Authors: Eric Anderson, MD, MBA, FACEP, Associate Director of Clinical Operations, Cleveland Clinic, OH; Assistant Professor of Emergency Medicine, The Ohio State University, Columbus; and Jonathan Glauser, MD, MBA, FACEP, Cleveland Clinic Foundation, Assistant Clinical Professor of Medicine, Case Western Reserve University; Faculty, Residency Training Program in Emergency Medicine, MetroHealth Medical Center, Cleveland, OH.
Peer Reviewers: Charles V. Pollack, Jr., MA, MD, FACEP, Chair, Department of Emergency Medicine, Pennsylvania Hospital, Associate Professor of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia; and William B. Ignatoff, MD, FACEP, Emergency Physician, Carondelet Health Network, St. Joseph’s and St. Mary’s Hospitals, Tucson, AZ.
Part I of this two-part series covered gastrointestinal causes of chest pain and aortic dissection. This second and final part of the series will focus on pulmonary, psychiatric, and musculoskeletal causes of chest pain.—The Editor
Pulmonary Causes of Chest Pain
The lung parenchyma itself is insensitive to pain.1 Painful sensations are generated by the pleura, tracheobronchial tree, and chest wall. Inflammation of the upper part of the parietal pleura causes pain in the chest itself. The lower six intercostal nerves innervate the lower portion of the parietal pleura, the outer portion of the diaphragmatic pleura, and the abdominal wall. Lower pleural inflammation can cause pain in the upper abdomen or flank. The phrenic nerve innervates the central part of the diaphragm, so inflammation here can manifest as pain in the neck and top of the shoulder.1 The diaphragm also can be irritated by inflammatory processes in the upper abdomen, i.e., pancreatitis, cholecysitis, subphrenic abscess, viscous perforation, or peritonitis.
As mentioned in part I of this series, the most lethal cause of pneumomediastinum is esophageal perforation. Other causes of pneumomediastinum include hyperinflation of the lungs in persons who smoke illicit drugs, asthma, dental drills, and pneumothorax (PTX). Rapidly lethal causes of chest pain that arise from the pulmonary system include tension PTX and pulmonary embolus (PE).
Spontaneous Pneumothorax. Overview, Definitions and Epidemiology. PTX occurs when air enters the chest in the potential space between the parietal and visceral pleura. Primary spontaneous PTX occurs without clinically apparent lung disease. Secondary spontaneous PTX is a complication of pre-existing lung disease. Secondary PTX potentially is life-threatening because patients with associated lung disease have limited cardiopulmonary reserve.
Tension PTX is a diagnosis made on clinical grounds, with jugular venous distension, tachycardia, and absent breath sounds on the affected side. With compression of the vena cava, there is decreased cardiac output from decreased diastolic filling of the heart. This requires immediate diagnosis and decompression with expeditious chest tube insertion, sometimes preceded by emergency needle thoracostomy.
Primary spontaneous PTX occurs with an estimated incidence of between 7.4 and 18 cases per 100,000 population per year among men, and 1.2-6 cases per 100,000 population per year among women.2,3 It typically occurs in tall, thin males between the ages of 10 and 30 years, and becomes rare after age 40.4 Smoking increases the risk of spontaneous PTX by as much as a factor of 20.5 Drug use, including crack cocaine and ecstasy, is an important cause of PTX in patients with normal lung function.6
The peak incidence of secondary PTX is approximately age 60-65 years, reflecting the peak incidence of chronic lung disease in the general population. Secondary PTX also is more common in men, with approximately six cases per 100,000 population per year among men, and two cases per 100,000 population per year among women.2 Among patients with chronic obstructive pulmonary disease, the incidence of secondary PTX is 26 per 100,000 patients per year.7 There are approximately 20,000 cases of new spontaneous PTX in the United States each year. (For information on etiology, see Table 1.)
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Clinical Presentation of Pneumothorax. Most episodes of primary PTX occur at rest and present with ipsilateral pleuritic chest pain and dyspnea.8-10 Pain typically is described as sharp, then as a steady ache, and may resolve within 24 hours even if the PTX is untreated.8 Dyspnea may be severe, even with a small PTX.
