Pulmonary

Thromboembolism
Cheng Zhang ， Respiratory Medicine ， Affiliated
Hospital of Jining Medicine college
23,Feb
 GENARAL CONSIDRATIONS
• Many substances can embolize to the pulmonary
circulation, including air (during neurosurgery,
fron central venous catheters, ),amniotic fluid
(during active labor), foreign bodies (talc in
intravenous drug users), parasite eggs
(schistosomiasis), septic emboli(acute infectious
endocarditis), and tumor cells
 GENARAL CONSIDRATIONS
• The most common embolus is thrombus, which may
arise anywhere in the venous circulation or heart
but most often originates in the deep veins of the
major calf muscles
• The majority of cases are not recognized
antemortem, and fewer than 10% of patients with
fatal emboli have received specific treatment for the
condition
 GENARAL CONSIDRATIONS
• 50-60 percent of patients with proximal deep venous
thrombosis(DVT) will develop pulmoary emboli;
half of these embolic events will be asymptomatic
• Nearly 70% of patients who present with
symptomatic pulmonary emboli will have lower
extremity DVT
• The risk factors for pulmonary emboli are the risk
factors for thrombus formation within the venous
circulation: venous stasis, inlury to the vessel wall,
and hypercoagulability(Virchow’s triad)
• Predisposing factors (risk)
• Operation (especially spinal bone and joint
(hip replacement),neurologic
• Traum
• Stay bed for long time
• Elderly (aged)
• Underlying diseases( heart lung kidney)
• Tumor
• Medicine (contraceptive,women of child-
bearing age)
 epidemiology
• High morbidity
• High missed diagnosis and
misdiagnosis
• Prognosis without delay
 GENARAL CONSIDRATIONS
• Pulmonary thromboembolism(PE) has multiple
physiologic effects. Physical obstruction of the
vascular bed and vasoconstricction from
neurohumoral reflexes both increase pulmonary
vascular resistance. Massive thrombus may cause
right ventricular failure
• Vascular obstruction increases physiologic dead
space (wasted ventilation)(V/Q ratio )and leads to
hypoxemia through right –to –left shunting,
decreased cardiac output, and surfactant depletion
causing atelectasis. Reflex bronchoconstriction
promotes wheezing and increases work of breathing
 CLINICAL FINDINGS
• SYMPTOMS AND SIGNS
• The clinical findings depend on both the size of the
embolus and the patient’s preexisting
cardiopulmonary status. Dyspnea and chest pain on
inspiration occur in 75%-85% and 65%-75% of
patients, respectively. Tachypnea is the only sign
reliably foud in more than half of patients
• Hemoptysis accompany infarction; syncope may
indicate massive embolism. dyspnea ,chest
pain,hemoptysis triad is less than 1/3. But no single
symptom or sign or combination of clinical findings
is specific to PE. To establish the diagnosis or to
exclude it definitively, further testing is required in
the majority of patients
 CLINICAL FINDINGS
• LABORATORY FINDINGS
• a. The ECG is abnormal in 70% of patients
with PE. The most common abnormalities
are sinus tachycardia and nonspecific ST
and T wave changes. Five percent or less of
patients had P pulmonale, right ventricular
hypertrophy, right axis deviation, and right
bundle branch block. Double-edged sword
• .
• b. Arterial blood gases usually reveal acute
respiratoy alkalosis due to hyperventilation.
The arterial PO2 and PA-aDO2 are most
often abnormal in patients with PE.
Profound hypoxia with a normal chest
