Download Edema

‫‪Hemodynamic Disorders‬‬
‫د‪.‬بنان برهان محمد‬
‫ماجستير‪ /‬هستوباثولوجي‬
The health of cells and tissue depends not only on
an intact circulation to deliver oxygen and
nutrients and to remove wastes but also on
normal fluid balance (homeostasis).
Normal homeostasis encompasses maintenance
of vessel wall integrity as well as intravascular
pressure and osmolarity within certain physiologic
ranges.
Hemodynamic Disorders
Edema
Hyperemia and congestion
Hemorrhage
Hemostasis and thrombosis
Disseminated intravascular coagulation
Embolism
Infarction
Shock
Edema
Approximately 60% of lean body weight is water,
of which 2/3 is intracellular, 1/3 extracellular
(mainly interstitial), only 5% of total body water
is plasma
Edema : means pathological accumulation of
fluid in the interstitial tissue spaces or body
cavities..
Collection of fluid in the different body cavities
are variously designated:
•
•
•
•
Peritoneal cavity → ascites (hydroperitoneum)
Pleural cavity →hydrothorax
pericardium→hydro pericardium
anasarca → means severe & generalized
edema with profound subcutaneous tissue
swelling.
Nature of accumulated fluid:
• Transudate: this is serous (thin), protein poor fluid with
specific gravity < 1.012, due to intravascular volume or
pressure overload or reduced plasma protein (e.g. in
heart failure, nephrotic syndrome).
• Exudate: it is protein rich fluid, specific gravity >1.020
due to ↑vascular permeability leads to escape of
intravascular fluid with protein especially albumin.
e.g. in inflammation.
There are 2 opposing factors which govern the
movement of the fluid between vascular &
interstitial spaces:
• hydrostatic pressure (intravascular pressure)
encouraging the passage of fluid through the
capillary wall to the extra vascular compartment.
• osmotic pressure (plasma protein) encourages
the↑ retention of the fluid to the capillaries .
Normally , At the arterial end the hydrostatic
pressure is greater than the osmotic pressure
→ fluid is forced out the capillaries , of the
microcirculation.
The reverse occurs at the venous end & the
fluid is attracted into the vessels.
So the exit of fluid into the interstitium from
the arteriolar end of the microcirculation is
nearly balanced by inflow at the venular end;
a small residual amount of excess interstitial
fluid is drained by the lymphatics, then to the
blood stream via thoracic duct
Factors affecting fluid transit across capillary walls
Pathophysiology of edema(causes):
Edema results from:
1. Increased hydrostatic pressure.
2. Reduced plasma osmotic pressure
(hypoproteinemia).
3. Lymphatic obstruction.
4. Sodium and water retention.
5. Increased capillary permeability.
1-Increased hydrostatic pressure
a.Generalized edema:
It occurs most commonly in congestive heart failure
(CHF), affecting Rt. ventricular function. The heart
fails to pump the blood, that is received from the
Rt atrium, this causes accumulation of blood that
is reflect back into the systemic veins, as an
increase in systemic venous pressure → generalized
chronic venous congestion, this ↑ in hydrostatic
pressure elicits edema formation.
CHF is associated with ↓ cardiac output and
therefore reduced renal perfusion → stimulate
renin –angiotensin -aldosterone axis , inducing
Na+ and water retention by the kidney
(secondary aldosteronism).
This
mechanism
normally
functions
to
↑intravascular volume and improve cardiac out
put to restore normal renal perfusion, however if
the condition untreated the extra fluid load causes
increased venous pressure and eventually ↑
edema .
B.Localized edema :
As a result of impared venous return →↑
intravascular pressure → transudation of fluid e.g.
**deep venous thrombosis(DVT)→edema restricted
to the affected leg .
**during pregnancy due to pressure on the veins by
the gravid uterus → edema of the legs.
**acute Lt ventricular failure →acute pulmonary
edema.
2-reduced plasma osmotic pressure:
(Hypoproteinemia)
Reduced plasma osmotic protein→ movement
of fluid into the interstitial tissue (edema).
