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An original recording and exploiting data programme has been built. It is in Basic language for Apple II. The data programme allows the care of obstetric peridural analgesic records. The medical interest is the record edition which is possible when the patient comes back. The scientific interest is statistics produced quickly from a great number of records. The record, record edition and statistical edition are described.

The choice of anesthesia is discussed in connection with a serie of 38 women cardiac and pregnant cared from 1976 to 1979, 32 of them having delivered a child. Peridural analgesia improves the labour and the delivery without inconveniene for either mother of child, but general anesthesia must be prefered for cesarean section. Anticoagulant therapy is a contra-indication for peridural analgesia.

Four intensive care beds for open heart surgery have been equipped with a computer aided monitoring system following J. W. Kirklin and L. L. Sheppard (University of Alabama). Choice and motivations are discussed and material and programs are briefly discussed in this paper.

Twenty-seven patients, four of whom had presented with a crisis of malignant hyperthermia and the 23 other being close relatives of such patients, underwent a muscle biopsy so as to determine their susceptibility to malignant hyperthermia. Halothane-caffeine contracture tests, interpreted in accordance with the criteria of the European Group on Malignant Hyperthermia, yielded the following results: 13 positive (MHS), 10 negative (MHN), 4 equivocal (MHE). The history, clinical examination, CPK level, histoenzymatic morphology and electron microscopic study did not provide information sensitive enough to use for the detection of susceptibility to malignant hyperthermia. This confirmed the literature: the halothane-caffeine contracture test remains the only reliable diagnostic test to detect this susceptibility, despite the search for non invasive tests. If the mechanism of triggering a contracture to increasing doses of caffeine is well known in normal muscle, it is the smaller concentrations required which suggests malignant hyperthermia abnormality. The halothane effect is less well understood. A concentration less than or equal to 2 vol % yields a contracture only in MHS muscle. Differences in protocols used by American authors emphasize the importance of standardization as used by the European Group, which is the only way of collecting and comparing results on well over a thousand patients. This confrontation should reduce the number of equivocal diagnoses and allow a correct classification of patients at risk or their relatives as MHS or MHN.

Two patients presenting an unsettled mitral cardiopathy had to receive a valve replacement under cardiopulmonary by-pass in spite of a circulating anticoagulant with antiprothrombinase activity. A higher risk of thromboembolic trouble required an increase of heparin administration, under a strict biological control. Nevertheless both patients died: the first of coronary thrombosis, the second of cataclysmic bleeding, associated to severe and diffused thrombosis. Thus it is essential to insist upon the risk occurred by those patients and the difficulty of adaptation and control of heparin administration.

Calcium blockers (CB) are routinely used. This could lead to possible interference with anaesthetic drugs. CB prevent calcium from entering the cell by inhibiting the slow voltage-dependent calcium channels. They act mostly on heart and smooth muscle. Of all the possible indications, the three that are confirmed are coronary heart disease, arterial hypertension and supraventricular rhythm disturbances. Most of the work published and the cases reported concerns interactions between CB and halogenated anaesthetic agents; the latter's actions on the heart depend on cellular calcium exchange. Also, the cardiovascular effects of these anaesthetics are similar to that of CB. Experimentally, halothane and enflurane have direct cardiac inhibitory effects similar to verapamil and diltiazem, whereas isoflurane's properties seem closer to the dihydropyridines (nifedipine and nicardipine). Giving verapamil or diltiazem increases the number of sino-atrial and atrio-ventricular blocks when using a halogenated agent. Clinically, interpreting the effects of CB during anaesthetic induction is difficult because of the pathology (coronary heart disease, cardiac failure), the other drugs (beta-blockers and nitrates) and the type of anaesthesia (emergency or elective). Interactions can give rise to anything from a severe cardiovascular collapse, requiring catecholamines, to a mild fall in blood pressure which responds well to plasma expansion, or even no effect on blood pressure. Rebound is seen on stopping CB in patients with coronary heart disease or arterial hypertension; stopping them before surgery does not therefore seem justified. However, extreme care must be taken when using halogenated agents for patients under treatment with CB and/or beta-blockers. A wary anaesthetist will be able to adapt the technique to the patient. It has been suggested that CB could be used to treat preoperatively myocardial ischaemia (diltiazem), hypertensive crises (nifedipine, nicardipine) and ventricular rhythm disturbances (verapamil); this must be done with caution, the patient being closely monitored (haemodynamic and electrocardiographic monitoring). Postoperatively, intranasal nifedipine, continuous intravenous nicardipine or diltiazem have been used to treat increases in arterial blood pressure during recovery and to adapt the cardiovascular system to the increased metabolic needs. Here again, close patient monitoring is essential. In any case, treatment with CB which has been stopped should be started up again as soon as possible.

Writing about a case of post-operative diaphragmatic bilateral palsy (bilateral thoracotomies for oesocoloplasty and oesophagectomy necessited by a caustic oesophagitis) on a 8 years old boy, palsy which was cured 6 months after, the authors tell about causes, prognostic and treatment of diaphragmatic palsies. In that observation, treatment consisted essentially in artificial ventilation for months and a half, and on intensive kinesitherapy.

