Non-Cardiogenic Lung Edema

• Noncardiogenic pulmonary edema is the

accumulation of fluid in the pulmonary
interstitial tissue and pulmonary alveolus
caused by cardiac abnormalities.
• Lung edema is an excessive accumulation of
serous flu or serosanguinose in the interstitial
space and alveolus of the lungs. If edema
appears acute and widespread, often followed
by death in a short time.
Etiology and risk factors
• Non cardiogenic pulmonary edema results from
transudation of fluid from the lung capillaries into the
interstitial space and alveolar lung resulting from
other than heart abnormalities.
1. Increased pulmonary capillary permeability (ARDS)
•Directly
–Aspiration of stomach acid, drowning, Pulmonary contusions,
Severe pneumonia Fat embolism, Amnion fluid embolism,
Inhalation of chemicals, Oxygen poisoning
•Indirect
–Sepsis, Severe Trauma, Hypovolemic Shock, Repeated Blood
Transfusion, Burns, Pancreatitis, Disseminated Intravascular
Coagulation, Anaphylaxis
2. Increase lung capillaries
• Venous congestion syndrome
• Excessive injecting
• Blood transfusion
• Kidney failure
• Neurogenic pulmonary edema
• Lung edema due to altitude (Altitude)
3. Oncotic decline
• Nephrotic syndrome
• Malnutrition
4. Hyponatremia
Pathogenesis and Pathophysiology
Increased pulmonary capillary
permeability
• Lung edemaincreased pulmonary capillary pressure and
increased alveolar capillary permeabilityacute respiratory distress
syndrome (ARDS).
• In the early stages of pulmonary edema there is an increase in fluid
content in the interstitial tissues between the capillaries and the
alveoli.
• Pulmonary edema: increased pulmonary capillary permeability
caused by inflammatory cascade
• Activated neutrophils aggregate and attach to endothelial cells
• Release of toxins, free radicals, and inflammatory mediators such as
arachidonic acid, quinine, and histamine.
• Increased alveolar capillary permeability. Alveoli become fully
loaded with protein-rich exudate and contains many neutrophils
and inflammatory cells to form hyaline membranes.
Venous congestion syndrome (fluid overload)

• Increased pulmonary capillary pressures and

pulmonary edema may occur in patients with
excess intravascular fluid with normal heart size.
Intravascular volume expansion does not need to
be too large for venous congestion, since
systemic vasoconstriction can cause a shift in
blood volume into the central circulation. This
syndrome often occurs in patients who received
crystalloid fluid or intravenous blood in large
numbers, especially in patients with impaired
kidney function, or due to renal failure itself
(water retention).
Neurogenic pulmonary edema
• This condition occurs in patients who have head
trauma, convulsions, or sudden increase of intracranial
pressure. Presumably the basic mechanism of
neurogenic pulmonary edema is the presence of
hypothalamic stimulation (due to the above causes)
which causes stimulation of the adrenergic system,
which then causes a shift in blood volume from the
systemic circulation to the pulmonary circulation and
decreased left ventricular "compliance". As a result
there is a decrease in left ventricular fillingleft atrial
pressure increases and pulmonary edema develops.
Nephrotic syndrome
• The mechanism of the formation of edema is very complex; several
factors are:
1. Decreased plasma osmotic colloid pressure due to decreased serum
albumin concentration of extracellular fluid shift from the intra-
vascular compartment into the interstitial
2. A marked decrease in urinary sodium excretion due to increased
tubular reabsorption.
3. Water retention.
• The decrease in plasma osmotic colloid pressure and all consumed
sodium retention alone are not sufficient for the development of
edema in nephrotic syndrome. For the occurrence of edema there
should be water retention.
• Malnutrition
The principle mechanism of pulmonary edema in
malnutrition is similar to nephrotic syndrome.
Hypoproteinemia is the basis of edema.

• Excessive activity
In a study conducted by Ayus JC and colleagues in marathon
runners there were 18% of 605 marathon runners who
suffered pulmonary edema due to hyponatremia. This
mechanism concludes that as the activity increases
(marathon) occurs sodium expenditure through the sweat
water, so the body lacks sodium. After completion of the
activity of the body trying to do homeostasis, by secreting
ADH and there is water retention. The result is pulmonary
edema
SYMPTOMS AND SIGNS
• The typical symptoms of non-cardiogenic pulmonary
edema are:
• Beginning with chest pain (-)
• Shortness of breath suddenly
• Cold sweat
• Sitting position
• Restlessness
• Ronki is full
• If it happens so patient blood transfusion => TRALI
(Transfusion Related Acute Lung Injury)
•
DIAGNOSIS
• Diagnosis is confirmedclinical symptoms and examinations
caused by pulmonary edema and clinical symptoms of the
underlying disease.
• Investigations that may be helpful in determining the diagnosis
include: Chest radiographs showing diffuse bilateral infiltrations
without the presence of signs of cardiogenic pulmonary edema.
• Blood gas analysis may also support and also as a reference to the
treatment of pulmonary edema. In pulmonary edema the blood gas
(AGD) examination shows severe hypoxemia.
• CT Chest scans may also be helpful in diagnosis and may be used to
evaluate the improvement of pulmonary edema.
Electrocardiography to distinguish pulmonary edema from cardiac
abnormalities.
TREATMENT
• The first treatmentprimary disease that causes pulmonary edema.
• supportive treatmentmaintaining adequate oxygenation and
hemodynamic optimization
• Giving oxygen relieves and relieves chest pain
– oxygenation with ventilator, ie Positive end expiratorypressure (PEEP) 25-15
mmH2O can be used to prevent alveoli to collapse.
– extra corporeal membrane oxygenation (ECMO) uses an artificial external
membrane to help transport oxygen and remove CO2.

• Optimization of hemodynamic function: fluid retention, use of diuretics

and pulmonary vasodilator drugs (nitric oxide / NO). Be careful: the
hypotension and perfusion of disturbed organs, for that use must be
careful. Inotropic drugs and vasopressors such as dobutamine and
noradrenaline may be necessary to maintain systemic blood pressure and
adequate cardiac output especially in patients with sepsis (systemic
vasodilatation).
• Recent supportive therapy strategies in trial:
1. Surfactant replacement therapy, using a synthetic surfactant aerosol, was
disappointing, but using natural surfactant mammals and aerosol repair tools
proved to improve alveolar stability, reducing the incidence of atelectasis /
intrapulmonary shunting. Increases antibacterial and anti-inflammatory effects.
2. Extra corporeal gas exchange
3. Prone positioning, proven good in oxygenation due to perfusion shift and exchage
gas repair
4. Fluorocarbon liquid-assisted gas exchange
5. Anti-inflammatory
a. high dose fluorocorticoids
b. anti endotoxin monoclonal antibody
c. anti-TNF-a
d. anti-IL-1
e. activated protein C
f. antioxidants
g. 1. N-acetylcysteine
PROGNOSIS
• The prognosis depends on the underlying
disease and the treatable cause / trigger.
Although much research has been done to
determine the mechanism of noncardiogenic
pulmonary edema due to increased
pulmonary capillary permeability, treatment
improvement, and ventilator technique but
the patient mortality rate is still high at> 50%.