Pulmonary
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.
December 2024 Pulmonary Case of the Month: Two Birds in the Bush Is Better than One in the Hand
University of Nebraska Medical Center
Omaha, NE USA
History of Present Illness
A 48-year-old man is referred for dyspnea on exertion and a nonproductive cough. He was well until 6 months prior to this visit. He feels he has had “flu-like symptoms” over the past month.
PMH, SH, and FH
He has had intermittent atrial fibrillation controlled by digoxin but also clopidogrel as an anticoagulant. He has symptoms of hay fever and had asthma as a child.
He has never smoked and rarely drinks. Pets include two dogs and a cat. He is a university English literature professor and his office is an old building but the building is clean and well maintained. Hobbies include playing guitar in a rock-n-roll band.
His family history is unremarkable.
Physical Examination
His physical examination including lungs and cardiovascular examination is unremarkable.
Which of the following are indicated for further workup? (Click on the correct answer to be directed to the second of six pages.)
June 2024 Pulmonary Case of the Month: A Pneumo-Colic Association
Pulmonary Department
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
The patient is a 57-year-old woman who presented to the emergency department with increasing cough and shortness of breath over several days. She has a history of ulcerative colitis complicated by toxic megacolon with subsequent colectomy.
Past Medical History, Family History and Social History
Ulcerative colitis with history of toxic megacolon (4 years prior), s/p total colectomy
History of recent respiratory failure thought secondary to ustekinumab (Stelara). The respiratory failure responded well to steroid therapy.
She has a history of latent Tb treated with rifampin
Anxiety
Medications
Clonazepam 1.0 mg daily at bedtime
Gabapentin 300 mg TID
Pantoprazole 40 mg BID
Prednisone 5 mg daily
Physical Examination
Mild-moderate respiratory distress
Afebrile. SpO2 87% on room air. Oxygen saturation 94% on 2 lpm supplemental oxygen.
Chest: crackles noted at left base
Cardiovascular: regular rhythm, no murmur
Extremities: scarring and erythema on both ankles consistent with resolving pyoderma gangrenosum
Laboratory
Hgb 9.7 g/dL
White Blood Cell Count 16.9 × 109/L
Increased neutrophils on differential
Electrolytes, creatinine, BUN and liver function tests within normal limits
Radiology
A portable AP of the chest was performed in the emergency department (Figure 1).

Figure 1. Portable AP of chest done in emergency department.
Which of the following are appropriate next step(s)? (Click on the correct answer to be directed to the second of six pages)
Cite as: Wesselius LJ. June 2024 Pulmonary Case of the Month: A Pneumo-Colic Association. Southwest J Pulm Crit Care Sleep. 2024;28(6):74-77. doi: https://doi.org/10.13175/swjpccs023-24PDF
March 2022 Pulmonary Case of the Month: A Sore Back Leading to Sore Lungs
Brandon T. Larsen MD PhD2
Departments of 1Pulmonary Medicine and 2Pathology
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
An 82-year-old woman from Colorado was referred because of progressive shortness of breath over the past year. Her primary care physician had prescribed Trelegy® which did not improve her dyspnea. An outside pulmonologist noted abnormal findings on her thoracic CT scan and a bronchoscopy with bronchoalveolar lavage (BAL) was preformed which was positive for Mycobacterium Avium Complex (MAC). She was treated with a 3-drug regimen (azithromycin, rifampin, ethambutol) for 6 months with mild improvement. After the treatment was stopped, she noted more dyspnea and required supplemental oxygen. She underwent a fundoplication and initially improved but a month later her shortness of breath seemed to worsen. She was started on prednisone which was tapered to 10 mg/day. She was referred to the Mayo Clinic for possible VATS lung biopsy.
Past Medical History (PMH), Social History (SH), Family History (FH)
PMH
- Hiatal Hernia/GERD
- Ulcerative Colitis
- Hypertension
- Chronic Back pain
- Prior breast implants
SH
- Former smoker (24 pack-years, quit 1988)
- Social use of alcohol, no drug use
- No exposure to birds or down
- No occupational dust exposures
- Home humidifier
- Has indoor hot tub used frequently for back pain
FH
- Unremarkable
Medications
- Prednisone 10 mg daily
- Pantoprazole 40 mg bid
- Pregabalin 25 mg at bedtime
- Oxycodone 5 mg q 6 hours prn pain
- Ondansetron 4 mg tablet q 8hhours prn nausea
Physical examination
- BMI 31.9
- Oxygen saturation at rest 95% on 4 lpm, 88% on RA
- Chest: scattered crackles
- Cardiovascular: regular rate without murmur
- Extremities: no clubbing or edema
Which of the following should be done next? (Click on the correct answer to be directed to the second of seven pages.)
