Delayed traumatic right diaphragmatic rupture.
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Biomedical subjects
Publications and source records attributed to Jacques Duranteau.
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BACKGROUND: Simultaneous pancreas-kidney (SPK) transplantation is an effective treatment for patients suffering from type 1 diabetes mellitus. Conventional immunosuppressive treatments include steroids that may induce insulin resistance and are responsible for many side effects. In de novo SPK, early withdrawal of corticosteroids may be an important issue. METHODS: A total of 24 consecutive patients with type 1 diabetes mellitus had been treated by SPK transplantation. All of them had a short induction therapy with anti-thymoglobulin (ATG) and steroids for only 4 days, association with CellCept and tacrolimus. The rate of acute rejection, graft and patient survival and side effects have been analysed. RESULTS: Patient and kidney survival was 100% and the pancreas survival was 95.6% at 1 year. The rate of acute rejection of kidney and pancreas was 4.2% and 8.3% at 6 months, respectively. The mean serum creatinine was 98.9+/-19.6 micromol/l and the mean HbA1c concentration was 5.1%+/-0.5% at 6 months. Only four patients developed a cytomegalovirus primo-infection, associated in one case with pneumonia, whereas 75% of patients developed a bacterial infection. Because of the occurrence of leucopenia and/or diarrhoea, CellCept has been dramatically decreased in 33% of cases and required the re-introduction of steroids. CONCLUSION: A short induction with ATG and steroids associated with a chronic therapy with CellCept and tacrolimus is safe and efficient in preventing acute renal rejection in SPK.
Hemorrhagic shock generates a prolonged alteration of organ perfusion due to the decrease in oxygen delivery. Hemorrhagic shock is mainly due to three etiologies: traumatology, gastrointestinal bleeding and high risk surgery. If intensive cares are not rapidly performed, severe complications occur, as organ failure with a high mortality rate. Primary cares aim at restoring a perfusion pressure to prevent tissue hypoperfusion while waiting for the radical therapy of bleeding. Priority during initial treatment is to restore tissue perfusion and achieve haemostasis in vital functions. Fluid resuscitation and transfusion are common to every case of hemorrhagic shock but the strategy to localise the hemorrhage and stop the bleeding differs between the situations. Key factors in the management of hemorrhagic shock are the communication between surgical, anaesthetic, and critical care teams and the application of pathology.
The aim of this study was to describe, in rats, brain energy metabolites changes after different levels of head trauma (T) complicated by hypoxia-hypotension (HH). Male Sprague Dawley rats (n = 7 per groups) were subjected to T by impact-acceleration with 450-g weight drop from 1.50 or 1.80 m (T 1.50 or T 1.80), or to a 15-min period of HH (controlled hemorrhage to mean arterial pressure [MAP] of 40 mm Hg, and mechanical ventilation with N(2) 90%/O(2) 10%), or to their association (T followed by HH). Invasive MAP, intraparenchymental intracranial pressure (ICP), and cerebral blood flow (CBF using Laser Doppler flowmetry) were recorded during the 5 post-traumatic hours. Cerebral microdialysis was used to measure each hour interstitial brain glucose, lactate, pyruvate, and glutamate. For the entire period, the levels of cerebral glucose, pyruvate, and glutamate were not statistically different between groups. In addition, there were no differences associated with the lactate-glucose ratio. Lactate was significantly higher overtime only in T 1.80 + HH group (p < 0.001 vs. every other groups). The lactate-pyruvate ratio increased with trauma level, and was significantly different vs. sham for the entire study period in T 1.50 + HH, in T 1.80, and in T 1.80 + HH. There was no correlation between CBF variations and the lactate-pyruvate ratio (r(2) = 0.00001). The cerebral perfusion pressure was greater than 70 mm Hg in all groups. The prolonged post-traumatic impairment in brain energy metabolism may be related to traumatic brain injury (TBI) severity. It became worse when T was complicated by HH, but was not related to changes in CBF.
