and nosocomial infections in critically ill patients.

OBJECTIVES: To document in intensive care unit (ICU) patients the effect of dental plaque antiseptic decontamination on the occurrence of plaque colonization by aerobic nosocomial pathogens and nosocomial infections. DESIGN: Single-blind randomized comparative study. SETTING: A 16-bed adult intensive care unit in a university hospital. PATIENTS: Patients consecutively admitted in the ICU with a medical condition suggesting an ICU stay of 5 days and requiring mechanical ventilation. INTERVENTIONS: After randomization, the treated group received dental plaque decontamination with 0.2% chlorhexidine gel, three times a day during the ICU stay. The control group received standard oral care. SPECIFIC MEASUREMENTS: Dental status was assessed by the Caries-Absent-Occluded index; the amount of dental plaque was assessed by a semi-quantitative plaque index. Bacterial sampling of dental plaque, nasal and tracheal aspirate, blood, and urine cultures were done on days 0, 5, 10, and every week. MAIN RESULTS: Sixty patients were included; 30 in the treated group and 30 in the control one (mean age: 51 +/- 16 years; mean Simplified Acute Physiological Score II: 35 +/- 14 points). On admission, no significant differences were found between both groups for all clinical and dental data. Compared with the control group, the nosocomial infection rate and the incidence densities related to risk exposition were significantly lower in the treated group (18 vs 33% days in the ICU and 10.7 vs 32.3% days of mechanical ventilation; P < 0.05). These results were consistent with a significant preventive effect of the antiseptic decontamination (Odds Ratio: 0.27; 95% CI: 0.09; 0.80) with a 53% relative risk reduction. There was a trend to a reduction of mortality, length of stay, and duration of mechanical ventilation. CONCLUSIONS: An antiseptic decontamination of dental plaque with a 0.2% chlorhexidine gel decreases dental bacterial colonization, and may reduce the incidence of nosocomial infections in ICU patients submitted to mechanical ventilation.