Download Disseminated intravascular coagulation (DIC),

‫‪Hemodynamic Disorders 3‬‬
‫د‪.‬بنان برهان محمد‬
‫ماجستير‪/‬هستوباثولوجي‬
Disseminated Intravascular
Coagulation (DIC),
It is a sudden or insidious onset of widespread
thrombi formation in the micro-circulation, which
are causing diffuse circulatory insufficiency,
especially in brain, lungs, heart and kidneys.
The multiple thrombi will lead to
rapid
consumption of platelets and coagulation proteins
(consumption coagulopathy) that results in
activation of fibrinolytic mechanisms.
So, a thrombotic disorder evolves into a serious
bleeding disorder.
DIC is not a primary disease but rather a
potential complication of many conditions (e.g.
obstetric complications, infections, advanced
malignancy, massive tissue injury).
Embolism:
Is a detached intravascular solid, liquid, or
gaseous mass that is carried by the blood to a
site distant from its point of origin with
subsequent impaction .
The site of impaction depends on the source of
the embolus.
The potential effect of embolism is ischemic
necrosis (infarction).
There are many types of emboli:
1. Thrombo-embolism (99%).
2. Fat.
3. Gas (air, nitrogen).
4. Amniotic fluid.
5.Atherosclerotic debris.
6. Tumor fragments.
7. Bone marrow.
8. Foreign body (bullet).
Pulmonary thrombo-embolism:
In more than 95% of instances, venous emboli
originate from DVT, (above the level of the knee).
Depending on the size of the embolus:
1. It may occlude the main pulmonary artery.
2. Impact across the bifurcation (saddle embolus).
3. Or pass out into the smaller branching arterioles.
Frequently there are multiple emboli.
Rarely, an embolus may pass through an interatrial ( patent foramen ovale) or inter-ventricular
defect to gain access to the systemic circulation
(paradoxical embolism).
Pulmonary embolism
Saddle embolus of main pulmonary trunk
Pulmonary embolus obstructing the main pulmonary
artery
Lung hilum thromboembolus with lines of
Zahn
Paradoxical embolus through a patent foramen ovale
Microscopic appearance of a pulmonary thromboembolus in a large
pulmonary artery. There are interdigitating areas of pale pink and
red that form the "lines of Zahn" characteristic for a thrombus
.
Clinical consequences include:
1. Most pulmonary emboli are silent.
2.Sudden death, cardiovascular collapse or acute Rt.
ventricular failure (more than 60% of pulmonary
circulation is obstructed).
3. Obstruction of medium-sized arteries may result in
pulmonary hemorrhage.
4. Obstruction of small end-arterioles result in
infarction.
5. Multiple emboli over time → pulmonary
hypertension → Rt. ventricular failure.
Systemic thrombo-embolism:
They may originate from:
1. Intra-cardiac mural thrombi (about 80% of
emboli).
2. Thrombi on ulcerated atherosclerotic plaques
3. Aortic aneurysm.
4. Fragmentation of a valvular vegetation.
5. Very small % from Paradoxical emboli.
The main sites involved are;
In contrast to venous emboli which lodge
primarily in one vascular bed (lung), arterial
emboli can travel to wide variety of sites:
1. Lower extremities (75%).
2. Brain (10%).
3. Intestines.
4. Kidneys.
5. Spleen.
Fat embolism,
it may result from;
1. Fractures of long bones (most common).
2. Soft tissue trauma and burns (rare).
Gas embolism,
Air embolism may enter the circulation during:
1. Obstetric procedures.
2. Chest wall injury.
More than 100 ml of air are required to produce a clinical
effect, bubbles can coalesce to form frothy mass
sufficiently large to occlude major vessels.
***Decompression sickness***
Is a particular form of gas embolism occurring in
individuals who are exposed to sudden changes in
atmospheric pressure (deep sea divers). When air is
breathed at high pressure, increased amounts of
gas (particularly nitrogen) become dissolved in the
blood and tissues. If the diver ascends
(depressurizes) too rapidly,
the nitrogen expands in
the tissues and bubbles
out of solution in the blood to
form gas emboli.
Clinically, the diver suffers from;
1.Muscle and joint pain.
2. Infarctions in various tissues.
3. Respiratory distress(chokes).
Amniotic fluid embolism:
Is a grave but uncommon complication of labor.
The underlying cause is the infusion of amniotic
fluid or fetal tissue into the maternal circulation
via a tear in the placental membranes or rupture
of uterine veins.
1. Sudden severe dyspnea.
2. Cyanosis.
3. Hypotensive shock.
4. Seizure and coma.
5. If the patient survives, pulmonary edema and
DIC develop.
Infarction :
It is an ischemic necrosis caused by occlusion of
either the arterial supply or the venous drainage
in a particular tissue.
Causes, include:
1. Thrombosis or embolism (99%).
2. Local vasospasm.
3. Expansion of atheroma due to hemorrhage in
plaque
4. Extrinsic compression of a vessel e.g. tumor,
twisting, edema, hernia).
5. Traumatic rupture of blood supply.
Morphology
Infarcts are classified on the basis of their color
and the presence or absence of infection, into;
1) Red (hemorrhagic).
2) White (anemic)
And 1) Septic.
2) Sterile.
Red infarcts: occur in the following situations;
1. Venous occlusion (ovarian torsion).
2. Loose tissue (lung).
3. Tissues with dual circulation(lung, small
intestine).
4. Previously congested tissues.
5. Re-established blood flow to site of necrosis.
White infarcts: Occur in
1. arterial occlusions.
2. solid organs with end-arterial circulation (e.g.
heart, spleen, kidney).
Pulmonary infarction ( wedge- shaped area & has begun to
organize at the margins) caused by a medium-sized
thromboembolus to the lung.
Infarctions of the spleen (wedge –shaped pale areas(
caused by obstruction of spleenic artery
Coagulative necrosis
(infarction) of kidney
Clinical correlation
The consequences of a vascular occlusion can
range from no or minimal effect, to death of a
tissue or even the individual.
The factors that influence the outcome include;
1. Nature of the vascular supply.
2. Rate of development of occlusion.
3. Vulnerability to hypoxia.
4. Oxygen content of blood