OBJECTIVE: Circulatory shock results in hypoxia/reoxygenation processes that lead to the release of reactive oxygen species, endothelial injury, and multiple organ failure. Previous data suggest that beta2-adrenergic agonists prevent endothelial dysfunction. The study aimed at determining whether the beta2-adrenergic agonist formoterol protects endothelial cells against hypoxia/reoxygenation injury in vitro. DESIGN: Prospective controlled trial. SETTING: University hospital research laboratory. SUBJECTS: Cultured human umbilical vein endothelial cells (HUVECs). INTERVENTIONS: Confluent HUVECs were sealed in a flow-through chamber mounted on an inverted microscope and perfused with a constant flow of Krebs medium. After 1 hr of equilibration, HUVECs underwent 2 hrs of hypoxia and 1 hr of reoxygenation. Cell death at the end of reoxygenation and reactive oxygen species formation were assessed with fluorescent probes propidium iodide and 2',7'-dichlorodihydrofluorescein diacetate, respectively. The effects of the beta2-adrenergic agonist formoterol, the beta2-adrenergic antagonist ICI 118,551 and the nitric oxide synthase inhibitor L-NNA were investigated. Statistical analysis was performed with analysis of variance followed by post hoc Fisher's test. MEASUREMENTS AND MAIN RESULTS: Hypoxia/reoxygenation increased cell death (hypoxia/reoxygenation 29 +/- 4% vs. control 1 +/- 5%, p < .05) and endothelial reactive oxygen species production (hypoxia/reoxygenation 126 +/- 4% vs. control 108 +/- 4%, p < .05). Formoterol reduced cell death in a concentration-dependent manner (EC95 = 10 mol/L) and reduced endothelial reactive oxygen species production (hypoxia/reoxygenation + formoterol EC95 109 +/- 4% vs. hypoxia/reoxygenation 126 +/- 4%, p < .05). When added to formoterol EC95, ICI 118,551 and L-NNA abolished the formoterol-induced cell protection and reduced reactive oxygen species production. CONCLUSIONS: These results indicate that formoterol reduces endothelial cell death and reactive oxygen species production in this in vitro hypoxia/reoxygenation model. These effects are beta2-adrenergic specific and are partially mediated by nitric oxide synthase.
OBJECTIVE: The effects of vasopressin, norepinephrine, and L-arginine alone or combined on intestinal microcirculation were evaluated in the septic mouse by intravital microscopy, with which we measured the erythrocyte flux and velocity in villus tip arterioles and the density of perfused villi. DESIGN: Controlled animal study. SETTING: University research laboratory. SUBJECTS: Female BALB/c mice weighing between 18 and 21 g. INTERVENTIONS: Anesthetized and ventilated mice received at t0 an intravenous injection of Escherichia coli endotoxin (2 mg/kg bolus intravenously), inducing after 1 hr (t60) a decrease in mean arterial blood pressure to 40-50 mm Hg associated with a significant decrease in erythrocyte flux and velocity in villus tip arterioles and in the density of perfused villi. The mice then received a randomly different treatment for endotoxin-induced shock. Treatments consisted in continuous intravenous infusion for 1 hr with either saline (control group), norepinephrine, vasopressin, L-arginine, vasopressin+L-arginine, or norepinephrine+L-arginine. The doses of vasopressors (used alone or combined with L-arginine) were titrated to restore mean arterial pressure to the baseline level. MEASUREMENTS AND MAIN RESULTS: At the end of the treatment (t120), we observed in the control group further decreases in arteriolar flux and velocity and in the density of perfused villi. In the groups treated by a vasopressor alone, mean arterial pressure returned to baseline and there were no additional decreases in arteriolar flux and velocity or in the density of perfused villi. However, these latter three variables did not return to their preshock baseline values. Even though L-arginine did not restore mean arterial pressure, the infusion of L-arginine alone prevented the decrease in flux or erythrocyte velocity occurring between t60 and t120 and conserved to some extent the density of perfused villi compared with that in the control groups. In addition, we found that simultaneous administration of norepinephrine or vasopressin with L-arginine improved all microcirculation variables more efficiently than either vasopressor alone. CONCLUSIONS: From these data, we conclude that a) restoring mean arterial pressure after 1 hr of endotoxemia was not sufficient to restore ad integrum intestinal mucosa microvascular perfusion; b) L-arginine could have a beneficial effect at the microcirculatory level, which was independent of mean arterial pressure; and c) administration of L-arginine combined with the maintenance of perfusion pressure by vasopressive drugs allowed a better preservation of intestinal microcirculation at an early stage of endotoxemia.
The incidence of hemostatic abnormalities in the early hours after traumatic incident is high and represents an independent predictor of mortality. Key factors in the development of traumatic coagulopathy include the severity of injury, hypothermia, acidosis, hemorrhagic shock, hemodilution, clotting factor consumption, and fibrinolysis. Assessment of bleeding includes evaluation of the mechanism of injury, vital signs, biochemistry, detection of external and internal bleeding sources, injuries found upon secondary investigation, and response to treatment. Priority in treating the bleeding trauma patient should be given to prevention of further bleeding, hypothermia, acidosis, coagulopathy, and maintenance of tissue oxygenation, achieved by careful physical handling, damage control surgery, analgesia, maintenance of normothermia, correction of coagulopathy, control of blood pH, and serum calcium. Priority during initial treatment is to restore tissue perfusion and achieve hemostasis in vital functions; other nonvital procedures may generally be delayed. This state-of-the-art review aims to address key issues in acute control of bleeding in the trauma patient.
