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Glauser, D’Amore • CPC: HEMOPTYSIS
Clinicopathological Conference: A Previously Healthy 40-year-old Woman with Hemoptysis
JONATHAN GLAUSER, MD, JASON Z. D’AMORE, MD
RESIDENT CASE PRESENTATION
A 40-year-old Chinese woman presented to the emergency department (ED) with a two-week history of a cough productive of blood-tinged sputum. She also complained of fevers, occasional diaphoresis (no night sweats), fatigue, and intermittent shortness of breath with mild dyspnea on exertion. The patient denied chest pain, palpitations, nausea, vomiting, diarrhea, rash, coryza/congestion, epistaxis, hematuria, arthralgias/myalgias, headache, trauma, recent travel history, or any known sick contacts. She had been in her usual state of health until recently and denied any signiﬁcant past medical history. There was no history of past surgical procedures; she took no medications (including any herbal preparations); she had no known drug or environmental allergies; and she was puriﬁed protein derivative (PPD)-negative in 1997. The patient was born in China and immigrated to the United States 11 years prior to presentation. She lived in ‘‘Chinatown’’ (Lower East Side Manhattan) in a modern, well-maintained, apartment building with her husband and two children (ages 8 and 10). She worked in a local restaurant as a hostess and waitress and denied tobacco, ethanol, and intravenous (IV) or other drug abuse. On examination the patient was alert, fully oriented, and sitting up comfortably on the stretcher. She spoke in complete sentences without difﬁculty, though she did appear to be in mild respiratory distress with tachypnea and obvious supraclavicular retractions. Her rectal temperature was 101ЊF; pulse was regular at 115 beats/min; blood pressure was 110/80 mm Hg; respiratory rate was 25 breaths/min; and pulse oximetry reading on room air was 93% saturation. The head and scalp examination was normal; the pupils were equal and reactive with normal extraocular movements. The nose and throat were clear. The neck was supple without jugular venous distention or lymphadenopathy. The pulmonary examination was significant for coarse rhonchorous breath sounds throughout with scattered ﬁne crackles at the bases bilaterally. The heart was tachycardic with a loud S1 without any appreciable murmurs, rubs, or gallops. The abdomen was ﬂat with normal bowel sounds. There was no tenderness to palpation, no distention, and no hepatosplenomegaly. The patient had 1ϩ non-pitting edema of her lower extremities. Pulses were 2ϩ throughout and there was no peripheral cyanosis or clubbing. The skin was warm and dry without any rash. A neurologic examination including assessment of cognition, memory, cranial nerves, gross motor and sensory function, cerebellar function, and gait was unremarkable. Initial arterial blood gases, measured while breathing room air, were pH 7.38; pCO2 37 torr; pO2 85 torr; HCO3 26 mEq/L; 98% saturation. Her hemoglobin was 12 g/dL; white blood cell (WBC) count was 14 ϫ 109/L with a differential of 88% neutrophils and no bands; platelet count was 255 109/L. Serum electrolyte, hepatic, and renal function studies were unremarkable. It was determined that the patient was clinically stable enough to be transported for a chest xray (Fig. 1) and was sent to radiology on 3 liters of oxygen by nasal cannula. She received 1 gram of acetaminophen orally. Approximately 10 minutes after the patient returned from radiology, she became acutely short of breath and began to complain of a rapid heart rate and palpitations. Repeat vital signs revealed an irregular heart rate of 130– 150 beats/min; a blood pressure of 90/60 mm Hg, a respiratory rate of 40 breaths/min, and a room air oxygen saturation of 88%. The patient was placed on 100% O2 by non-rebreather mask, a second large-bore IV was placed, and full monitoring with electrocardiogram (ECG), automated blood pressure cuff, and pulse oximetry was instituted. Airway and cardiac resuscitation equipment was assembled and an ECG was rapidly performed (Fig. 2). In lieu of cardioversion, the patient received 20 mg of IV diltiazem with a subsequent decrease in heart rate to the low 90s and a concomitant increase in blood pressure to 110/70 mm Hg. The respiratory rate also improved, decreasing to
From Case Western Reserve University, the Department of Emergency Medicine, Cleveland Clinic Foundation, and Metro Health Medical Center Residency Program (JG), Cleveland, OH; and the Department of Emergency Medicine, Bellevue New York University (JZD), New York, NY. Received October 17, 2000; revision received December 4, 2000; accepted January 4, 2001. Section editors: Andy Jagoda, MD, Mt. Sinai School of Medicine, New York, NY; and Joseph LaMantia, MD, North Shore University Hospital, Manhasset, NY. Address for correspondence and reprints: Jonathan Glauser, MD, Department of Emergency Medicine, Cleveland Clinic Foundation, 9500 Euclid Avenue (E-19), Cleveland, OH 44195.