Sixty-two suspected crises of anaesthetic malignant hyperthermia (MH) were collected between 1969 and 1988 by a retrospective inquiry which lasted four years. 33 patients (53%) died whilst 29 survived. 20 cases were confirmed to be MH, either directly or indirectly by way of muscle biopsy and halothane and caffeine contracture tests carried out according to the European MH group protocol by two laboratories. This group included 11 of the deaths, one family member of whom, at least, is sensitive (MHS), 7 MHS survivors and 2 survivors too young to undergo muscle biopsy but belonging to MHS families. 21 cases were highly suspect of MH: 15 of the deaths which occurred in a typical way, and 6 patients of three different families who have suffered from anaesthetic deaths which, clinically, suggested MH. Another 15 were possible MH cases, all survivors, including one case of Steinert's disease and a brother of a case of central core disease. 2 cases were still being debated, because they had equivocal results for the caffeine test (MHEc); the last 4 had negative muscle biopsies and were excluded. 33 close relatives of the MH patients were diagnosed as MHS. 44 others were found to be free from the genetic predisposition. It was strongly recommended to yet 11 others that they carry the MHS card because they were MHEc. The clinical, surgical and anesthetic pictures were always as described in the literature. The anaesthetic protocols included inhalational agents in 90% of cases; these were combined with suxamethonium in 55% of cases. Dantrolene was only used in 32% of cases, and then at inadequate doses and very often too late; this probably explains the large number of treatment failures. The number of severe forms of MH was also very high in this series (70%). The need to increase the means of prevention and screening for MH in France is stressed.

The ideal screening test for malignant hyperthermia susceptibility (MHS) has yet to be discovered. It should be simple noninvasive, yet totally specific and sensitive. Until such an ideal test becomes available, allowing simple routine preoperative screening, tests should only be used in certain specific situations. These include: patients in whom a clinical crisis was suspected; the members of the family of a subject labeled MHS because of a fatal, or otherwise, crisis, or in whom tests were positive; patients with other pathological conditions which could be linked to malignant hyperthermia (MH) (some myopathies, effort or stress MH, neuroleptic malignant syndrome). The various tests proposed in the literature aim at revealing MHN subjects, using or not a triggering agent, halothane most often. However, detecting these abnormalities sometimes gives greater insight into the physiopathology of MH than in the detection of an individual patient's susceptibility. The tests have been classified as in vivo, electrophysiological, blood, and in vitro muscle biochemical, morphological, and pharmacological tests. The discovery of new tests gives renewed hope: CPK levels, platelet tests, calcium sarcoplasmic reticular reuptake, lymphocyte Quin 2 test, nuclear magnetic resonance spectroscopy. However, experts worldwide agree that the only reference test to this day remains the in vitro halothane caffeine contracture tests. These tests have shown their reliability; they must be performed on muscle strips obtained from surgically removed muscle biopsies, by laboratories used to this technique and who have at their disposal a sufficiently large group of MHS subjects with a clear-cut clinical crisis, as well as controls. The patients must therefore travel to these laboratories. The design of common protocols for European laboratories on one hand, and the North American laboratories on the other, is a good guarantee of the reliability of these tests.

The authors analysed a series of 400 aorto-coronary bypasses performed between 1970 and April 1978. A notable improvement in the statistics was seen during the second period between 1976 and April 1978. During this period, 248 patients were operated upon with a mortality of 4 per cent. The progress made was in large part attributed to improved preoperative assessment, in particular a complete ventricular assessment, improved peroperative myocardial protection and the use of the intra-aortic counter-pressure balloon and of sodium nitroprussiate.

The authors report the case of a 57-year old woman who was susceptible to malignant hyperthermia (MH) and also had central core disease (CCD) of muscle. The latter was asymptomatic and was discovered when muscle biopsy was performed for in vitro tests of susceptibility to malignant hyperthermia. This case was compared with the 117 cases of CCD and 33 cases of CCD associated with MH published in the literature. Anaesthesia-induced MH is lethal in 80 per cent of the cases without treatment and in 20 per cent with treatment. CCD and MH are both transmitted as autosomal dominant traits. Susceptibility to MH is a functional abnormality of unknown mechanism. CCD is a disease of muscle fibre structure. One may hope that molecular studies and genetic probes will show whether or not these two diseases are transmitted by genes that are similar but distinct and independent.

A moderate controlled hypotension has been performed with isoflurane in the presence of nimodipine (4 mg.h-1) on ten patients anesthetized for cerebral aneurysm clipping. The administration of both drugs induced a dose-dependent hypotension secondary to the reduction of the systemic vascular resistance without impairment of cardiac index. Nimodipine did not modify the cardiovascular effects of isoflurane. It is concluded that intravenous administration of nimodipine should be continued during the operative period.

The child with a severe head injury requires a three component's treatment: against cerebral edema, against restlessness and vegetative trouble, against shock in case of scalp-hemorrage or attendant traumatism. As there is no agreement neither about the treatment of cerebral edema nor that of sedative treatment, we continue to use systematically artificial ventilation, sometimes corticoids, rarely mannitol. Decerebration is treated by a lytic coktail enclosing always diazepam and in case of failure, sodium gamma-hydroxybutyrate.