Category Archives: CIRCULATORY DISTURBANCES
GANGRENE
Posted by DAM
on February 2, 2012
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GANGRENE
Definition: it is necrosis of tissue with super-added putrifaciton.
Gangrene may be:
- Primary.
-
Secondary.
The difference lies in the cause of the tissue necrosis.
- Primary gangrene: is brought about by infection with pathologic bacteria which both kill the tissue by secreting potent exotoxins and then invade and digest the dead tissue e.g. gas gangrene.
- Secondary gangrene: in which necrosis is due to some other cause usually loss of blood supply from vascular obstruction or tissue laceration and saprophytic bacteria then digest these dead tissues e.g. dry and moist gangrene.
Types of gangrene: There are three types:
I- Dry gangrene:
Usually occurs in the limbs which are exposed to dryness by evaporation of the tissue fluid. Lower limbs are more commonly affected than upper limbs, starting from the big toe which is the farthest point of circulation.
Causes:
1 – The Cause of necrosis is cut of blood supply in tissues with poor collateral circulation due to:
a- Atheroma or arteriosclerosis is the commonest cause especially in old age and it is called senile gangrene. It leads to inadequate collateral circulation followed by thrombosis in a main artery with cut of blood supply.
b- Embolism.
c- Spasmodic contraction of arteries as occurs in Raynaud’s disease.
- Causes of putrefaction: are usually putrefactive micro-organisms which ingest and digest the dead tissues.
Pathogenesis:
- Early manifestations of gangrene, the affected limb, cold, pale, with loss of sensation and loss of function.
- The process of gangrene starts in the big toe and gradually ascends up the limb until there is an adequate blood supply where it stops.
- The affected part becomes dry, shrunken and mummified.
- A series of colors appear in the form of red, green, and then black depending on the increasing amount of iron sulphate (due to action of hydrogen disulphide produced by bacteria on the hemoglobin of the red blood cells).
- Putrefaction is minimal and spread of gangrene is slow due to lack of fluids. The toxemia is minimal and that is why the general condition of the patient is good.
-
The living tissue just near the gangrenous part, become irritated forming thin line of granulation tissue which appears red in color and is called “line of demarcation” later on it is transformed into fibrous part and so it will be called “line of separation”. The separated gangrenous part is called “slough” and the remaining part is called “stump” which appears conical in shape because the blood supply of the skin and subcutaneous tissue is less abundant than that of the muscle and bones.
II- Moist or wet gangrene: it is very serious and usually fatal. It usually develops in parts where there is excess tissue fluids as occurs in the following sites:
1- Moist gangrene of the limbs: gangrene of limbs may be of the moist type in the following conditions:
a- Diabetic patients: where the arteries and collaterals are already narrowed due to accompanying arteriosclerosis. In addition, the excess sugar in tissues favors bacterial infection inducing thrombosis in arteries and veins to occur. The limb becomes edematous and thus the gangrene is going to occur in the moist type. Diabetic gangrene occurs in younger people.
b- In old persons: if there is edema of lower limbs, due to any cause, and gangrene is going to occur, it will be of the moist type due to presence of excess edema fluid.
c- Following severe crushing injury of the limb, a thrombus will occur in both arteries and veins. Thrombosis in veins leads to edema of lower limbs and thrombosis in arteries lead to cut of blood supply followed by gangrene which in this condition will be of the moist type due to edema.
Internal organs such as:
a- Intestines: Necrosis of a loop of the intestine occurs due to cut of blood supply as occurs in strangulated hernia, thrombosis or embolism of one of the mesenteric arteries. This is followed by invasion of this dead segment by the putrefactive organisms, present normally in the lumen of the intestine as B. Lactis aerogenes. The color of this part rapidly turns black due to iron sulphide with very offensive odor. The general condition of patient is very bad due to marked toxemia and the manifestations of acute intestinal obstruction.
b- Lungs: Especially if there is severe infection such as bronchopneumonia, lung abscess, in a patient with marked lowering of resistance, senility and diabetes.
c- Appendix: In acute suppurative appendicitis if thrombosis occurs in appendicular artery leading to cut of blood supply.
Moist gangrene of the skin of the back (known as “bed sores”: It is a common complication in prolonged recumbancy due to paralysis or fracture. It occurs over the sacrum and buttocks due to pressure opposite boney prominences leading to cut of blood supply in the arteries of the skin. Important predisposing factors as old age, long standing illness with malnutrition and deficiency of proteins. The dead tissues are cast off, lead to a sore which exposes the underlying bone.
Pathogenesis of wet gangrene:
- The affected part is swollen, edematous and there may be ulcerated and shows blebs containing bubbles of gas.
-
The series of colors usually appears very rapidly.
