Hospital Practice

ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20

A Nonclassic Case of Pulmonary Embolism Elliot Rapaport & Rolf M. Gunnar To cite this article: Elliot Rapaport & Rolf M. Gunnar (1992) A Nonclassic Case of Pulmonary Embolism, Hospital Practice, 27:9, 86-102, DOI: 10.1080/21548331.1992.11705485 To link to this article: http://dx.doi.org/10.1080/21548331.1992.11705485

Published online: 17 May 2016.

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Date: 20 June 2016, At: 18:55

DECISION MAKING IN MEDICINE

A N onclassic Case of Pulmonary Embolism ELL 1o T RAPAPoRT

University of California, San Francisco

Case Commentary:

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R 0 L F M. GUNNAR

Loyola University

Case Presentation A 55-year-old woman had an episode of rightsided chest pain, which radiated to her right shoulder and was associated with mild fatigue and shortness of breath. The pain faded, but it recurred the next morning when she arose from bed. That day she sought medical care in the emergency department. She said that the pain on arising had lasted only about five minutes and that she had not had any associated symptoms, such as nausea, vomiting, excessive sweating, light-headedness, or palpitations. The patient had been well until the onset of the pain. She had not experienced similar episodes in the past and had no history of myocardial infarction or other cardiac disorder. She had known, however, that she had an elevated circulating total cholesterol level, which was of some concern to her and for which she apparently had been on a diet. She had been taking estrogen for hot flushes and depression secondary to her menopause. She had no history of high blood pressure or dia-

Dr. Rapaport is Professor of Medicine, University of California, San Francisco, School of Medicine. Dr. Gunnar is Professor Emeritus, Department of Medicine, Loyola University of Chicago Stritch School of Medicine.

86

Hospital Practice September 15, 1992

betes, and there was no family history of cardiac disease. She had never smoked. She had no leg discomfort or varicosities, no recent trauma to the pelvis, and no history of cancer. On physical examination, she appeared well and somewhat younger than her stated age but anxious. There was no evidence of peripheral vascular disease: She had good pedal pulses and no pedal edema. Homan sign was negative. A short grade 2/6 systolic murmur could be heard at the left sternal border and at the apex without radiation. Laboratory results were unremarkable except for the electrocardiogram, which contained a 2mm ST-segment depression in leads V3 to V5 , with a strainlike pattern in V5 • Because of the abnormal ECG f"mdings, the patient was hospitalized and placed on a protocol to rule out myocardial infarction. Although this patient was admitted to rule out myocardial infarction, the differential diagnosis would also have included unstable angina and pulmonary embolism. Given her relative lack of risk factors for those disorders, however, one might also give strong consideration to psychosomatic chest pain. Rounding out the list of possible causes would be such conditions as acute intercostal muscle strain, costochondral junction problems, osteoarthritis with referred pain into the chest, osteoporotic fracture or rib fracture, trauma, peri-

Hospital Practice September 15. 1992

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carditis, cholecystitis and biliary colic, gastroesophageal reflux disease with esophageal spasm, and even aortic dissection or aortic aneurysm. The location of chest discomfort in this patient was slightly atypical for acute myocardial infarction. When chest pain is a component of infarction, as it usually is, it tends to be at least partially substernal. It may, however, occasionally occur at highly aberrant locations. Often in such cases the pain is referred to areas of underlying somatic disease. For example, an MI patient with a tooth abscess may well have jaw pain; one with bursitis may have discomfort in the affected bursa. Thus, while substernal chest pain is classic for acute myocardial infarction and diagnostically helpful. it is not an absolute requirement. Weighing against the atypical location of the pain were the ST-segment changes in leads V3 to V5 on the electrocardiogram, which suggest anteroseptal or anteroapical ischemia from coronary artery disease. Those electrocardiographic abnormalities are not strongly suggestive of pulmonary embolism; the ECG changes most often associated with acute pulmonary embolism are a right axis shift in the frontal plane, perhaps with S waves in leads I, II, and III or an incomplete right bundle branch block. In sum, the electrocardiographic abnormalities, combined with the history of hypercholesterolemia in a postmenopausal woman, raised the issue of potential non-Q-wave myocardial infarction or acute unstable angina.

