Intermittent positive pressure ventilation in the treatment of severe crushing injuries of the chest.

Maintenance of metabolism during intensive patient care

“…Equally, however, attempts to ventilate the hypovolaemic subject nearly always lead to systemic hypotension, impaired renal function, and further metabolic problems. The importance of maintaining metabolism and particularly the hydration of such patients has been stressed elsewhere (Ambiavagar et al, 1966;Ambiavagar & Jones, 1967;Riding, 1967). If adequate oxygenation is preserved, then the resultant additional metabolic complications of tissue hypoxia are avoided, and metabolic acidosis is prevented.…”

Treatment of respiratory failure following chest injuries

“…In a thoughtful review of the subject, Harley (1961) concluded that mechanical, haemodynamic and neurogenic factors caused increased bronchial secretions with a reduced ability to expel them, increased the permeability of alveolar capillaries and disturbed the ventilation-perfusion ratio of the lungs. The evidence leading to these conclusions is somewhat fragmentary but the main point I wish to make is that 'traumatic wet lung' was not seen during IPPV (Ambiavagar et al, 1966), and Griffiths (1960) observed that two of his patients who died during treatment with IPPV showed no evidence of wet lung at autopsy. One patient we treated was admitted 48 hr after he had sustained fractures of five right ribs in a traffic accident.…”

“…In conclusion, it must be pointed out, a large number of patients with minor chest trauma never go into respiratory failure, but it is seldom possible to predict with certainty which patients will. It is known that patients with concomitant head injuries (Schrire, 1962), slowly developing haemothorax (D'Abreu, 1965) and pre-existing lung disease (Ambiavagar et al, 1966) are particularly liable to this fate following minor chest trauma.…”

“…But death steps in suddenly, peacefully, naturally and unnecessarily.' Respiratory failure following a chest injury is a good example of a reversible breakdown in the mechanisms of breathing and if this vital function can be adequately substituted for a short period, complete recovery can be expected (Ambiavagar et al, 1966). Particular emphasis will therefore be placed on describing these relatively obscure processes in terms of currently acceptable concepts of respiratory failure.…”

“…The complex disturbances of physiology are due to interference with: (1) the bellows action of the chest wall because of loss of rigidity and uniformity, and reflex splinting due to pain; (2) 'alveolarcapillary block' from pulmonary oedema; (3) diffuse reversible 'airways obstruction' (Ciba Foundation Symposium, 1959) from retained bronchial secretions; (4) atelectasis (Pasteur, 1914) and lung infections; and (5) perfusion of unventilated areas of contused lung (Ambiavagar et al, 1966).…”