Case report: recovery of Calliphora vicina first-instar larvae from a human traumatic wound associated with a progressive necrotizing bacterial infection.

Human myiasis caused by Calliphora vicina is rare in Europe. Here we report a case of C. vicina infection occurring in the traumatic leg wound of a healthy 21-year-old man. Firstly, a progressive necrotizing infection developed in the wound despite administration of antibiotics. Aeromonas hydrophila was isolated from the wound samples. Secondly, during debridement, C. vicina first-instar larvae were isolated from the wound. To our knowledge, this is the first European case of C. vicina wound myiasis associated with severe A. hydrophila infection.

Inhaled NO reduces leukocyte-endothelial cell interactions and myocardial dysfunction in endotoxemic rats.

Inhaled nitric oxide (NO) has been shown to have some protective effect in the peripheral distal inflamed vasculature. The objective of the study was to determine whether inhaled NO would reduce endotoxin-induced leukocyte activation and myocardial contractile dysfunction. Rats were treated with either saline or endotoxin (10 mg/kg iv) and then allowed to breathe (4 h) either air or air plus NO (10 ppm). In endotoxemic rats, mesenteric venular endothelium leukocyte firm adhesion increased compared with control rats (1.15 +/- 0.32 vs. 4.08 +/- 0.96 leukocytes/100 microm; P < 0.05). Inhaled NO significantly attenuated endotoxin-induced venular endothelium leukocyte adhesion (4.08 +/- 0.96 vs. 1.86 +/- 0.76 leukocytes/100 microm; P < 0.05) and FITC-conjugated anti-intercellular adhesion molecule-1 fluorescence intensity. Endotoxin-induced myocardial dysfunction and leukocyte content increases were reduced in inhaled NO-treated rats. These observations suggest that inhaled NO reduces the degree of cardiovascular dysfunction and inflammation in endotoxemic rats.

Inhaled nitric oxide modulates leukocyte kinetics in the mesenteric venules of endotoxemic rats.

OBJECTIVE: to determine whether inhaled nitric oxide (NO) would alter leukocyte kinetics in the septic microvasculature. DESIGN: Randomized, controlled trial. SETTING: Experimental laboratory. SUBJECTS: Male Sprague Dawley rats. INTERVENTIONS: Rats were treated with either saline or endotoxin (10 mg/kg, iv) and then allowed to breathe either air or air plus NO (10 ppm). MEASUREMENTS AND MAIN RESULTS: After a 4-hr period, rolling, firm adhesion, and emigration of leukocytes and endothelial dysfunction were monitored in mesenteric venules by using intravital videomicroscopy. Compared with controls, endotoxemic rats exhibited a profound influx in mesenteric venule rolling leukocytes (55+/-17 vs. 70+/-19 leukocytes/min; p < .05), associated with a reduction of leukocyte rolling velocity (83+/-14 vs. 34+/-3 microm/sec; p < .05). In endotoxemic rats, venular endothelium leukocyte firm adhesion (1.15+/-0.32 vs. 4.08+/-0.96 leukocytes/ 100 microm; p < .05) and emigration (0.84+/-0.47 vs. 4.23+/-1.2 leukocytes/100 microm; p < .05) increased compared with controls. Inhaled NO had no effect on leukocyte kinetics in control rats. Inhaled NO significantly attenuated endotoxin-induced venular endothelium leukocyte adhesion (4.08+/-0.96 vs. 1.86+/-0.76 leukocytes/100 microm; p < .05) and emigration (4.23+/-1.2 vs. 1.68+/-0.72 leukocytes/100 microm; p < .05). Compared with control rats, macromolecular (FITC-dextran) vascular leakage, expressed as the perivenular/intravenular fluorescence intensity ratio, increased in endotoxemic rats (0.56+/-0.02 vs. 0.81+/-0.05; p < .01). Endotoxin-induced macromolecular vascular leakage increases were partially prevented by inhaled NO (0.66+/-0.01 vs. 0.56+/-0.02; p < .05). CONCLUSION: These observations suggest that inhaled NO reduces leukocyte adhesion and the degree of vascular permeability dysfunction in mesenteric venule of endotoxemic rats.

