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Last 50 Pulmonary Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

September 2015 Pulmonary Case of the Month: Holy Smoke
August 2015 Pulmonary Case of the Month: Holy Sheep
Reducing Readmissions after a COPD Exacerbation: A Brief Review
July 2015 Pulmonary Case of the Month: A Crazy Case
June 2015 Pulmonary Case of the Month: Collapse of the Left Upper
Lung Herniation: An Unusual Cause of Chest Pain
Valley Fever (Coccidioidomycosis): Tutorial for Primary Care Professionals
Common Mistakes in Managing Pulmonary Coccidioidomycosis
May 2015 Pulmonary Case of the Month: Pneumonia with a Rash
April 2015 Pulmonary Case of the Month: Get Down
March 2015 Pulmonary Case of the Month: Sticks and Stones May
   Break My Bronchi
Systemic Lupus Erythematosus Presenting As Cryptogenic Organizing 
   Pneumonia: Case Report
February 2015 Pulmonary Case of the Month: Severe Asthma
January 2015 Pulmonary Case of the Month: More Red Wine, Every
December 2014 Pulmonary Case of the Month: Bronchiolitis in Adults
November 2014 Pulmonary Case of the Month: BAL Eosinophilia
How Does Genetics Influence Valley Fever? Research Underway Now To
   Answer This Question
October 2014 Pulmonary Case of the Month: A Big Clot
September 2014 Pulmonary Case of the Month: A Case for Biblical
Role of Endobronchial Ultrasound in the Diagnosis and Management of
Bronchogenic Cysts: Two Case Descriptions and Literature Review
Azathioprine Associated Acute Respiratory Distress Syndrome: Case Report
   and Literature Review
August 2014 Pulmonary Case of the Month: A Physician's Job is 
   Never Done
July 2014 Pulmonary Case of the Month: Where Did It Come From?
June 2014 Pulmonary Case of the Month: "Petrified"
May 2014 Pulmonary Case of the Month: Stress Relief
Giant Cell Myocarditis: A Case Report and Review of the Literature
April 2014 Pulmonary Case of the Month: DIP-What?
Wireless Capsule Endo Bronchoscopy
Elevated Tumor Markers In Coccidioidomycosis of the Female Genital Tract
March 2014 Pulmonary Case of the Month: The Cure May Be Worse
   Than the Disease
February 2014 Pulmonary Case of the Month: Faster Is Not Always
January 2014 Pulmonary Case of the Month: Too Much, Too Late
32 Year Old Man with “Community-Acquired” Pneumonia
December 2013 Pulmonary Case of the Month: Natural
November 2013 Pulmonary Case of the Month: Dalmatian Lungs
October 2013 Pulmonary Case of the Month: A Hidden Connection
Bronchoscopic Cryoextraction: A Novel Approach for the Removal
   of Massive Endobronchial Blood Clots Causing Acute Airway
September 2013 Pulmonary Case of the Month: Chewing the Cud
IgG4-Related Systemic Disease of the Pancreas with Involvement 
   of the Lung: A Case Report and Literature Review
August 2013 Pulmonary Case of the Month: Aids for Diagnosis
Variation in Southwestern Hospital Charges for Pulmonary
   and Critical Care DRGs
July 2013 Pulmonary Case of the Month: Swan Song
June 2013 Pulmonary Case of the Month: Diagnosis
   Makes a Difference
May 2013 Pulmonary Case of the Month: the Cure Can be
   Worse than the Disease
April 2013 Pulmonary Case of the Month: 
   A Suffocating Relationship
Doxycycline Decreases Production of Interleukin-8
   in A549 Human Lung Epithelial Cells
March 2013 Pulmonary Case of the Month:
   Don’t Rein Me In
February 2013 Pulmonary Case of the Month: 
   One Thing Leads to Another
January 2013 Pulmonary Case of the Month:
   Maybe We Should Call GI


For complete pulmonary listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles broadly related to pulmonary medicine including thoracic surgery, transplantation, airways disease, pediatric pulmonology, anesthesiolgy, pharmacology, nursing  and more. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.



Azathioprine Associated Acute Respiratory Distress Syndrome: Case Report and Literature Review

Dmitriy Scherbak, D.O.

Ruth Wyckoff, M.D.

Clement Singarajah, M.D.


