4. Edema
Normal body water distribution:Two compartments:
1. Intracellular – comprising of two- thirds of
total body fluid.
2. Extracellular – comprising of one- third of
total body fluid.
1. Interstitial compartment- 75%
2. Intra vascular compartment – 25%
5. Normal fluid exchange
There
are two ends for a capillary
1. Arteriolar end
2. Venous end
The pressure is high in the arteriolar end
then the venous end.Normally the fluid
moves out from the vessel in arteriolar
end into interstitial tissue. From
interstitial tissue same fluid moves back
into vessel at venous end.The small
amount of fluid which is left in interstitial
space is cleared by lymphatics.
9. Normal fluid pressures
1. Osmotic pressure
Is exerted by the chemical constituents of the
body fluids
Eg. Electrolytes – crystalloid osmotic
pressure
proteins (albumin)- oncotic osmotic
pressure.
2. Hydrostatic pressure
Pressure within the blood vessel.
11. Classification of edema according to
distribution of fluid
Localized edema
involving one organ or part of the body.
eg-pleural effusion,ascitis,pericardial
effusion ,etc.
2. Generalized edema
Involving the entire body- ANSARCA
1.
12. Pathogenesis of edema:1.
2.
3.
4.
5.
Increased hydrostatic pressure
Increased permeability of the vessel
wall
Decreased oncotic pressure
Sodium retention in the kidneys
Obstruction of lymph flow
13. 1. Hydrostatic edema
Results
from increased intra
vascular pressure (hydrostatic
pressure).
15. 2. Increased vascular
permeability
Commonest
cause is
inflammation.Release of inflammatory
mediators like histamine, bradykinin,
PAF & others leads to increased
permeability.
Other causes: Injury,
16. 3.Decreased plasma oncotic
pressure
1.Decresed synthesis in the liver – end
stage liver disease.
2.Incresed loss in urine(nephrotic
syndrome) or stool (protein losing
enteropathy)
3.Inadequte intake-kwashiokar
17. Sodium Retention
Excessive salt intake with renal
insufficiency
Increased tubular reabsorption of
sodium
Renal hypoperfusion
Increased renin-angiotensinaldosterone secretion
18. Lymphatic obstruction
Elephantiasis
Edema
of the arm following surgical
resection of axillary lymph nodes
Edema of hand following post irradiation
fibrosis.
40. Classification based on origin
1. Cardiac- penetrating wound
rupture of ventricles in MI
2. Arterial – trauma
rupture of aneurysm
3. Capillary – trauma, surgery
4. Venous – trauma, surgery
41. Petechiae, Pupura, Ecchymoses
Refers
to the hemorrhage into the skin
& mucosae.
Petechiae- pinpoint hemorrhage ( < 1mm)
Purpura- 1mm- 1cm in diameter
Echymoses- >1cm
45. Hematoma
Is
grossly visible accumulation of
extravasted blood in tissue.
First it is red, then as the blood is
deoxygenated it becomes dusky &
bluish red.
46. Body cavity hemorrhage
Hemothorax – accumulation of blood in
pleural cavity
Hemopericardium – in pericardial cavity
Hemoperitonium – in peritonial cavity
Hemoarthrosis – in intra – articular space
Hematocephalus – in ventricles of brain
47. Hematuria
Is appearance of blood in urine.
1. Microscopic – detectable by
microscopic examination of urine.
2. Macroscopic – visible to naked eye
Hematuria signifies disease of kidney or
urinary tract
48. Hematemesis
Is
vomiting of blood.
Sign of esophageal & gastric
hemorrhage like rupture of esophageal
varices & peptic ulcer bleeding.
50. Melena
Black
colored blood in stools.
Indicates bleeding in upper GIT.
Blood is partialy digested by HCLof
gastric juice & transformed into a black
pigment called hematein.This pigmentis
not digested in the intestines & is
passed in the feces.
51. Epistaxis & Hemoptysis
Epistaxis
is bleeding from the nose.
Hemoptysis is bleeding from lungs.
52. Menorrhagia & Metrorrahagia
Menorrhagia
is heavy menstrual
bleeding.
