Pulmonary embolism resident survival guide

Jump to: navigation, search

For pulmonary embolism prevention resident survival guide click here.

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]; Pratik Bahekar, MBBS [3]; Chetan Lokhande, M.B.B.S [4]

Pulmonary embolism Resident Survival Guide Microchapters
Overview
Causes
FIRE
Diagnosis
Long term treatment
Do's

Overview

Pulmonary embolism (PE) is the acute obstruction of the pulmonary artery or one of its branches by a thrombus, air, tumor, or fat. Most often, PE is due to a venous thrombus which has been dislodged from its site of formation in the deep veins of the lower extremities, a process referred to as venous thromboembolism. PE is a potentially lethal condition. The patient can present with a range of signs and symptoms; however, the typical presentation is characterized by dyspnea (78-81% of the cases), pleuritic chest pain (39-56% of the cases), and/or syncope (22-26% of the cases).[1] The diagnostic approach of PE depends on whether the patient is a high-risk patient due to the presence of hypotension and/or shock or a non-high risk patient, as well as on the pre-test probability of this disease. While fibrinolytic therapy is the treatment of choice for patients with massive PE, patients with non-massive PE are treated with anticoagulation therapy.[2]

Causes

Life Threatening Causes

Pulmonary embolism is a life-threatening condition and must be treated as such irrespective of the underlying cause.

Common Causes

Classification

Massive Pulmonary Embolism

Massive pulmonary embolism falls under the category "high risk patients" in the European guidelines. High risk PE patients have a risk of PE-related early mortality of > 15%.[3]
Massive PE is characterized by the presence of:

OR

OR

Submassive Pulmonary Embolism

Submassive pulmonary embolism falls under the category "intermediate risk patients" in the European guidelines. Intermediate risk PE patients have a risk of PE-related early mortality ranging between 3 and 15%.[3]
Submassive PE is characterized by:

AND

Right Ventricular Dysfunction

Right ventricular (RV) dysfunction is characterized by the presence of AT LEAST ONE of the following:[4][5]

Myocardial Necrosis

Myocardial necrosisis defined as the presence of:[4][5]

OR

Low-Risk Pulmonary Embolism

Low risk PE patients have a risk of PE-related early mortality of <1%.[3] Low risk PE is characterized by the absence of hypotension, shock, RV dysfunction, and myocardial necrosis.[4]

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.[3][4][2]

Abbreviations: CT: Computed tomography; IV: Intravenous; IVC: Inferior vena cava; PE: Pulmonary embolism; PERC: PE Rule-Out Criteria; RV: Right ventricle; SC: Subcutaneous; VKA: Vitamin K antagonist

Step 1: Confirm PE

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Identify cardinal findings that increase the pretest probability of PE
Dyspnea
Pleuritic chest pain
Syncope
Tachycardia
Tachypnea
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Does the patient who is suspected to have PE have hypotension or shock?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Suspected high-risk PE
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Suspected non-high risk PE
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Administer parenteral anticoagulation
(in case there are no contraindications)
during the diagnostic workup
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is a CT available immediately?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
What is the pretest probability of PE?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No
 
 
 
 
 
 
 
 
 
Yes
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Order Echocardiography
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Does the patient have RV overload?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Low pretest probability
 
Intermediate pretest probability
 
High pretest probability
OR
PE is likely
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Administer parenteral anticoagulation
(in case there are no contraindications)
during the diagnostic workup
 
Administer anticoagulation
(in case there are no contraindications)
during the diagnostic workup
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No
 
 
 
Yes
 
 
 
 
 
Order CT
 
 
 
 
 
Order D-dimer
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Positive
 
Negative
 
Positive
 
Negative
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is the patient unstable
OR
no other tests are available?
 
Is the patient stabilized
AND
CT is now available?
 
 
 
 
 
 
 
 
 
 
 
Order CT
 
PE is excluded
 
Order CT
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Positive
 
Negative
 
Positive
 
Negative
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PE is excluded
 
❑ Consider thrombolytic therapy
OR
Embolectomy
 
❑ Order CT
 
PE is confirmed
 
PE is excluded
 
PE is confirmed
 
PE is excluded
 
PE is confirmed
 
PE is excluded
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Positive for PE
 
Negative for PE
 
Click here for the initial treatment
 
 
 
 
 
Click here for the initial treatment
 
 
 
 
 
Click here for the initial treatment
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PE is confirmed
 
PE is excluded
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Click here for the initial treatment
 
 
 

Assessment of the Pretest Probability of PE

The assessment of the pretest probability of PE can be achieved through scoring systems. The most commonly used score is the Wells score. Other scores, such as Geneva score and PERC can also be used.