Number 4 375 Figure 1. and she denied night sweats. While there. and a heparin infusion was started at 1. Volume 8. Her PPD was negative in 1997. The patient received heparin. In the ED she had a fever to 101ЊF. 5. A diagnostic procedure was performed. and blood-tinged sputum. Her initial cardiac rhythm was regular. The patient’s electrocardiogram. The patient’s chest x-ray.ACADEMIC EMERGENCY MEDICINE • April 2001. she developed Figure 2. There was no recent travel history. Signiﬁcant negatives in the history included absence of arthralgias or myalgias. .000 IU IV as a bolus. and she was deemed stable for transport to radiology for a chest radiograph. She received 1 gram of IV vancomycin and 80 mg of IV gentamicin. dyspnea on exertion. FACULTY DISCUSSION Reviewing the salient features of this case. She had no chest pain and no sick contacts. 15–20 breaths/min.000 IU/hr. this patient was a 40-year-old female of Asian extraction presenting with a two-week history of fatigue.
though serious consideration must be given to possible infectious etiologies in this patient since she had a fever. calciﬁed spots. elevated pulmonary venous and capillary pressures. There is no evidence of extrapulmonary involvement in the skin. Hemoptysis is usually minor in extent unless there is rupture into the abscess cavity. The differential is quite broad. von Willebrand’s disease. or exudate. uremia Other disorders related to systemic illness: systemic lupus erythematosus (SLE) pneumonitis. No such cavity is visible on the radiograph. It may be con- . TB was the most common etiology for massive hemoptysis in this country. dizziness. patchy opacities. AIDS with Kaposi’s sarcoma. and visual disturbances. atypical mycobacterium. and conﬁrmed on culture. Blood from the stomach is acidic and dark red. or meninges. trimetallic anhydride Pneumoconiosis Cryptogenic in 2% to 30% *Based on data obtained from references 4 and 8–19 in the reference list. it would account for her fever. producing a mycetoma. or pleural effusions. isocyanates. nitrofurantoin. Metacercariae are ingested in crustaceans such as crab or crayﬁsh. hemoptysis. amebiasis or ecchinococcal cysts are unlikely diagnoses in this patient. Diagnosis is based on visualization of budding yeast forms within tissue. Africa. necrotizing vasculitides arteritis of the pulmonary artery (Behc ¸ et’s syndrome). and migrate to the lung. cough. Lung abscess may present with fever. became somewhat hypotensive.1 Patients with cerebral paragonimiasis may experience headaches. Simple tuberculous erosion into the bronchial mucosa may cause massive hemoptysis by erosion into bronchial vessels. aortic aneurysms. Lung ﬂukes form cystic cavities 1–5 cm in diameter. tetralogy of Fallot Other congenital illness: cystic ﬁbrosis. and is frequently encountered in cultures that ingest raw or undercooked crustaceans. Fungal diseases can present with fever. D’Amore • CPC: HEMOPTYSIS TABLE 1. Osler-Weber-Rendu disease (atrioventricular malformations). bronchogenic cysts Related to drug toxicity: amiodarone. migrate through the small bowel wall into the peritoneal cavity. aortic dissection Bleeding disorders. While Paragonimus westermani is most frequently encountered. An