October - LRS Institute of Tuberculosis & Respiratory Diseases

REVIEW ARTICLE Ind, .J. Tub., 1986, 33, 155
ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)
D.D.S. KULPATI*
ARDS represents a final common pathway
of injury due to a variety of massive, often
unrelated insults to the lungs, resulting in
respiratory distress, decreased pulmonary
compliance and severe arterial hypoxaemia
along with acute diffuse infiltrative lung lesions.
It is a form of acute respiratory failure with
noncardiogenic pulmonary oedema (Fein et al,
1982; Petty and Fowlder, 1982; Rinaldo and
Rogers., 1982: Tranbaugh and Lewis, 1982;
Bernard and Brigham, 1985).
The awareness of Adult Respiratory
Distress Syndrome can be traced to World
War II but the magnitude and nature was
appreciated in Vietnam War. Soldiers with
nonthoracic injuries were treated and sent
to regional hospital where during convalescence
unexpectedly life threatening respiratory distress
occurred. Lungs seemed to be full of water.
It was called ‘wet lung’, ‘shock lung’ or ‘Da-
Nang lung’ - the site of hospital in Vietnam.
Various synonyms (Wilson and Bone, 1979)
for ARDS are given in Table I.
The term was coined (Ashbaugh et al, 1967)
due to clinico-pathologic similarities with
infantile respiratory distress syndrome (1RDS).
However, in infants, the alveoli are small,
the chest wall is highly compliant, distending
pressure at the end of expiration is small and
these combined with lack of decrease in surface
tension at the alveolo-capillary membrane leads
to atelectasis which is characteristic of IRDS,
while, in ARDS, diffuse injury to pulmonary
capillary membrane leads to increased permeability
and pulmonary edema. The surfactant
deficiencies are secondary to diffuse lung
injury in ARDS in contrast to a deficiency
of surfactant as primary eticlogy in IRDS.
Similar clinical profile of ARDS may result
from different specific conditions which may
require specific diagnostic and therapeutic
measures. Thus, this term may obscure clinically
important differential diagnosis with serious,
therapeutic implications. Therefore, specific
etiologic conditions should always be retained
with this diagnosis. The term ARDS emphasises
the respiratory element of the syndrome
but conceals the fact that there is extensive
damage throughout the body (Wallace and
Spence, 1983).
Etiology : ARDS occurs following a variety
of catastrophic events which represent risk
factors (Table II). These include shock,
overwhelming in feet ions, trauma, aspiration
and damage due to various drugs and. physiochemical
agents. More and more specific
entities are being recognized to be associated
with ARDS, Some risk factor for the development of
ARDS are more lik ely to produce the syndrome
than other. A recent study suggested that sepsis
syndromeu results in development of ARDS
in 36 % whereas less than 1%, of patients
undergoing cardiopulmonary bypass, develop
ARDS (Demling. 1980; Modig, 1980; Pope et al,
1983).
Pathogenesis : Different noxious
stimuliproduce uniformly diffuse damage to
alveolo-capillary membrane. Damage to either
alveolar or capillary surface of this membrane
can produce ARDS (Fig.I ) Diffuse alveolar
injury i.e. to alveolar lining cell, type I alveolar
cell results from contact with toxins like gasses
hydrocarbons or gastric acid. Diffuse capillary
endothelial injury is probably the commonest
mechanism of ARDS. Implicated humoral and
cellular mechanisms of capillary endo-thelial
injury are :
4. Others : Serotonin, bradykinin,histamine,
B-endorphin, complement, platelets, free
fatty acids.
5. Direct injury :Gastric acid, hyperoxia
toxins
Neutrophil injury
Thu polymorphonuclear neutrophil, by
producing potentially toxic ,edoators of injury,
plays a central role in the enesis of certain forms
of ARDS. Fowler et al (1983) and Fowler et al
(1983) demostrated large numbers of
*Professor and Head, Department of Medicine and Respirators
Associated LNJPN and G.B. Hant Hospital, New Delhi-110002.
Unit Maulana Azad Medical College,