The document discusses edema, hyperaemia, and hemorrhage, defining edema as an abnormal increase in interstitial fluid and outlining various types such as localized and generalized edema. It explains the factors influencing fluid transit across capillary walls, the pathogenesis of edema, and mechanisms leading to various conditions like cardiac, renal, and pulmonary edema. Additionally, the document covers hyperaemia, detailing active and passive types, and provides information on hemorrhage, its causes, effects, and consequences.

1. Edema, Hyperaemia,
Congestion, Haemorrhage
Dr Soumya Kanti Pramanik

2. Edema
 Definition of Edema : An abnormal increase in interstitial fluid within tissues is
called edema.
 fluid collections in the different body cavities are variously designated
hydrothorax (within thorax cavity) , hydropericardium (within pericardial
cavity), and hydroperitoneum/ Ascites (within peritoneal cavity)
 Anasarca is a severe and generalized edema with widespread
subcutaneous tissue swelling.

3. Factors influencing fluid transit across
capillary walls (Starling Forces)
 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.

4.  Disturbance in the normal Starling forces leads to edema i.e.,
1. Hydrostatic pressure
2. Oncotic pressure
3. Obstruction to venous/lymphatic flow
4. Capillary permeability

5. Classification :
Edema
Localized Generalized special type
1. Venous edema 1. Cardiac edema 1. Pulmonary edema
2. Lymphatic edema 2. Renal edema 2. Cerebral edema
3. Inflammatory edema 3. Hepatic edema
4. Allergic edema 4. Nutritional edema
5. Idiopathic edema

7. PATHOGENESIS OF OEDEMA
 The following mechanisms may be operating singly or in combination to
produce oedema:
1. Decreased plasma oncotic pressure
2. Increased capillary hydrostatic pressure
3. Lymphatic obstruction
4. Increased capillary permeability
5. Sodium and water retention

8. 1. DECREASED PLASMA ONCOTIC
PRESSURE-
 A fall in the total plasma protein level (hypoproteinaemia of less than 5 g/dl),
results in lowering of plasma oncotic pressure in a way that it can no longer
counteract the effect of hydrostatic pressure of blood. This results in
increased outward movement of fluid from the capillary wall and decreased
inward movement of fluid from the interstitial space causing oedema.
 The examples are -
i) Oedema of renal disease e.g. in nephrotic syndrome, acute
glomerulonephritis.
ii) Ascites of liver disease e.g. in cirrhosis of the liver.
iii) Oedema due to other causes of hypoproteinaemia e.g. in protein-losing
enteropathy

9. 2. INCREASED CAPILLARY HYDROSTATIC
PRESSURE -
 A rise in the hydrostatic pressure at the venular end of the capillary which is
normally low (average 12 mmHg) to a level more than the plasma oncotic
pressure results in minimal or no reabsorption of fluid at the venular end,
consequently leading to oedema.
 The examples are :
i) Oedema of cardiac disease e.g. in congestive cardiac failure, constrictive
pericarditis.
ii) Passive congestion e.g. in mechanical obstruction due to thrombosis of veins
of the lower legs, varicosities, pressure by pregnant uterus, tumours etc.
iii) Postural oedema.

10. 3. LYMPHATIC OBSTRUCTION-
 Obstruction to outflow of these channels causes localised oedema, known as
lymphoedema.
 The Examples are –
i) Removal of axillary lymph nodes in radical mastectomy for carcinoma of the breast
ii) Pressure from outside on the main abdominal or thoracic duct such as due to tumours,
effusions in serous cavities etc.
iii) Inflammation of the lymphatics as seen in filariasis (infection with Wuchereria
bancrofti) results in chronic lymphoedema of scrotum and legs known as elephantiasis.
iv) Occlusion of lymphatic channels by malignant cells may result in lymphoedema.
v) Milroy’s disease or hereditary lymphoedema is due to abnormal development of
lymphatic channels.

