Pulmonary Embolism Clinical Presentation
- Author: Daniel R Ouellette, MD, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more...
The challenge in dealing with pulmonary embolism is that patients rarely display the classic presentation of this problem, that is, the abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia. Studies of patients who died unexpectedly from pulmonary embolism have revealed that often these individuals complained of nagging symptoms for weeks before death. Forty percent of these patients had been seen by a physician in the weeks prior to their death.
The following risk factors can be indications for the presence of pulmonary embolism:
Surgery and trauma
Oral contraceptives and estrogen replacement
Hereditary factors resulting in a hypercoagulable state
Acute medical illness
Drug abuse (intravenous [IV] drugs)
Drug-induced lupus anticoagulant
Warfarin (first few days of therapy)
Inflammatory bowel disease
The PIOPED II study listed the following indicators for pulmonary embolism:
Travel of 4 hours or more in the past month
Surgery within the last 3 months
Malignancy, especially lung cancer
Current or past history of thrombophlebitis
Trauma to the lower extremities and pelvis during the past 3 months
Central venous instrumentation within the past 3 months
Stroke, paresis, or paralysis
Prior pulmonary embolism
Chronic obstructive pulmonary disease
Physical examination findings are quite variable in pulmonary embolism and, for convenience, may be grouped into 4 categories as follows:
Massive pulmonary embolism
Acute pulmonary infarction
Acute embolism without infarction
Multiple pulmonary emboli or thrombi
The presentation of pulmonary embolism may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea. (Prior poor cardiopulmonary status of the patient is an important factor leading to hemodynamic collapse.) Most patients with pulmonary embolism have no obvious symptoms at presentation. In contrast, patients with symptomatic DVT commonly have pulmonary embolism confirmed on diagnostic studies in the absence of pulmonary symptoms. Sickle cell disease often creates a diagnostic difficulty with regard to pulmonary embolism. A chest infection is often the presenting symptom.
Patients with pulmonary embolism may present with atypical symptoms. In such cases, strong suspicion of pulmonary embolism based on the presence of risk factors can lead to consideration of pulmonary embolism in the differential diagnosis. These symptoms include the following:
Decreasing level of consciousness
New onset of atrial fibrillation
Flank pain 
Delirium (in elderly patients) 
The diagnosis of pulmonary embolism should be sought actively in patients with respiratory symptoms unexplained by an alternative diagnosis. The symptoms of pulmonary embolism are nonspecific; therefore, a high index of suspicion is required, particularly when a patient has risk factors for the condition.
Acute respiratory consequences of pulmonary embolism include the following:
Increased alveolar dead space
In patients with recognized pulmonary embolism, the incidence of physical signs has been reported as follows:
Tachypnea (respiratory rate >16/min) - 96%
Rales - 58%
Accentuated second heart sound - 53%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%
Diaphoresis - 36%
S 3 or S 4 gallop - 34%
Clinical signs and symptoms suggesting thrombophlebitis - 32%
Lower extremity edema - 24%
Cardiac murmur - 23%
Cyanosis - 19%
The PIOPED study reported the following incidence of common symptoms of pulmonary embolism :
Pleuritic chest pain (66%)
Fever of less than 39°C may be present in 14% of patients; however, temperature higher than 39.5°C is not from pulmonary embolism. Chest wall tenderness upon palpation, without a history of trauma, may be the sole physical finding in rare cases.
Pleuritic chest pain without other symptoms or risk factors may be a presentation of pulmonary embolism. Pleuritic or respirophasic chest pain is a particularly worrisome symptom. Pleuritic chest pain is reported to occur in as many as 84% of patients with pulmonary emboli. Its presence suggests that the embolus is located more peripherally and thus may be smaller.
Pulmonary embolism has been diagnosed in 21% of young, active patients who come to emergency departments (EDs) complaining only of pleuritic chest pain. These patients usually lack any other classical signs, symptoms, or known risk factors for pulmonary thromboembolism. Such patients often are dismissed inappropriately with an inadequate workup and a nonspecific diagnosis, such as musculoskeletal chest pain or pleurisy.
Massive pulmonary embolism
Patients with massive pulmonary embolism are in shock. They have systemic hypotension, poor perfusion of the extremities, tachycardia, and tachypnea. In addition, patients appear weak, pale, sweaty, and oliguric and develop impaired mentation.
Signs of pulmonary hypertension, such as palpable impulse over the second left intercostal space, loud P2, right ventricular S3 gallop, and a systolic murmur louder on inspiration at left sternal border (tricuspid regurgitation), may be present.
Massive pulmonary embolism has been defined by hemodynamic parameters and evidence of myocardial injury rather than anatomic findings because the former is associated with adverse outcomes. Although previous studies of CT scans in the diagnosis of pulmonary embolus suggested that central obstruction was not associated with adverse outcomes, a new multicenter study clarifies this observation. Vedovati et al found no association between central obstruction and death or clinical deterioration in 579 patients with pulmonary embolus. However, when a subset of 516 patients who were hemodynamically stable was assessed, central localization of emboli was found to be an independent mortality risk factor while distal localization was inversely associated with adverse events. Thus, anatomic findings by CT scan may be important in assessing risk in hemodynamically stable patients with pulmonary embolus.
Acute pulmonary infarction
Approximately 10% of patients have peripheral occlusion of a pulmonary artery, causing parenchymal infarction. These patients present with acute onset of pleuritic chest pain, breathlessness, and hemoptysis. Although the chest pain may be clinically indistinguishable from ischemic myocardial pain, normal ECG findings and no response to nitroglycerin rules out myocardial pain. Patients with acute pulmonary infarction have decreased excursion of the involved hemithorax, palpable or audible pleural friction rub, and even localized tenderness. Signs of pleural effusion, such as dullness to percussion and diminished breath sounds, may be present.
Acute embolism without infarction
Patients with acute embolism without infarction have nonspecific physical signs that may easily be secondary to another disease process. Tachypnea and tachycardia frequently are detected, pleuritic pain sometimes may be present, crackles may be heard in the area of embolization, and local wheeze may be heard rarely.
Multiple pulmonary emboli or thrombi
Patients with pulmonary emboli and thrombi have physical signs of pulmonary hypertension and cor pulmonale. Patients may have elevated jugular venous pressure, right ventricular heave, palpable impulse in the left second intercostal space, right ventricular S3 gallop, systolic murmur over the left sternal border that is louder during inspiration, hepatomegaly, ascites, and dependent pitting edema. These findings are not specific for pulmonary embolism and require a high index of suspicion for pursuing appropriate diagnostic studies.
Pulmonary emboli in children
Many physical findings are typically less marked in children 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.
Because of the rarity of pulmonary emboli in children, these patients are probably underdiagnosed. For the same reason, much of the information pertaining to diagnosis and management of pulmonary embolism has been derived from adult practice.
Cough is present in approximately 50% of children with pulmonary emboli; tachypnea occurs with the same frequency. Hemoptysis is a feature in a minority of children with pulmonary emboli, occurring in about 30% of cases. 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 ventilation-perfusion (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.
A gallop rhythm signifies ventricular failure, while peripheral edema is a sign of congestive heart failure. Various heart murmurs may be audible, including a tricuspid regurgitant murmur signifying pulmonary hypertension.
Fever is an unusual sign that is nonspecific, and 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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