ICL 3.2: Pulmonary Embolism and Hemorrhage

Question 1

what is a DVT?

Answer 1

the formation of thrombi in the deep veins, most commonly the large veins of the legs or pelvis

Popliteal vein most commonly affected

Ileofemoral most common source of embolus

Question 2

what are the screening and diagnostic tests for DVT?

Answer 2

D-dimer is sensitive screening test; sensitive but not specific

dopper/US is the diagnostic test

Question 3

when does a pulmonary thromboembolism occur?

Answer 3

when thrombi dislodge from clots in vein walls and travel through the heart to pulmonary arteries

there is a 50% chance for patients with untreated proximal DVT to develop symptomatic PTE within 3 months

for 25% of patients, the presenting manifestation of PTE is sudden death; yikes

Question 4

what are the heredity risk factors for pulmonary thromboembolism?

Answer 4

1. factor V leiden (A506G mutation)
2. anti-thrombin deficiency (SERPINC1 variants)
3. protein S or C deficiency

Question 5

a 65 year old patient was diagnosed with DVT in common femoral vein. anti-coagulation is contraindicated due to recent hemorrhagic stroke. what is the likelihood that PE will occur within 3 months if no action is taken?

Answer 5

50%

Question 6

what is the clinical presentation of pulmonary thromboembolism?

Answer 6

highly variable signs and symptoms so conduct history and physical with Virchow’s triad in mind:

1. stasis: travel, prolonged bedrest, or other cause
2. venous endothelial injury: e.g.: fracture, hip or knee replacement, recent percutaneous venous cath
3. hypercoagulability: Hereditary or acquired (e.g. cancer or antiphospholipid antibody)

Wells criteria developed to standardize risk analysis in ER

Question 7

what is Virchow’s triad?

Answer 7

1. stasis
2. venous endothelial injury
3. hypercoagulability

Question 8

what is the importance of classifying a PTE as provoked vs. unprovoked pulmonary thromboembolism?

Answer 8

understanding of provoked or unprovoked and the persistent nature of risk factors is very important for creating anticoagulation therapy plans with appropriate duration of treatment to address the risk of VTE recurrence after cessation of treatment

Question 9

what is a provoked PTE?

Answer 9

a provoked PTE refers to a thrombotic event that has been caused by an acquired known risk factor for PTE

acquired risk factors may be transient or persistent

transient risk factors are usually related to stasis and/or endothelial injury; if it’s transient there is lower risk of recurrence after stopping anticoagulation

progressive and persistent risk factors are usually due to hypercoagulability and/or stasis factors; there is a higher risk of recurrence after stopping anticoagulation

Question 10

what are some transient risk factors for a PTE?

Answer 10

1. bed rest
2. trauma
3. surgery
4. pregnancy
5. OCP

Question 11

what are some progressive/persistent risk factors for PTE?

Answer 11

1. active cancer
2. CHF
3. obesity
4. varicose veins
5. membranous glomerulopathy nephrotic syndrome = loss of antih tomrbin III in urine
6. autoimmune diseases

Question 12

what is an unprovoked pulmonary thromboembolism?

Answer 12

a thrombotic event that is not associated with an acquired risk factor

may be associated with host risk factors, typically related to hypercoagulability like hereditary thrombophilia, male gender, or older age

Question 13

70 year old man with lung cancer presents to ER with sudden onset of pleuritic chest pain. on exam he has pulse is 105 and he’s hypoxic. you diagnose PTE on a CT pulmonary angiogram and start treatment. what type/category of PTE is it?

Answer 13

provoked with persistent risk

cancer is persistent which is a hypercoagulability factor

Question 14

what is the pathophysiology of the lung’s response to a pulmonary thromboembolism?

Answer 14

Infarction and inflammation of the lungs and pleura can occur which causes:

1. pleuritic chest pain and/or hemoptysis and/or hemothorax
2. leads to atelectasis (collapse) through loss of blood flow and surfactant dysfunction
3. impaired gas exchange due to V/Q mismatch, evidenced as increase A-a gradiant
4. hypoxia triggers respiratory drive with hyperventilation (hypocarbia) to maintain oxygenation

Question 15

what is the pathophysiology of the heart’s response to a pulmonary thromboembolism?

Answer 15

SUBMASSIVE PE
1. decreased LV filling and stroke volume due to PA obstruction resulting in tachycardia

2. elevated pulmonary artery pressure due to blockage
3. right ventricular overload, decreased cardiac output, tachycardia, hemodynamic instability

MASSIVE PE
1. obstructive shock –> pulseless electrical activity PEA) (aka electromechanical dissociation)

2. death

Question 16

what is the presentation of a person with a PTE?