In this article we describe the current use of recombinant activated factor VII (rFVIIa; NovoSeven) in trauma patients. Emphasis is placed on current uses as defined by key studies, efficacy data, and safety data. Most published studies in trauma patients are retrospective case studies and reports, although an international, double-blind, randomized, controlled, phase II study has been conducted that reported on the efficacy of rFVIIa in reducing the amount of blood products transfused in blunt trauma patients. That study demonstrated the efficacy and safety profile of this hemostatic agent as compared with placebo as adjunctive therapy in the management of severe bleeding associated with trauma. Further prospective, randomized, and placebo-controlled clinical trials will yield more information on the role of rFVIIa in the management of traumatic bleeding.
OBJECTIVE: Shock induces oxidative stress by ischemia-reperfusion phenomenon. Endothelial cells are involved in the inflammatory response and oxidative stress responsible for microcirculation impairment and organ failure. We examined the potential of serum from patients to induce in vitro reactive oxygen species production by cultured human umbilical vein endothelial cells (HUVECs). PATIENTS: Three groups were compared: hemorrhagic shock trauma patients, isolated brain injured patients, and healthy volunteers. METHODS: In the hemorrhagic shock group we sought a correlation between reactive oxygen species production and severity of shock. Serum was separated and perfused in an in vitro model of perfused HUVECs. Ex vivo reactive oxygen species production was assessed by fluorescence microscopy using dichlorodihydrofluorescein, an intracellular dye oxidized by H2O2. Results are expressed in proportional change from baseline and normalized by protidemia to control for variation related to hemodilution. RESULTS: Reactive oxygen species production by endothelial cells exposed to serum from hemorrhagic shock patients (46.2+/-24.9%) was significantly greater than in those with brain injury (3.9+/-35.1%) and in healthy volunteers (-6.8+/-5.8%). In the hemorrhagic shock group dichlorodihydrofluorescein fluorescence was strongly correlated positively to Simplified Acute Physiology Score II and lactatemia and negatively to [HCO3-]. CONCLUSIONS: Serum from trauma patients with hemorrhagic shock induces reactive oxygen species formation in naive endothelial cells which is correlated to shock severity.
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BACKGROUND: Left ventricular ejection time (LVET) measured in central arteries is modified during hypovolemia. We compared modifications of the pulse wave in a central artery (carotid) and in a peripheral artery (digital) during central hypovolemia induced by lower body negative pressure (LBNP) in conscious volunteers. METHODS: Hypovolemia was simulated with progressive LBNP (baseline, -10, -20, and -30 mm Hg) in nine young healthy volunteers. The carotid arterial pressure waveform was recorded using a Millar tonometric method. The digital pulse wave was measured with a volume-clamp method (Finapres) and the stroke volume with a thoracic impedance method (Biomed). RESULTS: Mean arterial pressure did not change during LBNP. Compared with baseline values, heart rate increased significantly at the -30 mm Hg level (68 +/- 13 beats/min vs. 59 +/- 11 beats/min), and stroke volume decreased as soon as -10 mm Hg was achieved (113 +/- 41 mL vs. 127 +/- 35 mL). Both carotid and digital LVET decreased significantly at the -10 mm Hg level (337 +/- 26 and 339 +/- 24 ms vs. 360 +/- 35 and 361 +/- 24 ms, respectively). CONCLUSION: Peripheral LVET could reflect variation of central LVET during LBNP and be a reliable noninvasive parameter for monitoring hypovolemia.
PURPOSE: To expand the pool of suitable organ donors we developed an organ procurement program of non-heartbeating donors during the last 15 years. We compare graft survival in patients receiving renal transplants procured from non-heartbeating with recipients of kidneys from heartbeating donors. MATERIALS AND METHODS: From 1986 to 1999, 60 renal transplantations were performed with kidneys harvested from non-heartbeating donors (Mastrich category IV). Kidneys were procured using a double balloon triple lumen catheter inserted into the femoral artery. The 60 kidneys were selected from 70 non-heartbeating donors based on age younger than 50 years, warm ischemia less than 30 minutes, creatinine less than 200 micromol./l., and no hypertension or major histological lesions. Long-term results of graft survival and complications were compared with a series of 1,065 renal transplantations performed during the same period with kidneys procured from heartbeating donors. RESULTS: Mean age of the recipients was statistically different as non-heartbeating donors were older. However, the 10-year graft survival rates were similar in both groups (50% versus 53%). Incidence of ureteral stenosis and fistula, arterial stenosis and thrombosis was not statistically different in both groups. On the other hand, delay graft function was more frequent in non-heartbeating donors (60% versus 40%, p = 0.01). CONCLUSIONS: Despite a high rate of acute tubular necrosis, kidneys harvested from non-heartbeating donors had the same graft survival rates as those procured from heartbeating donors. Surgical complications were not different. Transplantation of selected kidneys procured from non-heartbeating donors should be promoted as a response to organ shortage.
