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2. HDS Pulmonary > Pulmonary Embolism > Flashcards

Pulmonary Embolism Flashcards

1
Q

Pulmonary Embolism

Definition

A

Blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream.

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2
Q

PE

Epidemiology

A

In the US:

  • DVT ⇒ 2 mil/yr
  • PE ⇒ 500-600 k/yr
  • 300k hospitalizations/yr
  • 50-60k deaths/yr
  • 3rd most common acute CV disease
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3
Q

PE

Pathogenesis

A

Virchow’s Triad

  • Venous stasis ⇒ ↑ coagulation factors & activation of clotting cascade
  • Vascular damage ⇒ release of IL-1, TNF-α, plasminogen activator inhibitor, tissue factor
  • Alteration in coagulation ⇒ thrombogenic / hypercoagulable state
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4
Q

Venous Thromboembolism

Risk Factors

A
  • Hypercoagulable state
  • Prior DVT
  • Immobilization ⇒ long drive or flight, bed rest
  • Cancer
  • Major orthopedic fracture or procedure
  • Estrogen/oral contraceptive agents
  • Obesity
  • Inflammatory bowel disease
  • HIT syndrome
  • Pregnancy
  • Smoking
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5
Q

Hypercoagulable States

A
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin III deficiency
  • Factor V Leiden (protein C resistance)
  • Anticardiolipin Ab / Lupus anticoagulant
  • Dysfibrinogenemia
  • Hyperhomocysteinemia
  • Prothrombin gene mutations (FIIG20210A)
  • Elevated factor VIII, IX, or XI
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6
Q

PE

Symptoms

A

Sx may be acute or subacute and can be subtle.

Keep index of suspicion high in at-risk patients.

  • Dyspnea at rest or with exertion
  • Pleuritic pain
  • Cough
  • Orthopnea
  • Calf/thigh pain, swelling, or erythema
  • Wheezing ⇒ especially unilateral wheezing
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7
Q

PE

Signs

A
  • Tachypnea
  • Tachycardia
  • Rales
  • Decreased breath sounds
  • Accentuated P2 ⇒ can sound like a gallop, due to RV strain
  • JVD

Pts with PE can be asymptomatic or have a normal exam.

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8
Q

PE

Diagnosis

A
  • D-dimer levels
  • Wells’ Score
  • CXR
  • EKG
  • CTA Chest
  • CT Venogram
  • Ventilation/perfusion (V/Q) scans
  • Duplex US Lower Extremity Veins
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9
Q

D-Dimer

A
  • D-dimers released by endogenous fibrinolysis of a fibrin clot
  • Sensitive but non-specific
  • False positives in surgical, MI, and other pts
  • Levels < 500 ng/ml are strongly predictive of a normal angiogram

A positive test is unhelpful.

A negative test indicates PE is very unlikely.

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10
Q

Wells’ Score

A

Model for pretest probability of PE.

< 2 ⇒ Low PTP

2-6 ⇒ Moderate PTP

> 6 ⇒ High PTP

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11
Q

PE

CXR Abnormalities

A

CXR changes are non-specific and can be normal.

  • Focal consolidation
    • Caused by bleeding into area of PE
  • Atelectasis
    • Tissues in area less likely to make surfactant
  • Pleural effusion (small)
  • Diaphragm elevation
    • Usually due to splinting from the pain
  • Westermark’s sign ⇒ focal decrease in pulmonary vasculature markings
  • Hampton’s hump ⇒ peripheral wedge/semicircle abutting pleura
    • Indicates a pulmonary infarction
  • Enlarged PA with decreased peripheral size
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12
Q

PE

EKG Changes

A
  • Sinus tachycardia ⇒ 50-70%
  • Nonspecific ST or T wave changes ⇒ 49%
  • “S1, Q3, T3” pattern ⇒ 12%
    • S-wave in I, Q-wave in III, and TWI in III
    • Suggestive of right strain
  • “S1, S2, S3” pattern ⇒ < 10%
  • RBBB ⇒ < 5%
  • P pulmonale ⇒ <5%
  • RAD ⇒ < 5%
  • Atrial fibrillation/flutter ⇒ 5%
  • Normal ⇒ 30%
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13
Q