Phoenix VA Healthcare System

Phoenix, AZ



A 58-year-old Caucasian man treated with azathioprine to prevent rejection of an orthotopic liver transplant, presented to the Carl Hayden VA Medical Center with rapid respiratory decline and appeared septic. He required urgent intubation, mechanical ventilator support and empiric antibiotics. His clinical picture and imaging studies were consistent with acute respiratory distress syndrome; however, extensive infectious work up failed to reveal an offending organism. Review of his current medications implicated azathioprine and upon discontinuation of this agent, the patient made a rapid recovery. He was subsequently extubated, transferred out of the ICU and soon discharged home in good health.

Prescribed for organ transplant rejection and a wide array of autoimmune diseases, azathioprine has been rarely correlated with pneumonitis and rapid respiratory failure. No reported cases were found in which azathioprine was used to treat liver transplant rejection and associated with development of the adult respiratory distress syndrome (ARDS). However, there have been ARDS cases in which azathioprine was used for other purposes. We review all the available cases of azathioprine associated ARDS. The patients in these reports had similar clinical symptoms on presentation as our patient: hypoxia, febrile episodes and rapid development of ARDS with no infectious etiology. Most notable is the rapid resolution of ARDS after discontinuation of azathioprine.

Although azathioprine toxicity related respiratory failure is rare, this correlation should still be considered in the differential for immunosuppressed patients presenting with rapid pulmonary decline. Further studies are needed and warranted to better correlate this connection, but it is imperative to recognize that the relationship exists.


Since its first use in 1961, azathioprine (a derivative of 6-mercaptopurine) has been used as a steroid sparing immunosuppressive agent in numerous disorders including prevention of graft rejection for solid organ transplantation (1-2). Azathioprine side effects are commonly gastrointestinal complaints such as nausea and vomiting, occurring in ~19% of patients. Laboratory abnormalities such as leukopenia are also common (17%) with thrombocytopenia and anemia being less common (3-4%) (3). Hepatotoxicity has been reported as well. Pulmonary toxicity is not usually noted as a side effect (1). Sixteen cases have been reported in the literature implicating azathioprine with pulmonary toxicity (1-2, 4-12). In 10 of these cases, the patient developed acute respiratory distress syndrome (ARDS) (1,2,6,8,9,11).

Pulmonary infections have been the leading cause of complications in immunosuppressed recipients of solid organs (13). Therefore, when a patient presents with respiratory distress, an abnormal chest x-ray and fevers, such infections are high on the differential, but the possibility of lung injury resulting from the immunosuppressive agent is often overlooked (1). We present a case of azathioprine induced ARDS in a liver transplant recipient and review the available ARDS cases associated with azathioprine use.

Case Report

We present a 58-year-old white man with a past medical history of end-stage liver disease due to hepatitis C cirrhosis and hepatocellular carcinoma who received an orthotopic liver transplant (OLT) 9 months prior to presentation. He was being treated with azathioprine 150mg daily and tacrolimus 1.5 mg daily to prevent rejection. He presented to the emergency department 9 months after his transplant with shortness of breath and increasing hypoxia. He was admitted to the intensive care unit where he developed respiratory failure that night requiring intubation and ventilator support. He had fevers as high as 105.1⁰F. He had pancytopenia with white blood cell count (WBC) 2.3 thousand cells at presentation, hemoglobin (HGB) 9.8 g/dL and platelets (PLT) 119 thousand cells.

Chest x-ray showed bilateral patchy pulmonary infiltrates. CT of the chest was done as well showing bilateral ground glass opacities and diffuse scattered pulmonary consolidations (Figure 1).

Figure 1. Representative images from chest CT with contrast done on admission showing diffuse ground glass opacities and scattered pulmonary consolidations.

Since he was immunosuppressed he was started on empiric antibiotic coverage with vancomycin, levofloxacin, pipercillin/tazobactam, gancyclovir and fluconazole. Trimethoprim-sulfamethoxazole was added on day 2 of hospitalization. A bronchoscopy with bronchial alveolar lavage (BAL) was done prior to antibiotics. Cell count and differential showed 160 white blood cells, 11% segmented neutrophils and 3% eosinophils, the other 86% of cells were pulmonary macrophages/monocytes and reactive respiratory epithelial cells. No organisms or evidence of malignancy were seen. BAL cultures showed no growth on bacterial, viral, acid fast or mycology cultures. Influenza A and B and a pneumocystis smear were also negative. Blood cultures were taken twice during the patient’s hospitalization during febrile episodes and showed no growth both times in two sets of cultures. On day 6 of hospitalization anti-microbial therapy was discontinued.