Wells Score

The Wells score is a simple, commonly used clinical risk prediction tool to evaluate the need for further testing in patients suspected to have pulmonary embolism.[6][7][8][9]

Calculation of Wells Score

Pulmonary embolism Wells Score Calculator

Variable Wells Score[8]
Clinically suspected DVT (leg swelling, pain with palpation) 3.0
Alternative diagnosis is less likely than PE 3.0
Immobilization/surgery in previous four weeks 1.5
Previous history of DVT or PE 1.5
Tachycardia (heart rate more than 100 bpm) 1.5
Malignancy (treatment for within 6 months, palliative) 1.0
Hemoptysis 1.0
Interpretation of Wells Score
Wells Criteria

Shown below is the pretest probability of PE according to Wells criteria.[8][9][10]

  • Score >6.0: High probability (Rate of PE: ~66.7%)
  • Score 2.0 to 6.0: Moderate probability (Rate of PE: ~20.5%)
  • Score <2.0: Low probability (Rate of PE: ~3.6%)
Modified Wells Criteria

Shown below is the pretest probability of PE according to the modified Wells Criteria.[8][9][10][11]

  • Score > 4: PE likely (Rate of PE: ~40.7%)
  • Score 4 or less: PE unlikely (Rate of PE: ~7.8%)

Step 2: Initial Treatment

 
 
 
 
 
 
 
 
 
 
Assess the severity of pulmonary embolism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Massive PE
(also known as high-risk PE)
Cardiogenic shock
OR
Persistent hypotension (≤90mmHg)
OR
Drop of the blood pressure by ≥ 40mmHg for > 15 min[12]
OR
Pulselessness
OR
Profound bradycardia (<40 bpm) with findings of shock[4]
 
 
 
 
 
Submassive PE
(also know as intermediate-risk PE)
Right ventricular dysfunction
AND/OR
Myocardial injury (Troponin +)
 
 
 
 
 
Low-risk PE
No cardiogenic shock
AND
No hypotension
AND
No right ventricular dysfunction
AND
No myocardial injury (Troponin -)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Provide hemodynamic and respiratory support

❑ Begin high dose unfractionated heparin[12]

❑ Bolus 10.000 U
❑ Continuous infusion of at least 1250 U/hour for a targeted aPTT of at least 80 s

❑ Administer rapidly 500-1000 mL of normal saline (caution with fluid overload)[12]
❑ Have a low threshold for ionotropes (dopamine or dobutamine)[12]

❑ Administer oxygen for hypoxemic patients[12]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is there any contraindication to fibrinolytic therapy?
 
 
 
 
 
Is there any contraindication for anticoagulation therapy?
 
 
 
 
 
Is there any contraindication for anticoagulation therapy?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
NO
 
YES
 
NO
 
YES
 
NO
 
YES
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
❑ Discontinue unfractionated heparin
AND
❑ Begin fibrinolytic therapy
 
❑ Surgical pulmonary embolectomy
OR
❑ Percutaneous catheter embolectomy
 
Anticoagulation therapy
AND
❑ Hospital admission
 
IVC filter
AND
❑ Hospital admission
 
Anticoagulation therapy
AND
❑ Early discharge/home treatment
 
IVC filter
AND
❑ Early discharge/home treatment
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Does the patient fail to improve
OR
Develop cardiogenic shock
OR
Develop hypotension?
 
 
 
 
 
 
 
Does the patient fail to improve
OR
Develop cardiogenic shock
OR
Develop hypotension (<90 mmHg)
OR
Develop respiratory distress (SaO2<95% with Borg score>8 or altered mental status)
OR
Have moderate to severe RV dysfunction (RV hypokinesis or estimated RVSP>40 mmHg)
OR
Have elevated biomarkers (troponin> upper limit of normal, BNP>100 pg/mL, or pro-BNP>900 pg/mL)?[4]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
YES
 
NO
 
YES
 
NO
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Surgical pulmonary embolectomy
OR
Percutaneous catheter embolectomy
 
❑ Continue with the same treatment
 
Is there any contraindication for fibrinolytic therapy?
 