CTA Chest

A
  • Most useful for central emboli
  • Sensitivity ~ 90%
  • Specificity ~ 90%
  • False ⊖ rate is lower when leg US also ⊖
  • ⊖ study does not totally r/o PE but very unlikely
  • May dx other causes of symptoms
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14
Q

CT Venogram

A

Can be performed with CT angiogram

Adds additional sensitivity but also adds radiation dose.

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15
Q

V/Q Scan

A
  • Injection and inhalation of radioactive tracers
    • Defects on perfusion not seen on ventilation indicative of a clot
  • Best uses
    • Suspected PE with normal CXR
    • Contraindication to IV contrast
  • Results
    • High probability ⇒ 2 large regions of ventilation without perfusion which follow anatomic segments
    • Intermediate probability ⇒ Not high and not low
    • Low probability
      • Non-segmental perfusion defects
      • Matching defects
      • Ventilation defect greater than the perfusion defect
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16
Q

US Duplex BLE

A

Can show:

Limited or no flow in region of clot

Non-compressible clot in vein

17
Q

PE

Treatment

A
  • Anticoagulation
    • Prevents further clot deposition
    • Allows natural fibronolytic mechanisms to lyse clot
  • Thrombolysis
    • Accelerates rate of thrombus dissolution
  • Thrombectomy / Suction embolectomy
    • Surgical or catheter directed removal of clot or embolus
    • High risk
  • Vena caval interruption (IVC filter)
    • Prevent of (recurrent) embolization
18
Q

Anticoagulation

A
  • Begin heparin, LMWH, or oral factor Xa inhibitor immediately unless contraindicated
    • Do not wait for results of work-up
  • Warfarin may be started within 24 hours if heparin is started
    • May cause initial pro-coagulant effect from decrease in Protein C and S levels
    • Don’t start without “cover” of heparin or LMWH
  • Oral direct thrombin inhibitor may be used after heparin/LMWH instead of warfarin after 5 days
19
Q

Massive PE

A

Acute PE with any of the following:

  • Sustained hypotension ⇒ SBP < 90% mmHg for at least 15 minutes or requiring inotropic support
  • Pulselessness
  • Persistant profound bradycardia ⇒ HR < 40 w/o signs or sx of shock
20
Q

Submassive PE

A

Acute PE without shock but with either RV dysfunction or myocardial necrosis.

  • RV dysfunction ⇒ at least 1 of the following
    • RV dilation on ECHO (RV:LV > 0.9) or CT
    • ↑ atrial volume
      • Cardiac biomarkers ⇒ BNP > 90 pg/mL or N-terminal pro-BNP > 500 pg/mL
    • EKG changes
      • New complete/incomplete RBBB
      • Anteroseptal ST elevation or depression
      • Anteroseptal TWI
      • S1, Q3, T3 pattern
  • Myocardial necrosis
    • ↑ cardiac ischemic biomarkers ⇒ troponin I or troponin T
21
Q

Thrombolytics

Indications

A
  • Generally accepted indication ⇒ massive PE w/ shock
    • Acceptable risk of bleeding complications
    • Given within 2 weeks of event
  • Consider in pts with submassive PE and:
    • Hemodynamic instability
    • Severe respiratory insufficiency
    • Severe RV failure
    • Major myocardial necrosis
    • Low bleeding risk
22
Q

Thrombolytics

Absolute Contraindications

A
  • Prior intracranial hemorrhage
  • Known structural intracranial cerebrovascular disease (e.g. AVM)
  • Known malignant intracranial neoplasm
  • Recent ischemic stroke w/in last 3 months
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis
  • Recent surgery encroaching on spinal canal or brain
  • Recent significant closed-head or facial trauma with radiographic e/o bony fracture or brain injury
23
Q

