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Pulmonary embolism and infarction

Pulmonary embolism and infarction: Excerpt from Handbook of Diseases

Pulmonary embolism is an obstruction of the pulmonary arterial bed by a dislodged thrombus or foreign substance. Although pulmonary infarction (tissue death) may be so mild as to be asymptomatic, massive embolism (more than 50% obstruction of pulmonary arterial circulation) and infarction can be rapidly fatal.

Causes

Pulmonary embolism generally results from dislodged thrombi originating in the leg veins. More than half of such thrombi arise in the deep veins of the legs and are usually multiple.

Other less-common sources of thrombi are the pelvic veins, renal veins, hepatic vein, right side of the heart, and upper extremities. Such thrombus formation results directly from vascular wall damage, venostasis, or hypercoagulability of the blood.

Rare causes

Rarely, the emboli contain air, fat, amniotic fluid, talc (from drugs intended for oral administration that are injected I.V. by addicts), or tumor cells. Thrombi may embolize spontaneously during clot dissolution or may be dislodged during trauma, sudden muscular action, or a change in peripheral blood flow.

Rarely, pulmonary infarction may evolve from pulmonary embolism, especially when pulmonary embolism occurs with chronic cardiac or pulmonary disease. However, if the embolus obstructs a large vessel, bronchial circulation may provide an inadequate oxygen supply to the lung supplied by the occluded vessel.

Risk factors

Predisposing factors to pulmonary embolism include:

❑ long-term immobility

❑ chronic pulmonary disease

❑ heart failure or atrial fibrillation

❑ thrombophlebitis, polycythemia vera, thrombocytosis, autoimmune hemolytic anemia, and sickle cell disease

❑ varicose veins and vascular injury

❑ recent surgery

❑ advanced age

❑ pregnancy

❑ lower-extremity fractures or surgery

❑ burns

❑ obesity

❑ malignancy

❑ use of hormonal contraceptives.

Signs and symptoms

Total occlusion of the main pulmonary artery is rapidly fatal; smaller or fragmented emboli produce symptoms that vary with the size, number, and location of the emboli. Usually, the first symptom of pulmonary embolism is dyspnea, which may be accompanied by angina or pleuritic chest pain.

Other clinical features include tachycardia, productive cough (sputum may be blood-tinged), low-grade fever, and pleural effusion. Less-common signs include massive hemoptysis, splinting of the chest, leg edema and, with a large embolus, cyanosis, syncope, and jugular veins distention .

In addition, pulmonary embolism may cause pleural friction rub and signs of circulatory collapse (weak, rapid pulse; hypotension) and hypoxia (restlessness).

Diagnosis

The patient’s history reveals any predisposing conditions for pulmonary embolism. The following diagnostic tests are also helpful:

Chest X-ray helps to rule out other pulmonary diseases; it also shows areas of atelectasis, an elevated diaphragm, pleural effusion, a prominent pulmonary artery and, occasionally, the characteristic wedge-shaped infiltrate suggestive of pulmonary infarction.

Spiral computed tomography scan may identify a thrombus in the pulmonary vasculature.

Lung scan shows perfusion defects in areas beyond occluded vessels; however, it doesn’t rule out microemboli.

Pulmonary angiography is the most definitive test but requires a skilled angiographer and radiologic equipment; it also poses some risk to the patient. Its use depends on the uncertainty of the diagnosis and the need to avoid unnecessary anticoagulant therapy in high-risk patients.

Electrocardiography (ECG) is inconclusive but helps distinguish pulmonary embolism from myocardial infarction. In extensive embolism, the ECG may show right-axis deviation; right bundle-branch block; tall, peaked P waves; ST-segment depression and T-wave inversions (indicating right heart strain); and supraventricular tachyarrhythmias.

Auscultation occasionally reveals a right-sided ventricular S3 gallop and increased intensity of the pulmonic component of S2. Also, crackles and a pleural rub may be heard at the site of embolism.

Arterial blood gas (ABG) analysis showing decreased partial pressures of arterial oxygen and carbon dioxide are characteristic but don’t always occur.

If pleural effusion is present, thoracentesis may rule out empyema, which indicates pneumonia.

CLINICAL TIP: When the patient’s condition is stabilized, a thorough diagnostic evaluation for hematologic hypercoagulability should be performed.

Treatment

In pulmonary embolism, treatment is designed to maintain adequate cardiovascular and pulmonary function during resolution of the obstruction and to prevent recurrence of embolic episodes.

Oxygen and anticoagulants

Because most emboli resolve within 10 to 14 days, treatment consists of oxygen therapy, as needed, and anticoagulation with heparin to inhibit new thrombus formation. Heparin therapy is monitored by daily coagulation studies (partial thromboplastin time [PTT]). Low-molecular-weight hep-arin has been used successfully for intramuscular injections.

Long-term therapy with oral anticoagulants such as warfarin is used to prevent recurrence.

Drug therapy

Patients with massive pulmonary embolism and shock may need fibrinolytic therapy with urokinase, streptokinase, or a tissue plasminogen activator to enhance fibrinolysis of the pulmo-nary emboli and remaining thrombi. Emboli that cause hypotension may require the use of vasopressors. Treatment of septic emboli requires antibiotics, not anticoagulants, and evaluation for the infection’s source, particularly endocarditis.

Surgery

Interruption of the inferior vena cava is used for patients who can’t take anticoagulants, who have recurrent emboli during anticoagulant therapy, or who have been treated with thrombolytic agents or pulmonary thromboend-arterectomy.

Surgery (which shouldn’t be done without angiographic evidence of pulmonary embolism) consists of vena caval ligation, plication, or insertion of a device (umbrella filter) to filter blood returning to the heart and lungs. To prevent postoperative venous thromboembolism, a combination of heparin and dihydroergotamine may be given.

Special considerations

❑ Give oxygen by nasal cannula or mask. Check ABG levels in the event of fresh emboli or worsening dyspnea.

❑ Be prepared to provide endotracheal intubation with assisted ventilation if breathing is severely compromised.

❑ Administer heparin, as needed, through I.V. push or continuous drip. Monitor coagulation studies daily. Effective heparin therapy raises PTT to 1½ to 2½ times normal.

❑ Watch closely for nosebleed, pete-chiae, and other signs of abnormal bleeding; check stools for occult blood. Tell the patient to prevent bleeding by shaving with an electric razor and by brushing his teeth with a soft toothbrush.

❑ After the patient’s condition is stable, encourage him to move about frequently, and assist with isometric and range-of-motion exercises.

❑ Check pedal pulses, temperature, and color of the feet to detect venostasis. Never vigorously massage the patient’s legs.

❑ Help the patient walk as soon as possible after surgery to prevent veno-stasis.

❑ Use incentive spirometry to assist in deep breathing. Provide tissues and a bag for easy disposal of expectorations.

❑ Warn the patient not to cross his legs because it promotes thrombus formation.

❑ Advise patients taking anticoagulants to watch for signs of bleeding (bloody stools, blood in urine, large ecchymoses), to take the prescribed medication exactly as ordered, and to avoid taking any additional medication (even for headaches or colds) or changing doses of medication without consulting their physicians.

❑ Stress the importance of follow-up laboratory tests (prothrombin time) to monitor anticoagulant therapy.

❑ To prevent pulmonary emboli in patients predisposed to this condition, encourage early ambulation. With close medical supervision, low-dose heparin may be useful prophylactically.

Book Source Details

  • Book Title: Handbook of Diseases
  • Author(s): Springhouse
  • Year of Publication: 2003
  • Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.




More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5

 » Next page: Pulmonary Embolism (The 5-Minute Pediatric Consult)

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