110 THE NEW ENGLAND JOURNAL OF MEDICINE
12, 1995
CASE RECORDS
OF THE
MASSACHUSETTS GENERAL HOSPITAL
Weekly Clinicopathological Exercises
FOUNDED BY RICHARD C . CABOT
ROBERT E. SCULLY, M.D., Editor
EUGENE J. MARK, M.D., Associate Editor
WILLIAM F. MCNEELY, M.D., Associate Editor
BETTY U. MCNEELY, Assistant Editor
CASE 1-1995
PRESENTATION OF CASE
An 80-year-old man was admitted to the hospital be-
cause of an enlarging lung tumor of long duration, re-
current bouts of postobstructive pneumonia, and recent
respiratory distress.
There was a history of a slowly growing mass in the
left main bronchus that had first been noted on radio-
graphs of the chest obtained 22 years earlier. The pa-
tient refused to undergo a thoracotomy, and the find-
ings at bronchoscopic examination were considered to
be consistent with a carcinoid tumor; no biopsy speci-
men was obtained. During the ensuing 15 years there
were no symptoms referable to the mass.
Seven years before admission, the patient began to
have bouts of left-sided pneumonia once or twice annu-
ally, which responded to antibiotic treatment. Because
of its slow growth the mass continued to be regarded
as a carcinoid tumor, although the patient never had
episodes of flushing, tachycardia, wheezing, dyspnea,
or diarrhea. In more recent years the patient was fol-
lowed closely by his internist and a pulmonary special-
ist; periodic radiographs of the chest and pulmonary-
function studies revealed no change. Two-and-a-half
years before admission, a computed tomographic (CT)
scan of the chest (Fig. 1) showed a nodular soft-tissue
mass in the distal trachea with extension into the left
main bronchus and the proximal left-upper-lobe bron-
chus. The mass contained stippled calcifications; no
mediastinal extension was noted; the left lung was par-
tially collapsed.
Two-and-a-half weeks before admission the patient’s
temperature rose to 39.4°C, and cough, anorexia, and
fatigue developed, without chills, chest pain, or dysp-
nea. He was admitted to another hospital and treated
for pneumonia of the left lower lobe. A CT scan of the
chest (Fig. 2), performed after the intravenous injec-
tion of contrast material, showed that the mass had
enlarged since the earlier CT examination, with com-
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Jan.
Figure 1. CT Scan of the Chest Obtained 2 1⁄ 2 Years before Ad-
mission, Showing a Soft-Tissue Mass in the Left Main Bronchus
Containing Peripheral Stippled Calcifications, with Partial Col-
lapse of the Left Lung.
plete obstruction of the left main bronchus and total
collapse of the left lung; there was no mediastinal ex-
tension or lymphadenopathy. Bronchoscopic examina-
tion revealed an increase in the size of the tumor, which
extended above the tracheal carina and occluded 80
percent of the tracheal lumen. In the hospital the pa-
tient had three bouts of respiratory distress, two of
which were relieved when he coughed up mucous plugs.
The fever resolved after the administration of several
antibiotics, and he was transferred to this hospital.
The patient was a retired teacher in good general
health. He had never smoked and did not drink alco-
hol; he was able to walk 12 blocks and climb two flights
of stairs without difficulty. There was no history of he-
moptysis or endocrine neoplasia.
The temperature was 36.7°C, the pulse was 60,
and the respirations were 20. The blood pressure was
130/70 mm Hg.
On physical examination the patient was a pleasant,
spry man who appeared younger than his chronologic
age. No rash or telangiectases were seen, and no lym-
phadenopathy was found. The head and neck were nor-
mal. Breath sounds were diminished over the left lung,
and a few rhonchi and respiratory stridor were heard
over the right lung. The heart and abdomen were nor-
mal. There was no peripheral edema, digital clubbing,
or cyanosis. Neurologic examination was negative.
The hematocrit was 32.3 percent, and the mean cor-
puscular volume was 89 mm3. The prothrombin and
partial-thromboplastin times were normal. The values
for urea nitrogen, creatinine, calcium, phosphorus,
electrolytes, aspartate aminotransferase, and alanine
aminotransferase were normal. In a specimen of arte-
rial blood, drawn while the patient was breathing room
air, the partial pressure of oxygen was 57 mm Hg, the
partial pressure of carbon dioxide 41 mm Hg, and the
pH 7.47. An electrocardiogram revealed a normal
rhythm at a rate of 84, with evidence of left atrial en-
largement, and was otherwise normal. Radiographs of
Vol. 332 No. 2 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL
Figure 2. CT Images of the Chest Obtained 2 1⁄ 2 Weeks before
Admission, with Enhancement after the Intravenous Injection of
Contrast Material.
