648 THE NEW ENGLAND JOURNAL OF MEDICINE Sept. 7, 1995 CLINICAL PROBLEM-SOLVING In this Journal feature, information about a real patient also be caused by reactivation of the old tuberculosis in- is presented in stages (boldface type) to an expert clinician, who fection. She could also be having pulmonary emboli, responds to the information, sharing his or her reasoning with since there is an increased incidence of pulmonary em- the reader (regular type). The author’s commentary follows. boli in pregnancy. I would also worry that hemoptysis and breathless- STUDYING THE CLASSICS ness could be due to left heart failure. In heart failure hemoptysis is caused by the rupture of fragile anasto- GEORGE E. THIBAULT, M.D. moses between the pulmonary and bronchial veins when they are subjected to high pressure. The patient A 25-year-old Hispanic woman in the 27th week is Hispanic; we have not been told where she spent her of pregnancy came to the emergency room com- childhood. Acute rheumatic fever and rheumatic heart plaining of cough and shortness of breath. She re- disease are still endemic in many developing countries. ported that she had been well until two days ear- This could be the clinical presentation of mitral steno- lier. In the past day she had also been nauseated, sis in a previously asymptomatic woman who became and she had vomited once. In the emergency room symptomatic only in the third trimester of pregnancy, she was found to have a temperature of 38°C when the cardiac output is at its maximum. The failure (100.5°F) and was thought to be dehydrated. In- to hear a murmur on cardiac examination does not ex- travenous fluids, ampicillin, and gentamicin were clude mitral stenosis, particularly in the presence of administered. She was given a prescription for tachycardia and a lot of respiratory noise. She could erythromycin and sent home. She returned the also have heart failure due to other causes, such as car- next day because she was more dyspneic and ex- diomyopathy. It is a bit early in the pregnancy for peri- plained that she had coughed up a half-cup of partum cardiomyopathy. blood. She also reported that she had been treat- ed with antibiotics one month earlier for a pre- The serum sodium and potassium, blood urea sumed upper respiratory infection. Since then nitrogen, and serum creatinine concentrations she had been tired and short of breath. Four pre- were normal. The hematocrit was 35 percent; the vious pregnancies and deliveries had been unre- white-cell count was 9900 per cubic millimeter markable. Four years earlier she had been treated with 82 percent neutrophils and 4 percent band for tuberculosis. On examination her tempera- forms; the platelet count was 230,000 per cubic ture was 38.6°C (101.4°F), her pulse was 120 to 130 millimeter. The urinalysis was unremarkable. Ar- beats per minute, her blood pressure was 94/50 terial-blood gas values measured while the pa- mm Hg, and the respiratory rate was 30 per tient was breathing 2 liters of supplemental oxy- minute. The cardiac examination was considered gen per minute were as follows: partial pressure to be unremarkable, but the chest examination of oxygen, 61 mm Hg; partial pressure of carbon revealed bibasilar rhonchi and wheezes. Her arte- dioxide, 26 mm Hg; pH 7.44; and calculated bicar- rial oxygen saturation was 94 percent while she bonate concentration, 17 mmol per liter. Her chest was breathing oxygen at a rate of 2 liters per film is shown in Figure 1. minute. The patient is mildly anemic and has no leukocyto- At the time of her first visit to the emergency room, sis, but there is a slight leftward shift. She has a sub- the patient’s fever and symptoms were most suggestive stantial arterial–alveolar pressure gradient. The blood of a respiratory infection, but there also seemed to be a gas values are consistent with chronic respiratory alka- gastrointestinal component. A community-acquired fe- losis but she could also have a mild degree of metabolic brile illness with respiratory and gastrointestinal symp- acidosis. toms would be consistent with legionella infection; The chest film is quite interesting. The hilar vessels erythromycin may have been an appropriate drug. I do are plump, the upper-lobe vessels also appear to be en- not know how sick she looked at the time of the first larged, and there are increased interstitial markings. visit, so I cannot say whether further investigation This could be interstitial inflammation or interstitial should have been undertaken then. Because hemoptysis pneumonia, but it looks more like heart failure to me. is not a common feature of community-acquired pneu- There is also straightening of the left heart border, monias, I would want to consider either a more aggres- which is suggestive of left atrial enlargement, and some