Patients with a small (< 15%) PTX may have no physical findings or only a resting tachycardia. Decreased or absent breath sounds on the affected side may be present, with hyperresonance to percussion. Hypotension or cyanosis may occur if a tension PTX is present. If an arterial blood gas is checked, there may be an increased alveolar-arterial oxygen gradient and acute respiratory alkalosis. Hypercapnea often occurs due to underlying pulmonary disease in secondary spontaneous PTX. A large PTX results in a decrease in vital capacity and an increase in the alveolar-arterial oxygen gradient, causing varying degrees of hypoxemia. Because the underlying lung function is normal, hypercapnea does not develop in patients with primary spontaneous PTX.
The diagnosis is suggested by the patient’s history and confirmed by the presence of a thin, radiolucent visceral pleural line that is displaced from the chest wall on a posterior-anterior chest radiograph. An expiratory chest film is favored by some, but has not been shown to reliably increase the diagnostic yield.11,12 Patients with bullous emphysema may have a giant bulla that appears to be a PTX, although bullous lesions that abut the chest wall generally have a concave appearance, while a PTX should produce a visceral line that runs parallel to the chest wall. Pseudo-pneumothorax may be due to scapular border or skin fold. Vascular markings should be sought outside the confines of the radiolucent line. Most patients with PTX do not have evidence of pleural effusion on standard chest radiography.
If the diagnosis is not clear by chest x-ray (CXR), computed tomography (CT) of the chest should be performed. Since severe bullous emphysema may mimic PTX, and insertion of a chest tube into a large bulla can result in bronchopleural fistula and large PTX, an accurate diagnosis is imperative. Patients with acute dyspnea who have a disease such as idiopathic pulmonary fibrosis, which predisposes them to PTX, may benefit from chest CT if the chest radiograph fails to identify extra-alveolar air.13 CT of the chest shows ipsilateral bullae in 89% of patients with primary spontaneous PTX, as compared with 20% of controls matched for age and smoking status.14
Treatment of Pneumothorax. The treatment of PTX centers on evacuating air from the pleural space and preventing recurrences. Treatment options include simple observation, simple aspiration with a catheter with immediate removal of the catheter after pleural air is evacuated, insertion of a chest tube, pleurodesis, thoracoscopy and video-assisted thoracoscopic surgery (VATS), and thoracotomy. Treatment choice depends on the size of the PTX, whether it is primary or secondary, whether it is recurrent, the degree of distress of the patient, and whether there is a persistent air leak.
Patients with a small (< 15%) primary PTX may be minimally symptomatic. In patients breathing room air, resorption of air by the pleura occurs at a rate of approximately 1.25-2% per day. Administration of supplemental oxygen can increase resorption three- to fourfold, and should be employed. Observation and discharge after six hours with repeat chest films documenting no expansion of the PTX may be a legitimate option,15 although 23-40% of patients treated expectantly eventually require tube thoracostomy.16 Discharged patients should be given instructions to avoid strenuous activity and return immediately if shortness of breath or dyspnea develop, and to follow up in 24 hours for a recheck and a repeat CXR.
For larger PTX, drainage may be accomplished by aspiration with a small-bore catheter (7-14 French) or by insertion of a chest tube. The catheter may be placed, under sterile conditions, in the second anterior intercostal space, mid-clavicular line, or laterally at the fourth or fifth intercostal space in the anterior axillary line. In older (> 50 years old) patients, or if more than 2.5 L are aspirated, this method is more likely to be unsuccessful.17 If aspiration shows resolution of the PTX by CXR obtained six hours after aspiration, the patient may be discharged with follow-up in 24 hours for CXR.
Alternatively, the catheter may be left in place and attached to a one-way Heimlich valve or a water-seal device and used as a chest tube. The Heimlich valve allows ambulation18,19 and out-patient treatment. Water-seal devices have been recommended mainly for patients in whom Heimlich devices fail or in those patients with respiratory problems in whom a recurrent PTX would be poorly tolerated. Therefore, a 20-28 French chest tube has been recommended for drainage and water-seal for secondary spontaneous PTX.8
Chest tube drainage has a success rate of 90% for treatment of a first PTX, decreasing to 52% for treatment of a first recurrence and 15% for treatment of a second recurrence.20 Complications of chest tube drainage include pain, pleural infection, hemorrhage, injury from incorrect tube placement, and re-expansion pulmonary edema.21
Surgical procedures may include resection or stapling of small apical bullae, and pleurodesis by mechanical pleural abrasion or by insufflation of talc.22 VATS has been advocated for patients who experience recurrent PTX following tube thoracostomy for the initial event, for persistent air leak or hemopneumothorax, for incomplete lung expansion, and for bilateral involvement.23
Prognosis and Recurrence. Rates of recurrence of secondary spontaneous PTX range from 39% to 47%.24-26 Patients should be advised of activities that may increase the risk of recurrent PTX, such as flying or diving. Discontinuance of tobacco and cocaine smoking should be encouraged.
