SUMMARY. In cases of severe burning the pulmonary damage causing respiratory insufficiency may result from a double mechanism: direct toxic activity on bronchial and alveolar epithelium from the gases and fumes caused by combustion or by explosion; or indirect metabolic derangement induced by multiparenchymal failure resulting from the severe effect of heat on the tissues. In both cases the clinical picture is almost identical and coincides with the pattern of ARDS.
Dyspnoea, cyanosis, restlessness and severe hypoxaemia resistant to 02 treatment are the typical symptoms. Chest XR shows interstitial or interstitial-alveo tar diffuse oedema. Prevention is difficult and consists mainly of 02 administration, humidification of respiratory gases and prompt correction of the metabolic derangements.
As soon as clinical manifestation of respiratory failure becomes evident the patient must be immediately transfered to the I.C.U. where respiratory assistance is promptly adopted: PEEP and in less severe cases CPAP. If the hypoxaemia is associated with a significant reduction of current volume, endotracheal intubation and mechanical ventilation are needed.
In addition to the specific ventilatory assistance, all the measures to prevent the negative evolution of the metabolic derangements are fundamental. Particular attention must be paid to caloric and hydroelectrolyte balances and to monitoring of the kidney and heart functions.

Acute respiratory insufficiency is a fairly common occurrence in the severe burn patient. The clinical picture is comparable to that seen in the Adult Respiratory Distress Syndrome (ARDS). In most cases the pulmonary modifications are due to carbon monoxide poisoning and to grave lesions of the airways caused by inhalation of high-temperature irritant gas.
The airways are more frequently affected in victims who suffer burning in closed spaces. The extent of the damage to the airways is not directly related to the gravity of the skin lesions and in some cases it may become the greatest therapeutic problem in a gravely burned patient. The objective examination of the patient usually evidences burns to the face, particularly around the mouth and nostrils, oedema of the uvula and pharyngeal phlogosis. The patient may be aphonic, present laryngeal stridor and expectorate a very viscid mucus. Dyspnoea, expectorate containing soot, and rale and sibilus detected on chest auscultation are usually an indication of parenchymal damage.
Complete obstruction of the upper airways, mainly caused by oedema of the mucosae, may develop acutely. Even slight obstruction of the upper airways therefore justifies endotracheal intubation. If possible, tracheostomy should be avoided, as this may facilitate infection at pulmonary level, especially when the neck is burned.
Parenchymal damage, in contrast, develops slowly and insidiously. Normally, burn lesions are limited to the upper airways (pharynx, larynx, upper part of the trachea) and do not affect the pulmonary parenchyma, owing to the considerable cooling of inhaled gases that occurs in the upper airways and to the glottis closure reflex. Only the inhalation of vapour can cause burns as far as the most distal portions of the large bronchi.
The pathogenesis of ARDS is linked both to direct pulmonary damage due to the chemical irritation produced at alveolar level by the inhaled substances, which may contain high concentrations of aldehydes, ketones and organic acids, and to indirect damage caused by the metabolic and haernatological modifications induced by extensive skin burns. Another possible cause of not inconsiderable damage is the intensive fluid therapy adopted in such cases and associated infections. The end result is however the same: grave impairment of the integrity of the alveolocapillary membrane, caused by activation of the neutrophil leukocytes which effect their cyto'toxic action essentially by liberating oxygen free radicals in the extracellular space. The pulmonary lesion manifests itself with partial or total alveolar collapses, which cause a reduction of residual functional capacity and pulmonary compliance. This results in an increase of respiratory labour and the consequent appearance of a hypoxaemia which is refractory to oxygen administration, even in high concentrations. Prevention is difficult and consists mainly in the administration of oxygen, the humidification of inhaled gases and the rapid correction of any associated metabolic disturbances.
In the initial phase the patient's symptoms are unremarkable: a fine, mainly basal, rale, moderate hyperventilation, slight hypoxaemia associated with hypocapnia. Chest radiography is usually negative. Early recognition of these features and symptoms should make it possible to diagnose ARDS in its initial stages, when effective therapeutic measures can be adopted in time to reduce the gravity of the syndrome.