❑ Continue with the same treatment
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
NO
 
YES
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
❑ Hold anticoagulation and give thrombolytics
 
Surgical pulmonary embolectomy
OR
Percutaneous catheter embolectomy
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Does the patient fail to improve?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
YES
 
NO
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Surgical pulmonary embolectomy
OR
Percutaneous catheter embolectomy
 
❑ Continue with the same treatment

Dosage of Fibrinolytic Therapy

Shown below is the dosage schedule for the thrombolytic agents:[4]

  • Streptokinase (FDA-approved)
    • Loading dose: 250 000 IU over 30 min
    • Maintenance dose: 100 000 IU/h over 12–24 hr
    • Accelerated regimen: 1.5 million IU over 2 hr
  • Urokinase (FDA-approved)
    • Loading dose: 4400 IU/kg over 10 min
    • Maintenance dose: 4400 IU/kg/h over 12–24 hr
    • Accelerated regimen: 3 million IU over 2 hr
  • Recombinant tissue plasminogen activator (rtPA)[13]
    • Alteplase (FDA-approved): 10-mg IV bolus followed by 90 mg IV infusion over 2 hours
    • Reteplase: 10-U IV bolus followed in 30 mins by another 10-U IV bolus
    • Tenecteplase: 0.5-mg/kg IV bolus (max 50mg)

Contraindications to Fibrinolytic Therapy

Shown below is a table summarizing the absolute and relative contraindications to fibrinolytic therapy among pulmonary embolism patients.[3]

Absolute contraindications Relative contraindications
❑ Previous hemorrhagic stroke or stroke of unknown origin

Ischemic stroke within the last 6 months
Central nervous system tumor or damage
❑ Major trauma, head injury, or surgery within the last 3 weeks
Gastrointestinal bleed within the last month
❑ Known bleeding

Transient ischemic attack within the last 6 months

Oral anticoagulant therapy intake
❑ Advanced liver disease
Infective endocarditis
Peptic ulcer disease that is currently active
Pregnancy or within 1 week post partum
❑ Punctures that are non-compressible
Traumatic resuscitation
Systolic blood pressure >180 mmHg refractory to treatment

Choice of Initial Anticoagulation Therapy

 
 
 
Begin initial anticoagulation therapy in:
Confirmed PE
OR
High or intermediate probability of PE while awaiting the diagnostic tests
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is the patient high risk or non-high risk?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
High risk
 
 
 
Non-high risk
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
❑ Administer IV unfractionated heparin
❑ 80 U/kg as bolus, followed by 18 U/kg/h, OR
❑ 70 U/kg as bolus, followed by 15 U/kg/h for stroke or cardiac patients[14]
❑ Adjust the dosages according to the aPTT
 
 
 
Does the patient have:
High risk of bleeding
OR
Severe renal failure?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes
 
No
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
❑ Administer unfractionated heparin:[3]
IV injection
❑ 80 U/kg as bolus, followed by 18 U/kg/h, OR
❑ 70 U/kg as bolus, followed by 15 U/kg/h for stroke or cardiac patients[14]
❑ Adjust the dosages according to the aPTT
OR
SC injection
❑ 333 U/kg as bolus, followed by 250 U/kg[14]
❑ Administer VKA as an overlap anticoagulation if VKA is planned for long term treatment
 
❑ Administer ONE of the following:
❑ SC low molecular weight heparin (1st line)
❑ Enoxaparin 1.0 mg/kg every 12 hours OR 1.5 mg/kg once daily
❑ Tinzaparin 175 U/kg once daily
❑ SC fondaparinux (1st line)
❑ 5 mg once daily (if body weight <50 kg)
❑ 7.5 mg once daily (if body weight <50-100 kg)
❑ 10 mg once daily (if body weight >100 kg)
❑ IV unfractionated heparin
❑ 80 U/kg as bolus, followed by 18 U/kg/h, OR
❑ 70 U/kg as bolus, followed by 15 U/kg/h for stroke or cardiac patients[14]
❑ Adjust the dosages according to the aPTT
❑ SC unfractionated heparin
❑ 333 U/kg as bolus, followed by 250 U/kg[14]
❑ Administer VKA as an overlap anticoagulation if VKA is planned for long term treatment