Pulmonary Embolism. There are an estimated 630,000 cases per year of PE in the United States.27 The age-adjusted incidence is approximately 69 per 100,000, with risk increasing in the older population in part due to malignancy, immobility, serious cardiac disease, and hospitalization for trauma or surgery.28 Insurance statistics indicate that PE is diagnosed at least 300,000 times per year.29 The mortality has been cited as 2-10 % in treated patients, although the International Cooperative Pulmonary Embolism Registry (ICOPER) gives mortality overall at three months as 17.4%.30 PE has been estimated to cause or contribute to 50,000-200,000 deaths annually in this country,31 and to be responsible for up to 15% of all in-hospital deaths. More than 16,000 people die each year despite treatment, making PE the third leading cause of death in this country. It is the most common nonsurgical cause of maternal death in the peripartum period. The real scope of PE in the United States is unknown. It has been reported that 8% of asymptomatic postoperative general surgical patients have new unmatched perfusion defects.
The difficulty in diagnosing PE has been recognized for a long time, and only 25-30% of patients with symptoms compatible with PE are confirmed to have thromboembolism on objective testing.32,33 Antemortem diagnosis of fatal PE has remained at approximately 30% for the past four decades.34 Furthermore, each diagnostic test has its limitations, further complicating the task of reliably confirming or excluding the disorder. The treatment for thromboembolic disease is not benign. Anticoagulation has long been a leading cause of drug-related toxicity in young hospitalized patients. Nonetheless, PE is quite treatable, and the risk for death has been shown to be reduced significantly with anticoagulation.
Pulmonary emboli arise predominantly from deep venous thromboembolism (DVT), of which 80-90% arise from lower extremity veins and 10-15% from upper extremity veins. The latter especially are associated with indwelling central venous catheters. Other sources include septic emboli and emboli from right-sided endocarditis, pelvic vein thrombosis, amniotic fluid or fat emboli, and right heart thrombosis.
Predisposing factors for pulmonary emboli include those causing Virchow’s triad of hypercoagulability, venous stasis, and endothelial damage in deep veins. (See Table 2.)
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Signs and Symptoms of Pulmonary Embolus. Chest pain, which typically is pleuritic, and dyspnea are the most common presenting complaints, and each is present in more than 80% of documented cases of PE.35 The clinician’s index of suspicion must be particularly high when risk factors for DVT are present. Since symptoms may be caused either by direct mechanical obstruction of the pulmonary arterial system or from release of mediators such as prostaglandins, serotonin, histamine, and catecholamines, patients may present with a variety of findings.
On physical examination, the patient may have tachypnea, tachycardia, altered mental status, or apprehension. Jugular venous distention due to right heart failure may be present. Hemoptysis occurs in only 30% of documented PE. Syncope and near syncope also can occur.
Classic findings on physical examination include an accentuated pulmonary component of the second heart sound (P2 > S2). Pleural friction rub or rales may be present. Evidence for phlebitis may be found in approximately 20-32% of cases.32,36
Massive pulmonary embolism should be considered in all patients with unexplained hypotension, syncope, cardiac arrest, or hypoxemia and respiratory failure.
Pulmonary Embolus: Diagnostic Testing in the Emergency Department (ED). The CXR is normal in approximately one-third of patients with PE. Evidence for regional oligemia should be sought. Westermark’s sign represents oligemia distal to engorged pulmonary arteries. Evidence for lung volume loss, such as atelectasis, may be present, and an elevated hemidiaphragm may be present in up to 40% of patients with PE. Pleural effusion is nonspecific. Pleural-based, wedge-shaped pulmonary infiltrates constitute the so-called Hampton’s Hump.
