Chapter 300 - Deep Venous Thrombosis and Pulmonary Thromboembolism

Question 1

What is the anual death rate estimative for Pulmonary Embolism (PE)?

Answer 1

“In the United States, the Surgeon General estimates there are 100 000 to 180 000 deaths anually from PE and has declared that PE is the most common preventable cause of death among hospitalized patients.”

Question 2

Name two caues of morbidity related to Deep Venous Thrombosis and Pulmonary Thromboembolism.

Answer 2

Chronic thromboembolic pulmonary hypertension and postthrombotic syndrome (also known as chronic venous insufficiency).

Question 3

Explain the prothrombotic mechanisms of the neutrophils.

Answer 3

“Virchow’s triad of inflammation, hypercoagulabity, and endothelial injury leads to recruitment of activated platelets, which release microparticles. These microparticles contaain proinflammatory mediators that bind neutrophils, stimulating them to release their nuclear material and form web-like extracellular networks called neutrophil extracellular traps. These prothrombotic networks contain histones that stimulate platelet aggregation and promote platelet-dependent thrombin generation.”

Question 4

C protein is responsible for the inactivation of factor V aswell as VIII.
True or False?

Answer 4

True.

Question 5

What is the most common acquired cause of trombophilia?

Answer 5

Antiphospholipid syndrome.

Question 6

How is it possible that a clot in the venous system embolizes to the systemic arterial circulation?

Answer 6

“Paradoxically, these thrombi occasionally embolize to the arterial circulation through a patent foramen ovale or atrail septal defect.”

Question 7

Anatomic dead space and physiologic dead space are both increased in pulmonary embolism. How do you explain this phenomenon?

Answer 7

“Anatomic dead space increases because breathed gas does not enter gas exchange units of the lung. Physiologic dead space increases because ventilation to gas exchange units exceeds venous blood flow through the pulmonary capillaries.”

Question 8

How do you explain a largte alveolar-arterial O2 gradiente in the set of a small pulmonary embolism (PE)?

Answer 8

“Release of vasoactive mediators [from the platelet] can produce ventilation-perfusion mismatching at sites remote from the embolus, thereby accounting for discordance between a small PE and a large alveolar-arterial O2 gradient.”

Question 9

In Pulmonary embolism one might say that there is alveolar hyperventilation and alveolar hypoventilation.
True or False?

Answer 9

True.
The nonobstructed lung migth have alveolar hypoventilation relative to perfusion, which might result in hypoxemia. On the other hand, there might be alveolar hyperventilation due to reflex stimulation of irritant receptors.

Question 10

How does one explain decreased cardiac output in pumonary embolism?

Answer 10

“When right ventricle (RV) wall tension rises, RV dilation and dysfunction ensue, with release of the cardiac biomarker, brain natriuretic peptide. The interventricular septum bulges into and compresses an intrinsically normal left ventricle (LV). Diastolic LV dysfunction redues LV distensibility and impairs LV filling. (…) Underfilling of the LV may lead to a fall in LV cardiac output and systemic arterial pressure, with consequent circulatory collapse and death.”

Question 11

Pulmonary Embolism might lead to myocardial infarction.

True or False?

Answer 11

True.
“Increased right ventricle (RV) wall tension also compresses the right coronary artery, limits myocardial oxygen supply, and precipitates right coronary artery ischemia and RV microinfarction, with release of cardiac biomarkers such as troponin.”

Question 12

How frequent is massive pulmonary embolism (PE), submassive PE and low-risk PE?

Answer 12

5-10%, 20-25% and 70-75%, respectively.

Question 13

What defines massive PE?

Answer 13

Massive PE is defined by right ventricular dysfunction with decreased systemic arterial pressure. It is characterized by extensive thrombosis affecting at least half of the pulmonary vasculature, in order to have these consequences.

Question 14

What are the main risks for upper extremity deep venous thrombosis?

Answer 14

Pacemakers, internal cardiac defibrillators, or indwelling central venous catheters.

Question 15

What is the most common symptom for pulmonary embolism (PE) and Deep Vein Thrombosis (DVT)?

Answer 15

PE’s “most common symptom is unexplained breathlessness.”
“With DVT, the most common symptom is a cramp or “charley horse” in the lower calf that persists and intensifies over several days.”

Question 16

Low-to-moderate likelihood of Deep Venous Thrombosis should indicate the need for D-dimer testing, while high risk should skip this test, indicating the need for imagiologic testing as the next step in the diagnostic algorithm.
True or False?

Answer 16

True.

Question 17

Name three conditions for the differential diagnosis of deep vein thrombosis.

Answer 17

Rupture Baker’s cyst, cellulitis and postthrombotic syndrome.

Question 18

Name causes for nonthrombotic pulmonary embolism (PE).

