Pulmonary Infarction Clinical Presentation

Updated: Jan 16, 2015
  • Author: Lennox H Huang, MD, FAAP; Chief Editor: Michael R Bye, MD  more...
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Presentation

History

Classic symptoms of pulmonary embolism (PE) are rarely encountered. The frequency with which the diagnosis is missed in both adults and children is striking. Adding to the clinical dilemmas is the fact that few symptoms are sensitive or specific for pulmonary embolism. In adult series, clinical diagnosis has a sensitivity of 85% but a specificity of 38%, reflecting the vast differential diagnosis found in both adults and children. Symptoms vary according to the severity of the pulmonary embolism and the presence of underlying conditions. Pulmonary emboli of small-to-moderate size are generally asymptomatic.

Respiratory symptoms

Pleuritic chest pain is reported to occur in as many as 84% of children and adults with pulmonary emboli. Its presence suggests that the embolus is located more peripherally and, thus, may be smaller.

Tachypnea and dyspnea are observed in as many as 60% of adult patients with pulmonary emboli but are generally less frequent in children.

Cough is present in approximately 50% of children with pulmonary emboli. Hemoptysis is a feature in a minority of children with pulmonary emboli, occurring in about 30% of cases.

Other symptoms

A feeling of apprehension is a manifestation of arousal of the sympathetic system. Sweating and syncope are rarely present.

Risk factors to elicit on history taking

Obtain a detailed history of any previous pulmonary embolism/thromboembolism, oral contraceptive use, recent pregnancy, termination of pregnancy, drug history, and family history.

Sickle cell disease

Patients with sickle cell disease may present with manifestations of sickle cell anemia other than acute chest syndrome. These may include anemia, sequestration crisis, pain crisis, stroke, and priapism.

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Physical

The use of physical findings as a diagnostic aid in suspected cases of pulmonary embolism brings the same problems as are outlined in History. Many physical findings are typically less marked than they are in adults, presumably because children have greater hemodynamic reserve and, thus, are better able to tolerate the significant hemodynamic and pulmonary changes.

Pulmonary findings include the following:

  • Tachypnea is a feature in almost 50% of children with pulmonary emboli.

  • Crackles are heard in a minority of cases.

  • Cyanosis and hypoxemia are not prominent features of pulmonary embolism. If present, cyanosis suggests a massive embolism leading to a marked V/Q mismatch and systemic hypoxemia. Some case reports have described massive pediatric pulmonary embolism with normal saturation.

  • A pleural rub is often associated with pleuritic chest pain and indicates an embolism in a peripheral location in the pulmonary vasculature.

  • Signs that indicate pulmonary hypertension and right ventricular failure include a loud pulmonary component of the second heart sound, right ventricular lift, distended neck veins, and hypotension. An increase in pulmonary artery pressure is reportedly not evident until at least 60% of the vascular bed has been occluded.

Cardiovascular findings include the following:

  • A gallop rhythm signifies ventricular failure.

  • Peripheral edema is a sign of congestive heart failure.

  • Various heart murmurs may be audible, including a tricuspid regurgitant murmur signifying pulmonary hypertension.

Other signs include the following:

  • Fever is an unusual sign that is nonspecific.

  • Diaphoresis is a manifestation of sympathetic arousal.

  • Signs of other organ involvement in patients with sickle cell disease would be elicited, such as sequestration crisis, priapism, anemia, and stroke.

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Causes

In contrast with adults, most children (98%) diagnosed with pulmonary emboli have an identifiable risk factor or a serious underlying disorder. DVT is associated with a pulmonary embolism in 30-60% of cases. Thrombosis may also arise from intracardiac thrombi or intracerebral sinus thrombosis.

Acquired thrombosis has 3 broad etiological risk factors: (1) a relative stasis of blood flow due to either immobilization or the presence of a nidus on which a thrombus may form, (2) a prothrombogenic tendency (hypercoagulability), and (3) injury to a vascular wall. These 3 factors have been termed the Virchow triad.

The following conditions predispose to some or all of these factors for acquired thrombosis:

  • Central venous catheters: This is one of the most common acquired risk factors for pediatric PE. In 1993, David et al reported that 21% of children with DVT, pulmonary emboli, or both had an indwelling central venous catheter. [1] Additional series report presence of central lines in as many as 36% of patients. [10] A clot may form as a fibrin sleeve that encases the catheter. When the catheter is removed, the fibrin sleeve is often dislodged, releasing a nidus for embolus formation. In another scenario, a thrombus may adhere to the vessel wall adjacent to the catheter.

  • Surgery: Recent surgery and postsurgical immobilization are associated with approximately 15-29% of pulmonary embolism and DVT cases.

  • Heart disease: Thrombi may be associated with dilated cardiomyopathy, a situation in which sluggish blood flow is combined with an enlarged cardiac chamber.

  • Sickle cell disease: This condition often creates a diagnostic difficulty. A chest infection is often the presenting symptom. Hypoxemia, dehydration, and fever lead to intravascular sludging within pulmonary (among others) vasculature. This promotes a vicious cycle, further exacerbating local hypoxemia, ultimately leading to local tissue infarction. This process is further worsened by bone marrow infarction, which may cause release of fat emboli that lodge in the pulmonary circulation. [11]

  • Trauma: Whether the increased risk of pulmonary embolism in trauma patients is independent of the role of immobilization and surgery is unclear. [8]

  • Neoplasm: Pulmonary emboli have been reported to occur in association with solid tumors, leukemias, and lymphomas. This is probably independent of the indwelling catheters often used in such patients. [12]

  • Hyperalimentation: A recent study reported that major thrombosis or pulmonary embolism was present in more than 33% of children treated with long-term hyperalimentation and that pulmonary embolism was the major cause of death in 30% of these children. Fat embolization may exacerbate this clinical picture. [13]

  • Dehydration: Dehydration, especially hyperosmolar dehydration, is typically observed in younger infants with pulmonary emboli.

  • Inherited disorders of coagulation: In 1993, David et al reported that 5-10% of children with venous thromboembolic disease have inherited disorders of coagulation, such as antithrombin III, protein C, or protein S deficiency. [1] In 1997, Nuss et al reported that 70% of children with a diagnosis of pulmonary embolism have antiphospholipid antibodies or coagulation-regulatory protein abnormalities. [14] However, this was a small study in a population with clinically recognized pulmonary emboli; hence, its applicability to the broader pediatric population is uncertain.

Miscellaneous causes

Other causes of pulmonary embolism include the following:

  • Obesity (BMI ≥ 25 kg/m2)

  • Estrogen use, including oral contraceptives

  • Pregnancy

  • Pregnancy termination

  • Nephrotic syndrome

  • Ventriculoatrial shunt: The tip of the atrial shunt may act as a nidus for thrombus formation.

  • Autoimmune disorders: These may be associated with antibodies that predispose to a hypercoagulable state.

In a retrospective review of pediatric patients presenting to a pediatric emergency department, the most common risk factors identified for pulmonary embolism were BMI ≥ 25 kg/m2, oral contraceptive use, and history of previous pulmonary embolism. [15]

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