ulmonary Edem

DR. HAR
UNDER
D
M.

Outline

Definition

Epidemiology

Pathophysiology

Classifications & causes

Pathogenesis

Staging

Clinical manifestations

Complications

Differential diagnosis

Treatment

Definition
is a condition
characterized by fluid accumulation in
the lungs caused by extravasation
of fluid from pulmonary
vasculature in to the
interstitium and alveoli of the
lungs
Pulmonary Edema ;

The extent to which fluid accumulates in the interstitium of the

lung depends on the balance of hydrostatic and oncotic forces
within the pulmonary capillaries and in the surrounding tissue.

Hydrostatic pressure

-favors movement of fluid from the capillary into the

interstitium

Oncotic pressure
-favors movement of fluid into the vessel

Maintenance

-lymphatic in the tissue carry away the small amounts of

protein that may leak out
-tight junction of endothelium are impermeable to protein

Epidemiology

Pulmonary edema occurs in about 1% to 2% of the general

population.

Between the ages of 40 and 75 years, males are affected

more than females.

After the age of 75 years, males and females are affected

equally.

The incidence of pulmonary edema increases with age and

may affect about 10% of the population over the age of 75
years.

Pathophysiology

imbalance of starling force

-increase pulmonary capillary pressure
-decrease plasma oncotic pressure
-increase negative interstitial pressure

damage to alveolar- capillary barrier

lymphatic obstruction
Disruption of endothelial barrier allow protein to
escape capillary bed and enhance movement of
fluid in to the tissue of the lung
idiopathic or unknown

Classification

based on inciting mechanism

1.

Imbalance of Starling force

A. Increased pulmonary capillary pressure

-left ventricular failure
-Volume overload
B. Decreased plasma oncotic pressure
- Hypoalbuminemia due to different cause
C. Increased negativity of interstitial pressure
-Rapid removal of pneumothorax with large
applied negative pressures (unilateral)

Classification
Based on inciting agent..

. Altered alveolar-capillary membrane

permeability
o Infectious pneumonia
o Inhaled toxins
o Circulating foreign substances
o Aspiration
o Endogenous vasoactive substances
o Disseminated intravascular coagulation
o Immunologichypersensitivity pneumonitis, drugs
o Shock lung in association with non-thoracic trauma
o Acute hemorrhagic pancreatitis
2

Classification

Based on inciting agent.

Lymphatic insufficiency

-After lung transplant

- Lymphangitic carcinomatosis

-Fibrosing lymphangitis
4. Unknown or incompletely understood
- High-altitude pulmonary edema
- Neurogenic pulmonary edema
- Narcotic overdose
- Pulmonary embolism
- Eclampsia
-After anesthesia
- After cardiopulmonary bypass
3.

Classification
Base on underlining cause

Cardiogenic pulmonary edema

Non-cardiogenic pulmonary edema

Cardiogenic
pulmonary edema
Is Pulmonary edema due to
increased pressure in the
pulmonary capillaries because of
cardiac abnormalities that lead to
an increase in pulmonary venous
pressure.
o

Hydrostatic pressure is increased

and fluid exit capillary at
increased rate

Cardiogenic PE

Basic pathophysiology:

A rise in pulmonary venous and

pulmonary capillary pressures
pushes fluid into the pulmonary
alveoli and interstitium.
CXR: B/L perihilar bats wing
appearance,symmetric opacification
of lung fields

Pathogenesis of CPE
Left sided heart failure

Decrease pumping ability to the systemic circulation

Congestion & accumulation of blood in the pulmonary area

Fluid leaks out of the intravascular space to the interstitium

Accumulation of fluid

Pulmonary edema

Risk Factors

Vary by cause

Leading risk factor is clearly

underlying cardiac disease.
-

Causes of Cardiogenic PE
LV

failure is the most common

cause.

Dysrhythmia
LV

hypertrophy and
cardiomyopathy

LV volume over load

Myocardia

infarction

left ventricular outflow obstruction

Non cardiogenic
pulmonary edema
It is defined as the evidence of alveolar
fluid accumulation with out
hemodynamic evidence that suggest
a cardiogenic etiology.
Hydrostatic pressure is normal
Leakage of protein and other molecule
in to the tissue

Non cardiogenic PE
o

Associated with dysfunction of

surfactant lining the alveoli,
increased surface force and a
propensity for the alveoli to
collapse at low volume.

Characterized by intra pulmonary

shunt with hypoxemia and
decrease lung compliance

Non cardiogenic
pulmonary edema
Mechanism include:

Increased

alveolarcapillary
membrane permeability

Decreased

plasma oncotic

pressure
Increased

negativity of
pulmonary interstitial pressure

Lymphatic

insufficiency or
obstruction

Non- cardiogenic PE

cause

I.

