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is important to note that the metastatic lesions in our
case were discovered only incidentally, the patient
discovering them after undergoing a screening EBCT to
assess his cardiac function. As EBCT is being used more
often to evaluate cardiac function and disease, the
conundrum of lung cancer screening is resurfacing.12
EBCT scans performed as screening procedures have
the ability to provide high-resolution images and often
present us with diagnostic dilemmas: to what extent is it
cost-effective to pursue pulmonary irregularities incidentally discovered on cardiac screening? The findings
of two previous Japanese nonrandomized studies13,14 on
prevalence screening using low-dose CT with sputum
sampling did not demonstrate clear decreases in mortality. A 1999 Mayo Clinic trial and the American
College of Radiology Imaging Network have ongoing
investigations, but no definitive evidence exists as to
whether radiography for screening purposes has any
impact on mortality.15 Our case highlights the efforts
necessary to pursue the diagnosis entailed by the
discoveries made available by these newer modalities;
cost effectiveness remains to be elucidated.
References
1 Inoue N, Shimojyo M, Iwai H, et al. Malignant ameloblastoma with pulmonary metastasis and hypercalcemia. Am J
Clin Pathol 1988; 90:474 – 481
2 Mathew S, Rappaport K, Ali S, et al. Ameloblastoma: cytologic findings and literature review. Acta Cytol 1997; 41:955–
960
3 Newman L, Howells GL, Coghlan KM, et al. Malignant
ameloblastoma revisited. Br J Oral Maxillofac Surg 1995;
35:47–50
4 Clay R, Weiland H, Jackson I. Ameloblastoma metastatic to
the lung. Ann Plast Surg 1989; 22:160 –162
5 Lanham R. Chemotherapy of metastatic ameloblastoma: a
case report and review of the literature. Oncology 1987;
44:133–134
6 Houston G, Davenport W, Keaton W, et al. Malignant
metastatic ameloblastoma case report. J Oral Maxillofac Surg
1993; 51:1152–1155
7 Vorzimer J, Perla D. An instance of adamantinoma of the jaw
with metastases to the right lung. Am J Pathol 1932; 8:445– 453
8 Laughlin E. Metastasizing ameloblastoma. Cancer 1989; 64:
776 –780
9 Sheppard B, Temeck B, Taubenberger J, et al. Pulmonary
metastatic disease in ameloblastoma. Chest 1993; 104:1933–
1935
10 Atkinson CH, Harwood AR, Cummings BJ. A meloblastoma
of the jaw: a reappraisal of the role of megavoltage irradiation.
Cancer 1984; 53:869 – 873
11 Eliasson A, Moser R, Tenholder M. Diagnosis and treatment
of metastatic ameloblastoma. South Med J 1989; 82:1165–
1168
12 Rumberger J, Brundage B, Rader D, et al. Electron beam
computed tomographic coronary calcium scanning: a review
and guidelines for use in asymptomatic persons. Mayo Clin
Proc 1999; 74:243–252
13 Kaneko M, Eguchi K, Ohmatsu H, et al. Peripheral lung
cancer screening and detection with low-dose spiral CT
versus radiography. Radiology 1996; 201:798 – 802
14 Sone S, Takashima S, Li F, et al. Mass screening for lung
cancer with mobile spiral CT scanner. Lancet 1998; 351:
1242–1245
15 Patz E, Goodman P. Current concepts: screening for lung
cancer. N Engl J Med 2000; 343:1627–1633
Venous Dilatation Seen on
Routine Mammography*
A Clue to Superior Vena Cava
Obstruction
Padmanabhan Krishnan, MD, FCCP; Lalith Uragoda, MD;
Hemalatha Rao, MD; and Santi R. Dhar, MD, FCCP
A diagnosis of superior vena cava obstruction
(SVCO) generally is made on clinical grounds and
can be confirmed by SVCO-specific diagnostic tests.
When the obstruction is long-standing, clinical recognition may be compromised as venous drainage of
the head, neck, chest, and upper extremity is diverted via collateral venous channels that bypass the
obstructed superior vena cava. In such situations,
only the visualization of this collateral flow will
suggest the presence of SVCO. We describe a patient
in whom the unanticipated diagnosis of SVCO was
first suggested when routine mammography revealed grossly dilated superficial veins of both
breasts, which were the result of collateral flow.
(CHEST 2002; 121:1361–1363)
Key words: mammogram; radionuclide venography; superior
vena cava obstruction
Abbreviation: SVCO ⫽ superior vena cava obstruction
linical recognition of superior vena cava obstruction
C (SVCO)
rests on the presence of a constellation of
symptoms and signs that result from impaired venous
drainage of the head, neck, chest, and upper extremities. SVCO-specific diagnostic tests such as radionuclide venography, contrast venography, and contrastenhanced chest CT scan can be performed to confirm
the diagnosis of SVCO. Obstruction of the superior vena
cava results in collateral circulation diverted via the
internal mammary, azygos, hemiazygos, lateral thoracic,
thoracoepigastric, and vertebral veins.1 The improvement of venous drainage by collateral flow that bypasses
the obstructed superior vena cava can allow SVCO to
remain unrecognized. If these collateral venous channels are not visualized, SVCO is not suspected and
SVCO-specific diagnostic tests are not performed.