Further Investigation The patient had no further chest pain during her hospitalization. Serial creatine kinase levels were negative, and myocardial infarction was ruled out. A second ECG taken during the hospital stay showed ongoing resolution of the ST-segment depression seen on the first ECG. Nevertheless, because of the history of hypercholesterolemia and her ECG changes, on the third hospital day she underwent cardiac catheterization, which demonstrated completely clear coronary arteries and good left ventricular function. 88

Hospital Practice September 15, 1992

At the time of cardiac catheterization, a rightsided percutaneous Swan-Ganz catheter was introduced via the femoral artery into the pulmonary circulation to record central circulatory pressures. Pulmonary artery pressure was 35/9 mm Hg, and mean pulmonary artery pressure was in the low 20s. Wedge pressure was normal. Cardiac output was 3.8 L/min. Because of the elevated pulmonary pressures and the location of the chest pain, the possibility of pulmonary embolism was entertained, and a ventilation-perfusion scan was performed. The scan showed multiple partially matched perfusion defects, much larger than ventilation defects, in the left apex and lower lobe and the right upper and middle lobe. Pleural-based wedgeshaped perfusion defects were seen in the anterior basal segment of the right lower lobe and the anterior segment of the right upper lobe. The scan was interpreted as indicating a high probability of acute pulmonary embolism, with the perfusion patterns suggesting a combination of recent and older emboli. The classic presentation in pulmonary embolism includes pleuritic chest pain, cough, hemoptysis, grunting respirations, friction rub, fever, palpitations and tachycardia, and a wedge-shaped defect on the chest x-ray. Thinking of pulmonary embolism in terms of that classic picture may be almost dangerous, however, because it tends to obscure the wide clinical variability of the disorder. Pulmonary embolism runs the gamut, from repeated showers of silent pulmonary emboli to massive pulmonary embolus causing sudden death. Unless one has a high index of suspicion for pulmonary embolism, one might miss the diagnosis in a patient such as this, whose symptoms did not fit the typical pattern. A fmding that may suggest the diagnosis in nonclassic cases, provided the patient is seen acutely, is a low arterial Po2 or an increased alveolar-arterial pressure gradient. The arterial hypoxemia is usually minor and often resolves quickly, but it is evidence of the ventilation-perfusion abnormality in the lungs. Indeed, a normal blood gas reading in a patient with acute symptoms argues against the diagnosis of pulmonary embolism. Since blood gas studies are often performed when patients present to the emergency room, the hypoxemia may alert the clinician to the possibility of pulmonary embolism. Hypoxemia is a particularly useful clue in patients whose chest x-ray

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shows no pulmonary edema or congestion to account for that finding. In this patient, however, blood gas studies were not performed initially, and the pulmonary embolism did not receive strong consideration at that time. Once non-Q-wave myocardial infarction was ruled out, it was natural to think that perhaps the patient had acute unstable angina. That, along with her history of hypercholesterolemia, led to her cardiac catheterization. The choice of catheterization was a cost-effective one, since the procedure eliminated coronary artery disease from consideration and turned the physicians' attention to pulmonary embolism. Right heart catheterization revealed pulmonary hypertension-not severe but with systolic pressure about 10 mm Hg higher than normal. Had the patient not demonstrated pulmonary hypertension, we would have entertained the possibility of coronary artery spasm. Attempting to reproduce the spasm with ergonovine would have been an appropriate maneuver at that point. The combination of pulmonary hypertension and the earlier symptoms, however, brought up the question of whether the patient had had one or more pulmonary emboli recently. Consequently, immediately after catheterization, the patient was sent for a ventilation-perfusion scan, which is probably the single most valuable test in suspected pulmonary embolism. Ventilation-perfusion scans are quite reliable as long as a chest x-ray has confirmed that the patient does not have pneumonia or some other potentially misleading parenchymal lesion. The scans are read as normal or as showing a high, intermediate, or low probability of embolism. If a ventilation-perfusion scan indicates a low probability of pulmonary emboli in a patient with strong clinical evidence of embolism, the physician should try to establish the diagnosis by some other test, such as pulmonary arteriography or venography. It is not appropriate to initiate therapy on the basis of clinical suspicion alone. In any case, discrepancy between the clinical findings and scan results is not common. At present, most physicians believe that the scan provides the closest thing to a definitive answer in suspected pulmonary embolism. Pulmonary arteriography may be especially useful in patients who have no history of a recent acute episode, or in whom one is worried about repeated pulmonary emboli in the absence of acute ventilation-perfusion abnormalities. Gaps in the pul(continues)

Hospital Practice September 15. 1992

89

PULMONARY EMBOLISM

(continued)

monary circulation on arteriography suggest occlusion of those arteries by emboli at some point in the past.