Contrast enhancement shows that the mass in the left main
bronchus has enlarged; the left lung is collapsed (top). The mass
is nodular, extending into the distal trachea; an enlarged aorto-
pulmonic lymph node is visible (bottom).
the chest disclosed a smooth, well-defined mass, 2.5 by
2 cm, in the distal trachea, with complete collapse of
the left lung; the left main bronchus and lobar bronchi
were not visible, probably because of obstruction by the
mass; the heart and mediastinum were shifted to the
left; the right lung was hyperinflated and clear.
A diagnostic procedure was performed.
DIFFERENTIAL DIAGNOSIS
DR. JOSEPH LOCICERO III*: May we review the ra-
diologic findings?
DR. JO-ANNE O. SHEPARD: Images from the CT scan
of the chest obtained 21/2 years before admission (Fig.
1) show a well-circumscribed, nodular soft-tissue mass
protruding into the lumen of the distal trachea laterally
and posteriorly and extending into the mediastinal fat.
An oval intraluminal mass with peripheral stippled cal-
*Chief, general thoracic surgery, and codirector, Surgical Intensive Care Unit,
New England Deaconess Hospital; associate professor of surgery, Harvard Med-
ical School.
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Copyright © 1995 Massachusetts Medical Society. All rights reserved.
111
cifications is visible at the level of the left main bron-
chus, with a partial collapse of the left lung. A CT scan
with intravenous contrast material, obtained 21/2 weeks
before admission (Fig. 2), shows a polypoid mass in the
distal trachea, with extension into the adjacent medias-
tinal fat. The left main bronchus is occluded by the
mass, which had increased in size since the earlier CT
study and appears enhanced with contrast material;
the left lung is totally collapsed. Representative radio-
graphs of the chest obtained on admission show the
mass in the distal trachea and the left main bronchus,
with distal complete collapse of the lung.
DR. LOCICERO: In summary, this elderly man had a
long-standing history of a slowly growing intraluminal
tumor in the distal trachea and left main bronchus. He
had had multiple bouts of pneumonia, culminating in
total collapse of the left lung. The only laboratory
abnormality was normocytic anemia, consistent with
chronic disease. The radiographs showed a slowly
growing, well-circumscribed mass with peripheral stip-
pled calcifications.
Masses in the airway can be benign or malignant.1
The 22-year duration of the lesion in this case does not
rule out the diagnosis of a malignant tumor.
Most lung cancers are bronchogenic, such as squa-
mous-cell carcinoma and adenocarcinoma.2 These tu-
mors typically double in size in 100 to 150 days, a rate
of growth more rapid than that of this patient’s tumor.
In addition, the average five-year survival of patients
with lung cancer is 12 to 25 percent. With time, most
lung carcinomas metastasize to regional lymph nodes
and subsequently to other organs. This patient had no
evidence of metastasis.
Several less-common malignant tumors have to be
considered in this case. Three in particular are adenoid
cystic carcinoma, previously known as cylindroma,
low-grade mucoepidermoid carcinoma, and chondro-
sarcoma. Adenoid cystic carcinoma is a low-grade ma-
lignant tumor originating in the bronchial gland3 that
can occur up to the age of 65 years.4 It usually forms
an annular mass or an ill-defined nodule in the bron-
chial tree. Histologic examination shows an infiltrative
pattern, and the patients often present with secondary
obstructive symptoms. Calcification is usually not a
feature of an adenoid cystic carcinoma. After complete
resection, the five-year survival rate is approximately
80 percent. Mucoepidermoid carcinoma is a rare, usu-
ally low-grade tumor of bronchial-epithelial origin. It
may occur at any age, ranges in diameter from a few
millimeters to 6 cm, does not calcify,5 and tends to in-
filtrate surrounding tissue. If the tumor is of low grade
the prognosis is excellent, but if it is of high grade the
outlook is very poor.6 Chondrosarcoma is an unusual
pulmonary tumor, which rarely calcifies and tends to
infiltrate surrounding tissue, although it is associated
with an excellent prognosis.7 The absence of evidence
of infiltration of the tumor in the case under discussion,
as well as the presence of calcification, which does not
occur in mucoepidermoid and adenoid cystic carcino-
mas and is rare in chondrosarcomas, makes these tu-
mors improbable in this case.