aneurysm in the wall of a tuberculous cavity may cause massive hemoptysis. complex cyanotic heart disease. This is a bronchoscopic diagnosis. pulmonary arteriovenous ﬁstulae.3 For similar reasons. and the Asian Paciﬁc islands.2 None of these were present in this patient. Chest x-ray may reveal nonspeciﬁc linear streaking. This parasitic infection is most frequently associated with India. In older series. Paragonimiasis is a parasitic infection with a predilection for pulmonary involvement. which is reported in most cases of pulmonary paragonimiasis. sarcoid. transposition of the great arteries. In most instances of bronchiectasis. paratracheal and hilar lymph node enlargement. Table 1 presents the differential diagnosis of hemoptysis. though it is not clearly seen in Figure 1. other immune complex diseases. The initial approach to the patient with a chief complaint of coughing blood is to ensure that the blood is not coming from the nasopharynx or gastrointestinal tract. and pneumonia. Diagnosis is established by identifying eggs in the cytologic preparation of bronchioalveolar lavage ﬂuid. hemophilia. there is a typical history of chronic productive cough. and dropped her oxygen saturation from 92% on room air to 88% on 3 liters of oxygen by nasal cannula. anticoagulant use. In endemic areas. syphilitic aortitis. cavitary lesions. South America. nor was there an eosinophilia. atrial ﬁbrillation. carcinoma.6 The lack of apical lesions or of cavitation in a patient recently tested PPD-negative strongly militates against TB as a cause for her hemoptysis.4 although a study of patients who had hemoptysis between 1986 and 1995 indicated that bronchitis. drugs that cause thrombocytopenia. leukemia Idiopathic pulmonary hemosiderosis Congenital in children: ventricular septal defect. tuberous sclerosis Hamartomas Disorders primarily affecting the pulmonary vasculature: pulmonary embolus with infarction. If this were the case. Asia.376 HEMOPTYSIS Glauser. paragonimiasis presents in similar fashion to tuberculosis (TB). and pneumonia were more common than TB (8%). Differential Diagnosis of Hemoptysis* Inﬂammation: Bronchitis acute or chronic. lung abscess. purulent sputum. aspirates. Hemoptysis is a frequent presenting sign in bronchiectasis and chronic bronchitis. tracheobronchitis Infection: pneumonia. This patient had no evidence of a cavity. they may live up to ﬁve years or more. mycetoma from Aspergillus or Candida. especially in a patient originally from Asia. bone. and purulent expectoration. and recurrent ﬂares of pneumonitis. D-penicillamine. truncus arteriosus. The radiologist read the chest radiograph as demonstrating a right lower lobe inﬁltrate.5 Large-volume hemoptysis can complicate fungal invasion of a tuberculous cavity. tuberculosis. Tuberculosis is in the differential diagnosis of any patient with fever and hemoptysis. and parasites Broncholithiasis Trauma Foreign-body aspiration Neoplasm Catamenial Processes diffusely affecting the lung parenchyma: Goodpasture’s syndrome. Wegener’s granulomatosis. trans-retinoic acid. fungi. bronchiectasis. Patients with chronic bronchitis have a chronic productive cough. other Paragonimus species cause a similar picture.
