Transcript Pulmonary Embolism

Pulmonary Embolism
M.A.ZOHAL
PULMUNOLOGIST
• Venous thromboembolism (VTE), which
encompasses deep venous thrombosis
(DVT) and pulmonary embolism (PE), is
one of the three major cardiovascular causes
of death, along with myocardial infarction
and stroke.
• VTE can cause death from PE or, among
survivors, chronic thromboembolic
pulmonary hypertension and postphlebitic
syndrome
• PE is the most common preventable cause
of death among hospitalized patients
• Approximately three of four symptomatic
VTE events occur in the community, and
the remainder are hospital acquired
• Approximately 14 million (M) hospitalized
patients are at moderate to high risk for
VTE in the United States annually: 6 M
major surgery patients and 8 M medical
patients with comorbidities such as heart
failure, cancer, and stroke.
• The long-term effects of nonfatal VTE
lower the quality of life. Chronic
thromboembolic pulmonary hypertension is
often disabling and causes breathlessness. A
late effect of DVT is postphlebitic
syndrome, which eventually occurs in more
than one-half of DVT patients
PE
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Epidemiology
Pathophysiology
Prevention/Risk factors
Screening
Diagnosis
Treatment
PE
• Epidemiology
– Five million cases of venous thrombosis each
year
– 10% of these will have a PE
– 10% will die
– Correct diagnosis is made in only 10-30% of
cases
– Up to 60% of autopsies will show some
evidence of past PE
PE
• Epidemiology
– 90-95% of pulmonary emboli originate in the
deep venous system of the lower extremities
– Other rare locations include
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Uterine and prostatic veins
Upper extremities
Renal veins
Right side of the heart
Virchow’s Triad
• Rudolf Virchow postulated more than a
century ago that a triad of factors
predisposed to venous thrombosis
– Local trauma to the vessel wall
– Hypercoagulability
– Stasis of blood flow
• It is now felt that pts who suffer a PE have
an underlying predisposition that remains
silent until a acquired stressor occurs
Risk Factors
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CHF
Malignancy
Obesity
Estrogen/OCP
Pregnancy (esp post
partum)
• Lower ext injury
• Coagulopathy
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Venous Stasis
Prior DVT
Age > 70
Prolonged Bed Rest
Surgery requiring > 30
minutes general
anesthesia
• Orthopedic Surgery
Risk Factors
cancer,
obesity, cigarette
smoking, systemic
arterial hypertension,
chronic
obstructive pulmonary
disease, chronic kidney
disease, blood
transfusion,
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long-haul air travel, air
pollution, oral
contraceptives,
pregnancy,
postmenopausal
hormone replacement,
surgery, and trauma
Risk Factors
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immobilization
surgery
malignancy
previous thrombophlebitis
lower extremity trauma
estrogen use
Stroke
3 months post-partum.
Hypercoagulability state
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Factor V Leiden mutation
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
Prothrombin gene mutation A20210
Anticardiolipin antibodies
Lupus anticoagulant
Hyperhomocystinemia
common predisposing factors
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cancer,
systemic arterial hypertension,
chronic obstructive pulmonary disease,
long-haul air travel,
air pollution, obesity,
cigarette smoking,
eating large amounts of red meat,
oral contraceptives, pregnancy,
postmenopausal hormone replacement,
surgery, and trauma
Factor V Leiden
• Most frequent inherited predisposition to
hypercoagulability
• Resistance to activated Protein C
• Single point mutation (Factor V Leiden)
• Single nucleotide substitution of glutamine for
arginine
• Frequency is about 3% in healthy American male
physicians participating in the Physicians’ Health
Study
PE
• When venous emboli become dislodged
from their site of origin, they embolize to
the pulmonary arterial circulation or,
paradoxically to the arterial circulation
through a patent foramen ovale
– About 50% of pts with pelvic or proximal leg
deep venous thrombosis have PE
– Isolated calf or upper extremity venous
thrombosis pose a lower risk for PE
Pathophysiology
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Increased pulmonary vascular resistance
Impaired gas exchange
Alveolar hyperventilation
Increased airway resistance
Decreased pulmonary compliance
Increased pulmonary vascular
resistance
• vascular obstruction
• platelet secretion of vasoconstricting
neurohumoral agent such as serotonin
Impaired gas exchange
increased alveolar dead space from
• vascular obstruction,
• hypoxemia :
– alveolar hypoventilation relative to perfusion in
the nonobstructed lung,
– right-to-left shunting,
– impaired carbon monoxide transfer due to loss
of gas exchange surface.
