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Postmortem computed tomography can easily demonstrate gas collections after diving accidents. Thus, it is often used to support the diagnosis of air embolism secondary to barotrauma. However, many other phenomenons (putrefaction, resuscitation maneuvers, and postmortem tissue offgassing) can also cause postmortem gas effusions and lead to a wrong diagnosis of barotrauma.The aim of this study is to determine topography and time of onset of postmortem gas collections respectively due to putrefaction, resuscitation maneuvers, and tissue offgassing.A controlled experimental study was conducted on nine pigs. Three groups of three pigs were studied postmortem by CT from H0 to H24: one control group of nonresuscitated nondivers, one group of divers exposed premortem to an absolute maximal pressure of 5 b for 16 min followed by decompression procedures, and one group of nondivers resuscitated by manual ventilation and thoracic compression for 20 min. The study of intravascular gas was conducted using CT scan and correlated with the results of the autopsy.The CT scan reveals that, starting 3 h after death, a substantial amount of gas is observed in the venous and arterial systems in the group of divers. Arterial gas appears 24 h after death for the resuscitated group and is absent for the first 24 h for the control group. Concerning the putrefaction gas, this provokes intravenous and portal gas collections starting 6 h after death. Subcutaneous emphysema was observed in two of the three animals from the resuscitated group, corresponding to the thoracic compression areas.In fatal scuba diving accidents, offgassing appears early (starting from the first hour after death) in the venous system then spreads to the arterial system after about 3 h. The presence of intra-arterial gas is therefore not specific to barotrauma. To affirm a death by barotrauma followed by a gas embolism, a postmortem scanner should be conducted very early. Subcutaneous emphysema should not be mistaken as diagnostic criteria of barotrauma because it can be caused by the resuscitation maneuvers.

Exposure to nitrogen-oxygen mixture at high pressure induces narcosis, which can be considered as a first step toward general anaesthesia. Narcotic potencies of inert gases are attributed to their lipid solubility. Nitrogen narcosis induces cognitive and motor disturbances that occur from 0.3 MPa in man and from 1 MPa in rats. Neurochemical studies performed in rats up to 3 MPa have shown that nitrogen pressure decreases striatal dopamine release like argon, another inert gas, or nitrous oxide, an anaesthetic gas. Striatal dopamine release is under glutamatergic and other amino acid neurotransmission regulations. The aim of this work was to study the effects of nitrogen at 3 MPa on striatal amino acid levels and to compare to those of 3 MPa of helium which is not narcotic at this pressure, by using a new technique of microdialysis samples extraction under hyperbaric conditions, in freely moving rats. Amino acids were analysed by HPLC coupled to fluorimetric detection in order to appreciate glutamate, aspartate, glutamine and asparagine levels. Nitrogen-oxygen mixture exposure at 3 MPa decreased glutamate, glutamine and asparagine concentrations. In contrast, with helium-oxygen mixture, glutamate and aspartate levels were increased during the compression phase but not during the stay at maximal pressure. Comparison between nitrogen and helium highlighted the narcotic effects of nitrogen at pressure. As a matter of fact, nitrogen induces a reduction in glutamate and in other amino acids that could partly explain the decrease in striatal dopamine level as well as the motor and cognitive disturbances reported in nitrogen narcosis.

Premature birth is a factor of increased blood pressure in adulthood. Little is known about the physiologic characteristics of the arterial bed in neonates. The aim of this study was to characterize in vivo the arterial compliance in neonates and its maturation profile in very low birth weight (VLBW) premature infants. A group of stable, VLBW premature infants was compared with a control group of near term neonates. The abdominal aortic wall distensibility coefficient (DC) and whole-body arterial compliance (WBAC) were determined using specifically designed noninvasive methods, based on ultrasonic measurements in combination with synchronous, beat-to-beat recording of aortic pulse pressure (PP). On the fifth day of life, WBAC and the CD were lower in VLBW premature infants than in controls. Furthermore, WBAC and the DC remained unchanged in VLBW premature infants 7 wk after birth. In conclusion, VLBW premature infants are characterized as early as the fifth day of life by high arterial stiffness, which persists when they reach their theoretical term. It can be speculated that early alteration of arterial elastic properties may pave the way for long-term elevation of arterial pressure in VLBW premature infants.

