Pathophysiology of Oedema

Dr.Sunil P.V
Courtesy: Dr.Arun Kumar
Department of Pathology, IMU

Learning outcomes
Recapitulate: Plenary on microcirculation and
oedema (Foundation)
Explain how capillary pressure and
plasma/interstitial colloid osmotic pressure affect
fluid movements
Outline different causes of oedema
Pathophysiology of Pulmonary oedema

Factors influencing fluid transit across capillary walls. Capillary hydrostatic and osmotic forces are normally balanced so
that there is no net loss or gain of fluid across the capillary bed. However, increased hydrostatic pressure or diminished
plasma osmotic pressure will cause extravascular fluid to accumulate. Tissue lymphatics remove much of the excess
volume, eventually returning it to the circulation via the thoracic duct; however, if the capacity for lymphatic drainage is
exceeded, tissue edema results

Pathways leading to systemic edema from primary heart failure, primary renal failure, or reduced
plasma osmotic pressure (e.g., from malnutrition, diminished hepatic synthesis, or protein loss from
nephrotic syndrome).

OEDEMA
Increased fluid in interstitial tissue space
Other fluid accumulation: Pleural effusion,
Pericardial effusion, Ascites
Anasarca: Generalized body oedema
Pathophysiology:
- Increased Hydrostatic pressure
- Reduced plasma Osmotic pressure (Proteins &
bicarbonates)
- Lymphatic obstruction
- Sodium retention & Inflammation

Raised Capillary Pressure

Cardiac failure

Right ventricular failure - systemic oedema

Left ventricular failure - pulmonary oedema
Congestive cardiac failure - both

Local venous obstruction

Deep vein thrombosis

External compression
SVC obstruction

Pathophysiologic categories of
edema

E
D
E
M
A

Increased hydrostatic pressure

Impaired venous return
- Congestive heart failure
-Ascites
-Constrictive pericarditis
-Venous obstruction or compression
Thrombosis, mass,Lower extremity inactivity
Arteriolar dilatation
-Heat and neurohumoral dysregulation
Reduced Plasma Oncotic pressure
- Protein-losing glomerulopathies
-Liver cirrhosis
-Malnutrition
-Protein losing gastroenteropathy

Pathophysiologic categories of
edema

E
D
E
M
A

Sodium retention
- Excessive salt intake with renal insufficiency
-Increased tubular reabsorption of sodium
Renal hypoperfusion
Increased Renin-Angiotensin-aldosterone secretion
Inflammation
- Acute
-Chronic
-Angiogenesis

Lymphatic obstruction
-Inflammation
Neoplastic
Postsurgical
-Postirradiation

Pitting type pedal Oedema in dependent parts of the body

Right Heart failure or Congestive heart failure (Combined)

Reduced Oncotic Pressure

Renal disease

Hepatic disease

Loss of albumin across glomerulus

Inadequate albumin synthesis

Malnutrition

Inadequate albumin synthesis

Ascites in Liver failure

Reduced Plasma Osmotic Pressure(Hypoproteinemia)

Malnutrition (Protein
energy Malnutrition)
Kwashiorkor

Protein loosing
Enteropathy
(Intestinal lesions)

Lymphatic Obstruction
Tumours
Fibrosis
Inflammation
Surgery
Congenital abnormality

Oedema due to eye

inflammation

Oedema in hypersensitivity
Before and after steroids

Non pitting oedema- Filariasis

Post Mastectomy Lymphoedema

Laryngeal oedema

Cerebral
Oedema

Cerebral Oedema

Causes increased
intracranial pressure
Fatal if left untreated
Generalised in
hypoxia, injury
Surrounding other
lesions eg tumour,
abscess

Generalised Oedema
Congestive cardiac failure
Right ventricular failure
Renal disease
Liver disease

Anasarca

Generalised Oedema

Swelling of ankles,
limbs, face,
effusions
Sacral oedema in
recumbent patients

Fluid in Body Cavities

Pleural effusion

Pericardial effusion

heart failure, inflammation, tumour

inflammation, tumour

Ascites (peritoneal effusion)

cirrhosis, heart failure, tumour

Pericardial effusion

Pleural effusion

Ascitis in Cirrhosis

Oedema in Heart faliure

Right ventricular failure Generalised
oedema (Pitting), hepatomegaly, ascites,
raised JVP
Hepatomegaly: Nut meg liver

Left ventricular failure Pulmonary

oedema
Congestive heart failure (CHF)
Combination of LHF and RHF

Nutmeg liver

Pulmonary edema
Life threatening emergency
Extreme breathlessness
Gradual increase in grades of breathlessness
proceeding to Orthopnea & PND
Increased Left atrial pressure Increased
pulmonary venous pressure ( Normal pressure
is 5-14 mm of hg) Increased Pulmonary
capillary pressure Increased fluid
sequestration into alveoli Alveolar edema

CAUSES OF PULMONARY EDEMA

Atrial outflow obstruction: Mitral stenosis,
Atrial myxoma
LV systolic dysfunction: Congestive heart
failure (CHF) or cardiomyopathy. Acute MI
or ischemia
Diastolic dysfunction, Arrhythmias
Other causes of LHF

CLINICAL FEATURES-Pulm
Oedema
Breathlessness
Wheezing (Cardiac Asthma)
Cough, productive, Pink frothy sputum
Tachypnea with peripheral circulatory
failure
Crackles & Wheez heard at lung bases &
throughout

INVESTIGATIONS-Pulm Oedema
ABG:
Initially Arterial Po2 falls and also PCo2 falls due to
rapid breathing
Later PCo2 increases due to impaired gas exchange

CXR: (Video)
Diffuse haziness due to alveolar fluid
Inter lobar & inter lobular septa (Kerly B lines)
Prominent upper lobe veins
Bat wing appearance
Summary of Pulm Edema

INVESTIGATIONS
Electrocardiography ( EKG)
Features of Left atrial enlargement and LV
hypertrophy
Arrhythmia
Myocardial ischemia or infarction

PCWP measurement by using pulmonary

arterial catheter (Swan-Ganz catheter)

PCWP
Pulmonary capillary wedge pressure
(PCWP) provides an indirect estimate of
left atrial pressure (LAP)
Normal pressure is 8- 10 mm
of Hg
Pressure more than 30 mm
Of Hg Pulm edema

Learning outcomes
Recapitulate: Plenary on microcirculation and
oedema (Foundation)
Explain how capillary pressure and
plasma/interstitial colloid osmotic pressure affect
fluid movements
Outline different causes of oedema
Pathophysiology of Pulmonary oedema