Effects of breathing air at 4 atm abs: evidence for a change in strategy.

The effect of breathing air at 4 atm abs on two tasks was investigated. For the recognition memory task, subjects learned a list of symbols in anticipation of a recognition test. The second task was a speed test in which subjects were instructed to detect all occurrences of a given target. A signal detection analysis of performance to the recognition test showed that sensitivity index was invariant, but the criterion (beta) became stricter under hyperbaric pressure. For the speed test, the results showed that under pressure the error rate increased progressively with time while the working speed remained constant. It is argued that strategic variables may be particularly sensitive to the hyperbaric environment.

[Role of microcirculation in multiorgan failure of infectious origin]. / Rôle de la microcirculation dans la défaillance multiviscérale d'origine infectieuse.

The normal host response to infection is a complex process which serves to localize and control bacterial invasion and to initiate repair of injured tissue. This inflammatory process is accompanied by activation of circulating and fixed phagocytic cells and generation of pro-inflammatory and anti-inflammatory mediators. Sepsis results when the prerequisite inflammatory response to infection becomes generalized, and thereby extends to involve otherwise normal tissue which is remote from the initial site of injury or infection. Sepsis is typically associated to cardiovascular alterations that have been characterized by increases in oxygen delivery to the tissues. Paradoxically, the host's systemic inflammatory response syndrome may simultaneously disturb the ability to adequately match tissue oxygen needs and availability at a time when tissue oxygen needs are typically increased. Depressed tissue oxygen availability relative to augmented needs may result from dysfunction at all of the central, regional, and microregional levels of the circulation. Significant dysregulation in the process by which oxygen availability is usually matched to changing tissue oxygen needs is typical associated with changes the microvascular blood flow behavior, vascular reactivity and endothelial and leukocyte activation. Specific tools developed to explore the microcirculation have been applied in the setting of both human and animal models sepsis. Abnormalities observed in the septic microvasculature are characterized by reductions in cutaneous and skeletal muscle blood flow and in mucosal intestinal ischemia and hypoxia. Regarding the skeletal muscle organ system, microvascular abnormalities were further characterized by an impairment of blood flow to increase in response to oxygen need increase. Also, microvascular abnormalities in the intestine were associated with evidence of endothelial and leukocyte activation leading to epithelial dysfunction. Thus, sepsis appears to be associated with early onset microvascular dysfunction. The relationship between microvascular dysfunction and endothelial and leukocyte activation leading to organ failure has been suggested by numerous studies.

Gastric mucosal pH and blood flow during weaning from mechanical ventilation in patients with chronic obstructive pulmonary disease.

To determine if gastric intramucosal pH changes during weaning from mechanical ventilation are related to gastric mucosal blood flow modifications, we studied 16 ventilator-supported patients with chronic obstructive pulmonary disease (COPD) who tolerated a 2-h trial of spontaneous breathing with pressure support ventilation and were successfully extubated and 11 patients with COPD who failed such a trial. Gastric mucosal perfusion was assessed using gastric intramucosal pH (pH(i)) by tonometry and laser-Doppler flowmetry. During the weaning attempt, the failure weaning group developed a rapid, shallow breathing pattern with acute respiratory acidosis. The pH(i) was lower and gastric intramucosal PCO(2) (PCO(2)im) was higher in the failure weaning group than in the successful weaning group (p < 0.05). No change in gastric intramucosal-arterial PCO(2) difference was observed and a linear correlation was found between arterial PCO(2) and PCO(2)im (r(2) = 0.70; p < 0.001). Cardiac index increased in the failure group (p < 0.05) and remained stable in the success group whereas gastric mucosal blood flow decreased in the failure group (H(120) (min): -22 +/- 11% from baseline; p < 0.05) and increased in the success group (H(120) (min): 85 +/- 27% from baseline; p < 0.05). We conclude that gastric intramucosal pH changes during a 2-h weaning trial are mainly due to arterial PCO(2) variations. Nevertheless, gastric mucosal blood flow changes do occur and differ according to the weaning success or failure.