ACADEMIC EMERGENCY MEDICINE • April 2001. Although LA enlargement is the striking feature of her chest ﬁlm. more pronounced in the lower lobes). On the posteroanterior (PA) examination.7 There are many other causes for hemoptysis presented in Table 1. In lateral view. There is no history of drug or toxin exposure. which demonstrates atrial ﬁbrillation with a rapid ventricular response of approximately 135 beats/min. caused by an enlarged left atrium behind the right atrium 3. and <7. The double density in the mid-portion of the cardiac silhouette to the right of the spine repre- sents the blood-ﬁlled left atrium. bacterial pneumonias. There is no lung mass visible on the chest radiograph. There is no left ventricular hypertrophy (LVH) by voltage which in this case is a signiﬁcant ﬁnding. a retrocardiac mass representing the enlarged left atrium 5. The distance between the midpoint of the double density and the midpoint of the left mainstem bronchus is normally <7. In patients with mitral regurgitation (acute or chronic). the LA appendage is the only portion of the left atrium that forms part of the left border of the heart and can be seen. double atrial density. It is deﬁned by identiﬁcation of the LA border medial to the right atrial portion of the right cardiac border (double atrial shadow). producing frank pulmonary edema. Pulmonary hemosiderin deposition may cause a chronic interstitial radiodensity (a ﬁne diffuse nodulation. A and C lines are randomly distributed linear densities found in mid-lung ﬁelds. producing fuzziness of the hila. On lateral. although by history the patient is a nonsmoker and had no signiﬁcant occupational exposures. Notable ﬁndings include the following: 1. I am unable to assess LA size on her ECG because of the absence of P waves. Any convexity is abnormal and indicates LA enlargement. There is neither mention of menstrual history nor indication that her hemoptysis coincided with menses. Further evaluation of this patient’s x-ray reveals radiographic signs of pulmonary venous hypertension. Hemoptysis is rarely the sole clinical manifestation of a hemorrhagic diathesis. inducing an intrapulmonary shunt of pulmonary blood ﬂow from the lower lobes to the upper lobes. If LA outﬂow obstruction exists alone. There are other useful ﬁndings on chest x-ray that may help to differentiate causes of LA enlargement.4.8–19 There is no evidence by history that this patient had congenital heart disease. Local increases in pulmonary resistance in the lower lobe pulmonary vessels ensue from local arteriolar hypoxemia. and a superior. sarcoidosis. so that increased LA pressure is transmitted through the pulmonary veins to the pulmonary bed. The Chest X-ray in LA Enlargement. the left atrium forms the superior posterior border of the heart. or thickening of the pulmonary septa due to chronic venous engorgement. It occupies the portion of the left heart border between the main pulmonary segment and the superior portion of the left ventricular (LV) contour. the LV size should be normal and there should be . posterior displacement of the left mainstem bronchus (a line drawn between the centers of the right and left mainstem bronchi when extended superiorly should pass within the main tracheal air column). Early LA enlargement is manifested by straightening of this segment of the left heart border. With these considerations in mind. The pulmonary hila may become dense and appear enlarged. If mitral stenosis is the cause of the LA pressure elevation and hypertrophy. There is no history of expectoration of gravel. posterior mass behind the heart. Volume 8. Other signs of LA enlargement include: posterior displacement of the left bronchial tree. there is a discrete convex bulge to the superior posterior cardiac contour below the carina. possible right lower lobe inﬁltrate 6. Further enlargement causes a convexity of the LA appendage portion of the left heart border. let us turn to the patient’s chest radiograph. Edematous interstitial tissues overlap. Elevation of the LA pressure above 25 mm Hg ﬂoods the alveolar space. so it is unlikely that her LA pressure was as high as 25 mm Hg. or malignancy.20 Enlargement is an indicator of previous rheumatic disease.5 cm in males. prominent right pulmonary artery We are also given the patient’s ECG. When LA pressure and volume are normal. focal right upper lobe pulmonary edema may be found. A number of neoplasms may cause hemoptysis.0 cm in females. elevation of the left mainstem bronchus. This patient did not have frank pulmonary edema visible. making lower lobe pulmonary vessels appear indistinct. Number 4 377 fused on x-ray with TB. posterior and superior displacement of the left mainstem bronchus 4. trauma. the hemosiderin does not resolve after the relief of the stenosis. carinal angle of 90 degrees or more (normally 75 degrees). or any systemic inﬂammatory disorder that would explain the hemoptysis. Recall that pulmonary veins are valveless. Plump pulmonary veins 7. Further edematous swelling of the bronchial walls and peribronchial tissues results in peribronchial cufﬁng and Kerley B lines. left atrial (LA) enlargement with splaying of the bronchi 2. possibly related to the jet of regurgitant blood directed toward the right upper pulmonary vein. this segment of the left heart border is concave.
