Search

Two cases of fatal lightning injury are described. Fixed dilated pupils should not be taken as an indicator of death after a lightning strike. Persons who fail to breath spontaneously within one minute of lightning shock should receive external cardiac massage and mouth-to-mouth resuscitation. Paralysis may persist as result of cerebral oedema or prolonged hypoxia—it is therefore suggested that adequate ventilation and metabolic balance should be maintained until recovery or death.

Drowning remains one of the three leading causes of accidental death in the world, yet few textbooks deal with its evaluation and treatment. Because of overemphasis placed upon distinguishing between fresh- and sea-water drowning, the importance of immediate attention to simple and effective resuscitative procedures has been bypassed. We have outlined a continuum of evaluation and treatment in four stages: (1) emergency care at the scene and during transportation, (2) hospital admission resuscitation, (3) intensive care, and (4) return to normal. Four representative cases are presented in order to review pathophysiological concepts in this serious problem.

Experience gained with a wide variety of missile injuries of the brain is presented. Clinical signs and intracranial pressure (ICP) studied in the early post-injury period have been correlated with survival and treatment. Stress is laid on fluid requirements and the importance of controlled ventilation in the management of the labile clinical condition of such patients. Coughing and struggling caused extrusion of blood and brain from the wound, and this was reduced considerably with endotracheal intubation and mechanical ventilation. Post-operatively high ICP could be controlled in potential survivors with continued ventilation.

The results of mechanical ventilation for severe hyaline membrane disease (HMD), and the changes in technique which took place, during the 6-year period 1967-72 are described. A pilot study of the effect of hydrocortisone among the most severely affected infants showed no benefit. After the introduction at the beginning of 1970 of a regimen for ventilating the infants at low peak airway pressures, slow respiratory frequencies, and high inspiration: expiration ratios, there was a sudden increase in survival rate which was largely accounted for by a reduction in the incidence of bronchopulmonary dysplasia. Evidence is presented that in infants with HMD mechanical factors are more important than oxygen toxicity in the pathogenesis of this condition.

The objectives of this study were to test the hypothesis in awake dogs that during control conditions endocardial vessels are maximally dilated and to determine whether variables introduced by general anesthesia and thoracotomy modify distribution of myocardial blood flow or impair capacity for augmentation of flow in response to a coronary vasodilator stimulus. Myocardial blood flow was measured in relatively small, 2-3 g, left ventricular epicardial and endocardial samples by using 7-10-mum radioisotope-labeled microspheres during control conditions and during infusion of adenosine in dosages which produced maximum increases in coronary blood flow. Measurements were made initially in awake resting animals and were repeated after pentobarbital anesthesia, thoracotomy, and pericardiotomy. Blood flow (mean+/-SEM) in the epicardium and endocardium, respectively, was 0.75+/-0.06 and 0.83+/-0.06 during control conditions and 4.98+/-0.28 and 4.49+/-0.27 cm(3)/min/g during adenosine. These data demonstrate considerable capacity for vasodilation in both myocardial layers and thus refute the hypothesis that endocardial vessels are maximally dilated during control conditions. During control conditions blood flow within epicardial and endocardial layers was essentially homogeneous around the circumference of the left ventricle. In contrast to previous studies in anesthetized animals, however, transmural gradients were present in most regions, i.e., endocardium: epicardium ratio (endo/epi) 1.06-1.16. During adenosine, circumferential epicardial flows were homogeneous; however, circumferential endocardial flows were inhomogeneous and increased less than epicardial flows, endo/epi 0.81-0.99.Anesthesia, thoracotomy, and pericardiotomy increased epicardial and endocardial flow, mean values 1.08+/-0.10 and 1.11+/-0.08 cm(3)/min/g, respectively. Transmural gradients remained in only papillary muscle regions. Adenosine increased epicardial flow comparably before and after anesthesia. Although adenosine increased endocardial flow three- to fourfold after anesthesia, the increase was considerably less than epicardial flow, i.e., endo/epi 0.63-0.78.