- Putrefaction is maximal with very bad odor and marked acute toxemia which is the usual cause of death.
- The line of demarcation will not appear because the process of gangrene is rapid.
- Putrefaction is maximal with very bad odor and marked acute toxemia which is the usual cause of death.
Ill- Gas gangrene: It is a rare disease usually affecting the muscle in neglected wound particularly those of wars, may follow surgical operations when there are septic conditions. The commonest cause are spores of Clostridium which are introduced into deep wounds germinate rapidly under anaerobic conditions, proliferate and produce toxins which cause extensive necrosis of muscles and at the same time produce putrefaction in dead muscles which acquires a green or black color. Toxemia is severe and fatal.
Cancrum oris: It is caused by bacteria e.g. Borrelia vincenti and fusiform bacteria (normal flora of the mouth) which cause necrosis of the gum and then spread to the cheek then the dead tissues undergo putrefaction. Deficient intake of vitamin B complex predisposes to the condition. Usually this condition occurs in poorly nourished children.
Difference between dry and moist gangrene
|
Point of comparison |
Dry |
Moist |
|
Mode of onset |
Gradual |
Sudden |
|
Site of gangrene |
Limbs |
Limbs and internal organs |
|
Site of occlusion |
Artery |
Artery and veins |
|
Cause of necrosis |
Tissue anoxia |
Tissue anoxia or toxins |
|
Tissue fluids |
Decreased |
Increased |
|
Size of affected part |
Shrunken |
Swollen |
|
Line of demarcation |
Well formed |
Poorly formed |
|
Toxemia |
Mild |
Severe |
|
Course |
Slow, may end in self-separation |
Rapid and fatal |
EDEMA
Posted by DAM
on February 1, 2012
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EDEMA
Definition:
It is excessive accumulation of fluids in tissue spaces and serous sacs.
Normally:
A certain amount of fluid is distributed in the interstitial tissues of the body, which is regulated by:
1- The normal capillary permeability.
2- The normal hydrostatic pressure in the venous capillaries.
3- By the normal osmotic pressure of the plasma proteins. Causes of edema:
1- Increase in the permeability of the capillaries caused by toxins and anoxia.
2- Increase in the venous hydrostatic pressure of the capillaries as occurs in chronic venous congestion.
3- Decrease of the colloidal osmotic pressure of the plasma proteins below 5%. The decrease in albumin is more important because it has stronger osmotic pressure than globulin.
4- Lymphatic obstruction: The interstitial fluid is removed by lymphatics.
Types of edema:
It may be local or generalized.
I- Local edema which may be:
A- Inflammatory edema: This appears in acute inflammation and is due to increased capillary permeability and increase of the osmotic pressure in the interstitial tissues due to the high protein content in the inflammatory exudate.
B- Edema due to venous obstruction: As occurs in thrombosis of the femoral vein with edema of the lower limb. It is usually due to increased venous pressure due to stagnation of venous blood, helped by increased capillary permeability due to anoxia. It also occurs in a loop of intestine in volvulus and in strangulated hernia.
II- Generalized edema (anasarca) is of 3 main types:
a- Cardiac edema
b- Renal edema. 1 – Nephritic 2- Nephrotic c- Nutrional edema.
III- Lymphatic edema:
Due to lymphatic obstruction as in elephantiasis and edema of the skin of the breast and the arm in carcinoma of the breast where the lymphatics are obstructed by the malighant infiltration.
IV- Allergic edema:
Appears in some allergic diseases or due to hypersensitivity and is known as angioneurotic edema and is due to increased capillary permeability.
V- Other types of edema:
1- In normal pregnancy, edema of the ankles, which may
be accompanied by generalized edema may develop.
This is due to increased retention of fluids which occurs
in normal pregnancy. This may be helped in late months
of pregnancy by pressure of the enlarged uterus on the
veins and lymphatics of the lower limbs.
- In toxemia of pregnancy or pre-eclampsia, edema may appear due to hypertension and proteinurea which occurs in this disease.
2- Edema due to adrenal hormones:
In Cushing’s syndrome and during therapeutic administration of cortisone and ACTH, edema may develop and this is due to salt and water retention.
Generalized edema:
A- Cardiac edema: which occurs in right-sided heart failure with chronic generalized venous congestion. It is directly related to gravity and first appears in the ankles when the patient is walking and in sacral region when he is sleeping.
Pathogenesis or causes: It is usually due to the following factors:
1- Increase in the venous pressure of the capillaries.
2- Increased capillary permeability due to anoxia from congestion.
3- Accumulation of waste products in the tissues which by their osmotic action will tend to attract more water from blood.
4- Salt and water retention due to disturbance of the renal and adrenal functions resulting from decrease in the cardiac output. This is the main factor.