27 Bleeding may be massive. In 1944. the differential diagnosis list can be revised (Tables 2 and 3). D’Amore • CPC: HEMOPTYSIS TABLE 2.26 It is now generally believed that most bleeding from mitral stenosis results from rupture of thin-walled.31 The patient in this case did have hemoptysis with desaturation and atrial ﬁbrillation. This patient’s symptoms were not positional. My clinical diagnoses in this case therefore are: 1. and physical ﬁndings are consistent with mitral stenosis. Left atrial enlargement from mitral regurgitation is associated with LV enlargement.12. and that by deﬁnition an abnormally high left atrioventricular pressure gradient must be present to diagnose mitral stenosis. Fever. and there may be frank parenchymal pulmonary hemorrhage.29 In 1952. the patient may experience dyspnea. Physical ﬁndings may include a diastolic murmur. 2. has been reported in 14% of patients with pulmonary emboli and no other source for fever. Having established that the single striking ﬁnding on this patient’s chest x-ray was LA enlargement and not LV enlargement. This patient had dyspnea and evidence for PVH. Anastomoses of small bronchial veins (pulmonary–bronchial venous connections) develop from elevated backup pressure. Did This Patient Have Mitral Stenosis? Severity of mitral stenosis can be graded using the criteria presented in Table 4. from rheumatic heart disease.25 Several mechanisms have been proposed by which mitral stenosis causes hemoptysis. as seen in patent ductus arteriosus.20.28. Atrial tumors often calcify and may present with radiographic evidence of calciﬁcation in the left atrium. and enlargement of the central and peripheral pulmonary arterial segments. from a microvascular source.24 Recall that the normal cross-sectional area of the mitral valve oriﬁce is 4– 5 cm2. ventricular septal defect may result in LA dilatation *Based on data obtained from references 20 and 21 in the reference list. Causes for Mitral Stenosis* Rheumatic fever Congenital Acute infective endocarditis Massive annular calciﬁcation Systemic lupus erythematosus Carcinoid Methysergide therapy Hunter’s syndrome/Hurler’s syndrome Fabry’s disease Whipple’s disease Rheumatoid arthritis *Based on data obtained from reference 22 in the reference list. elevated serum IgG. but not pulmonary edema. and she had no evidence of systemic emboli. the diagnosis is by two-dimensional echocardiography.22 The chest x-ray presented . or elevated erythrocyte sedimentation rate (ESR). Gilroy et al. Mitral stenosis. which can be conﬁrmed using echocardiography (Table 5). and therefore should not have predisposed the patient to embolic phenomena. The x-ray picture is that of LA enlargement. What Causes Hemoptysis in Patients with Mitral Stenosis? Hemoptysis has been reported in 9–38% of patients with mitral stenosis. †Mitral stenosis is the most common cause for LA enlargement in an adult (see Table 3). and exsanguination or asphyxiation may be a genuine concern. as from LA myxoma Massive LA ball thrombus Cor triatriatum: congenital membrane present in the left atrium Increased pulmonary blood ﬂow. Differential Diagnosis of Left Atrial (LA) Enlargement* Mitral stenosis† Chronic rheumatic mitral stenosis Congenital mitral stenosis LA obstruction. missed 10–20 years ago. thus clinically. This patient had left-sided heart disease that could explain her presentation.23. Infective endocarditis is unlikely since it is unusual TABLE 3. thus making the above considerations unlikely. dilated bronchial veins.25. Shunt lesions resulting in LA enlargement present most notably with shunt vascularity. Fever from a right lower lobe pneumonia.21 If LA emptying is obstructed by a tumor. signs of pulmonary venous hypertension (PVH). which may vary with body position. Bleeding may be minor. it appears that the atrial ﬁbrillation was of sudden onset. fever. possibly less if she contracted the disease in China. and thus PE is unlikely unless two separate processes were occurring simultaneously. Ferguson et al. her mitral stenosis is classiﬁed as being moderately severe. as deﬁned by a temperature of >100ЊF. However. systemic emboli. Pulmonary hemosiderosis results from passage of formed blood products into the pulmonary interstitium. and any emboli from the left atrium would be expected to be systemic. noted dilated pleurohilar veins communicating freely with both the pulmonary and azygous venous beds. demonstrated varices of the bronchial veins in cases of mitral stenosis and thought that these were responsible for the hemoptysis seen. though massive hemoptysis may be the presenting sign of mitral stenosis.30 A ﬁnal note on pulmonary embolus (PE) is in order. The patient most likely had rheumatic fever.378 HEMOPTYSIS Glauser. Left atrial myxoma may be associated with weight loss. anemia. and not pulmonary.