Treatment

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The patient was started on anticoagulation therapy with heparin, then switched to warfarin. She had no further episodes of chest pain during her hospital stay. This patient received the management of choice for mild to moderate pulmonary embolism: immediate heparinization, continued for several days and followed by prolonged oral anticoagulation with warfarin. Although in the past heparin was gtven for as long as 10 days before starting warfarin, recent studies indicate that warfarin can safely be started within three days of heparinization. (Personally, I like to treat a little longer with heparine.g.. for one week.) Heparin acts quickly to prevent further thrombus formation and prevent the release of vasoconstrictive substances from platelets adherent to pulmonary emboli. Those vasoactive substances are thought to cause pulmonary hypertension in acute pulmonary embolism. In contrast. stable pulmonary hypertension is a late finding. It suggests that the patient has sustained repeated episodes of silent pulmonary embolism, with obstruction and obliteration of large areas of the pulmonary circulation. The increased resistance to flow across the remaining pulmonary circulation raises the pulmonary perfusion pressure. If sufficiently severe, the pulmonary hypertension may eventually lead to congestive heart failure. There is very little the physician can do when a patient presents with stable pulmonary hypertension. Giving anticoagulants would be closing the barn door after the horse has escaped. In this case, however, one is dealing with a patient who has mild pulmonary hypertension that presumably is due to recent pulmonary embolism. Here anticoagulation should be effective in stabilizing pulmonary pressure and preventing further embolic episodes until (continues) Hospital Practice September 15, 1992

93

NAPROSYNi (NAPROXEN) 500 mg tablets Brief Summary:

Contralndlcatlons:

Patients who have had allergic reactions to NAPROSYN, ANAPROX or ANAPROX OS or In whom asp1nn or other NSA\Ds induce the syndrome of asthma, rh1n1t1S, and nasal polyps. Because anaphylactic reactions usually occur '" patients with a history of such reactions, question pat1ents for asthma. nasal polyps, urt1cana, and hypotension associated with _NSA\Ds before starting therapy. If such symptoms occur, d1scont~nue the drug. Warnings: Serious Gl toxicity such as bleeding, ulceratiOn. and perforation can occur at any tHt:1e, With_ or Without warn1~g symptoms, in patients treated chromcally w1th NSAIDs. Remain alert for ulceration and bleeding m such patients even m the absence of previous Gl tract symptoms. In clinical tnals, symptomatic upper Gl ulcers, gross bleeding or perforation appear to occur in approximately 1% of pat1ents treated for 3-6 months . and 1n about 2-4% of patients treated for one year. lnf~rm pat1ents about the signs and/or symptoms of senous Gl tox1c1ty and what steps to take if they occur. Studies have_ not 1dent1fled any subset of patients not at risk of developing peptic u1cerat1on and bleeding. Except for a prior h1story of serious Gl events and other r1sk factors known to be associated with peptic ulcer disease, such as

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seem to tolerate ulceration or bleeding less well than others and most spontaneous reports of fatal Gl events are 1n this population. In considering the use of relatively large doses (within the recommended dosage range), sufficient benefit should be anticipated to offset the potential increased risk of Gl toxicity. Precautions: DO NOT GIVE NAPROSYN• (NAPROXEN~ CONCOMITANTLY WITH ANAPROX~ (NAPROXEN SODIUM OR ANAPROX~ OS (NAPROXEN SODIUM) SINCE THEY BO H CIRCULATE IN PLASMA AS THE NAPROXEN ANION. Acute interstitial nephritis with hematuria, proteinuria, and nephrotic syndrome ~as be_en reported. Patients with impaired renal function, heart failure, liver dysfunction. patients taking diuretics, and the elderly are at greater nsk of overt renal decompensation. If thts occurs, discontinue the drug. Use with caution and monitor serum creatinme and/or creatinine clearance in patients with significa_ntly impai~ed renal function. Use caution in patients with baselme creatimne clearance less than 20 mliminute. Use the lowest effective dose in the elderly or in patients with chronic alcoholic liver disease or cirrhosis. With NSA\Ds, borderline elevations of liver tests may occur in up to

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manifestations occur (e.g., eosmophilia or rash), discontinue ther-

