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Case Records of the Massachusetts General Hospital

Founded by Richard C. Cabot

Eric S. Rosenberg, M.D., Editor Nancy Lee Harris, M.D., Editor
Jo‑Anne O. Shepard, M.D., Associate Editor Alice M. Cort, M.D., Associate Editor
Sally H. Ebeling, Assistant Editor Emily K. McDonald, Assistant Editor

Case 8-2016: A 71-Year-Old Man

with Recurrent Fevers, Hypoxemia,
and Lung Infiltrates
Kai Saukkonen, M.D., Amita Sharma, M.D., and Eugene J. Mark, M.D.​​

Pr e sen tat ion of C a se

Dr. Jason P. Cooper (Medicine): A 71-year-old man was admitted to this hospital be- From the Departments of Pulmonary and
cause of recurrent fevers, dyspnea, and hypoxemia, with associated fluctuating Critical Care (K.S.), Radiology (A.S.), and
Pathology (E.J.M.), Massachusetts Gen‑
pulmonary infiltrates. eral Hospital, and the Departments of
The patient had reportedly been well until approximately 6 months before this Pulmonary and Critical Care (K.S.), Radi‑
admission, when fatigue, fever, chills, shortness of breath, and erythema in the ology (A.S.), and Pathology (E.J.M.), Har‑
vard Medical School — both in Boston.
right leg developed. He was admitted to another hospital. A chest radiograph
showed band atelectasis in the left lower lobe. Computed tomography (CT) of the N Engl J Med 2016;374:1077-85.
DOI: 10.1056/NEJMcpc1505680
chest that was performed on the same day revealed multifocal bilateral ground- Copyright © 2016 Massachusetts Medical Society.
glass opacities throughout the lungs, consolidation in the lingula and lower lobes,
and enlarged mediastinal lymph nodes. A diagnosis of cellulitis of the right leg
was reportedly made. Therapy with doxycycline and cefazolin was begun; the pa-
tient’s condition improved, and he was discharged home with a plan to continue
a 7-day course of the antibiotic agents.
During the next 6 months, multiple episodes occurred that consisted of fatigue
and decreased appetite, followed by chills, severe weakness, dyspnea, fevers (to a
temperature of 39.4°C), and hypoxemia. During that time, the patient was admitted
at least six additional times to two different hospitals. Multiple CT scans of the
chest, the most recent of which had been obtained 6 weeks before this admission,
showed improvement of the air-space opacities in the lower lobes but persistence
of the upper-zone ground-glass opacities. Antibiotics were administered during
the episodes, and symptoms improved within 1 to 4 days; without the administra-
tion of glucocorticoids, the patient’s condition returned to baseline within 8 days.
No infectious causes were identified. Bronchoscopic examination with broncho­
alveolar lavage (BAL) was performed 3.5 months before this admission, and the
BAL fluid reportedly contained 30% neutrophils, 24% lymphocytes, 32% macro-
phages, and 2% eosinophils; microbiologic testing and cytologic examination were
negative. Results of transthoracic echocardiography were normal, and a videofluo-
roscopic swallowing study revealed mild oropharyngeal dysphagia that cleared
with spontaneous subsequent swallows. A diagnosis of possible hypersensitivity
pneumonitis was made.

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 The n e w e ng l a n d j o u r na l of m e dic i n e

