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

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

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

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)

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

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

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

30. Increased hydrostatic pressure
Results in increased outflow of fluid
Causes:
Impaired venous return
Congestive heart failure / constrictive
pericarditis
Arteriolar dilatation - heat / neurohumoral
dysregulation

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

37. 2nd Year Pathology 2010
Pitting Subcutaneous Oedema

38. 2nd Year Pathology 2010
Cerebral Oedema & Herniation
Flattened sulci and uncal herniation

39. 2nd Year Pathology 2010
Cerebral Oedema & Herniation
Tonsillar herniation and
pontine haemorrhage

40. 2nd Year Pathology 2010
Effusions
Similar pathogenesis and aetiology as oedema
 Increased hydrostatic pressure
Left heart failure:
 Hypoproteinaemia
Cirrhosis - ascites
 Fluid overload (salt and water retention)
Renal failure
 Inflammation
Pleural effusion associated with pneumonia /
TB

41. Grossly
1. organomegaly or tissue swelling
2. subcutaneous tissues /dependent body parts:
sacrum / legs, pitting oedema
3. Tissues with loose extracellular matrix (ECM):
eyelids
4. Lungs - heavy, contain frothy blood-tinged fluid
5. Brain swollen with narrowed sulci and flattened
gyri , +/- evidence of herniation

42. 2nd Year Pathology 2010
Serous pleural effusion

43. 2nd Year Pathology 2010
Serosanginous pleural effusion

44. 2nd Year Pathology 2010
Fibrinous
pericarditis

45. 2nd Year Pathology 2010
Chylous Ascites

46. 2nd Year Pathology 2010
Effusions
Transudates:
Serous:
mainly edema fluid, very few cells
pleural effusion = hydrothorax
pericardial effusion = hydropericardium
peritoneal effusion = hydroperitoneum / ascites
Exudate :
 Fibrinous (serofibrinous):
 protein-rich exudate containing fibrin strands
 Purulent:
 numerous inflammatory cells, mainly neutrophils
 (also called "empyema" in the pleural space)

47. 2nd Year Pathology 2010
• Haemorrhagic (blood):
hemo-thorax/pericardium/peritoneum
Cause: trauma, ruptured MI / aortic aneurysm
• Chylous (lymphatic fluid):
chylo-thorax/pericardium/peritoneum
Cause: trauma (often surgical) to major lymphatic
vessels