Adjustment of Heparin Dosage According to aPTT

aPTT Variation in the dosage[3]
< 1.2 x control (<35 s) Bolus: 80 U/kg
Infusion rate: increase by 4 U/kg/h
1.2-1.5 x control (35-45 s) Bolus: 40 U/kg
Infusion rate: increase by 2 U/kg/h
1.5-2.3 x control (46-70 s) Continue the same dosage
2.3-3.0 x control (71-90 s) Infusion rate: decrease by 2 U/kg/h
> 3.0 x control (>90s) Stop infusion for a period of 1 hour, then
Infusion rate: decrease by 3 U/kg/h

Contraindications to Anticoagulation

Complete Diagnostic Approach

A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.

Abbreviations: DVT: Deep venous thrombosis; JVD: Jugular venous distention; P2: Second heart sound; RV: right ventricle; S3: Third heart sound ; S4: Fourth heart sound

Characterize the symptoms:

Dyspnea (78–81%)[16]
Pleuritic chest pain (39–56%)[16]
Fainting (22–26%)[16]
Cough (20%)[3]
Substernal chest pain (12%)[3]
Hemoptysis (11%)[3]
Wheezing
Cyanosis (11%)[16]
Fever (7%)[16]
❑ Asymptomatic
❑ Findings suggestive of DVT (15%)[3]

❑ Calf or thigh pain and swelling
Edema, erythema, tenderness, or a palpable cord in the calf or thigh

❑ Symptoms suggestive of shock (in case of massive PE)

Altered mental status
Cold extremities
Cyanosis
Oliguria
 
 
 
 
 
 
Elicit a detailed history:

Risk factors[3][17]

Chemotherapy
Chronic heart failure
Respiratory failure
Hormone replacement therapy
Cancer
Oral contraceptive pills
Stroke
Pregnancy
Postpartum
❑ Prior history of VTE
Thrombophilia
❑ Advanced age
Laparoscopic surgery
❑ Prepartum
Obesity
Varicose veins

Triggers[3][17]

Bone fracture (hip or leg)
Hip replacement surgery
❑ Knee replacement surgery
Major general surgery
Significant trauma
Spinal cord injury
❑ Athroscopic knee surgery
Central venous lines
Chemotherapy
❑ Bed rest for more than 3 days
❑ Prolonged car or air travel
Laparoscopic surgery
❑ Prepartum

Previous episode of VTE

❑ Age
❑ Location

Past medical history of diseases associated with hyperviscosity

Atherosclerosis
Collagen vascular disease
Heart failure
Myeloproliferative disease
Nephrotic syndrome
Autoimmune diseases
Polycythemia vera
Hyperhomocysteinemia
Paroxysmal nocturnal hemoglobinuria
Waldenstrom macroglobulinemia
Multiple myeloma

History of thrombophilia

Factor V Leiden mutation
Prothrombin gene mutation G20210A
Protein C or Protein S deficiency
Antithrombin (AT) deficiency
Antiphospholipid syndrome (APS)

Abortion

Abortion at second or third trimester of pregnancy (suggestive of an inherited thrombophilia or APS)

Drugs that may increase the risk of VTE

Hydralazine
Phenothiazine
Procainamide
Tamoxifen
Bevacizumab
Glucocorticoids

Family history (suggestive of inherited thrombophilia)

Deep vein thrombosis
Pulmonary embolism
❑ Recurrent miscarriage

Social history

❑ Heavy cigarette smoking (>25 cigarettes per day)
Intravenous drug use (if injected directly in femoral vein)
Alcohol
 
 
 
 
 
 
 
Examine the patient:

Vital signs
Blood pressure

Blood pressure lower than baseline, suggestive of cardiogenic shock (associated with tachycardia and end organ hypoperfusion)

Tachycardia (26%)[3]
Tachypnea (70%)[3]
Low grade fever

Skin
❑ Lower extremity swelling, erythema, and/or tenderness suggestive of DVT
Edema (suggestive of right heart failure)
Cyanotic and cold skin, lips, nail bed (suggestive of cardiogenic shock)

Heart
❑ Cardiac murmur

Graham-Steell murmur (suggestive of pulmonary regurgitation)

❑ Accentuated P2
S3 or S4 gallop (suggestive of RV dysfunction)
JVD (suggestive of right heart failure)

Lungs
Rales
Crackles
Pleural friction rub

 
 