Inhaled NO preadministration modulates local and remote ischemia-reperfusion organ injury in a rat model.

Inhaled nitric oxide (iNO) has been shown to have a protective effect in lung ischemia-reperfusion (I/R)-induced injuries. We studied the role of iNO (10 parts/million for 4 h) administered before I/R. In an isolated perfused lung preparation, iNO decreased the extravascular albumin accumulation from 2,059 +/- 522 to 615 +/- 105 microl and prevented the increase in lung wet-to-dry weight ratio. To study the mechanisms of this prevention, we evaluated the role of nitric oxide (NO) transport and lung exposure with matched experiments by using either lungs or blood of animals exposed to iNO and blood or lungs of naive animals. iNO-exposed blood with naive lungs did not limit the extravascular albumin accumulation (2,561 +/- 397 microl), but iNO-exposed lungs showed a leak not significantly different from the group in which both lungs and blood were iNO exposed (855 +/- 224 vs. 615 +/- 105 microl). An improvement in heart I/R left ventricular developed pressure in the animals exposed to iNO showed that blood-transported NO was, however, sufficient to trigger remote organ endothelium and reduce the consequences of a delayed injury. In conclusion, preventive iNO reduces the consequences of lung I/R injuries by a mechanism based on tissue or endothelium triggering.

Dobutamine improves gastrointestinal mucosal blood flow in a porcine model of endotoxic shock.

OBJECTIVE: To test the hypothesis that saline solution plus dobutamine increases gastrointestinal mucosal perfusion better than saline solution alone in a model of endotoxic shock. DESIGN: Prospective, randomized, unblinded study. SETTING: Animal research laboratory affiliated with a university teaching hospital. SUBJECTS: Twelve female pigs, weighing 30 to 32 kg. INTERVENTIONS: Animals were anesthetized, and their lungs were mechanically ventilated. Catheters were inserted into the right atrium, pulmonary artery, and carotid artery for blood sampling and blood pressure and cardiac output measurements. A tonometer and a laser Doppler probe were placed in the lumen of the stomach and the ileum for determination of mucosal acid-base status and measurement of mucosal blood flow. Group 1 animals (n = 6) received an infusion (T = 0 min) of 150 mcirog/kg Escherichia coli endotoxin and normal saline solution (0.3 mL/kg/min). Group 2 animals (n = 6) received an infusion of endotoxin and were resuscitated with the same method as used in group 1, but an infusion of dobutamine (5 microg/kg/min) was begun at T = 60 mins, and continued for the duration of the experiment. MEASUREMENTS AND MAIN RESULTS: Both experimental regimens produced shock, with decreased mean arterial pressure and systemic vascular resistance, without change in cardiac output and oxygen delivery. Endotoxin plus saline infusion decreased gastrointestinal mucosal blood flow to <60% of baseline and decreased gastrointestinal pH. In contrast, gastrointestinal mucosal blood flow returned to baseline values, and intramucosal pH tended to normalize by the end of the saline solution plus dobutamine resuscitative protocol. CONCLUSION: Compared with saline solution alone, saline solution plus dobutamine increased blood flow to the gastrointestinal mucosa, and may have partially improved oxygenation.

[Anaerobic infections of the soft tissues]. / Les infections anaérobies des tissus mous.

