Pulmonary Thromboembolism

Prof. Sevda Özdoğan MDChest Diseases

Pulmonary Thromboembolism

Pulmonary embolism is caused by the obstruction of the pulmonary arteries by clots from the veins of the systemic circulation that embolise to lungs

Obstructive material other than blood (fat, amnion fluid etc) can also cause pulmonary embolism in certain cituations but venous thromboembolism (VTE) is the most common cause

Epidemiology In USA there are 300-650.000 new

case /year and the incidence rate is higher among older age groups

The mortality rate was reported as 51/100000 in 1995

Mortality rate is very high in the first hour

Among the survivors after the first hour 2/3 of the patients remain undiagnosed

The mortality for this group is around 30%

With the right diagnosis and treatment this rate declines to 3-8%

% 90 of the thrombus comes from the lower extremities

Pathophysiology

Virchow Triade

1. Venous stasis2. Vascular endothelial (wall)

damage 3. Hypercoagulation

Risk factorsGenetic Acquired

Antithrombin III deficiency

Autosomal dominantRisk of VTE x5

DVT Previous PE

30% DVT pts develop symptomatic PE50%-60% DVT pts develop asymptomatic PE

Protein C and S (cofactor) deficiency

Autosomal dominantRisk od VTE x6

Age 40 years or more

Activated protein C (APC) resistance

Factor V Leiden mutationPositive in 21% of VTE patients

Surgery and trauma*(Lover extremity fracture or surgery,Neurosurgery)

Blood stasis due to immobilizationGeneral anesthetic disturbs the balance of coagulation factors and their inhibitorsLocal tissue trauma, vessel damage

Prothrombin G20210A

A single nucleotide change in prothrombin gene results in elevated prothrombin levelsRisk of DVT x5

Medical conditions

Left ventricular failureMalignancyNephrotic syndromeStrokeCrohn diseasePrevious VTE

Hyperhomocystinemia

Defects in enzymes of homocystein disposalRisk of VTE x2

Oral contraceptives

Estrogen content increases the risk x7If heterozygot Fac V leiden mut. Than x30

Genetic Acquired

Increased Factor VIII

RR for VTE x4.8 Smoking Cause the vessel wall damage

Blood group other than O

RR of DVT x2 Pregnancy HypercoagulabilityVenous stasis

Combination of the genetic risk factors

Platelet abnormalities

Polistemia vera

Obesity

Testing for genetic risk factors is considered in patients who have: VTE at a young age Family history of VTE No evidence of acquired risk factors PE that originates from a spontaneous

venous thrombosis other than leg vein thrombosis

Clinical features and Diagnosis

Clinical suspicion*** Medical history:

To identify the patient at risk Family history Medical or acquired risk factors

Symptomatology:

Unexplained acute dyspnea Tachypnea Substernal chest discomfort Pleuretic chest pain Cyanosis Shock / sencope Fever Hemopthysis Asymptomatic

97%

Tachycardia, tachypnea Pleural rub Late inspiratory rales, wheese İncreased pulmonary component of the

second heart sound (p2) Right ventricular S3 Elevated jugular venous pulse Tender liver Fever (in infarction)

Physical findings: (nonspecific)

Diagnostic approach

There are significant difficulties in the accurate diagnosis of pulmonary embolism as there is a broad differential diagnosis.

PE can present in a variety of ways depending on the size, location, number of emboli and the underlying condition of the patient.

Objective diagnostic test result are needed for definite diagnosis of VTE and deep venous thrombosis (DVT)

Diagnostic approach

Semptomatology and signs Chest radiology Arterial blood gas analysis (ABG) Electrocardiography Standard laboratory tests Echocardiography (Cardiac and venous doppler

of the lower extremity) D-Dimer Spiral CT Ventilation / perfusion scan Pulmoner angiography (gold standard) MRI

Estimating Clinical Probability of Pulmonary Embolism

High Risk factor present(80-100% probable) Otherwise unexplained dyspnea, tachypnea, or pleuritic chest pain

Otherwise unexplained radiographic or gas exchange abnormality

Intermediate Neither high nor low clinical probability(20-79% probable)

Low Risk factor not present(1-19% probable) Dyspnea, tachypnea, or pleuritic pain possibly present but explainable by another condition

Radiographic or gas exchange abnormality possibly present but explainable by another condition

Chest Radiography Negative chest radiogram is a common

presentation so does’t exclude the diagnosis

80% Abnormal chest radiograph but nonspecific Peripheral regional oligemia (Westermark’s sign) (7%) A prominant pulmonary hilus with little tapering of

vessels (Fleischner’s sign) (15%) Peripheral wedge shaped densities (Hampton’s hump)

(35%) Plate like atelectasis Diaphragmatic elevation (%24) Pleural effusion (%48)

Linear atelectasisPulmonary infarct

Frontal chest radiograph obtained from a patient with an acute pulmonary embolism. The left pulmonary artery is enlarged (small arrow), and a wedge-shaped peripheral opacity is present at the left costophrenic angle (large arrow)

ABG Analysis

Hypoxemia, hypocapnia and respiratory alcalosis PaO2 <%80 PaO2 may be normal in submassive embolism if no

underlying pulmonary disease is present

(A-a)O2 gradient is increased in almost all the patients

ECG Abnormalities of ECG are nonspecific

Acute right ventricular strain in massive embolism Sinus tachicardia Negative T wave and/or ST segment depression in

leads V1-3 S1Q3T3 patern (Deep S wave in lead D1, deep Q wave

in lead D3, inverted T waves in D3) Right bundle branch block (complete or incomplete) P-pulmonale