Thrombolytics

Relative Contraindications

A
  • Age > 75 years
  • Current use of anticoagulation
  • Pregnancy
  • Noncompressible vascular punctures
  • Traumatic or prolonged CPR
  • Recent internal bleeding w/in 2-4 weeks
  • Hx of chronic, severe, and poorly controlled HTN
  • Severe uncontrolled HTN on presentation ⇒ SBP > 180 mmHg or DBP > 110 mmHg
  • Remote ischemic stroke w/in > 3 months
  • Major surgery w/in 3 weeks
24
Q

Embolectomy

Indications

A
  • Massive PE after failed thrombolysis
  • Massive PE with contraindication to lysis
  • Submassive PE and e/o adverse prognosis (respiratory failure, myocardial necrosis)
25
Q

IVC Filter

Indications

A
  • Effective at preventing early recurrence only
  • Generally accepted indications
    • Anticoagulant-induced bleeding
    • When anticoagulants are contraindicated
    • Failure of therapeutic anticoagulation
  • Consider if you think the next PE would kill the pt
  • Can be a nitus for clot formation
26
Q

Chronic PE

A

WHO Group 4 Pulmonary HTN

  • Suspect if sx persist and PA pressures on ECHO remain high after full course of anticoagulation therapy
  • Can also occur with subclinical PEs that build up over time
  • Best diagnostic test is V/Q scan
  • Treatment
    • Surgical pulmonary artery endarterectomy (preferred)
    • Riociguat (if not a surgical candidate)
27
Q

Fat Embolism

A
  • Causes
    • Long bone fx
    • Amniotic fluid
    • Blunt trauma to fatty organ (e.g. liver)
  • Manifestations
    • Latent interval 12-72 hrs
    • ARDS
    • Change in mental status (e.g. confusion, coma)
    • Thrombocytopenia and petechiae
  • Treatment
    • Supportive
    • Anticoagulation and steroids ineffective
28
Q

Acute Chest Syndrome

Definition

A

Broad category of acute lung injury due to:

  • Hb-S related causes
    • Pulmonary vaso-occlusion
    • Fat embolism from bone marrow ischemia/necrosis
    • Hypoventilation from rib/sternal bone infarction
    • Pulmonary edema from narcotics or fluid overload
  • Indirect consequences of Hb-S
    • Atypical, bacterial, or viral infection
    • Staph, pneumococcus, haemophilus, RSV, Parvovirus B19, mycoplasma, chlamydia
  • Unrelated to Hb-S
    • Fibrin thromboembolism
    • Other pulmonary disease (asthma, aspiration)
29
Q

Acute Chest Syndrome

Diagnosis

A

New pulmonary infiltrate and any one of the following:

  • Chest pain
  • Fever > 38.5° C / 101.4° F
  • Tachypnea
  • Wheezing
  • Cough
  • Hypoxia
30
Q

Acute Chest Syndrome

Treatment

A
  • Prophylaxis
    • Pneumococcal and H. influenza vaccination
    • Parvovirus, flu vaccinations
    • Hydroxyurea (if 2 prior episodes)
  • Supportive treatment
    • Antibiotics
    • Pain management
    • Incentive spirometry
    • Bronchodilators
    • Exchange transfusion for Hb-S related causes
31
Q

PE

Summary

A
  • PE presentations
    • Subtle subacute dyspnea
    • Acute dyspnea or chest pain
    • Sub-massive PE with RV strain
    • Massive PE with shock
  • Index of suspicion should be high for people at risk
    • Hypercoagulable states
    • Clinical risks ⇒ pregnancy, travel, surgery, inflammatory bowel
  • Dx made by imaging clot w/ CT, VQ scan, or US of extremities
  • Treatment is determined by severity of PE and risks of bleeding

2. HDS Pulmonary (28 decks)

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