ARDS (adult respiratory distress syndrome) Disease
Table Of Contents:
? Alternative names
? Causes, incidence, and risk factors
? Prognosis / Mortality
? Signs and tests
? Calling your health care provider
stiff lung; shock lung; pump lung; acute respiratory distress syndrome;
Adult (acute) respiratory distress syndrome (ARDS) is the rapid onset
of progressive malfunction of the lungs, especially with regard to
the ability to take in oxygen, usually associated with the malfunction
of other organs. The condition is associated with extensive pulmonary
inflammation and small blood vessel injury in all affected organs.
ARDS has a fatality rate of approximately 50% despite supportive therapy,
including assisted respiration. It is difficult to estimate the incidence
of ARDS because it is often associated with other severe illnesses. But
it is a common problem in hospital intensive care units. The incidence
of ARDS has been difficult to determine, due partly to the variety of
causes. Various published estimates have ranged from 1.5 to 71 cases
per 100,000 population. Other figures suggest the occurrence of 13,000
to 27,000 cases annually.
Pathophysiology ARDS is the end result of acute alveolar injury caused by
a variety of insults and probably initiated by different mechanisms. The
initial injury is to either the capillary endothelium or alveolar
epithelium. There is increased capillary permeability, Organization and
scarring follows. The capillary defect is produced by an interaction
of inflammatory cells and mediators, including leukocytes, cytokines,
oxygen radicals, complement and arachidonate metabolites, that damages the
endothelium and allows fluid and proteins to leak. Endotoxin, neutrophils
and macrophages may also play key roles in the pathogenesis of ARDS.
ARDS results from widespread acute injury to the alveolar capillary
membrane. This produces high permeability edema, visible on the chest
x-ray. It also inhibits surfactant function (especially fibrin monomers).
Epithelial injury also impairs new surfactant synthesis. Inflammation
may exacerbate the injury because of release of oxidants and lysosomal
enzymes from activated leukocytes. Lung compliance (delta V) / (delta
P) is decreased because many airspace?s contain edema (and hence cannot
accept air) and because abnormally high surface tension counteracts the
negative intrapleural pressure.
Causes, incidence, and risk factors: ARDS is a medical emergency. It may
be caused by a variety of conditions that directly or indirectly cause
the blood vessels to “leak” fluid into the lungs. The ability of the
lungs to expand is severely decreased and damage to the air sacs and
lining (endothelium) of the lung is extensive. Blood concentration of
oxygen remains very low in spite of high concentrations of supplemental
oxygen given to the patient. Systemic causes of lung injury include
trauma, head injury, shock, sepsis, multiple blood transfusions,
and medications. Pulmonary causes include pulmonary embolism, severe
pneumonia, smoke inhalation, radiation, high altitude, near drowning,
and more. Symptoms usually develop within 24 to 48 hours of the injury
or illness. Cigarette smoking may be a risk factor. The incidence is 1
out of 100,000 people.
ARDS is commonly precipitated by trauma, sepsis (systemic infection),
diffuse pneumonia and shock. It may be associated with extensive surgery,
and certain blood abnormalities. Less common causes include drowning
and inhalation of toxic gases. In half the cases, onset occurs within
24 hours of the original illness or injury; in nearly all, it occurs
within three days.
Prognosis / Mortality The death rate estimates a range from 30-70%
Although survivors usually recover normal lung function, some
individuals may suffer permanent lung damage, which can range from mild to
severe. Recent data suggests that on average more than 40 percent die from
ARDS. This data accounts for direct deaths resulting from not recovering
from ARDS. The data does not account for deaths among survivors which
may be causally related due to medical conditions arising or effected
by the encounter with ARDS.
Since ARDS was first described in 1967, the prognosis has
improved slightly despite rapid advancements in medical science and
technology. Statistical data reveals that approximately one half of
who develop ARDS each year will survive in the United States and other
countries which have well trained medical personnel and facilities for
treating ARDS patients.
Younger people and those who have fewer chronic health problems are more
likely to recover. It is known that people with a milder form of ARDS
tend to have a better chance of recovering than those with a more severe
form of the illness. It is also known that the cause of a patient’s
ARDS helps predict that patient’s chances for survival. For example,
patients who develop ARDS due to sepsis usually do not do as well as
patients whose ARDS is related to trauma. Finally, those patients who
do survive after developing ARDS usually improve over several months
with a return to normal or near normal lung function.
? No measures to prevent ARDS are presently known.