Metrorrhagia occurs at any time & is
not related to menstrual cycle.
53. Effects of Hemorrhage
Site
of hemorrhage
– brain, pericardium, pleural spac
Rate
of blood loss
– acute
• loss of > 20% of blood volume may cause
hypotension or hypovolemic shock
• hemoglobin concentration not altered
– non-acute
• volume loss compensated by shift of fluid from
extravascular to intravascular compartment
• hemoglobin concentration decreased
54. HYPEREMIA &
CONGESTION
Is
increase in volume of blood in a
particular tissue.
Hyperemia is an “active process” , the
increased blood influx results from
arteriolar dilatation.
Congestion, also known as “passive
hyperemia”, results due to stagnation of
blood because of venous obstruction.
58. Examples:Hyperemia:1. Inflammation
2. Blushing – adrenergic stimulation
3. Exercise – incresed blood flow to the
muscle.
Congestion:Obstruction of veins due to thrombi or
backward pressure due to heart failure.
59. Color of hyperemic & congested
tissue: Hyperemic
tissue contains increased
amounts of oxygenated blood &
therefore the tissue appears bright red.
Congested tissue contains increased
amounts of deoxygenated blood &
appears blue.
Hyperemic tissue is warm, while
congested blood is cold & clammy.
60. Chronic venous congestion
(CVC): In
CVC there is long standing there is
accumulation of deoxygenated blood &
hence there is damage to the tissue.
61. Mechanism
heart failure
left heart failure
Pressure into
Pulmonary vein
CVC LUNGS
right heart failure
pressure into the
systemic venous system
CVC LIVER SPLEEN KIDNEY
62. CVC Lung
Causes:Left heart failure
Gross :The lungs are heavy. Lungs appear
brown- BROWN INDURATION OF
LUNGS.
63. CVC Lungs
Micro:Rupture of congested vessel results in
edema & hemorrhage. Lysis of RBC’s
releases hemosiderin pigment which is
taken up by macrophages – HEART
FAILURE CELLS.
64.
65.
66. CVC Liver
Causes:1. Right heart failure
2. Occlusion of inferior vena cava or
portal vein.
GROSS APPEARANCE:NUTMEG APPEARANCE – Alternate
areas of red & yellow .
68. CVC Liver (MICRO)
Blood fills up the central vein & sinusoids
around it. Followed by centrilobular
hepatocytes necrosis.
In the long standing cases the necrotic
area is replaced by fibrous tissue.
The areas with blood appears red &
areas with fibrosis appears whitish
yellow- NUTMEG APPEARANCE.
Caused by abnormalities in number or function of platelets or abnormalities in capillary wall (e.g. scurvy)
The palpable purpura on the foot of this nearly 3-year-old boy are associated with the disease Henoch-Schönlein Purpura.
Henoch-Schönlein Purpura involves small vessels, not capillaries. Another common cause of purpura is vasculitis induced by an allergic reaction to drugs.
The purpura and ecchymosis on the skin of this 12-year-old boy were the presenting symptoms of his acute myelogenous leukemia.
The hemoglobin is converted to bilirubin (greenish) and hemosiderin (brown)
Figure 4-3 Hyperemia versus congestion. In both cases there is an increased volume and pressure of blood in a given tissue with associated capillary dilation and a potential for fluid extravasation.
In hyperemia, increased inflow leads to engorgement with oxygenated blood, resulting in erythema.
In congestion, diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and resulting in cyanosis.
View of pulmonary congestion and edema. Often caused by an increase in hydrostatic pressure, a protein poor transudate seeps into interstitial and alveolar spaces. Note the engorged alveolar wall capillaries. If capillaries rupture, RBCs will escape into the alveolar space
Heart failure cells are hemosiderin laden macrophages. Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst. Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.
Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.
Nutmeg liver compared with actual nutmeg.
Courtesy of Dr. Ed Friedlander
This view shows a close up of hemorrhagic central necrosis. Necrotic cells in the central area have been removed (cell dropout) and been replaced by cellular debris and hemorrhge. There is evidence that the passive congestion and hemorrhage is chronic, as many of the RBCs have been degraded into hemosiderin.
