GENERAL PATHOLOGY

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EMBOLISM, ISCHAEMIA,
INFARCTION & SHOCK
Dr.Murali B M M.D(path)

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E M B O L I S M
An embolism is a process of detached
intravascular solid, liquid, or gaseous mass that is
carried by the blood, ultimately lodges in a vessel
too small to permit further passage, resulting in
partial or complete vascular occlusion leading to
ischemic necrosis of distal tissue (infarction).
An embolus is a detached intravascular solid,
liquid or gaseous mass that is carried by blood.
Embolus may have arisen from within the body or
may be introduced from outside. Most common (
over 90%) emboli is thrombus. Emboli that lodge
in cerebral or coronary blood vessels may be
rapidly fatal.

4. Types of embolism
• The material may be solid (Thrombus, fat), liquid
(amniotic fluid) or gas (air, nitrogen).
1. Thromboembolism (over 90% of embolism): In
Thrombo-embolism a thrombus that breaks loose
and travels through circulation. Common sites for
lodging of emboli are the small pulmonary blood
vessels of the lungs (pulmonary embolism) or
systemic circulations (systemic embolism).
2. Fat embolism
3. Air embolism
4. Amniotic fluid embolism

5. Angiogram showing embolism and infarction

6. PULMONARY THROMBO-EMBOLISM
• Originate from thrombosis of lower limb veins.
Most pulmonary emboli (60% to 80%) are
clinically silent because they are small.
• Embolic obstruction of small end-arteriolar
pulmonary branches may result in infarction.
Sudden death, right heart failure (cor pulmonale),
or CVS occurs when 60% or more of the
pulmonary circulation is obstructed with emboli

7. SYSTEMIC THROMBO-EMBOLISM
• Emboli traveling within the arterial
circulation. Mostly (80%) from intra-
cardiac mural thrombi. The major sites for
arteriolar embolization are the lower
extremities (75%) and the brain (10%). In
general, arterial emboli cause infarction of
tissues supplied by the artery

8. FAT EMBOLISM
• Microscopic fat globules may be found in
the circulation after fractures of long
bones (which have fatty marrow) or,
rarely, in soft tissue trauma and burns.
Less than 10% of patients with fat
embolism have any clinical findings.

9. AIR EMBOLISM
• Gas bubbles within the circulation can obstruct
vascular flow acting as thrombotic masses.
Bubbles may coalesce to form frothy masses
sufficiently large to occlude major vessels.
• Air may enter the circulation during obstetric
procedures or as a consequence of chest wall
injury or an injection of air in Intra-venous or
Intra-arterial lines .
• An excess of 100 cc is required to have a clinical
effect.

10. Decompression sickness
• Occurs when individuals are exposed to sudden changes
in atmospheric pressure as in deep sea divers. When air
is breathed at high pressure (e.g., during a deep sea
dive), increased amounts of nitrogen become dissolved
in the blood and tissues. If the diver then ascends
(depressurizes) too rapidly, nitrogen expands in the
tissues and bubbles out of solution in the blood to form
gas emboli.
• Treatment: placing the individual in a compression
chamber where the barometric pressure may be raised,
thus forcing the gas bubbles back into solution followed
by subsequent gradual decompression

11. AMNIOTIC FLUID EMBOLISM
• A grave and uncommon complication of labor
and the immediate postpartum period,
characterized by sudden severe dyspnea,
cyanosis, and hypotensive shock, followed by
seizures and coma.
• Caused by infusion of amniotic fluid or fetal
tissue into the maternal circulation via a tear in
the placental membranes or rupture of uterine
veins.
• If the patient survives the initial crisis,
pulmonary edema develops, along with DIC,
owing to release of thrombogenic substances
from amniotic fluid.

12. Ischaemia
• Ischaemia is the result of impaired vascular
perfusion, depriving the affected tissue vital
nutrients and oxygen.
• The effect of ischemia on tissue can be
reversible, but this depends on duration (brief
ischemic espisodes may be recoverable) &
metabolic demands of the tissue ( cardiac and
brains cells more vulnarable)
• No organs are exempt from the effects of
ischaemia
• If ischemia is sustained then death of tissue or
Infarction results.