112 THE NEW ENGLAND JOURNAL OF MEDICINE
A benign lesion of the tracheobronchial tree is a
more likely diagnosis. Benign lesions to be considered
include neoplasms and nonneoplastic lesions, both in-
fectious and noninfectious. Granulomatous infections,
such as tuberculosis and histoplasmosis, often produce
enlarged, calcified lymph nodes and are the most com-
mon types of infection that present as masses in the
airway. Several features, however, make these diag-
noses improbable in this case. Granulomatous infec-
tions usually result in calcification in many lymph-node
groups, which is easily detectable on a CT scan, where-
as only one calcified mass was found in this patient.
Moreover, granulomatous infectious lesions arise out-
side the bronchus and tend to erode into the lumen,
causing hemoptysis. Finally, patients with intraluminal
granulomatous disease often cough up small calcified
lymph nodes, known as broncholiths. The patient un-
der discussion did not have any of these manifestations.
Of the noninfectious tumorlike lesions of the lung,
amyloidosis is the most likely to occur in the airway.8
This lesion may be associated with systemic amyloido-
sis.9,10 Tracheobronchial amyloidosis enlarges slowly
and may present with recurrent pneumonia and ate-
lectasis, but usually the patients have no pulmonary
symptoms.11 The lesion occurs in a wide range of age
groups but is most common in the fourth decade, un-
like the nodular pulmonary form of amyloidosis, which
presents in the sixth decade. Tracheobronchial amyloi-
dosis may form nodules 1 to 4 cm in diameter and may
be characterized by stippled calcification. The airway
itself is often thickened, and the mucosa is eroded. The
CT scan in this patient showed no thickening of the tra-
chea or bronchus around the lesion. In addition, labo-
ratory tests showed no abnormalities of liver or kidney
function that might suggest systemic amyloidosis.
Several other non-neoplastic, noninfectious lesions
that are less likely to present in this manner deserve
mention. Plasma-cell granuloma, known variously as
inflammatory pseudotumor, histiocytoma, endothelio-
ma, and fibromyxoma, usually presents with hemopty-
sis and a parenchymal mass. Bahadori and Liebow12
described 40 cases of plasma-cell granuloma; the le-
sions arise most commonly in the lower lobes, surround
and obstruct small bronchi, and often calcify. Scleros-
ing hemangiomas, also known as xanthomas or histio-
cytomas, are well-demarcated lesions, usually in the
lower lobes, with large areas of hemorrhage.13 The pa-
tient under discussion had no history of hemoptysis.
Castleman’s disease, or giant lymphoid hyperplasia
of the hyaline-vascular type, may present as a large
central mass in the chest and can involve any lymph-
node group.14 CT scanning is most helpful diagnosti-
cally, because the giant lymph nodes are well demar-
cated and separate from vascular structures but are
enhanced readily with contrast material because of
their rich blood supply. They are often associated with
enlargement of nearby lymph nodes.
The final category of intraluminal lesions is that of
benign neoplasms. There is a wide variety of such le-
sions. Almost any cell line of epithelial, endothelial, or
mesenchymal origin can produce a tumor of the air-
way. I shall concentrate on the three most likely to be
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Copyright © 1995 Massachusetts Medical Society. All rights reserved.
Jan. 12, 1995
characterized by the constellation of findings in this
case: carcinoid tumor, hamartoma, and leiomyoma.
Carcinoid tumor, which was the working diagnosis in
this case, was first described in 188215 and was
classified as a bronchial adenoma16 in 1930. Over the
years the term “adenoma” has been applied to several
other tumors of the airways, making the nomenclature
confusing.17 Therefore, this term has been dropped as
a designation for carcinoid tumors. These tumors orig-
inate from neuroendocrine Kulchitsky’s cells and
present as slowly enlarging lesions.18 They infiltrate
bronchial cartilage and may grow in a dumbbell shape,
presenting as intraluminal or extraluminal lesions.
They may be focally calcified. In a series of 124 patients
at the Memorial Sloan-Kettering Cancer Center,19 only
1 presented with manifestations of the carcinoid syn-
drome. The rarity of this association was confirmed by
a report on a series at the Mayo Clinic.20 Patients with
carcinoid tumors present more commonly with Cush-
ing’s syndrome than with the carcinoid syndrome be-
cause of the secretion of corticotropin by the tumor
cells.21-23 This patient had no symptoms of Cushing’s
syndrome. Reports over the years have suggested that
a biopsy of a carcinoid tumor is unsafe because of the
potential for hemorrhage. However, Paulson and Gins-
berg24 have pointed out that with a careful technique
and use of laser or electrocautery, bleeding can easily
be controlled, and a biopsy can be successfully per-
formed with a minimum of complications.
