4. Typesofemboli
A. Depending upon the matter in the emboli.
Solid e.g. tumour cell clumps, tissue fragments,parasites.
Liquid e.g. fat globules, amniotic fluid, bone marrow.
Gaseous e.g. air, other gases.
B. Depending upon whether infected or not:
Bland, when sterile.
Septic, when infected.
C. Depending upon the source of the emboli:
Cardiac emboli from left side of the heart
Arterial emboli e.g. in systemic arteries in the brain, spleen, kidney,
intestine.
Venous emboli e.g. in pulmonary arteries.
Lymphatic emboli can also occur.
5.
6. Thromboembolism
Adetachedthrombusorpartofthrombusconstitutes.
Themostcommontypeofembolism.
Arterial (systemic) thromboembolism. Arterial emboli may be derived from the following
sources:
A. Causes within the heart (80-85%): These are mural thrombi in the left atrium or left ventricle.
B. Causes within the arteries: These include emboli developing in relation to atherosclerotic
plaques, aortic aneurysms.
The effects of arterial emboli
1. Infarction of the organ or its affected part e.g. ischaemic necrosis in the lower
limbs.
2. Gangrene following infarction in the lower limbs if the collateral circulation is
inadequate.
3. Arteritis and mycotic aneurysm formation from bacterial endocarditis.
4. Myocardial infarction may occur following coronary embolism.
5. Sudden death may result from coronary embolism
11. Decompression Sickness
This is a specialised form of gas embolism known by various
names such as caisson’s disease, divers’ palsy or aeroembolism.
PATHOGENESIS. Decompression sickness is produced when the
individual decompresses suddenly, either from high atmospheric
pressure to normal level, or from normal pressure to low
atmospheric pressure.
Amniotic Fluid Embolism.
This is the most serious, unpredictable and unpreventible cause
of maternal mortality. During labour and in the immediate
postpartum period, the contents of amniotic fluid
may enter the uterine veins and reach right side of the heart
resulting in fatal complications.
12. Theclinicalsyndromeofamnioticfluidembolism
• Sudden respiratory distress and dyspnoea
• Deep cyanosis
• Cardiovascular shock
• Convulsions
• Coma
• Nexpected death
Tumour Embolism.
Malignant tumour cells invade the local blood vessels and may
form tumour emboli to be lodged elsewhere, producing
metastatic tumour deposits.
13. INFARCTION
DEFINITION. Infarction is the process of tissue necrosis
resulting from some form of circulatory insufficiency.
Causes of infarction
o Most commonly, infarcts are caused by interruption in
arterial blood supply, called ischaemic necrosis.
o Less commonly, venous obstruction can produce
infarcts termed stagnant hypoxia. Generally, sudden,
complete, and continuous occlusion (e.g. thrombosis or
embolism) produces infarcts.
14. o TYPES OF INFARCTS
o 1. According to their colour:
o Pale or anaemic.
o Red or haemorrhagic, seen in soft loose tissues.
2. According to their age:
o Recent or fresh
o Old or healed
3. According to presence or absence of infection:
o Bland, when free of bacterial contamination
o Septic, when infected.
18. Edema
Definition of edema : Abnormal accumulation of fluids in the
body extravascular.
The oedema may be of 2 main types:
1. Localised when limited to an organ or limb e.g. lymphatic oedema, inflammatory
oedema, allergic oedema.
2. Generalised (anasarca or dropsy) when it is systemic in distribution, particularly
noticeable in the subcutaneous tissues e.g. renal oedema, cardiac oedema,
nutritional oedema.
19.
20. PATHOGENESIS OF OEDEMA
1. Decreased plasma oncotic pressure.
i. Oedema of renal disease e.g. in nephrotic syndrome, acute glomerulonephritis.
ii. Ascites of liver disease e.g. in cirrhosis of the liver.
iii. Oedema due to other causes of hypoproteinaemia e.g. in protein-losing
enteropathy.
2. Increased capillary hydrostatic pressure.
i. Oedema of cardiac disease
ii. Ascites of liver disease.
iii. Passive congestion.
3. Lymphatic obstruction.
i. Pressure from outside
ii. Inflammation of the lymphatics as seen in filariasis.
iii. Occlusion of lymphatic channels by malignant cells
21. 4. Tissue factors:
i. Elevation of oncotic pressure of interstitial fluid.
5. Increased capillary permeability.
i. Generalised oedema occurring in systemic infections.
ii. Localised oedema(Inflammatory oedema)
6. Sodium and water retention:
i. Oedema of cardiac disease e.g. in congestive cardiac failure.
ii. Ascites of liver disease e.g. in cirrhosis of liver.
iii. Oedema of renal disease e.g. in nephrotic syndrome, acute glomerulonephritis.
