Pulmonary Embolism Dr Samah M Shehata MD Associate

Pulmonary Embolism Dr. Samah M. Shehata; MD Associate Prof. Of Chest diseases

Pulmonary Embolism n Thrombosis (Thrombo-embolic) that originates in the venous system and embolizes to the pulmonary arterial circulation: ü Thrombus in the popliteal segment of the femoral vein is the cause of PE in > 60% of cases. ü PE can arise from DVT anywhere in the body. ü Fatal PE often results from thrombus that originates in : Ø Ø Ø Veins of the pelvis. Axillary or subclavian veins (deep veins of the arm or shoulder) Thrombus that forms around indwelling central venous catheters. n Air embolism. n Fat embolism.

How Common? n n 650, 000 cases in the US each year 150, 000 – 200, 000 US deaths each year Most common preventable cause of hospital death 3 rd most common acute cardiovascular emergency (MI and stroke)

Predisposing factors for venous thromboembolism Strong predisposing factors Fracture (hip or leg) Hip or knee replacement Hospitalization for heart failure or atrial fibrillation/flutter (within previous 3 months) Myocardial infarction (within previous 3 months) Previous VTE Major general surgery Major trauma Spinal cord injury Moderate predisposing Weak predisposing factors Arthroscopic knee surgery Central venous lines Chemotherapy Congestive heart or respiratory failure Hormone replacement therapy Malignancy Oral contraceptive therapy Paralytic stroke Pregnancy/postpartum Thrombophilia Bed rest >3 days Immobility due to sitting (e. g. prolonged car or air travel) Increasing age Laparoscopic surgery (e. g. cholecystectomy) Obesity Pregnancy/antepartum Varicose veins Diabetes mellitus Arterial hypertension

Virchow’s Triad: n n n Stasis: mainly caused by heart failure, prolonged immobility Endothelial injury: mainly caused by either direct trauma (severed vein) or local irritation (by chemotherapy, past DVT, phlebitis) Hypercoagulability: inherited (AT III def. , protein C, S deficiency) or acquired (malignancy, pregnancy, AT III def. , protein C, S deficiency as in nephritic syndrome, DIC and liver failure.

Clinical Presentation n n n Asymptomatic Sudden onset of unexplained dyspnea Pleuritic chest pain Tachypnea Tachycardia Anxiety/agitation, cough, hemoptysis, syncope, fever, cyanosis, isolated crackles, pleural friction rub, loud P 2, right-sided S 3, pulmonary insufficiency murmur, elevated JVP, right ventricular heave, acute worsening of heart failure or lung disease

Differential Diagnosis n n n n Pneumothorax Myocardial ischemia Pericarditis Pneumonia MI with cardiogenic shock Cardiac tamponade Aortic dissection etc, etc

Elevated left diaphragm, denoting volume loss at left lung

Hampton Hump Radiologic sign which consists of a shallow wedgeshaped opacity in the periphery of the lung with its base against the pleural surface.

Westermark Sign • represents a focus of oligemia (vasoconstriction) seen distal to a pulmonary embolism. While the chest x-ray is normal in the majority of PE cases, the Westermark sign is seen in 2% of patients. • The sign results from a combination of: – The dilation of the pulmonary arteries proximal to the embolus and – the collapse of the distal vasculature creating the appearance of a sharp cut off on chest radiography.

EKG Findings

Unfortunately, only 20% of patients with proven PE have any of these classic ECG abnormalities. • ECG abnormalities in the setting of PE are: Tachycardia (the most common) S 1 -Q 3 -T 3 (nonspecific and insensitive) Classic findings of Right heart strain and acute cor pulmonale are: o. Right axis deviation, and Right bundle-branch block, o. P pulmonale (Tall, peaked P waves in lead II), o. T-wave inversion in leads III and a. VF or in leads VI-V 4 o. Atrial fibrillation. • The following ECG abnormalities have been associated with poor prognosis(from above) : 1. Right bundle branch block 2. Precordial T-wave inversion 3. Atrial arrhythmias

Evaluation and Diagnosis n Evaluation and imaging is dependent upon estimated pretest probability (Modified Wells’ Criteria) n Pretest probability: n n n Low (<2 points) Intermediate (2 -6 points) High (>6 points) VARIABLE POINTS S/S of DVT 3. 0 HR >100 1. 5 Immobilization (bed rest >/= 3 d) OR surgery within 4 weeks 1. 5 Prior DVT or PE 1. 5 Hemoptysis 1. 0 Malignancy (treated within the past 6 months or palliative 1. 0 Other diagnoses less likely than PE 3. 0

D-dimer in evaluation of PE n n D-dimer levels are elevated in plasma in the presence of acute thrombosis as it is a degradation product of cross-linked fibrin. The negative predictive value of D-dimer testing is high, and a normal D-dimer level renders acute PE or DVT unlikely. On the other hand, the positive predictive value of elevated Ddimer levels is low and D-dimer testing is not useful for confirmation of PE. D-dimer is also more frequently elevated in patients with cancer, in hospitalized patients , in severe infection or inflammatory disease, and during pregnancy. Negative ELISA has >95% negative predictive value and can be used to exclude PE in patients with either low or intermediate pre-test probability.