- Pulmonary function testing
- Open surgical lung biopsy
- Review thoracic CT scan
- 1 and 3
- All of the above
Cite as: Wesselius LJ, Larsen BT. March 2022 Pulmonary Case of the Month: A Sore Back Leading to Sore Lungs. Southwest J Pulm Crit Care Sleep. 2022;24(3):36-39. doi: https://doi.org/10.13175/swjpccs011-22 PDF
Adjunctive Effects of Oral Steroids Along with Anti-Tuberculosis Drugs in the Management of Cervical Lymph Node Tuberculosis
Adjunctive Effects of Oral Steroids Along with Anti-Tuberculosis Drugs in the Management of Cervical Lymph Node Tuberculosis
Babulal Bansiwal1
Maneesha Jelia2
Ramesh Chand Meena2
Satyam Agarwal2
Shinu A2
Departments of 1Respiratory Medicine and 2Anatomy
Government Medical College, Kota
Rajasthan 324010, India
Abstract
Background: Tuberculosis (TB) can infect both pulmonary and extra-pulmonary organs. In India pulmonary TB accounts for 80% of cases and extrapulmonary TB (EPTB) accounts for 20% cases. Cervical lymph nodes are the most location for EPTB.
Aims and Objectives: To study the efficacy of treatment with oral steroids along with anti-tuberculosis treatment in cervical lymph node tuberculosis.
Methods: A total of 60 patients were enrolled in the study all with EPTB and cervical lymphadenitis. These 60 study patients were randomised into two groups. Group-I consisted of 30 patients given anti-tuberculosis therapy along with prednisolone 1mg/kg body weight for 4 weeks followed by tapering at 0.5 mg/kg body weight over 4 weeks. Group-II was comprised of 30 patients given antituberculosis treatment plus placebo
Results: After completion of treatment 27 patients in Group 1 (90%) showed complete resolution and 3 patients (10%) had residual evidence of lymphadenitis with no change. In contrast, only 19 patients (63.3%) showed complete resolution in Group 2 and 11 patients (36.7%) had residual lymphadenitis present (10 had no change, 1 had increase in size).
Conclusion: We conclude that steroids given with antituberculosis treatment to patients with cervical lymphadenitis led to faster and earlier resolution of tuberculous lymphadenitis.
Introduction
Tuberculosis (TB) is an ancient disease that affects both pulmonary and extra-pulmonary organs. In India most TB cases are pulmonary (80%) but extrapulmonary TB (EPTB) accounts for a substantial proportion (20%) (1). Peripheral lymph node tuberculosis is observed in about 5% of all TB patients and 30-55% of extra-pulmonary TB cases (2). Cervical lymph nodes are the most common lymph nodes affected, classically termed as “scrofula”, although supraclavicular, axillary, inguinal nodes may also be involved (3-5). Lymphadenopathy may lead to complications by compression of adjacent structures, organs, and blood vessels or fistula formation (6-10). Multiple studies have shown better outcomes with addition of steroids to anti-tuberculosis treatment in extrapulmonary tuberculosis including pleural effusion, pericardial effusion, tubercular meningitis, and mediastinal lymphadenopathy (11,12). However, the safety and efficacy of this approach remains largely unproven except in cases of intrathoracic obstruction where it was found to relieve the pressure on the compressed bronchus (13).
Aims and Objectives
To study the efficacy of treatment with oral steroids along with anti-tuberculosis treatment in cervical lymph node tuberculosis.
Materials and Methods
Patients: Sixty patients with cervical lymph node tuberculosis seen from 1st October 2013 to 30th September 2014 in the Department of Respiratory Medicine, Government Medical College, Kota, India participated in the study. All cases of cervical lymph node tuberculosis found to have cyto-pathological, histo-pathological, immunological and/or bacteriological evidence of TB and who had not received any anti- tuberculosis therapy in the past, were included in the study. Patients were excluded if they were pregnant or had a chronic disease such as diabetes mellitus, hypertension, peptic ulcer disease, alcoholism, or HIV-AIDS. Patients were also excluded if they had a detectable abscess.
Study Design: The study was an open label, randomized, prospective and placebo-controlled interventional study comparing the efficacy of the addition of two months treatment with oral corticosteroids along with Revised National Tuberculosis Control Programme (RNTCP) recommended anti-TB therapy.
Sixty patients were randomised into two groups by a computer-generated random table. All patients were given category I anti-tuberculosis therapy (ATT) consisting of INH 600 mg and rifampicin 450 mg daily for 6 months with pyrazinamide 1500 mg daily for the first 2 months. Group-I consisted of 30 patients given category I RNTCP-recommended therapy along with prednisolone 1mg/kg body weight for 4 weeks followed by tapering at 0.5mg/kg body weight for 4 weeks. Group-II was comprised of 30 patients given category I RNTCP-recommended therapy plus placebo.
All the study cases were monitored clinically by visits after 1, 2 and 6 months.
Statistical Analysis: Pearson’s x2 test or Fisher’s exact test was used to evaluate correlations between categorical variables, as appropriate. Relationships among continuous variables was evaluated using Student’s t- test. All tests of significance are two-tailed, and p < 0.05 was considered to reflect significance.
Results
The patients were well matched between groups in age (27.5 + 12.9 years vs. 26.3 + 11.7 years, p=0.612) and sex (12M/18F vs. 11M/19F). The groups were well-matched in other clinical characteristics (Table 1).
Table 1. Clinical characteristics of patients at beginning of therapy.
In addition to the above, the patients were well-matched by the extent of both upper and lower lymphadenopathy (Group I, 25/30; Group 2, 28/30), absence of chest lesions (Group I, 1/30; Group 2, 2/30), and positive histopathology on needle aspiration (Group I, 27/30; Group 2, 26/30). Out of 26 patients of Group II, 4 (13.3%) patients were diagnosed by AFB smear of the needle aspirate as well as cytopathological examination, 2(6.7%) had only AFB smear positivity and 22 (86.7%) had only cytopathological confirmation. None had a positive sputum smear.