Answer 16

1. sudden onset of symptoms
2. dyspnea, SOB
3. sudden pleuritic chest pain
4. tachypnea and hypoxia
5. achycardia
6. cough and possibly hemoptysis
7. dullness on percussion of chest (due to hemothorax and or atelectasis)
8. hypotension
9. split second heart sound and increased jugular venous distension
10. syncope, shock, and/or sudden death if large embolus (e.g., saddle embolus)
11. fever
12. signs of DVT; unilateral leg swelling, tenderness

consider PE in differential diagnosis of recurring or progressive dyspnea

Question 17

what is the Wells criteria?

Answer 17

tests the pre-test probability that someone has PTE

0-4 points means PE is unlikely and get high sensitivity D-dimer testing; if it’s negative stop the workup but if it’s positive get a CTA

over 4 points means you should get a CTA

1. clinical signs and symptoms (3)
2. if the clinician believes PE is the #1 diagnosis based on what they’ve seen (3)
3. HR > 100 (1.5)
4. immobilization at least 3 day for surgery in the past 4 week (1.5)
5. previous objectively diagnosed PE or DVT (1.5)
6. hemoptysis (1)
7. malignancy treatment within 6 months (1)

Question 18

which tests support a PTE diagnosis but are not diagnostic themselves?

Answer 18

1. echocardiogram

2. lower-extremity duplex scan (doppler/ultrasound)

Question 19

when would you get an echocardiogram when evaluating a PTE? what would you see?

Answer 19

echocardiogram is done to detect signs of right ventricular and PA pressure elevation

it would show:
1. tricuspid valve regurgitation consistent with elevated systolic RV and PA pressure

2. dilation and hypokinesis of the right ventricle which is evidence of new right heart strain
3. D-sign: flattening of inter-ventricular septum causing LV to appear D-shaped rather than donut shaped

Question 20

when would you get a lower extremity duplex scan when evaluating a PTE?

Answer 20

Indications
1. symptoms/signs of DVT and PE

2. contraindications to CT angiogram like pregnancy, renal failure

supportive findings are a hypoechoic material in lumen of veins that does not collapse under compression, and lack of venous flow augmentation when calf squeezed

important consideration is that a negative duplex scan may not be sufficient to rule out PE because maybe you had a clot that was there but then went to the lungs

Question 21

what are the EKG changes you’ll see with a PTE?

Answer 21

1. may be normal if a submissive PTE
2. tachycardia
3. bradycardia if distortion of the conduction pathways
4. S1-Q3-T3 pattern
5. new RBBB
6. right axis deviation
7. P pulmonale
8. ST-segment elevation or depression
9. T-wave inversions in anterior precordial leads
10. atrial arrhythmias

Question 22

a 65 year old patient present to clinic with swelling and pain of right leg for 10 days after an 18 hour flight home. on exam, you confirm the leg swelling and tenderness and patient also has a HR of 110 . what should you do?

Answer 22

tachycardia and swelling and flight suggest PTE so the wells score is at least a 4

so do a CT pulmonary angiogram!

Question 23

what are the markers of PTE severity?

Answer 23

1. using sPESI score
2. right ventricular dysfunction from echo; do you have RV dilation?
3. what is the pulmonary artery systolic pressure based on tricuspid regurgitant jet velocity?
4. clot burden observed via extent of DVT visually, D-dimer level and extend of PE clot on CTA
5. myocardial injury (cardiac troponin)

Question 24

what is sPESI?

Answer 24

it predicts 30-day outcome of patients with PE (1 point for each criterion)

1. Age > 80
2. Cancer (hypercoagulable)
3. Cardiopulmonary disease (stasis and poor reserve)
4. Heart Rate ≥ 110
5. Systolic BP < 100 mm Hg
6. O2 Saturation < 90%
   Patients who have none of these are considered low risk

Question 25

what are the 3 risk categories of PTE?

Answer 25

1. non-massive pulmonary embolism (low risk PE)
2. submassive pulmonary embolism
3. massive pulmonary embolism

Question 26

what is a non-massive pulmonary embolism?

Answer 26

this is a low risk PE

1. normal BP
2. no right ventricular dysfunction
3. normal cardiac biomarkers; no elevated BNP or troponin

Question 27

what is a submassive pulmonary embolism?