Direct injury to the lung

II.

Hematogenous injury to the

lung

III.

possible lung injury plus

elevated hydrostatic
pressure

Staging of PE
Three stages of PE can be distinguished based on
the degree of fluid accumulation:
Stage-1 : all excess fluid can still be cleared by
lymphatic drainage.
Stage-2 : characterized by the presence of
interstitial
edema.
Stage-3 : characterized by alveolar edema due to
altered alveolor- capillary permeability

Mild:

Only engorgement of
pulmonary vasculature is seen.

Moderate:

There is
extravasation of fluid into the
interstitial space due to
changes in oncotic pressure.

Severe:

Alveolar filling occurs.

Unusual type
pulmonary edema

Neurogenic pulmonary edema

Patients with central nervous system disorders

and without apparent preexisting LV dysfunction

Re-expansion pulmonary edema

Develops after removal of air or fluid that has

been in pleural space for some time, postthoracentesis

Patients may develop hypotension or oliguria

resulting from rapid fluid shifts into lung.

Unusual type
pulmonary edema

High altitude pulmonary edema

occurs in young people who have quickly

ascended to altitudes above2700m and who
then engage in strenuous physical exercise at
that altitude, before they have become
acclimatized.

Reversible (in less than

48 hours)

Pathophysiology

on ascending to high altitude, falling level of Po2 trigger hypoxic

pulmonary vasoconstriction

This directs blood flow away from hypoxic areas of lung towards
area that are well oxygenated

This results in a rise in mean pulmonary artery pressure & a

heterogeneous blood flow to different parts of the lung

Cont

In areas that receive high blood flow the capillary

trans-mural pressure rises & walls of the capillary
&alveolus are exposed to stress failure

Extensive damage to alveolar capillary membrane

Edema which is rich in high molecular weight

proteins & RBCs to pass freely in to the alveoli &
impair oxygenation.

patient present with

Headache, Insomnia, Fluid retention, Cough,Shortness

of breath

Symptom of pulmonary
edema
ACUTE

Shortness of breath

A Feeling of suffocating

Anxiety ,restlessness

Cough-frothy sputum that may be tinged with

blood

excessive sweating

pale skin

chest pain if PE is cause by cardiac abnormality

palpitation

Symptom
Long term(chronic)

Paraxosomal nocturnal dyspnea

orthopnea

Rapid weight gain

Loss of appetite

fatigue

ankle and leg swelling

Signs

Tachycardia

Tachypnea

Confusion

Agitation

Anxious

Diaphoric

Hypertension

Cool extremities

Rales

Wheezing

CVS findings ; S3 ,accentuation of pulmonic component

of S2, jugular venous distention..

Special considerations

Unilateral pulmonary edema after rapid

evacuation of large pneumothorax

Findings may be apparent only by radiography.

Occasionally, dyspnea with physical findings

localized to edematous lung

Special consideration

Lymphatic blockade secondary to fibrotic and

inflammatory diseases or lymphangitic
carcinomatosis

Both clinical and radiographic

manifestations are dominated by the
underlying disease process.

Neurogenic pulmonary edema

Symptoms usually occur within minutes to hours

of the injury

Complications

leg swelling(edema),

abdominal swelling(ascites),

Pleural effusion,

Congestion & swelling of liver,

acute heart attack (myocardial infarction [MI]),

cardiogenic shock,

arrhythmias,

electrolyte disturbances,

mesenteric insufficiency,

protein enteropathy,

respiratory arrest, and death.

Differential diagnosis
Pneumothorax
Bronchitis
Cardiac

tamponed

COPD
Pericarditis
Pneumonia
Pulmonary

(bacterial ,viral , PCP)

embolism

Shocks

(cardiogenic ,septic ,anaphylactic)

Venous

air embolism

Distinguishing Cardiogenic from

Non-cardiogenic Pulmonary Edema
Finding

suggesting cardiogenic edema

-S3 gallop
-elevated JVP
-Peripheral edema

Findings

suggesting non-cardiogenic edema

-Pulmonary findings may be relatively normal in

the early stages
-.

Distinguishing ..
Chest

radiography

A cardiogenic cause is favored with

Cardiomegaly
Kerley B lines and loss of distinct vascular margins
Cephalization: engorgement of vasculature to the apices
Perihilar alveolar infiltrate
Pleural effusion
Non cardiogenic cause
-Heart size is normal
-Uniform alveolar infiltrate
-pleural effusion is uncommon
-lack of cephalization

Distinguishing..