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ing adrenal insufficiency and exacerbation of art~rit1s symptoms Determine hemoglobin values periodically for patients with initial values of 10 grams or less who receive long-term therapy. Penpheral edema has been reported. Therefore, use with cautiOn in patients with fluid retention, hypertension or heart failure. The

r:~:r\;~'i~l!~e~~a;~n.a~1~~i~~n~a~g~rr ~f~~v~~~fic~~1u~~~uoc;_ duct ophthalmic studies if any change or disturbance in vision occurs. For patients with restricted sodium intake, note that the 0

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there are more serious side effects, such as Gl bleeding, which may result in hospitalization and even fatal outcomes. Physicians may wish to discuss with patients the potential risks and likely

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an acceptable alternative. Patients should use caution for activities requiring alertness if they experience drowsiness, diuiness, vertigo or depression during therapy. Laboratory Tests: Because serious Gl tract ulceration and bleeding can occur without warn-

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PULMONARY EMBOLISM

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the source of the emboli has resolved. Anticoagulation alone is not adequate for major pulmonary embolism, however. A large embolus can migrate to a major pulmonary artery and completely obstruct blood flow. causing severe circulatory impairment. Such patients are in significant respiratory distress, are hypotensive, and have a pronounced right ventricular lift and oligemic lung fields on chest x-ray. Usually the diagnosis is fairly evident. The other main diagnostic consideration is myocardial infarction, which is usually distinguishable by ECG. Major pulmonary embolism can be life threatening. In addition to intravenous heparin, morphine, and oxygen, these patients require prompt restoration offlow through obstructed pulmonary circulation. Flow can be restored by various means, including pulmonary embolectomy and extraction of emboli via transvenous suction catheter. Increasingly, however, thrombolytic therapy is assuming foremost importance. Studies have suggested that, along with lysing the pulmonary embolus itself, thrombolytic therapy has the additional benefit of reducing residual peripheral venous insufficiency. Peripheral or pelvic veins are usually the source of emboli in these cases. Consequently, when a patient has major pulmonary emboli from phlebothrombosis in the legs, a 24-hour infusion of a thrombolytic agent is probably the treatment of choice.

follow-up. Drug Interactions: Use caution when giving concoml-

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probenecid: or methotrexate. Drug/Laboratory Test Interactions: The drUQ may decrease platelet aggregation and prolong bleeding time or 1ncrease urinary values for 17-ketogemc steroids. Temporarily stop therapy for 72 hours before doing adrenal function

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genicity. Pregnancy: Category B. Do not use during pregnancy

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doses of 2.5-5 mglk~. with total daily dose not exceeding 15 mg/kg/day, are safe '" children over 2 years of age. Adverse Reactions: In a study, Gl reactions were more frequent and severe in rheumatoid arthritis patients on 1,500 mglday than in those on

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tions a~out the same, and other reactions less frequent than 1n adults. Incidence Greater Than 1%; Probable Causal RelatiOnship: Gl: The most frequent complaints related to the Gl tract: constipation~ heartbum; abdominal pain; nausea; dyspepsia, diarrhea, stomatitis. CNS: headache: dizziness: drowsiness: light-headedness, vertigo. Dermato\ogic: itching (pruritus): skin eruptions: ecchymoses; sweating, purpura. Special Senses: tmmtus; hearing disturbances, visual disturbances. Cardiovascular: edema.· 1

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cohtis. G\ bleeding and/or perforation, hematemesis, jaundice. melena, peptic ulceration with bleeding and/or perforation, vomitinQ. Renal: glomerular nephntis, hematuria, hyperkalemia, interStitial nephntis, nephrotic syndrome, renal disease, renal failure, ren~l papillary necrosis. Hematoloqic: agranulocytosis .. eosino· phifla, Qranulocytopenia, leukopema, thrombocytopema. CNS depression, dream abnormalities, inability to concentrate, insom-

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hearing impairment. Cardiovascular: congestive heart failure. Respiratory: eosinophilic pneumonitis. General: anaphylactoid reactions, menstrual disorders, py~exia (chills and fever). Causal

A Doppler scan for deep venous thrombosis detected no abnonnalities. An echocardiogram showed no thrombi or structural abnonnalities-particularly tricuspid insufficiency-that could result in thrombus formation. Serum lipids were in the normal range, with a total cholesterol of 195 mgtdl, an HDL of 44 mgtdl, and an LDL of 130 mgtdl. Her fasting blood sugar was 88mgtdl.