- The reduction in cardiac output, leads to renal vasoconstriction which helps the reabsorption of sodium with water retention.
- The generalized edema, leads to a decrease in the blood volume because increased fluid is retained in tissues. This decrease in blood volume stimulates the secretion of antidiuretic hormone and aldosterone, leading to salt and water retention.
B- Renal edema: which is of two forms.
1- Nephritic edema: which occurs in acute glomerul-
onephritis. It is a mild type of generalized edema which
affects mainly the face and eyelids and sometimes the
ankles and genital region. It is due to increase in the
capillary permeability based on allergic mechanism with
damage of the capillary walls. Another important factor
is the accompanying oligemea in acute glomerul-
onephritis, which leads to water retention.
2- Nephrotic edema: It is a severe type of generalized edema
which appears in nephrosis and in the nephrotic syndrome such as rapidly progressive glomerulonephritis and renal amyloidosis. It is mainly due to decrease in the osmotic pressure of the plasma proteins due to heavy albuminurea.
C- Nutritional edema: also known as "famine edema" which usually develops with prolonged malnutrition, chronic starvation and cachectic disease. It is usually due to decrease in the osmotic pressure of plasma proteins due to marked hypoproteinaemia.
Features of edema:
1- Generalized edema cannot be evident unless at least five liters of fluid had accumulated in tissues.
2- When we press with the finger on the edematous part, the fluid moves from one place to another and a pit is formed and this is known as pitting edema.
3- In severe generalized edema, fluid accumulates in the serous sacs leading to hydrothorax and hydroperitoneum. This fluid is known as transudate, which is quite different from the fluid which accumulates in the same sites as a result of inflammation and is called exudate.
Differences between transudate and exudates
Transudate
Exudates
1-protein content
Less than 1%
More than 3%
2- Aspect
Does not clot
May clot due to presence of fibrinogen.
3- Specific gravity
Less than 1015
More than 1015
4- Cells
Few or absent
Present in large numbers and their type depends on the type of inflammation.
EMBOLISM
Posted by DAM
on February 1, 2012
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EMBOLISM
Definition:
It is the circulation of undissolved material known as embolus and its impaction in small arteries. Embolism occurs only in arteries, never in veins except in the portal veins.
Type of emboli:
1- Detached part of a thrombus:
Non-infected thrombotic emboli lead to infarction while infected ones lead to pyemia.
2- Tumor emboli: formed of malignant cells that produce secondary deposits in distant organs known as metastases.
3- Parasitic emboli: e.g. Bilharzial ova.
4- Air emboli: This occurs in cut wounds in the neck.
5- Fat emboli: in fracture of bone and in marked fatty change.
6- Atheromatous emboli.
7- Amniotic fluid emboli: fatal.
THROMBOSIS
Posted by DAM
on February 1, 2012
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THROMBOSIS
Definition
It is a vital process with the formation of a solid mass (thrombus) from blood element essentially platelets inside the cardio-vascular system during life.
Causes of thrombosis:
1. Damage of endothelial wall: as in atherosclerosis, direct pressure, trauma or inflammation of the arterial wall.
2. Slowing of the circulation:
• In leg veins as post-operative or after labor due to recumbency.
• Chronic venous congestion.
• Acute inflammation.
• Aneurysm and varicose veins.
3. Changes in blood constitutents:
• Increase in viscosity of blood as in dehydration and after operation.
• Decrease in heparin.
Pathogenesis:
At first the platelets adhere to the site of endothelial damage, and then more platelets precipitate and accumulate in growing columns against the current of blood which appear as whitish lamina known as lines of Zhan. Stasis of blood occurs in between these lamina, in which fibrin threads are formed, entangling red and white blood cells.
Types of thrombi:
- Pale thrombus formed mainly of platelets.
- Mixed thrombus formed of different elements of blood.
Sites of thrombosis:
1- Thrombosis in veins: phlebothrombosis or thrombophlebitis.
2- Thrombosis in the arteries.
3- Thrombosis in the heart.
Fate of thrombus:
1- If small, it may be liquefied and dissolved.
2- Contraction with re-passing of blood again.
3- Detachment with embolic manifestation leading to infarction.
4- Infection with disintegration leading to septic emboli causing pyemia.
5- Organization or replacement with fibrous tissue with our without canalization.
6- Dystrophic calcification (phlebolith).
INFARCTION
Posted by DAM
on February 1, 2012
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INFARCTION
Definition
It means necrosis of some part due to complete ischemia. All infarcts present as coagulative necrosis except the brain which presents as liquifactive necrosis.
Types of infarction:
A. Red or hemorrhagic infarction:
Sites: lung, intestine.