Most of the patients in Group-I had earlier lymph node resolution compared to Group-II (Table 2).
Table 2. Initial lymph node status and after varying durations of treatment.
This table shows the status of the lymph node initially and after varying duration of treatment. After completion of treatment 27 patients (90%) showed complete resolution and only 3 patients (10%) had no change in Group-I. In contrast, only 19 patients (63.3%) in Group-II showed complete resolution and 11 patients (36.7%) had residual lymph nodes (10 with no change, 1 with an increase in size). Most patients had a negative AFB smear from the needle aspirate after 6 months in both Group-I (27 patients) and group-II (26 patients).
Only 2 patients in Group-I (6.67%) had complications as compared to 09 (30.0%) in Group-II (p<0.001). The complications were in the form of abscess, sinus and/or new lymph node/s. All these patients needed surgical exploration during the course of treatment. Sequelae in form of residual lymph node was also higher in Group II patients (10 out of 30 patients) as compared to Group I (3 out of 30, p<0.001).
Overall, the incidence of side effects was greater in Group-II. This difference was mostly due to a higher occurrence of joints pain and skin rashes in Group-II than Group-I, (8 and 4 patients vs. 1 and 1 patients respectively).
Discussion
The present study was done to determine the role of steroids in the management of cervical lymph node tuberculosis. In contrast to 20 patients (66.67%) in the non-steroid group-II who had complete resolution after 6 months, 27 patients (90%) in the steroid group had complete resolution. Blaikely et al. (14) reported complete resolution in 82% of their non-steroid study patients which was similar to results of our study.
In the present clinical study, only 2 patients (6.66%) in the steroid group had complications as compared to 9 (30.0%) in the non-steroid group. The complications were in the form of abscess, sinus and/or new lymph node/s. In Group II, fresh lymph nodes appeared in 4, existing lymph node increased in 1, abscess formation occurred in 3 while 2 patients developed sinuses. Sequela in the form of residual lymph node was also higher in the non-steroid patients (10 out of 30, 33.33%) as compared to the steroid treated patients (3 out of 30 patients, 5%, p<0.001). Results were comparable to other studies (15).
We used a moderate dose of steroids for 2 months. The major concern against the use of steroids when given along with anti-TB treatment in tubercular lymphadenitis are adverse systemic effects. However, the overall incidence of side effects with anti-TB treatment were more in the non-steroid group in the form of joint pains and skin rashes, (8 and 4 patients v/s 1 and 1 patients respectively). Gastro-intestinal side effects i.e. nausea/vomiting and pain abdomen, were slightly higher in the steroid-treated patients.
Conclusion
We conclude that steroids when given along with anti-tubercular treatment led to faster and earlier resolution of tuberculous lymphadenitis. Complication and sequela in form of residual lymph node are also less in steroid group as compared to non-steroid group. It is unclear if long-term outcomes are affected. However, this data suggests that justification for routine use of corticosteroids could be made in tubercular cervical lymphadenitis.
References
- Arora V, Jaiswal AK, Gupta S, Gupta MB, Jain V, Ghanchi F. Implementation of RNTCP in a private medical college: five years' experience. Indian J Tuberc. 2012 Jul;59(3):145-50. [PubMed].
- Asghar RJ, Pratt RH, Kammerer JS, Navin TR. Tuberculosis in South Asians living in the United States, 1993-2004. Arch Intern Med. 2008 May 12;168(9):936-42. [CrossRef] [PubMed]
- Lazarus AA, Thilagar B. Tuberculous lymphadenitis. Dis Mon. 2007 Jan;53(1):10-5. [CrossRef] [PubMed]Thompson MM, Underwood MJ, Sayers RD, Dookeran KA, Bell PR. Peripheral tuberculous lymphadenopathy: a review of 67 cases. Br J Surg. 1992 Aug;79(8):763-4. [CrossRef] [PubMed]
- Dandapat MC, Mishra BM, Dash SP, Kar PK. Peripheral lymph node tuberculosis: a review of 80 cases. Br J Surg. 1990 Aug;77(8):911-2. [CrossRef] [PubMed]
- Singh B, Moodley M, Goga AD, Haffejee AA. Dysphagia secondary to tuberculous lymphadenitis. S Afr J Surg. 1996 Nov;34(4):197-9. [PubMed]
- Gupta SP, Arora A, Bhargava DK. An unusual presentation of oesophageal tuberculosis. Tuber Lung Dis. 1992 Jun;73(3):174-6. [CrossRef] [PubMed]
- Ohtake M, Saito H, Okuno M, Yamamoto S, Ohgimi T. Esophagomediastinal fistula as a complication of tuberculous mediastinal lymphadenitis. Intern Med. 1996 Dec;35(12):984-6. [CrossRef] [PubMed]
- Wilson RS, White RJ. Lymph node tuberculosis presenting as chyluria. Thorax. 1976 Oct;31(5):617-20. [CrossRef] [PubMed]
- Puri S, Khurana SB, Malhotra S. Tuberculous abdominal lymphadenopathy causing reversible renovascular hypertension. J Assoc Physicians India. 2000 May;48(5):530-2. [PubMed]
