Post on 07-Apr-2018
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Pulmonary
ThromboembolismCheng Zhang Respiratory MedicineAffiliated
Hospital of Jining Medicine college
23,Feb
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GENARAL CONSIDRATIONSGENARAL 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
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GENARAL CONSIDRATIONSGENARAL 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
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GENARAL CONSIDRATIONSGENARAL CONSIDRATIONS
50-60 percent of patients with proximal deep venousthrombosis(DVT) will develop pulmoary emboli;half of these embolic events will be asymptomatic
Nearly 70% of patients who present withsymptomatic pulmonary emboli will have lowerextremityDVT
The risk factors for pulmonary emboli are the riskfactors for thrombus formation within the venouscirculation: venous stasis, inlury to the vessel wall,and hypercoagulability(Virchows triad)
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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)
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epidemiologyepidemiology
High morbidity
High missed diagnosis and
misdiagnosis
Prognosis without delay
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GENARAL CONSIDRATIONSGENARAL CONSIDRATIONS
Pulmonary thromboembolism(PE) has multiplephysiologic effects. Physical obstruction of thevascular bed and vasoconstricction fromneurohumoral reflexes both increase pulmonary
vascular resistance. Massive thrombus may causeright ventricular failure
Vascular obstruction increases physiologic deadspace (wasted ventilation)(V/Q ratio )and leads tohypoxemia through right to left shunting,decreased cardiac output, and surfactant depletioncausing atelectasis. Reflex bronchoconstrictionpromotes wheezing and increases work of breathing
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CLINICAL FINDINGSCLINICAL FINDINGSSYMPTOMSANDSIGNS
The clinical findings depend on both the size of theembolus and the patients preexistingcardiopulmonary status. Dyspnea and chest pain oninspiration occur in 75%-85% and 65%-75% ofpatients, respectively. Tachypnea is the only signreliably foud in more than half of patients
Hemoptysis accompany infarction; syncope mayindicate massive embolism. dyspnea ,chest
pain,hemoptysis triad is less than 1/3. But no singlesymptom or sign or combination of clinical findingsis specific to PE. To establish the diagnosis or toexclude it definitively, further testing is required inthe majority of patients
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CLINICAL FINDINGSCLINICAL FINDINGS
LABORATORYFINDINGS a. The ECGis abnormal in 70% of patients
with PE. The most common abnormalities
are sinus tachycardia and nonspecific STand 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
.
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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
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CLINICAL FINDINGSCLINICAL FINDINGS
Plasma levels ofD-dimer are elevated in the
presence of the thrombus. Usin a D-dimer
threshold between 300 and500 ng/mL has shown
a sensitivity for PEof 95%-97% and a specificity
of 45%
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CLINICAL FINDINGSCLINICAL FINDINGS
IMAGINGANDSPECIAL EXAMINATIONS
Chest Radiography
The most frequent findings were atelectasis,parenchymal infliltrates, and pleural effusions. A
prominent central pulmonary artery with localoligemin(westermarks sign) or pleural-based areasof increased opacity that representintraparenchymal hemorrhage (Hamptons hump)
are uncommon. The chest radiograph does notestablish the diagnosis by itself. But it is necessaryto exclude other common lung diseases
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CLINICAL FINDINGSCLINICAL FINDINGS
CT
Helical CT arteriography is very sensitive for the
detection of thrombus in the proximal pulmonary
arteries but less so in the segemental andsubsegemental arteries (with sensitivity of53%-60%
and specificity of 81%-97%). False-negative results
may occur in up to 20% of helical CTs
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CLINICAL FINDINGSCLINICAL FINDINGS
LungScanning
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 PEin the most
instances (positive predictive value of 88%)
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CLINICAL FINDINGSCLINICAL FINDINGS
Venous ThrombosisStudies
Commonly available diagnostic techniques include
venous ultrasonography, impedance
plethysmography, and contrast venography. The
venous ultrasonography is the test of choice to
detect proximalDVT and is diagnostic of first-
episodeDVT (positive predictive value of 97%). An
intraluminal filling defect in the contrastvenography is diagnostic of venous thrombosis
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CLINICAL FINDINGSCLINICAL 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 PEinclude abrupt arterial cutoff,
asymmetry of blood flow-especially segmental
oligemiaor a prolonged arterial phase with slowfilling
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CLINICAL FINDINGSCLINICAL 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