radiograph in the absence of preexisting
lung disease is highly suspicious for PE
 CLINICAL FINDINGS
• Plasma levels of D-dimer are elevated in the
presence of the thrombus. Usin a D-dimer
threshold between 300 and 500 ng/mL has shown
a sensitivity for PE of 95%-97% and a specificity
of 45%
 CLINICAL FINDINGS
• IMAGING AND SPECIAL EXAMINATIONS
• Chest Radiography
• The most frequent findings were atelectasis,
parenchymal infliltrates, and pleural effusions. A
prominent central pulmonary artery with local
oligemin(westermark’s sign) or pleural-based areas
of increased opacity that represent
intraparenchymal hemorrhage (Hampton’s hump)
are uncommon. The chest radiograph does not
establish the diagnosis by itself. But it is necessary
to exclude other common lung diseases
 CLINICAL FINDINGS
• CT
• Helical CT arteriography is very sensitive for the
detection of thrombus in the proximal pulmonary
arteries but less so in the segemental and
subsegemental arteries (with sensitivity of 53%-60%
and specificity of 81%-97%). False-negative results
may occur in up to 20% of helical CTs
 CLINICAL FINDINGS
• Lung Scanning
• A normal perfusion scan excludes the diagnosis of
clinically significant PE(negative predictive value of
91%). A high-probability V/Q scan is most of ten
defined as having two or more segmental perfusion
defects in the presence of normal ventilation and is
sufficient to make the diagnosis of PE in the most
instances (positive predictive value of 88%)
 CLINICAL FINDINGS
• Venous Thrombosis Studies
• Commonly available diagnostic techniques include
venous ultrasonography, impedance
plethysmography, and contrast venography. The
venous ultrasonography is the test of choice to
detect proximal DVT and is diagnostic of first-
episode DVT (positive predictive value of 97%). An
intraluminal filling defect in the contrast
venography is diagnostic of venous thrombosis
 CLINICAL FINDINGS
• Pulmonary Arteriography
• Pulmonary arteriography remains the reference
standard for the diagnosis of PE. An intraluminal
filling defect in more than one projection establishes
a definitive diagnosis. Secondary findings highly
suggestive of PE include abrupt arterial cutoff,
asymmetry of blood flow-especially segmental
oligemiaor a prolonged arterial phase with slow
filling
 CLINICAL FINDINGS
• A definitive diagnosis was established in 97%.
Pulmonary arteriography is a safe but invasive
procedure with well-defined morbidity and
mortality. Arteriography is indicated in patient in
whom the diagnosis is in doubt when there is a high
clinical pretest probabity of PE
 CLINICAL FINDINGS
• MRI
• The test is noninvasive and avoids the use if
potentially nephrotoxic adiocontrast dye. However,
it remains expensive and not widly available
 CLINICAL FINDINGS
• Integrated Approach
• The integrated approach uses the clinical likelihood
of venous thromboembolism along with the
overlapping results of noninvasive testing to come to
one of three decision points: to establish venous
thromboemblolism(PE or DVT) as the diagnosis; to
exclude venous thromboembolism with sufficient
confidence to follow the patient without therapy; or
to refer the patient for pulmonary arteriography. An
ideal diagnositic algorithm would proceed in a
stepwise fashion to come to these decision points in
a cost-effective way at minimal risk to the patient
 Standard algorithm
Clinical suspicion of Pulmonary Thromboembolism