The patient’s clinical status continued to deteriorate. Chest x-rays continued to show increasing bilateral pulmonary infiltrates (Figure 2).

Figure 2. Chest x-ray at worst (hospital day 8) showing worsening bilateral pulmonary infiltrates.

The diagnosis of acute respiratory distress syndrome (ARDS) was established. His ventilator settings followed the NHLBI ARDS Network protocol, and on day 6 he was even placed in a prone position. On day 7 of hospitalization his white blood cell count dropped to a nadir of 0.5 thousand cells, hemoglobin dropped to 6.5 g/dL and platelets down to 69 thousand cells). Azathioprine was discontinued due to the pancytopenia and due to finding a few case reports in which it was implicated in ARDS. Within 3 days of azathioprine discontinuation (day 10 of hospitalization), the patient’s chest x-rays and pulmonary function had dramatically improved and he was successfully extubated by the fifth day of azathioprine being withdrawn (day 12 of hospitalization). Daily chest x-rays showed continued resolution of infiltrates (Figure 3).

Figure 3. Chest x-ray from hospital day 15 showing dramatic improvement of infiltrates after azathioprine discontinuation.

He improved rapidly and was discharged from the ICU on day 17 and discharged home from the hospital on day 18 with complete resolution of his pulmonary symptoms. His azathioprine was not restarted but he resumed tacrolimus for immunosuppression. Six months after admission, the patient was in good health with no clinical symptoms.


Azathioprine is a nitroimidazole derivative of 6-mercaptopurine (4). It was first used in 1961 and has since become a common medication for treatment of numerous auto-immune disorders and as an immunosuppressant in transplant recipients (1). It has been described to have several reversible dose dependent side effects including bone marrow suppression, hepatotoxicity, anorexia, nausea and vomiting (4). Hypersensitivity reactions have also been described and include fevers, rigors, arthralgia, myalgia, cutaneous reactions, headaches, interstitial nephritis, pancreatitis, dyspnea, cough and pneumonitis (1-4, 6).

In our case the patient developed pneumonitis and ARDS which resolved rapidly after the discontinuation of azathioprine. A review of the literature using broad search terms in OVID, Pub-Med and Google Scholar revealed only 10 articles constituting 16 cases of pulmonary toxicity linked to azathioprine. Detailed analysis showed only 5 reported cases of ARDS linked to azathioprine toxicity (2,6,8,9,11), and a single case series of 7 cases of which 2 also have an infectious etiology (1). Data from these cases are summarized on table 1.

Table 1. Cases of Azathioprine induced ARDS in the literature.

The four remaining articles not appearing in table 1 were excluded because they either represented an immediate hypersensitivity reaction to azathioprine or had infectious pneumonitis which could have contributed to the development of ARDS (4,5,10,12).

Neither our case nor those in the literature contain irrefutable proof that azathioprine was directly responsible for lung injury. However, the similarities between the cases in which the patient survived lead us to conclude that azathioprine is involved in this adverse reaction. First, all 8 cases in which the patient survived show a rapid improvement within one to two weeks after discontinuation of azathioprine. Second, all of these patients present in the same way with hypoxia, pulmonary infiltrates, and fevers. Third, none of the cases show any other possible causes and the ones that go to biopsy have non-specific findings (UIP or diffuse alveolar damage) (1,2,6,7,11). These observations are circumstantial, but the diagnosis of drug-induced pulmonary toxicity is usually based on clinical history of drug exposure and the absence of other known causative agents. Additionally, diffuse interstitial pulmonary disease is the most common form of lung pathology caused by drugs (1,14).

Leukopenia or pancytopenia were present in our case as well as 4 of the 10 reported cases (6,8,9,11). No other side effects from azathioprine were reported in any of the cases. Therefore ARDS is likely a unique effect and unrelated to other potential side effects of azathioprine. The dose of azathioprine was widely variable in the known cases (25-150mg daily) leading us to believe that the development of ARDS is not dose-dependent. All of the cases had patients who had been on azathioprine for months (years in one case) prior to developing pneumonitis or ARDS, leading us to speculate that ARDS is not an acute hypersensitivity. It may be that ARDS development is a function of dose effect over time.