11. 4. INCREASED CAPILLARY
PERMEABILITY-
 Any injury to capillary endothelium leading to increase of capillary permeability to plasma
proteins, due to development of gaps between the endothelial cells, leading to leakage of
plasma proteins into interstitial fluid. This, in turn, causes reduced plasma oncotic pressure
and elevated oncotic pressure of interstitial fluid which consequently produces oedema.
 The examples are –
i) Generalised oedema occurring in systemic infections, poisonings, certain drugs and
chemicals, anaphylactic reactions and anoxia.
ii) Localised oedema-
a. Inflammatory oedema as seen in infections, allergic reactions, insect-bite, irritant drugs and
chemicals.
b. Angioneurotic oedema is an acute attack of localised oedema occurring on the skin of
face and trunk and may involve lips, larynx, pharynx and lungs. It is possibly neurogenic or
allergic in origin

12. 5. SODIUM AND WATER RETENTION-

13.  The Examples are –
i) Oedema of cardiac disease e.g. in congestive cardiac failure.
ii) Ascites of liver disease e.g. in cirrhosis of liver.
iii) Oedema of renal disease e.g. in nephrotic syndrome, acute
glomerulonephritis

14. PATHOGENESIS AND MORPHOLOGY OF
IMPORTANT TYPES OF OEDEMA
 Renal Edema-
1. Oedema in nephrotic syndrome- persistent and heavy proteinuria
(albuminuria) in nephrotic syndrome, there is hypoalbuminaemia causing
decreased plasma oncotic pressure resulting in severe generalised oedema.
2. Oedema in nephritic syndrome- due to excessive reabsorption of sodium
and water in the renal tubules via renin-angiotensin-aldosterone mechanism.
3. Oedema in acute tubular injury- loss of reabsortive capacity of glomeruli
and excessive retention of Na, water and toxic metabolites leading to
edema.

15. Cardiac Edema

16. Pulmonary Oedema
1. Elevation in pulmonary hydrostatic pressure (Haemodynamic oedema)-
left heart failure, mitral stenosis, pulmonary vein obstruction etc.
2. Increased vascular permeability (Irritant oedema)- fulminant pulmonary
and extrapulmonary infections, inhalation of toxic substances, aspiration,
shock, radiation injury, hypersensitivity to drugs or antisera, uraemia and
adult respiratory distress syndrome (ARDS).
3. Acute high altitude oedema- anoxic damage to the pulmonary vessels.

17. Cerebral Edema
1. VASOGENIC OEDEMA- Vasogenic oedema is prominent around cerebral
contusions, infarcts, brain abscess and some tumours.
2. CYTOTOXIC OEDEMA- the blood-brain barrier is intact and the fluid
accumulation is intracellular due to disturbance in the cellular
osmoregulation.
3. INTERSTITIAL OEDEMA- the excessive fluid crosses the ependymal lining of
the ventricles and accumulates in the periventricular white. This mechanism
is responsible for oedema in non-communicating hydrocephalus.

18. Morphology
 Subcutaneous edema mainly seen at the areas of high hydrostatic pressure,
most commonly at the dependent part of the body.
 Finger pressure over substantially edematous subcutaneous tissue displaces
the interstitial fluid and leaves a depression, a sign called pitting edema.
 periorbital edema is thus a characteristic finding in severe renal disease.
 pulmonary edema, the lungs are often two to three times their normal
weight, and sectioning yields frothy, blood-tinged fluid—a mixture of air,
edema, and extravasated red cells.
 cerebral edema could be Localized (due to abscess; neoplasms) or
Generalized (due to encephalitis; hypertensive crisis venous
obstruction). The brain is grossly swollen with narrowed sulci; distended gyri
show evidence of compression against the unyielding skull.

20. HYPERAEMIA AND CONGESTION
 the increased volume from arterial and arteriolar dilatation being referred to
as hyperaemia or active hyperaemia.
 the impaired venous drainage is called venous congestion or passive
hyperaemia.
 If the condition develops rapidly it is called acute, while more prolonged
and gradual response is known as chronic.

