COPD

PULMONARY EDEMA
Dr Sunil Arora
Professor
Deptt of Pathology
Definition
 A disease state characterized by the
presence of airflow obstruction due to
chronic bronchitis or emphysema;
 The airflow obstruction is generally
progressive, may be accompanied by
airflow hyperactivity
 Includes emphysema and chronic
bronchitis
Types of COPD
 Emphysema
 Permanent and destructive enlargement of
airspaces distal to the terminal bronchioles without
obvious fibrosis and with loss of normal architecture
 Always involves clinically significant airflow
limitation
 Chronic Bronchitis
 Presence of a cough productive of sputum not
attributable to other causes on most days for at
least 3 months over 2 consecutive years
 May be present in the absence of airflow limitation
Pathogenesis of Emphysema

• Cigarette smoking and other pollutants

• Inflammatory mediators and leucocytes

• Protease - Antiprotease imbalance

• Oxidative stress

• Infections
Pathogenesis of Chronic Bronchitis

• Cigarette Smoking / Pollutants

• Mucus Hypersecretion

• Gland Hypertrophy

• Inflammation

• Infection
Pathogenesis of Emphysema
Morphology of COPD
 Emphysema
 Centriacinar:
 focal destruction limited to the respiratory bronchioles and the central
portions of acinus
 associated with cigarette smoking
 most severe in the upper lobes
 Panacinar:
 involves the entire alveolus distal to the terminal bronchiole

 develops in patients with homozygous alpha1-antitrypsin (AAT)

deficiency
 most severe in the lower lung zones

 Distal acinar:
 Also called paraseptal

 involves distal airway structures, alveolar ducts, and sacs

 localized to fibrous septa or to the pleura and leads to formation of

bullae
 Irregular
 Chronic Bronchitis
 Mucus gland enlargement
 Airway atrophy, focal squamous metaplasia, ciliary
abnormalities, smooth muscle hyperplasia,
inflammation, and bronchial wall thickening
 Respiratory bronchioles display a mononuclear
inflammatory process, lumen occlusion by mucous
plugging, goblet cell metaplasia and distortion due to
fibrosis
 Airway walls deform and narrow the airway lumen
Patterns of Emphysema
Risk Factors
 Smoking!
 48 million smokers in the USA & 120
million in India
 Nearly all patients with symptomatic
COPD are current or former smokers
 10-20% of smokers will develop
symptomatic COPD.
 In men who smoke one pack/day, the
drop in FEV1 per year was 9 mL more
than in non-smokers
 Occupational Exposures
 Dusts, gases, fumes
 Alpha1-antitrypsin deficiency
 Alpha1-antitrypsin is an important
protease inhibitor that usually prevents
elastases from causing lung destruction
Symptoms

 Dyspnea
 Cough (with sputum )
 Wheezing
 Cyanosis
 Right heart failure
 Weight loss, anorexia
Emphysema – Pink Puffers

Over ventilated and well oxygenated

Chronic Bronchitis - Blue Bloaters

Hypercapnia and mild cyanosis

LAB EXAMINATION
Centriacinar & Panacinar emphysema
OTHERS FORMS OF EMPHYSEMA

• Compensatory

• Obstructive overinflation

• Bullous Emphysema

• Interstitial Emphysema
BULLOUS EMPHYSEMA
Emphysema
Take Home Points
 Smoking is the number one cause of
COPD!
 If smoking is stopped once COPD
diagnosed, the progression of disease
can slow down
 Treat COPD exacerbations with
antibiotics and possibly with steroids
 Continuous oxygen is shown to decrease
morbidity and mortality in COPD
WORLD NO TOBACCO DAY – MAY 31
Pulmonary edema is a condition characterized
by fluid accumulation in the lungs caused by
extravasation of fluid from pulmonary
vasculature into the interstitium and alveoli of
the lungs
• 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
 Based on underlying cause
 Cardiogenic pulmonary edema
 Non-cardiogenic pulmonary edema

 Neurogenic PE

 High Altitude PE

 Post Aspiration PE

 Re-expansion PE

 Other ( inhaled toxins, lymphatic obstruction,

post lung transplant, etc.)

 Due to cardiac abnormalities, pulmonary
capillary pressure is increased that increases
the pulmonary venous pressure.
CAUSES

• LV failure
• Dysrhythmia
• LV hypertrophy and cardiomyopathy
• LV volume overload
• Myocardial infarction
• LV outflow obstruction
Left sided heart failure

Decreased pumping ability to the systemic

circulation

Congestion and accumulation of blood in

pulmonary area

Fluid leaks out of intravascular space to the

interstitium

Accumulation of fluid

Pulmonary edema
 Neurogenic PE
Patients with CNS disorders and without
apparent preexisting LV dysfunction
 Re-expansion PE

Develops after removal of air or fluid,

post-thoracocentesis
 High Altitude PE
 Occurs in young people who have
quickly ascended to altitudes above
2700m and engage in strenuous physical
exercise without acclimatization
 Reversible when altitude is

dropped (in less than 48 hours)

 Based on the degree of fluid
accumulation
 Stage- 1:all excess fluid can still be
cleared by lymphatic drainage
 Stage- 2 presence of interstitial
edema
 Stage- 3 alveolar edema
Symptoms: Acute
 Severe shortness of breath

 Cough- with pink frothy sputum

 Profuse sweating

 Cyanosis

 Anxiety, restlessness

 Palpitation

 Chest pain
 Long Term (Chronic)
 Paroxysmal nocturnal dyspnea

 Orthopnea
 Rapid weight gain
 Loss of appetite
 Fatigue
 Ankle and leg swelling
 Tachycardia
 Tachypnea
 Confusion
 Agitation, anxious
 Diaphoresis
 Hypertension
 Cool extremities
 Crepitant rales, rhonchi or wheeze
 CVS findings: S3, accentuation of S2,
jugular venous distension
Leg edema
 Ascites
 Pleural effusion
 Congestion of liver
 Myocardial infarction
 Cardiogenic shock
 Arrythmias
 Electrolyte disturbances
 Mesenteric insufficiency
 Respiratory arrest and death
 CBC – severe anemia
 Serum electrolytes – Hypokalemia, Hypomagnesemia

 Pulse oximetry – assess Hypoxia

Response to supplemental oxygenation

 ABGs – Initially hypoxia and hypocapnia with

respiratory Alkalosis
- Later Hypercapnia with respiratory and metabolic
acidosis
 ECG- tachydysrhythmia
-Brady dysarhythmia
-acute MI

Chest x-ray-
1. Enlarged heart
2.Inverted blood flow
3.Kerley lines
4.Basilar edema (vs diffuse edema)
5.Absence of air bronchograms
6.bilateral and symmetrical pleural effusions
Pulmonary edema
Pulmonary edema
Bat wing
edema in a
71-year-old
woman with
fluid overload
and cardiac
failure
Neurogenic PE
in a patient with
subdural
hematoma
Bilateral
alveolar filling
process and a
normal- sized
heart
Patient admitted
with progressive
respiratory distress
24 hours after
arriving at 2700 m
above sea level
HAPO

Right greater than

left indistinct
airspace opacity