24.

Oedema

Dr. Damodar Sedhai

Date :
 Oedema
• is a condition in which there is an excess amount of
fluid in the intercellular space, extracellular space or
body cavity.
• Exchange between intracellular and interstitial fluid is
governed by the Starling force (i.e. Hydrostatic and
osmotic pressure).
• Fluid moves from intravascular to interstitial
component at the arterial end of the capillary beds by
the hydrostatic pressure (BP) of the blood.
• But it enters to the venules end because of osmotic
pressure. Here, albunin determines the OP of the
plasma.
• Volume of interstitial fluid depends on
– the hydrostatic pressure (BP) at the arterial end of
the capillary,
– the level of plasma protein and
– the adequacy of the lymphatic drainage.

Remember: BP and OP of artery or vein vary from

organ to organ. But principles of edema are the same.
 Normal situation in leg
• In normal condition no fluid enters into the lymph
vessels or lymph capillaries.
• Interstitial fluid does not contain Plasma Protein.
• i.e. 15mm long of Hg of fluid goes in the capillary
endothelium and then to the cells of the body.
• Then 15mm of Hg of water comes to the venule part of
the veins.
• Hence, the B.P of veins become (15+15=30) equal to
that of artery.
• Again the B.P of vein falls to 15mm of Hg immediately.
Fluid balance – leg in resting condition
( Normal)
Pressure in normal condition in the leg
part ( for understanding)
Arterial side
• OP = 30 mm of Hg
• BP = 45
• Diff 45 – 30= 15 mm of Hg
Venous side
• OP =30 mm of Hg
• BP = 15 mm of Hg
• Difference 30-15 = 15 mm of Hg which goes out
from vein
 Classification of oedema
• A On the basis of area involved:
1. Local oedema: - occurs in one part of body
due to the local congestion/passive hyperemia
or obstruction of lymph vessels.
2. General oedema:-generally affect the whole
body caused by cardiac, renal and pulmonary
lesions.
 B. On the basis of cause:

1. Parasitic oedema
2. Nutritional oedema / cachectic oedema
3. Lymphoedema (oedema by lymphatic
obstruction).
 C. On the basis of organ involved
a. Renal oedema (common in man)
b. Sub-cut oedema
c. Pulmonary oedema
d. Cardiac oedema (due to venous obstruction in heart –
e. g. coronary vein)
e. Gastric oedema (due to gastric or intestinal ulcers there
is hindrance in the protein absorption from the intestine
and hence leads to the hypoproteinaemia- hence the
name given)

f. Ventral edema (oedema of lower body parts)

 Etiology of edema
1. Increase in intravascular hydrostatic
pressure(BP) in venous side
2. Fall in colloidal osmotic pressure of plasma (OP)
3. Impairment in the flow of blood due to
inflammation, mechanical injury, thermal injury
4. Renal retention of salt and water
5. Obstruction in the lymph vessels by CAT, worms
or fibrosis
6. Increased permeability of capillary endothelium
due to injury
 1. Increase in intravascular BP in
venous side
• when there is serious obstruction in the veins
of either in heart or lungs or local congestion,
there is an increase in hydrostatic pressure
(BP) in the venous side, whereas Osmotic
pressure remains constant.
BP increased in vein
 Example
• B.P increase slightly but the osmotic pressure
does not increase. Then there will be the diff. of
O.P with (30- 45=15mm of Hg) in the arterial side
.
• But 15mm of Hg of water is coming from the
capillaries to the venules side. So, rest (30-20) =
10mm of Hg of water) - 5mm of Hg of water= 5
mm of Hg will be accumulated in the venous side
leading to the mild Oedema in the vein.
• This condition generally occurs in case of venous
destruction or in the central obstruction.
 2. Fall in osmotic pressure of plasma
in arterial side
• Osmotic pressure decreases sharply when
there is oedema due to hypo-protenemia
 Causes of hypo-protenemia
• Haemorrhage for a longer period
• Hook worm infection or stomach warm
infection (cattle, sheep or horse)
• Malnutrition for a longer period (esp. for
protein)
• Bleeding due to gastric or intestinal ulcers (in
pig dog)
 Hypo-protenemia …
• Injury to the glomerulus: Injury of glomerulus
permits the protein to excrete through urine
(in man) .
– Ex: Excess blood protein is lost through glomeruli
only in case of oak poisoning and renal
amyloidosis in cattle and sheep
• Advanced liver damage (cirrhosis)
 3. Obstruction in the lymph vessels
Obstruction in the lymph vessels – leading to
slightly decrease in O.P. in arterial side
Fall in OP in arterial side
 If OP falls in artery
• OP= 20 at arterial side (say)
• BP = 45
• Diff in pressure = 25mm of Hg.
So, 25mm of Hg of water enters into the capillaries.
Venous side
• OP = 20
• BP = 15
• The pressure difference =B.P-O.P
=20-15 = 5mm of Hg
• So only 5mm of Hg of water comes to the venules from the
capillaries resulting into the retention of 20mm of Hg of
water in the arterial side – Severe Oedema.
4. Sodium retention:
• Causes expansion of the intravascular fluid
volume and secondarily, the interstitial fluid
volume.
• Failure to excrete sodium in the urine results
in water retention in tissues of various organs
(leads to generalized oedema). e.g. congestive
heart failure, nephrosis/ nephritis, acute renal
failure.
5. Disturbance in the flow of blood in b/v due
to increase in permeability of the capillary
endothelium – leading to decrease in O.P. in
arterial side
(e.g.inflammation, thermal, mechanical injury
and allergic condition)
 Terms used according to the location of
accumulation of fluid ( hydro + organ)
• Hydrocephalus- fluid in brain.
• Hydrothorax-fluid thoracic cavity
• Hydropericardium- fluid pericardial sac
• Hydroperitoneum-fluid peritoneum
• Hydrocele –fluid tunica vaginalis of testis
• Anasarca –means, generalized oedema of the
s/c tissue of the whole body
 Gross changes in oedema /How to
identify oedema?
1 Swelling of the part
2 Cool in touch a (sub normal temp)
3 No pain
4 Pits on pressure
5 Increase in weight of affected organ
6 Fluids come out when incised/ cut the oedema
part
7 Less intense colour than normal
 Microscopic change in oedema