Table 1. Laboratory Data.*

5.5 Wk before 3 Wk before

Reference Range, Admission, Admission, On Admission,
Variable Adults† Third Hospital Third Hospital This Hospital
Hematocrit (%) 41.0–53.0 (men) 32.6 38.2 38.3
Hemoglobin (g/dl) 13.5–17.5 (men) 10.7 12.5 12.2
White-cell count (per mm3) 4500–11,000 6230 15,120 17,900
Differential count (%)
Neutrophils 40–70 68.6 90.4 92.4
Lymphocytes 22–44 18.0 4.7 3.2
Monocytes 4–11 8.5 4.6 3.6
Eosinophils 0–8 4.7 (ref 0 to 5) 0.1 0.3
Basophils 0–3 0.2 0.2 0.2
Erythrocyte sedimentation rate (mm/hr) 80 (ref 0 to 12) 62 (ref 0 to 12)
Reticulocyte count (%) 0.5–2.5 0.9
Glucose (mg/dl) 70–110 95 119 119
Total protein (g/dl) 6.0–8.3 5.8
Phosphorus (mg/dl) 2.6–4.5 2.0 1.1
Magnesium (mg/dl) 1.7–2.4 1.5 1.6
C-reactive protein (mg/liter) <8.0 85.8 70.7
Haptoglobin (mg/dl) 16–199 246
Iron (μg/dl) 45–160 20
Iron-binding capacity (μg/dl) 230–404 218
Angiotensin-converting enzyme (U/liter) 8–53 63
25-Hydroxyvitamin D (ng/ml) >32 desired 29
1,25-Dihydroxyvitamin D (pg/ml) 18–64 69
Venous blood gases
Oxygen supplementation Not specified Ambient air
pH 7.30–7.40 7.43 7.43
Partial pressure of carbon dioxide 38–50 39 46
(mm Hg)
Partial pressure of oxygen (mm Hg) 35–50 57 <29
Base excess (mmol/liter) 1 (ref −3 to 3) 4.6

* The term ref denotes the reference range at the third hospital. To convert the values for glucose to millimoles per liter,
multiply by 0.05551. To convert the values for phosphorus to millimoles per liter, multiply by 0.3229. To convert the val‑
ues for magnesium to millimoles per liter, multiply by 0.4114. To convert the values for iron and iron-binding capacity
to micromoles per liter, multiply by 0.1791. To convert the values for 25-hydroxyvitamin D to nanomoles per liter, multi‑
ply by 2.496.
† Reference values are affected by many variables, including the patient population and the laboratory methods used. The
ranges used at Massachusetts General Hospital are for adults who are not pregnant and do not have medical conditions
that could affect the results. They may therefore not be appropriate for all patients.

Approximately 5 weeks before this admission,
the patient was discharged from one hospital
and admitted on the same day to a third hospital
for further evaluation. Blood levels of N-termi-
nal pro–B-type natriuretic peptide (NT-proBNP)
and thyrotropin were normal; serum testing for
galactomannan, 1,3-β-d-glucan, and antibodies
to strongyloides was negative. Other test results
are shown in Table 1. Blood and urine cultures
were sterile. CT of the sinuses revealed moderate