Answer 18

“Nonthrombotic PE etiologies include fat embolism afterpelvic or long bone fracture, tumor embolism, bone marrow, and air embolism. Cement embolism and bony fragment embolism can occur after total hip or knee replacement. Intravenous drug users may inject themselves with a wide array of substances that can embolize such as hair, talc, and cotton. Amniotic fluid embolism occurs when fetal membranes leak or tear at the placental margin.”

Question 19

What does the elevation of D-dimer mean?

Answer 19

It occurs following fibrinolysis, corresponding to the breakdown of fibrin by plasmin.

Question 20

What is the main factor for the use of D-dimer if you suspect Deep Venous Thrombosis or Pulmonary Embolism?

Answer 20

A normal D-dimer is a useful “rule out” test.

Question 21

Why is that D-dimer has rarely a useful role among hospitalized patients?

Answer 21

“Levels increase in patients with myocardial infarction, pneumonia, sepsis, cancer, and the postoperative state and those in the second or third trimester of pregnancy. Therefore, D-dimer rarely has a useful role among hospitalized patients, because levels are frequently elevated due to systemic illness.”

Question 22

What do you expect to find more frequently in an electrocardiogram following pulmonary embolism?

Answer 22

RV strain and ischemia cause the most common abnormality, T-wave inversion in leads V1 to V4.”

Question 23

What is McGwinn-White sign?

Answer 23

S1Q3T3 sign: “an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III.”

Question 24

Acute thrombus has a low echogenicity.

True or False?

Answer 24

True.

Question 25

Which signs might one observe on a pulmonary embolism (PE) thorax radiography?

Answer 25

“A normal or nearly normal chest x-ray oftern occurs in PE. Well-established abnormalities include focal oligoemia (Westermark’s sign), a peripheral wedged-shaped density above the diaphragm (Hamtpon’s hump), and an enlarged right descending pulmonary artery (Palla’s sign).”

Question 26

Which gases might be used for a ventilation scanning?

Answer 26

Xenon or krypton.

Question 27

What is the positive preditive value for pulmonary embolism in the presence of a high-probability scan?

Answer 27

90%.

Question 28

Name the main limitations for ventilation-perfusion scan in detecting pulmonary embolism (PE).

Answer 28

“The diagnosis of PE is very unlikely in patients with normal and nearly normal scans and is about 90% certain in patients with high-probability scans. Unfortunately, most patients have nondiagnostic scans, and fewer than one-half of patients with angiographically confirmed PE have a high probability scan. As many as 40% of patients with high clinical suspicion for PE but “low-probability” scans do, in fact, have PE at angiography.”

Question 29

Echocardiography is a useful diagnostic tool for pulmonary embolism.
True or False?

Answer 29

False.
“echocardiography is a very useful diagnostic tool for detecting conditions that mimic PE, such as acute myocardial infarction, pericardial tamponade, and aortic dissection.”

Question 30

How do you descibre McConnel’s sign?

Answer 30

“McConnel’s sign: hypokinesis of the right ventricle (RV) free wall with normal or hyperkinetic motion of the RV apex.”

Question 31

What are the secondary signs for pulmonary embolism (PE) on angiography?

Answer 31

“Secondary signs of PE include abrupt occlusion (“cutoff”) of vessels, segmental oligemia or avascularity, a prolonged arterial phase with slow filling, and tortuous, tapering peripheral vessels.”

Question 32

If Chest CT scan is not diagnostic of pulmonary embolism, which imaging test would you choose next?

Answer 32

Lung scan which in turn, if nondiagnostic, would indicate a venous ultrasound which, if negative, would indicate the need for other techniques, such as transesophageal echocardiography, MRI or invasive angiography.

Question 33

How often should one replace graduated compression stockings for secondary prevention of venous thromboembolism?

Answer 33

Every 3 months.

Question 34

What patients following a pulmonary embolism are candidates for anticoagulation alone?

Answer 34

“When right ventricle (RV) function remains normal in a hemodynamically stabel patient, a good clinical outcome is highly likely with anticoagulants alone.” Thus, normotensive patients with normal RV function should undergo secondary prevention with anticoagulation alone (Inferior Vena Cava filter is an alternative for patients who are not candidates for anticoagulation).

Question 35

What are the dosages one uses for unfractionated heparin as anticoagulation for treatment of pulmonary embolism?

Answer 35

Bolus: 80U/Kg
Infusions: 18U/Kg per hour

Question 36

Which conditions advocate for dosage adjustment for low-molecular weight heparins?

Answer 36

Markedly obese patients and chronic kidney disease.

Question 37

Why is that foundaparinux doesn’t cause heparin-induced thrombocytopenia?

Answer 37

Foundaparinux is synthesized in a laboratory and unlike UFH and LMWH, it is not animal derived.

Question 38

Give two examples of the usefulness of pharmacogenomics concerning warfarin dosage.