Anaerobic soft tissue infections are still life threatening infections. Although their frequency is actually moderate; they remain severe because physicians are often insufficiently aware of them. Although the classification between myonecrosis and necrotizing fasciitis is still valid, these infections share so many points in common that they can be considered together. Their origin is often traumatic or surgical but may also be secondary to an ulcer or a small wound in a high-risk patient: arteriosclerotic, diabetic. Hypoxia, traumatic muscle crush, heavy bacterial contamination as well as incorrect antibiotic prophylaxis are the major reasons for their occurrence. Management consists of antibiotics adapted to both anaerobic and associated aerobic bacteria, large and early surgical debridement, but with conservative excision, and intensive hyperbaric oxygen therapy. Strict prevention measures must be applied to avoid their occurrence.

The contrasting effects of dobutamine and dopamine on gastric mucosal perfusion in septic patients.

To test the hypothesis whether or not dobutamine or dopamine infusion increases gastric mucosal perfusion, a prospective randomized crossover trial was conducted on 10 septic patients in the intensive care unit of a university hospital. Systemic hemodynamic, oxygen transport, and gastric perfusion assessed by gastric intramucosal pH and laser Doppler flowmetry were measured at baseline and after administration of dobutamine or dopamine (5 micrograms/kg/min). Both increased oxygen transport. In response to dobutamine, gastric mucosal blood flow increased (+32 +/- 14% from baseline; p < 0.05), gastric tonometered PCO2 and gastric arterial PCO2 difference decreased (58 +/- 7 versus 52 +/- 7 mm Hg; p < 0.05; 16.8 +/- 7.0 versus 10.5 +/- 7.2 mm Hg; p < 0.05), and intramucosal pH increased (7.23 +/- 0.05 versus 7.29 +/- 0.06; p < 0.05). In response to dopamine, gastric mucosal blood flow decreased (-28 +/- 8% from baseline; p < 0.05), gastric tonometered PCO2, gastric-arterial PCO2 difference, and calculated intramucosal pH were unchanged (58 +/- 7 versus 61 +/- 9 mm Hg, ns; 16.8 +/- 7.0 versus 18.9 +/- 8.4 mm Hg, ns; 7.24 +/- 0.05 versus 7.21 +/- 0.06, ns). We speculated that despite an oxygen transport increase, dobutamine and dopamine have affected differently gastric mucosal perfusion in septic patients.

[Carbon monoxide poisoning]. / L'intoxication au monoxyde de carbone.

Carbon monoxide (CO) poisoning still represents a frequent and severe casualty in France. Aside from the well-known effect of CO on hemoglobin, the role of CO binding to other hemoproteins like myoglobin and cytochrome a3 has been more recently recognized. Moreover, in addition to these hypoxic injuries, the reoxygenation phase may itself induce toxic effects by a mechanism close to the ischemia-reperfusion phenomenon. Clinical manifestations include neurologic disturbances, cardiac arrhythmia, respiratory and circulatory failures which usually disappear with removal from toxic atmosphere and administration of oxygen. However, long term neurologic manifestations may occur and lead to important functional impairment and disability. Hyperbaric oxygen is actually the treatment of choice to avoid the occurrence of delayed sequelae. HBO is advocated in every patient who remains comatose on hospital admission, who has lost consciousness during toxic exposure or with persisting neurologic abnormalities. CO poisoned pregnant women should also undergo HBO.

[Indications for hyperbaric oxygen therapy. Organization of the treatment unit. Training of personnel]. / Les indications de l'oxygénothérapie hyperbare. Organisation d'une unité de traitement. Formation des personnels.