This was the case in our patient in whom chronic SVCO
*From the Departments of Pulmonary Medicine (Drs. Krishnan,
Uragoda, and Dhar) and Nuclear Medicine (Dr. Rao), Coney
Island Hospital, Brooklyn, NY.
Manuscript received May 22, 2001; revision accepted September
5, 2001.
Correspondence to: Padmanabhan Krishnan, MD, FCCP, Associate Director, Department of Pulmonary Medicine, Coney Island
Hospital, 2601 Ocean Pkwy, Brooklyn, NY 11235
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was not recognized until collateral flow was first visualized,
in the form of grossly dilated superficial veins of the
breasts, on routine mammography. A radionuclide superior venacavagram confirmed SVCO.
Case Report
An 80-year-old woman was referred for the evaluation of
possible SVCO after a routine mammogram revealed grossly
dilated superficial veins of the breast (Fig 1). A radionuclide
superior venacavagram (Fig 2) confirmed that the superior vena
cava was obstructed. The superior vena cava was not visualized,
and the collateral venous pathways were outlined clearly in the
form of the internal thoracic vein on the left, the lateral thoracic
vein on the right, and intercostal veins bilaterally.
A review of hospital records indicated that 8 years before,
central venous catheter-induced superior vena cava thrombosis
and obstruction were suspected during a prolonged and complicated postoperative course following resection of a rectal carcinoma. Since that time, the patient had noted facial and upper
Figure 2. A radionuclide superior venacavagram reveals no
visualization of the superior vena cava. Clearly visible is the
collateral flow via the lateral thoracic vein (oriented vertically on
the right, small arrow), the internal thoracic vein (oriented
vertically on the left, large arrow), and the intercostal veins
(oriented horizontally on both sides, arrowheads).
arm swelling, headaches in the supine position, and exertional
dyspnea, all of which had decreased over the years.
An examination of the patient following the mammographic
findings of venous dilatation revealed no facial or upper
extremity swelling. The jugular veins were not distended and
a few dilated veins were present over the upper anterior chest
wall. The chest radiograph revealed no lung or mediastinal
masses. The patient was thought to have chronic SVCO as a
result of the thrombotic occlusion of the superior vena cava
that had been induced by central venous catheter placement in
the past.
Discussion
Figure 1. A mammogram reveals the dilated superficial veins of
the breast.
Evidence of impaired venous drainage of the head,
neck, chest, and upper extremities leads to the recognition
of SVCO. Symptoms include dyspnea, headache, visual
disturbances, epistaxis, hoarseness, dizziness, syncope,
tongue swelling, and hemoptysis. Recumbency or bending
over can exacerbate these symptoms. Physical signs include swelling of the face and upper extremities, jugular
venous distension, facial plethora, chest or shoulder swelling, distended thoracic veins, proptosis, glossal or laryngeal edema, conjunctival suffusion, mental status change,
impaired visual acuity, and Horner syndrome.2
Bronchogenic carcinoma remains the most common
cause of SVCO. Benign causes include superior vena cava
thrombosis and fibrosis following the insertion of central
venous catheters, mediastinitis and fibrosis secondary to
histoplasmosis and tuberculosis, and benign intrathoracic
mass lesions.3
In acute SVCO, the presence of symptoms and signs of
impaired venous drainage of the superior vena cava territory makes the diagnosis obvious. In patients with longstanding SVCOs, the development of collateral venous
pathways can allow the SVCO to go unrecognized. These
collateral pathways provide venous drainage to the head,
neck, chest, and upper extremities, and they empty into
the azygos vein and inferior vena cava. These pathways
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Selected Reports
include the following: the internal thoracic-superior-inferior epigastric veins on the left; the lateral thoracicsuperficial epigastric veins on the right; the anterior and
posterior intercostal veins; the azygos-accessory hemiazygos-hemiazygos veins; the jugular veins; the vertebral
plexus; and the small tributaries of the thoracoabdominal
wall and the breast.4,5 On radionuclide venography, the
lateral thoracic veins, the internal thoracic veins, the
accessory hemiazygos veins, and the azygos veins can be
seen running vertically (with the latter two veins being
medially located), while the intercostal veins run horizontally.4 The superficial collateral flow via the small tributaries of the chest wall can be visualized on chest inspection
and by contrast chest CT scan as dilated veins over the
anterior chest wall. Dilated superficial veins of the breast
that provide collateral flow have been visualized by mammography.5
In this patient, we have described the presence of
dilated superficial veins of the breast, which were first
noted on routine mammography, served to alert the
physician to a possible SVCO. As a result, a radionuclide
superior venacavagram was performed, and the diagnosis
of SVCO was established.