Ventilation-perfusion lung scan

normal Low or indeterminate probability high probability

Pulmonary Testing for deep venous treatment

Thromboembolism thrombosis
excluded
positive negtive

treatment Pulmonary arteriogram or

serial noninvasive testing
for venous thrombosis

positive negtive

treatment Pulmonary
Thromboembolism excluded
 TREATMENT
• ANTICOAGULATION
• Heparin binds to and accelarates the ability of an
antithrombin III to inactive thrombin, factor Xa,
and factor Ixa. It thus retards additional thrombus
formation, allowing endogenous fibrinolytic
mechanisms to lyse existing clot. The standrd
regimen of heparin followed by 6 months of oral
warfarin results in an 80%-90% reduction in the
risk if both recurrent venous thrombosis and death
from PE
 TREATMENT
• Once the diagnosis of proximal DVT or pulmonary
thromoembolism is established, it is critical to
ensure adequate therapy (full anticoagulation with
heparin without contraindications). The
weightbased regimen in (Table 1-7-1) is superior to
standard dosing. It is necessary to monitor the
activated partial thromboplastin time (APTT) and
ajust dosing to maintain the aPTT 1.5-2.5 times
control
 TREATMENT
• LMW heparins appear to carry an equivalent or
lower risk of hemorrhage ， and immune-mediated
thrombocytopenia is less common
• They are as effective as heparin in the treatment of
venous thromboembolism
• They are administered in dosages determined by
body weight once or twice daily without the need for
coagulation monitoring
 TREATMENT
• Anticoagulation therapy for venous
thromboembolism is continued for a minimum of 3
months ， so oral anticoagulant therapy with
warfarin is usually initiated concurrently with
heparin ， initially at a dose of 2.5-10mg/d
• The lower dose is preferred in elderly patients
• Maintenanse therapy usually requires 2-15mg /d
• Adequacy of therapy must be monitored by
following the prothrombin time ， most often
adjusted for differences in reagents and reported as
the international normalized ratio ， or INR
 TREATMENT
• The target INR is 2.5 ， with the acceptable range
from 2.0 to 3.0
• When oral anticoagulation with warfarin is
contraindicated ， LMW heparin is a convenient
alternative
• It is reasonable to continue therapy for 6 months
after a first episode when there is a reversible risk
factor ， 12 months after a first-episode idiopathic
thrombus ， and 6-12 months to indefinitely in
patients with nonreversible risk factor or recurrent
disease
 TREATMENT
• Thrombolytic therapy
• Streptokinase ， urokinase ， and recombinant
tissue plasminogen activator （ rt-PA ；
altepiase ） increase plasmin levels and thereby
directly lyse intravascular thrombi
• In patients with established PE ， thrombolytic
therapy accelerates resolution of emboli within the
first 24 hours compared with standard heparin
therapy
 TREATMENT
• However ， at 1 week and 1 month after
diagnosis ， these agents show no difference in
outcome compared with heparin and warfarin
• There is no evidence that thrombolytic therapy
improves mortality
• The major disadvantages of thrombolytic therapy
compared with heparin are its greater cost and a
significant increase in major hemorrhagic
complications
 TREATMENT
• Currents evidence supports thrombolytic therapy for
PE in patients at high risk for death in whom the
more rapid resolution of thrombus may be lifesaving
• Such patients are usually hemodynamically
unstable despite heparin therapy
• Absolute contraindications to thrombolytic therapy
include active internal bleeding and stroke within
the past 2 months
• Major contraindications include uncontrolled
hypertension and surgery or trauma within the past
6 weeks
 TREATMENT
• Additional measures
• Interruption of the inferior vena cava may be
indicated in patients with a major contraindication
to anticoagulation who have or are at high risk for
development of proximal DVT or PE
• Placement of an inferior vena cava filter is also
recommended for recurrent
thromboembolism ， for chronic recurrent
thromboembolism with pulmonary hypertension ，
and with the concurrent perfomance of surgical
pulmonary embolectomy or pulmonary
thromboendarterectomy
 TREATMENT
• These devices reduce the short-term incidence of PE
in patients presenting with proximal lower extremity
DVT
• Pulmonary embolectomy is an emergency procedure
of last resort with a very high mortality rate
• Several catheter divices to fragment and extract
thrombus through a transvenous approach have
been reported in small numbers of patients
 Prognosis
• In the majority of deaths ， PE is not recognized
antemortem or death occurs before specific
treatment can be initiated
• The outlook for patients with diagnosed and
appropriately treated PE is generally good
• Overall prognosis depends on the underlying disease
rather than the PE itself
• Approximately 1% of patients develop chronic
thromboembolism pulmonary hypertension
 Prevention
• It is a prevalent disease ， clearly associated with
identifiable risk factors
• There is unambiguous evidence of the efficacy of
prophylactic therapy ， yet it remains underused
• Options for venous thromboembolism therapy begin
with machanical devices such as graduated-
compression stockings and intermittent pneumatic
compression
• Stanard pharmacologic therapy in medical patients
is low-dose unfractionated heparin ， 5000 units
subcutaneously every 8-12 hours