The electrocardiogram (ECG) may demonstrate sinus tachycardia, and/or non-specific ST-T abnormalities in the anterior leads. A new right bundle-branch block (RBBB) or right heart strain may be present. Mention of S1Q3T3 is largely of historic interest, dating from a report in 1935 of seven patients with PE-induced cor pulmonale.37 Rhythm disturbances are uncommon. The ECG equivalent of cor pulmonale is right axis deviation, complete or incomplete RBBB, P pulmonale, and S1Q3T3. In two studies, the pattern of anterior T-wave inversions in the precordial leads has been shown to represent the ECG finding that best correlates with the severity of the PE.38,39
D-dimers represent the fibrinolytic degradation products of cross-linked fibrin, and have emerged as the most useful of the procoagulant activity and ongoing fibrinolysis markers.40 D-dimer is released into the circulation when cross-linked fibrin is degraded by plasmin, and becomes positive within one hour of thrombus formation. D-dimer measurements are very sensitive in excluding the diagnosis of PE in the setting of normal values, non-diagnostic lung scans, and low clinical suspicion. They have limited specificity, as venous thromboembolism, trauma, cancer, infection, and myocardial infarction (MI) all are associated with fibrin formation. Pregnancy and acute inflammatory states also may elevate D-dimer levels.41 Therefore, high values are not as helpful in establishing the diagnosis of PE as normal values are in excluding the diagnosis.42 However, negative ultrasound and D-dimer measurements may preclude the need for serial imaging for DVT. A threshold value of 500 ng/mL has been used in many assays.
There are at least five assays available. There is evidence that missed venous thromboembolism is rare if the more sensitive enzyme-linked immunosorbent assays (ELISA) are used. ELISA requires a spectrophotometer and takes 2-4 hours to complete. Turbidometric and rapid ELISA tests require a spectrophotometer, but provide an objective quantifiable result within one hour.
Latex agglutination assays are quicker D-dimer tests, but sacrifice some sensitivity. Prospective outpatient studies of the SimpliRED D-dimer assay have validated the negative predictive value of the assay.40 It takes two minutes to perform. NycoCard, a D-dimer assay that uses monoclonal antibodies directed against the D-dimer, takes 35 minutes. Instant 1A and SimpliRED are read by visual inspection for color changes and are semi-quantitative and, therefore, somewhat subjective. For example, SimpliRED requires an observer to render an opinion as to whether agglutination is present or absent on visual inspection.
The overall sensitivity of D-dimer testing for thromboembolic disease is approximately 85%, with specificity of approximately 70%, although some have found the sensitivity to be greater than 95%, with a negative predictive value of greater than 90%.43,44 The patients deemed safest for D-dimer assay use in the ED in one report were those patients judged to not be of high clinical risk. High-risk patients for PE in that study were those with shock index (heart rate/systolic blood pressure) greater than 1.0, age greater than 50 years, unexplained hypoxemia (SaO2 less than 95% with no pre-existing lung disease), unilateral leg swelling, recent major surgery, or hemoptysis.45
Arterial blood gases frequently have been advocated as a screen for PE. Unfortunately, there is limited usefulness of the alveolar-arterial (A-a) gradient, which is normal in 20-25% of patients with PE. A standard definition of normal A-a gradient is either less than 20 or less than (10 + age/10). Approximately 10-15% of patients with documented PE have a pO2 greater than 80 mmHg. In the prospective investigation of pulmonary embolism diagnosis (PIOPED) study, among patients with no previous cardiopulmonary disease who had a normal A-a gradient with a pO2 greater than 80 and pCO2 greater than 35, 38% had angiographically proven PE.33 Therefore, while A-a gradients have been employed for many years in the assessment of these patients, their diagnostic value for PE is limited.
Expired CO2 monitoring has shown promise in the diagnosis of PE. The rationale for bedside testing of expired CO2 (Vd/Vt) is that PE significantly decreases alveolar CO2 content and increases alveolar dead space. Anesthesiologists have recognized that a rapid fall in end-tidal CO2 may be the first indicator of a clinically significant PE.46 Its screening sensitivity approaches that of V/Q scans. The normal ratio compares arterial carbon dioxide (PaCO2) with end-tidal CO2 (PetCO2) measured simultaneously. The ratio (PaCO2-PetCO2)/PaCO2 should be less than 0.20. Combined with D-dimer less than 0.50 mcg/L, the sensitivity for ruling out PE in ambulatory patients approaches 100%.47
Radiographic Screening for Pulmonary Embolus. There is no uniform approach to non-invasive screening for PE. Historically, ventilation-perfusion scanning has been employed heavily, as vasoconstriction may cause pulmonary infarction and hemorrhage, and may be manifested by ventilation-perfusion (V/Q) mismatch on V/Q scanning. Imaging modalities employed may include the following tests used either singly or in combination with other testing such as D-dimer screening: duplex ultrasonography (U/S) of the extremities, MRI, CT of the chest, or echocardiography.