? labored, rapid breathing
? nasal flaring
? cyanosis blue skin, lips, and nails caused by lack of oxygen to the tissues
? breathing difficulty
? anxiety, stress, and tension
Additional symptoms that may be associated with this disease:
? joint stiffness
? joint pain
? breathing, absent temporarily
Signs and tests:
? Chest auscultation (examination with a stethoscope) reveals abnormal breath sounds.
Tests used in the diagnosis of ARDS include:
? chest X-ray
? arterial blood gas
? The objective of treatment is to provide compensation for the severe
dysfunction of the respiratory system and treat the underlying cause of
the lung injury.
? Oxygen is used to treat hypoxia, often at high concentrations (100%
oxygen concentration may be needed).
? Intubation, passing a tube through the nose or the mouth into the
trachea (airway), is often necessary. Mechanical ventilation or a
respirator (a machine used to aid the breathing) is usually necessary for
further support of the respiratory system. This treatment is continued
until gradual weaning from the mechanism is tolerated.
? Medications may be indicated to treat infections, reduce inflammation,
and eliminate fluid within the lungs.
? The stress of illness can often be helped by joining support groups
where members share common experiences and problems. See lung disease -
Treatment for ARDS consists of mechanical ventilation along with
fluid removal and a supportive breathing technique called positive end
expiratory pressure (PEEP). These are combined with continuing treatment
of the precipitating illness or injury. There are many experimental
therapies that show promise for the treatment of ARDS. These include
replacement surfactant and the use of anti-inflammatory agents.
? multiple organ system failures
Calling your health care provider:
? If breathing difficulty or other symptoms of ARDS develop call the
local emergency number (such as 999) or go to the emergency room.
injuries that have in common the activation of the complement system.
? The first well-described cause of ARDS was traumatic shock sustained
after non-thoracic injury (shock lung).
? ARDS is a clinical syndrome characterized by the sudden onset of severe
shortness of breath, tachycardia, and profound hypoxia refractory to
oxygen therapy. Some degree of pulmonary edema is present on chest X-ray.
? Common causes of ARDS include: septic shock, traumatic shock, diffuse
viral pneumonia?s, oxygen therapy toxicity, inhaled toxins and irritants,
narcotic overdose, hypersensitivity reactions to organic solvents,
cardiac surgery with an extracorporeal pump and aspiration pneumonitis.
? The currently accepted pathogenesis of ARDS begins with the
release of mediators (like complement C5a, platelet activating factor,
leukotriene B4) into the blood that result in leukocyte aggregation in
the lungs. Stimulated neutrophils release oxygen free radicals, lysosomal
enzymes and products of arachidonic acid that damage the lung capillaries
and alveolar epithelium.
? Damaged endothelium of the capillaries allows fluid to leak from
the blood. Further chemical damage by neutrophils destroys alveolar
? The result is the accumulation of serum, fibrin and dead cell debris
in the alveoli.
? Pink glassy membranes form on the insides of the alveoli. These pink
membranes are called hyaline membranes.
? Once hyaline membranes have formed, no surfactant is present in the
alveoli so they tend to collapse (atelectasis). The combination of
atelectasis and edema make the lung stiff and noncompliant.
? Many patients with ARDS progress to a phase of the disease where
healing occurs by fibrosis of the lung (organizing stage).
? Most patients who develop ARDS have some other condition that brings
them to the hospital. Once ARDS develops, there is a 50% mortality.
? There is no effective therapy for ARDS once it has begun. Only resolving
the initial injury (e.g. treating the initial sepsis) and supportive
care are useful. Some patients will resolve their ARDS completely with
QUESTIONS TO CONSIDER AS LEARNING OBJECTIVES:
? The Vietnam conflict highlighted this war-related etiology of ARDS.
? This component of the compliment system is the first to be triggered
? This cellular event is the second step in the pathogenesis of ARDS.
? These toxic substances are produced by neutrophils and are felt to
induce vascular and epithelial damage with permeability and resultant
? While many pulmonary diseases may produce “white-out” on the chest
? A hallmark of ARDS pathologically are these glassy pink membranes that
line the insides of alveoli.
? The mortality rate for ARDS may be as high as this figure.
? The chest X-ray in ARDS can be described best by this term.
? Some therapies may inherently aggravate ARDS which is what makes this
manifestation of ARDS, the most difficult to manage.
? The stiff lungs of ARDS are produced initially by these two related