[A 25-year study (1983-2008) of children's health outcomes after hyperbaric oxygen therapy for carbon monoxide poisoning in utero]. / Devenir des enfants intoxiqués au monoxyde de carbone en période foetale et traités par oxygéno- thérapie hyperbare--etude d'une cohorte constituée sur 25 ans de 1983 a 2008.

Carbon monoxide (CO) poisoning during pregnancy can be fatal for the fetus, or cause bone malformations or encephalopathy, depending on the stage of pregnancy at which the poisoning occurs. Fewer cases of death and encephalopathy have been reported since the adoption of maternal hyperbaric oxygen (HBO) therapy in this setting, but these children's long-term psychomotor development and growth remains to be documented. A prospective single-center cohort study spanning 25 years (1983 - 2008) included all pregnant women living in the Nord-Pas-de-Calais region of France who received HBO for CO poisoning and who gave birth to a living child. A descriptive analysis of the women and children was performed first. A control group of children was created by matching with anonymous files from local authorities. The results of the children's compulsory health & development assessments were used to compare the two groups. 406 women were included in the study, of whom 6 were expecting twins. The psychomotor development of 412 children was monitored, up to the day 8 assessments in 388 cases, the year 2 assessments in 276 cases, and the year 6 assessments in 232 cases. Sixty children have not yet reached the age of 6 years. No significant differences in psychomotor or height/weight criteria (p > 0.05 for both) were found between the exposed and unexposed children. No malformations were reported. These findings support the use of HBO therapy for all expectant mothers exposed to CO poisoning. No specific follow-up of the children is necessary if their neonatal status is normal.

[Pre-hospital management of adults with life-threatening emergencies]. / Prise en charge pré-hospitalière des urgences vitales de l'adulte en pratique civile.

In France, acute life-threatening situations are handled by the French Secours a Personne (assistance to persons) and emergency medical facilities. An unequivocal success, this early management of life-threatening emergency situations relies upon centralized call reception, medical dispatching, and immediate on-site emergency medical care. We describe the different emergency care providers and steps involved in the response to emergency situations. Each call centre (Samu, phone number 15; Sapeurs-Pompiers, 18) provides a response tailored to the nature of incoming calls for assistance. A check-list of grounds for an "automatic response" by the SDIS (Service Départemental d'Incendie et de Secours--the French fire brigade) is in use, ensuring that firefighters are often the first on the spot, while the knowledge and skills of the dispatching physician are essential to ascertain the patient's needs, to preserve life and vital functions, and to ensure the patient is sent to the appropriate emergency healthcare facility. In life-threatening emergency situations, patients must be brought straight to the appropriate reference emergency healthcare facility, as quickly as possible, without prior admittance to an emergency department. This is the procedure for extremely acute emergency situations in the following areas: trauma (multiple trauma and/or uncontrolled bleeding, spinal cord trauma), delivery bleeding, other life-threatening situations such as ischemic heart disease, cardiac arrest (sudden death), cerebrovascular stroke and ensuing brain damage, some acute respiratory situations such as anaphylactic shock, foreign-body inhalation, electrocution, drowning, drug overdose, certain forms of poisoning, and conditions requiring initial hyperbaric oxygen (diving accidents, acute carbon monoxide and smoke poisoning). The reasons for suboptimal emergency care in life-threatening situations are currently a major issue, with medical facilities being reduced in some areas, fewer voluntary firemen, hospital reorganization, tight funding, difficulties of medical dispatching, and the varying skills of "first-on-the-scene "emergency workers. Grievances include late emergency responses, inappropriate medical care, and dispatching to the wrong facility. This raises the question of equal opportunity for all in a country with widely varying geographic features and population density. Improvement in the system's efficiency will require a series of objectives to be met in varied and complementary--Enhanced functional coordination, by speeding up the deployment of the ANTARES digital radio-frequency transmission network (Adaptation Nationale des Transmissions Aux Risques Et aux Secours).--Implementation of a network of emergency services with varying degrees of emergency healthcare management related to the technical nature of the facilities. Three levels of emergency healthcare must be made available: level 1 is provided by local hospitals, level 2 includes support facilities available in general hospitals (not necessarily the nearest hospital), and level 3 provides specialized healthcare in large and/or training hospitals with specialized departments. Life-threatening emergency situations are to be handled by level 2 or 3 facilities. Specific facilities must be selected as reference centers. In France, the ARS (Agences Régionales de Santé) is in charge of this procedure, as it provide funding for healthcare continuity--Reducing inequalities in access to emergency care. This will involve improving the network of SDIS brigades, making local medical facilities more responsive, delegating more medical procedures, on-site telemedicine, providing more helicopters equipped with healthcare facilities, more automated external defibrillators, and more dedicated neuro-vascular units.--First aid training must be made widely available. The French National Academy of Medicine has approved ten recommendations regarding organization and facilities.

