2. PULMONARY THROMBOEMBOLISM
• Fatal form of thromboembolism where occlusion of pulmonary
arterial tree occurs by thromboemboli
• Pulmonary emboli originates from deep vein thrombosis more
commonly
• Incidence – 100 – 200 cases/100,000 people in US
• Sex –more commonly seen in males than in females
3. PULMONARY THROMBOEMBOLISM
• Obstruction by thrombosis is uncommon but more commonly by thromboembolism
FEATURE PULMONARY THROMBUS PULMONARY
THROMBOEMBOLISM
Pathogenesis Locally formed Disseminated from thrombus
Location In small arteries and
branches
In major arteries and branches
Attachment to vessel
wall
Firmly adherent Loosely attached or lying freely
Gross appearance Head pale, tail red No distinct head and tail,
smooth surfaced which is dull
and dry
Microscopy Platelets and fibrin in layers.
Lines of zahn are seen
Mixed with blood clot.
Lines of zahn are rare
4. PULMONARY THROMBOEMBOLISM
Risk factors
• Stasis of venous blood and hypercoagulable state
Causes
• Most commonly seen in hospitalized and bed ridden patients
• Thrombi originating in large vein of lower legs (deep veins in
95% of thromboemboli)
• Less common sources
• Thrombus in the varicosities of superficial veins of legs
• Pelvic veins such as periprostatic, periovarian, uterine and
broad ligament veins
5. PULMONARY THROMBOEMBOLISM
• If the thrombus is large, it is impacted
• at the bifurcation of main pulmonary
artery - saddle thrombus
• In right ventricle
• Its out flow tract
6. PULMONARY THROMBOEMBOLISM
• Mostly large emboli is fragmented into
multiple small emboli which are impacted
in lower lobes of lungs
• Rarely paradoxical embolism occurs – by
passage of an embolus from right heart to
left heart through atrial or ventricular
septal defect
8. PULMONARY THROMBOEMBOLISM
CONSEQUENCES OF
PULMONARY
THROMBOEMBOLISM
Sudden death
Due to massive pulmonary
embolism or emboli
obstructing 60% or more
of pulm circulation
Acute
corpulmonale
Numerous small
emboli obstruct most
of the pulmonary
vessels
Right heart
failure
Pulmonary
infarct
Obstruction
of small
vessels
Pulmonary
hemorrhage
Obstruction of
terminal branches
(endarteries) leads to
central pulmonary
hemorrhage
Resolution
Pulmonary
hypertension
Chronic cor
pulmonale
Pulmonary
arteriosclerosis
Multiple small
emboli undergoing
organization rather
than resolution
Multiple emboli
9. AMNIOTIC FLUID EMBOLISM
• 5th most common cause of maternal mortality world wide
• Though incidence is 2 to 6 in 100,000 deliveries death rate is
80%
• AFE is rare obstetric complications in which amniotic fluid, hair,
fetal cells or other debris enters the maternal circulation
leading to cardiorespiratory failure
• Process is more similar to anaphylaxis than embolus
(anaphylactoid syndrome of pregnancy)
10. AMNIOTIC FLUID EMBOLISM
Common causes of amniotic fluid embolism
• Old age
• Trauma
• Abortion
• Caesarian section
• Instrumental delivery
11. AMNIOTIC FLUID EMBOLISM
Pathogenesis
• Cause is infusion of amniotic fluid or fetal tissue into maternal circulation via a tear in
the placental membranes or rupture of uterine veins
12. AMNIOTIC FLUID EMBOLISM
• Morbidity and mortality in amniotic fluid embolism is not because
of obstruction of pulmonary veins but is due to
• Components of amniotic fluid producing anaphylactic reaction
• Release of vasoactive substances result from degranulation of
mast cells releasing histamine and tryptase
• Biochemical activation of coagulation factors, components of
complement pathway
13. AMNIOTIC FLUID EMBOLISM
Amniotic fluid components
Amniotic fluid (biochemical mediators)
• Surfactant
• Endothelin
• Leukotriene C4 and D4
• IL – 1 and TNF – α
• Thromboxane A2
• Prostaglandins
• Arachidonic acid
• Thromboplastin
• Collagen and Tissue factor III
• Phospholipase A2
• PF III
Anaphylactic reaction with
multisystem involvement
Fetal components
• Lanugo hair
• Vernix caseosa
• Fetal squames
