EDEMA & INFARCTION

Prof Noor Khan Lakhnana

Head Pathology Department
Al Nafees Medical College
Islamabad
LEARNING OBJECTIVES
1. Define edema

2. Enlist causes of edema

3. Describe the pathogenesis of edema

4. Describe morphology of edema

5. Describe clinical features of edema

6. Differentiate between transudate and exudate

7. Define infarction
8. Enlist causes of infarction
9. Enumerate types of infarct
10. Describe of morphology of infarct
11. Enlist factors affecting infarct development
Edema
 Edema is “an excessive accumulation of body fluid in
interstitial space or serous body cavity, which is a
pathologic process caused by diseases rather than a
disease entity.
 Anasarca is severe generalized edema marked by
profound swelling of subcutaneous tissues and
accumulation of fluid in body cavities.
 Fluid collection in body cavities is called------
 Pleural cavity (hydrothorax)
 Pericardial cavity (hydropericardium)
 Peritoneal cavity (hydroperitoneum, Ascites)
Classification
 According to the range that edema fluid spreads
to:
– Anasarca (generalized edema)
– Local edema
 According to the cause of edema:
– Renal edema
– Hepatic edema
– Cardiac edema
– Malnutritional edema
– lymphedema
– Inflammatory edema
Edema
 75 % of total body weight is water
 - 50 % - Intracellular volume
 - 20 % - Interstitial volume
 - 5 % - Intravascular volume

 Edema is increasing of fluid volume in tissues.

 It is usually used to define the increasing of
extracellular and extravascular fluid volume
Starling law of capillary filtration
 Total Pressure Differences Inside and Outside Capillary

HP c Arteriolar end: 35 mm Hg HPc Ven end: 17 mm Hg COP if: 1

COP c: :26 mm Hg COPc : 24 mm Hg HP if: 0
Arteriolar end: Hydrostatic pressure > Oncotic pressure  Fluid passes into interstitium
Venule end: Oncotic pressure > Hydrostatic pressure  Fluid returns capillary bed
Edema: Mechanisms and Causes:

 imbalance of fluid exchange between plasma and

interstitial compartment

 Increased hydrostatic pressure

 Decreased osmotic pressure

 Lymphatic obstruction

 Sodium retention

 Inflammation
1. Increased capillary blood pressure

↑capillary blood  Causes:

pressure  •Elevated plasma volume
 •Increased venous pressure
↑force driving fluid - Increased general venous
into interstitium pressure i.e.
congestive heart failure
 - Increased local venous
↑formation of
interstitial fluid pressure, i.e.
When greater than venous thrombosis
lymphatic  •Arteriolar dilation i.e.
compensatory
return
acute imflammation
Edema
2. Decreased plasma colloid osmotic pressure

 Causes: plasma protein

↓ plasma colloid
osmotic pressure decrease
 ―Decrease of protein
↓force drawing water production i.e. hepatic
back into capillary from cirrhosis, malnutrition
interstitium
 ―Excessive loss of protein
i.e. nephrosis
↑formation of nterstitial fluid
 ―Elevated catabolism of
 When greater than protein i.e. chronic
lymphatic
compensatory return debilitating diseases, such as
Edema malignant tumor
3. Obstruction of lymphatics

 During the process of interstitial fluid formation,

one-tenth of fluid that leaves the capillary at its
arterial end returns to the venous circulation via
lymphatics. So obstruction of lymphatic will result in
edema.
Causes:
•Blockage by cancer
•Blockage by infection, especially with filarial
infection (elephantiasis)
• Following surgery and radiation therapy
4. Increased capillary permeability
↑capillary permeability
 Causes: inflammation

•Infection
` Filtration of more protein
from capillary to interstitium •Burn

↓Plasma colloid osmotic pressure •Allergic response

•Trauma
↑formation of interstitial fluid
•Anoxia

•Acidosis
edema
Edema
 Common sites of edema:
 Subcutaneous edema: occurs in heart failure in the
dependent part of the body eg. Legs and sacral
area (dependent edema, or pitting edema)
 Pulmonary edema: is accumulation of fluid in the
alveolar space. It occurs in heart failure (Left side
failure). It can occur with renal failure or pulmonary
infection.
 Brain edema:
o Localized: in abscess or around tumors
o Generalized: in encephalitis, hypertensive crisis.
See a