Pathophysiologic mechanisms involved in the application of HBO therapy are poorly understood that may limit its clinical use. However, useful indications are well standardized in the setting of critical care medicine, CO poisoning, decompression sickness, gas gangrene and soft tissue anaerobic infections, crush syndrome, burns, sudden deafness... HBO therapy is also indicated in the management of chronic limb ischemia, diabetic foot lesion, osteomyelitis, osteoradionecrosis. These clinical indications have been evaluated in a Consensus Conference on Hyperbaric Medicine that has classified its application according to its efficiency. Indications were classified as strongly recommended (positively affects the patient's survival), recommended (does not influence the patient's survival but is important for the prevention of serious disorders) and optional (regarded as a additional treatment modality). Clinical application of HBO therapy requires specific equipment including a multiplace hyperbaric chamber and specific educational program and training for personnel employed in the clinical hyperbaric center. Lastly, HBO therapy is related to accurate rules defining its indications as well as its evaluation that are minimal prerequisites for safety and clinical results.

[Carbon monoxide poisoning: current aspects]. / Intoxication par le monoxyde de carbone: aspects actuels.

Carbon monoxide (CO) poisoning still represents a frequent and severe casualty in France. Aside the well-known effect of CO on hemoglobin, the role of CO binding to other hemoproteins like myoglobin and cytochrome a3 have been more recently recognized. Moreover, in addition to these hypoxic injuries, the reoxygenation phase may itself induce toxic effects by a mechanism close to the ischemia-reperfusion phenomenon. Clinical manifestations include neurologic disturbances, cardiac arrythmia, respiratory and circulatory failures which usually disappear with removal from toxic atmosphere and administration of oxygen. However, long term neurologic manifestations may occur and lead to important functional impairment and disability. Hyperbaric oxygen in actually the treatment of choice to avoid the occurrence of delayed sequelae. HBO is advocated in every patient who remains comatose on hospital admission, who had lost consciousness during toxic exposure or with persisting neurologic abnormalities. CO poisoned pregnant women should also undergo HBO. Well designed prevention programs are urgently needed in our country to decrease the incidence and the consequences of CO poisoning.

Skeletal muscle microvascular blood flow and oxygen transport in patients with severe sepsis.

To compare skeletal muscle microvascular blood flow at rest and during reactive hyperemia in septic patients, a prospective, controlled trial was conducted on 16 patients with severe sepsis and a control group of 10 patients free of infection in the intensive care unit of a university hospital. Systemic hemodynamics, whole-body oxygen transport, and skeletal muscle microvascular blood flow at rest and during reactive hyperemia were measured. Reactive hyperemia was produced by arrest of leg blood flow with a pneumatic cuff; on completion of the 3 min ischemic phase the occluding cuff was rapidly deflated to 0. Hemodynamic and oxygen-derived variables were determined invasively. Skeletal muscle microvascular blood flow data were obtained using a laser Doppler flowmetry technique and values expressed in millivolts. Whole-body oxygen delivery in septic patients was increased compared with control subjects. Resting skeletal muscle blood flow was decreased in septic patients compared with control subjects (233 +/- 52 versus 394 +/- 93 mV; p < 0.05). Peak flow during reactive hyperemia was also decreased in septic patients compared with control subjects (380 +/- 13 versus 2,033 +/- 853 mV; p < 0.05). Cyclic variation in blood flow (vasomotion) was observed in control subjects but not in septic patients. Skeletal muscle microvascular perfusion is altered in patients with severe sepsis despite normal or elevated whole-body oxygen delivery. These microvascular abnormalities may further compromise tissue nutrient flow and may contribute to the development of organ failure in septic patients.

[Inhaled nitric oxide test for patients with stable chronic obstructive pulmonary disease: value and feasibility]. / Test au monoxyde d'azote chez l'insuffisant respiratoire chronique à l'état stable: intérêt et faisabilité.