 
 
 
 
 
Order tests:

CBC
Electrolytes
ABG

Hypoxemia
Hypocapnea
Respiratory alkalosis

EKG

Sinus tachycardia
❑ Stress on the right ventricle
Right axis deviation
Right bundle branch block
❑ S1Q3T3
❑ Deep S in lead I
Q wave in lead III
Inverted T wave in lead III

Chest X ray[18]

Atelectasis (most common)
Fleishner sign: enlarged pulmonary artery
Hampton hump: peripheral wedge-shaped density above the diaphragm that implies lung infarction
Westermark's sign: vasoconstriction distal to the pulmonary embolus
Pleural effusion
❑ Elevated diaphragm
❑ Enlarged hilum
❑ Normal (in 12%)
 

Long Term Treatment

The long term treatment of PE depends on whether the episode is the first one or not, whether it is provoked or unprovoked, and on the risk of bleeding of the patient. Among non cancer patients, the first line therapy for long term management of PE is vitamin K antagonists (VKA); whereas the first line treatment among cancer patients is low molecular weight heparin. If long term treatment with VKA is decided, VKA should be started at the same day with heparin allowing for at least 5 days of overlap until the INR is ≥2 for at least 24 hours. Among patients on extended anticoagulation therapy, the risk vs benefits of the anticoagulation therapy should be assessed regularly (for example annually).[2]

 
 
 
 
 
 
 
 
 
Is this the first episode of PE?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
YES
 
 
 
 
 
 
 
NO
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is PE provoked?
 
 
 
 
 
 
 
What is the risk of bleeding?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes, transient reversible risk factor
 
Yes, cancer
 
No (unprovoked)
 
Low or moderate
 
High
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Therapy for 3 months
VKA (first line)
OR
LMWH
OR
Dabigatran
OR
Rivaroxaban
 
Extended therapy or until cancer is cured
LMWH (first line)
OR
VKA
OR
Dabigatran
OR
Rivaroxaban
 
Therapy for ≥ 3 months
VKA (first line)
OR
LMWH
OR
Dabigatran
OR
Rivaroxaban
 
Extended therapy
VKA (first line)
OR
LMWH
OR
Dabigatran
OR
Rivaroxaban
 
Therapy for 3 months
VKA (first line)
OR
LMWH
OR
Dabigatran
OR
Rivaroxaban
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Re-assess the risk of bleeding
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Low or moderate
 
High
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Extended therapy
 
Do not extend the therapy beyond the initial 3 months
 
 
 
 
 
 


Note that edoxaban[19] has been evaluated for the treatment of VTE and is currently seeking approval for this indication.

Vitamin K Antagonist

  • Begin with 5 mg warfarin for 2 days followed by dosing based on the INR.
  • Start at the 1st or 2nd day of the initial parenteral therapy.
  • Target INR is 2-3.
  • Monitor INR monthly.
    • If the INR is stable but there is one value 0.5 below or above the target range, continue the same dose and repeat INR within 1-2 weeks.
  • Avoid NSAIDs, COX2 selective NSAIDs and some antibiotics[14]

Assessment of Risk of Bleeding

The risk factors of bleeding with anticoagulation therapy are:[2]

Shown below is a table summarizing the risk of bleed based on the number of risk factors. Note that, although the presence of one risk factor signify moderate risk of bleeding, if the single risk factor is severe (such as severe thrombocytopenia or recent major surgery) then the patient is at high risk of bleeding despite the presence of a single risk factor.

Risk of bleeding Number of risk factors[2]
Low Risk 0
Moderate Risk 1
High Risk ≥2

Do's

  • When indicated, administer fibrinolytic therapy for a short infusion time (for 2 hours) rather than over prolonged perfusion (for 24 hours).[2]