Ventilation-Perfusion (V/Q) Scanning. To reduce the need for angiography, less invasive tests usually are favored for PE screening. By comparing the distribution of Technetium99m labeled al-bumin in the pulmonary vasculature with the distribution of radioactive aerosol inhaled into the lung airspace, mismatches (differences in the perfusion and ventilation patterns) can help diagnose PE. Unfortunately, V/Q scanning is only diagnostic if the scan is normal or high probability, and this occurred in only 174/887 (19.6%) of cases in the PIOPED study.71 Falsely positive scans may result if an infiltrate is present on CXR, or if the patient has preexisting cardiopulmonary disease or has sustained a prior PE. Nonetheless, it is a familiar and readily available test to many physicians.
The disadvantages of use of V/Q scanning are several: It cannot make other diagnoses as CT can. Nondiagnostic tests may result if the patient has a pulmonary infiltrate or a history of heavy smoking. Further diagnostic evaluation, therefore, must be done in approximately 50-60% of patients with suspected PE.48
It is worth reviewing the PIOPED study, which was published in 1990, because it has been cited widely as defining the role of V/Q scanning in the diagnosis of PE. In this report, clinical likelihood of PE prior to V/Q scanning was compared with results of pulmonary arteriography, then considered the gold standard for diagnosis of PE. It is noteworthy that the incidence of PE was 4% in patients with normal or near-normal V/Q scans and low clinical suspicion. However, the incidence of PE was 40% in patients with low probability scans, if the pre-test clinical likelihood was deemed to be high. (See Table 3.)
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There were several problems with the PIOPED study. No defined pretest clinical probability scoring system was developed. Furthermore, 78% of scans in PIOPED read as intermediate, indeterminate, or low probability, meaning that V/Q scanning did not give a definitive result more than three-quarters of the time. Conversely, most (59%) patients with angiographically proven PE had a high probability scan. To address the latter problem, an objective scale for pre-test probability for PE was developed.49 (See Table 4.)
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Spiral CT of the chest may detect intrathoracic pathology other than PE. Spiral CT shows a clear advantage over V/Q scanning in this regard. Nonembolic explanations for symptoms may be found in 33% of patients.50 CT is especially useful in patients with abnormal chest radiographs or underlying cardiopulmonary disease. As with other imaging technologies, its accuracy is dependent upon the scanner and the interpreter. The sensitivity reportedly ranges from 53% to 100%, with specificity of 81-100%.50,51 It is less sensitive for detecting emboli involving subsegmental arteries or more distal segments.52 A CT scan that is negative for PE portends a good outcome; the three-month risk for venous thromboembolism was 1.7% in one study of patients with a negative CT who were not anticoagulated.53
Disadvantages to utilization of CT in the diagnosis of PE include its inaccuracy in diagnosing subsegmental branch PE, although this may not be clinically significant. A high-speed scanner and expert interpretation are needed. It requires a 20-30 second breath hold—or possibly two 10-second breath holds. The contrast load is 300 cc of 60% iodine, which is acceptable if the patient’s creatinine is less than 2 mg/dL. While approximately 1.7% of patients in whom PE was excluded based upon negative CT findings may have a PE during three-month follow-up, one can expect greater than 90% positive and negative predictive values compared with angiography.
Magnetic resonance angiography (MRA) using gadolinium highlights the pulmonary vasculature. It does not expose the patient to ionizing radiation. It can be used in patients with renal insufficiency and in those with iodine allergy. Intravenous (IV) gadolinium is administered for optimal imaging. It has shown a specificity of 95-100% and a sensitivity approaching 100% when compared to conventional pulmonary angiography.54
MRA has the potential advantage of visualizing the pulmonary vasculature and pelvic and thigh veins with a single study. The patient is required to lie supine with arms overhead, and to be able to hold his breath for 16 seconds. Disadvantages to routine use of MRA include that it is difficult to evaluate peripheral vessels and that it is not readily available. With availability and improvements in technology, MRA eventually may become the reference standard for diagnosis of PE.
Echocardiography has been proposed as a useful diagnostic modality in the evaluation of possible PE. Unfortunately, its value as a screening test is limited. Its sensitivity has been reported to be in the 51-67% range, with a specificity of 87-94%.55-57 Problems with echocardiography in the evaluation of PE are several. TEE is invasive and does not visualize the left pulmonary artery well because the bronchus obstructs the view. Right heart strain and pulmonary hypertension are detectable only if at least 30-40% of the pulmonary vascular bed is occluded. There has been no study in stable ambulatory patients of the utility of TEE as a screening test for PE. TEE requires a specialist to perform the test at this time.