Objectives: To assess the relationship between the time period before hyperbaric oxygenation therapy (HBO) and clinical outcome in patients with iatrogenic cerebral air embolism. Design and setting: Retrospective study in a hyperbaric chamber and medical intensive care unit of a university hospital. Patients: All patients with air embolism from 1980 to 1999. Interventions: We retrieved the cases of 86 patients who benefited from an identical HBO and analyzed the relationship between the time period before HBO and clinical outcome. Results: Patients treated with HBO less than 6 h had a better outcome than those treated later. In patients treated within this delay the cause was venous air embolism in 84% and arterial air embolism in only 16% of cases. After this delay the cause was venous air embolism (53%) and arterial air embolism (47%). Patients with venous air embolism and recovery had a shorter delay than patients with sequelae or death (2 h 15 min vs. 4 h). Patients with venous air embolism treated less than 6 h had a better outcome than those treated later. In patients with arterial air embolism the time period before HBO was longer than in venous air embolism (8 h vs. 3 h) and the outcome worse (recovery in 35% vs. 67%). In patients with arterial air embolism no difference in the time period was found between patients with recovery and sequelae or death. Conclusions: We stress the beneficial effect of an early HBO in air embolism, the importance of an increased awareness of physicians concerned with this severe complication, and the need to develop techniques to detect air emboli in the cerebral circulation.

Objective: To evaluate the economic impact of a rational policy in antibiotic treatment. Design: Comparative study with a retrospective and a prospective part. Setting: An 11-bed intensive care unit (ICU) in a general hospital. Patients: All patients admitted to the unit in 1994, 1995 and 1996. Interventions: In 1995, a program of cost control was started and a contract of agreed objectives signed with the director of the hospital. This contract included a commitment to refund the eventual savings in order to improve the quality of care. Prescribing protocols were established by consensus as guidelines for a rational policy in antibiotic therapy. Measurements and results: The cost of antibiotic therapy, the patients' characteristics and the incidence of nosocomial infection were compared prior to and during the program. The expenses for antibiotic drugs decreased by 19 % in 1995 and by 22 % in 1996. Most of the savings were refunded to the ICU and contributed to the employment of an additional nurse and the purchase of new material. In number of patients, type of disease, mean age, Simplified Acute Physiology Score, occupancy rate, length of stay, omega score, artificial ventilation, readmission within 7 days, mortality and incidence of nosocomial infection, no significant difference was found. Conclusions: We proved a positive economic impact of a rational policy in antibiotic therapy realized with a contract of agreed objectives. The savings made while applying our program of cost control were used to improve the quality of care.

Patients in the intensive care unit (ICU) have many risks factors for gallbladder stasis or acute acalculous cholecystitis (ACC), including fasting, total parenteral nutrition, sedation, mechanical ventilation, infection and shock. We have performed a prospective study to estimate the prevalence of ultrasonographic gallbladder abnormalities in 30 consecutive medical ICU patients during the first 2 days of their stay in the ICU. Two patients had previously undergone cholecystectomy and were excluded from the study. Seventeen (61%) of the remaining 28 patients presented with gallbladder abnormalities. Considering three major criteria of ACC, 14 patients (50%) presented with either sludge (25%), wall thickening (22%) or hydrops (11%). However, none of the patients needed a surgical procedure during the study because of gallbladder disease. We conclude that an important proportion of ICU patients presented with gallbladder abnormalities shown by ultrasonography and that this may have implications for establishing a diagnosis of ACC using ultrasonographic criteria.

In our intensive care unit, the cost of the antibiotherapy is reduced in a 20 percent ratio, using a rational politic antibiotic usage.