References

  1. Miniati M, Cenci C, Monti S, Poli D (2012). "Clinical presentation of acute pulmonary embolism: survey of 800 cases". PLoS One. 7 (2): e30891. doi:10.1371/journal.pone.0030891. PMC 3288010. PMID 22383978.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ; et al. (2012). "Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e419S–94S. doi:10.1378/chest.11-2301. PMC 3278049. PMID 22315268.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P; et al. (2008). "Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)". Eur Heart J. 29 (18): 2276–315. doi:10.1093/eurheartj/ehn310. PMID 18757870.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ; et al. (2011). "Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association". Circulation. 123 (16): 1788–830. doi:10.1161/CIR.0b013e318214914f. PMID 21422387.
  5. 5.0 5.1 5.2 Cannon CP, Goldhaber SZ (1996). "Cardiovascular risk stratification of pulmonary embolism". Am. J. Cardiol. 78 (10): 1149–51. PMID 8914880. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)
  6. Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, Kearon C, Weitz J, D'Ovidio R, Cogo A, Prandoni P (1995). "Accuracy of clinical assessment of deep-vein thrombosis". Lancet. 345 (8961): 1326–30. PMID 7752753. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  7. Wells PS, Ginsberg JS, Anderson DR, Kearon C, Gent M, Turpie AG, Bormanis J, Weitz J, Chamberlain M, Bowie D, Barnes D, Hirsh J (1998). "Use of a clinical model for safe management of patients with suspected pulmonary embolism". Ann Intern Med. 129 (12): 997–1005. PMID 9867786.
  8. 8.0 8.1 8.2 8.3 Wells P, Anderson D, Rodger M, Ginsberg J, Kearon C, Gent M, Turpie A, Bormanis J, Weitz J, Chamberlain M, Bowie D, Barnes D, Hirsh J (2000). "Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer". Thromb Haemost. 83 (3): 416–20. PMID 10744147.
  9. 9.0 9.1 9.2 Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D, Forgie M, Kovacs G, Ward J, Kovacs MJ (2001). "Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer". Ann Intern Med. 135 (2): 98–107. PMID 11453709.
  10. 10.0 10.1 Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, Sos TA, Quinn DA, Leeper KV, Hull RD, Hales CA, Gottschalk A, Goodman LR, Fowler SE, Buckley JD (2007). "Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II Investigators". Radiology. 242 (1): 15–21. doi:10.1148/radiol.2421060971. PMID 17185658.
  11. van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW; et al. (2006). "Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography". JAMA. 295 (2): 172–9. doi:10.1001/jama.295.2.172. PMID 16403929.
  12. 12.0 12.1 12.2 12.3 12.4 Kucher N, Goldhaber SZ (2005). "Management of massive pulmonary embolism". Circulation. 112 (2): e28–32. doi:10.1161/CIRCULATIONAHA.105.551374. PMID 16009801.
  13. Fengler BT, Brady WJ (2009). "Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm". Am J Emerg Med. 27 (1): 84–95. doi:10.1016/j.ajem.2007.10.021. PMID 19041539.
  14. 14.0 14.1 14.2 14.3 14.4 14.5 Holbrook A, Schulman S, Witt DM, Vandvik PO, Fish J, Kovacs MJ; et al. (2012). "Evidence-based management of anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e152S–84S. doi:10.1378/chest.11-2295. PMC 3278055. PMID 22315259.
  15. Stein PD, Hull RD, Raskob GE (2000). "Withholding treatment in patients with acute pulmonary embolism who have a high risk of bleeding and negative serial noninvasive leg tests". Am J Med. 109 (4): 301–6. PMID 10996581.
  16. 16.0 16.1 16.2 16.3 16.4 Cohen AT, Dobromirski M, Gurwith MM (2014). "Managing pulmonary embolism from presentation to extended treatment". Thromb Res. 133 (2): 139–48. doi:10.1016/j.thromres.2013.09.040. PMID 24182642.
  17. 17.0 17.1 Anderson FA, Spencer FA (2003). "Risk factors for venous thromboembolism". Circulation. 107 (23 Suppl 1): I9–16. doi:10.1161/01.CIR.0000078469.07362.E6. PMID 12814980.
  18. Worsley DF, Alavi A, Aronchick JM, Chen JT, Greenspan RH, Ravin CE (1993). "Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study". Radiology. 189 (1): 133–6. doi:10.1148/radiology.189.1.8372182. PMID 8372182.
  19. Hokusai-VTE Investigators. Büller HR, Décousus H, Grosso MA, Mercuri M, Middeldorp S; et al. (2013). "Edoxaban versus warfarin for the treatment of symptomatic venous thromboembolism". N Engl J Med. 369 (15): 1406–15. doi:10.1056/NEJMoa1306638. PMID 23991658. Review in: Ann Intern Med. 2014 Jan 21;160(2):JC4 Review in: Ann Intern Med. 2014 Mar 18;160(6):JC4

Linked-in.jpg