Pulmonary angiography traditionally has been considered the gold standard for diagnosis of PE. However, approximately 4% of studies are nondiagnostic, and 10-20% of patients are unable to undergo angiography. It is invasive, not readily available, and requires expertise. It is contraindicated if pulmonary artery pressures are high. The reported mortality is 0.1-0.5%, with major morbidity in 4% of procedures.58,59 It may be too sensitive a test if clinical outcome is the primary endpoint measured. Angiography may miss subsegmental emboli, and interobserver agreement may be very low.33
PE may be excluded without any imaging at all. Of 437 patients deemed to have low clinical probability, and a negative D-dimer result, only one developed PE during three-month follow-up.49 In that study, if a patient was not deemed to be low probability for PE by clinical and D-dimer testing, patients underwent V/Q scanning, bilateral ultrasonography, and pulmonary angiograms, in that order, until a diagnosis was made.
In another report, of 177 patients with low pretest probability of DVT and negative bedside D-dimer testing, only one had DVT during three-month follow-up.60
Therapy for Pulmonary Embolism. Supportive care includes fluid hydration and use of norepinephrine or dopamine if vasopressors are needed. Etomidate may be an ideal sedative for intubation, since it preserves hemodynamic status. The goals of care are to reduce mortality, prevent recurrent events, minimize adverse effects of anticoagulation, and, possibly, restore right ventricular function.61 Medical therapy includes anticoagulants with or without thrombolytics. Surgical therapy may include placement of venous filters or catheter or surgical embolectomy.
Standard anticoagulation entails treatment with heparin followed by at least three months of oral anticoagulation.62 The usual loading dose of IV heparin is 80 units (U)/kg, followed by 18 U/kg/hr. Heparin impairs clot propagation and prevents recurrent PE. Oral warfarin is started within 24 hours of heparin initiation, with the therapeutic goal of keeping the international normalized ratio (INR) between 2 and 3 for three months. Patients should be fully anticoagulated before therapy with warfarin is started; otherwise medications such as the warfarin may induce a paradoxical hypercoagulable state.63
The role of low molecular weight heparins (LMWHs) such as enoxaparin or tinzaparin in the management of PE has yet to be clearly defined. LMWH has not been approved for the outpatient treatment of PE. For patients with heparin-induced thrombocytopenia who require anticoagulation, the role of agents such as lepirudin has not been defined clearly in PE.
The role for thrombolysis in the management of PE has not been delineated clearly. Thrombolysis has been advocated to prevent chronic vascular obstruction that can lead to pulmonary hypertension and postphlebitic syndrome. It provides for more rapid clot resolution than heparin. Rapid improvement in hemodynamic measurements (RV function) vs. heparin at 24 hours can be demonstrated.64 However, no difference in mortality as compared to heparin therapy has been established if the patient is not in shock. Correction of hypoxemia, improved systemic hemodynamics as measured by cardiac output, pulmonary artery pressure, and pulmonary vascular resistance are goals of thrombolytic therapy. Based upon available data, thrombolytic therapy is indicated for hemodynamically unstable patients, including those with hypoxemia or right ventricular failure due to PE or hypotension. Agents employed have included urokinase, streptokinase, and tissue plasminogen activator (tPA).
The only thrombolytic approved by the FDA for PE in the presence of hemodynamic instability is tPA, given as 100 mg over two hours. All three thrombolytic agents are probably equally effective and safe. The role of thrombolytic therapy in normotensive patients with evidence of right ventricular dysfunction, either by echocardiography or by physical examination has not been defined. The risk of major hemorrhage is 8-14%, and the risk of intracranial hemorrhage is approximately 2%.65,66 Thrombolysis may be effective in the treatment of PE for up to 14 days.64
Other Therapy. Vena caval filters (Greenfield and others) traditionally have been utilized for patients who are bleeding actively, for failure of anticoagulant therapy, or for patients with risk of serious bleeding that precludes use of anticoagulant therapy. One randomized study showed no difference in mortality after two years between filter and non-filter groups.67
Mechanical thrombolysis using a rotational catheter tip or high-pressure saline jets to break up thrombus has been described.68,69 Surgical embolectomy for acute PE is used infrequently.
The role of ultrasound in the diagnosis and management of PE is evolving, especially as it relates to the presence of right ventricular dysfunction and the potential use of thrombolytic therapy. The role for LMWHs for outpatient therapy also has not been defined, especially for the stable PE patient.
