III.

THROMBOSIS
A thrombus is a solid mass of blood constituents
formed within the vascular system in life.
Predisposing factors (virchows triad)
- abnormalities of the vessel wall (injury to
endothelium).
- abnormalities of blood flow.
- abnormalities of the blood constituents
(alteration in the blood, hypercoagulability)
Arterial thrombosis is most commonly
superimposed on atheroma.
Venous thrombosis is most commonly due to stasis.
Cinica conse!"ences inc"de#
Arterial thrombosis (tissue infarction distally)
Venous thrombosis (oedem due to impaired venous
drainage and emboli).
T$pe of thro%&i
- Pale thrombi composed of fibrin and platelet
with few entrapped erythrocytes.
!sually they occur in arteries.
- "ed thrombi which contain large numbers of
erythrocyte.
!sually they occur in veins.
Sites of thro%&osis
'. (rteria thro%&osis.
#s common, it typically occurs after endothelial
damage and local turbulence caused by
atherosclerosis.
$arge and medium si%ed arteries such as the aorta,
carotid arteries, circle of willis, coronary arteries
are mainly affected.
$ess commonly, its follows polyarteritis nodosa,
giant cell arteritis, or thromboangitis obliterans.
). Cardiac thro%&osis*
thrombi from within the chambers of the heart in
the following circumstance.
-inflammation of cardiac valves endocarditis and
valvulitis lead to local turbulence and deposion of
platelet&fibrin thrombi (vegetation) on the valves.
- damage to mural endocardium endocardial
thrombi from following infarction of the subjacent
myocardium.
- turbulence and stasis in arterial chambers large
ball thrombi may form in atrial fibrillation.
+. ,eno"s thro%&osis
- thro%&ophe&itis
denotes venous thrombosis occurring secondary to
acute inflammation.
#nvolve the superficial veins of e'tremities.
#s characteri%ed by the thrombus being firmly
attached to the vessel wall, and rarely forming
emboli.
- Phe&othro%&osis
denotes venous thrombosis occurring in the
absence of obvious inflammation.
(ccurs mostly in the deep veins of the leg (deep
vein thrombosis).

-ate of the thro%&"s
-Propagation
the thrombus may propage and eventually cause
obstruction of some critical vessel.
-emboli%ation
thrombi may dislodge to distal sites in the vascular
tree.
-dissolution
they may be removed by fibrinolytic activity.
-organi%ation and recanali%ation
thrombi may induced inflammation and fribosis
termed organi%ation, and may eventually become
recanali%ide.
.isse%inated intravasc"ar coag"ation (.IC)
)he widespread development of small thrombi in
the microcirculation throughout the body is serious
and often fatal.
*auses
#n many cases, the cause of disseminated
intravascular cuogulation is un+nown. #ts occurs as
a complication of many disease.
,ffects -
- decreased tissue perfusion
due to multiple occlusions of small vessels,
disseminated intravascular coagulation may lead to
microinfarction and shoc+.
- bleeding
is due to e'haustion of clotting factors factors
(consumption coagulopathy), e'cess fibrinolysis,
and release of fibrin degradation products, which
have anticoagulant properties. (ften the main
clinical effect is hemorrhage.
)reatment
.eparin is administered to inhibit the formation of
thrombi. #nfusion of platelets and plasma can
restore the depleted coagulation factors.
/MBO0ISM
An embolus is a mass of material in the vascular
system able to became lodged within a vessel and
bloc+ its lumen.
/ost emboli are derivated from thrombi
(thromboembolism).
(ther type of embolic material include
Atheromatous pla0ues material, vegetation on
heart valves (infective endocarditis), fragmen of
tumor (causing metastasis), amniotic fluid, gas, fat.
/ost common occurrence is pulmonary embolism
from deep leg vein thrombosis.
Origin of e%&oi
A. (rigin in systemic veins
,mboli that originate in systemic vein and the right
side of the heart lodge in the pulmonary arterial
system unless.
)hey are so small that they can pass through the
pulmonary capillaries.
,mboli that originate in the portal vein lodge in the
liver.
1. (rigin in heart and systemic arteries.
,mboli originating in the left side of the heart and
systemic arteries lodge in a distal systemic artery
in brain, heart, +idney, e'tremity, intestine, etc.
T$pes 1 sites of e%&ois%
(. Thro%&oe%&oi
2etached fragments of thrombi are the
commonest form of embolus.
3. P"%onar$ e%&ois%.
Pulmonary emboli are the most serious form of
thromboembolism.
(ver 456 of pulmonary emboli originate in the
deep veins of the leg (phlebothrombosis).
)hey are more common with certain states that
predispose to phlebothrombosis
- post operative and postpartum periods.
- cardiac failure.
- oral contraceptives.
*linical effects- si%e is the factor most influencing
the clinical effects of pulmonary embolism.
). S$ste%ic arteria e%&ois%.
*auses, origins of emboli
- #nfective endocarditis , emboli arise from
vegetation on the mitral and aortic valves.
- /ural endocardial thrombi in patients who have
suffered myocardial infarction.
- Atrial thrombi in patients with atrial fibrillation.
- /ural thrombi in patients with aortic and
ventricular aneurism.
*linical effects depend on the si%e, the site, and
the collateral supply.
#nfarction is common in brain, heart, +idney and
spleen. $ess common in intestine and limb.
B. (ir e%&ois%
#s rare, about 375 ml of air causes death.
*auses
- 8urgery of or trauma to internal jugular veins.
- *hild birth or abortion.
- )herapeutic pneumothora'.
- !terotubal insufflation.
C.2itrogen gas e%&ois%(decompression sic+ness
is also called caisson disease.
*auses
Air breathed at high underwater pressure
e0uilibrate with the tissue (nitrogen is selectively
soluble in adipose tissue.
#f decompression is too rapid , nitrogen comes out
of solution and forms bubbles in the tissues and
blood stream.
)he bubbles act as emboli.
8cuba divers who ascend rapidly from depths as
shallow as 35 m are at ris+.
*linical effects
Platelets adhere to nitrogen bubbles, leading to
disseminated intravascular coagulation.
#mpaction of gas bubbles in capillaries adds to the
ischemia.
#nvolvement of the brain in severe cases may cause
death.
9erve and muscle involvement causes pain.
$ung emboli cause difficulty in breathing.

.. -at e%&ois%.
*auses
)ypically follows fractures of large bones (eg,
femur) that e'pose fatty bone marrow.
*linical effects
$arge fat globules, are arrested in the lung and
cause respiratory distress.
8maller fat globules pass into the systemic
circulation, and may produce a hemorrhagic s+in
rash or acute diffuse neurologic dysfunction.
About 356 of patients with clinical fat embolism
die. :at can be demonstrated in vessel at autopsy.
/. Bone %arrow e%&ois%
:ragments of bone marrow may also form emboli
after trauma, but produce little clinical effect.
-. (thero%ato"s (choestero) e%&ois%.
!lcerated pla0ues often release atheromatous
material into the circulation.
8uch emboli lodge in small systemic arteries.
#n the brain they produce transient ischemic
attac+s.
3. (%niotic f"id e%&ois%.
)his is rare, but a mortality rate of about ;56.
)hromboplastic substances in amniotic fluid induce
disseminated intravascular coagulation.
,mboli composed of fetal hair or s0uamous cell may
be found in the lungs at autopsy.
H. T"%or e%&ois%.
)hese are usually too small to constitute
significant emboli.
"enal carcinoma has a propensity to grow into the
inferior vena cava, and form large emboli.