Voluntary reporting system in anaesthesia: is there a link between undesirable and critical events?

BACKGROUND: Reporting systems in anaesthesia have generally focused on critical events (including death) to trigger investigations of latent and active errors. The decrease in the rate of these critical events calls for a broader definition of significant anaesthetic events, such as hypotension and bradycardia, to monitor anaesthetic care. The association between merely undesirable events and critical events has not been established and needs to be investigated by voluntary reporting systems. OBJECTIVES: To establish whether undesirable anaesthetic events are correlated with critical events in anaesthetic voluntary reporting systems. METHODS: As part of a quality improvement project, a systematic reporting system was implemented for monitoring 32 events during elective surgery in our hospital in 1996. The events were classified according to severity (critical/undesirable) and nature (process/outcome) and control charts and logistic regression were used to analyse the data. RESULTS: During a period of 30 months 22% of the 6439 procedures were associated with anaesthetic events, 15% of which were critical and 31% process related. A strong association was found between critical outcome events and critical process events (OR 11.5 (95% confidence interval (CI) 4.4 to 27.8)), undesirable outcome events (OR 4.8 (95% CI 2.0 to 11.8)), and undesirable process events (OR 4.8 (95% CI 1.3 to 13.4)). For other classes of events, risk factors were related to the course of anaesthesia (duration, occurrence of other events) and included factors determined during the pre-anaesthetic visit (risk of haemorrhage, difficult intubation or allergic reaction). CONCLUSION: Undesirable events are associated with more severe events and with pre-anaesthetic risk factors. The way in which information on significant events can be used is discussed, including better use of preoperative information, reduction in the collection of redundant information, and more structured reporting.

[Infectious complications of implantable infusion ports in patients with HIV infection]. / Complications infectieuses des chambres implantables chez les patients VIH.

Thirty-four implantable ports were consecutively implanted in 27 AIDS patients (mean CD4 lymphocyte count: 39/mm3) from January 1993 to December 1995. We observed 33 complications in these patients. Perioperative complications included: one pneumothorax (3%), one haematothorax (3%) and one septic shock (3%). Later complications included one venous thrombosis (3%) and 26 infectious complications (79%). Fever of unknown origin was observed in three patients (9%). A total of 19 bacteremias occurred in 12 patients. The global rate of infection for 100 catheter-days was 0.51 for a total of 5,096 catheter-days. The following microorganisms were isolated: Staphylococcus (n = 21; 72%), Pseudomonas (n = 3; 11%) and others (n = 5; 17%). Thirty-eight percent of the ports (n = 13) were removed, after a mean of 89 days. During the study, 21 patients died. Two patients died from a catheter infection with septic shock (8%). It seems to be important to clearly define the indications of implantable infusions ports in AIDS patients with respect to their life expectancy.

[Effect of halothane on ventilation and arterial blood gases in rats with and without diaphragmatic paralysis]. / Effets de l'halothane sur la ventilation et les gaz du sang arteriel chez le rat avec ou sans paralysie diaphragmatique.

Some patients with diaphragmatic paralysis or dysfunction maintain ventilation by use of other muscles. Anaesthesia, in modifying the performance of these muscles, presents a potential risk to such patients. To evaluate this risk, the effects of halothane on ventilation and arterial blood gases were studied on a model of bilateral diaphragmatic paralysis, the phrenectomized rat. The study was performed on 43 rats. Success of phrenectomy was confirmed at laparotomy, which did not result in blood gas changes. Laparotomy was performed in 23 rats and a carotid artery was catheterized. In 11 control rats, phrenic nerves were exposed but not sectioned, and in 12 other rats, the phrenic nerves were sectioned. Ventilation was measured by plethysmography in awake rats before and after surgery and in the same rats anaesthetized with halothane 1.1%. In the 23 rats, a decrease in weight and core temperature was observed after operation and this was more marked in phrenectomized than in control rats. In the 11 control rats, ventilation increased postoperatively without change in blood gases. In these rats, halothane caused a decrease in minute ventilation and PaO2 and an increase in PaCO2. Phrenectomy in awake rats led to an increase in minute ventilation, hypoxaemia and hypercapnia. In these rats, halothane led to death in three and a decrease in minute ventilation, with hypercapnia and hypoxaemia in the nine other rats. Blood gas changes were greater than in anaesthetized controls. In the intact rat, halothane leads to blood gas changes comparable to those observed in other species and humans. The present study confirms the effects of halothane on respiratory muscles other than the diaphragm and demonstrates the severe respiratory risk of anaesthesia in patients whose ventilation is maintained by these muscles.