It is infarction which remains red as occurs in the lungs and intestine due to increased blood content in these organs. Blood escapes from the damaged capillaries in the necrosed part and lies free in the infarct area.
B. Pale infarction:
Sites: heart, kidney, spleen.
Usually starts as red then the blood is gradually removed and the infarct area becomes pale in color.
C. Soft infarction: (liquifactive necrosis)
Occurs in the central nervous system, because of the high lipid content of the C.N.S, the necrotic tissue becomes softened and liquefied, then the fluid material is absorbed leaving a cyst.
HYPEREMEA
Posted by DAM
on February 1, 2012
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HYPEREMEA
Definition: It is increased accumulation of blood in tissues. Hyperemia may be: a) Active (arterial) Or b) Passive (Venous)
- Active or arterial hyperemia: In which the arterioles and capillaries are dilated and filled with blood, it may be physiological e.g. in muscular exercise or pathological e.g. in acute inflammation (the vascular response).
- Passive hyperemia or venous congestion:
It is increased accumulation of blood in the venous side of the circulation.
It is of two types local or general (systemic)
I- Generalized venous congestion or chronic venous
congestion (C.V.C): In which blood accumulates in the venous side of the circulation all over the body.
A- Causes in the heart: leading to congestive heart failure such as martial incompetence and aortic valvular disease.
B- Causes in lungs: leading to pulmonary hypertension such as:
- Emphysema.
- Increased fibrosis in the lungs as in pulmonary TB, chronic lung abscess, bronchiectasis and silicosis.
Effect of Generalized venous congestion:
1- The lungs:
Congestion of the lungs occurs only in cases of mitral stenosis and left sided heart failure.
Gross appearance:
1 – Both lungs are enlarged and heavy.
2- They are firm in consistency and brown (brown
induration) due to:
a- Hemosiderin pigmentation.
b- Fibrosis in alveolar septa induced by hemosiderin.
3- On cut section a big amount of frothy blood comes
out if the lungs are squeezed.
Microscopically:
1- Alveolar capillaries are dilated, tortuous and packed with red blood cells. Upon rupture, the extravasated red cells haemolyse and hemoglobin breaks into hematoidin (absorbed) and hemosiderin. Macrophages move into alveolar spaces and engulf red cells and yellowish granules of hemosiderin and are called cardiac or heart failure cells.
2- Alveoli are distended and filled with red blood cells and heart failure cells (which are diagnostic).
3- The interstitial tissues show increased fibrosis.
2- Liver:
Gross appearances:
1 – The liver is enlarged and firm in consistency.
2- Both outer and cut surfaces show a nut-meg appearance; mottled red due to congested centers of lobules and yellow streaks due to fatty change of the periphery of lobules.
Microscopically:
1- The central vein and sinusoids in the central zone of each hepatic lobule are distended with blood.
2- Liver cells in the center of lobules show at first fatty change and in long standing cases show atrophy of the central zonal cells. With advance of the case, fatty change appears in the mid-zonal area this is due to stagnation of blood in the sinusoids giving rise to tissue anoxia. In old cases, there is increased fibrosis around the central veins in the lobules, a condition known as "cardiac cirrhosis". Hemosiderin granules arc seen in kupffer cells.
3- Spleen
Gross appearance:
1- Dark red and enlarged up to 250 gm.
2- Red pulp is congested and appears almost black.
Microscopically:
1- The spleen shows congestion of the venous sinuses in the red pulp.
2- Thickening of reticulin framework.
3- Atrophy of medullary cords. 4- Kidney
Gross appearance:
1 – Kidney is enlarged and dark red.
2- Cut surface shows small dark red dots (congested
glomeruli) and dark red streaks (congested vessels) in
a rather pale cortex.
3- Medulla is dark red.
Microscopically:
1- Glomerular capillaries are distended with red cells.
2- Convoluted tubules show cloudy swelling or fatty change.
C.V.C. is also apparent in other organs as brain, stomach, intestine, adrenals.
II- Localized venous congestion: Occurs when the main vein of a tissue or an organ is obstructed. It may be acute or chronic.
a- Acute local venous congestion as occurs in strangulated hernia and thrombosis in a vein. The venules and capillaries in this local area are markedly engorged with venous blood.
b- Chronic local venous congestion for example.
1- In portal hypertension due to liver cirrhosis, leading to the following manifestations:
Venous blood accumulates in the radicals of the portal vein.
The spleen is enlarged in size and red in colour.
The anastomotic veins between the portal and systemic circulations become dilated, tortuous and engorged with blood i.e. varicosities at the lower end of oesphagus (oesophageal varices) and at the lower end of the rectum (piles).
In chronic cases, fluid may pass to the peritoneal cavity leading to ascites.
2- Gradual pressure on a vein from outside e.g by a tumor.
