EMBOLISM
Dr. Hussain Bilal
CONTENT
Definition
Types
Pathological features.
DEFINITION
Embolus is an intravascular solid, liquid or
gaseous mass that is carried by the blood to a site
distant from its point of origin.
majority of emboli derive from a dislodged
thrombus hence the term thromboembolism.
TYPES
1. Pulmonary
Depending on the size, a PE can occlude the main
pulmonary artery, lodge at the bifurcation of the right and
left pulmonary arteries or pass into smaller, branching
arterioles.
TYPES
2. Systematic
80% arise from intracardiac mural thrombi. the remainder
originate from aortic aneurysms, thombi overlying
ulcerated atherosclerotic plaques, fragmented valvular
vegetations or the venous system.
PE
Major clinical and pathological features.
Most PE are small and clinically silent. With time they undergo
organization and become incorporated into vascular wall; this
leaves behind bridging fibrous webs.
A large embolus that blocks a major pulmonary artery can cause
sudden death.
PE
Embolic obstruction of medium sized arteries and subsequent rupture
of capillaries rendered anoxic can cause pulmonary hemorrhage. Such
embolization does not usually cause pulmonary infarction since the
area also receives blood through an intact bronchial circulation.
However, a similar embolus in the setting of left sided cardiac failure
can lead to a pulmonary infarct.
Multiple emboli occurring over time can cause pulmonary
hypertension and right ventricular failure ( corpulmonale).
FAT EMBOLISM
Soft tissue crush injury or rupture of marrow vascular sinusoids releases
microscopic fat globules into the circulation.
Minority of patients develop a symptomatic fat embolism syndrome
characterized by pulmonary insufficiency, neurological symptoms,
anemia, thrombocytopenia and diffused petechial rash which is 10% fatal.
Clinical sign and symptoms appear 1 to 3 days after injury as a sudden
onset of tachypnea, dyspnea, tachycardia, irritability and restlessness
which can progress rapidly to delirium or coma.
FAT EMBOLISM
Pathogenesis of fat emboli syndrome involves both mechanical
obstruction and biochemical injury. Fat micro-emboli occlude
pulmonary and cerebral microvasculature, both directly and by
triggering platelet aggregation. This deleterious effect is exacerbated by
fatty acid release from lipid globules, which causes local toxic
endothelial injury. Platelet activation and granulocytes recruitment
complete the vascular assault.
AMNIOTIC FLUID EMBOLISM
It is an uncommon and grave complication of labor and
immediate postpartum period.
Onset is characterized by sudden severe dyspnea, cyanosis
and hypotensive shock followed by seizures and coma.
AMNIOTIC FLUID EMBOLISM
The underlying cause is entry of amniotic fluid into the
maternal circulation via tears in the placental membranes
and/or uterine vein rupture.
Histological analysis reveals squamous cells shed from
fetal skin, lanugo hair, fat from vernix caseosa and mucin
derived from fetal respiratory or gastrointestinal tracts in
the maternal pulmonary microcirculation.
AIR EMBOLISM
Gas bubbles within the circulation can coalesce and obstruct
vascular flow and cause distal ischemic injury.
A small volume of air trapped n a coronary artery during
bypass surgery or introduced into a cerebral arterial circulation
by neurosurgery performed in an upright sitting position can
occlude flow with dire consequences.
AIR EMBOLISM
Small venous gas emboli have sufficient air that can enter
pulmonary circulation during obstetric procedures or as a
consequence of a chest wall injury to cause hypoxia.
Air embolism can occur upon rapid decompression, most
commonly in diverse; it results from sudden bubbling of
nitrogen dissolved in blood at high pressures.
MORPHOLOGY