typical gradient is 15 mm Hg (SD Ϯ 7) Estimate of mitral oriﬁce size to within 0.23 Blood culture should be obtained and the patient should be treated with standard therapy for community-acquired pneumonia. Hemoptysis is an unusual presenting complaint in mitral stenosis.25–1. Additionally. Auscultatory signs when the patient is in sinus rhythm: Presystolic murmur Loud S1—The elevated left atrial (LA) pressure (transmural gradient) keeps the mitral valve open throughout diastole until the left ventrical closes it with a loud closing sound Opening snap (early—<0. need 25 mm Hg left atrial pressure to maintain a normal cardiac output *Based on data obtained from reference 12 in the reference list. Number 4 379 in pure mitral stenosis (endocarditis is more likely if mitral regurgitation is present). Volume 8.0 cm2 valve gradient 15 mm Hg).75–2 cm2 Moderate stenosis: 1. CASE OUTCOME The chest radiograph demonstrated left atrial hypertrophy (LAH) with a double density sign and signiﬁcant horizontal displacement of the left mainstem bronchus. The shortness of breath was most likely due to the loss of atrial kick and especially to the decreased diastolic ﬁlling time in atrial ﬁbrillation and an increased heart rate through a stenotic mitral valve. The infection with its attendant fever and tachycardia created a hyperdynamic state leading to decompensation and atrial ﬁbrillation. or diltiazem.ACADEMIC EMERGENCY MEDICINE • April 2001. Suggested therapy therefore must address this patient’s tachycardia initially. The fever should be managed with antipyretics. A transthoracic echocardiogram demonstrated LAH. digoxin. Atrial ﬁbrillation. The treatment goal is to stabilize the patient’s cardiovascular status by slowing the ventricular rate.4 cm2 Presence and severity of accompanying mitral regurgitation Restriction of mitral valve leaﬂets Decreased E to F slope on M-mode Multiple echoes (thickening or calciﬁcation of the valve) *Based on data obtained from references 23 and 24 in the reference list. Finally. It is thought that the patient developed a communityacquired pneumonia in the setting of increasing CHF secondary to her mitral stenosis. Shortness of breath most likely resulted from decreased diastolic ﬁlling time and loss of atrial kick. the sooner the falling left ventricular pressure of early ventricular relaxation equilibrates with LA pressure Mid-diastolic murmur (diastolic rumble) heard best in left lateral recumbent position With severe mitral stenosis: S1 is soft Opening snap is not usually heard Often mitral regurgitation with holosystolic murmur Other physical ﬁndings that may be present in mitral stenosis: On jugular venous pulse examination: prominent a wave if right ventricular hypertrophy.0–1. Diagnosing Mitral Stenosis* TABLE 4. Congestive heart failure is most likely the predisposing factor for the patient’s hemoptysis.5 and 3.5. Grading Mitral Stenosis* Mild stenosis: cross-sectional area 1. She may be cardioverted out of atrial ﬁbrillation immediately. If the patient remains in chronic atrial ﬁbrillation.32 TABLE 5.75 cm2 Moderately severe stenosis: 1.06 sec after S2—if high LA pressure)—The higher the LA pressure. She needs longer diastolic ﬁlling time to maintain an adequate cardiac output. there were small bilateral effusions consistent with pneumonia or congestive heart failure (CHF) and a small right lower lobe inﬁltrate consistent with pneumonia. and severe mitral stenosis (valve area <1. then her fever and possible infection. 