A hamartoma is the most common benign tumor of
the lung, found in a quarter of all autopsies.25,26 The le-
sion may occur at any age and grows slowly, at a rate
of 1 to 10 mm a year. It is nearly always calcified, with
a stippled or “popcorn” appearance, which is demon-
strated best by standard tomograms of the trachea. A
CT scan can be helpful, particularly if it shows a low
Hounsfield number within the lesion, indicating the
presence of fat. This tumor is diagnosed and managed
by excision. Dr. Shepard, do you have any information
on the attenuation of the lesion in this case?
DR. SHEPARD: The attenuation was not measured,
but there were no low-density areas suggesting fat.
DR. LOCICERO: Leiomyomas usually occur in the
airway but may arise peripherally in the parenchyma
as well.27 Patients with these tumors commonly present
with cough, hemoptysis, or pneumonia.28,29 Pulmonary
leiomyomas rarely contain calcium.
On the basis of the presentation, chronicity, and ra-
diologic appearance of this lesion, it was probably be-
nign. The normocytic anemia is most compatible with
an inflammatory process, including a chronic infection;
the patient had recurrent pneumonia over the years
and evidence of long-standing atelectasis, as demon-
strated on the CT scan obtained 21⁄ 2 years before ad-
mission. Wintrobe’s textbook of hematology30 lists in-
fection (specifically, pulmonary infection) as a common
cause of anemia associated with chronic disease.
This patient’s lesion was partially inside and partial-
ly outside the tracheal and bronchial lumens and was
the site of stippled calcification. There was no area of
hypodensity indicating the presence of fat, and the le-
sion enlarged slowly, doubling in roughly 900 days, with
Vol. 332 No. 2 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 113

a growth rate of 0.5 mm per year. The best method of

establishing the diagnosis would have been a biopsy,
which could have been performed safely regardless of
the nature of the lesion. The least invasive approach
would have been endoscopic curettage of the lesion. If
the patient consented to a thoracotomy, a cure could
have been achieved by excision of the lesion and re-
anastomosis of adjacent normal bronchus.
In conclusion, the prompt enhancement of this lesion
on CT scanning and its very slow growth lead me to
suspect that the diagnosis was Castleman’s disease.
DR. EUGENE J. MARK: What diagnostic or therapeu-
tic procedure would you have undertaken at that point?
DR. LOCICERO: The patient had refused thoracoto-
my in the past. In my experience involved lymph nodes
in patients with Castleman’s disease can bleed consid-
erably. Bronchoscopic biopsy would have been difficult.
I would have recommended a thoracotomy for both di-
agnosis and treatment.
DR. MARK: Dr. Wright, what was your diagnosis?
DR. CAMERON D. WRIGHT: In view of the long histo-
ry I favored the diagnosis of a carcinoid tumor. The op-
Figure 3. Endoscopic View of the Smooth, Glistening Pink Mass
tions for therapy included endoscopic débridement of Projecting into the Tracheal Lumen.
the tumor or debulking with laser. Neither of these A prominent vein passes along the surface.
choices was considered appropriate in this case, and
therefore resection was offered and accepted by the
patient. right main bronchus after a frozen-section analysis
showed that the resection margins were uninvolved.
CLINICAL DIAGNOSIS The patient was well after the operation.
Carcinoid tumor of left main bronchus. DR. MARK: The resected mass was 6 cm in length
and solid with rounded ends; it was loosely attached to
DR. JOSEPH LOCICERO III’S DIAGNOSIS the cartilage of the bronchial wall by a membranous
Castleman’s disease. stalk and plugged the bronchial lumen. Sectioning of
the bronchus showed that the lesion virtually occluded
PATHOLOGICAL DISCUSSION the lumen (Fig. 4). There was no ulceration or necrosis.
DR. WRIGHT: Bronchoscopic examination demon-
strated a large, smooth, benign-appearing polypoid tu-
mor arising from the left main bronchus and occluding
approximately 80 percent of the distal tracheal lumen.
The lesion was tannish red and appeared very vascular,
in a pattern compatible with a carcinoid tumor (Fig. 3).
A biopsy was not performed because of the nearly total
occlusion of the trachea and fear that the right trache-
obronchial tree would be flooded with blood. The man-
agement of the patient’s care would not have been
changed by an endoscopic biopsy, since the lesion ap-
peared to be resectable.
