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Pulmonary Embolism and Deep Vein Thrombosis

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Pulmonary Embolism and Deep Vein Thrombosis

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Pulmonary Embolism & Deep Vein Thrombosis

Introduction

Overview

Pulmonary embolism occurs when the pulmonary arteries are obstructed. This is most often due to emboli that travel from the deep veins of the thighs/pelvis.

Because deep vein thrombosis and pulmonary embolism so often occur together, we have a term for their combined condition: venous thromboembolism.

Nonthrombotic sources of pulmonary embolism include: air, fat, amniotic fluid, bacterial (septic), foreign bodies, and, tumors.

Pulmonary embolism is a leading cause of cardiovascular-related death; denote that key complications of pulmonary embolism include pulmonary hypertension, right heart failure, and pulmonary infarction.

Treatments

Supportive therapy, which includes administration of oxygen, saline, and vasopressors.

Anti-coagulation therapies, which can include heparin/enoxaparin or fondaparinux for short-term treatment, and warfarin for longer-term treatment.

In some cases, embolectomy or clot dissolution is required to restore blood flow through the pulmonary arteries.

Deep Vein Thrombosis

DVT/PE Relationship

DVT is the leading cause of pulmonary embolism.

Virchow Triad

The "Virchow Triad" comprises three factors that predispose an individual to deep vein thrombosis; each of the three elements of the Virchow Triad contribute to the formation of clots in the blood vessels.

Endothelial injury promotes clotting – endothelial injury can be due to fracture, surgery, trauma, or even previous deep vein thrombosis.

  • Upon injury, the endothelium responds by triggering the clotting cascade (review of hemostasis). If this process goes unchecked, and the clots are not ultimately dissolved, they can be problematic.

Venous stasis is another predisposing factor – venous stasis can be caused by immobility (if a person is bed-ridden or on a long flight, for example), elevated central venous pressure, heart failure, and obesity.

  • To prevent DVT in hospitalized patients, we use SCD's (sequence compression devices), which prevent venous stasis in the legs.
  • In select patients, we use prophylactic anticoagulants, which includes low doses of enoxaparin or heparin.
  • Note that heparin-induced thrombocytopenia is a worrisome complication of anticoagulant, but, overall, in the correct population, prophylactic anticoagulants can be an important way of preventing DVT.

Hypercoagulation states are predisposing medical conditions

  • Pregnancy (which is also associated with inferior vena cava stasis)
  • The post partum period
  • Smoking (which is also associated with endothelium damage)
  • Cancer
  • Medications, including combined hormonal contraceptives and some hormonal replacement therapies
  • Coagulation disorders, such as Factor V Leiden disorder.
    • Be aware that individuals with multiple predisposing factors (i.e., pregnant women who are put on bed rest, for example), are at higher risk for developing deep vein thrombosis.

Symptoms

When present, symptoms of deep vein thrombosis tend to arise unilaterally in the legs, leaving them swollen, tender, and with signs of venous dilation.

Deep vein thrombosis can occur in the upper body, too, but this is less common.

Post thrombotic syndrome

Post thrombotic syndrome occurs when the venous valves are damaged.

Diagnosis of DVT

For the diagnosis of deep vein thrombosis, we rely on the Wells Score for Deep Vein Thrombosis, which gives points based on several factors including the presence of swelling, edema, and the likelihood of alternative diagnosis.

D-dimer level is an important way to try to rule out low-probability DVTs.

  • If deep vein thrombosis is highly suspected, imaging with contrast venography or venous ultrasonography with compression can verify the presence of thrombus.

Pulmonary Embolis

Pathogenesis

We'll begin by showing how a clot can reach the lungs and become lodged in the pulmonary arteries.

  • First, show a clot in a deep vein of the thigh: show red blood cells, platelets, white blood cells, and fibrin.
  • Then, indicate that a piece of this clot can break off and travel to the inferior vena cava.
  • From here, the clot can pass through the right atrium and ventricle, and be pumped through the pulmonary trunk and arteries to reach the pulmonary blood supply.
  • This clot blocks blood flow so that downstream alveoli will not be perfused and gas exchange will be impaired.

Symptoms

As a result of pulmonary artery obstruction and impaired gas exchange, show that patients may experience dyspnea, tachypnea (rapid breathing), and chest pain.

Tachycardia and right heart failure are possible.

We also look for altered mental state in elderly patients.

Classification

We can classify PE by risk level: pulmonary embolisms are considered massive (high risk), intermediate (submassive), and low risk.

Risk is determined by assessing hemodynamic instability (i.e., the presence of hypotension).

Emboli can also be classified by their location:

  • Saddle emboli are located where the pulmonary trunk bifurcates.
  • Other emboli may become lodged in the lobar, segmental, or subsegmental arteries.

Diagnosis of PE

Diagnosis of pulmonary embolism can be difficult due to the nonspecific symptoms and signs.

The Pulmonary Embolism Wells Score gives points based on a variety of factors, including heart rate, presence of signs/symptoms, and likelihood of an alternative diagnosis.

Wells score of 4 or greater indicates that pulmonary embolism is likely.

  • Some calculators say less than 2 is low probability, 2-6 is moderate probability, and higher than 6 is highly probable.

We can also measure D-dimer in the blood to rule out pulmonary embolism.

  • D-dimer is a product of fibrin degradation, and levels greater than 500 nanograms per milliliter indicate that pulmonary embolism is possible and more tests are needed.