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 Case Records of the Massachuset ts Gener al Hospital
opacification in the left maxillary sinus and left
infundibular obstruction. On the fourth day, the
percentage of eosinophils in the peripheral
blood rose to 5.9% (reference range, 0 to 5), with
an absolute eosinophil count of 320 per cubic
millimeter. No ova or parasites were seen in a
stool specimen. A diagnosis of hypersensitivity
pneumonitis was considered.
After discharge, the patient moved into a
hotel. However, 3 weeks before this admission,
fevers and dyspnea recurred and he was readmit-
ted to the third hospital. Testing for antineutro-
phil cytoplasmic antibodies, anti-PR3 and anti-
MPO antibodies, antibodies to double-stranded
DNA, and antinuclear antibodies was negative,
as were thick and thin blood smears for para-
sites; blood levels of total tryptase, mature
tryptase, IgG, IgA, IgM, and IgE were normal.
Other test results are shown in Table 1. Blood
cultures were sterile, and results of urine cul-
tures were consistent with contamination. The
next day, combined positron-emission tomogra-
phy and CT revealed widespread bilateral ground-
glass opacities and associated peribronchiolar
consolidation predominantly in the lower lobes;
these findings had minimal 18F-fluorodeoxyglu-
cose avidity. Bronchoscopic examination with
BAL was performed, and the BAL fluid con-
tained 58% macrophages, 18% neutrophils, 10%
lymphocytes, 2% monocytes, and 12% eosino-
phils; the fluid also contained 19% CD4+ T lym-
phocytes (reference range, 40 to 58) and 57%
CD8+ T lymphocytes (reference range, 10 to 40),
with a CD4:CD8 ratio of 0.33 (reference range,
0.56 to 4.27). Polymerase-chain-reaction testing
for adenovirus was negative. No organisms or
malignant cells were seen, and pathological ex-
amination of a transbronchial-biopsy specimen
reportedly showed evidence of acute focal lung
injury (including hyaline membranes), hyperpla-
sia of type II pneumocytes, and mild chronic
interstitial pneumonitis. Surgical lung biopsy
was recommended, and the patient was dis-
charged on the fifth hospital day.
Eighteen days later, the patient and his wife
came to the outpatient pulmonary clinic of this
hospital. He reported the onset of fatigue and
shortness of breath beginning earlier that day
and suspected another episode was beginning.
He reported night sweats, weight loss of 6.4 kg
that he attributed to multiple hospitalizations,
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and no wheezing, cough, chest pain, difficulty
swallowing, or known aspiration. He was not
aware of any precipitating factors. He had hyper-
tension, dyslipidemia, mild psoriasis, venous sta-
sis, and depression. He lived with his wife and
three adult dogs, worked primarily in an office,
and reported no known exposure to asbestos,
birds, reptiles, or hay. He smoked cigars on rare
occasions, previously drank one alcoholic bever-
age per day until he stopped drinking several
months before this presentation, and did not use
illicit drugs. He had traveled to coastal Massa-
chusetts 7 months earlier and had no other re-
cent travel. Medications were atorvastatin, ome­
prazole, and fluoxetine. He was allergic to
cephalosporins (which caused a rash and elevat-
ed aminotransferase levels). There was no family
history of lung or autoimmune disease.
On examination, the patient appeared fatigued
and was shivering. The temperature was 36.4°C,
the blood pressure 148/67 mm Hg, the pulse 89
beats per minute, the respiratory rate 12 breaths
per minute, and the oxygen saturation 96%
while he was breathing ambient air and 99%
while he was breathing oxygen through a nasal
cannula at a rate of 2 liters per minute. The
height was 193 cm, the weight 104.5 kg, and the
body-mass index (the weight in kilograms di-
vided by the square of the height in meters) 28.1.
The chest rose symmetrically, without use of
accessory muscles or wheezing. Sparse crackles
were heard at the right lung base, and 1+ leg
edema was present, without cyanosis or club-
bing. The remainder of the examination was
normal. He was referred to the emergency de-
partment for admission to this hospital.
On examination in the emergency department,
the temperature was 38.9°C, the blood pressure
155/76 mm Hg, the pulse 104 beats per minute,
the respiratory rate 24 breaths per minute, and
the oxygen saturation 93% while the patient was
breathing ambient air. The remainder of the
examination was unchanged. The platelet count,
red-cell indexes, plasma anion gap, and results
of serum electrophoresis and tests of coagula-
tion and renal and liver function were normal,
as were blood levels of electrolytes, calcium, ionic
calcium, albumin, globulin, lactic acid, troponin T,
NT-proBNP, lactate dehydrogenase, ferritin, vita-
min B12, folate, IgG, IgA, and IgM. Other test
results are shown in Table 1. An electrocardio-
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 The n e w e ng l a n d j o u r na l of m e dic i n e

A B

C D

Figure 1. CT Scan of the Chest.

A CT scan of the chest was obtained at the lung‑window setting (Panels A through D). Multiple bilateral ground‑
glass opacities are present throughout the lungs (arrows). Peripheral consolidation is present in the lower lobes
(arrowhead). These findings waxed and waned on subsequent CT scans.

gram revealed sinus tachycardia at a rate of
102 beats per minute. A chest radiograph showed
minor bibasilar patchy opacities, which had im-
proved during the previous 3 weeks.
On the second day, CT of the chest, per-
formed without the administration of intrave-
nous contrast material, revealed improvement in
the bilateral ground-glass opacities in the lower
lobes. The previously noted consolidation had
resolved. Mildly enlarged mediastinal and hilar
lymph nodes had not changed during the previ-
ous 3 months.
The next day, a diagnostic procedure was
performed.
Im aging S t udie s
Dr. Amita Sharma: Multiple CT scans of the chest
show dependent consolidation in the lower lobes Dr. Kai Saukkonen: I am aware of this patient’s
and diffuse bilateral nondependent ground-glass diagnosis, although I did not participate in his
opacities that waxed and waned over a period of
6 months (Fig. 1). These findings may be seen
with episodic aspiration pneumonitis and super-
imposed aspiration pneumonia. The differential
diagnosis of chronic peripheral consolidation
includes organizing pneumonia, chronic eosino-
philic pneumonia, sarcoidosis, and cancer, includ-
ing lymphoma and adenocarcinoma; however,
diffuse ground-glass opacities would be unusual
in patients with these conditions. Chronic diffuse
ground-glass opacities can be seen in patients
with hypersensitivity pneumonitis or desquama-
tive interstitial pneumonia; however, dependent
consolidation is not typical in patients with these
entities.
Differ en t i a l Di agnosis