Changes can be similar to MI

Standard laboratory tests Nonspecific changes

WBC can be slightly elevated LDH, bilirubine can be slightly elevated D-Dimer (fibrin degradation product) can be

elevated ELISA or Latex agglutination Sensitivity % 95-97 but specificity is low <500 ng/ml PE can be excluded if there is also low

clinical probability Elisa is more sensitive but slow compared to Latex

ECHOCARDIOGRAPHY (Doppler) Can be performed rapidly at the bedside Features that suggest acute massive PE include

A dilated, hypokinetic right ventricle With the absence of right ventricular hypertrophy Distortion of the interventriculer septum toward the

left ventricle Tricuspit regurgitation the elevation of pulmonary

artery pressure Identified trombi in the central pulmonary arteries Absence of significant pathologic left ventricular

conditions

Spiral Computed Tomography Angiography (SCTA) Allows rapid investigation of the pulmonary vasculature

at peak contrast opasification within a single breath hold

Three dimentional reconstruction is possible Sensitivity and specificity is around 90% up to

subsegmental defects May demonstrate or exclude other abnormalities in the

lung Bolus contrast is used for the visualization of the

pulmonary vasculature Filling defects are diagnostic

Partial filling defect in right middle lobe and lover lobe artery

Wedge shaped infiltration on the right upper lobe posterior segment

Sagital-oblique CT image showing thrombus narrowing left lover lobe pulmonary artery

Ventilation-Perfusion Scintigraphy Detection of the perfusion abnormalities subsequent to

the embolic event Classically to display that a segment distal to an

obstructing embolus is not perfused but is still ventilated

99Tc is usually used for perfusion and 133Xe for ventilation scaning. The two studies are analysed together.

In clinical practice the results of V/Q scintigraphy are interpreted together with the clinical estimate of the likelihood of acute PE

A normal V/Q virtually excludes clinically relevant PE

Patient with multiple embolisms in both lungs: segmental mismatch defect in left lung was detected by both SPECT (A and B) and planar scintigraphy (C and D). Defects are marked by arrows in B and D. Subsegmental mismatch defects are present in right lung. CT angiography found thrombotic clots in branches of middle lobe artery and both lower lobe arteries

Estimate of the likelihood of PE

Normal Perfusion (Q): exclude PE Q defects—Ventilation (V) is normal on these

regions: (V/Q mismatch defect) High probability of PE If Chest x ray is normal on the regions of V/Q

mismatch: higher probability If V/Q mismatch areas are segmental or larger:

higher probability Q defects—V defect on these regions: (V/Q

match defect) Low probability, undetermined

MRI Magnetic resonance angiography with the use of

contrast material can demonstrate the pulmonary arteries beyond the segmental level

A potential advantage is that it allows the study of the pulmonary arteries and the deep veins of the lower extremities within a single examination

Pulmonary Angiography (gold standard) Detects emboli in the subsegmental or even

more peripheral arteries Unfortunately it is invasive and there is lack of

availability in an urgent investigation Can be used if V/Q scan is nondiagnostic and

the clinical probability is high Not performed if perfusion scintigraphy is

normal Mortality %0,5 Major complications %0,4

Deep Venous Thrombosis (DVT)

Compression ultrasound Doppler ultrasonography Venography (gold standard)

Suspect Pulmonary Embolism ?

Give heparin IV and order V/Q scan

Low V/Q probability,low clinical probability

High V/Q probability +high clinical probability

Intermediate V/Q probability,Low or high V/Q prob with

discordant clinical probability

Probability V/Q Clinical1. Low Mid2. Mid Low

No treatment

Probability V/Q Clinical3. Low High4. Mid Mid / High5. High Low / Mid

Leg Ultrasound Treat_

PulmonaryAngiography

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Am J Respir Crit Care Med. Vol 159: 1-14; 1999

BT

BT (-) BT (-) high cl prob. BT (+)

Treatment of PTE and DVT Supportive treatment

Oxygen Intravenous fluid Vasopressor agents Resuscitary measures depending on the clinical status of the

patient Anticoagulant therapy

Unfractionated heparin (UFH) Low molecular weight heparin (LMWH) Oral anticoagulants (Warfarin)

Thrombolytic treatment Vena Cava Filters Surgical treatment

Treatment duration Reversible risk factor, first event, age<60 : 3-6 months

Reversible risk factor, first event, age>60: 6-12 months

First event, unknown risk factor: 6-12 months

Recurrent event: >12months- life long

Irreversible risk factor, first event: >12 months- life long

Primary Prevention Determined by the thrombotic risk of the

clinical situation in conjunction with the patients profile of risk factors Ortopedic surgery (post-traumatic) ICU Neurosurgery carry the highest risk

LMWH or UFH can be used LMWH’s can be used preoperatively safely Prophylaxis should be continued up to 4

weeks after surgery

Patients with congenital risk factors: Homozygot : Lifelong anticoagulation Heterozygot: During the periods of

high risk Recurrent embolism or continious

risk factor: lifelong anticoagulation

Non medical Prophylaxis Graduated compression stockings İntermittent pneumatic compression Foot impulse pumps Can be used for patients who have

contraindications to anticoagulants.