3. with some LVH. not from a pulmonary embolus. surgical intervention for her mitral stenosis with mitral valvular commissurotomy or mitral valve replacement should be considered. Mitral valve surgery has been associated with rapid and sustained cessation of hemoptysis. or tricuspid stenosis (must be in sinus rhythm) Gradual pressure decline after mitral valve opening ( y descent) No presystolic murmur if atrial ﬁbrillation present Systolic blood pressure usually normal or low Hoarseness in left recurrent laryngeal nerve impinged (Ortner’s syndrome) Esophageal impingement from the enlarged left atrium (dysphagia) Echocardiographic ﬁndings in mitral stenosis: Doppler-derived mitral gradient is reliable and actually provides a more accurate measurement than conventional cardiac catheterization using pulmonary capillary wedge pressure. . Alternatively.25 cm2 Severe stenosis: <1 cm2. she may have her ventricular rate slowed with esmolol. amiodarone. the INR should be kept between 2.
endometriosis. tachycardia. probably represents only 2% to 4% of all cases. orthopnea. RESIDENT DISCUSSION This was a 40-year-old Asian female with hemoptysis who was febrile. exertion. dyspnea. This .. they are both insensitive and nonspeciﬁc. and atrial ﬁbrillation with a rapid ventricular response can all cause acute decompensation. fever. • Any condition that increases ﬂow through the stenotic valve will exacerbate symptoms of mitral stenosis. moderate (<500 mL). where she underwent a porcine mitral valve replacement on the third hospital day. the transvalvular pressure gradient increases. a history of tobacco smoking.37 This patient did not have these risk factors. Common risk factors for pulmonary neoplasia include age >40 years. while more common in certain populations (immigrants from Asia). and pulmonary hypertension. • Fever and tachycardia should be addressed aggressively in patients with mitral stenosis and atrial ﬁbrillation.35 Hemoptysis is generally classiﬁed as being mild (<5 mL blood/day). and hemoptysis. and pulmonary hypertension (from Eisenmenger’s complex.33 Pulmonary embolus is rarely the etiology of hemoptysis. infection. pulmonary edema. mitral stenosis.12 seconds in lead I. or pulmonary edema. or hematuria made the diagnosis of a systemic vasculitis such as Wegener’s or Goodpasture’s similarly unlikely.38. Congestive heart failure. As the valve area decreases. Tuberculosis. Several clinical entities came to mind. Key Teaching Points • Mitral stenosis usually presents in the fourth or ﬁfth decade of life as a remote sequela of childhood rheumatic fever. tachycardia. A loud S1 is a nonspeciﬁc ﬁnding that can be found in hyperdynamic states (as might occur with fever and infections). and tachypnea. paroxysmal nocturnal dyspnea. Once considered.e. Physical ﬁndings did not signiﬁcantly alter the differential diagnosis of this case. • Increasing left atrial pressure with resulting left atrial dilatation and hypertrophy and pulmonary hypertension may result in dyspnea. asbestos or beryllium). The classic opening snap. and because 50% of fatal PEs go undiagnosed until necropsy. The diagnosis that rises quickly to the top of the differential in light of the above ﬁndings is mitral stenosis. Fever. Lack of arthralgias/ myalgias. Mitral stenosis usually presents in the fourth or ﬁfth decade of life as a remote sequela of childhood rheumatic fever. ﬁsh-mouthed valve with a small oriﬁce. • Infectious causes for fever and hemoptysis in patients of foreign extraction may include tuberculosis and paragonimiasis (lung ﬂukes) in addition to more common etiologies.40 Rheumatic heart disease is slowly progressive and the initial bout of rheumatic fever is often undiagnosed. can occur in 30% to 40% of cases and usually indicates severe mitral