It is likely that a clinical outcome approach may be used as an endpoint for optimal diagnosis and therapy, rather than angiography as a gold standard. Although failure to use pulmonary angiography may result in a reduced detection of pulmonary emboli, the most important question may not be, "Who has had a PE?" but rather, "Who will have another embolism that may be fatal?"
Finally, there may be the possibility of stopping the diagnostic evaluation for PE in the ED without ordering any imaging study if there is a low clinical probability, normal expired CO2 and a normal D-dimer test.
Other Pulmonary Causes of Chest Pain. Pneumonia and lung abscess (bacterial, protozoan, fungal, or viral) can cause an inflammatory reaction with the parietal and visceral pleura that can result in a pleuritic type of chest pain. Clues to this diagnosis include productive cough, fever, lethargy, shortness of breath, and pleuritic chest pain. Patients with immunocompromising conditions are especially at risk for pneumonia. Conditions that place a patient at particular risk for pneumonia include but are not limited to: advanced age, positive HIV status, malignancy and chemotherapy, IV drug abuse, chronic alcoholism, gastric and jejunostomy tubes, stroke, neck extension contractures, and known difficulties with swallowing.
Treatment includes recognition of the condition, beginning with a CXR in the ED, and antibiotics appropriate for the circumstances of the pneumonia. Admission or ambulatory treatment appropriate for the patient’s physical status and social resources must be evaluated.
Chronic obstructive pulmonary disease, asthma, and bronchitis can cause chest pain as a result of the work of breathing and pleural inflammation secondary to concomitant pulmonary infection.
Pulmonary oncologic processes can cause pain as a result of direct pressure or traction on pain sensitive structures.70
Psychiatric Disorders Manifesting with Chest Pain
Various psychiatric conditions may present in the ED with complaints of chest pain. Several studies indicate that panic disorder affects approximately 30% of noncardiac chest pain (NCCP) patients.71-75 Panic disorder is present in 1-4% of the general population.76,77 By definition, panic disorder is characterized by at least three attacks in a three-week period. The attacks consist of intense fear, anxiety, or discomfort accompanied by at least four of the following symptoms: chest pain, restlessness, choking sensation, palpitations, sweating, dizziness, nausea, abdominal pain, paresthesias, flushing, trembling, or a sense of dying or impending doom.78 The symptoms characterizing panic disorder and the increased public awareness of acute coronary syndromes make it easy for the patient to confuse the symptoms of panic attack with those of an acute MI. Concerns of an acute coronary syndrome may heighten the level of anxiety.
Treatment of the acute panic episode typically begins with quiet reassurance while preparations are made for oral or IV benzodiazepines. Options include oral or IV diazepam, 2-10 mg IV q 3-4 h; lorazepam, 0.5-2 mg q 6 h oral; or alprazolam, 0.25-0.5 mg q 8 h. A typical outpatient regimen for panic disorder is alprazolam, 0.25-0.5 mg po tid as needed for symptoms. Dosage is titrated upward every 3-4 days by 1 mg/day until desired effect. The mean dosage is 6-7 mg per day.78 Referral is to a primary care provider or psychiatric follow-up. Patients often are frustrated with the lack of resolution of their symptoms and often will welcome the referral if they think it will help. Initiation of antidepressant medication is best left to their primary care physician or with psychiatry since follow-up of the patient’s status after initiation of the new medication will be necessary. Patients can be discharged safely home when the acute symptoms have subsided.
Musculoskeletal Causes of Chest Pain
Pain secondary to abnormalities of the chest wall tend to be sharper and more focal in character than chest pain secondary to coronary artery disease (CAD). Certain body movements or manipulations may exacerbate the pain of chest wall origin. Chest wall pain secondary to minor chest wall trauma, costochondritis, shingles, or spinal nerve radiculopathies are considered here. (See Table 5.)
Minor chest wall trauma can cause pain secondary to contusions, rib fractures, or frank open chest injuries. While open chest wall injuries may be obvious, contusions and rib fractures may be more subtle, especially in patients who are unable to give a history of events leading up to the ED visit (such as in patients with dementia, retardation, intoxication, or in young children).
In awake, alert patients, the history will make the diagnosis much easier. The physical exam may reveal an area of pain and tenderness with or without bruising or deformity. It is important to assess for more significant underlying injury (i.e., pulmonary contusion, hemothorax, PTX, or injury to the great vessels). This can be aided by a thorough history noting the energy forces involved in the injury. A CXR may be helpful when there is doubt about the extent of the traumatic injury.