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epidermal necrolysis, erythema multiforme, photosenSitivity reactions resembling porphyria cutanea tarda and epidermolysis bul\osa, Stevens-Johnson syndrome, urticaria. Gl: non-peptic Gl ulceration, ulcerative stomatitis. Cardiovascular: vasculitis. General: angioneurotic edema, hyperglycemia, hypoglycemia. OVenlosage: May have _drowsiness, heartburn, indiges11on, nausea, vom1tmg. A few pat1ents have had seizures. Empty stomach and use usual supportive measures. In animals 0.5 g/kg of activated charcoal reduced plasma levels of naproxen. Caution: l~gic:

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of reported reaction 3%-9%. ~:VJ~.~: Where unmarked, incidence less than 3% . ..,. ""' ·~ U.S. patent nos. 3,904,682. 3,998,966 and others. © 1991 Syntex Puerto Rico, Inc. Rev. 39 September 1990

* Incidence

The source of pulmonary emboli in this woman remains unknown. Occult cancer is a concern in such patients, as is pelvic thrombosis. This wom-

96

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PULMONARY EMBOLISM

(continued}

an had been on estrogen replacement, which was discontinued because estrogen has been reported to produce thromboembolism. Admittedly, thromboembolism is not usually associated with estrogen replacement in postmenopausal women; it was most often associated with use of older oral contraceptives that contained higher doses of estrogen than ones generally used today. Although this patient had a heart murmur initially, suggesting a possible cardiac origin of the emboli, the murmur was soft and faded during hospitalization. Echocardiography then confirmed the absence of a possible cardiac source for the embolism. It is not rare for the source of emboli to remain unidentified, but in most cases of pulmonary embolism, the patient will have a history of trauma, surgery (particularly pelvic surgery), childbirth, deep venous thrombosis, or some other condition that offers an obvious explanation. The physician should bear in mind that pulmonary emboli need not come from a venous source; they can originate in the right atrium in a patient with chronic atrial fibrillation, just as emboli can stem from the left atrium and cause stroke or peripheral embolic phenomena. One line of inquiry we did not follow in this patient was to measure levels of antithrombin III, protein C. and protein S. Abnormally low levels of those endogenous anticoagulants would explain a propensity toward embolism. Coagulation disorders of that nature usually manifest at an early age, however, and they tend to be familial (although patients often are unaware that their relatives are affected). If this patient were to have another episode we would consider investigating her coagulation system more thoroughly. There might be some who would do that immediately, rather than just providing empiric management.

which showed partial resolution of the defects that had been visible on her previous scan. An ultrasound study of her lower legs was negative for deep venous thrombosis. She was discharged from the hospital. Anxiety is a very important symptom of pulmonary embolism; in some cases it is the only symptom. Such asymptomatic patients may present quite late, with pulmonary hypertension due to repeated pulmonary emboli, but no history of clinical manifestations that could have marked episodes of pulmonary infarction. When queried, however, those patients may recall that they felt nervous or anxious, or had sudden, unexplained shortness of breath lasting for 10 to 30 minutes. Those symptoms are quite nonspecific, and when a patient does seek medical care, physicians not infrequently attribute them to emotional upset. The sudden onset of anxiety is cause for concern, thereforeparticularly in a patient such as this, who has labo-

A Recurrence? The patient was discharged after six days in the hospital. The day after discharge she returned to the emergency room complaining of anxiety and fatigue. She was readmitted and underwent a second ventilation-perfusion scan, Hospital Practice September 15, 1992

99

ratory evidence of pulmonary embolism. In this case, however, the ventilation-perfusion scan showed no evidence of fresh pulmonary embolL It did show resolution of some of the abnormalities apparent on the initial scan, which suggested that some of the embolic phenomena had been relatively recent.