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 Case Records of the Massachuset ts Gener al Hospital

care. This 71-year-old man presented with a
6-month history of episodes of intermittent
fatigue, decreased appetite, fever, dyspnea, hy-
poxemia, pulmonary infiltrates, and elevated
inflammatory markers that typically resolved
within 8 days, usually after the administration
of antibiotics and without the administration of
systemic glucocorticoids. There were no definite
inciting events or environmental exposures and
no clearly effective interventions. The recurring
nature of his pulmonary infiltrates is consistent
with congestive heart failure, recurrent aspira-
tion, recurrent pneumonia, or one of the many
kinds of interstitial lung diseases, including those * Data are adapted from Ryerson and Collard.
Table 2. Underlying Causes of Interstitial Lung Diseases.*
Disorders related to occupational, avocational, environmental, or medication
exposures (e.g., hypersensitivity pneumonitis)
Connective-tissue diseases (e.g., scleroderma, rheumatoid arthritis, dermato‑
myositis, polymyositis, Sjögren’s disease)
Sarcoidosis
Idiopathic causes (e.g., idiopathic pulmonary fibrosis, nonspecific interstitial
pneumonitis, respiratory bronchiolitis–associated interstitial lung disease,
desquamative interstitial pneumonitis, cryptogenic organizing pneumonia,
acute interstitial pneumonitis)
Other causes (vasculitis, diffuse alveolar hemorrhage, Langerhans’-cell histio‑
cytosis, chronic eosinophilic pneumonia, lymphangioleiomyomatosis)
3

that might involve alveolar hemorrhage. How-

ever, this patient’s history and imaging studies
of the chest are not consistent with any of these does not rule out this diagnosis. However, blood
entities except interstitial lung diseases. tests for anti-PR3 and anti-MPO antibodies were
negative, and no blood was reportedly present
Interstitial Lung Diseases in the BAL fluid; therefore, vasculitis-associated
Interstitial (or diffuse parenchymal) lung dis- alveolar hemorrhage is unlikely.
eases are a group of disorders characterized by The diagnoses that are most consistent with
various types of inflammation and fibrosis, and this patient’s presentation are hypersensitivity
the diagnosis is best approached by a multidisci- pneumonitis, cryptogenic organizing pneumo-
plinary team. A surgical biopsy may be required nia, and chronic eosinophilic pneumonia. All
if it becomes clinically important to establish a these entities may have a waxing and waning
firm diagnosis.1,2 Interstitial lung diseases may clinical course and are associated with findings
be categorized on the basis of their underlying on imaging studies similar to those seen in this
causes, such as exposure-related disorders (in- patient.
cluding hypersensitivity pneumonitis), connective-
tissue diseases, sarcoidosis, and idiopathic and Hypersensitivity Pneumonitis
other causes (Table 2).3 Hypersensitivity pneumonitis is caused by an
Several connective-tissue diseases — includ- immune response to inhaled proteins.4 Affected
ing scleroderma, rheumatoid arthritis, dermato- patients typically present with dyspnea and
myositis, polymyositis, and Sjögren’s disease — cough, which may be acute, subacute, or chron-
may be associated with interstitial lung diseases, ic.5 There is a long list of descriptively named
but this patient’s clinical course and laboratory entities that are associated with specific expo-
findings are not consistent with these diagnoses. sures to fungal or bacterial proteins, including
Sarcoidosis is unlikely because of the rapidly farmer’s lung, bird-fancier’s lung, hot-tub lung,
relapsing and remitting nature of the pulmonary and shower-curtain disease.4
infiltrates, the atypical findings on imaging This patient’s history suggests acute exposure-
studies, and the absence of noncaseating granu- related hypersensitivity pneumonitis, since his
lomas on examination of the transbronchial- condition seemed to rapidly improve when he
biopsy specimens. was in the hospital, presumably after he was
Most idiopathic and other interstitial lung dis- removed from exposure to the unidentified of-
eases have a gradually progressive course, with fending agent. The absence of any known suspi-
patterns on imaging studies that differ from the cious occupational, avocational, or medication
waxing and waning peripheral ground-glass exposures does not rule out the diagnosis of
opacities that were seen in this patient. Alveolar hypersensitivity pneumonitis.5 However, the pa-
hemorrhage can have an intermittent course, tient had a relapse when he stayed in a hotel,
and the absence of hemoptysis in this patient suggesting either that he was exposed to the

