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Hyperemia and congestion edema
1. Haemodynamics
The principles of blood flow are called
haemodynamics
Hyperemia and congestion
are the terms used for localised increase in
the volume of blood within the dilated vessels
of an organ/tissue
2.
3. Hyperemia Congestion
Eg:
1. At sites of
inflammation
2. In skeletal muscle
during exercise
3. Blushing – flushing
of skin of face in
response to emotions
4. Menopausal flush
Increased blood flow
Eg:
1. systemic in cardiac
failure
2. Isolated in venous
obstruction
3. Reduced outflow of
blood from a tissue
4.
5.
6. Hyperemia and congestion
Hydrostatic pressure is increased in both the
conditions,
hence, hyperemia and congestion are
always associated with edema
Edema: Accumalation of fluid in tissues
Effusion: When the serosal surface is involved,
fluid may accumalate in the adjacent body
cavity as an effusion
7. Left sided heart failure
Etiology –
1. Systemic hypertension – most common cause
2. Ischemic heart disease
3. Aortic or mitral valve disease
4. Primary myocardial disease
8. Clinical presentations of LHF
1. Obstruction to pulmonary vascular
outflow leads to pulmonary congestion
and edema
2. Reduced renal perfusion leads to
- salt and water retention
- reduced excretion of waste products -
azotemia
- ischemic tubular necrosis
3. Reduced CNS perfusion causes hypoxic
encephalopathy ( irritation to coma)
9. Clinical presentation of RHF
1. Congestion and edema of portal and
dependent peripheral area
Eg: feet, ankle and sacrum, effusions in
pleura and peritoneum
2. CVC spleen
3. CVC Liver
4. Acute tubular necrosis
10.
11.
12. CVC Liver
Etiology- Right heart failure
Occlusion of inferior vena cava and hepatic vein
Gross – Liver enlarged and tender
Capsule tense
C/S – nutmeg appearance
Central regions of hepatic lobules are grossly red-
brown and slightly depressed owing to loss of
cells and are accentuated against the sorrounding
zones of uncongested tan liver (nut meg liver)
13.
14. Microscopy –
Congestion more marked in the centrilobular
zone due to severe hypoxia than at
peripheral zone. So, fatty change in the
hepatocytes
Centrilobular hemorrhagic necrosis
Long cases – fibrosis and regeneration of
hepatocytes leading to cardiac cirrhosis
15.
16.
17. CVC Lung
Etiology –
left heart failure in rheumatic mitral stenosis
Gross –
Lungs – heavy and firm in consistency
C/S – dark, sometimes rusty brown in color
referred to as brown induration of lungs
brown induration is due to pigmentation and
fibrosis
18. Histology: Acute pulmonary congestion
Alveolar septa widened
( due to dilated and congested capillaries)
Focal intra-alveolar hemorrhage
Alveolar septal edema
Chronic pulmonary congestion
Alveolar septa thickened – increased fibrous
tissue
rupture of dilated and congested capillaries
leads to hemosiderin laden macrophages in
alveoli called as heart failure cells
19.
20. CVC Spleen
Etiology – Right heart failure
Portal hypertension from cirrhosis of liver
Gross – Spleen enlarged
Organ – congested, tense and cyanotic
C/S – grey tan
21. Microscopy: Red pulp – enlarged
Congestion and marked sinusoidal dilatation
Foci of recent and old hemorrhages
Hyperplasia of reticuloendothelial cells in red
pulp
Fibrous thickening of capsule and trabeculae
Gamma-gandy bodies / haemosiderofibrotic
nodules
Advanced stage – firm spleen
hepatic cirrhosis (congestive splenomegaly)
22. 2nd Year Pathology 2010
Oedema
Extravascular fluid collections can be classified
as follows:
Exudate: rich in protein and/or cells (grossly
cloudy)
Transudate: an ultrafiltrate of plasma with little
protein and few or no cells (grossly clear)
Oedema = increased volume of fluid in
interstitial space
Effusion = increased fluid in a body cavity
Oedema and effusions have similar
pathogenesis
23. 2nd Year Pathology 2010
Normal homeostasis
Movement of fluid between
microcirculation (arterioles, capillaries,
veins) and interstitium dependent on
intravascular hydrostatic pressure
intravascular colloid osmotic pressure
24. Normally
Net outflow at arteriolar end
(hydrostatic > osmotic)
No net flow across capillaries
(hydrostatic = osmotic)
Net inflow at venular end
(hydrostatic < osmotic)
Any excess interstitial fluid removed by
lymphatics
No net increase in interstitial fluid volume
25. 2nd Year Pathology 2010
Normal homeostasis
ARTERIOLE VENULECAPILLARY BED
Net flow
in
No net flowNet flow
out
LYMPHATICS
Excess
fluid
hydrostatic P
oncotic P
26. 2nd Year Pathology 2010
Increased hydrostatic pressure
ARTERIOLE VENULECAPILLARY BED
No net flow
Net flow
out
hydrostatic P
oncotic P
Net flow
out
Overall excess flow out
27. 2nd Year Pathology 2010
Decreased oncotic pressure
ARTERIOLE VENULECAPILLARY BED
No net flow
Net flow
out
hydrostatic P
oncotic P
Net flow
out
Overall excess flow out
28. 2nd Year Pathology 2010
Lymphatic obstruction
ARTERIOLE VENULECAPILLARY BED
Net flow
in
No net flowNet flow
out
Excess
fluid
hydrostatic P
oncotic P
Excess fluid collects
LYMPHATIC
29. 2nd Year Pathology 2010
Pathogenesis of Oedema
Increased hydrostatic pressure
Reduced plasma oncotic pressure
Lymphatic obstruction
Sodium and water retention
Inflammation
Protein-
poor
transudate
Protein-
rich
exudate
31. 2nd Year Pathology 2010
Results in decreased resorption of fluid
Causes:
nephrotic syndrome
cirrhosis
protein losing enteropathies
malnutrition
Reduced oncotic pressure
32. 2nd Year Pathology 2010
Lymphatic obstruction
Results in decreased resorption of fluid
Usually localised
Causes:
Surgical removal of lymph nodes and
lymphatics
Tumour metastases to lymph nodes
Irradiation
Filariasis (parasitic infection)
33. 2nd Year Pathology 2010
Sodium and water retention
Results in:
Expansion of intravascular fluid volume
Increased hydrostatic pressure
Dilutional decrease in vascular osmotic
pressure
34. 2nd Year Pathology 2010
Sodium and water retention
Causes:
1. Excessive salt intake
2. Renal diseases
- Acute renal failure
- Renal hypoperfusion
- Chronic renal disease
3. Cardiac failure Decreased cardiac output
renal hypoperfusion
4. Hypoproteinaemia Contraction of blood
volume renal hypoperfusion
35. 2nd Year Pathology 2010
Inflammation
Due to vasodilation and hyperpermeable vessels
vasoactive mediators
e.g. Histamine, cytokines e.g. IL-1, TNF
Characterised by:
protein-rich and inflammatory cell-rich exudate
Usually localized to sites of acute inflammation
Can be generalised and life-threatening e.g.
anaphylaxis
36. 2nd Year Pathology 2010
Localised oedema - blister
Generalised oedema –
laryngeal oedema in
anaphylaxis