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Follow-up The patient remained well, and warfarin was discontinued after six months. A follow-up ventilation-perfusion scan has been scheduled for the near future. How long to keep a patient like this on anticoagulation therapy is an arbitrary decision. We do not know how the duration of therapy affects the balance of risks and benefits. One factor favoring prolonged therapy is that bleeding complications with chronic warfarin anticoagulation are much less common than they used to be. Better understanding of the differences in the tissue thromboplastins used for prothrombintime testing in Europe and the United States has brought standardization of the results and fostered the realization that we could anticoagulate at a shorter prothrombin time. In the past, physicians in the United States generally anticoagulated patients to 2 to 2.5 times control. which probably was inappropriately high; now the standard is 1.25 to 1.5 times control. The net effect of the change is that one can continue to give warfarin for long periods with fewer episodes of bleeding. Once patients have been weaned from chronic anticoagulant therapy, they should return for a follow-up visit within one to six months, to check for recurrence of clinical symptoms and perhaps for another ventilation-perfusion scan. How closely one follows the patient should depend on the clinicalcourse. Aspirin has been proposed as an alternative agent for preventing pulmonary embolism, but its role is not fully elucidated. Some years ago, a trial of chronic aspirin administration in patients who had undergone hip replacement suggested a beneficial effect. A more established method is the use oflow-dose heparin to prevent embolism in immobilized surgical patients during prolonged periods of hospitalization. 100

Hospital Practice September 15. 1992

Finally, a patient who repeatedly breaks through anticoagulant therapy from dependent peripheral venous sources may be a candidate for placement of an umbrella filter. The filter, which is placed in the inferior vena cava through a catheter, intercepts emboli and prevents them from reaching the lungs. This technique has been available for about 20 years but is not widely used today. Insertion is something of a technical tour de force, with its risk of perforation and other complications. Also, the umbrella filter may not be completely protective, since emboli may reach the lungs through collateralization above it. For the most part, clinicians currently rely on more vigorous medical management for those patients. D

Case Commentary

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ROLF M. GUNNAR

Loyola University

This is an interesting case of an important disorder. There are about 200,000 deaths in the United States each year associated with pulmonary embolism, and in about half of those pulmonary embolism is the principal cause of death. As in this patient, pulmonary embolism can occur in people who are seemingly healthy. Many of those, however, have an obvious predisposing factor. The classic example is the person who presents with pulmonary embolism after a trip that involved sitting for prolonged periods in an airplane or a car. Evidence of chronic venous stasis is also common, particularly in older patients. In the absence of an obvious predisposing factor, there is always the question of occult carcinoma. I would agree with the differential diagnosis Rapaport provides. I would, however, suggest two other disorders that merit consideration. One is pleurodynia, or Bornholm's disease. This widespread Coxsackie infection occurs in the fall and early winter. It can produce severe chest wall pain and may present a diagnostic challenge. The other syndrome that must be considered is chronic pulmonary embolism presenting as pulmonary hypertension with heart failure. Higher pulmonary artery pressures can develop in this setting, and diagnosis is occasionally made only after lung biopsy in the workup for primary pulmonary hypertension. The syndrome may require treatment with extensive pulmonary embolectomy. Rapaport does not stress physical findings that may provide some diagnostic hints. In some patients one can hear a fourth heart sound from the right ventricle; it is particularly distinct along the left sternal border or in the supraclavicular area. With a large pulmonary embolus, there may be wide splitting of the second heart sound and sometimes a very subtle parasternal lift. This patient had a systolic murmur, apparently from the right ventricular outflow tract. Such murmurs, which can have a scratchy quality, are not uncommon in pulmonary embolism. They have been attributed to subtle outflow tract distention. The ECG changes in this patient are noteworthy because they are ones not usually associated with pulmonary embolism. Normally, patients have Twave changes in leads V1 to V3 ; she had ST depression in leads V3 to V5 . Rapaport mentions the typi-

cal S 1 , Q3 , T 3 pattern and right bundle branch block; patients who do not have bundle branch block may at least have anterior and rightward shifts in the terminal forces of the QRS. A positive ventilation-perfusion scan is of course very helpful. In a patient such as this, whose clinical story is compatible with pulmonary embolism and whose ventilation-perfusion scan shows clearcut abnormalities, there is no need for angiography. If on the other hand, the ventilation-perfusion picture is somewhat obscure, angiography may indeed be necessary. Pulmonary angiography is considered the gold standard in the diagnosis of pulmonary embolism. There is some risk of false-negative findings, however, unless the procedure includes selective views of the pulmonary vasculature. If the initial views are not obviously positive-as in a patient who does not have a large embolus-selective views may be necessary. Selective views are particularly important in patients with chronic recurrent emboli. A simpler alternative to pulmonary angiography in patients with indeterminate ventilation-perfusion scans is venous angiography, which usually will show a clot in a leg or pelvic vein. Venous angiography is especially useful in patients who present late in the course of disease. After seven days, the pulmonary abnormalities may have substantially resolved, and deep venous thrombosis in the pelvis or legs may be the only remaining evidence. Noninvasive assessment for deep venous thrombosis can be made with Doppler ultrasound scanning. The choice between Doppler scanning and venography depends on one's level of clinical suspicion. Doppler scanning did not show deep venous thrombosis in this case, which could have been misleading if the ventilation-perfusion scan had been indeterminate. Rapaport mentions thrombolytic therapy for pulmonary embolism. Some physicians advise widespread use of thrombolytic therapy in pulmonary embolism because they think there is evidence that patients treated with heparin alone may have some long-term limitation of pulmonary function. The other side of the coin is that if the patient still has a large, poorly attached clot in a leg or pelvic vein, thrombolysis may unseat that clot, which may then cause mischief. I think there is little doubt that in the patient who has a massive embolus, thrombolytic therapy is very useful. In a patient who is tolerating the pulmonary embolism well, however, there is a serious question of whether thrombolysis has any advantage over heparin. That question is not completely settled yet. Hospital Practice September 15. 1992