• Bile stained meconium
• Fetal gut mucin
• Trophoblasts
Mechanical obstruction
(minor effects)
14. AMNIOTIC FLUID EMBOLISM
Progression occurs in 2 phases (Cotton1996)
Phase I
Amniotic fluid and fetal cells in maternal circulation
Release of biochemical mediators
Pulmonary artery vasospasm
Pulmonary hypertension
Elevated right ventricular pressure
Hypoxia
Myocardial and pulmonary
capillary damage
Left heart failure
Acute respiratory
distress syndrome
15. AMNIOTIC FLUID EMBOLISM
Phase II Biochemical mediators
DIC
Activation of complement pathway and coagulation
factors
Hemorrhagic phase
Massive hemorrhage and uterine atony
16. AMNIOTIC FLUID EMBOLISM
Clinical features
• Characterized by severe dyspnea, cyanosis and
shock followed by neurologic impairment ranging
from headache to seizures, coma and by DIC
17. AMNIOTIC FLUID EMBOLISM
Findings at autopsy
• Presence of the following substances in pulmonary
microvasculature
• Squamous cells shed from fetal skin
• Lanugo hair
• Fat from vernix
• Mucin derived from the fetal respiratory or GIT
18. FAT EMBOLISM
• Refers to presence of microscopic fat globules (sometimes with
hematopoietic bone marrow) in the vasculature after the
fractures of long bones or rarely in the setting of soft tissue
trauma or burns
• Injuries rupture sinusoids in the marrow or small veinules
allowing marrow or adipose tissue to herniate into the vascular
spaces and travel into lung
21. FAT EMBOLISM
Non- traumatic causes
• Agglutination of chylomicrons and VLDL by high levels of plasma CRP
• Disease related
• Diabetes, acute pancreatitis, burns, SLE and sickle cell crisis
• Drug related
• Parenteral lipid infusion
• Procedure related
• Orthopedic surgery, liposuction
22. FAT EMBOLISM
Fat embolism syndrome –
• Term applied to the minority of
patients who become symptomatic
• Characterized by
• Pulmonary insufficiency
• Neurologic symptoms
• Anemia
• Thrombocytopenia
Fatal in 5 – 15% of cases
Hypoxemia
Neurological
abnormalities
Petechial rash
TRIAD OF FES
23. FAT EMBOLISM
• Platelets adhere to fat globules and subsequent
aggregation or splenic sequestration - leading to
thrombocytopenia
• RBCs adhere around fat globules and or subsequent
hemolysis – leading to anemia
• Rapid onset of thrombocytopenia –leads to petechial rash
which is useful diagnostic clue
24. FAT EMBOLISM
Pathogenesis
• Both mechanical obstruction and biochemical injury
Mechanical obstruction –
• Fat emboli with associated red cell and platelet aggregates can occlude the pulmonary
and cerebral microvasculature
Biochemical injury
• Release of free fatty acids from fat globules exacerbate the situation by Causing local
toxic injury to endothelium and platelet activation and granulocyte recruitment
• With release of free radicals, proteases and eicosanoid, more vascular damage occurs
25. FAT EMBOLISM
1 to 3 days after injury there is sudden onset of
• Tachypnea
• Dyspnea
• Tachycardia
• Irritability and restlessness
• Further progresses to delirium and coma
26. 3 types of fat embolism syndrome (Sevitts classification)
• Subclinical FES
• Non fulminant FES
• Fulminant FES
27. FAT EMBOLISM
Subclinical FES
• Occurs around 3 days after trauma
• Characterized by decreased PaO2, hemoglobin and
platelets
• No clinical signs and symptoms of respiratory
insufficiency
28. FAT EMBOLISM
Non fulminant FES
• Occurs at any time upto 6 days after trauma
• Clinical signs and symptoms are evident
• Petechiae, tachycardia, respiratory failure and signs of CNS
embolism
• Thrombocytopenia, anemia, coagulation abnormalities,
• Chest X-ray- pulmonary alveolar and interstitial opacities
30. FAT EMBOLISM
Fulminant FES
• Occurs suddenly and rapidly, progressing quickly to death with in few
hours of trauma
• Clinical features are acute respiratory failure, acute cor pulmonal and
neurological embolic changes
• These changes result in death of patient shortly after injury
