pulmonary thromboembolism
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Pulmonary Thromboembolism. Prof. Sevda Özdoğan MD Chest 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 - PowerPoint PPT PresentationTRANSCRIPT
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.