101

Report to Readers on the

Hospital Practice Series Decision Making in Medicine Edited by Norton J. Greenberger

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Professor and Chairman Department of Medicine University of Kansas

In coming months look for A Strategy for the Isolated Thyroid Nodule by Hossein Gharib, Mayo Clinic with commentary by Ernest L. Mazzaferri Ohio State University

Acute Recurrent Viral Meningitis by J. Richard Baringer University of Utah with commentary by Jay P. Sanford University of Texas Southwestern Medical Center, Dallas

Diagnosis of Cushing's Disease by James W. Findling, Jr. St. Luke's Medical Center, Milwaukee

with commentary by Ernest L. Mazzaferri Ohio State University

Sudden Onset of Purpura by Robert W. Lightfoot University of Kentucky with commentaries by John S. Davis IV, University of Virginia William J. Williams SUNY Health Science Center, Syracuse

AIDS-Related Diarrhea by John Cello University of California, San Francisco with commentaries by Norton J. Greenberger and Jay P. Sanford

Regarding chronic therapy, the consensus is that long-term warfarin is the treatment of choice. Some physicians continue warfarin for three months; I prefer six months in view of the switch to dosages lower than those traditionally used in the United States. As Rapaport observes, we no longer see many of the complications previously associated with long-term warfarin therapy now that we are keeping the prothrombin time in the range of 1.25 to 1.5 times the control. I agree that warfarin should be started early, because ideally the patient should get about five days of warfarin therapy before the heparin is stopped. The reason is that the prothrombin time reflects not only prothrombin level but factor VII activity as well. When warfarin is begun, the factor VII level drops first, so the prothrombin time may be prolonged before prothrombin levels fall. Reducing factor VII levels does not protect against thrombosis, of course, so one could have a false sense of security in that early phase. Rather than getting measurements of prothrombin itself, which requires a coagulation laboratory, most clinicians prefer to give five days of D warfarin before stopping heparin.

Selected Reading Morrell Nw. Seed WA: Diagnosing pulmonary embolism. Br Med J 304 : 1126, 1992 Carson J et al: The clinical course of pulmonary embolism. N Engl J Med 326: 1240, 1992 Caracci BF et al: How accurate are ventilation-perfusion scans for pulmonary embolism? Am J Surg 156: 4 77. 1988 Stein PD et al: Complications and validity of pulmonary angtography in acute pulmonary embolism. Circulation 85:462, 1992 Amstutz HC et al: Warfarin prophylaxis to prevent mortality from pulmonary embolism after total hip replacement. J Bone Joint Surg[Am]71: 321, 1989 Todd GJ et al: Recent clinical experience with the vena cava filter. AmJ Surg 156:353, 1988 Dalen JE, Alpert JS: Natural history of pulmonary embolism. Prog Cardiovasc Dis 17: 259, 1975 Saltzman HA et al: Value of the ventilation/perfusion scan in acute pulmonary embolism. JAMA 263 :2753, 1990 Hull RD et al: Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 98:891, 1983 Levine M et al: A randomized trial of a single bolus dosage regtmen of recombinant tissue plasminogen activator in patients with acute pulmonary embolism. Chest98:1473, 1990 Lyerly HK, Sabiston D Jr: Surgical treatment of chronic pulmonary embolism. Annu Rev Med 42: 507, 1991

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A nonclassic case of pulmonary embolism.

Hospital Practice ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20 A Nonclassic Case of Pulmonary...
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