[Carbon monoxide and the heart: unequivocal effects?]. / Monoxyde de carbone et coeur: des effets univoques?

UNLABELLED: Carbon monoxide is the leading cause of fatal poisoning in many countries. At least two mechanisms of CO toxicity are currently recognized: carboxyhemoglobin formation and CO binding to haeme proteins such as mitochondrial cytochrome C oxidase and myoglobin. However, a growing body of evidence also suggests interference with NO pathways such as nitrosative stress and peroxynitrite formation. Cardiac manifestations of CO poisoning include myocardial ischemia, cardiogenic pulmonary edema, and arrhythmias. Their pathophysiology is unclear, and conflicting observations have been made in animal models, with either an improvement or a deterioration of cardiac function. We therefore explored the functional effects of CO on isolated perfused rat hearts. MATERIALS AND METHODS: Conscious adult rats were intoxicated with various concentrations of CO in a closed chamber for 90 minutes. Cardiac function was assessed on isolated perfused hearts, along with dose-response, calcium sensitivity and pharmacological studies. Simultaneous biological studies included iNOS Western blot, plasma nitrate assay and high-resolution respirometry. RESULTS: cardiac function was improved by CO exposure, as shown by the dP/dtmax ratio, reflecting a rise in coronary perfusion pressure, at concentrations as low as 100 ppm; these effects plateaued after 250 ppm and lasted for 96 hours. No change in mean arterial pressure or cardiac frequency occurred. Cardiac rhythm disturbances occurred immediately and lasted until 3 hours of reoxygenation. Calcium sensitivity was increased Vasoreactivity was also modified, with a decreased response to acetylcholine and to an NO donor. Beta-blockade and NO synthase inhibition with L-NAME had no preventive effect. In contrast, N-acetylcysteine and FeTPPS, a peroxynitrite decomposition catalyst, partially prevented the increase in contractility, without affecting coronary pressure. Interestingly, ODQ, a guanylate cyclase inhibitor, had no preventive effect, but when given alone it led to an increase in contractility and coronary pressure. Protein expression of iNOS increased as early as 24 hours and peaked at 96 hours. Plasma nitrate levels were slightly increased High-resolution respirometry showed marked inhibition of cytochrome C oxidase at H3 but not at later times. DISCUSSION: mechanism of cardiac toxicity could be explained as follows:--Nitrosative stress, due to peroxynitrite formation but without NO formation may occur as in cerebral CO toxicity. That could explain in part the increase in contractility in this model. It may act by increasing cardiac fiber calcium sensitivity.--Considering the vasoreactivity partial loss, CO may act as a partial guanylate cyclase agonist, that may explain disequilibrium in GMPc/AMPc pathway, leading to an increase in AMPc levels and therefore in enhanced contractility.--For the first time in the heart, NO related endothelium dysfunction has been proved in a CO poisoning animal model. NO pathways are incriminated Endothelium dysfunction seems to trigger coronary vasoconstriction and increase of cardiac function. In the context of cellular hypoxia as demonstrated here, it could explain ischemic situation in vivo and all its detrimental consequences.

[Oxygen and wound healing]. / Oxygène et processus de cicatrisation.

It has long been recognized that normal healing is dependent on the oxygen gradient in the wound Hypoxia can slow or arrest the healing process and augments the risk of infection. While hypoxia triggers neoangiogenesis, normal tissue oxygen pressures are mandatory for migration of repair cells (macrophages, fibroblasts), production of collagen precursors and, thus, for wound repair with good mechanical properties. Recent studies have identified the underlying molecular mechanisms of wound repair. In clinical practice, hyperbaric oxygen therapy is to treat problem wounds like diabetic foot lesions, arterial ulcers, and radionecrosis. Direct or indirect measurement of oxygen tissue pressure can help to select patients and to monitor treatment outcome.

