[Impact of a trauma network on mortality in patients with severe pelvic trauma]. / Impact de la mise en place d'un réseau de soins en traumatologie sur la mortalité des patients traumatisés graves du bassin.

AIM: To evaluate the impact of a regional trauma network on intra-hospital mortality rates of patients admitted with severe pelvic trauma. STUDY: Retrospective observational study. PATIENTS: Sixty-five trauma patients with serious pelvic fracture (pelvic abbreviated injury scale [AIS] score of 3 or more). METHODS: Demographic, physiologic and biological parameters were recorded. Observed mortality rates were compared to predicted mortality according to the Trauma Revised Injury Severity Score methodology adjusted by a case mix variation model. RESULTS: Twenty-nine patients were admitted in a level I trauma centre (reference centre) and 36 in level II trauma centres (centres with interventional radiology facility and/or neurosurgery). Patients from the level I trauma centre were more severely injured than those who were admitted at the level II trauma centres (Injury Severity Score [ISS]: 30 [13-75] vs 22 [9-59]; P<0.01). Time from trauma to hospital admission was also longer in level I trauma centre (115 [50-290] min vs 90 [28-240] min, P <0.01). Observed mortality rates (14%; 95% confidence interval, 95% CI, [1-26%]) were lower than the predicted mortality (29%; 95% CI [13-44%]) in the level I trauma centre. No difference in mortality rates was found in the level II trauma centres. CONCLUSION: The regional trauma network could screen the most severely injured patients with pelvic trauma to admit them at a level I trauma centre. The observed mortality of these patients was lower than the predicted mortality despite increased time from trauma to admission.

Accidental potassium dichromate poisoning. Toxicokinetics of chromium by ICP-MS-CRC in biological fluids and in hair.

Intoxications by chromium (Cr) compounds are very life threatening and often lethal. After oral ingestion of 2 or 3g of hexavalent Cr (Cr(VI)), gastrointestinal injury, but also hepatic and renal failure, often occurs which each leads to a fatal outcome in most patients. Cellular toxicity is associated with mitochondrial and lysosomal injury by biologically Cr(VI) reactive intermediates and reactive oxygen species. After Cr(VI) has been absorbed, there is not much that can be done except to control the main complications as the treatment is only symptomatic. The biotransformation of Cr(VI) to Cr(III) reduces the toxicity because the trivalent form does not cross cellular membranes as rapidly. In fact, more than 80% of Cr(VI) is cleared in urine as Cr(III). We report the case of a 58-year-old male patient who was admitted to hospital after accidental oral ingestion of a 30 g/L potassium dichromate (the estimated amount of ingested Cr is about 3g). ICP-MS equipped with a collision/reaction cell (CRC) and validated methods were used to monitor plasma (P), red blood cells (RBCs), urine (U) and hair chromium. For urine the results were expressed per gram of creatinine. After 7 days in the intensive care unit, the patient was discharged without renal or liver failure. P, RBC and U were monitored during 49 days. During this period Cr decreased respectively from 2088 µg/L to 5 µg/L, 631 µg/L to 129 µg/L and 3512 µg/g to 10 µg/g. The half-life was much shorter in P than in RBC as the poison was more quickly cleared from the P than from the RBC, suggesting a cellular trapping of the metal. Hair was collected 2 months after the intoxication. We report a very rare case of survival after accidental Cr poisoning which has an extremely poor prognosis and usually leads to rapid death. For the first time, this toxicokinetic study highlights a sequestration of chromium in the RBC and probably in all the cells.

Beneficial effects of helium:oxygen versus air:oxygen noninvasive pressure support in patients with decompensated chronic obstructive pulmonary disease.

OBJECTIVE: To test the hypothesis that, in decompensated chronic obstructive pulmonary disease (COPD), noninvasive pressure support ventilation using 70:30 helium:oxygen instead of 70:30 air:oxygen could reduce dyspnea and improve ventilatory variables, gas exchange, and hemodynamic tolerance. DESIGN: Prospective, randomized, crossover study. SETTING: Medical intensive care unit, university tertiary care center. PATIENTS: Nineteen patients with severe COPD (forced 1-sec expiratory volume of 0.83+/-0.3 l) hospitalized in the intensive care unit for noninvasive pressure support ventilation after initial stabilization with noninvasive pressure support for no more than 24 hrs after intensive care unit admission. INTERVENTIONS: Noninvasive pressure support ventilation was administered in the following randomized crossover design: a) 45 min with air:oxygen or helium:oxygen; b) no ventilation for 45 min; and c) 45 min with air:oxygen or helium:oxygen. MEASUREMENTS AND MAIN RESULTS: Air:oxygen and helium:oxygen decreased respiratory rate and increased tidal volume and minute ventilation. Helium:oxygen decreased inspiratory time. Both gases increased total respiratory cycle time and decreased the inspiratory/total time ratio, the reduction in the latter being significantly greater with helium:oxygen. Peak inspiratory flow rate increased more with helium:oxygen. PaO2 increased with both gases, whereas PaCO2 decreased more with helium:oxygen (values shown are mean+/-SD) (52+/-6 torr [6.9+/-0.8 kPa] vs. 55+/-8 torr [7.3+/-1.1 kPa] and 48+/-6 torr [6.4+/-0.8 kPa] vs. 54+/-7 torr [7.2+/-0.9 kPa] for air:oxygen and helium:oxygen, respectively; p<.05). When hypercapnia was severe (PaCO2 >56 torr [7.5 kPa]), PaCO2 decreased by > or =7.5 torr (1 kPa) in six of seven patients with helium:oxygen and in four of seven patients with air:oxygen (p<.01). Dyspnea score (Borg scale) decreased more with helium:oxygen than with air:oxygen (3.7+/-1.6 vs. 4.5+/-1.4 and 2.8+/-1.6 vs. 4.6+/-1.5 for air:oxygen and helium:oxygen, respectively; p<.05). Mean arterial blood pressure decreased with air:oxygen (76+/-12 vs. 82+/-14 mm Hg; p<.05) but remained unchanged with helium:oxygen. CONCLUSION: In decompensated COPD patients, noninvasive pressure support ventilation with helium:oxygen reduced dyspnea and PaCO2 more than air:oxygen, modified respiratory cycle times, and did not modify systemic blood pressure. These effects could prove beneficial in COPD patients with severe acute respiratory failure and might reduce the need for endotracheal intubation.