In patients with chronic SVCO, the development of
collateral venous pathways that bypass the obstructed
superior vena cava can make SVCO clinically occult. In
such cases, only the visualization of these collateral pathways will suggest the unanticipated diagnosis of SVCO.
Our experience is unique in that a routine mammogram
served this purpose.
References
1 Yedlicka JW Jr, Cormier MG, Gray R, et al. Computed
tomography of superior vena cava obstruction. J Thorac
Imaging 1987; 2:72–78
2 Chen JC, Bongard F, Klein SR. A contemporary perspective on
superior vena cava syndrome. Am J Surg 1990; 160:207–211
3 Strimlan CV. Superior vena cava syndrome [letter]. Cleve
Clin J Med 1992; 59:356
4 Sy WM, Lao RS. Collateral pathways in superior vena cava
obstruction as seen on gamma images. Br J Radiol 1982;
55:294 –300
5 Jackson VP, Jahan R, Yao S, et al. Benign breast lesions. In:
Bassett LW, Jackson VP, eds. Diagnosis of disease of the
breast. Philadelphia, PA: WB Saunders, 1997; 36
Pamidronate Results in
Symptom Control of
Hypertrophic Pulmonary
Osteoarthropathy in Cystic
Fibrosis*
Luke A. Garske, MBBS; and Scott C. Bell, MD
Hypertrophic pulmonary osteoarthropathy (HPOA)
may complicate the advanced lung disease that is
associated with cystic fibrosis, resulting in severe
joint pain and early-morning stiffness. Symptoms are
usually controlled with the administration of nonsteroidal anti-inflammatory drugs, physiotherapy, and,
on occasions, oral corticosteroids. This report describes a case of refractory HPOA with complete
remission following the administration of IV pamidronate, which is a potent inhibitor of osteoclastic
bone resorption. Symptom relief resulted for up to 3
months, but repeated courses of pamidronate have
been required to maintain symptom control.
(CHEST 2002; 121:1363–1364)
Key words: biphosphonates; cystic fibrosis; hypertrophic pulmonary osteoarthropathy; pamidronate
Abbreviations: CF ⫽ cystic fibrosis; HPOA ⫽ hypertrophic
pulmonary osteoarthropathy; NSAID ⫽ nonsteroidal anti-inflammatory drug
pulmonary osteoarthropathy (HPOA) is a
H ypertrophic
well-recognized complication of cystic fibrosis (CF)
and occurs more frequently in patients with advanced lung
disease.1 Joint pain, stiffness, mastalgia, and gynecomastia
may complicate HPOA in patients with CF and are usually
controlled by therapy with nonsteroidal anti-inflammatory
drugs (NSAIDs), physical therapy, and occasionally therapy with systemic corticosteroids.
Case Report
We report the case of a 27-year-old woman with CF who
presented with severe diffuse bone pain and HPOA, which
responded to therapy with IV pamidronate. The patient had
moderate bronchiectasis (FEV1, 65% of predicted), and chronic
Pseudomonas aeruginosa infection. The treatment of pulmonary
disease included physiotherapy, therapy with aerosolized bronchodilators, therapy with intermittent nebulized aminoglycosides,
and two previous hospital admissions for therapy with IV antibiotics. The patient was well-nourished (body mass index,
24.6 kg/m2), but a liver biopsy had confirmed the presence of
biliary cirrhosis, which was complicated by portal hypertension
(ie, splenomegaly, thrombocytopenia, and esophageal varices,
which had been controlled with sclerotherapy).
In June 1999, the patient presented with an 8-week history
of severe bilateral ankle and knee pain, and right elbow and
right wrist pain. The pain was being poorly controlled with
simple analgesia and was impairing the patient’s sleep at night.
The pain was associated with severe early-morning stiffness
and required leave from full-time employment as a clerical
officer. A clinical examination revealed bony tenderness proximal to both ankles, which was associated with minimal ankle
edema. There was no clinical evidence of synovitis or of an
inflammatory arthritis. The findings of chest and abdominal
examinations were unchanged from those of earlier examinations, and the results of spirometry testing were consistent
with earlier values. Rheumatoid factor was negative, and
antinuclear antibody level was weakly positive (nucleolar
pattern, titer 160; the normal reference is ⬍40 titre). How*From the Adult Cystic Fibrosis Unit and University of Queensland, The Prince Charles Hospital, Brisbane, Australia.
Received January 26, 2001; revision accepted October 2, 2001.
Correspondence to: Scott C. Bell, MD, Department of Thoracic
Medicine, University of Queensland, The Prince Charles Hospital, Rode Road, Chermside, Brisbane, QLD, Australia 4032;
e-mail: [email protected]
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