sive, necrotizing bacterial pneumonia or another proc- enlargement of her central pulmonary arteries. The ess responsible for the hemoptysis. Hemoptysis could x-ray film makes me suspect heart failure more strong- ly; the findings would be quite consistent with mitral From Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115, stenosis. I still cannot exclude the diagnosis of intersti- where reprint requests should be addressed to Dr. Thibault. tial pneumonitis. The chest film does not show evi- Downloaded from www.nejm.org at COLUMBIA UNIV HEALTH SCIENCES LIB on September 8, 2006 . Copyright © 1995 Massachusetts Medical Society. All rights reserved. Vol.333 No.10 CLINICAL PROBLEM-SOLVING 649 perform Gram’s staining of the fluid to look for bacte- ria and white cells. The fact that her jugular venous pressure is elevated means that she has right atrial hy- pertension and, by definition, right heart failure. That does not prove that she has left heart failure, although that is the most common cause of right heart failure. However, patients with severe pneumonia or recurrent pulmonary emboli can present with acute cor pulmo- nale and isolated right heart failure. Given her earlier x-ray film, these findings are most consistent with left heart failure leading to or coincident with right heart failure. We are told no gallops were heard. If this were a case of severe, dilated cardiomyopathy caused by acute myocarditis or of peripartum cardiomyopathy, I would expect to hear a loud third heart sound. In a patient Figure 1. Chest Film Obtained in the Emergency Room. who has a rapid heartbeat with a lot of respiratory noise, murmurs of mitral stenosis and the opening snap may not be recognized. There was only slight cardio- dence of lobar pneumonia, active tuberculosis, or find- megaly on the chest film. That would still be consistent ings suggestive of pulmonary emboli, though chest with early acute myocarditis or mitral stenosis. I would films are both insensitive and nonspecific with respect do an echocardiogram to evaluate the valves and myo- to the last diagnosis. cardial function. On the basis of the chest film, I believe tuberculosis, necrotizing bacterial pneumonia, and pulmonary em- The electrocardiogram is shown in Figure 2 and boli are unlikely. The probability of heart failure has the chest film obtained after the patient was intu- gone up, and I am particularly concerned about the bated in Figure 3. possibility that she has rheumatic heart disease. I would want to repeat the cardiac examination in a quiet room The electrocardiogram shows sinus tachycardia and and obtain an echocardiogram. I also would want to a vertical axis. This axis could be normal, but it could obtain expectorated sputum for examination, because I also be indicative of right heart strain. There is also ev- have not entirely excluded the possibility that she has idence of left atrial enlargement. The vertical axis and an atypical pulmonary infection. left atrial enlargement are consistent with mitral steno- sis, though neither of these abnormalities is specific. The patient was treated with fluids and intrave- She now has progressive opacification of both lung nous erythromycin (500 mg every six hours), but fields. What was previously an interstitial process is she became increasingly dyspneic and was airlift- now an alveolar process. With this degree of radio- ed to a tertiary care center. On arrival she had an graphic abnormality, one cannot be specific about the arterial oxygen saturation of 40 percent, and she cause. It is consistent with cardiogenic pulmonary ede- was immediately intubated. The fluid suctioned ma, but it is also consistent with noncardiogenic pulmo- from the endotracheal tube was pink and frothy. nary edema or any progressive lung injury leading to The physical examination revealed jugular venous the adult respiratory distress syndrome. distention to the angle of the jaw. The cardiac ex- amination disclosed tachycardia (120 beats per minute and regular); S1 and S2 were audible; no gallops or murmurs were heard. Examination of I aVR V1 V4 the chest revealed diffuse rhonchi. She had no cyanosis, clubbing, or edema of the arms and legs. II aVL V2 V5 The patient did not get better on erythromycin and got worse when she received a large volume load. If she did have rapidly progressive pneumonia, the failure to III aVF V V improve in the first 24 hours does not necessarily mean 3 6 that the wrong antibiotic was chosen. But I am even more suspicious that she has something other than in- fection. Pink frothy fluid coming from the endotracheal II tube is characteristic of pulmonary edema and points Figure 2. Electrocardiogram and Lead II Rhythm Strip Obtained strongly to severe heart failure. I would still want to at the Time of Transfer to a Tertiary Care Center.