The latent period concludes with the onset of manifest acute respiratory insufficiency. The patient is agitated, dyspnoeic and cyanotic. Radiography reveals interstitial and alveolar oedema and blood gas analysis shows marked hypoxaemia and hypocapnia. At this point the patient has to be admitted to an Intensive Care Unit where immediate therapy must be given to maintain an adequate exchange of gases at pulmonary level.
The most effective technique is the application of the positive end expiration pressure (PEEP). The mechanism by which PEEP improves oxygenation is essentially linked to the increase in residual functional capacity (RFC) obtained both by increasing the volume of partially collapsed alveoli and by reopening totally collapsed alveoli. In this way the surface available for respiratory exchanges increases and Pa02 improves. The increase in RFC caused by PEEP also improves pulmonary compliance, which in turn leads to a reduction in respiratory labour.
In less serious cases the application of continuous positive airways pressure (CPAP) in spontaneous ventilation can prove to be very effective. This technique makes it possible to maintain spontaneous breathing, with lower pleural pressures than in mechanical ventilation; it also has the advantage of reducing negative haemodynamic effects. It can be applied using an endotracheal tube or an airtight face mask.
If spontaneous respiration is impossible, because of excessive rigidity of the pulmonary tissue or increased fatigue in the patient, mechanical ventilation becomes necessary. This will ensure, adequate alveolar ventilation and a PEEP that opposes the closing of the small airways and alveolar collapse.
If there is a predominantly , unilateral pneumonopathy or a bronchopleural fistula, separate ventilation of the lungs with two different eircuits'and ventilators, using a double-lumen endotracheal tube, can considerably improve gas exchanges. In this way it is possible to choose for each lung the tidal volume, the FiO 2 and the PEEP most appropriate for the type of pulmonary pathology.
When mechanical ventilation is not effective and does not provide sufficient oxygenation, it may be advisable to carry out extracorporeal elimination of C02 together with low frequency positive ventilation. This technique makes use of an iron lung (similar to that used in heart surgery with extracorporeal circulation); oxygenation is maintained by diffusion through the lungs ventilated at a rate of 3-4 acts per minute. The lungs are thus kept at rest until they have recovered, and they are spared the trauma caused by mechanical ventilation. The results obtained are very encouraging, but this technique requires adequate operating facilities and considerable staff resources.

RÉSUMÉ. Dans les brûlures graves le dommage pulmonaire qui cause l'insuffisance respiratoire peut être le résultat d'un double mécanisme: l'activité toxique directe sur l'épithélium bronchique et alvéolaire de part des gaz et des vapeurs causés par la combustion ou l'explosion; ou bien un dérangement métabolique indirect provoqué par l'insuffisance multiparenchymale qui dérive de la gravité de l'effet de la chaleur sur les tissus. En tous les deux cas le tableau clinique est presque identique et il c6incide avec celui du syndrome de l'insuffisance respiratoire aiguë. Les symptomes typiques sont: la dyspnée, la cyanose, l'agitation et l'hypoxémie grave résistante au traitement avec 02. La radiographie thoracique indique un oedème diffus interstitiel ou interstitiel-alvéolaire. La prévention est difficile et consiste principalement en l'administrations d'02, l'humidification des gaz respiratoires et la correction immédiate des dérangements métaboliques.
Dès que l'insuffisance respiratoire se manifeste cliniquement, il faut porter immédiatement le patient au Centre de Réanimation pour lui administrer une thérapie respiratoire: il PEEP (pression positive à fin de respiration), et dans les cas moins graves il CPAP (pression continuelle positive des voies aériennes). Si l'hypoxémie est accompagnée d'une réduction significative du volume courant, il faut effectuer l'intubation endotrachéale et la ventilation mécanique.
Non seulement la thérapie ventilatoire spécifique mais aussi toutes les mesures'pour prévenir l'évolution négative des dérangements métaboliques sont fondamentales. Il faut prêter une attention particulière aux équilibres caloriques et hydroélectrolytiques et au monitorage des fonctions rénales et cardiaques.