Answer 38

“Pharmacogenomics may provide more precise initial dosing of warfarin. CYP2C9 variant alleles impair the hydroxylation of S-warfarin, thereby lowering the dose requirement. Variants in the gene encoding the vitamin K epoxide reductase complex 1 (VKORC1) can predict wether patients require low, moderate, or high warfarin doses.”

Question 39

Which novel oral anticoagulant was approved for the treatment of acute Venous Thromboembolism?

Answer 39

Rivaroxaban.

Question 40

Name the heparin’s antidote.

Answer 40

Protamine Sulfate.

Question 41

In case of major bleeding event from warfarin, which is the best management available?

Answer 41

Prothrombin complex concentrate.

“With serious but non-life-threatening bleeding, fresh-frozen plasma or intravenous vitamin K can be used.”

Question 42

Name the indications for oral vitamin K regarding a patient on warfarin.

Answer 42

“Oral vitamin K is effective for managing minor bleeding or an excessively high INR in the absence of bleeding.”

Question 43

How do you anticoagulate a patient with cancer and venous thromboembolism?

Answer 43

Low-Molecular-Weight Heparin.

Question 44

For how long should you anticoagulate a patient with provoked proximal leg Deep Venous Thrombosis?

Answer 44

3 to 6 months.

Question 45

For how long should you anticoagulate a patient with Deep Venous Thrombosis provoked by trauma or surgery and antiphospholipid antibody syndrome?

Answer 45

Indefinitely.

Question 46

Regarding unprovoked deep venous thrombosis, how long is anticoagulation recommended? (ACCP guidelines)

Answer 46

Indefinetly.

Question 47

The presence of genetic mutations such as heteryzgous factor V Leiden and prothrombin gene mutation increases the likelihood of recurrent venous thromboembolism.
True or False?

Answer 47

False.

Question 48

Name the two principal indications for insertion of an Inferior Vena Cava filter.

Answer 48

“(1) active bleeding that precludes anticoagulation and (2) recurrent venous thrombosis despite intensive anticoagulation.”

Question 49

What are the indications for inferior vena cava retrievable filters?

Answer 49

“Retrievable filters can now be placeted for patients with an anticipated temporary bleeding disorder or for patients at temporary high risk of pulmonary embolism (PE), such as individuals undergoing bariatric surgery who have a prior history of perioperative PE.”

Question 50

How come a retrievable filter can become a permanent one?

Answer 50

“The filters can be retrieved up to several months after insertion unless thrombus forms and is trapped within the filter. The retrievable filter becomes permanent if it remains in place or if, for technical reasons such as rapid endothelialization, it cannot be removed.”

Question 51

Which drugs are first-line inotropic agents for the treatment of pulmonary embolism related shock?

Answer 51

Dopamine and dobutamine.

Question 52

How does fibrinolysis lower the rate of death and recurrent pulmonary embolism?

Answer 52

“(1) dissolving much of the anatomically obstructing pulmonary arterial thrombus, (2) preventing the continued release of serotonin and other neurohumoral factors that exacerbate pulmonary hypertension, and (3) lysing much of the source of the thrombus in the pelvic or deep leg veins, thereby decrasing the likelihood of recurrent PE.”

Question 53

What is the dosage for tissue plasminogen activator?

Answer 53

100mg as a continuous peripheral intravenous infusions over 2h.

Question 54

The only indication FDA-approved for fibrinolysis is massive pulmonary embolism (PE).
True or False?

Answer 54

True.
“For patients with submassive PE, who have preserved systolic blood pressure but moderate or severe right ventricle dysfunction, use of fibrinolysis remains controversials.”

Question 55

Tenecteplase reduces the risk of death by 56% within 7days in submassive pulmonary embolism but increases the likelihood of hemorrhagic stroke to~2%.
True or False?

Answer 55

True.

Question 56

What is the usual range of alteplase dosage using pharmacomechanical catheter-directed therapy?

Answer 56

20-25mg instead 100mg using peripheral intravenous systemic dosage.

Question 57

How many patients develop chronic thromboembolic pulmonary hypertension following acute pulmonary embolism?

Answer 57

2-4%

Question 58

Pulmonary tromboendarterectomy might cure chronic thromboembolic pulmonary hpertension.
True or False?

Answer 58

True.

Question 59

What is the mortality rate for pulmonary thromboendarterectomy in experiencied centers?

Answer 59

Approximately 5%.
“The operation requires median sternotomy, cardiopulmonary bypass, deep hypothermia, and periods of hypothermic circulatory arrest.”

Question 60

Extended-duration prophylaxis after hospital discharge with enoxaparin, apixaban or rivaroxaban is effective and safe.
True or False?

Answer 60

False.

Question 61

How long should be the duration of prophylaxis after hip replacement or extensive cancer surgery?

Answer 61

At least 1 month.