stenosis. paroxysmal atrial ﬁbrillation. or >600 mL/ day). or primary/idiopathic causes) each contribute less than 2% to 3% of cases.43 Clinically. • Atrial ﬁbrillation as a result of left atrial hypertrophy usually indicates severe mitral stenosis. The patient was admitted to the cardiothoracic surgery department.44 The echocardiogram measures both the valve area and the transvalvular pressure gradient. i. a loud S1. In this case the diagnosis must unify the following subjective and objective elements: hemoptysis. and mitral stenosis.38 The most common clinical presentation is dyspnea. The ECG is insensitive in diagnosing mitral stenosis. The lung ﬁndings would be consistent with either CHF or an infectious etiology. PE often presents with fever.e. parasites. any condition that increases ﬂow through the stenotic valve will exacerbate symptoms. occurring in less than 20% of cases. mycetomas. suggest the diagnosis. and diastolic rumble (best heard at the apex in the left lateral decubitus position) may be very difﬁcult to appreciate or may be masked by tachycardia or adventitial breath sounds such as wheezing. and en- vironmental/occupational exposures (i. rash.380 HEMOPTYSIS Glauser. or severe (massive single episodes >100 mL.41 Atrial ﬁbrillation. atrioventricular ﬁstulas.. as a result of LA hypertrophy and alterations in the conduction system.34 However.42 Hemoptysis may occur secondary to the rupture of thin-walled. though these designations should be interpreted cautiously as patients with mild hemoptysis can unexpectedly change course. which can also include dyspnea on exertion. dilated pulmonary vessels and in rare cases can be massive and life-threatening. rales. a loud S1. the diagnosis can usually be made with twodimensional echocardiography. we entertained certain considerations. although ﬁndings of LAH. She did well and was discharged on the fourth postoperative day. Without repeating the entire differential diagnosis. and LAH. systemic vasculitides. This leads to increasing LA pressure with resultant LA dilatation and hypertrophy. and tachypneic.39 The best diagnosis is usually the unifying diagnosis. The pathophysiology is explained by fusion of the mitral valve apparatus ultimately resulting in a funnel-shaped. male gender. D’Amore • CPC: HEMOPTYSIS TABLE 6. it remained an important part of the differential diagnosis. tachycardic. The same applies to radiographic ﬁndings of LAH. Diastolic ﬁlling time must be increased in patients with hemodynamic instability.36 This patient fell within the ﬁrst category. such as ‘‘P mitrale’’ or a P-wave duration >0. tachycardia.
1311–7. Chest. 1:1113–24. J Rheumatol. Marty AM. 43:560–8. 80:967–71. 1954. management should be directed toward decreasing ﬂow across the stenotic valve by treating the tachycardia and fever. . Santiago S. Martin R. Weder W. Am Heart J. 28. Very early onset of acute amiodarone pulmonary toxicity presenting with hemoptysis. Dietrick JE. Guerra-Bautista G. Br Med J. 43. Marshall TJ. 9. Wood P. Clin Radiol. and treatment in a tertiary referral hospital. Pneumococcal abscess manifesting as an anterior mediastinal mass and fatal hemoptysis. Diffuse alveolar hemorrhage with underlying pulmonary capillaritis in the retinoic acid syndrome. In the ED. Maw GM. Role of bronchoscopy in massive hemoptysis. 1998. 1997. Natural history of mitral stenosis: a review. et al. Kobilak RE. 30. evaluation. 1997. Marchand P.ACADEMIC EMERGENCY MEDICINE • April 2001. Feigenbaum H. An appreciation of mitral stenosis: part I. 1954. pp 196– 7. An appreciation of mitral stenosis: part II. 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