This document discusses different types of thromboembolism including pulmonary embolism, fat embolism, air embolism, and amniotic fluid embolism. It provides details on the definition, causes, risk factors, symptoms, diagnosis, treatment and prognosis of pulmonary embolism, which is the most common type of thromboembolism. The document also discusses the pathophysiology and mechanisms of the different embolism types.

1. Thromboembolism
DR MUHAMMAD ALI BASHIR.
PATHALOGY DEPT.

2. EMBOLISM
 An
embolus is an intravascular solid,
liquid, or gaseous mass that is carried by
the blood to a site distant from its point of
origin.
 The vast majority of emboli derive from a
dislodged thrombus—hence the term
thromboembolism.

3. Key Terms
Emboli
● Thrombosis
● Deep vein thrombosis
●

4. • Emboli
Clots or other substances that
travel through the blood stream and
get stuck in a blood vessel, blocking
circulation.

5. • Thrombosis
The development of a blood clot
inside a blood vessel.

6. •Deep vein thrombosis
The development of a blood clot
in the calf's deep vein. This frequently
leads to pulmonary embolism if
untreated.

7.  Most
common is pulmonary embolism.
 Less common types include: fat embolism,air
embolism,amniotic fluid embolism.

8. • Pulmonary embolism
The occlusion of one or more
vessels in the pulmonary arterial tree
by matter from a source extrinsic to
the lung. The process is almost
invariably acuate but may on
occasion be chronic.

9. How dose pulmonary embolism
occur ?

10. Prevalence & Incidence
of P.E
The term 'prevalence' of pulmonary
embolism usually refers to the estimated
population of people who are managing
pulmonary embolism at any given time.
●
The term 'incidence’ of pulmonary
embolism refers to the annual diagnosis rate,
or the number of new cases of pulmonary
embolism diagnosed each year.
●

11. Incidence (annual): approximately
650,000 cases in the USA
Incidence Rate: approx 1 in 418 or
0.24% in USA

12. Etiology
Pulmonary embolism is caused by emboli
that travel through the blood stream to the
lungs and block a pulmonary artery. When
this occurs, circulation and oxygenation of
blood is compromised. The emboli are usually
formed from blood clots but are occasionally
comprised of air, fat, amniotic fluid, tumor
tissue, or particulate matter from intravenous
injection, etc.

14. Common risk factors for pulmonary embolism:
congestive heart
failure;
leukemia;
polycythemia;
sickle cell anemia;
dysproteinemias;
massive obesity;
immobility;
cancer;
pregnancy;
oral contraceptives;
the early postpartum
period;
surgery;
DVT;
hypercoagulable
states;
right heart failure;
fractures of the pelvic
and lower extremities
etc.

15. Risk factors for pulmonary thromboembolism
include:
any cause of venous stasis
such as: ① venous valvular insufficiency
② right-side HF
③ the postoperative period
④ prolonged bed rest

16. Pathophysiology
Pulmonary embolism can have the following
pathophysiological effects:
Increased pulmonary vascular resistance due
to vascular obstruction, neurohumoral agents,
or pulmonary artery baroreceptors.
 Alveolar hyperventilation due to reflex
stimulation of irritant receptors.

17. Impaired gas exchange due to increased
alveolar dead space from vascular obstruction
and hypoxemia, V/Q mismatch.
Increased airway resistance due to bronchoconstriction.
Decreased pulmonary compliance due to lung
edema, lung hemorrhage,and loss of surfactant.

18. Symptoms
Each individual may experience
symptoms differently, which depend
on the size and number of emboli.

19. chest pain
● labored breathing, dyspnea, cyanosis
● cough
● syncope
● anxiety
● a rapid pulse.
● a low fever
● hypotension, shock
● fluid build-up in the lungs
●

20. Diagnosis
The diagnosis of pulmonary embolism
should be based on the patient's history,
physical exam, and diagnostic tests.