Although there are very few reported cases, It is possible that azathioprine induced lung injury is more common than it appears. When an immunosuppressed patient presents with respiratory distress, some form of infectious etiology is usually involved and the immunosuppressants are often discontinued (1). It is possible that in some of these cases azathioprine itself is the cause or may at least contribute to the development of ARDS. We believe it is important that azathioprine lung toxicity be included in the differential for ARDS causes because prompt discontinuation of azathioprine has led to rapid recovery and good outcome in 8 of the 10 known cases (1,2,6,8,9,11).


Sarah Waybright, Pharm.D. and Lindsay Kittler, Pharm.D. The clinical pharmacists who noted case reports of azathioprine causing pulmonary toxicity and recommended it’s discontinuation in our patient.


  1. Bedrossian CW, Sussman J, Conklin RH, Kahan B. Azathioprine-associated interstitial pneumonitis. Am J of Clin Pathol. 1984;82(2):148-54. [PubMed]
  2. Weisenburger DD. Interstitial pneumonitis associated with azathioprine therapy. Am J of Clin Pathol. 1978;69(2):181-5. [PubMed]
  3. Whisnant JK, Pelkey J. Rheumatoid arthritis: treatment with azathioprine (IMURAN (R)). Clinical side-effects and laboratory abnormalities. Ann Rheum Dis. 1982;41:44-47. [CrossRef] [PubMed]
  4. Stetter M, Schmidl M, Krapf R. Azathioprine hypersensitivity mimicking Goodpasture's syndrome. Am J of Kidney Dis. 1994;23(6):874-7. [CrossRef] [PubMed]
  5. Krowka MJ, Breuer RI, Kehoe TJ. Azathioprine-associated pulmonary dysfunction. Chest. 1983;83(4):696-8. [CrossRef] [PubMed]
  6. Rubin G, Baume P, Vandenberg R. Azathioprine and acute restrictive lung disease. Aust N Z J Med. 1972 Aug;2(3):272-4. [CrossRef] [PubMed]
  7. Bidinger JJ, Sky K, Battafarano DF. Henning JS. The cutaneous and systemic manifestations of azathioprine hypersensitivity syndrome. [Review] J Am Acad Dermatol. 2011;65(1):184-91. [CrossRef] [PubMed]
  8. Carmichael DJS, Hamilton DV, Evans DB, Stovin PGI, Calne RY. Interstitial pneumonitis secondary to azathioprine in a renal transplant patient. Thorax. 1983;38:951-952. [CrossRef] [PubMed]
  9. Perreaux F, Delphine Z, Capron F, Trioche P, Odievre M, Labrune P. Azathioprine-induced lung toxicity and efficacy of cyclosporine a in a young girl with type 2 autoimmune hepatitis. J Ped Gastroenterol Nutr. 2000;31:190-192. [CrossRef]
  10. Ananthakrishnan AN, Attila T, Otterson MF, Lipchik RJ, Massey BT, Komorowski RA, Binion DG. Severe pulmonary toxicity after azathioprine/6-mercatopurine initiation for treatment of inflammatory bowel disease. J Clin Gastroenterol. 2007;41(7):682-688. [CrossRef] [PubMed]
  11. Brown AL, Corris PA, Ashcroft T, Wilkinson R. Azathioprine-related interstitial pneumonitis in a renal transplant recipient. Nephrol Dial Transplant. 1992;7:362-364. [PubMed]
  12. Frost J, Carion G, Mazer J. A case of azathioprine hypersensitivity syndrome, acute respiratory distress syndrome, and shock. Crit Care Med Suppl. 2011;32(12):926.
  13. De Gasperi A, Feltracco P, Ceravola E, Mazza E. Pulmonary complications in patients receiving a solid-organ transplant. Curr Opin Crit Care. 2014;20(4):411-419. [CrossRef] [PubMed]
  14. Camus P, Fanton A, Bonniaud P, Camus C, Foucher P. Interstitial lung disease induced by drugs and radiation. Respir. 2004;71:01-326. [CrossRef] [PubMed]

Reference as: Scherbak D, Wyckoff R, Singarajah C. Azathioprine associated acute respiratory distress syndrome: case report and literature review. Southwest J Pulm Crit Care. 2014;9(2):94-100. doi: PDF



August 2014 Pulmonary Case of the Month: A Physician's Job is Never Done

Elijah Poulos, MD*

Kristine Saunders, MD


Pulmonary and Critical Care Medicine*

Department of Pathology

Phoenix VA Medical Center

Phoenix, AZ


Pulmonary Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity.

