Emergency management of Pulmonary Embolisms

What is a Pulmonary Embolism?

Blockage of the main artery of the lung or one of

its branches by a substance that has travelled from elsewhere in the body through the bloodstream.

Goldhaber SZ (2005). "Pulmonary thromboembolism". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 156165

Risk Factors
Recent surgery, especially abdominal/pelvic or

hip/knee replacement Thrombophilia Leg fracture Prolonged bed rest Malignancy Pregnancy/postpartum;pill/HRT

Goldhaber SZ (2005). "Pulmonary thromboembolism". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 156165

Approach to treatment:
Assessment of Severity:

-Low-risk PE is diagnosed when all checked right

ventricular dysfunction and myocardial injury markers are found negative.

-Intermediate-risk PE is diagnosed if at least one RVD or one myocardial injury marker is positive. -High-risk PE is diagnosed in the presence of shock or
persistent arterial hypotension (defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused by new-onset arrhythmia, hypovolaemia orand sepsis) Guidelines on the diagnosis management of acute pulmonary embolism- European Heart
Journal, Volume 29- Issue 18.

Approach to treatment:
RESUSCITATION: - Respiratory Support: Supplemental oxygen

should be administered if hypoxemia exists. Severe hypoxemia or respiratory failure should prompt consideration of intubation and mechanical ventilation.
- Haemodynamic support: patients presenting

with acute PE and hypotension. Intravenous fluid administration is first-line therapy. Administration of 500 mL of dextran significantly increased the cardiac index from a mean of 1.6 to 2.0 L/min/m2.
Guidelines on the diagnosis and management of acute pulmonary embolism- European Heart Journal, Volume 29- Issue 18.

Approach to treatment:
Which anticoagulant should be administered?

How much and for how long?

Should thrombolytic therapy be administered?

Should an inferior vena caval filter be placed?

Is embolectomy indicated?

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension- American Heart Association 2011.

Anticoagulation:
Rapid anticoagulation can only be achieved with

parenteral anticoagulants, such as intravenous unfractionated heparin, subcutaneous low-molecularweight heparin (LMWH) or subcutaneous fondaparinux. Treatment with parenteral anticoagulants is usually followed by the administration of oral vitamin K antagonist. Anticoagulation with unfractionated heparin, LMWH or fondaparinux should be continued for at least 5 days and stopped when the international normalized ratio (INR) lies between 2.0 and 3.0 for at least 2 consecutive days. If warfarin is used, a starting dose of 5 or 7.5 mg and is preferred over higher doses. Guidelines on the diagnosis management of acute pulmonary embolismEuropean Heart Journal,
Volume 29- Issue 18.

Anticoagulation:
Warfarin should be continued for a minimum of 3

months after stopping heparin.

Thrombolysis for a high risk PE is 50mg bolus of

alteplase.

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension- American Heart Association 2011.

Empirical parenteral anticoagulation:

Therapeutic anticoagulation with subcutaneous LMWH,

intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients

with objectively confirmed PE and no contraindications

to anticoagulation.
Therapeutic anticoagulation during the diagnostic

workup should be given to patients with intermediate

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension- American Heart Association 2011.

or high clinical probability of PE and no

Thrombolytic Therapy:
First-line treatment in patients with high-risk PE

presenting with cardiogenic shock and/or persistent arterial hypotension.

Intermediate-risk PE- after thorough consideration of

conditions increasing the risk of bleeding. Not used routinely.

Thrombolytic therapy should be not used in patients

with low-risk PE.

Guidelines on the diagnosis and management of acute pulmonary embolism- European Heart Journal, Volume 29- Issue 18.

Thrombolytic Therapy:
Streptokinase

-250 000 IU as a loading dose over 30 min, followed by 100 000 IU/h over 1224 h -Accelerated regimen: 1.5 million IU over 2 h Urokinase -4400 IU/kg as a loading dose over 10 min, followed by 4400 IU/kg/h over 1224 h Accelerated regimen: 3 million IU over 2 h Recombinant tissue Plasminogen Activator -100 mg over 2 h or 0.6 mg/kg over 15 min (maximum dose 50 mg)
Guidelines on the diagnosis and management of acute pulmonary embolism- European Heart Journal, Volume 29- Issue 18.

Embolectomy
Used in: - High risk PE - Intermediate risk PE with right ventricular dysfunction

when contraindications exclude thrombolysis.

- Low risk PE to remove a right atrial thrombus or

paradoxical embolus.

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension- American Heart Association 2011.

Embolectomy
Catheter embolectomy and fragmentation or surgical

embolectomy is reasonable for patients with high riskPE and contraindications to fibrinolysis High risk PE who remain unstable after receiving fibrinolysis
Intermediate risk PE judged to have clinical evidence

of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis)
low-risk PE or intermediate risk PE with minor RV
Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension- American Heart Association 2011.

dysfunction, minor myocardial necrosis, and no

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