1 Microscopic amount of fluid in intercellular

space, cells swollen.
2. Cytoplasm contains vacuoles. Nucleus pushed
on periphery
3 In long-standing case atrophy or fibrosis of
organ’s parenchyma.
4. Microscopic sections contain a finely granular
material, which stain faintly pink with eosin due
to the presence of albumin in the transudate.
Anasarca / General edema
Pulmonary odema
Hydropericardium/ body cavity
Oedema disease
Ventral oedema
Oedema of musculatures

HS
 Thank you
• Any question?
 Lect. 25. Shock

• Shock is a serious circulatory disturbance in

which there is a decrease in total blood volume
and also decrease in flow of blood. Here the
blood will be thick due to haemoconcentration.
 Types of shock

• I Generic classification:
1. Primary shock
caused by stimuli of nervous system and there
will be immediate death. Shock is usually
associated with fright and emotional crisis
2. Secondary shock:
Example: - Case of accident, profuse
haemorrhage, severe burns, surgery.
II Classification on the basis of cause:

• Neurogenic shock e.g. psychological, castration,

surgical manipulation, etc.
• Hypovolumic shock; Dehydration
• Haemorrhagic shock: accident leading to
haemorrhage
• Toxic shock. e. g. chemical / plant toxin, burn,
burn and retained placenta in women.
• Traumatic shock e.g. accident, surgery
• Endotoxic shock e.g. by bacterial toxins
 III Classification On the basis of
pathophysiology

• Hypovolumic shock. e.g. due to severe burn, vomition,

diarrhoea, severe haemorrhage
• Cardiogenic shock. e. g. due to myocardial infarction,
Cardiac tamponade due to haemopericardium.
• Septic or endotoxic shock . e. g.E.coli, Proteus sp. ,
Pseudomonas infection. The most notorious bacteria
are gram negative ones although gram positive
bacteria also produce endotoxins.
• Neurogenic shock e. g. due to anaesthesia, spinal cord
injury. Herethe principal mechanism of shock is due to
peripheral vasodilatation with pooling of blood.
 Stages of shock

• Early shock: If there is slight decrease in blood

volume the heart rate will increase and the skin
becomes pale
• Progressive shock: If there is decrease in blood
pressure the volume of blood pumped by the
heart will be less. In oligourea such condition
occurs.
• Irreversible shock: Here there will be progress
reduction in BP and cardiac output. This
condition leads to coma followed by renal failure,
uremia and death of the individual.
 Mechanism of secondary shock ( step by
step)

• Injury to the tissue ( say, burn or toxin)

• Release of histamine
• Dilatation of capillary endothelium / increase
in the space of tight junction
• Blood fluid escape from capillaries to other
tissues.
• Less blood in the venous side/ large vessels.
• Less blood in heart and large b/v
 Mechanism of ……….
• Increased Hb % in blood
• Heart and b/v cannot maintain normal pressure
• Availability of less oxygen, nutrients to the tissue
• Accumulation of waste products in the tissues
• Degeneration and necrosis of the tissue of bod
• Shock and death result due to asphyxia.
 Symptoms of shock

• Coldness of skin, animal depressed, lethargic and

worried
• Subnormal temperature
• Rapid pulse, heart rate very rapid.
• Shallow breathing and irregular
• Rapid heart rate
• Sharp fall in B.P
• Animal becomes gradually depressed,
unconsciousness and finally death due to
circulatory failure.
 Gross lesion in shock
• 1. Small amount of blood in body cavities
• 2. Acute general passive hyperaemia, capillaries
dilation
• 3. Severe congestion of liver, kidney, intestine,
lungs, intestine, lymph nodes, etc.
• 4. Petechial haemorrhage in the different organs
• 5. Anaemia of Spleen but normal in size.
• 6. Organ cyanotic
 Microscopic lesions in shock

• Small veins and capillaries are distended with

blood
• Pin point haemorrhage at places
• Cells and tissue fibres are separated by
transudate
Thank you for your kind attention !