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Elijah Poulos, MD. The author(s)/contributor(s) state that they do not have any financial arrangements that could constitute a conflict of interest. Detailed Information

Learning Objectives:
As a result of this activity I will be better able to:

  1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
  2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
  4. Will integrate new treatment options in discussing available treatment alternatives for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at the Arizona Health Sciences Center Credit Designation and Accreditation Statements.

Current Approval Period: January 7, 2013 - January 6, 2015

Original Release Date: August 1, 2014

Most Recent Review by Author: August 1, 2014

Most Recent Review by CME Sponsor: August 1, 2014

Financial Support Received: None


History of Present Illness

A 75-year-old man presented with recurrent minimally productive cough, dyspnea, fatigue, low-grade fevers, and weight loss in November 2013. The patient had been treated twice as an outpatient with antibiotics in the previous 6 weeks for pneumonia.


The patient has a history of obstructive sleep apnea but is not compliant with his prescribed continuous positive airway pressure. He also as a history of obesity, dyslipidemia, and peripheral vascular disease.

There is no significant family history.  

He is a retired brick layer with a 50 pack-year smoking history but quit a few weeks prior to admission.  He drinks a case of beer/week.

Physical Examination

VS stable. There were no significant findings on physical examination.


A chest radiograph (Figure 1) was performed.

Figure 1. Admission PA (Panel A) and lateral (Panel B) chest radiograph.

What should be done next? (Click on the correct answer to proceed to the next panel)

  1. Bronchoscopy with bronchoalveolar lavage
  2. Bronchoscopy with transbronchial biopsy
  3. Needle biopsy
  4. Thoracentesis
  5. Video-assisted thorascopic surgery (VATS)

Reference as: Poulos E, Saunders K. August 2014 pulmonary case of the month: a physician's job is never done. Southwest J Pulm Crit Care. 2014;9(2):59-67. doi: PDF



July 2014 Pulmonary Case of the Month: Where Did It Come From?

Colin B. Fitterer, MD

James M. Parish, MD


Mayo Clinic Arizona

Scottsdale, AZ


History of Present Illness

A 67 year old man presented with worsening cough and shortness of breath. He has a history of metastatic colon cancer first diagnosed in 2010. He was treated with radiation and chemotherapy (FOLFOX) but unfortunately developed new pulmonary nodules in October, 2013 which were metastatic colon cancer on biopsy. In February 2014 he developed a right parietal brain mass which was resected. Thoracic CT scan at that time showed progression of the pulmonary nodules. He has also noted a 30 pound weight loss over the past 6 months and an enlarging right supraclavicular lymph node.


In addition to the colon cancer, he has previous diagnoses of type 2 diabetes mellitus, hypertension, allergic rhinitis, and vitamin D deficiency. He is married and a recently retired railroad engineer. He has no history of tobacco use. There is a positive family history of lung cancer but no colon cancer.

Physical Examination

Vital Signs:  Temperature 36.8, pulse 98, respirations 18, blood pressure 144/70, SpO2 91% on 3 L via nasal cannula.

Pertinent findings include:

  • A large firm and fixed right supraclavicular lymph node that is nonpainful on palpation.
  • Diminished breath sounds across all right posterior lung fields with dullness to percussion. 
  • Palpable liver edge is palpable approximately 2cm below the right costal margin.

Laboratory Analysis

Admission laboratory values include a hemoglobin of 11.1 g/dL but with a normal white blood cell count and platelet count. Electrolytes, blood urea nitrogen, creatinine, and liver enzymes were all within normal limits.  Serum chemistries are within normal limits.


A chest x-ray (Figure 1A) and chest CT (Figure 1B) were performed.


Figure 1. Admission AP (Panel A) and representative image from the thoracic CT scan (Panel B).

