patho sheet # 5 of Dr Faisal - Sari Ma7aseh

by **Shadi Jarrar** 5/12/2010, 2:27 pm

بسم الله الرحمن الرحيم

_________________________________________________________________
https://cid-5cd521ed790e48d5.office.live.com/self.aspx/patho%20sheet%2029-11/patho29-11.doc
_________________________________________________________________

Last lect. We introduced the term embolus which is a traveler in the cardiovascular system circulating away from the origin, it may be solid, semisolid or fluid.(ex. nitrogen embolus, fat embolus).The most common form is thrombus.
Frequently an embolus might result in infarction if there are certain conditions that might facilitate the infarction such as the lack of a collateral circulation (ex. The lung has 2 circulations the pulmonary and the bronchial circulations).
If these factors are not satisfied completely they might result in either ischemia of the target organ (ex. Embolus in a small artery or a rich anastomatic channel) or hemorrhage so infarction might not occur.
remarks about pulmonary embolization:
1-Some researches stated that 15% of hospitalized patients have a sort of pulmonary embolization, some might show hemorrhage or ischemia to a part of the lung.
However the researches are widely variable depending on the hospital and the country.
2-Deep vein thrombosis especially at or about the popliteal fossa in the lower limb, this is most common site of thrombosis for the embolization of the pulmonary circulation.
That is the reason for the recommendation to move or dorsi-flex your feet while sitting for a long period of time because it prevent the formation of a thrombus in the deep veins but not in the superficial veins.
3-massive occlusion it's in the form of either a large no of small emboli obstruct a large no of pulmonary small vessels or a large embolus obstruct a large artery such as the main pulmonary artery (if the obstruction involves the right and left pulmonary trunks it is named saddle because it will look like a saddle).
Roughly speaking If the embolus resulted in death then a min. of 60% of the pulmonary circulation were obstructed which means that a large thrombus was formed in the illiofemoral (deep), femoral or the popliteal vessels, usually the thrombus is big and the patient may present signs and symptoms (edema in the lower limb, pain and cyanosis).
So a long thrombus might result in massive embolization resulting in death (60% of the pulmonary circulation is usually obstructed due to the big thrombus)
Sometimes the thrombus might arise from the heart in the case of the congenital abnormalities of the heart.
One of the commonest congenital abnormalities of the heart is the VSD (ventricular septal defect),if the pressure of the left side of the heart is higher than that of the right side then emboli might present in the right side coming from the left side because there will be left to right shunting and vice versa.
But if there was a right to left shunting and there was an embolus and a VSD then the embolus will move to the left side of the heart and travels along the arteries and may reach the brain, the lower limbs, the circle of Willis, the coronary arteries or any other artery branch.
Right to left or left to right shunting is called paradoxical (which means the movement from one side to the other).
The vast majority of systemic emboli (arterial emboli) arise from the heart which in turn arise from acute myocardial infarction, rheumatic heart diseases (stenosis of the mitral valve which cause stasis of blood in the left ventricle and a thrombus is formed) may participate in the systemic emboli.
Turbulence causes arrhythmia in the left ventricle which leads to thrombus formation.
Atherosclerotic lesion of abdominal aorta and aneurism of other arteries might give rise to an embolus.
The most common is the aneurism of the lower abdominal aorta which is caused by an atherosclerosis.
Another cause is Infective endocarditis, in the past they used to call it bacterial endocarditis or subacute endocarditis but sometimes it’s not subacute so they don't use the subacute or bacterial terms unless they are sure and to specify the type of endocarditis.
Usually the valve surface is smooth but if get infected with Microorganism, they may cause irregular elevations at the valves (different valves of the heart),they are called vegetations.
The most common form of vegetation is the infective endocarditis because there are other vegetation formed by other ways and may cause embolization.
Replacement of the original valve because of its injury or damage, this replacement by another valve whether mechanical (metal or plastic) or bio (heart valve taken from an animal such as pigs), this is called prosthesis.
These factors (endocarditis, prosthesis and paradoxical) promote embolization.
The source of embolus in about 15% of patients is not known but with modern technologies this percentage decreased to less than 7%.
As I mentioned before embolism could lead to ischemia, hemorrhage and infarction.
There are certain factors that could lead to one of the above:
1-vulnerability of the tissue,ex.end artery which means that one artery enters the organ and one vein exits the organ so there is no collateral circulation in the organ so if an embolus obstructs the artery infarction will occur, the classical example is the ovary/testes.
The same principle applies to the brain if one artery is obstructed by an embolus so if ischemia takes place the neurons will die in 3-4 minutes.
Usually systemic embolization will affect the lower limb (because of the aorta which ends in the lower limbs) and sometimes it might affect the brain.
Fat embolus is an example, fat acts as a passenger within the cardiovascular system, and it's mainly formed by a trauma to a fat depot, severe burn or by a fracture of a long bone.
Once the bone fractures the fat is introduced into the systemic veins forming fat embolism (usually it affects the pulmonary circulation).
Duration is about 2-3 days, after the 3rd day of fracture the symptoms start to appear. Fortunately only 10% of these reach a severe case and shows serious symptoms.
Only 1/1000 of the 10% dies.
It causes:
1-mechanical obstruction of circulation
2-pulmonary embolization causes respiratory embarrassment (adult respiratory distress syndrome) ex. hyaline membrane disease in neonates which causes atelectasis.
3-changes in CNS (ex. Restlessness, coma)
4-anemia because it causes hemolysis and aggregation of the RBCs.
5-rash because thrombocytes and platelets are used to surround the fat globules.
Pulmonary embolization and changes in the CNS are the most important changes.