21. Symptoms ＆ Signs
● Plasma D-dimer levels
● ECG
● Arterial Blood Gas
● Chest Radiograph
● Ventilation/Perfusion Lung Scanning
● Pulmonary Angiography
●

22. Plasma D-dimer levels
●
●
Low specificity (40-43%)
High sensitivity (92-100%)
Plasma D-dimer levels <500ug/L by
ELISA may exclude PE

23. ECG
S1-Q3-T3
● RBBB (right bundle branch block)
● right axis deviation
● ischemia
● prominent P waves
● tachycardia
● atrial arrhythmia
0
●Ⅰ AVB(atrioventricular block)
●

24. S1-Q3-T3

25. Arterial Blood Gas
● hypoxemia ( Po )
2
●
●
respiratory alkalosis ( Pco2 )
increased A-a(Alveoli-artery) gradient

26. Chest Radiograph
can be normal
● pulmonary infiltrate
● pleural effusion
● elevated hemidiaphragm
● atelectasis
● Hampton’s hump ( a pleural-based,
wedge-shaped infiltrate )
●

27. Posteroanterior chest film of patient with pulmonary
embolism showing "Hampton's hump" in right lower lung
field, a homogeneous, wedge-shaped density in the
peripheral field, convex to the hilum.

28. Ventilation/Perfusion Lung Scanning
Ventilation Lung Scanning is normal,
and perfusion Lung Scanning can show
poor flow of blood in areas beyond
blocked arteries.

29. Normal
ventilation,
perfusion
Lung
Scanning
show poor
flow of
blood.

30. Pulmonary Angiography
The most reliable test for diagnosing
pulmonary embolism (“gold standard”)

31. Right
pulmonary
arteriogram
showed
multiple
filling defects
clustered
mainly
around the
hilum
(arrow)

32. Pulmonary
angiogram
with digital
subtraction
demonstrates a
large, acute
embolus in the
right lower
lobar
pulmonary
artery
(arrowhead).

34. Treatment






Bed rest
Haemodynamic and respiratory support
Anticoagulation Therapy
Thrombolytic Therapy
IVC Filter
Surgical Therapy

35. Left, A large embolus in the right pulmonary artery (arrow). Right,
After a 2-hour infusion of rt-PA through a peripheral vein, there is
pronounced resolution, with only a small amount of residual
thrombus in segmental branches.

37. Inferior vena caval filters. Most filters are placed percutaneouslv via
the right femoral vein. Bird's Nest Filter

38. Prognosis
About 10% of patients with pulmonary
embolism die suddenly within the first hour of
onset of the condition. The outcome for all
other patients is generally good; only 3% of
patients who are properly diagnosed and
treated die. In cases of undiagnosed pulmonary
embolism, about 30% of patients die.

39. Prevention
Pulmonary embolism risk can be
reduced in certain patients through
judicious use of antithrombotic drugs
such as heparin, venous interruption,
gradient elastic stockings and/or
intermittent pneumatic compression of
the legs.

40. Fat embolism
 Soft
tissue crush injury or rupture of
marrow vascular sinusoids (long bone
fracture) releases microscopic fat globules
into the circulation.
 fat and marrow embolism occurs in some
90% of individuals with severe skeletal
injuries but less than 10% show any clinical
findings.

41.  The
pathogenesis of fat emboli syndrome
involves both mechanical obstruction and
biochemical injury. Fat microemboli
occlude pulmonary and cerebral
microvasculature, both directly and by
triggering platelet aggregation.

42. Air embolism
 Gas
bubbles within the circulation can
obstruct vascular flow and cause distal
ischemic injury.
 a small volume of air trapped in a coronary
artery during bypass surgery or introduced
into the cerebral arterial circulation by
neurosurgery performed in an upright
“sitting position” can occlude flow, with
dire consequences

43. 
A particular form of gas embolism called decompression
sickness is caused by sudden changes in atmospheric
pressure. Thus, scuba divers, underwater construction
workers, and persons in unpressurized aircraft who
undergo rapid ascent are at risk. When air is breathed at
high pressure (e.g., during a deep sea dive), increased
amounts of gas (particularly nitrogen) become dissolved in
the blood and tissues. If the diver then ascends
(depressurizes) too rapidly, the nitrogen expands in the
tissues and bubbles out of solution in the blood to form gas
emboli, which cause tissue ischemia.

44. Amniotic fluid embolism
 The
underlying cause is entry of amniotic
fluid (and its contents) into the maternal
circulation via tears in the placental
membranes and/or uterine vein rupture.