A left-sided thoracotomy was performed, and the
polypoid mass was found to be filling the lumen of the
entire left main bronchus, protruding into the most
proximal portion of both the left-upper-lobe bronchus
and the left-lower-lobe bronchus. The left main bron-
chus was detached at its origin from the trachea, en-
abling us to pull the tumor out of the distal end of the
trachea. The entire left main bronchus was then resect-
ed to the origin of the left-upper-lobe and left-lower-
lobe bronchi. A frozen-section examination led to the
diagnosis of an amyloidoma. Inspection of the left lung
showed that the upper lobe was destroyed by obstruc-
tive pneumonitis and could not be reinflated, and we Figure 4. Cross-Section of the Tumor Occluding the Left Main
therefore resected it. A left carinal pneumonectomy Bronchus, after Fixation in Formalin.
was performed, with reattachment of the trachea to the The surface is tan and solid with pits.
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114 THE NEW ENGLAND JOURNAL OF MEDICINE
Figure 5. Amyloidoma Filling the Lumen and Apposing Bronchial
Cartilage (10).
Microscopical examination revealed an amyloidoma
(Fig. 5). The mass was composed of pale eosinophilic
amyloid, which formed lamellae and spherules and was
stained with Congo red and crystal violet. Multinucle-
ated histiocytes had ingested chunks of amyloid (Fig.
6). Calcium was present in the outer layer of the amy-
loidoma but not in its center.
This case is an example of the tumorous form of
tracheobronchial amyloidosis,11,31-35 which is generally
not associated with diffuse interstitial amyloid deposi-
tion and impairment in the diffusing capacity or re-
strictive lung disease. Nodular tracheobronchial amy-
Figure 6. Two Multinucleated Histiocytes Adjacent to Deposits of
Amyloid (Left and Right) (350).
Plasma cells (middle) are clustered between the amyloid deposits.
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Copyright © 1995 Massachusetts Medical Society. All rights reserved.
Jan. 12, 1995
loidosis and nodular parenchymal amyloidosis in the
lung are viewed as surgical diseases, whereas diffuse al-
veolar septal amyloidosis is regarded as a medical dis-
ease. Because the patient had received a clinical di-
agnosis of carcinoid tumor and because bronchial
carcinoid tumor has been associated with an extensive
amyloid stroma,36 we sectioned the lesion carefully in
search of evidence of a carcinoid tumor but found none.
Calcification or ossification occurs in many cases of
nodular amyloidosis.11,34,35
Deposits of amyloid were present in mediastinal
lymph nodes (Fig. 7) in amounts sufficient to cause the
radiologically detectable nodal enlargement. Mediasti-
nal or hilar lymphadenopathy due to amyloid deposits
can develop in patients who have nodular bronchopul-
monary amyloid tumors without plasma-cell disease37
and in patients with systemic amyloidosis and multiple
myeloma.38
Clusters of 10 to 20 plasma cells were found through-
Figure 7. Lymph Node Expanded by Spherical Deposits of Pink
Amyloid (60).
out the amyloidoma. In nodular pulmonary amyloidosis
the plasma cells produce light chains locally that are
precursors of amyloid with a special affinity for lung
tissue.39,40 Nodular pulmonary amyloidosis is generally
not associated with hypergammaglobulinemia, plasma-
cell dysplasia, multiple myeloma, or lymphoma, but
there are exceptions to every rule.41,42
Dr. Wright, after the diagnosis of amyloidoma was
established, did you investigate the blood or bone mar-
row for abnormal gamma globulins or plasma cells?
DR. WRIGHT: The results of protein electrophoresis,
performed subsequently at the referring institution,
were normal. The patient has been well during the six
months since the operation.
DR. LOCICERO: My initial differential diagnosis was
hamartoma versus amyloidosis, and my resident en-
couraged me to choose the latter. I did not favor this
diagnosis, however, particularly because amyloidosis
tends to infiltrate the wall of the bronchus and trachea
and cause ulceration.
Vol. 332 No. 2 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 115

DR. SHEPARD: Will you comment on the vascularity
of this mass, Dr. Mark, as it appeared radiographically
and during the surgical procedure, in terms of amy-
loidomas in general?
DR. MARK: The amyloidoma was not particularly
vascular, but the blood vessels that we saw were im-
pregnated with amyloid and might not have been able
to constrict well after biopsy. Bronchoscopic biopsy of
an amyloidoma carries a risk of bleeding,35 and bleed-
ing after resection has occasionally been fatal.32,43
ANATOMICAL DIAGNOSIS
Tracheobronchial amyloidoma.
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