[The effects of halothane on the changes in PaCO2, acid-base equilibrium and ventilation induced by hypoxia in the rat]. / Effets de l'halothane sur les modifications de la PaCO2, de l'équilibre acido-basique et de la ventilation provoquées par l'hypoxie chez le rat.

The effects of progressive hypoxia, obtained by decreasing FIO2 from 0.21 to 0.12, on arterial blood gases and acid-base balance were studied in 13 awake rats and 13 rats anaesthetized with halothane (inspired concentration 1.1%). The effects on ventilation of the decrease in FIO2 from 0.21 to 0.12 were studied in eight rats, awake and then anaesthetized. Halothane causes a decrease in PaO2 and an increase in PaCO2; it abolishes the ventilatory response to hypoxia. The effects of hypoxia on PaCO2 were identical in awake and in anaesthetized rats. In the awake rats, PaO2 decreased from 90.3 +/- 5.9 mmHg to 42.3 +/- 3.6 mmHg, and PaCO2 decreased from 36.7 +/- 3.3 mmHg to 28.1 +/- 1.8 mmHg. In the anaesthetized rats, PaO2 decreased from 78.8 +/- 6.2 mmHg to 34.8 +/- 4.2 mmHg, and PaCO2 decreased from 40.7 +/- 2.8 mmHg to 31.9 +/- 3.7 mmHg. The decrease in PaCO2 during acute hypoxia in the anaesthetized rat could be explained by a decrease in CO2 production, secondary to a decrease in oxygen consumption due to the metabolic and circulatory effects of halothane and hypoxia.

[The effect of halothane on blood gases and arterial acid-base equilibrium in intact rats and in chemo-denervated rats]. / Effets de l'halothane sur les gaz du sang et l'équilibre acido-basique artériels chez le rat intact et chez le rat chémodénervé.

Halothane decreases the ventilatory response to hypoxia and the activity of peripheral arterial chemoreceptors, resulting in "chemical chemodenervation." In order to evaluate the role of this halothane-induced "chemical denervation" in acid-base and arterial blood gas changes, these values were measured in intact and chemodenervated rats, awake and under anaesthesia. Since the depth of anaesthesia could be modified by the anatomical chemodenervation, the ED50 of inspired halothane was determined in six rats before and after anatomical chemodenervation. To prevent haemodynamic changes due to halothane and/or anatomical chemodenervation from interfering with the results, systemic arterial blood pressure and heart rate were measured in six intact rats, awake and then anaesthetized, and in the same rats after chemodenervation, awake and then anaesthetized. In nine intact rats and in 19 chemodenervated rats, arterial pH, arterial bicarbonate concentration, and arterial blood gases (PaO2 and PaCO2) were measured before and after administration of halothane. Anatomical chemodenervation modified neither the inspired ED50 (1.1%), nor the mean arterial blood pressure or heart rate. The haemodynamic effects of halothane were comparable in intact and in chemodenervated rats. Changes in arterial blood gases and acid-base balance due to halothane in intact rats and due to chemodenervation in awake rats were not different, but there was a decrease in PaO2 and pHa, and an increase in PaCO2. In chemodenervated rats, halothane caused a further decrease in PaO2 and a further increase in PaCO2. The fact that halothane and anatomical chemodenervation have similar effects on arterial blood gases and acid-base balance favours a "chemical chemodenervating" action of halothane. However, the additional effects of halothane in the anatomically chemodenervated animal show that the action of halothane on blood gases and acid-base balance is the result of multiple sites of impact on the respiratory system.

[Respiratory effects of moderate hypothermia (36 degrees C-28 degrees C) in dogs under halothane anesthesia]. / Effets ventilatoires d'une hypothermie modérée (36 degrees C-28 degrees C) chez le chien anesthésie à l'halothane.

Changes in systemic haemodynamic variables (mean arterial pressure, MAP; heart rate, HR; cardiac output, Qc), in oxygen consumption, VO2, and in ventilation (minute ventilation, V; respiratory frequency, f; tidal volume, VT; and arterial blood gases) with particular attention to respiratory times (duration of inspiration, TI; duration of expiration, TE; duration of the breathing cycle, TTOT), to respiratory timing (TI/TTOT) and respiratory drive (VT/TI) were studied during moderate progressive hypothermia (36 degrees C to 28 degrees C) during stable halothane anaesthesia (MAC = 1.5) in six dogs. MAP, HR and Qc decreased; V and f decreased, the decrease in f being correlated with that in temperature (r = 0.66; P < 0.01). Tidal volume did not change. The PaO2 and pHa decreased while PaCO2 increased slightly. The decrease in ventilation was related to changes in respiratory times (TI and TE) which increased (TE more than TI) and in respiratory drive (VT/TI which decreased due to the increase in TI). The relation between VT/TI and TI/TTOT changes was not constant during cooling. Changes in respiratory times and drive could be due to the effect of cold on medullar respiratory control.