Arterial blood gases n ABGs usually reveal : n n Hypoxemia, Hypocapnia, Respiratory alkalosis. Massive PE with hypotension and respiratory collapse can cause Hypercapnia n Combined respiratory and metabolic acidosis (the latter due to lactic acidosis). n

Helical CT (CT pulmonary angiography) n n n Sensitivity 85% (more sensitive for proximal emboli) Specificity 95% Values vary widely in literature

Bilateral PE

Duplex US with compression of the lower extremities n n n Lower extremity ultrasound is sometimes performed in the diagnostic evaluation of PE. Only 30 -50% of patients with PE had venous thrombosis detected by compression ultrasound. Procedures: n n Ultrasound transducer is placed against the skin and then is pressed inward firmly enough to compress the vein being examined. In an area of normal veins, the veins are easily compressed completely closed, while the muscular arteries are extremely resistant to compression. Where DVT is present, the veins do not collapse completely when pressure is applied using the ultrasound probe. A negative ultrasound scan does not rule out DVT, because many DVTs occur in areas that are inaccessible to ultrasonic examination.

Pulmonary Angiography “Gold Standard” n Invasive study n 5% morbidity n < 0. 5% mortality n Indicated if the diagnosis remains uncertain after noninvasive testing n

PE on pulmonary angiogram

2019 ESC GUIDELINES ACUTE PULMONARY EMBOLISM

Unfractionated heparin therapy • If IV UFH is chosen, an initial bolus of 80 U/kg or 5000 U followed by an infusion of 18 U/kg/h or 1300 U/h should be given. • The efficacy of heparin therapy depends on achieving a critical therapeutic level of heparin within the first 24 hours of treatment. The critical therapeutic level of heparin is 1. 5 times the baseline control value or the upper limit of normal range of the activated partial thromboplastin time (a. PTT).

Low-molecular-weight heparin therapy • Current guidelines for patients with acute nonmassive pulmonary embolism recommend LMWH over UFH (grade 1 A). • LMWH can be administered safely in an outpatient setting. This has lead to the development of programs in which clinically stable patients with pulmonary embolism are treated at home, at substantial cost savings.

VKA: Warfarin therapy. • A prothrombin time ratio is expressed as an INR and is monitored to assess the adequacy of warfarin therapy. The recommended therapeutic range for venous thromboembolism is an INR of 2 -3. • Initially, INR measurements are performed on a daily basis; once the patient is stabilized on a specific dose of warfarin, the INR determinations may be performed every 1 -2 weeks or at longer intervals.

Vitamin K containing food

Mechanism of action of the non-vitamin K antagonist oral anticoagulants (NOACs).

Prothrombin time (PT) is specific for factors VII and X and as such is more suitable for measuring Xa blockers. while activated partial thromboplastin time (APTT) is specific to clotting factors VIII, IX, and XI and thus measures thrombin generation which is affected by dabigatran. The most sensitive test for dabigatran is thrombin time (TT) which measures conversion of fibrinogen to fibrin by the action of thrombin.

Burnett A. , Ansell J. (2019) Anticoagulants and Treatment of Venous Thromboembolism. In: Lazarus H. , Schmaier A. (eds) Concise Guide to Hematology. Springer, Cham

2019 ESC GUIDELINES ACUTE PULMONARY EMBOLISM

What is the hemodynamic instability? Any One of the following clinical presentations: 1. cardiac arrest, 2. obstructive shock (systolic BP <90 mm. Hg or vasopressors required to achieve a BP � 90 mm. Hg) , in combination with endorgan hypoperfusion (altered mental status; cold, clammy skin; oliguria/anuria; increased serum lactate) Who is the high-risk PE category ? ? Haemodynamic instability, combined with PE confirmation on CTPA and/or evidence of RV dysfunction on TTE, is sufficient to classify a patient into the high-risk PE category {the risk of early (in-hospital or 30 day) death} After haemodynamic stabilization of the patient, continue with anticoagulation treatment as in non high-risk PE

Recommendations for inferior vena cava filters 2019 ESC GUIDELINES ACUTE PULMONARY EMBOLISM

2019 ESC GUIDELINES ACUTE PULMONARY EMBOLISM

Recommendations for pulmonary embolism in pregnancy 2019 ESC GUIDELINES ACUTE PULMONARY EMBOLISM

Duration of anticoagulation in pregnancy • Patients who sustain a DVT or PE antepartum should receive anticoagulation therapy with heparin throughout the pregnancy. • After delivery, heparin treatment may be replaced by anticoagulation with VKA. Anticoagulant treatment should be administered for at least 6 weeks after delivery and with a minimum overall treatment duration of 3 months. VKAs can be given to breast-feeding mothers.