- Mansour AA, Al-Rbeay TB. Adjunct therapy with corticosteroids or paracentesis for treatment of tuberculous pleural effusion. East Mediterr Health J. 2006 Sep;12(5):504-8. [PubMed]
- Reuter H, Burgess LJ, Louw VJ, Doubell AF. The management of tuberculous pericardial effusion: experience in 233 consecutive patients. Cardiovasc J S Afr. 2007 Jan-Feb;18(1):20-5. [PubMed]
- Nemir RL, Cardona J, Vaziri F, Toledo R. Prednisone as an adjunct in the chemotherapy of lymph node-bronchial tuberculosis in childhood: a double-blind study. II. Further term observation. Am Rev Respir Dis. 1967 Mar;95(3):402-10. [CrossRef] [PubMed]
- Jha BC, Dass A, Nagarkar NM, Gupta R, Singhal S. Cervical tuberculous lymphadenopathy: changing clinical pattern and concepts in management. Postgrad Med J. 2001 Mar;77(905):185-7. [CrossRef] [PubMed]
- Blaikley JF, Khalid S, Ormerod LP. Management of peripheral lymph node tuberculosis in routine practice: an unselected 10-year cohort. Int J Tuberc Lung Dis. 2011 Mar;15(3):375-8. [PubMed]
- Allen MB, Cooke NJ. Corticosteroids and tuberculosis. BMJ. 1991 Oct 12;303(6807):871-2. [CrossRef] [PubMed]
Cite as: Bansiwal B, Jelia M, Chand Meena RC, Agarwal S, A S. Adjunctive Effects of Oral Steroids Along with Anti-Tuberculosis Drugs in the Management of Cervical Lymph Node Tuberculosis. Southwest J Pulm Crit Care. 2021;22(1):16-20. doi: https://doi.org/10.13175/swjpcc067-20 PDF
December 2020 Pulmonary Case of the Month: Resurrection or Medical Last Rites?
Lewis J. Wesselius, MD
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
An 88-year-old man who has been short of breath and febrile up to 101.5° F for the past day presented on October 20, 2020. He has no known sick contacts or exposure to COVID-19.
PMH, SH, and FH
- No reported pulmonary history although he had a Xopenex MDI which he rarely used.
- Coronary artery disease with prior coronary artery bypass grafting (1978); multiple subsequent stents; chronic atrial fibrillation; pacemaker (Micra)
- Stage 3-4 CKD (creatinine 1.95)
- Chronically on warfarin
Physical Examination
- Temp 37.3, Sat 92% on RA, 95% on 2 lpm,
- Lungs: Few crackles in right upper chest
- CV: regular, no murmur
- Ext: 1 to 2+ edema (chronic, uses TED hose)
Which of the following is/are the most likely diagnosis? (Click on the correct answer to be directed to the second of seven pages)
Cite as: Wesselius LJ. December 2020 Pulmonary Case of the Month: Resurrection or Medical Last Rites? Southwest J Pulm Crit Care. 2020;21(6):128-37. doi: https://doi.org/10.13175/swjpcc065-20 PDF
Severe Respiratory Disease Associated with Vaping: A Case Report
Evan Denis Schmitz MD
La Jolla, CA USA
Abstract
A case of severe respiratory disease associated with vaping cannabinoid oil is reported in a 38-year-old woman. She presented with shortness of breath and nonproductive cough. Chest x-ray and CT scan showed diffuse ground glass opacities and consolidation. Bronchoscopy showed diffuse bronchial erythema and bronchoalveolar lavage contained an increased percentage of eosinophils (59%). She was treated with high dose corticosteroids and rapidly improved.
Case Report
History of Present Illness
A 38-year-old woman complained of worsening shortness of breath and nonproductive cough for four weeks. She used to be able to climb three flights of stairs but now can barely walk ten feet. She had been treated with various forms of antibiotics, inhalers and steroids and was taking 20 mg of prednisone a day on the day of hospitalization. She also received opiates to help control her cough. She denied any hemoptysis, fever, chills, or sputum production. Because of her progressive symptoms she was hospitalized for further evaluation and management.
Past Medical History, Social History and Family History
She has a history of obesity and fibromyalgia. She has a prior history of smoking one to two packs a day for five years quitting approximately 15 years ago. Because of a family crisis she tried vaping cannabidiol (CBD) oil approximately one month prior to admission. She also resumed smoking tobacco one half a pack per day. Her family history was unremarkable.
Medications
She was taking prednisone 20 mg/day and cyclobenzaprine (Flexeril®) for her fibromyalgia. She was also taking codeine cough syrup.
Review of Symptoms
She did have some chest pain associated with her shortness of breath as well as chronic muscle aches and intermittent lower extremity edema. Her review of systems was otherwise unremarkable.
Physical Examination
Vital Signs: BP 137/72 mm Hg, Pulse 84 beats/min, temperature 98.8 °F, respirations 22 breaths/min, height 5’0, weight 231 lbs, SpO2 96%
General: She was morbidly obese and only able to speak in short sentences.
Mouth: Moist. Mallampati 3.
Pulmonary: Faint expiratory crackles. No wheezing.
Cardiovascular: Normal rate, regular rhythm, normal heart sounds and intact distal pulses. Exam reveals no gallop and no friction rub. No murmur heard.
