_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

_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

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

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.

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

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.

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

Pulmonary Embolism Flashcards by Quynh Tran

Pulmonary Embolism

Definition

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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Epidemiology

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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Pathogenesis

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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Venous Thromboembolism

Risk Factors

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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Hypercoagulable States

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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Symptoms

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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Signs

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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Diagnosis

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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D-Dimer

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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Wells’ Score

Model for pretest probability of PE.

< 2 ⇒ Low PTP

2-6 ⇒ Moderate PTP

> 6 ⇒ High PTP

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CXR Abnormalities

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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EKG Changes

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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CTA Chest

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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CT Venogram

Can be performed with CT angiogram

Adds additional sensitivity but also adds radiation dose.

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V/Q Scan

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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US Duplex BLE

Can show:

Limited or no flow in region of clot

Non-compressible clot in vein

Treatment

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

Anticoagulation

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

Massive PE

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

Submassive PE

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

Thrombolytics

Indications

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

Thrombolytics

Absolute Contraindications

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

Thrombolytics

Relative Contraindications

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

Embolectomy

Indications

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

IVC Filter Indications

* **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**

Chronic PE

**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)

Fat Embolism

* _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

Acute Chest Syndrome Definition

_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)

Acute Chest Syndrome Diagnosis

**New pulmonary infiltrate** and any one of the following: * Chest pain * Fever \> 38.5° C / 101.4° F * Tachypnea * Wheezing * Cough * Hypoxia

Acute Chest Syndrome Treatment

* **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**

PE Summary

* **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**