Alveolar hyperventilation
• reflex stimulation of irritant receptors.
Increased airway resistance
constriction of airways distal to the bronchi
Decreased pulmonary
compliance
• lung edema,
• lung hemorrhage,
• loss of surfactant
Right Ventricular Dysfunction
• Progressive right heart failure is the usual
immediate cause of death from PE
• As pulmonary vascular resistance increases,
right ventricular wall tension rises and
perpetuates further right ventricle dilation
and dysfunction
• Interventricular septum bulges into and
compresses the normal left ventricle
Clinical Syndromes
• Pts with massive PE present with systemic
arterial hypotension and evidence of
peripheral thrombosis
• Pts with moderate PE will have right
ventricular hypokinesis on echocardiogram
but normal systemic arterial pressure
• Pts with small to moderate PE have both
normal right heart function and normal
systemic arterial pressure
Diagnosis
• Clinical Syndromes
– Pulmonary Infarction usually indicates a small
PE, but is very painful, because it lodges near
the innervation of the pleural nerves
Physical Signs & Symptoms
 Dyspnea 73%
 Pleuritc Pain 66%
 Cough 43%
 Leg Swelling 33%
 Leg Pain 30%
 Hemoptysis 15%
 Palpitations 12%
 Wheezing 10%
 Angina-Like pain 5%
Common symptoms
Common physical signs
Cyanosis 19%
Cardiac murmur 23%
Thrombophlebitis 32%
S3 OR S4 34%
Fever 43%
Tachycardia 44%
Rales 58%
Tachypnea 92%
Diagnosis
• H&P
• Always ask about prior DVT, or PE
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Family History of thromboembolism
Dyspnea is the most frequent symptom of PE
Tachypnea is the most frequent physical finding
Dyspnea, syncope, hypotension, or cyanosis
suggest a massive PE
– Pleuritic CP, cough, or hemoptysis
Differential Diagnosis
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PE is known as “the great masquerader”
pericarditis, acute coronary syndrome , MI
Pneumonia, bronchitis, copd
CHF
Asthma
Costochondritis, Rib Fx,
Pneumothorax
PE can coexist with other illnesses!!
A Summary so Far…
• History alone is unreliable
• Physical exam is close to useless
• However, studies have shown that our
clinical suspicion of PE is useful in
interpreting diagnostic tests
WELLS CRITERIA
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Suspected DVT
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An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats / min
1.5
Immobilization>3 days or surgery within four
weeks 1.5
• Pervious DVT / PE
1.5
• Hemoptysis
1
• Malignancy(on treatment or treated in past 6 1
months )
Imaging tests to diagnose PTE
Diagnosis
• Serum Studies
– D-dimer
• Elevated in more than 90% of pts with PE
• Reflects breakdown of plasmin and endogenous thrombolysis
• Not specific: Can also be elevated in MI, sepsis, or almost any
systemic illness
• Negative predictive value
– ABG-contrary to classic teaching, arterial blood gases
lack diagnostic utility for PE
Diagnosis
• CXR
• A normal or nearly normal chest x-ray often
• occurs in PE
– Classic abnormalities include:
• Westermark’s Sign - focal oligemia
• Hampton’s Hump - wedge shaped density above the
diaphragm
• Enlarged Right Descending Pulmonary Artery
(Palla’s sign)
Hamptons
Hump
PE
Westermark’s Sign
PE
PE which
appears like
a mass.
