الفهرس 
Pulmonary Responses to Smoke InhalationOnly 14 pages are availabe for public view
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Abstract
The real cause of approximately 80 percent of deaths following thermal trauma caused by fire is
not the burn itself, but the inhalation of products of combustion of different materials. These
products cause hypoxia and exert a toxic chemical effect upon the respiratory tract with
subsequent development of adult respiratory distress syndrome (ARDS). ARDS is a leading cause of
death in burned patients with concomitant inhalation injury.
Major histophysiologic fmdings in these patients include deposition of fibrin casts in the airways
and progressive carbon dioxide retention secondary to a ball-valve effect. Recent studies suggest
that the lung lesions result from the action of free oxygen radicals (FOR) released from the
polymorphonuclear leukocytes (PNL) marginating in the pulmonary microcirculation and tracheo
bronchial region. Peroxide and hydroxyl ions have been implicated as mediators in the increased
microvascular permeability and consequently pulmonary edema seen in inhalation injury. Conventional
therapies, directed at the reduction of arterial C02,
maintenance of airway patency and adequate oxygenation are
associated with barotrauma related complications and often are unsuccessful. So, it appears
reasonable that a treatment regimen that reduces the number of FOR and inhibits fibrin cast
formation would be beneficial in the management of such patients.
Multiple experimental studies were undertaken to evaluate the role of the FOR scavengers in
the management of cases of
inhalation injury. Several authors (Kimura et aL, 1988; Brown et aL, 1988; ... etc) had got
significant improvement in the outcome of the treated animals insufflated with smoke. Desai et a/.
(1998), using also the same regimen on burned children suffering from concomitant inhalation
injury, had the same significant successful results. So, we followed the same regimen in a trial to
improve our results. This study was conducted on 43 patients, thirteen of them served as a control
group (receiving only the conventional therapy) while 30 patients received the suggested therapy of
the antioxidant combined with an agent which dissolves the fibrin casts (bisolvon or heparin). This
group was divided into two subdivisions. The first one is group B 1 which includes eleven patients,
they received the antioxidant in a continuous intravenous infusion route (as an early trial of our
study) and group B2 which includes 19 patients who received the antioxidant via the nebulized route
combined with heparin. We used four variables to study and evaluate the effectiveness of each
route. These are the analysis of arterial blood gases, the post-treatment fiberoptic bronchoscopy,
the serum peroxide level, and the mortality rate. Tracheobronchial lesions in each group were
graded, according to a grading system introduced by the author with the aid of the bronchoscope,
into four grades. Grade I lesions shows erythema, edema and petechial hemorrhage while in grade II
injury, in addition to the findings of grade I, there is ulceration of the mucosa, blisters and
sooting. More severe signs seen in grade ill injury were mucosal sloughing, and bronchiolar
obstruction by mucosal plugs and shedded epithelium. The severest injury, in the form of charring
and hemorrhage seen in grade IV.
The results of the control group (A) was disappointing as regards the parameters used for
evaluation, i.e. the mortality rate was 84.6o/o with the wor ening of arterial blood gases
and the
picture of bronchoscopy following treatment. While the results of the patients who received
the FOR scavenger and bisolvon by the intravenous infusion route were more satisfactory.
There was significant improvement in the arterial blood gas analysis (ABO), the fmdings
of the second bronchoscopy, with lowering of the serum peroxide level and lowering
of mortality rate (36.4%). However, on qualitative analysis of these results, it was found
that the patients suffering from severe degree of injury (grade III) were not ideal candidates
of such route of therapy. The mortality rate in such patients was 100% without improvement in
the bronchoscopic lesions detected (and even worsening of their tracheobronchial mucosal
signs). Those patients were in need of direct agent going, without any dilutional effect
exerted by the cardiac output, to the target tissues of the respiratory tract. So, we shifted
(in the second part of our study) to the nebulized therapy with the addition of nebulized
heparin to the antioxidant used. These nebulized agents succeeded in improving our previous
results of the group of patients suffering from third degree inhalation injury. The
mortality rate decreased from 100% to 80% taking into account that the commonest
cause of death was the multiorgan failure syndrome rather than the ARDS or respiratmy
failure. this means that the inhalation injury was not the actual cause of death as those
patients who suffered from concomitant extensive cutaneous burn died of secondary effects
of burn toxins and -multiple activated in:flarrunatory cascades. In addition to the
improved survival rate, the other parameters studied were also changed indicating improvement in
the lung function, tissue perfusion and the local bronchoscopic signs of injury. Furthermore,
there was significant improvement of patients having grade I and II inhalation injury as regards
the whole study variables used including the mortality rate.
from the present study, it is concluded that the combined regimen of the nebulized FOR scavenger
and heparin are effective therapy in treating the cases of inhalation injwy (whatever the grade
is). This is so long as the cutaneous burn is dealt with properly and promptly preventing the
perpetuating effect of burn toxins (from the cutaneous burn) upon the already cytokine loaded
lWlgs.