[The measurement of pH and gases in the blood using microanalysis: the effect of storage at 4 degrees C for an hour. A study in the rat]. / Mesure du pH et des gaz du sang sur des micro-echantillons: effets de la conservation à 4 degrees C pendant une heure. Etude chez le rat.

The effects of one hour storage at 4 degrees C on micro blood gas samples (150 microliters) were studied for a wide range of values (pH: 7.11-7.58; PCO2: 26-97 mmHg; PO2: 31-503 mmHg) in 20 rats with indwelling carotid artery catheters. Blood gas values were modified by varying the composition of inspired gases: normoxia, hypocapnic hypoxia, hyperoxia, hypercapnia (in this case eight animals were anaesthetized with halothane 1.1%). One hundred and eight double micro-samples were taken. For each double sample, one was analysed immediately (H0) and compared with the second sample after one hr storage at 4 degrees C (H1). The Bland and Altman method was used for the statistical analysis of results. After one hr storage at 4 degrees C, the PCO2 was slightly higher than at H0 (mean difference +/- SD: +1.08 +/- 1.7 mmHg) and arterial pH was slightly lower (mean difference +/- SD: -0.016 upH +/- 0.011 upH). These results show that for these two variables, in the range studied, one hour storage at 4 degrees C had little effect. In contrast, for arterial PO2 the mean difference between all measurements between H1 and H0 was -17 +/- 25 mmHg. If results lower than 200 mmHg (56 double samples) are considered separately, the mean difference between values at H1 and H0 was only -0.98 +/- 5.3 mmHg. For PaO2 greater than 200 mmHg (52 double samples), the mean difference was -34 +/- 26.3 mmHg; this may be due to low reproducibility of measurements of elevated PO2 levels and to the effects of cellular metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory effects of almitrine bismesilate in dogs breathing normoxic, hyperoxic and hypoxic mixtures.

The ventilatory effects of 1 mg.kg-1 i.v. almitrine were studied in five dogs anaesthetized with halothane 2% under conditions of normoxia, hyperoxia and hypoxia. Ventilation (minute ventilation, respiratory frequency, tidal volume, duration of inspiration and expiration, ratio TI/Ttot and VT/TI), Pao2, Paco2, pHa, systemic arterial pressure and heart rate were measured in air before and following almitrine; in air, after inhalation of pure oxygen and after almitrine in hyperoxia; in air, during hypoxia with Fio2 progressively decreased from 0.21 to 0.12 and after almitrine in hypoxia (FIO2 = 0.12). Halothane decreased ventilatory response to hypoxia. Almitrine stimulated ventilation irrespective of the level of oxygenation and restored the ventilatory response to hypoxia. Hyperoxia did not suppress ventilatory action of almitrine whose action is probably partly central. Hypoxia and almitrine did not induce major systemic haemodynamic modification.

[Respiratory effects of almitrine on various levels of the fraction of inspired oxygen. A study in the anesthetized dog]. / Effets ventilatoires de l'almitrine à différents niveaux de FIO2. Etude chez le chien anesthésié.

The effects of intravenous almitrine under normoxic, hyperoxic, and hypoxic conditions were studied in 5 male beagle dogs (mean weight 15.2 +/- 5 kg) anaesthetized with thiopentone. Plasma concentrations of thiopentone were maintained constant at 27-29 mg.1(-1). Each animal underwent twice the three different experiments, with a lapse of a fortnight between each experiment: a) breathing room air, with intravenous administration of 1 mg.kg-1 almitrine over 30 s, b) breathing room air, then pure oxygen for 15 min, followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing pure oxygen, and c) breathing room air, then progressively less oxygen (FIO2 0.18, 0.16, 0.14, 0.12 for 5 min each), followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing a mixture with 12% oxygen. Tidal volume, respiratory rate, minute ventilation, inspiratory and expiratory duration, arterial pH, PaO2 and PaCO2 were measured respectively in room air, after 100% oxygen, in hypoxia (FIO2 = 0.12), before, 5 and 10 min after the injection of almitrine. Hyperoxia depressed ventilation (-21%), whilst hypoxia stimulated it (+126%), although significantly less than in the awake animal. Almitrine restored the respiratory response to hypoxia, but hyperoxia did not suppress respiratory stimulation due to the drug. It would therefore seem likely that almitrine acts on peripheral arterial chemoreceptors, but also on other structures. The results of this study suggest that almitrine may be useful in restoring the respiratory response to hypoxia during recovery from anaesthesia.