Answer 27

intermediate risk PE

1. stable blood pressure (SBP > 90 mm Hg)
2. right ventricular dysfunction or evidence of myocardial necrosis (increased cardiac enzymes and/or BNP)

Question 28

what is a massive pulmonary embolism?

Answer 28

high risk PE

1. persistent hypotension and shock
2. RV failure

Question 29

you diagnose a 68 year old woman with PE. her bP is 110/60, HR is 110 and she has elevated cardiac enzyme troponin and RV dysfunction on echo. what risk categories of PTE is she?

Answer 29

submassive pulmonary embolism

BP is fine, HR is elevated and RV has dysfunction

Question 30

what is the acute management checklist for someone with a SUSPECTED pulmonary embolism?

Answer 30

1. give hemodynamic support in patients with hypotension
2. give supplemental oxygen as needed (RR >25 and/or oxygen saturation <88%)
3. analgesics for typical pleuritic chest pain
4. consult Pulmonary Embolic Response Team (PERT) if available
5. assess bleeding risk and consider empiric parenteral anticoagulation while awaiting definitive diagnosis

Question 31

what is the acute management for a diagnosed non-massive and sub-massive pulmonary embolism?

Answer 31

give initial anticoagulation If bleeding risk is low to moderate, start anticoagulation (ensure no recent surgery, hemorrhagic stroke, active bleeding)

1. IV unfractionated heparin, NOAC (e.g. rivaroxaban or apixaban), or low molecular weight heparin (LMWH)
2. LMWH or NOAC preferred in patients with cancer-associated hypercoagulability –> LMWH contraindicated in renal failure or morbid obesity

if bleeding risk is high, consider Inferior Vena Cava (IVC) filter placement to prevent further clots from going from the lower extremities to the lungs

in select patients with very low risk PE (sPESI score of 0), consider outpatient therapy with LMWH or NOAC

Question 32

what is the long-term management for a diagnosed non-massive and sub-massive pulmonary embolism?

Answer 32

long term anticoagulation

1. NOAC preferred over vitamin K antagonist (VKA, e.g. Coumadin) in general
2. if VKA, target INR of 2-3

Question 33

what is the treatment for PTE?

Answer 33

immediate anticoagulation remains the cornerstone of therapy for low and intermediate risk patients

low risk patients can often be treated entirely as outpatient = sPESI criteria: score of zero.

direct oral anticoagulants are now recommended as first line therapy for acute VTE

more aggressive options for high risk patients and intermediate risk patients at high risk of short-term morbidity/mortality include:

1. systemic full or half-dose thrombolysis
2. pharmacomechanical catheter-directed therapy
3. surgical embolectomy
4. IVC filter placement

Question 34

what is novel oral anticoagulant treatment?

Answer 34

NOACs are useful for acute and long term anti-coagulant treatment

1. apixaban
2. riveroxaban

direct factor 10 inhibitors

don’t give to patients with CKD

Question 35

how long do you treat someone with a PTE?

Answer 35

3 months in patients with transient risk

at least three months in unprovoked VTE or those with continuing risk factors*

Question 36

what is the acute management for massive pulmonary embolism?

Answer 36

1. evaluate need for mechanical ventilation
2. transfer to ICU for Hemodynamic support with fluids and pressors as needed.
3. be prepared for cardiopulmonary arrest
4. check candidacy for thrombolytic therapy (i.e., no contra-indications)
5. indications for thrombolytic therapy = massive PE causing right heart failure associated with hypotension; non-massive PE if the patient deteriorates after initiation of anticoagulation and low bleeding risk

if thrombolytic therapy ineffective or there are contraindications, consider catheter directed thrombolysis and/or embolectomy

Question 37

what do you do if you have a pulseless patient with suspected PE?

Answer 37

1. start ACLS

2. consider administration of thrombolytic therapy like tPA

Question 38

what is the agreed upon standard of care for patients presenting in shock from a PTE?

Answer 38

thrombolysis

patients who are hemodynamically stable without evidence of RV strain should NOT

Question 39

what are the treatment options for a severe acute PE?

Answer 39

1. surgical embolectomy
2. local/intra-thrombus thrombolysis
3. catheter fragmentation +/- local thrombolysis
4. IVC filter placement

Question 40

what is IVE filter placement?

Answer 40

use when there’s a contraindication to anticoagulation like GI bleed, hemorrhagic stroke or trauma

you also put one in if you’re unable to achieve/maintain adequate anticoagulation or if there’s recurrent PTE despite adequate anticoagulation

resume anticoagulation as soon as possible!