INTRODUCTION: The cold ischaemia time of a kidney before transplantation has a negative impact on the risk of acute tubular necrosis and graft survival. This cold ischaemia time can be reduced by a different organization of harvesting, organ distribution and transplantation. MATERIAL AND METHODS: Seventy nine organ donor case files from the same hospital were reviewed from reception of the donor until transplantation. 135 renal transplantations, including 60 kidneys and 14 kidney-pancreas transplants were performed on site with organs harvested from these donors. The various phases of harvesting were studied: reception and resuscitation of the patient took 30 hours, and the diagnosis of brain death, information of the families and transfer of the donor to the operating room for harvesting took 11 hours. RESULTS: The mean cold ischaemia time was 6 hours when kidney-pancreas transplantation was performed and 22 hours 30 minutes for isolated local renal transplantation. The decisive factor is the time required to obtain HLA typing, which is only performed during organ harvesting for isolated renal transplantation. HLA typing and lymph node sampling in the intensive care unit would save 7 hours. CONCLUSION: The authors recommend that HLA typing and lymph node sampling for cross matches be performed in the intensive care unit in order to reduce the cold ischaemia time.
OBJECTIVES: To evaluate the effect of an early dobutamine infusion on gastrointestinal perfusion in patients with severe sepsis. DESIGN: Prospective, randomized, controlled, multicenter clinical study. SETTING: Six medical and/or surgical intensive care units (ICU) of teaching hospitals. PATIENTS: Forty-two patients with severe sepsis. INTERVENTIONS: Patients were divided into two groups according to gastric-to-arterial CO2 gap (DeltaCO2) [normal DeltaCO2 group ( n=17): DeltaCO2 < or = 8 mmHg; increased DeltaCO2 group ( n=25): DeltaCO2 > 8 mmHg]. Patients within each group were then randomized to receive either dobutamine (5 microg/kg per min) or saline for 72 h. MEASUREMENTS AND MAIN RESULTS: SAPS II was similar in both groups [group 1: 44.0 (33.0-56.5); group 2: 48.5 (40.5-59.0), p=0.27]. At ICU admission, mean arterial pressure was lower in the high DeltaCO2 group [73.0 (67.0-79.5) mmHg, p=0.03] than in the normal DeltaCO2 group [84.0 (73.7-104.0) mmHg] while blood lactate [normal DeltaCO2 group: 1.6 (0.8-2.3); high DeltaCO2 group: 1.6 (1.1-1.9) mmol/l] was similar for the two groups. DeltaCO2 was significantly lower in the normal DeltaCO2 group [5.0 (2.0-6.0) mmHg)] than in the high DeltaCO2 group [11.0 (10.0-19.0) mmHg]. Dobutamine infusion did not significantly change hemodynamics, blood lactate concentration or tonometric parameters in any group within the first 72 h and had no particular beneficial effect in this population. CONCLUSIONS: An early infusion of dobutamine at a fixed dose of 5 microg/kg per min during the first 72 h of severe sepsis does not influence gastric DeltaCO2.
UNLABELLED: The rules of organ allocation allow one of the two kidneys harvested to be transplanted locally while the other is exchanged. This rule of local priority does not exist in all countries. The purpose of this article is to determine whether this rule provides a benefit for the patient. 804 locally harvested kidneys were compared to 1196 exchanged kidneys transplanted between 1970 and 2000 by the same renal transplantation team. RESULTS: The cold ischaemia time was shorter (-6 h), the number of cases of HLA identity was lower (-0.8), the rate of acute tubular necrosis was lower (-9), and the median graft survival of was 7 months longer for local kidneys. DISCUSSION: An article analysing the North American register reached similar conclusions: the local attribution rule reduces the cold ischaemia and the graft loss at one year. CONCLUSION: The local attribution rule has the advantage of increasing the organ harvesting rate from borderline donors, reducing the cold ischaemia, and improving the results: this rule should therefore be maintained.