Abdominal: Soft, bowel sounds normal. No distension, mass or tenderness. No rebound or guarding. Centripetal obesity.
Extremities: Normal range of motion. No edema or tenderness.
Lymphatics: No cervical or supraclavicular adenopathy.
Neurological: Alert and oriented to person, place and time.
Skin: Warm and dry. No rash, erythema or pallor. Not diaphoretic. Capillary refill within normal limits. No skin tenting.
Psychiatric: Depressed mood.
Laboratory
Pertinent findings are on her laboratory evaluation include an elevated white blood cell count of 16,850 cells/µL with an increased number of neutrophils. Her electrolytes, liver enzymes, creatinine, blood urea nitrogen and urinalysis were within normal limits.
Radiology
Her admission chest x-ray is shown in Figure 1.
Figure 1. The admission portable chest x-ray showed bilateral patchy pulmonary infiltrates.
To better define the areas of consolidation, a thoracic CT scan was performed (Figure 2).
Figure 2. Representative images in lung windows from contrast enhanced thoracic CT scan showing nonspecific patchy areas of ground glass and alveolar opacities with septal thickening involving both lungs.
Hospital Course
Echocardiography was unremarkable. Bronchoscopy with bronchoalveolar lavage was performed. She had diffuse upper and lower airway erythema and considerable coughing during the procedure. The cell differential revealed an increase in eosinophils (59%) and multiple foamy macrophages. Smears and cultures of the lavage fluid were negative for pathogens. She was treated with high dose corticosteroids (methylprednisolone 1000 mg/day). She rapidly improved over four days with her cough and shortness of breath resolving. A chest x-ray at discharge revealed improvement of the pulmonary infiltrates (Figure 3).
Figure 3. Chest x-ray on the morning of discharge showing near resolution of her pulmonary infiltrates.
Discussion
At the time of this writing (9/21/19) there have been 530 cases of lung injury associated with e-cigarette product use or vaping reported with seven deaths (1). Nearly three fourths (72%) of cases have been male with two thirds (67%) 18 to 34 years old. Most patients have reported a history of using e-cigarette products containing tetrahydrocannabinol (THC). Many patients have reported using THC and nicotine. Some have reported the use of e-cigarette products containing only nicotine.
At present no specific e-cigarette or vaping product (devices, liquids, refill pods, and/or cartridges) or substance has been linked to all cases. It seems likely that there may be different mechanisms of lung injury from different substances. In support of this concept, the present case had high numbers of eosinophils in the bronchoalveolar lavage while other cases have shown an increase in neutrophils (2). Our patient was treated with high dose corticosteroids and did improve while on the corticosteroids. However, the time course does not establish a definite relationship between corticosteroid treatment and her improvement.
At present the CDC recommends refraining from using e-cigarette or vaping products (1). Anyone who uses an e-cigarette or vaping product should not buy these products (e.g., e-cigarette or vaping products with THC or CBD oils) off the street, and should not modify or add any substances to these products that are not intended by the manufacturer.
References
- CDC. Outbreak of lung injury associated with e-cigarette use, or vaping. September 19, 2019. Available at: https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html (accessed 9/21/19).
- Arizona Thoracic Society. September 2019 Arizona thoracic society notes. Southwest J Pulm Crit Care. 2019;19(3):99-100. [CrossRef]
Cite as: Schmitz ED. Severe respiratory disease associated with vaping: a case report. Southwest J Pulm Crit Care. 2019;19(3):105-9. doi: https://doi.org/10.13175/swjpcc062-19 PDF
June 2018 Pulmonary Case of the Month
Lewis J. Wesselius, MD
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
The patient is a 53-year-old man who presented in January 2018 for a second opinion on interstitial lung disease first diagnosed in 2011. He lives in Los Angeles and had one year of increasing dyspnea on exertion prior to diagnosis. He had an outside surgical lung biopsy and was treated with prednisone, then started on azathioprine and the prednisone tapered. He was followed regularly and had limited progression over next 7 years. However, recently he had increasing shortness of breath.
Past Medical History, Social History, Family History
He has no significant past medical history. He is a nonsmoker and denies any significant occupational exposures.
Physical Examination
Physical examination was unremarkable without rales or clubbing.
Which of the following should be obtained at this time? (Click on the correct answer to proceed to the second of five pages)
- Prior chest x-rays, CT scans, pulmonary function testing and lung biopsy
- Repeat CT scan, pulmonary function testing
- Rheumatological serologies
- 1 and 3
- All of the above
Cite as: Wesselius LJ. June 2018 pulmonary case of the month. Southwest J Pulm Crit Care. 2018;16(6):296-303. doi: https://doi.org/10.13175/swjpcc063-18 PDF
February 2018 Pulmonary Case of the Month
Lewis J. Wesselius, MD
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
A 75-year-old woman was diagnosed with a thymic carcinoid tumor in April, 2015 (Figure 1).
Figure 1. Representative image from the preoperative CT scan performed in April 2015 showing an anterior mediastinal mass (arrow).
This was treated with surgical resection followed by radiation therapy.
She began having cough and dyspnea 1 to 2 months later and in August, 2015 had a thoracic CT scan of her chest (Figure 2).
Figure 2. Representative image in lung windows from the second thoracic CT scan performed in August 2015.