21. Active Hyperaemia
 Cause : either through sympathetic neurogenic mechanism or via the release of
vasoactive substances.
 Example :
1. Inflammation e.g. congested vessels in the walls of alveoli in pneumonia
2. Blushing i.e. flushing of the skin of face in response to emotions
3. Menopausal flush
4. Muscular exercise
5. High grade fever
6. Arteriovenous malformations
 Clinically, hyperaemia is characterised by redness and raised temperature in the
affected part.

22. Passive Hyperaemia (Venous
Congestion)
 Due to impaired venous return.
 The affected tissue or organ is bluish in colour due to accumulation of
venous blood (cyanosis).
 In left-sided heart failure (such as due to mechanical overload in aortic
stenosis, or due to weakened left ventricular wall as in myocardial
infarction) pulmonary congestion results.
 In right-sided heart failure (such as due to pulmonary stenosis or pulmonary
hypertension) systemic venous congestion results.

23. MORPHOLOGY OF CVC OF ORGANS
 CVC Lung
 Gross- heavy and firm in consistency; brown induration of Lung.
 Microcroscopic- Widened and thickened Alveolar Septa. Minute intralvolar
haemorrhage, followed by breakdown of RBC and engulfment by Macrophages, So
called – Heart Failure Cell.
 CVC liver
 Grossly, the liver is enlarged and tender and the capsule is tense. Cut surface shows
characteristic nutmeg* appearance due to red and yellow mottled appearance,
corresponding to congested centre of lobules and fatty peripheral zone respectively.
 Microscopically, The centrilobular hepatocytes undergo degenerative changes, and
eventually centrilobular haemorrhagic necrosis. The peripheral zone of the lobule is less
severely affected by chronic hypoxia and shows some fatty change in the hepatocytes

25.  CVC Spleen
 Grossly, enlarged, firm and tense appearance.
 Microscopically, Red pulp is enlarged due to congestion and marked
sinusoidal dilatation. Sinusoids may get converted into capillaries
(capillarisation of sinusoids). There is hyperplasia of reticuloendothelial cells
in the red pulp of the spleen (splenic macrophages).
- There is fibrous thickening of the capsule and of the trabeculae. Some of
haemorrhages overlying fibrous tissue get deposits of haemosiderin pigment
and calcium salts; these organised structures are termed as Gamna-Gandy
bodies.

26. HAEMORRHAGE
 Haemorrhage is the escape of blood from a blood vessel.
 The bleeding may occur externally, or internally into the serous cavities or
into a hollow viscus.
 Extravasation of blood into the tissues with resultant swelling is known as
haematoma.
 Large extravasations of blood into the skin and mucous membranes are
called ecchymoses.
 Purpuras are small areas of haemorrhages (upto 1 cm) into the skin and
mucous membrane, whereas petechiae are minute pinhead-sized
haemorrhages.

27. Aetiology
1. Trauma to the vessel wall e.g. penetrating wound in the heart or great vessels,
during labour etc.
2. Spontaneous haemorrhage e.g. rupture of an aneurysm, scurvy etc
3. Inflammatory lesions of the vessel wall e.g. bleeding from
chronic peptic ulcer, typhoid ulcers etc
4. Neoplastic invasion e.g. haemorrhage following vascular
invasion in carcinoma of the tongue.
5. Vascular diseases e.g. atherosclerosis.
6. Elevated pressure within the vessels e.g. cerebral and retinal haemorrhage in
systemic hypertension.

28. Effect of Haemorrhage
 The effects of blood loss depend upon 3 main factors: (1) the amount of
blood loss; (2)the speed of blood loss; and (3)the site of haemorrhage.
 A sudden loss of 33% of blood volume may cause death, while loss of up to
50% of blood volume over a period of 24 hours may not be necessarily fatal.
 chronic blood loss generally produces iron deficiency anaemia, whereas
acute haemorrhage may lead to serious immediate consequences such as
hypovolaemic shock.

29. Thank you