13664779 Pulmonary Thromboembolism

8/6/2019 13664779 Pulmonary Thromboembolism

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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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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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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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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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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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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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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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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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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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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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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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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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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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13664779 Pulmonary Thromboembolism