Hypoxemia

Cardiogenic

- due to ventilation perfusion miss match

-respond to administration of oxygen

Non cardiogenic

-due to intrapulmonary shunting

-persist despite oxygen supplimentation

Approach a Patient with

Pulm.Edema
History Taking

Exertional Dyspnea

Orthopnea

Aspiration of food or foreign body

Direct Chest injuries

Walking High altitude

Chest Pain(right or left)

Leg pain or swelling(Pulmonary Embolism)

A cough that produces frothy sputum that may be tinged

with blood(cardiogenic)

Cont

Palpitations

Excessive sweating

Skin color change-Pale skin

Chest pain(if it is Cardiogenic)

Rapid weight gain(cardiogenic)

Fatigue

Loss of appetite

Smoking History

Past Medical History

COPD,

heart failure,

HIV risk factors

(pulmonary Kaposis sarcoma).

Prior chest X-rays,

CT scans,

tuberculin testing (PPD).

Medications

Anticoagulants

Aspirin

NSAIDs

Narcotic

Heroin

Morphine

Methadone and

Dextropropoxyphene

INVESTIGATIONS

CXR-PA view:

unilateral or bilateral involvement,cardiogenic pattern

or non cardiognic pattern(air bronchogram signs, fluffy
opacities, asymmetrical inhomogenous
involvement),lobar involvement in post infectious PE.

ABG analysis:

hypoxia and hypocapnia initially with respi. alkalois

hypercapnea in later stage with respi and metabolic
acidosis

Hemodynamic measurement with Swan-Ganz

catheter

Blood work up and septic screen

Management stretagy

Treat underlying cause : Sepsis,heart failure,high

altitude hypoxia,obstruction,fluid
overload,hypoproteinemia etc.

Respi support: NIV vs Intubation f/b venti support

Indication for intubation f/b venti support

Refractive hypoxia

Excessive work of breathing : rate > 35/min ,

MV>12L/min

Hemodynamic instability

Inability to protect airway

Anticipated rapid clinical deterioration

Management stretagy..

NIV support:CPAP

Reasonable initial venti settings are EPAP 7 cmH2O

and IPAP of around 15 cm H2O with adjustment
according to patient tolerance and maintaining
SaO2>90%
Decreases work of breathing,FRC is
increased,collapse of alveoli due to edema fluid is
prevented and helps in opening up of already
collapsed alveoli
Good response is generally observed in 30
minutes,if not so or worsening is seen, consider
elective intubation f/b venti support

Management stretagy

Principles of mechanical ventilation

Two fundamental principles

1.

Prevention of overdistension of alveoli-limiting

tidal volume or inspiratory pressure

2.

Choose the level of PEEP sufficiently high to

prevent derecruitment of alveoli at end of
expiration

1.

Limiting tidal volume

High TV 12-15 ml per kg are

dangerous in patient with PE
Can lead to VOLUTRAUMA
Tidal volume kept at 6-8 ml per
kg to start with in patient of PE
Then adjusted to keep the
plateau pressure below 30 cm of
H2O

2. Use of PEEP
Recruits collapsed alveoli,prevents collapse,improves
V/Q mismatch,decreases shunt and venous
admixture,increases FRC,reduces pathological dead
space
Can allow adequate oxygenation at lower
FiO2,protects from oxygen toxicity
Most patients with ARDS will need PEEP of more than
10 cm H2O at FiO2<0.6
If high level of PEEP causes hemodynamic instability,
use of pressure controlled inverse ratio ventilation ,
prone posture can be beneficial
Inverse ratio venti:changes inspiration-expiration
ratio,lower peak pressure can be achieved,auto-PEEP
develops,higher mean alveolar pressure with low
peak pressure

Treatment in special
conditions

High altitude pulmonary edema

Slow ascent ,prophylactically tab.nifedipine 20mg

sustained release 8hrly, or tab dexamethasone 8 mg
12hrly,or inhaled salmeterol
Descent and supplemental O2 are definitive Rx
If descent not possible and O2 not available,start
pharmacotherapy to reduce pulmonary artery
pressure
Tab nifedipine 10mg sublingual f/b 20 mg SR tab
6hrly
Also hydralazine,inhaled nitrous oxide acetazolamide
are helpful

Post Aspiration PE

Preop gastric emptying by physical means(ryles tube

aspiration) or pharmacological
means(perinorm,atropine,glocopyrolate)

Anti ematics ondensatron,granisatron injectable

Induction in lateral position

Head low position

Bronchoscopic removal of particulate aspirate

material

NO BRONCHO-ALVEOLAR LAVAGE-removes surfactant

and promotes collapse

Supportive sterids

PEEP and mechanical venti till edema clears

THANK YOU