on 31-May-2021 (Mon)

The most common presenting symptom is dyspnea followed by chest pain (classically pleuritic but often dull) and cough.

However, many patients, including those with large PE, have mild or nonspecific symptoms or are asymptomatic. For example, a meta-analysis of 19 studies (25,343 patients) found that clinical impression alone had a sensitivity and specificity of 85 and 51 percent, respectively, for the diagnosis of PE [ 10].Thus, it is critical that a high level of suspicion be maintained such that clinically relevant cases are not missed.

The most common symptoms in patients with PE were identified in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) group (table 1) [7]. They include the following:

● Dyspnea at rest or with exertion (73 percent)

● Pleuritic pain (66 percent)

● Cough (37 percent)

● Orthopnea (28 percent)

● Calf or thigh pain and/or swelling (44 percent)

● Wheezing (21 percent)

● Hemoptysis (13 percent)

Less common presentations include transient or persistent arrhythmias (eg, atrial fibrillation), presyncope, syncope, and hemodynamic collapse (<10 percent each) [11,12]. Hoarseness from a dilated pulmonary artery is a rare presentation (Ortner syndrome) [13]

The onset of dyspnea is frequently (but not always) rapid, usually within seconds (46 percent) or minutes (26 percent) [9]. Dyspnea may be less frequent in older patients with no previous cardiopulmonary disease. Dyspnea is more likely to be present in patients who present with PE in the main or lobar vessels.

Approximately 10 percent of patients present with the symptoms of an infarcted lung, usually due to smaller, more peripheral emboli. Pleuritic pain is typical in this population due to inflammation of the pleura. Hemorrhage from the infarcted lung is also thought to be responsible for hemoptysis. (See "Overview of acute pulmonary embolism in adults", section on 'Pathogenesis and pathophysiology'.)

Retrospective studies report syncope as the presenting symptom in 10 percent or less of cases. Conversely, among those presenting with syncope, rates of PE ranging from 1 to 17 percent have been reported [14-22]. Rates may be higher in those hospitalized with syncope [19,22]

Syncope may indicate a high burden of thrombus since up to two-thirds of patients with PE who present with syncope have large thrombi located in the mainstem or lobar arteries [11,12]. The reasons for syncope in patients with PE are poorly understood but may be partially explained by transient arrhythmias as thrombus travels through the heart or transient obstruction as the embolus transits the pulmonic valve.

Some patients have a delayed presentation over weeks or days. One prospective study reported that patients with a delayed presentation beyond one week tended to have larger, more centrally located PE compared with patients who presented within seven days (41 versus 26 percent) [23]

Symptoms and signs of PE may also evolve over time such that patients who initially present with mild symptoms may become increasingly symptomatic or hemodynamically unstable, sometimes very quickly (minutes to hours). This may be secondary to recurrent embolization or progressive pulmonary hypertension secondary to vasoconstriction. Similarly, as a pulmonary infarct evolves, patients may develop progressive dyspnea, hypoxemia, pleuritic pain, and hemoptysis.

Importantly, symptoms may be mild or absent, even in large PE [6,9,24]. Although the true incidence of asymptomatic PE is unknown, one systematic review of 28 studies found that, among the 5233 patients who had a deep vein thrombosis (DVT), one-third also had asymptomatic PE [24].

Common presenting signs on examination include [9]:

● Tachypnea (54 percent)

● Calf or thigh swelling, erythema, edema, tenderness, palpable cords (47 percent)

● Tachycardia (24 percent)

● Rales (18 percent)

● Decreased breath sounds (17 percent)

● An accentuated pulmonic component of the second heart sound (15 percent)

● Jugular venous distension (14 percent)

● Fever, mimicking pneumonia (3 percent)

PE is a common cause of sudden cardiac arrest or circulatory collapse (8 percent), especially among patients younger than 65 years old [9,25,26]. Among such patients, either dyspnea or tachypnea is present in 91 percent. Massive PE may be accompanied by acute right ventricular failure manifested by increased jugular venous pressure, a right-sided third heart sound, a parasternal lift, cyanosis, and obstructive shock

A transition from tachycardia to bradycardia, or from a narrow complex to a broad complex tachycardia (ie, right bundle branch block), is an ominous sign of right ventricular strain and impending shock

PE should be suspected anytime there is hypotension accompanied by an elevated central venous pressure that is not otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial tamponade, or a new arrhythmia [ 27,28].

Arterial blood gas (ABG) – Unexplained hypoxemia in the setting of a normal chest radiograph should raise the clinical suspicion for PE and prompt further evaluation. However, while often abnormal among patients suspected of having PE, ABGs can be normal in up to 18 percent of patients with PE [29].

Common abnormalities seen on ABGs include one or more of the following [7,29,31] (see "Arterial blood gases"):

• Hypoxemia (74 percent)

• Widened alveolar-arterial gradient for oxygen (62 to 86 percent)

• Respiratory alkalosis and hypocapnia (41 percent)

Hypercapnia, respiratory, and/or lactic acidosis are uncommon but can be seen in patients with massive PE associated with obstructive shock and respiratory arrest.

Abnormal oxygenation may be of prognostic value. As an example, patients with hypoxemia or room air pulse oximetry readings <95 percent at the time of diagnosis are at increased risk of complications, including respiratory failure, obstructive shock, and death [32].