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 The n e w e ng l a n d j o u r na l
offending agent while he was at the hotel or that
the diagnosis is not related to exposure.
The nodules and ground-glass opacities that
were seen on multiple imaging studies are con-
sistent with hypersensitivity pneumonitis; patients
with this diagnosis may have ground-glass opac-
ities, nodules, air trapping, reticular changes,
and in chronic cases, fibrosis. Blood testing
with a panel for hypersensitivity pneumonitis
(which detects precipitating IgG antibodies to a
variety of environmental antigens) is of unclear
value, because false positive and false negative
results commonly occur. Pathological examina-
tion of lung-biopsy specimens shows evidence
of bronchiolocentric granulomatous lymphocytic
alveolitis, which can progress to fibrosis.4
Treatment of hypersensitivity pneumonitis in-
cludes removing the patient from exposure to the
offending agent, if it can be identified. Therapy
with a tapered course of glucocorticoids over a
period of several months is typically prescribed
if the symptoms are severe enough to warrant
treatment.4
This patient had symptoms that resolved on
hospitalization, thus suggesting that removal
from exposure resulted in improvement. In addi-
tion, the BAL fluid contained less than 40%
lymphocytes and the CD4:CD8 ratio was low;
both of these findings are consistent with a diag-
nosis of cryptogenic organizing pneumonia or
hypersensitivity pneumonitis. However, the pa-
tient had no known exposures and his symptoms
recurred after he moved into a hotel; these fea-
tures are not consistent with an exposure-related
diagnosis, unless repeated exposure resulted in
persistent inflammation.
Organizing Pneumonia
Patients with organizing pneumonia typically
present with several weeks of prodromal consti-
tutional symptoms, followed by the abrupt onset
of cough and dyspnea. Imaging studies show
patchy migratory pulmonary infiltrates, possibly
with ground-glass opacities and consolidation
with air bronchograms. Pathological evaluation
of an affected lung shows inflammation around
small airways and plugs of granulation tissue
filling these airways.6
Organizing pneumonia can be a primary
phenomenon or it can be secondary to other
processes, including drug reactions, cocaine use,
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of m e dic i n e
collagen vascular diseases, hypersensitivity pneu-
monitis, infection, cancer, organ transplantation,
infarcts, tumors, necrotizing granulomas, radia-
tion therapy, toxic-fume exposure, and smoke
inhalation.6 The treatment for organizing pneu-
monia is glucocorticoid therapy that is often
administered for at least 1 year.
This patient had an indolent disease with
ground-glass opacities, and the BAL fluid had a
low CD4:CD8 ratio; these features are consistent
with a diagnosis of cryptogenic organizing pneu-
monia. However, organizing pneumonia would
not relapse and then spontaneously wane in the
absence of therapy.
Chronic Eosinophilic Pneumonia
There are several eosinophilic lung disorders,
including chronic eosinophilic pneumonia, acute
eosinophilic pneumonia, eosinophilic granulo-
matosis with polyangiitis (formerly known as the
Churg–Strauss syndrome), the hypereosinophilic
syndrome, and eosinophilia associated with one
of many other disorders.7 The features of this
patient’s clinical presentation are consistent with
chronic eosinophilic pneumonia but not with the
other eosinophilic disorders. Chronic eosino-
philic pneumonia tends to occur in nonsmoking
women who are in their 40s, and features of the
presentation include an indolent cough, dyspnea,
fever, and migratory pulmonary infiltrates.7 Af-
fected patients typically have eosinophilia in
peripheral blood and in BAL fluid. Inflamma-
tory markers in the peripheral blood may be ele-
vated. It is important to rule out other causes of
eosinophilia.7 Chronic eosinophilic pneumonia
generally does not resolve spontaneously but does
respond quickly to glucocorticoids.7
This patient had an indolent clinical presenta-
tion characterized by pulmonary infiltrates and
elevated inflammatory markers. However, he is
not a middle-aged woman, his lungs had spon-
taneous improvement without glucocorticoid
therapy, and there was a paucity of eosinophils
in the BAL fluid and peripheral blood.
Diagnostic Approach
The indolent nature of this patient’s illness al-
lowed his doctors to perform a stepwise evalu-
ation that proceeded from the least invasive
assessment to more invasive investigations, and
ultimately led to transbronchial biopsy. Trans-
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 Case Records of the Massachuset ts Gener al Hospital