PE with hemorrhage
or pulmonary edema
PE with effusion
and elevated diaphragm
Spiral CT Scan
• Identifies proximal PE (which are the ones
usually hemodynamically important)
• Not as accurate with peripheral PE
CT revealing pulmonary infarct
DIAGNOSIS OF VENOUS
THROMBOEMBOLISM
Spiral chest CT scan
DIAGNOSIS OF VENOUS
THROMBOEMBOLISM
Spiral chest CT scan
Venous Ultrasonography
• Relies on loss of vein compressibility as the
primary criterion
• About 1/3 of pts will have no imaging
evidence of DVT
• Clot may have already embolized
• Clot present in the pelvic veins (U/S usually
inadequate)
– Workup for PE should continue even if
dopplers (-) in a pt in which you have a high
clinical suspicion
V/Q Scan
• Historically, the principal imaging test for
the diagnosis of PE
– A perfusion defect indicates absent or
decreased blood flow
– Ventilation scan obtained with radiolabeled
gases
– A high probability scan is defined as two or
more segmental perfusion defects in presence
of nl ventilation scan
V/Q Scan
• Useful if the results are normal or near
normal, or if there is a high probability for
PE
– As many as 40% of pts with high clinical
suspicion for PE and low probability scans have
a PE on angiogram
High Probability V/Q Scan
Pulmonary Angiogram
• Most specific test available for diagnosis of
PE
• Can detect emboli as small as 1-2 mm
• Most useful when the clinical likelihood of
PE differs substantially from the lung scan
result or when the lung scan is intermediate
probability
Echocardiogram
– Useful for rapid triage of pts
– Assess right and left ventricular function
– Diagnostic of PE if hemodynamics by echo are
consitent with clinical hx
high risk of an adverse clinical
outcome
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Hemodynamic instability,
RV dysfunction on echocardiography,
RV enlargement on chest CT,
Elevation of the troponin level due to RV
microinfarction outcome
Primary therapy
• Fibrinolysis
• Pharmacomechanical catheter-directed
therapy
• surgical embolectomy
• pulmonary thromboendarterectomy
Fibrinolysis
(1) dissolving much of the anatomically obstructing
pulmonary arterial thrombus,
(2) preventing the continued release of serotonin and
other neurohumoral factors that exacerbate
pulmonary hypertension,
(3) lysing much of the source of the thrombus in the
pelvic or deep leg veins, thereby decreasing the
likelihood of recurrent PE.
fibrinolysis
• massive PE
• For patients with submassive PE, who have
preserved systolic blood pressure but
moderate or severe RV dysfunction, use of
fibrinolysis remains controversial
Secondary prevention
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Anticoagulant
Ivc filter
graduated compression stocking
Intermittent pneumatic compression devices
Treatment
• (1) the conventional strategy of parenteral
therapy “bridged” to warfarin,
• (2) parenteral therapy “bridged” to a novel
oral anticoagulant such as dabigatran (a
direct thrombin inhibitor) or edoxaban (an
anti-Xa agent)
• (3) oral anticoagulation with rivaroxaban or
apixaban (both are anti-Xa agents)
parenteral therapy
three heparin-based parenteral anticoagulants
are:
(1) unfractionated heparin (UFH),
(2) low-molecular-weight heparin (LMWH),
(3) fondaparinux.
For patients with suspected or proven heparininduced thrombocytopenia, there are two parenteral
direct thrombin inhibitors: argatroban and
bivalirudin
Treatment
• Begin treatment with either unfractionated
heparin or LMWH, then switch to warfarin
(Prevents additional thrombus formation and permits endogenous
fibrinolytic mechanisms to lyse clot that has already been formed,
Does NOT directly dissolve thrombus that already exists)
• Warfarin for atleast 3 months, INR 2-3
IVC filter indication
(1) active bleeding that precludes
anticoagulation
(2) recurrent venous thrombosis despite
intensive anticoagulation.
Softer indication:
• Prevention of recurrent PE in patients with right heart
failure who are not candidates for fibrinolysis
• prophylaxis of extremely high-risk patients
IVC filter
graduated compression stocking
Intermittent pneumatic compression devices
Conclusion
• PE is often a misdiagnosed clinical disorder.
• Rapid identification and appropriate
treatment may often prevent unnecessary
morbidity and mortality.