Air embolism (nitrogen embolism):
The divers are should rest for a while after getting out of the sea because in the deep sea the pressure is higher than that at the surface and because the divers use oxygen masks (scuba), with pressure some of the gas might dissolve within the plasma, if the diver gets out of the sea quickly, the air dissolved in the plasma might form a big embolus which might be lethal if it reaches the lungs.
The most subjected people to air embolus are the scuba divers and the people working in construction sites of the petroleum refineries.
One of the complications is severe pain (BEND), it's mainly because the air bubbles reaches the soft tissues around the joints causing a severe pain around the joints and pain in the soft tissues.
Some of the air bubbles causes aseptic necrosis, necrosis of the certain areas especially necrosis of the head of the femur, head of the tibia and the head of the humerus.
The necrosis is not infective, it mainly causes pulmonary embolism which may be fatal.
The air embolism aroused primary in the construction sites workers in the petroleum refineries and because they work in the deep sea in a structure similar to a cage so they named it kason (not sure of the spelling), then it was seen among scuba divers.

Amniotic fluid embolism:
It's very rare situation, the lady might die in 70-80% of cases, different measurements are taken to prevent disseminated intravascular coagulation because of the amniotic fluid absorbed in the circulation which causes chemical and immunological reactions and the end result will be extensive endothelial injury leading to DIC (disseminated intravascular coagulation) and hemorrhage so the mortality is very high.

INFARCTION
Mainly due to occlusion of an arterial blood supply or venous drainage.
It might result in gangrene.
Infarction mainly occurs by
1-thrombo-embolism either arterial or venous.
2-A drug that causes vasospasm (ex. alkaloids)
3-Atherosclerotic complication (ulceration or calcification of the atherosclerotic area)
4-compression by a tumor might compromise the venous drainage because the vein wall is thinner than that of the artery, this causes cyanosis. Stasis and stagnation.
5-hernia also causes infarction because it compromises the venous blood supply so the blood will pool with the viscous area of the hernia and because the venous drainage is compromised it will start to collect at the hernia site.
Factors which might influence the process are:
1-nature of the blood supply, ex. The size of the artery, presence of collateral circulation, presence of double the blood supply such as the hand which is supplied by 2 arteries the radial and the ulnar arteries.
2-tissue vulnerability, ex. If the tissue is cartilage the needed blood supply is minimal (can withstand blood supply cut for long period of time) while the neurons can't withstand blood supply cut for more than 4 minutes.
3- rate of vessel occlusion, ex. If the vessels are occluding slowly they might give the needed time for the collateral circulation to open and supply the tissues. However if the vessels occludes quickly no time is given for the collateral circulation to open so infarction occurs.
If the infarction was infective it's called septic infarct while if it was not infective then it's called sterile infarct.
2 types of infarctions:
1-hemorrhagic infarction
Usually affects soft tissues
2-anemic infarction
Usually affects hard tissues and arterial blood supply is obstructed.
Change that occurs during infarctions:
1-infarcted area is dull in the first 1-2 days
after a few days the hemorrhagic infarction stays as it is but the anemic infarct becomes yellowish and depressed.
2- In few days both infarcts are surrounded by hemorrhagic irregular border and can be separated from the healthy tissue easily.
3- On both infarcts the first 2 weeks the tissue is most soft especially the heart tissue so normal life should not be resumed until the end of the 2nd week.

4- 6-8 weeks are needed for regeneration to occur and the infracted tissue to be replaced with fibrous tissue.

DONE BY: SARI ADEL MAHASNEH
DATE OF LECT.:29-11-10