[Report of a case of malignant vesical pheochromocytoma. Diagnosis and therapy]. / A propos d'une observation de phéochromocytome vésical malin. Conduite diagnostique et thérapeutique.

Bladder pheochromocytoma is a rare, usually benign bladder tumor. An exceptionally malignant bladder pheochromocytoma is reported with more than 5 years follow-up. The study of our case, and the review of 15 other cases reported in the literature show that surgery is the only effective therapy. Partial cystectomy with regional lymphadenectomy, when feasible is the treatment of choice. Because metastatic occurrence may be late, we emphasize the importance of long term follow-up.

Ventilatory effects of oxygen in the dog under thiopentone anaesthesia.

The ventilatory effects of prolonged oxygen administration were examined in seven dogs during thiopentone anaesthesia. Ventilation, tidal volume (VT), ventilatory rate (f), minute ventilation (VE), inspiratory time (TI), expiratory time (TE), period (Ttot), TI/Ttot and mean inspiratory flow (VT/TI) were measured during the inhalation of room air, after 30 min of oxygen inhalation, and finally after a return to breathing room air. Arterial blood-gas tensions were measured before and after 5, 10, 20 and 30 min of oxygen administration and 15 min after return to breathing room air. Oxygen administration produced an immediate, significant and persistent decrease in ventilation, principally from a decrease in ventilatory rate and changes in ventilatory times. This was in contrast to what occurred in awake animals. Modifications in ventilatory mechanics or suppression of an hypoxic stimulus to ventilation were probably not involved. Anaesthesia may modify centrally mediated ventilatory responses to hyperoxia.

The effects of cremophor EL in the anaesthetized dog.

The effects of cremophor EL were studied in 13 anaesthetized, paralyzed and ventilated dogs. Twenty per cent cremophor EL in a dose of 4.3 +/- 0.92 ml was infused at a rate of 30 ml X hr-1. In seven dogs, thoracopulmonary compliance, heart rate, systemic arterial pressure (SAP), pulmonary pressures (PAP, PCWP, RAP), cardiac output (CO) and platelet and white cell counts, were measured before the injection of cremophor EL, at the end of infusion and 5, 10, 30 and 150 minutes after the end of infusion. In six dogs, SAP, CO, and blood volume were measured before the injection of cremophor EL, at the end of infusion and 10, 30, 90 and 150 minutes after the end of infusion. Plasma histamine and catecholamines were assayed before the injection of cremophor EL and 2, 5, 10, 30, 90 and 150 minutes after starting the infusion. Cremophor EL induced a marked, sustained and significant decrease in SAP at the end of infusion and at 5, 10 and 30 minutes after the completion of the infusion (-68, -71, -70 and -43 per cent respectively), in PCWP, RAP and CO (-78 per cent at the end of infusion, -32 per cent 150 minutes after the end of infusion). Heart rate and systemic vascular resistance did not vary significantly. Pulmonary vascular resistance increased at the end of infusion, five and ten minutes after the end of infusion (+734, +548 and +439 per cent respectively). Plasma volume decreased 10 and 30 minutes after the end of infusion (-28 and -30.5 per cent respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

[Legionnaires' disease: 21 cases observed over 2.5 years in a Parisian respiratory intensive care unit]. / La maladie des légionnaires: 21 cas observés en 2 ans et demi dans une unité parisienne de soins intensifs respiratoires.

The incidence of Legionnaire's disease is probably underestimated in France. Its clinical presentation is very suggestive, especially after the failure of a 48 hour therapeutic trial of beta-lactams, when a pneumococcal infection is initially suspected. This one sign is sufficient to orient the diagnostic survey and constitutes an indication for a therapeutic trial of macrolides for at least 72 hours. In fact, the delay in the diagnosis appears to be the determinant factor in the fatal outcome of the disease.

[Acute non-cardiogenic pulmonary edema during resection of a bladder paraganglioma (pheochromocytoma)]. / Oedème aigu pulmonaire non cardiogénique (O.A.P.N.C.) au cours de la résection d'un paragangliome (phéochromocytome) vésical.

The onset of non-cardiogenic acute pulmonary oedema during resection of a vesical paraganglioma is reported. Such oedema may be caused by the intravascular injection of massive doses of catecholamines in the animal. Aetiopathogenic mechanisms are suggested on the basis of experimental data.