Nonsteroidal anti-inflammatory drugs (NSAIDs) or lower potency narcotic analgesics are appropriate for discharge analgesia. Intercostal nerve block may be necessary for temporary relief of intractable pain of multiple rib fractures. Patients generally may be discharged with instructions about warning signs of decompensation and should follow up in the next few days.
Herpes zoster (shingles), caused by reactivation of varicella-zoster virus, may manifest as unilateral chest wall pain in a dermatomal distribution. Pain may be present 1-2 days before vesicles appear in the same dermatomal distribution as the pain. These patients typically are elderly or have some immunocompromising condition or medication. Culture of fluid from one of the vesicles is diagnostic.
These patients can be managed with analgesics and antiviral agents. Domboro soaks are soothing locally and may help to limit secondary infection. Oral antiviral medications include acyclovir and famciclovir. Parenteral antiviral agents, which are used for treatment failures and disseminated disease, include ganciclovir, cidofovir, and foscarnet. Those who are treatment failures, have disseminated disease, or have significant comorbid conditions require hospitalization.
Costochondritis is a common cause of anterior musculoskeletal chest wall pain. It is caused by inflammation of the costochondral and costosternal articulations. Common causes include preceding unusual physical activity or recent viral infection.70
Patients may present with sharp focal anterior chest pain that is made worse with deep inspiration or compression over the painful area. Certain trunk movements also may reproduce the pain.
Treatment with NSAIDs, acetaminophen, or lower potency narcotic analgesics will be helpful. Discharge instructions should include warnings about returning if pain worsens. Follow-up should be recommended in a clinic with a primary care physician.
Spinal and paraspinal causes of chest pain include osteoarthritis of the thoracic spine, herniated cervical or thoracic disc, costovertebral joint dysfunction, and interspinous ligament disruption. Typical presenting complaints are of a sharp, stabbing spinal or paraspinal pain. There may be a history of recent minor trauma or muscular strain. The area may be tender to palpation and pain may be increased by deep breathing or certain trunk movements.
Intercostal nerve block will provide significant relief of the symptoms. Nerve block is both a diagnostic and therapeutic procedure for this condition; however, oral analgesics usually are the initial treatment of choice.70
Pitfalls in Management of Patients with Noncardiac Chest Pain
There are several pitfalls that emergency physicians should be aware of regarding the management of patients with noncardiac chest pain. Emergency physicians should avoid the following:
- Thinking that the chest pain is not of cardiac origin and, therefore, that the patient does not have a potentially life-threatening condition. Tension PTX, aortic dissection, PE, and esophageal rupture all can present with normal coronary anatomy. A thorough history and physical examination is needed to evaluate for these conditions.
- Not considering PE in patients with stated chest pain and shortness of breath and normal or near normal arterial blood gas (ABG), ECG, and CXR. Physical examination and symptomatology can vary from mild to a patient in extremis. Consider use of other technologies to assist in clarifying the diagnosis, such as D-dimer, end tidal CO2, chest CT, V/Q scan, or MRI.
- Inadequate analgesia—remember, the patient presents with a painful condition. Address the patient’s pain while he or she is in the ED during workup. Provide adequate discharge analgesia.
Summary
The broad differential diagnosis of patients with chest pain quickly can be narrowed down to general categories by a thorough history and physical examination. It is important to remember the four causes of chest pain that rapidly can be fatal: MI, PE, aortic dissection/rupture, and tension PTX. Other lethal causes of chest pain include pericardial tamponade and esophageal rupture. (See Table 6.)
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The general approach to the chest pain patient is to assume the most lethal diagnosis first. This usually can be excluded reasonably by history, physical examination, and ancillary testing. When there is doubt about the cause of the pain after the initial workup, admission to an observation unit for further evaluation to rule out life-threatening conditions is reasonable.
Determine which organ system is involved in the patient’s symptoms. When the involved organ system has been determined, then a diagnostic/therapeutic plan can be developed. On many occasions the ultimate diagnosis will not be made in the ED. The emergency physician needs to determine if an emergency medical condition exists. If an imminent threat to life or limb does not exist, then the next goal is to alleviate anxiety and pain and initiate a diagnostic course that can be followed up and completed by the patient’s primary care provider or referral specialist.
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Part I of this two-part series covered gastrointestinal causes of chest pain and aortic dissection. This second and final part of the series will focus on pulmonary, psychiatric, and musculoskeletal causes of chest pain.
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