Troponin – Similarly, serum troponin I and T levels are useful prognostically but not diagnostically [35-39]. As markers of right ventricular dysfunction, troponin levels are elevated in 30 to 50 percent of patients who have a moderate to large PE [35,40] and are associated with clinical deterioration and death after PE. Troponin elevations usually resolve within 40 hours following PE, in contrast to the more prolonged elevation after acute myocardial injury [41].

Abnormalities historically considered to be suggestive of PE (S1Q3T3 pattern, right ventricular strain, new incomplete right bundle branch block) are uncommon (less than 10 percent) [47,48]. ECG abnormalities that are associated with a poor prognosis in patients diagnosed with PE include [42,43,45]:

● Atrial arrhythmias (eg, atrial fibrillation)

● Bradycardia (<50 beats per minute) or tachycardia (>100 beats per minute)

● New right bundle branch block

● Inferior Q-waves (leads II, III, and aVF)

● Anterior ST-segment changes and T-wave inversion

● S1Q3T3 pattern

Chest radiograph — Nonspecific abnormalities on chest radiography are common (eg, atelectasis, effusion) in PE, but a normal chest radiograph can be seen in 12 to 22 percent of patients [7,8,49].

A Hampton's hump and Westermark's sign are rare but, when present, should raise the suspicion for PE [50]. Hampton's hump is a shallow, hump-shaped opacity in the periphery of the lung, with its base against the pleural surface and hump towards the hilum (image 1). Westermark's sign is the demonstration of a sharp cut-off of pulmonary vessels with distal hypoperfusion in a segmental distribution within the lung (image 2).

For patients who remain hemodynamically unstable (eg, systolic pressure <90 mmHg for 15 minutes or longer or clear evidence of shock) despite adequate resuscitation, definitive testing is typically considered unsafe. In these circumstances, bedside lower extremity ultrasonography and transthoracic echocardiography may be used to obtain a presumptive diagnosis of PE. In this population of unstable patients, a presumptive diagnosis of PE may justify the administration of potentially life-saving therapies (eg, thrombolysis).

Whenever PE is suspected, the PTP for PE should be estimated by clinical gestalt assessment or calculated using a validated PTP score (eg, Wells score, Modified Wells score, or Modified Geneva score) [10,57,58,64-69]. Although gestalt estimates and calculating probability scores have comparable sensitivity when combined with D-dimer testing, meta-analyses suggest that probability scores may have higher specificity [10,69] and increase the diagnostic yield of CTPA [70].

Although use of Wells, Modified Wells (table 2) (calculator 1), or Modified Geneva score (table 3) (calculator 2) is acceptable, based upon extensive validation and our clinical experience, we prefer that the Wells criteria be applied and the score calculated to determine probability of PE into a three-tiered system of:

● Low (score <2) (see 'Low probability of pulmonary embolism' below)

● Intermediate (score 2 to 6) (See 'Intermediate probability of pulmonary embolism' below.)

● High (score >6) (see 'High probability of pulmonary embolism' below)

Wells criteria include the following (table 2) (calculator 1):

● Clinical symptoms of deep vein thrombosis (DVT) (3 points)

● Other diagnoses are less likely than PE (3 points)

● Heart rate >100 (1.5 points)

● Immobilization three or more days or surgery in previous four weeks (1.5 points)

● Previous DVT/PE (1.5 points)

● Hemoptysis (1 point)

● Malignancy (1 point)

Despite validation of the Wells criteria, for unclear reasons, clinicians do not use them or use them incorrectly in up to 80 percent of patients [71,72]. In addition, they may not be as accurate in older or critically ill patients [67,73]. Wells criteria have best validated in outpatients presenting with suspected PE. However, one study of hospitalized patients, reported a sensitivity and specificity of 72 and 62 percent, respectively [74]; the addition of D-dimer to Wells criteria improved the sensitivity to 99 and reduced the specificity to 11 percent.

The PERC rule was designed to identify patients with a low clinical probability of PE in whom the risk of unnecessary testing outweighs the risk of PE [2,76-78] (see 'Low probability of pulmonary embolism' above). The PERC rule has eight criteria (table 4):

• Age <50 years

• Heart rate <100 beats/minute

• Oxyhemoglobin saturation ≥95 percent

• No hemoptysis

• No estrogen use

• No prior DVT or PE

• No unilateral leg swelling

• No surgery/trauma requiring hospitalization within the prior four weeks

The application of PERC resulted in a reduction in the proportion of patients undergoing CTPA (13 versus 23 percent) and also reduced the ED stay by 36 minutes.

PERC is only valid in clinical settings (typically the ED) with a low prevalence of PE (<15 percent) [77]. In clinical settings with a higher prevalence of PE (>15 percent), the PERC-based approach has been shown to have a substantially poorer predictive value [77]. Thus, it should not be used in patients with an intermediate or high suspicion for PE or for inpatients suspected as having PE.

For patients in whom the risk of PE is thought to be low, a normal D-dimer (<500 ng/mL [fibrinogen equivalent units]) effectively excludes PE, and typically no further testing is required. This includes patients who have had a prior PE and those with a delayed presentation and hospitalized patients [23,74,81].

For patients in whom the risk of PE is thought to be high, a normal D-dimer is not as helpful for excluding the diagnosis and does not need to be performed. While a negative D-dimer result does reduce the likelihood of PE in this population, it does not reduce it sufficiently to rule out the diagnosis with some data suggesting a prevalence of PE of 5 percent or more in this population [82-86]

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