Which of the following are true? (Click on the correct answer to proceed to the second of six pages)
- Bronchoscopy should be performed
- She should be given an empiric course of antibiotics
- The most like diagnosis is radiation pneumonitis
- 1 and 3
- All of the above
Cite as: Wesselius LJ. February 2018 pulmonary case of the month. Southwest J Pulm Crit Care. 2018;16(2):55-61. doi: https://doi.org/10.13175/swjpcc020-18 PDF
January 2018 Pulmonary Case of the Month
Lewis J. Wesselius, MD
Departments of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
A 67-year-old man from Idaho was seen in November 2017 for a second opinion. He has a history of slowly progressive dyspnea on exertion for 7 to 8 years. He has a significant smoking history of 50 pack-years, but is still smoking “a few cigarettes”.
He saw an outside pulmonologist in September 2017 and was noted to have abnormal pulmonary function testing with the primary abnormality being a low DLco. A thoracic CT Scan was reported to be abnormal with evidence of interstitial lung disease. He underwent video-assisted thorascopic surgery and the biopsies were reported to show usual interstitial pneumonitis (UIP). His pulmonologist questioned whether this was interstitial pulmonary fibrosis or UIP associated with rheumatoid arthritis.
PMH, SH and FH
He has a history of rheumatoid arthritis and had been treated with methotrexate for approximately 8 years. His methotrexate had been discontinued in September with no change in symptoms. FH is noncontributory.
Medications
Prednisone 5 mg/daily and tiotropium (these also did not change his dyspnea).
Physical Examination
- Chest: bibasilar crackles.
- Cardiovascular: regular rhythm without murmur.
- Ext: no clubbing, no edema, no joint deformity noted
Which of the following are indicated at this time? (Click on the correct answer to proceed to the second of five pages)
- Obtain a complete blood count and rheumatoid factor
- Begin pirfenidone or nintedanib
- Review his pulmonary function testing and radiographic studies
- 1 and 3
- All of the above
Cite as: Wesselius LJ. January 2018 pulmonary case of the month. Southwest J Pulm Crit Care. 2018;16(1):8-13. doi: https://doi.org/10.13175/swjpcc157-17 PDF
Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia in a Patient with Multiple Pulmonary Nodules: Case Report and Literature Review
Hasan S. Yamin, MD1
Feras Hawarri, MD1
Mutaz Labib, MD1
Ehab Massad, MD2
Hussam Haddad, MD3
Departments of 1Internal Medicine Pulmonary & Critical Care Division, 2Thoracic Surgery and 3Pathology
King Hussein Cancer Center
Amman, Jordan
Abstract
Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is a rare pulmonary disease, where carcinoid tumorlets invade the pulmonary parenchyma and bronchioles. These nests of cells release a variety of mediators including bombesin and gastrin releasing peptide that cause heterogeneous bronchoconstriction, creating a mosaic appearance on chest imaging studies, especially on expiratory scans. Clinically patients usually have long standing symptoms of shortness of breath (SOB) and cough that are difficult to distinguish from asthma. In this article we describe a case of DIPNECH in a patient with several years’ history of SOB and cough, and review 179 cases of DIPNECH reported in the literature since 1992.
Case Presentation
A 72-year-old, non-smoking lady was admitted to the hospital in preparation for bilateral mastectomy. She recently received a diagnosis of bilateral breast invasive ductal carcinoma grade 2, estrogen receptor/progesterone receptor/human epidermal growth factor receptor 2 (HER-2) positive in the left tumor but negative in the right tumor.
Her past medical history was significant for hypertension, long standing cough and dyspnea on exertion labeled as asthma poorly responsive to nebulizers. Socially, she was a house wife with no history of occupational exposure.
The patient was found to be tachypneic (respiratory rate 22 breaths/minute) and hypoxemic (oxygen saturation 86% on room air). Heart rate and blood pressure were within normal limits. She had bilateral decreased breath sounds and diffuse expiratory wheezes.
Chest CT scan revealed diffuse mosaic pattern and multiple pulmonary nodules in both lungs suggestive of metastases (Figure 1).
Figure 1. Representative images form chest CT scan showing a diffuse mosaic pattern and multiple pulmonary nodules in both lung fields suggestive of metastases.
These lesions did not take up fludeoxyglucose (FDG) on positron emission tomography (PET) scan. Her pulmonary function tests (PFT) were unremarkable except for reduction in expiratory reserve volume (ERV) at 22%, and increased residual volume to total lung capacity ratio (RV/TLC) at 136% probably related to air trapping. Diffusion lung capacity was within normal limits.
Video assisted thoracoscopic biopsy of one of the nodules in left lower lobe was done. Pathology showed both a carcinoid tumor and tumorlets invading lung bronchioles (Figure 2A & B) and these tumorlets were positive for chromogranin (Figure 2C & D) and pancytokeratin (Figure 2 E & F).
Figure 2. A & B: histology (H&E stain) showing carcinoid tumorlets invading lung bronchioles; C & D: positive staining for chromogranin; E &F: positive staining for pancytokeratin.
A diagnosis of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) was made, and the patient was treated with intravenous steroids and nebulizers. Her oxygen saturation improved to 94% on room air. She was later discharged on oral steroids. Her CT scan also showed no significant improvement in changes described above.