Reduced plasma volume→↓renal perfusion →
2'ry aldosteronism (Na+ and water retention)
and edema precipitated by low protein is
exacerbated by 2'ry Na+ and water retention.
Causes of reduced plasma oncotic
pressure::
1) protein malnutrition as in kwashiorkor.
2) Malabsorption
3) reduced albumin synthesis as in liver
cirrhosis.
4) excessive loss of albumin e.g. nephrotic
syndrome, also in protein – losing
gastroenteropathy.
3-lymphatic obstruction : Impaired lymphatic
drainage to area of the body →localized edema of
the affected part (lymphedema). It is
characteristically a non pitting edema. Causes:
*inflammation: certain parasitic infestation e.g.
filariasis →fibrosis of lymphatic vessels & L.N. of
the inguinal region → edema of external genitalia
&lower limbs (elephantiasis).
*tumor invasion e.g. in carcinoma of breast →
infiltration & obstruction of superficial lymphatics
→ edema of overlying skin → "peau d 'orange“.
*resection of lymphatic channels or scarring
related to surgery and radiation.
Lymphadema : (elephantiasis) non pitting
edema of the legs
4. Sodium and water retention : e.g. acute renal
failure and acute poststreptococcal
glumerulonephritis.
5. increase capillary permeability : e.g. inflammation.
Morphology:
Grossly : the edema is most easily recognized .
Microscopically →edema fluid generally
manifested as subtle cell swelling with clearing
&separation of the extracellular matrix elements
Although any organ or tissue may be
involved, edema most commonly encountered
in subcutaneous tissues, lungs and brain.
Subcutaneous edema: it can be:
**dependent edema : edema more prominent in
depended part of the body, the region with highest
hydrostatic pressures (influenced by gravity) e.g. HF
(Rt side HF) (in the legs when standing, in the
sacrum when recumbent),
**diffuse edema: Generalized and more severe
edema, is usually due to renal failure or nephrotic
syndrome.
Finger pressure over significantly edematous
subcutaneous tissue will displace the interstitial fluid
and leaving a finger-shaped depression (pitting edema)
Pulmonary edema:
Is a common clinical problem and frequently follow
Left side heart failure.
The lungs are typically 2-3 times their normal weight.
On sectioning frothy, sometimes blood-tinged fluid
representing a mixture of air and edema fluid and
extra-vasated RBCs.
Hyperemia and congestion
Both terms indicate a local increased
volume of blood in a particular tissue.
Hyperemia
•It is an active process.
• resulting from augmented blood flow due to
arteriolar dilation.
•the affected tissue is redder than normal
because of engorgement with oxygenated
blood.
e.g. - physiological as in skeletal muscle during
exercise
- pathological as in acute inflammation
Congestion :
•it is a passive process
•resulting from partial obstruction to the venous
return from a tissue.
•the tissue has blue –red color (cyanosis) due to
accumulation of deoxygenated blood in the affected
tissue.
Morphology:
Grossly, the cut surface is hemorrhagic and wet.
Microscopically, there is engorgement of capillaries by
blood.
Hyperemia and congestion
General venous congestion:
Where the whole venous return is impaired by chronic
obstructions. Combined
Rt and Lt sided heart
failure(CHF) causes systemic congestion, Rt sided heart
failure alone causes also systemic congestion but here
the lungs are spared.
Causes of Rt sided heart failure:
1. Lt sided heart failure, as it eventually leads to Rt
sided heart failure.
2. Chronic obstructive airway disease such as
emphysema, chronic bronchitis.
3. Pulmonary valve disease e.g. stenosis and /or
incompetence.
Local venous congestion:
Follows mechanical interference with the
venous drainage from an organ e.g.
---pulmonary congestion occurs in
mitral
stenosis, Lt sided heart failure, systemic
hypertension.
---thrombosis of the vein as in deep venous
thrombosis (DVT).
--- mechanical compression of the veins by
tumor or bandage, strangulated hernias,
volvulus of intestine
venous congestion → edema then may →
ischemic necrosis.