bronchial biopsy may be diagnostic, especially in
patients with infection, lymphangitic tumor,
sarcoidosis, eosinophilic pneumonia, and pul-
monary alveolar proteinosis. However, the diag-
nostic yield of transbronchial biopsy is often
limited by inadequate sample size of alveolar
tissue and by crush artifact. In addition, a small
sample may not indicate the full scope of patho-
logical features that would be present in a larger
sample of lung tissue, particularly in a patient
with interstitial lung disease. In this case, trans-
bronchial biopsy did not yield the diagnosis.
Lung biopsy by means of video-assisted tho-
racic surgery (VATS), an approach that has mostly
supplanted thoracotomy and minithoracotomy
for this purpose, yields a larger sample of lung
tissue than does transbronchial biopsy, thus en-
abling the pathologist to see a wider area of the
lung architecture, with less crush artifact. The
procedure has a low risk of complications, and
therefore it is often the preferred method of lung
biopsy for interstitial lung diseases.2
Results of lung biopsy have been shown to
alter the management of nonspecific interstitial
pneumonitis, usual interstitial pneumonitis, acute
interstitial pneumonitis, honeycomb lung, orga-
nizing pneumonia, eosinophilic pneumonia, cap-
illaritis, granulomatosis with polyangiitis, and
sarcoidosis.8 I would recommend a lung biopsy
by means of VATS in this otherwise healthy man
who has a recurrent lung disease that appears to
be one of several plausible interstitial lung dis-
eases, each with a different prognosis and ap-
proach to management.
Dr . K a i S auk konen’s Di agnosis
Interstitial lung disease (hypersensitivity pneu-
monitis, cryptogenic organizing pneumonia, or
chronic eosinophilic pneumonia).
Pathol o gic a l Discussion
Dr. Eugene J. Mark: The patient underwent a thora-
coscopic lung biopsy. Three biopsy specimens
were obtained from the right lung: one each
from the upper lobe, the middle lobe, and the
lower lobe. On histopathological examination of
the frozen sections, some lobules of lung had
alveolar filling with histiocytes. Some alveoli
contained scattered eosinophils amid the histio-
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cytes, and other alveoli contained large numbers
of eosinophils that accounted for up to 10% of
the cells. Eosinophils could also be found in the
interstitium around blood vessels (Fig. 2A and
2B). The three biopsy specimens were relatively
similar. In the specimen from the right lower
lobe, a small degree of interstitial fibrosis with
architectural simplification was present (Fig. 2C
and 2D).
An intraoperative diagnosis of alveolar filling
with histiocytes was made, thus suggesting an
overall diagnosis of chronic eosinophilic pneu-
monia. The diagnosis of alveolar filling with
histiocytes was also made on examination of
permanent sections.
Chronic eosinophilic pneumonia can be its
own diagnosis, but it is sometimes considered to
be a facet of bronchiolitis obliterans organizing
pneumonia. In this case, a bronchiolar component
was not present, and therefore a diagnosis of
chronic eosinophilic pneumonia alone is a better
fit. Also, the fibrin or hyaline membranes that
might be observed in patients with acute eosino-
philic pneumonia were not present in this case.
Chronic eosinophilic pneumonia is associated
with a specific histologic pattern, but a specific
cause of this pattern is not usually identified.
Underlying asthma or colonization or infection
with aspergillus are some possibilities. Drug
reaction and vasculitis are other possibilities. A
moderate degree of histiocytic and eosinophilic
inflammation was seen in this case, and greater
degrees of cellularity are seen in other examples
of chronic eosinophilic pneumonia.
Dr. Nancy Lee Harris (Pathology): Dr. Cooper,
would you tell us what happened with this pa-
tient?
Dr. Cooper: After the diagnosis of chronic
eosinophilic pneumonia was confirmed, gluco-
corticoid therapy (prednisone, 40 mg daily) and
appropriate gastrointestinal and infectious pro-
phylaxis were administered. The patient was
discharged home on the seventh hospital day.
Six months after discharge, the patient had not
had a recurrence of the acute episodes, was
gaining weight, and had normal oxygen satura-
tion while he was breathing ambient air. He felt
that he still had decreased exercise tolerance but
that it was improving. Chest radiography was
stable, and pulmonary-function tests suggested
only a mild restrictive defect. The dosage of glu-
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 The n e w e ng l a n d j o u r na l of m e dic i n e