Recent correspondence in the British Medical Journall-4 has discussed the need for oxygen-failure devices and the philosophy of their design, so we shall not repeat this discussion here. Briefly, however, we think that very occasional oxygen failures are inevitable, during both anaesthesia and artificial ventilation with oxygen. Because the danger is so remote any safety device that is to gain the wide acceptance that is essential if it is to be of any value must be both cheap and reliable. Oxygen failures

Ninety-one infants with respiratory failure secondary to primary pulmonary disease and with a birth weight of 1000 g. or over have been managed in a negative-pressure respirator (Air-Shields) over a three-year period. Of these the failure in 87 was due to respiratory distress syndrome (RDS) and in four it resulted from massive meconium aspiration. Respiratory failure was indicated initially by arterial blood gas tensions (while breathing 100% O(2)) of Po(2)40 mm. Hg, pH7.10 and Pco(2)75 mm. Hg in the initial 47 cases; these levels were subsequently raised to Po(2)50 mm. Hg, pH7.20 and Pco(2)70 mm. Hg for the remainder. Fifty-four (59.3%) of the infants survived the use of the respirator and 47 of these (51.6%) were subsequently discharged alive and well. Mean time in hours to normalization of blood gas values while on the respirator were as follows: for Po(2), 10.5; for pH, 11.6; and for Pco(2), 22.6. These values indicate that the respirator is more efficient in promoting oxygenation (raising Po(2)) than ventilation (lowering Pco(2)). They also suggest that the observed acidosis is in large part secondary to the hypoxia rather than the result of co(2) retention. For the survivors the average time of total respirator dependency before commencement of weaning was 53.7 hours. All the infants were managed without the use of endotracheal tubes although the use of the respirator and/or administration of 100% oxygen were either continuous or intermittent for periods of up to two weeks. There have been no instances of so-called respirator lung disease in the survivors or in those who died, which suggests that the use of high oxygen concentration by itself is not the major factor in the pathogenesis of this complication.

A retrospective clinicopathological study was carried out on newborn babies who had died over a 5-year period, had received oxygen therapy, and had lived for 48 hours or longer. 23 of 81 babies had pulmonary fibroplasia at necropsy. Prolonged therapy in oxygen concentrations above 60% and prolonged artificial ventilation were associated with the development of pulmonary fibroplasia. All babies developing pulmonary fibroplasia had been treated in over 60% oxygen for at least 46 hours and the condition was invariably present in those who had over 60% oxygen for more than 123 hours or above 80% oxygen for more than 105 hours. The relation of pulmonary fibroplasia to mechanical ventilation was less constant. Hyaline membrane disease was associated with the development of fibroplasia in babies who lived for 3 days or longer, and the most severe histological changes were almost always associated with HMD. There was no correlation between gestational age and development of pulmonary fibroplasia. It is concluded that oxygen toxicity was probably the most important cause of pulmonary fibroplasia in the babies studied, though some histological features may be more closely related to artificial ventilation. The implications of these findings for oxygen and ventilator therapy in the newborn are discussed.

1. Arterial blood samples were obtained from anaesthetized dogs in which either a respiratory alkalaemia, a respiratory acidaemia or a non-respiratory acidaemia was produced and from animals in which no deliberate changes in acid—base balance were produced. The samples were analysed for pH, carbon dioxide tension and concentration, oxygen tension and concentration and haematocrit. From these determinations the plasma carbon dioxide concentration, the plasma bicarbonate ion concentration and pK′ were calculated. 2. The value of pK′ lay within the range 5·86-6·27. The temperatures of the animals studied were between 36·75 and 39·25° C but there was no significant relationship between pK′ and temperature. 3. The values of pK′ increased with an alkalaemia and decreased with an acidaemia. 4. In addition to the variation of pK′ with pH there was a considerable residual scatter of pK′ values at any one pH value. 5. It was concluded that in these experimental conditions the use of the Henderson—Hasselbalch equation in a form not dealing with activities was unacceptable and could lead to much larger errors than has hitherto been thought.

International audience

International audience

The results of a series of porcine orthotopic liver homotransplants have shown that hepatic damage is related almost entirely to the period of warm ischaemia following death. Low flow perfusion with modified plasma would seem to be a satisfactory method of preserving cadaveric livers for at least six hours. In man it would appear possible to use cadaver livers derived from patients who had or had not been treated with artificial ventilation during life, provided the period of warm ischaemia is not longer than 25 to 30 minutes.