Patients suffering from chronic lung disease (CLDP) often develop secondary pulmonary hypertension (HP), which contributes to right ventricular dysfunction and worsens their prognosis. In order to evaluate the severity of this HP, pharmacodynamics tests are periodically proposed to these patients. Therefore, the administration of vasodilators is limited by systemic and pulmonary side-effects. Inhaling nitric oxide gas (NO) has been reported to induce a selective pulmonary vasodilation. The purpose of this study was to evaluate the safety and efficacy of an inhaled NO test perfected in our service. Sixteen CLDP were investigated in the absence of acute pulmonary failure. All had severe pre-capillary HP, confirmed after placement of a thermodilution pulmonary-artery catheter (mean pulmonary artery pressure >20 mmHg, pulmonary capillary wedge pressure >12 mmHg). Each subject breathed spontaneously NO in a concentration of 10 ppm for 15 minutes. They were connected through a facial mask and a one-way valve put on the inspiratory connection of a ventilator (Drager-Evita), to a tank of nitrogen with a NO concentration of 900 ppm. Hemodynamic variables and gas exchange were measured before, during and after gas inhalation. The inspired fractions of NO and NO2 were determined using a Polytron analyser (Drager). The methemoglobin levels were measured with spectrophotometry (OSM3). Inhaled NO acts as a selective pulmonary arterial vasodilator, without systemic effect. The action on the shunt is variable. Methemoglobin levels are remained <0.01%. All the patients were satisfied with the way of NO administration. In view of the lack of systemic effects, its seems that the NO inhaled test proposed in this study may be used accurately to evaluate the HP of chronic lung disease patients.

Cervical necrotizing fasciitis: clinical manifestations and management.

Forty-five cases of cervical necrotizing fasciitis are reported, and their clinical, bacteriologic, and therapeutic implications are considered. Fasciitis was of dental origin in 78% of cases, pharyngeal in 16%, and surgical or posttraumatic in 6%. The condition extended to the face in 22% of cases, to the lower part of the neck in 56%, and to the mediastinum in 40%. Soft-tissue cultures were positive in 78% of cases. Anaerobes were isolated along with aerobes in 49% of cases (mean, 2.2 isolates per patient) and in pure culture in 22%. Treatment included surgical debridement and drainage and the administration of antibiotics active against both anaerobic and gram-negative aerobic bacteria. Hyperbaric oxygen was used for adjunctive treatment. The bacteria involved did not affect clinical manifestations, extension, or mortality. The survival rate among our patients was 78%. Mortality was significantly higher among cases with mediastinal extension (44% vs. 7%; P < .01); thus the prompt recognition and drainage of sites of mediastinal extension are of critical importance. Other risk factors for death were an age of > 70 years, underlying diabetes, the development of septic shock within 24 hours after admission, and prolonged prothrombin time.

Carbon dioxide rebreathing method of cardiac output measurement during acute respiratory failure in patients with chronic obstructive pulmonary disease.

OBJECTIVE: To compare measurement of cardiac output by the CO2 rebreathing method vs. the thermodilution cardiac output technique in the setting of acute respiratory failure in patients with chronic obstructive pulmonary disease. DESIGN: Prospective, comparative study of two methods in a consecutive sample. SETTING: Intensive care unit. PATIENTS: Twenty-five patients with chronic obstructive pulmonary disease with acute respiratory failure were studied. The patients were being mechanically ventilated and monitored with systemic and pulmonary artery catheters. MEASUREMENTS AND MAIN RESULTS: Cardiac output was determined, using both the thermodilution technique and an indirect CO2 Fick method. Veno-arterial CO2 content difference was calculated from an estimated mixed venous PCO2 obtained by an equilibrium CO2 rebreathing method and measured PaCO2. PCO2 was converted to content using the equation of the CO2 dissociation curve described by McHardy. A wide range of cardiac output was studied. There was a significant correlation between thermodilution and CO2 rebreathing methods (r2 = .92, p < .001). The mean difference between thermodilution and CO2 rebreathing methods was -0.06 L/min/m2, standard deviation for the bias was 0.028 L/min/m2, and 95% confidence interval for the bias was -0.120 to -0.001 L/min/m2. CONCLUSION: Our results suggest that the CO2 rebreathing method may be a reliable non-invasive technique to determine cardiac output in mechanically ventilated patients with chronic obstructive pulmonary disease.