Calibration of seven ICU ventilators for mechanical ventilation with helium-oxygen mixtures.

The study evaluated seven intensive care unit (ICU) ventilators (Veolar FT, Galileo, Evita 2, Evita 4, Servo 900C, Servo 300, Nellcor Puritan Bennett 7200 Series) with helium-oxygen (HeO2), using a lung model, to develop correction factors for the safe use of HeO2. A 70:28 helium-O2 mixture (heliox) replaced air and combined with O2 (HeO2). Theoretical impact of HeO2 on inspiratory valves and gas mixing was computed. True fraction of inspired oxygen (FIO2del) was compared with fraction of inspired oxygen (FIO2) set on the ventilator (FIO2set). True tidal volume (VTdel) was compared with VT set on the ventilator (VTset) in volume control and with control VTdel at FIO2 1.0 in pressure control. FIO2del minimally exceeded FIO2set ( FIO2set by 125%). In volume control, with the Veolar FT, Galileo, Evita 2, and Servo 900C, VTdel > VTset, with the 7200 Series VTdel < VTset (linear relationship, magnitude of discrepancy inversely related to FIO2set). With the Evita 4, VTdel > VTset (nonlinear relationship), whereas with the Servo 300 VTdel = VTset. In pressure control, VTdel was identical to control measurements, except with the 7200 Series (ventilator malfunction). Correction factors were developed that can be applied to most ventilators.

[Severe acute buflomedil poisoning]. / Intoxication aigué grave au buflomédil.

The severity of the acute intoxication from buflomedil, a vasodilator with papaverinic and alpha-adrenolytic effects, remains generally underestimated. We report the case of a 18-year-old girl who ingested a high amount of buflomedil. Two hours later, she developed seizures and ventricular arrhythmias. On admission to the ICU, she was in circulatory arrest followed by deep coma with mydriasis (GCS = 3). Buflomedil blood concentration, 2 hours after admission, was 97.3 mg.L-1. Toxicological screening for other drugs was negative. Therapy included external chest compressions tracheal intubation, mechanical ventilation, epinephrine and gastric lavage. The haemodynamic status improved within the first 24 h, although she remained comatose until the fifth day. She was discharged the eight day after her admission. This observation demonstrates that the potential severity of buflomedil poisoning is mainly due to early cardiac complications. Treatment remains purely supportive.

[Aneurysm of the gastroduodenal artery ruptured into the peritoneum. Treatment by embolization]. / Anévrysme de l'artère gastro-duodénale rompu en péritoine libre. Traitement par embolisation.

Aneurysms rarely occur in the gastroduodenal artery. We encountered such an aneurysm which bled into the peritoneum leading to a difficult diagnostic situation. A 58-year-old man was hospitalized for acute abdominal pain. Past history included alcohol intake (wine, 3/4 litre per day) and moderate increase in serum gamma-glutamyl transferase levels (100 IU/L). At admission there was abdominal contracture, vomiting and shock (blood pressure 70 mmHg). Based on the clinical picture and laboratory tests the diagnosis of acute pancreatitis was entertained, but after the haemodynamic situation was reestablished by intravenous fluids, echography and computed tomography of the abdomen failed to give confirmation. An effusion however was seen in the peritoneum together with a large mass in the head of the pancreas compatible with a haematoma. Arteriography rapidly demonstrated an aneurysm of the gastroduodenal artery. Embolization was preferred over surgery due to the precarious haemodynamic situation. Outcome was quite favourable and no complications have been observed with a follow-up of 6 months. Reports of true aneurysms of the gastroduodenal artery are rare but clinical manifestations are usually latent or absent. Reported complications include massive digestive haemorrhage and rarely jaundice, haemobilia or wirsungorrhagia due to compression. Excepting recognized trauma, few aetiological factors have been determined. Fragile arterial walls due to atheroma, isolated dysplasia or connective tissue disease appear to be damaged by successive systolic distension leading to rupture of certain elements of the arterial wall and finally aneurysm. Embolization carries less risk than surgical repair but must be indicated only after precise characterization including localization, size and local involvement.