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RESPIRATORY TRACT DAMAGE IN BURNS: PATHOPHYSIOLOGY AND THERAPY *
Author(s) -
Zikria Bashir A.,
Sturner William Q.,
Astarjian Nubar K.,
Fox Charles L.,
Ferrer Jose M.
Publication year - 1968
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1968.tb14714.x
Subject(s) - medicine , respiratory tract , atelectasis , respiratory system , anesthesia , pulmonary edema , pathophysiology , lung
Summary (1) Of the 27 burn fatalities with respiratory tract involvement, this internal damage was the primary cause of death in 20 cases. (2) The edema and sodium contents in the lungs become maximal in 12 to 48 hr following the burn. (3) The surface tension in the lungs is abnormally elevated in respiratory burns and may be one of the causes of nonobstructive atelectasis. (4) The venous clotting time becomes depressed in the acute phase of respiratory burn and returns to normal in 24 hr. (5) Lymph drainage into the left thoracic duct vestibule decreases during the acute phase of the burn in the dog. (6) In the acute phase of the burn, the respiratory insufficiency is secondary to edema and to patchy atelectasis which can be reduced by automatic positive pressure respiration. (7) Infection of pulmonary and tracheobronchial tree plays a major role after 48 hr and early antibiotic coverage may help to control it.