Review of the Literature
Methods
We searched PubMed for all cases of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia reported in the English literature since 1992 when the entity was first described. A total of 179 patients were identified in 55 articles, in the form of case reports and case series. In this article we contribute an additional patient (1-55).
Patient Characteristics
A total of 180 patients (including our patient) were identified. There were 161 females (89.5%) and only 19 males (10.5%). Mean age at diagnosis was 57.75 years (males tended to present at a younger age of 52 years, compared to 58.4 years in females). Most patients were never smokers 52.8%, smokers/exsmokers 27.2%, and in 20% smoking status was not mentioned.
The majority of patients presented with cough (91 patients, 50.5%), followed by exertional dyspnea (81 patients, 45%), and hemoptysis (6 patients, 3.3%). Incidental imaging findings led to diagnosis in 22 patients (12.2%). Mean duration of symptoms before diagnosis was 8.25 years (Table 1).
Table 1. Patients` characteristics and presenting symptoms.
Diagnosis, Therapy and Outcome
Most patients underwent imaging with chest CT scan, the most common findings were nodules in 148 patients (82.2%), ground glass opacities/mosaic pattern in 66 patients (36.6%), and bronchial wall thickening in 37 patients (20.5%). Most patients had an abnormal spirometry: obstructive pattern (48.9%), restrictive (5%), or mixed obstructive restrictive pattern (6.7%) (Table 2).
Table 2. Spirometry and imaging.
Because of their symptoms, and spirometry findings 45 patients (25%) were labeled with another disease including asthma in 29 patients (16.1%), COPD in 12 patients (6.6%) and bronchiolitis in 4 patients (2.2%).
The diagnosis was made using surgical lung biopsy in 148 patients (82.2%), bronchoscopic biopsy in 10 patients (8 transbronchial biopsy, 2 endobronchial biopsy) (5.6%), CT-guided biopsy in 7 patients (3.9%), postmortem diagnosis in 3 patients (1.7%), post lung transplantation in 2 patients (1.1%) and clinically in 2 patients (1.1%). The diagnostic method was not mentioned in 8 patients (4.4%).
Patients received a variety of therapies including inhaled bronchodilators, inhaled or systemic steroids, and somatostatin analogues among others. Response to treatment was mentioned for 89 patients, (59 patients reported that their symptoms remained stable, 11 patients improved with treatment, while 18 patients reported symptom progression and 2 patients died. (Table 3).
Table 3. List of DIPNECH articles ordered by publication year. This table shows number of patients in each article, diagnostic method, therapy given and outcome.
Of note, 15 out of 23 patients who received a somatostatin analogue reported stable, or improvement in their symptoms (65.2%), which did not necessarily translate into improvement in air flows on spirometry (27, 29, 46, 51).
Discussion
Pulmonary neuroendocrine cell hyperplasia was described early in the previous century (56), however the significance and role of the pathologic changes were not precisely determined. It was thought that they were secondary to other lung diseases such as interstitial lung disease, bronchiectasis, cystic fibrosis, smoking exposure, or in people who live at high altitude. In addition to the previously mentioned associations, hyperplasia of pulmonary neuroendocrine cells was also thought to be a pre-neoplastic process, since the lesions can potentially progress to carcinoid tumors even without causing symptoms or airflow limitation. In 2004 the changes were recognized by WHO as one end of the spectrum of pulmonary neuroendocrine tumors.
The relationship between carcinoid tumorlets and other pulmonary diseases and its role in precipitating respiratory symptoms remains puzzling. The term DIPNECH was coined in 1992 by Aguayo (1) who described a new entity where idiopathic hyperplasia or dysplasia of pulmonary neuroendocrine cells occurred in the absence of other lung disorders. The changes were associated with physiologic and radiologic airflow limitation similar to obliterative bronchiolitis. This was the first description of pulmonary neuroendocrine hyperplasia as a primary process.
Because of similar symptoms, an obstructive pattern on pulmonary function tests, and chest imaging suggestive of air trapping, many patients receive a diagnosis of asthma for several years before the correct diagnosis is made. This similarity to other obstructive lung diseases can be explained by the pathologic changes of airway obstruction seen on biopsy. Pulmonary neuroendocrine cells, or Kulchitsky cells, are normally present in small numbers in airways, where they release a myriad of bioactive amines and peptides like serotonin, chromogranin A, gastrin-releasing peptide (GRP), and calcitonin.
Airway obstruction is believed to occur both due to physical obstruction of bronchioles by tumorlets and smooth muscle constriction caused by active mediators released. Bombesin and related peptides like gastrin releasing peptide, neuromedin B and neuromedin C are thought to cause bronchoconstriction indirectly through the release of several other bronchoconstrictors that act on smooth muscle cells (57). However, in vitro studies in guinea pig lungs suggest that bombesin may act directly by binding to specific receptors on smooth muscle cells (58).
Pulmonary neuroendocrine pathology occurs in a spectrum of three forms: hyperplasia, tumorlets and carcinoid tumors. DIPNECH is characterized by proliferation of neuroendocrine cells initially limited to the basement membrane of airways, when disease extends beyond the lumen of airway it is called carcinoid tumorlets. Tumorlets larger than 0.5 cm become carcinoid tumors and appear as nodules on chest CT scans. Diagnosis requires lung biopsy, with a surgical biopsy procedure more likely to provide diagnostic tissue than bronchoscopic transbronchial biopsies.