Transudate vs. exudate

Transudate Exudate
↑ hydrostatic pressure,
Inflammation-Increased
Main causes ↓ colloid osmotic
vascular permeability
pressure
Appearance Clear Cloudy
Specific gravity < 1.012 > 1.020
Protein content < 2.5 g/dL > 3-0 g/dL
Cell count Low High
Mesothelial cells or
Polymorphs, lymphocytes
Differential count lymphocytes
or RBCs

fluid LDH
< 0.6 or < 2​ ⁄3 > 0.6[2] or > 2​ ⁄3
UNL for serum
Cholesterol content < 45 mg/dL > 45 mg/dL
Culture Sterile Posiitve
4. Effect of edema
• Generally, edema is harmful, i.e.
– Impedes nutritional supply to cells
– Edema of brain is life-threatening,
intracranial pressure increase, herniation
of brain.

• Protect effect: the edema fluid of

inflammatory edema can dilute, neutralize
toxin and transport the antibody.
MORPHOLOGY
INFARCTION
INFARCTION
 Def:. Localized area of ischemic necrosis in an
organ or tissue resulting most often from reduction
of arterial blood supply or occasionally its venous
drainage………………….ROBBINS
Aetiology
 Thrombosis or embolism 99%
 Venous outflow obstruction (single outflow organs)
 Others : Hypotension, local vasospasm,
 compression of vessel by hematoma or tumor,
 torsion
AETIOLOGY
 Most commonly, Infarcts are caused by Interruption in
arterial blood supply, called ischemic necrosis.
 Less commonly, venous obstruction can produce infarcts
termed stagnant hypoxia.

 Generally, sudden, complete and continuous occlusion

by thrombosis or embolism.

 Torsion of a vessel, e.g. in testicular torsion

 Traumatic rupture or vascular compromise by edema,
e.g. anterior compartment syndrome.
Classification of infarcts

 Depending on Colour
a. Pale/anemic/white
b. Red (hemorrhagic) Infarct
 Depending on Age
a. Recent or fresh.
b. Old or healed.
 Presence or absence of infection.
a. Bland – when free of bacterial contamination
b. Septic – when infected
Pale / White Infarct

Ischemia following obstruction of nutrient

artery or hypoperfusion of tissue
 Solid organs with end-arterial circulation such

as kidney, heart, spleen

 Wedge shaped. occluded vessel at the apex,

base at the serosal surface

 Better defined with time, paler, hyperemic
margins
Red (hemorrhagic)infarcts

 Sites : Venous occlusion of organ with single

venous outflow e.g. testicular torsion
 Loose tissues- e.g. lung
 Tissues with dual circulations: lung and gut
 Previously congested tissue
 With reperfusion of previously infarcted tissue
 Time Gross Features Microscopic Features

0 – 4 hr None None

4 – 12 hr None Early coagulation necrosis (nucleus: pyknosis,

cytoplasm: eosinophilia)

12 – 24 hr Dark mottling Further necrosis, haemorrhage, early neutrophil

infiltrate

1 – 3 days Mottled with yellow-tan Marked neutrophil infiltrate and necrosis

necrotic centre

3 – 7 days Hyperaemic border, central Early phagocytosis of dead cells by

yellow-tan softening macrophages (at border)

7 – 10 days Maximal yellow-tan Well-developed phagocytosis, early granulation

softening, depressed red-tan tissue formation
margins

10 – 14 days Red-gray depressed infarct Well-developed granulation tissue, early

borders collagen deposition

2 – 8 week Grey-white scar progresses Increased collagen deposition, decreased

from border toward centre cellularity

> 2 months Dense gray scar Acellular collagenous scar

 Infarct, day 1

Haemorrhage, necrosis and early neutrophil infiltrate

 Infarct, day 3

Myocyte necrosis, pyknosis and marked neutrophil infiltrate

2nd Year Pathology 2010
 Infarct, day 10

Granulation tissue after macrophage phagocytosis of infarcted cells

Infarct, day 90+

Subendocardial acellular fibrous scar

Septic infarct
 Following fragmentation of a bacterial vegetations
from a heart valve or following microbes seeding a
necrotic area.
 Converted into an abscess
 Greater inflammatory response
 scarring
Clinical Correlations
 Nature of blood supply
 end-artery blood supply
 dual blood supply

 Rate of development of occlusion

 role of collateral circulation
 Vulnerability of tissue to hypoxia
 brain: 3-4 minutes
 heart: 20-30 minutes

 Oxygen content of blood

 hemoglobin concentration and saturation
 GOD BLESS U ALL

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