Additional tests for pulmonary embolism:

  • Ventilation to perfusion scan is a noninvasive test that can indicate the presence of a blood clot.
  • Chest CT w/angiography is perhaps the most widely used assessment for Pulmonary Embolism. With this, we can actually visualize disruption of blood flow within the pulmonary arteries.
  • Chest X-Rays may show signs of:
    • Atelectasis
    • Hampton hump, which is indicative of pulmonary infarction; we'll learn more about in a moment)
    • Westermark sign, which is indicative of oligemic areas; show that this appears as an area of poor perfusion of pulmonary arteries.
    • Pulmonary effusion
  • ECG: may show sinus tachycardia; some patients may show an S wave in lead 1 with inverted Q and T waves in lead III (S1Q3T3 sign).
  • Thrombi formed premortem display lines of Zahn, which are formed by layers of fibrin, red blood cells, and platelet deposition.

Pulmonary infarction is most often due to small emboli that obstruct blood flow and cause tissue ischemia.
– As mentioned, these patients' x-rays may show the wedge-shaped "Hampton Hump," most often in the lower lobes.

Clinical Cases

Case 1: Pregnant patient with calf swelling

A 32-year-old pregnant female presents to your office with a 1 week history of right leg swelling. She denies any history of trauma or similar symptoms, though describes pain with ambulation. The patient reports returning 12 days ago from an overseas trip which entailed a 12-hour plane ride.

On physical examination, she is afebrile and in no acute distress. Her heart rate is 70/min, and blood pressure is 100/70 mmHg. Pulse oximetry measurement shows 98 percent oxygen saturation. No rashes or lesions are noted on the affected extremity. Her right calf is 4 cm greater in circumference than her left calf, and there is tenderness when you squeeze the gastrocnemius muscle.

What is the preferred initial therapy in management of this patient's diagnosis?

Answer

  • Low-molecular-weight heparin (LMWH)

Explanation

This patient most likely has a deep venous thrombosis (DVT). Pregnancy and recent extended travel history are common predisposing factors for DVT. She is at risk for development of a pulmonary embolism (PE) and should therefore be started on low-molecular-weight heparin (LMWH) without delay. Wells' Criteria should also be calculated and is used to estimate the probability for acute PE in patients in which history and examination suggest PE is a diagnostic possibility. This risk stratification score and clinical decision rule provides a pre-test probability which can then be used in conjunction with a negative D-dimer to rule out PE and avoid unnecessary imaging.

Thrombolytic therapy, such as tissue plasminogen activator (tPA) is reserved for clinically unstable patients (hypotension or shock) due to a host of possible serious complications. Intracranial hemorrhage is the most devastating complication of tPA therapy and occurs in 0.2-1 percent of patients treated with thrombolytic therapy. Anticoagulants are the standard treatment for DVT or a clot in a calf vein.

An inferior vena cava (IVC) filter (also known as a Greenfield filter) is a small device placed by surgical cutdown or by percutaneous insertion through the femoral or jugular veins, and is intended to stop blood clots from going up into the lungs. It is not considered first-line therapy, but rather indicated for recurrent DVT's or in patients with chronic risk factors such as paraplegia, malignancy, or genetic hypercoagulable conditions.

Warfarin (Coumadin) therapy is contraindicated in pregnancy. In a patient that warfarin is not contraindicated (no risk factors or bleeding disorders), a standard warfarin protocol would be initiated simultaneously with low-molecular-weight heparin, and would include oral treatment at 5 mg per day and titrating the dose of warfarin every three to five days to achieve an international normalized ratio (INR) between 2.0 and 3.0. Treatment for a DVT caused by a reversible risk factor should be continued for 3 months.

Case 2: Post-operative patient with dyspnea and chest pain

A 65-year-old female underwent surgery for a total hip replacement 3 days ago. The procedure was uneventful and the patient has recovered as expected. You are called to evaluate the patient because she has developed acute cyanosis, shortness of breath (dyspnea), and substernal chest pain.

On physical examination, the patient is diaphoretic and in obvious acute respiratory distress. She has no rashes or lesions. The patient is on a cardiac monitor and appears to be in normal sinus rhythm. Her respiratory rate is 40/min and her breathing is labored. Her blood pressure is 100/70 mm Hg. Cyanosis is present, and chest auscultation demonstrates decreased breath sounds in the lower lobe of the right lung, as well as adventitious breath sounds in all lobes.

Based on the information provided, what is the most likely diagnosis in this patient?

Answer

  • Acute pulmonary embolism

Explanation

An acute pulmonary embolism (PE) is the blockage of a pulmonary artery by a blood clot that forms in the legs or another part of the body (deep vein thrombosis) and travels to the lungs. The area of the lung fed by the blocked artery does not receive enough blood supply and can die (pulmonary infarction). An acute pulmonary embolism (PE) can be life-threatening, especially when the blockage occurs at the bifurcation of the main pulmonary artery, called a "Saddle PE" (see photo).

Signs and symptoms of acute PE include chest pain that worsens with inspiration (typically substernal), shortness of breath (dyspnea), coughing up blood (hemoptysis), low oxygen levels in the blood (hypoxemia), increased heart rate (tachycardia), low blood pressure (hypotension), and clammy or bluish skin (cyanosis).

Chest x-rays (CXR) are not sensitive or specific for diagnosing PE. When detected on CXR (rare), findings include decreased vascularization at the periphery of the lung (Westermark's sign), and a peripheral, wedge-shaped opacification adjacent to the pleural surface, which represents the pulmonary infarction distal to the pulmonary embolus (Hampton's hump). Pulmonary angiography is the gold standard for diagnosing a PE.

Management options include anticoagulants, such as heparin or low-molecular weight heparin, warfarin, or factor Xa inhibitors, and in severe cases, thrombolytics.

Board Review

Pulmonary Embolism

Getting ready for boards? Review these concise, bulleted high yield reviews for your exam.

USMLE & COMLEX-USA

Nurse Practitioner (NP)

Physician Assistant (PA)

Internal Medicine (ABIM)

References

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