Which of the following is the best interpretation of the radiographic findings? (Click on the correct answer to proceed to the next panel)

  1. Large right pleural effusion
  2. Right lung atelectasis
  3. Right lung pneumonia
  4. Right lung pulmonary edema
  5. None of the above

Reference as: Fitterer CB, Parish JM. July 2014 pulmonary case of the month: where did it come from? Southwest J Pulm Crit Care. 2014;8(6):1-7. doi: PDF



June 2014 Pulmonary Case of the Month: "Petrified"

Steven W. Purtle, MD

University of Colorado Hospital, Denver, CO


History of Present Illness

A 52 year old expatriated Iraqi man presents to pulmonary clinic with complaints of chronic dyspnea. While a young man living in Iraq, he had been disqualified from service in the Iraqi Air Force after a screening chest x-ray was found to be abnormal. He had no respiratory symptoms at the time of his disqualification, and he remained asymptomatic for the next twenty five years. Beginning five years ago, he had an insidious onset of breathlessness and exertional intolerance. Over the past several years, he has developed diffuse pleuritic chest pain, non-productive cough, and fatigue. He denies any fevers, chills, night sweats, arthralgias, rash, or visual symptoms. After moving to Denver, Colorado three years ago, he has developed a continuous oxygen requirement of two liters per minute.


He has no significant past medical or family history. While living in Iraq, he worked as a photographer, but he is currently unemployed. He is a lifelong non-smoker and uses no illicit drugs. He has never had any pets. He denies any exposure to inorganic dusts.



Physical Examination

Physical examination reveals a thin, middle-aged man in no acute distress. Vital signs were notable for an oxygen saturation of 90% on 2 liters per minute of supplemental oxygen. Pulmonary examination was notable for fine inspiratory crackles heard best at the bilateral bases. There was no clubbing or peripheral edema. The remainder of his physical examination was unremarkable.

Laboratory Analysis

Serum chemistries are within normal limits. Complete blood count shows a normal white blood cell count, hematocrit, and platelet count.

Pulmonary Function Tests

Pulmonary functions tests are shown in Figure 1.


A chest x-ray (Figure 2) and chest CT (Figures 3 and 4) were performed.

Figure 2. Admission AP (Panel A) and lateral (Panel B) chest x-ray.


Figure 3. Static thoracic CT images displayed in lung windows (Panels A-D) and soft tissue windows (Panels E-H).


Figure 4. Movies of thoracic CT scan in lung windows (Panel A, top) and soft tissue windows (Panel B, bottom).


Which of the following features best describes the pattern seen on the patient’s chest CT? (Click on the correct answer to proceed to the next panel)

  1. Diffuse microcalcifications
  2. Honeycombing
  3. Mosaicism
  4. Patchy ground glass opacifications
  5. Pleural plaques

Reference as: Purtle SW. June 2014 pulmonary case of the month: "petrified". Southwest J Pulm Crit Care. 2014;8(6):299-304. doi: PDF


May 2014 Pulmonary Case of the Month: Stress Relief

Robert W. Viggiano, MD


Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ


History of Present Illness

A 62 year old man was referred for an abnormal CT scan of the chest. He was found to have an abnormality in the lung as an incidental finding on a CT scan of the abdomen done 6 months earlier for abdominal pain. A CT-guided needle biopsy was performed but revealed only scant tissue and no diagnosis was made.

The patient was asymptomatic without dyspnea, wheezing or cough. He had no fevers, chills, history of pneumonia or sinus disease. He denied any symptoms of gastroesophageal reflux disease (GERD), regurgitation, dysphagia or aspiration.


The patient had a small melanoma excised from his arm several months earlier. Family history was noncontributory. He smoked a pack per day for 7 years but quit over 30 years earlier. He does not drink.


  • Vitamins
  • Mineral oil laxative

Physical Examination

Physical examination was unremarkable.


A CT scan of the chest was performed (Figure 1).

Figure 1. Representative images from the thoracic CT scan. Panels A-E: lung windows. Panels F-J: Corresponding soft tissue windows.

The thoracic CT shows which of the following abnormalities? (Click on the correct answer to proceed to the next panel)

  1. Left lower lobe mass
  2. Mediastinal mass
  3. Right middle lobe mass
  4. 1 and 3
  5. All of the above

Reference as: Viggiano RW. Pulmonary case of the month: stress relief. Southwest J Pulm Crit Care. 2014;8(5): . doi: PDF


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