Diagnosis Treatment Introduction

1. PULMONARY EDEMA
NALI SOMASHEKAR SANTHOSH

2. PULMONARYEDEMA
• Pulmonary edema is fluid accumulation in the Lung tissue
and air spaces.
• It leads to impaired gaseous exchange and may cause
respiratory failure.
• It is due to either :
Failure of the left ventricle of the heart to remove blood
adequately from the pulmonary circulation (cardiogenic
pulmonary edema), or
An injury to the lung parenchyma or vasculature of the
lung (noncardiogenic pulmonary edema).

4. CAUSES
• Neurogenic: seizures, head trauma, strangulation, electrocution.
• Respiratory Causes:
• Acute respiratory distress syndrome
• Inhalation of hot or toxic gases
• Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle
accidents)
• Aspiration, e.g., gastric fluid
• Re-expansion, i.e. post large volume thoracocentesis, resolution of
pneumothorax, post decortication, removal of endobronchial
obstruction, effectively a form of negative pressure pulmonary
oedema.
• Reperfusion injury, i.e. postpulmonary thromboendartectomy or
lung transplantation
• Swimming induced pulmonary edema also known as immersion
pulmonary edema.

5. • Other causes:
• Transfusion Associated Circulatory Overload (TACO) occurs
when multiple blood transfusions or blood-products (plasma,
platelets, etc.) are transfused over a short period of time.
• Transfusion associated Acute Lung Injury (TRALI) is a specific
type of blood-product transfusion injury that occurs when the
donors plasma contained antibodies against the donor, such as
anti-HLA or anti- neutrophil antibodies.
• Severe infection or inflammation which may be local or
systemic. This is the classical form of ALI-ARDS

7. PATHOPHYSIOLOGY
• Fluid accumulation in the lungs causes extravasation of fluid
from the pulmonary vasculature into the interstitium and the
alveoli
• It can be caused by the following pathophysiologic forces:
• 1. Imbalance of Starling forces
-increased Pulmonary Capillary pressure
Decreased plasma oncotic pressure
Increased negative interstitial pressure
• 2.Damage to the alveolar-capillary barrier
• 3. Lymphatic obstruction
• 4. Idiopathic mechanisms

8. • Hydrostatic pressure favors movement of fluid from the capillary
to the interstitium, while Oncotic pressure favors movement of
fluid into the vessel.
• In cardiogenic pulm. edema, there is increased pulmonary
capillary hydrostatic pressure secondary to elevated
pulmonary venous pressure which results from back flow of
pressure from the Left auricle.
• Hydrostatic pressure increases and fluid exits from the
capillaries at an increased rate causing interstitial and
alveolar edema.
• Lymphatics are vital in removing excess interstitial fluids and
solutes back to the vascular spaces. Increased pulmonary
arterial capillary pressure causes increased filtration to levels
that overwhelm lymphatic drainage causing edema.

9. • In non cardiogenic pulmonary Edema, there is altered
permeability of the alveolar-capillary barrier secondary to
inflammation, ARDS, or intense pulmonary Vasoconstriction and
high capillary pressure.
• Endothelial leakage occurs which results to influx of protein rich
fluid into the alveolar space (interstitium) causing alveolar
edema without diffuse alveolar damage.

10. CLINICALFEATURES
• Shortness of breath –Dyspnoea orthopnea, paroxysmal
nocturnal dyspnea, fatigue
• Coughing up blood-classically pink, frothy sputum and
wheezing
• Excessive sweating, anxiety, and pale skin-Shock.
• Cyanosis
• Low oxygen saturation
• Other signs of fluid overload-Pitting oedema, ascites,
Tender hepatospleenomegally. (CHF/RVF)
• Basal or generalized crepitations.

11. DIAGNOSIS
• Chest X RAY
• Lung ultrasound,
• Echocardiography,
• Chest computerized tomography (CT) scan,
• Electrocardiogram

13. TREATMENT
• Treatment is focused on three aspects
Improve respiratory functions
Treat underlying cause
Avoid further lung damage
• Supportive therapy- Oxygen, i.v line, prop up.
• LMNOP-Lasix, Morphine, Nitrates(NTG), Oxygen, Position-
upright vs flat
• ALMOND

14. • Lasix-0.5-1mg/kg- Reduces preload
• Morphin-2-4mg/kg i.v boluses. Reduces anxiety, dyspnea
and it’s a transient venodilator thus reduces preload.
• Nitrates-Nitroglycerine 0.4mg every 5 minutes and
isosorbide dinitrate are venodilators with coronary artery
vasodilation.
• Oxygen- with CPAP/NIPPV
• Position- prop up and dangle the legs on the side of the
bed.

15. THANKY YOU