[Necrotizing soft tissue infections: role of the localization for the antibiotic management]. / Les infections aiguës nécrosantes des tissus mous: importance de la localisation dans le choix de l'antibiothérapie de première intention.

Necrotizing soft tissue infections (NSTI) are infrequent but life-threatening, and require prompt empirical antibiotic therapy. Current nosologic classifications have limited value because the criteria used are imprecise and their bacteriological specificity is uncertain. The aim of this study was to describe the bacterial flora and its antibiotic sensitivity in a cohort of patients with NSTI, and to derive guidelines for the choice of antimicrobial chemotherapy. This prospective study involved 120 patients. Aerobic and anaerobic bacteriological samples were taken from infected soft tissues. The species distribution and susceptibility of the isolates to various antibiotic (ATB) combinations were analyzed. The data were analyzed according to the type (cellulitis versus myonecrosis) and anatomical location of NSTI (abdomen and perineum; uterine cervix; limbs). The chi-square test was used to analyze qualitative variables, and Student's t test was used for quantitative variables. A total of 232 samples yielded bacterial isolates (122 aerobic, 110 anaerobic). The species distribution of anaerobes did not differ according to the nature of the involved tissue or the anatomic location. Gram-negative aerobes were more frequently isolated from abdominal, perineal and limb sites than from the cervix (p<0.05), while gram-positive aerobes showed the reverse distribution (p<0.05). Metronidazole was more effective than clindamycin on cervical isolates (95% vs 88%, p=0.0093). Among the broad-spectrum antibiotics tested, imipenem/cilastatin and piperacillin/tazobactam were equally effective against the different groups of bacteria (94% vs 88%, p=0.14), and were clearly more active than the other antibiotics (p<0.05), whatever the site of isolation, the bacterial species, and the type of NSTI. The five antibiotics tested showed similar efficacy against cervical isolates. These results suggest that the choice of antibiotic therapy for NSTI should depend on the anatomical site of involvement rather than the nature of the infection. For abdominal, perineal and limb NSTI, we recommend first-line treatment with a betalactam-inhibitor combination (piperacillin/tazobactam or ticarcillin/clavulanate) plus an agent active on gram-negative species (aminoglycoside or fluoroquinolone). For cervical NSTI, we recommend penicillin G/metronidazole, or amoxicillin/clavulanic acid.

Small intestine intramucosal PCO(2) and microvascular blood flow during hypoxic and ischemic hypoxia.

OBJECTIVE: To determine whether small intestine intramucosal PCO(2) and mucosal blood flow changes would be different between ischemic and hypoxic hypoxia. DESIGN: Randomized animal experiment. SETTING: Research laboratory. SUBJECTS: Anesthetized, mechanically ventilated, and surgically instrumented pigs. INTERVENTIONS: Systemic oxygen delivery was lowered in a stepwise manner to decrease it beyond critical oxygen delivery by lowering either FIO(2) or blood volume. MEASUREMENTS AND MAIN RESULTS: In hypoxic hypoxia pigs (n = 6), arterial oxygen concentration and oxygen delivery decreases were achieved by progressively reducing arterial PO(2) while cardiac index remained unchanged. In ischemic hypoxia pigs (n = 5), oxygen delivery reduction was achieved by progressively reducing cardiac index while arterial PO(2) remained unchanged. In control pigs, oxygen delivery remained unchanged. The lowest oxygen delivery measured in both hypoxia and ischemia experiments was 3.60 +/- 0.26 vs. 2.93 +/- 0.77 mL x kg(-1) x min(-1), respectively (p =.23). At the lowest oxygen delivery level, differences between ischemic hypoxia and hypoxic hypoxia experiments were observed for arterial lactate concentration (468 +/- 308 vs. 1070 +/- 218 mmol/L, respectively; p =.03), mixed venous arterial PCO(2) difference (10 +/- 7 vs. 4 +/- 2 torr, respectively; p =.04), and small intestine mucosal blood flow (6.2 +/- 2.1 vs. 15.7 +/- 7.4 perfusion units, respectively; p =.02). Small intestine intramucosal-arterial difference was higher in ischemic hypoxia than in hypoxic hypoxia (52 +/- 15 vs. 31 +/- 12 torr, respectively; p =.03). CONCLUSION: Small intestine intramucosal PCO(2) increases may indicate systemic oxygen uptake supply limitation in ischemic and hypoxic hypoxia related to conditions of mucosal flow stagnation and CO(2) generation.