13. Causes of Ischemia
• Atheroma resulting from Atherosclerosis
• Thrombus
• embolism
• Vascular spasm
• Vascular compression
• Vasculitis
• Hyper viscosity of blood
• Shock

14. Clinical effects of ischaemia
• Angina pectoris
• Acute renal failure
• Secondary hypertension
• Intermittent claudications
• Transient ischemic attacks of brain
• Strokes
• Frost bites

15. INFARCTION
• An infarct is an area of ischemic necrosis
caused by occlusion of either the arterial
supply or the venous drainage in a
particular tissue
• e.g. myocardial, cerebral, pulmonary and
bowel infarction.
• Thrombotic or embolic events occur due to
arterial or venous occlusion.

16. Consequences of Infarction
• The consequences of a vascular occlusion can
range from no or minimal effect, all the way up
to death of a tissue or even the individual.
• The major determinants include:
(1) the nature of the vascular supply;
(2) the rate of development of the occlusion;
(3) the vulnerability of a given tissue to hypoxia;
(4) the blood oxygen content.

17. Classification of Infarcts
• Infarcts are classified on the basis of their color
(reflecting the amount of hemorrhage) and the
presence or absence of microbial infection.
• A. Red (hemorrhagic) infarcts occur with
venous occlusions (such as in ovarian torsion)
• B. White (anemic) infarcts occur with arterial
occlusions in solid organs (such as heart, spleen,
and kidney.
• C. Septic infarctions when embolization
occurs by fragments of a bacterial vegetation
from a heart valve or when microbes seed an
area of necrotic tissue. The septic infarct is
converted into an abscess

18. Morphology of infarcts
• Gross: Most infarcts are wedge-shaped, with
the occluded vessel at the apex and the
periphery of the organ forming the base.
• Microscopy: An inflammatory response at the
margins of infarcts followed by phagocytosis of
the cellular debris by neutrophils and
macrophages. Most infarcts are ultimately
replaced by scar tissue.

19. Clinical effects
• Myocardial infarction
• Strokes
• Thrombophlebitis migrans
• Gangrene

20. S H O C K
Dr. Murali B M M.D(path)

21. S H O C K
• Shock is a clinical condition of reduced blood
flow to organs and tissues (tissue hypo-
perfusion).
• Systemic hypoperfusion caused by reduction
either in cardiac output or in the effective
circulating blood volume.
• The end results are hypotension, followed by
impaired tissue perfusion and cellular hypoxia.
• Initially the cellular injury is reversible,
persistence of shock eventually causes
irreversible tissue injury.

22. Morphology
Hypoxic injury particularly evident in
brain, heart, lungs, kidneys, adrenals, and
gastrointestinal tract .
• brain -ischemic encephalopathy,
• heart -coagulation necrosis,
• kidneys -tubular ischemic injury (acute
tubular necrosis, with oliguria, anuria, and
electrolyte disturbances &
• lungs are resistant to hypoxic but not
septic injury.

23. Classification of Shock
• Shock may be classified into three main
categories based upon the cause of the
shock:
1. Distributive shock
2. Cardiogenic shock
3. Hypovolemic shock.

24. 1. Cardiogenic Shock
• Shock that occurs when the heart is
unable to maintain normal cardiac output.
• Results from myocardial pump failure
• Possible causes of cardiogenic shock:
1. Heart failure
2. Myocardial infarction
3. Cardiomyopathy
4. Cardiac tamponade
5. Pneumothorax

25. 2. Hypovolemic Shock
• Shock that occurs from decreased blood volume
• It results from loss of blood or plasma volume
• Possible causes of hypovolemic shock:
1. Hemorrhage & Trauma
2. Excess fluid loss from diarrhea, vomiting &
burns
3. Shifting of fluids from the vasculature to the
interstitial spaces (ascites).