A B

C D

Figure 2. Lung-Biopsy Specimens (Hematoxylin and Eosin).

Panel A shows alveolar filling with a histiocytic and eosinophilic infiltrate (oval). Panel B shows interstitial inflam‑
mation, as well as numerous eosinophils (circle). Panel C shows a terminal bronchiole filled with mucus (asterisk)
and scattered eosinophils in the interstitium around the bronchiole. Panel D shows slight interstitial fibrosis (arrows),
which causes moderate alveolar simplification, with rounding of the alveoli.

cocorticoids was gradually tapered to 7.5 mg
daily, with plans to continue the slow reduction.
The erythrocyte sedimentation rate and C-reac-
tive protein level were monitored every 3 months
and remain substantially lower than they were
during his hospitalization.
Dr. Mark: Dr. Sharma, in retrospect, do any
radiographic clues favor the diagnosis of chron-
ic eosinophilic pneumonia?
Dr. Sharma: Chronic eosinophilic pneumonia is
one of the causes of peripheral air-space opaci-
ties, so the consolidation in the lower lobes on
chest CT would be consistent with the diagnosis.
However, in patients with chronic eosinophilic
pneumonia, peripheral air-space opacities are
not typically seen only in the dependent portions
of the lower lobes; they are also seen peripher-
ally, in the nondependent regions of all lobes. The
radiographic differential diagnosis for peripheral
consolidation is quite limited and includes orga-
nizing pneumonia and chronic eosinophilic
pneumonia, as well as rare cases of sarcoidosis,
adenocarcinoma of the lung, and lymphoma.
Although the dependent opacities were atypical,
their peripheral nature is consistent with chron-
ic eosinophilic pneumonia.
Fina l Di agnosis
Recurrent chronic eosinophilic pneumonia.
Presented at the Seventh Annual Thoracic Pathology Course,
“Thoracic Pathology with Clinical Correlation” (held on Septem-
ber 13–15, 2014, and directed by Eugene J. Mark, M.D., and Wil-
liam D. Travis, M.D.).
Dr. Mark reports providing expert legal testimony on behalf
of patients who believe they have been injured by exposure to
asbestos. No other potential conflict of interest relevant to this
article was reported.
Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
We thank Drs. Christopher H. Fanta and Krishna Reddy for
their review of a draft of the case history and participation at the
conference.

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 Case Records of the Massachuset ts Gener al Hospital

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Lantern Slides Updated: Complete PowerPoint Slide Sets from the Clinicopathological Conferences
Any reader of the Journal who uses the Case Records of the Massachusetts General Hospital as a teaching exercise or reference
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shown at the live Clinicopathological Conference (CPC) that is the basis of the Case Record. This slide set contains all of the
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and photomicrographs, as well as unpublished text slides, tables, and diagrams, are included. Every year 40 sets are produced,
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