31. FAT EMBOLISM
• Special techniques like frozen section and stains for fat are required to demonstrate fat as
lipids dissolve in paraffin embedded sections
32. AIR EMBOLISM
• Gas bubbles within the circulation
can coalesce to form frothy
masses that obstruct vascular flow
and cause distal ischemic injury
• Air embolism occurs when there is
communication between the
vasculature and outside air and
negative pressure gradient “sucks”
in air
33. AIR EMBOLISM
Causes
Surgical
• During neurosurgery in sitting position creating a gravitational gradient and air
enters into the cerebral circulation
• Introduced during laproscopy and obstetric procedures
Non-surgical
• During endovascular and interventional procedures
• During mechanical ventilation
• As a consequence to chest wall injury
• Scuba diving, contrast infusion CT scan, CPR
34. AIR EMBOLISM
• More than 100ml is necessary to produce clinical affect in pulmonary
vasculature
• 300 to 500ml of air at 100ml/sec introduced may be fatal
• Emboli trapped in pulmonary vasculature causes
• Perfusion blockage of down stream region
• Microemboli in capillaries causes intense inflammatory response with
release of cytokines that may injure alveoli
• Bubbles in CNS may have mental impairment and even sudden onset
of coma
35. AIR EMBOLISM
Venous air entrapment
Massive air emboli
Entrapment of air in Superior vena cava or
Right Atrium or Right Ventricle
Impedes flow through heart
Decreased cardiac output and
decreased blood pressure
Small air bubbles
36. AIR EMBOLISM
Venous air entrapment
Massive air emboli Small air bubbles
Air lodges in
pulmonary capillaries
Functional decrease in
capillary bed
Increased pulmonary
arterial pressure and
central venous pressure
Decreased cardiac output and
decreased blood pressure
Increased alveolar dead
space
Decreased PO2 and
increased PCO2
Abnormal air blood interface in
pulmonary arteries denatures plasma
proteins
Amorphous proteinaceous and
cellular debris created on cell
surface
Attracts and activates WBC
Injury to pulmonary capillary
cells and increased permeability
Alveolar flooding
Non-cardiogenic
pulmonary edema
37. AIR EMBOLISM
Decompression sickness
• Occurs when individual experiences
sudden decrease in atmospheric pressure
• People at risk are
• Scuba and deep sea divers
• Under water construction workers
38. AIR EMBOLISM
• In underwater partial pressure of nitrogen in breathing air is
higher
• Nitrogen is not used by body but it gets dissolved in tissues
• As the partial pressure increases more and more nitrogen is
dissolved in tissues
• When the pressure decreases, nitrogen in the tissues comes out
39. AIR EMBOLISM
Pathogenesis
• If the diver ascends too rapidly, nitrogen comes out of solution in the tissues
and blood
• Rapid formation of gas bubbles with in skeletal muscles and supporting
tissues in and about joints is responsible for painful conditions called “the
bends” as in 1880 it was noted in those afflicted characteristically arched
their backs in a marren reminiscent of then popular womens fashion pose
called Grecian bend (photo)
40. AIR EMBOLISM
• In the lungs, gas bubbles in vasculature causes
• Oedema
• Hemorrhage
• Focal atelectasis
• emphysema
Respiratory distress called chokes
41. AIR EMBOLISM
Caisson disease
• More chronic form of decompression sickness
• Named for the pressurized vessels used in bridge
construction
• Workers in these vessels suffered both acute and
chronic form of decompression sickness
42. AIR EMBOLISM
• Caisson disease
• Persistence of gas emboli in skeletal system leads to multiple foci of
ischemic necrosis
• Common sites – femoral head, tibia and humerus
• Treatment – patients are placed in chambers under sufficiently high
pressure to force the gas bubbles back into solution
• Subsequently slow decompression permits gradual resorption and
exhalation of gases which prevents obstructive bubbles from