26. 3. Distributive Shock
• Occurs as a result of marked vasodilatation and loss of vascular
tone. Types of Distributive shock:
A. Neurogenic shock:
– Caused by loss of sympathetic input to blood vessels, leading to
loss of vascular tone and peripheral pooling of blood.
– Caused by brain or spinal cord injury, CNS depressant drugs &
Anaesthetic accidents.
B. Septic shock (endotoxic shock):
– Occurs most frequently with systemic infection by gram
negative bacteria, rarely with gram+ bacteria and fungi
– Widespread vasodilatation occurs in response inflammatory
mediators(examples: histamine, cytokines) and bacterial toxins.
C. Anaphylactic shock:
– An allergic reaction to antigens such as drugs, food, insect
venom, etc. initiated by a generalized IgE-mediated
hypersensitivity response
– Develops suddenly and manifests with marked systemic
vasodilatation, bronchospasm and hypotension. May be rapidly

27. Physiologic Responses to Shock
1) Decreased blood pressure is detected by baroreceptors
(pressure sensors) in the aortic arch and carotid arteries
which stimulate a centrally mediated increase in heart
rate and cardiac output.
2) The catecholamines epinephrine and norepinephrine are
also released by the adrenal medulla to increase
peripheral resistance, heart rate and cardiac output.
3) Reduced renal blood flow will also lead to activation of
the renin-angiotensin system with subsequent
vasoconstriction and fluid retention.
• Up to a certain point, these compensatory mechanisms
are able to maintain blood pressure and cardiac output;
however, as shock progresses these compensatory
mechanisms are no longer able to maintain adequate
blood pressure and as a result tissue and organ
perfusion will suffer.

28. Clinical Course
• The patient presents with hypotension; weak
rapid pulse; tachypnea; and cool, clammy,
cyanotic skin.
• In septic shock, skin is warm and flushed
because of Vasodilatation.
• Then, electrolyte disturbances and metabolic
acidosis (lactic acidosis) complicate the situation
followed by progressive fall in urine output .
• Prognosis: varies with origin and duration of
shock.80% to 90% of young healthy individuals
with hypovolemic shock survive with appropriate
management. Cardiogenic shock associated with
extensive myocardial infarction and gram-
negative septic shock carry mortality rates of up
to 75%, even with the best care.

29. Stages of Shock
Shock occurs in three stages:
1. mild (compensated),
2. Moderate (progressive) or
3. severe (irreversible).

30. 1. Mild or compensated shock
– Blood volume loss less than 25% of total
volume.
– Slight reductions in blood pressure.
– Mild peripheral vasoconstriction.
– Slight tachycardia (increased heart rate), cool
extremities.
– Possible activation of thirst centers of the
hypothalamus to increase fluid intake.

31. 2. Moderate or progressive shock
– Blood volume loss on the order of 25 to 35% of
total.
– Failure of compensatory mechanisms to
adequately maintain cardiac output.
– Significant tachycardia and peripheral
vasoconstriction.
– Tissues becoming hypoxic due to poor blood
perfusion; possible cyanosis (bluish tinge).
– Reduced urinary output (oliguria) to conserve
fluids.
– Evidence of symptoms of poor CNS blood flow
such as restlessness and impaired mental state

32. 3. Severe or irreversible shock
– Loss of blood volume that may approach 50%.
– Marked tachycardia.
– Rapidly falling blood pressure.
– Shallow, rapid breathing.
– Cessation of urine output (anuria).
– Unconsciousness.
– Organ and tissue damage from hypoxia.
– Shock irreversible at this point even if blood
volume is restored.
– Death from circulatory collapse

33. Complications of Shock
1. Adult respiratory distress syndrome (shock lung):
A potentially fatal respiratory failure that accompanies
severe shock, The exact cause is uncertain but the
condition may involve ischemic injury to lung tissues.
2. Acute renal failure: due to reduced renal perfusion.
3. Disseminated intravascular coagulation:
Formation of multiple small blood clots that may be
related to sluggish blood flow or abnormal clotting
activity.
4. Multiple organ failure, cerebral hypoxia, death.

34. Rationale for Therapy
1. The underlying cause of the shock must
be corrected if possible.
2. Maintenance of air ways (if required
mechanical ventilation
3. Plasma volume must also be restored
through the administration of fluids,
plasma or blood
4. Drugs that affect vascular tone or cardiac
output (Dopamine , Nitroprusside )may
also be of value.