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CLINICAL FINDINGSCLINICAL FINDINGS
MRI
The test is noninvasive and avoids the use if
potentially nephrotoxic adiocontrast dye. However,
it remains expensive and not widly available
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CLINICAL FINDINGSCLINICAL FINDINGS
Integrated Approach The integrated approach uses the clinical likelihood
of venous thromboembolism along with theoverlapping results of noninvasive testing to come to
one of three decision points: to establish venousthromboemblolism(PEorDVT) as the diagnosis; toexclude venous thromboembolism with sufficientconfidence to follow the patient without therapy; orto refer the patient for pulmonary arteriography. An
ideal diagnositic algorithm would proceed in astepwise fashion to come to these decision points ina cost-effective way at minimal risk to the patient
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Standard algorithmStandard algorithmClinical suspicion of Pulmonary ThromboembolismClinical suspicion of Pulmonary Thromboembolism
Ventilation-perfusion lung scan
normal Low or indeterminate probability high probability
PulmonaryThromboembolism
excluded
Testing for deep venousthrombosis
treatment
positive negtive
treatmentPulmonary arteriogram
or serial noninvasivetesting forvenous
thrombosis
positive
treatment
negtive
Pulmonary
Thromboembolism excluded
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TREATMENTTREATMENT
ANTICOAGULATION
Heparin binds to and accelarates the ability of an
antithrombinIIIto inactive thrombin, factorXa,
and factorIxa. 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
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TREATMENTTREATMENT
Once the diagnosis of proximalDVT or pulmonarythromoembolism is established, it is critical toensure adequate therapy (full anticoagulation withheparin without contraindications). The
weightbased regimen in (Table 1-7-1) is superior tostandard dosing.It is necessary to monitor theactivated partial thromboplastin time (APTT) andajust dosing to maintain the aPTT 1.5-2.5 timescontrol
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TREATMENTTREATMENT
LMW heparins appear to carry an equivalent orlower risk of hemorrhageand immune-mediatedthrombocytopenia 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 forcoagulation monitoring
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TREATMENTTREATMENT
Anticoagulation therapy for venousthromboembolism is continued for a minimum of 3
monthsso oral anticoagulant therapy with
warfarin is usually initiated concurrently with
heparininitially 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 timemost often
adjusted for differences in reagents and reported as
the international normalized ratioorINR
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TREATMENTTREATMENT
The targetINR is 2.5with the acceptable rangefrom 2.0 to 3.0
When oral anticoagulation with warfarin iscontraindicatedLMW heparin is a convenient
alternative It is reasonable to continue therapy for 6 months
after a first episode when there is a reversible riskfactor12 months after a first-episode idiopathic
thrombusand 6-12 months to indefinitely inpatients with nonreversible risk factor or recurrentdisease
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TREATMENTTREATMENT
Howeverat 1 week and 1 month after diagnosisthese 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 hemorrhagiccomplications
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TREATMENTTREATMENT
Additional measures Interruption of the inferior vena cava may be
indicated in patients with a major contraindicationto anticoagulation who have or are at high risk for
development of proximalDVT or PE Placement of an inferior vena cava filter is also
recommended for recurrent thromboembolismforchronic recurrent thromboembolism with
pulmonary hypertensionand with the concurrentperfomance of surgical pulmonary embolectomy orpulmonary thromboendarterectomy
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TREATMENTTREATMENT
These devices reduce the short-term incidence of PEin 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
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PrognosisPrognosis
In the majority of deathsPEis not recognized
antemortem or death occurs before specific
treatment can be initiated
The outlook for patients with diagnosed and
appropriately treated PEis generally good Overall prognosis depends on the underlying disease
rather than the PEitself
Approximately 1% of patients develop chronic
thromboembolism pulmonary hypertension
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PreventionPrevention It is a prevalent diseaseclearly associated with
identifiable risk factors
There is unambiguous evidence of the efficacy of
prophylactic therapyyet it remains underused
Options for venous thromboembolism therapy beginwith machanical devices such as graduated-
compression stockings and intermittent pneumatic
compression
Stanard pharmacologic therapy in medical patientsis low-dose unfractionated heparin5000 units
subcutaneously every 8-12 hours
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