Pulmonary Embolism

Description

Pulmonary embolism (PE) may manifest as a cardiovascular emergency secondary to mechanical obstruction and the release of inflammatory mediators in the pulmonary arterial system.
The majority result from blood clots in the pelvic and deep veins of the lower extremities, but can also occur with amniotic fluid, fat, air, and septic emboli.
Intraoperative and postoperative PE can result from venous stasis and inflammatory mediators related to surgery. Additionally, the choice of anesthetic technique (general versus regional) may have an impact on perioperative hypercoagulability. Epidural and spinal anesthesia have been shown to have a decreased incidence of deep venous thrombosis (DVT).
DVT/PE is regarded as an avoidable and preventable event. Thus, anesthesia providers play a role in implementing and ensuring that preventative measures are performed.

Epidemiology

Incidence

Annual incidence for DVT is estimated to occur in 23–69 cases per 100,000 surgical cases.

Prevalence

Varies depending on the population studied and coexisting diseases.
PE has been documented in 15–55% of cases after autopsy (death from all causes).

Morbidity

PE may occur in up to 50% of patients with DVT.

Mortality

In the US: 300,000 deaths annually.
If undiagnosed and untreated within 1 hour, 10% of patients may die.

Etiology/Risk Factors

Acquired factors:
- Obesity
- Pregnancy and post-partum period
- Estrogen use
- Surgery: Orthopedic (hip or knee), GI, gynecological, cancer.
- Age 40 years and older
- Trauma: Fractures (hip or leg).
- Spinal cord injury
- Malignancy: Secondary to chemotherapy, hormone therapy.
- Prolonged immobilization: Travel, surgery
- Central venous catheters
- Antiphospholipid antibody syndrome
- Polycythemia vera
Hereditary factors:
- Protein C and S deficiency
- Antithrombin III deficiency
- Factor V Leiden
- Prothrombin gene mutation
- Dysfibrinogenemia
- Plasminogen deficiency
Other factors:
- History of DVT, heparin-induced thrombocytopenia (HIT), varicose veins.
- Medical conditions such as: Congestive heart failure (CHF), arrhythmia, respiratory failure, and inflammatory disease (bowel, rheumatoid arthritis).

Physiology/Pathophysiology

Mechanical obstruction: PE may have various degrees of obstruction within the pulmonary circulation depending on the number and location of emboli. This can result in:
- Dead space ventilation (ventilation without perfusion)
- Increased right ventricular afterload
- Pulmonary infarct
Inflammatory mediators: Additionally, obstructive material may set off an inflammatory cascade that releases vasoactive products and serotonin. The effect is a constellation of:
- Pulmonary edema
- Shunting (impaired alveolar ventilation secondary to atelectasis) and hypoxemia
- Increased airway resistance (wheezing)
- Increased minute ventilation
- Decreased vital capacity
- Decreased diffusing capacity
- Tachycardia and hypotension
In severe cases, right ventricular dysfunction and respiratory collapse may result secondary to an elevation in wall tension, ventricular dilation, and ischemia. Cardiogenic shock and myocardial ischemia may occur.

Prevantative Measures

Avoid prolonged immobilization
Heparin/low-molecular-weight heparin (LMWH) may be administered preoperatively/postoperatively. Since most antithrombotic drugs are renally excreted, caution must be observed when administering to patients with renal dysfunction. LMWH has a better therapeutic profile than unfractionated heparin (UFH) and may provide superior DVT prophylaxis in high-risk surgical groups (trauma, hip, and knee replacement).
Intermittent pneumatic compression devices and elastic stockings applied during the perioperative period have shown benefit in patients with a moderate risk for DVT or with a known contraindication for anticoagulation.
An inferior vena cava (IVC) filter is indicated if there is a recent diagnosis of DVT/PE and the patient is unable to receive anticoagulation.
Utilize adjuvant therapies for pain management such as intravenous analgesics (PCA) or local regional techniques (nerve blocks, epidural, spinal, and wound infiltration). Regional techniques may control acute pain for hours to days depending on the technique used. Epidural and spinal anesthesia may decrease the rates of DVT, likely as a result of sympathetic blockade with improvement in circulation and decrease in hypercoagulability.
Fat emboli occurrence can be minimized with early treatment of the underlying cause: Surgical repair of long bone fractures, careful monitoring of fat content in total parenteral nutrition infusions, and surgical repair of cardiac wall defects (PFO).
Septic emboli must be ruled out in patients with persistent fever and positive blood cultures. A search for the embolic source (e.g., heart valves) is important in guiding therapeutic decisions.

Pregnancy Considerations

The risk of PE is ~15 times higher in the postpartum period than during pregnancy, and is likely related to venous stasis, alterations in circulating clotting factors (I, II, VII, VIII, IX, and X), declines in protein S, increased platelet activation, and elevated fibrin production. The therapeutic approach is the same as the non-pregnant patient.

Amniotic fluid emboli prevention requires avoidance of any uterine trauma (surgical and nonsurgical) or spontaneous rupture.

Clinical findings include tachycardia, tachypnea, calf pain or swelling, cough, hemoptysis, chest pain/pleural rub, increased jugular pressure, or syncope (lacking sensitivity and specificity)
Location: Central vascular zones include the main pulmonary artery, left and right main pulmonary arteries, anterior trunk, right and left interlobar arteries, left upper lobe trunk, right middle lobe artery, and right and left lower lobe arteries. Peripheral vascular zones include the segmental and subsegmental arteries of the right upper lobe, right middle lobe, right lower lobe, left upper lobe, lingula, and left lower lobe.
Extent: A PE is considered to be massive when it involves both pulmonary arteries or results in hemodynamic compromise.
Pre-test risk stratification is important for diagnosis and treatment. The Wells (2) and Geneva (3) scores factor in risk factors and clinical findings and may aid in guiding further diagnostic work-up.
Computerized tomography (CT) scan. A spiral chest CT scan produces a 3-D image by rotating the scanner around the body in a spiral and has a greater sensitivity (and is quicker) than plain CT imaging (2-D). Contrast material may be injected to provide delineation of the pulmonary vasculature and improve definition of nonvascular structures (CT angiogram). However, contrast may be harmful to the kidneys.
Pulmonary angiography use is reserved for cases requiring a catheter-based treatment.
Ventilation-perfusion (V/Q) lung scanning is an alternative to CT angiography if contrast dye is a concern. Highly sensitive in patients without cardiopulmonary disease.
Compression ultrasonography can detect proximal DVT in 20% of patients with PE; they have a high sensitivity and specificity for proximal DVT of the lower extremities (evidence grade A).
Chest radiography is useful to rule out acute conditions such as hemothorax and pneumothorax.
Echocardiography is an alternative if the patient is too unstable for transport. TEE has a sensitivity of 60–80% and specificity of 95–100%. TTE is useful in detecting right ventricular dysfunction. Findings include abnormalities in ventricular wall motion, ventricular dilation, paradoxical septal motion, tricuspid insufficiency, elevated pulmonary artery pressure, and IVC congestion.
PA catheter may be considered for management and differential diagnosis purposes.
ECG may have an S1, Q3, T3 pattern consistent with acute cor pulmonale. Right bundle branch block (RBBB) and right axis deviation may also be present. ECG findings in PE are neither specific nor sensitive. Helpful in MI diagnosis during an acute hemodynamic crisis.
Arterial blood gas analysis is useful to evaluate hypoxemia, hypercarbia, and can aid with the differential diagnosis of PE.
D-dimer levels: If there is a low pre-test probability, a negative test can be useful to rule out a PE (strong negative predictive value).

Differential Diagnosis

Congestive heart failure
Pulmonary hypertension
Acute coronary syndrome

Intravenous anticoagulation:
- Heparin enhances the activity of antithrombin III, which inhibits thrombin and other factors such as Xa, IXa, XIa, and XIIa. Thrombin also inhibits factors V, VIII, and thrombin-induced platelet activation. Initial treatment of PE and DVT consists of a heparin bolus (80 U/Kg) with a maintenance dose (18 U/Kg); aPTT levels should be titrated to 1.5–2.5 times normal levels or a plasma concentration of 0.3–0.7 IU/L within 24 hours. Current evidence suggests treatment for 5–6 days in combination with oral therapy (evidence level A).
- LMWH are derived from heparin after chemical and enzymatic depolymerization to create shorter compounds that have a decreased ability to combine with other molecules. Enoxaparin 1 mg/kg SQ q12 hours or 1.5 mg/kg SQ QD can be used for the treatment of PE and DVT (has been shown to be as effective as heparin for PE, and more effective for DVT). LMWHs have the benefit of SQ administration, lower rates of HIT, and do not require routine laboratory monitoring. If monitoring is necessary (obesity, pregnancy, renal failure), anti-factor Xa levels are checked.
Oral anticoagulation:
- Warfarin inhibits the enzymes that convert vitamin K epoxide to reduced vitamin K. The initial dose for PE and DVT treatment is 5–10 mg daily with individual factors requiring dose adjustments. INR levels should be titrated to a level of 2.0–3.0 for venous thromboembolism (VTE) for 2 consecutive days prior to the discontinuation of heparin. Treatment for 3 months is recommended for PE due to reversible causes (evidence level A).
Thrombolytic therapy (urokinase, streptokinase, alteplase) is indicated in proven cases of PE with cardiogenic shock. They rapidly dissolve thrombus, but carry significant risk of intracranial bleeding. It has the greatest benefit if used within 48 hours of the onset of symptoms.
Thrombin inhibitors: If HIT is suspected, consider therapy with argatroban, lepirudin, or bivalirudin.
Catheter-based pulmonary embolectomy and local intraembolic thrombolytic therapy can be lifesaving. Surgical embolectomy can be considered in patients with free-floating thrombi in the right atrium.

Acute intraoperative PE should be suspected in any patient with a strong preoperative history suggestive of DVT.
Intraoperative TEE (transesophageal echocardiogram) may be helpful with the diagnosis of PE.

Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med. 2008;359:2804–2813.
Wells PS , anderson DR , Rodger M , et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: Management of patients suspected of pulmonary embolism presenting to the emergency department by using a simple clinical model and D-Dimer. Ann Intern Med. 2001;135:98–107.
Le Gal G , Righini M , Roy PM , et al. Prediction of pulmonary embolism in the emergency department: The revised Geneva score. Ann Intern Med. 2006;144:165–171.
Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008;358:1037–1052.
Hirsch J , Guyatt G , Albers GW , et al. Antithrombotic and thrombolytic therapy: American College of Chest Physicians (ACCP) Evidence-Based Clinical Practice Guidelines Executive Summary. Chest. 2008;133:71S–105S.

See Also (Topic, Algorithm, Electronic Media Element)

ICD9

415.19 Other pulmonary embolism and infarction

ICD10

I26.99 Other pulmonary embolism without acute cor pulmonale

Diagnosis and treatment of PE requires a high index of suspicion and rapid risk stratification.
Hemodynamically unstable patients require immediate evaluation to exclude sepsis, hypovolemia, and new onset arrhythmia. If the initial assessment is negative, they are regarded as high risk for PE.
Prevention is essential in hospitalized patients with the use of heparin, LMWH, warfarin, and/or sequential compression devices.

Carlos A. Puyo , MD

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Pregnancy Considerations

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