According to Aguayo`s definition of DIPNECH, patients have pulmonary symptoms with radiographic and physiologic abnormalities suggestive of obstructive lung disease, but in our review 12.2% of patients had no symptoms at all, and 15.5% had normal spirometry. We believe hyperplasia, tumorlets and carcinoid tumors represent different aspects of the same disease, the occurrence of symptoms, radiologic and physiologic airflow limitation depends on the time frame at which diagnosis was made, should those patients be followed up, they could develop symptoms and airflow limitation in the future. Thus, we propose to expand the definition to include patients with no symptoms or spirometry abnormalities. However, it remains uncertain whether asymptomatic patients who are diagnosed at an earlier stage need specific treatment or not.
It is also clinically difficult to establish a causal relationship, or determine the direction of the relationship between pulmonary neuroendocrine cell hyperplasia and other concomitant lung disorders, or harmful exposures (1,59, 60). In our review 27.2% of patients were active or previous smokers, only one patient lived at high altitude (more than 2000m) (14), 29 patients had a history of previous or current malignancy including 8 lung cancers (not shown in table), 13 patients had evidence of bronchiectasis, and one patient had honeycombing on imaging. These findings are similar to data obtained from individual case reports and series (2, 6, 14, 17, 19, 22, 29, 33, 37, 46, 47 and 53).
When the diagnosis is made, therapeutic options may include observation for mild symptoms, inhaled or systemic steroids, in addition to bronchodilators, especially if patients who show reversible airway obstruction on PFT. Other potential therapies are somatostatin analogues, however more studies are needed to determine their precise role. (27, 29, 43, 46)
Conclusion
DIPNECH is a rare clinical entity that requires a high clinical suspicion. Because of clinical, spirometry, and imaging similarity to other obstructive lung diseases, and the requirement for lung biopsy to make the diagnosis, DIPNECH is probably an under-diagnosed entity, with still limited treatment options. The diagnosis should probably be considered in any patient with difficult to treat obstructive lung disease, unexplained bronchiolitis, particularly if there are multiple small lung nodules present on chest CT scan. We propose to expand the definition of DIPNECH to include patients with even no symptoms or spirometric evidence of airflow limitation, as development of these abnormalities depends on the time frame at which diagnosis is made. It is also difficult to establish a causal relationship with other concomitant lung conditions, the presence of which should not rule out a diagnosis of DIPNECH.
References
- Aguayo SM, Miller YE, Waldron JA, et al. Brief report: idiopathic diffuse hyperplasia of pulmonary neuroendocrine cells and airways disease. N Engl J Med. 1992;327:1285-8. [CrossRef] [PubMed]
- Miller RR, Müller NL. Neuroendocrine cell hyperplasia and obliterative bronchiolitis in patients with peripheral carcinoid tumors. Am J Surg Pathol. 1995 Jun;19(6):653-8. [CrossRef] [PubMed]
- Armas OA, White DA, Erlandson RA, et al. Diffuse idiopathic pulmonary neuroendocrine cell proliferation presenting as interstitial lung disease. Am J Surg Pathol. 1995;19(8):963-70. [CrossRef] [PubMed]
- Brown MJ, English J, Muller NL. Bronchiolitis obliterans due to neuroendocrine hyperplasia: high-resolution CT–pathologic correlation. AJR Am J Roentgenol. 1997;168:1561-2. [CrossRef] [PubMed]
- Alshehri M, Cutz E, Banzhoff A, et al. Hyperplasia of pulmonary neuroendocrine cells in a case of childhood pulmonary emphysema. Chest. 1997 Aug;112(2):553-6. [CrossRef] [PubMed]
- Lee JS, Brown KK, Cool C, et al. Diffuse pulmonary neuroendocrine cell hyperplasia: radiologic and clinical features. J Comput Assist Tomogr. 2002;26:180-4. [CrossRef] [PubMed]
- Ruffini E, Bongiovanni M, Cavallo A, et al. The significance of associated pre-invasive lesions in patients resected for primary lung neoplasms. Eur J Cardiothorac Surg. 2004;26(1):165-72. [CrossRef] [PubMed]
- Fessler MB, Cool CD, Miller YE, et al. Idiopathic diffuse hyperplasia of pulmonary neuroendocrine cells in a patient with acromegaly. Respirology. 2004;9(2):274-7. [CrossRef] [PubMed]
- Carmichael MG, Zacher LL. The demonstration of pulmonary neuroendocrine cell hyperplasia with tumorlets in a patient with chronic cough and a history of multiple medical problems. Mil Med. 2005;170:439-441. [CrossRef] [PubMed]
- Swigris J, Ghamande S, Rice TW, et al. Diffuse idiopathic neuropathic cell hyperplasia an interstitial lung disease with airway obstruction. J Bronchol. 2005;12:62-65. [CrossRef]
- Terminella L, Duarte A. Obliterative bronchiolitis due to diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Chest 2005; 128:467S–468S. [CrossRef]
- Adams H, Brack T, Kestenholz P, et al. Diffuse idiopathic neuroendocrine cell hyperplasia causing severe airway obstruction in a patient with a carcinoid tumor. Respiration. 2006;73(5):690-3. [CrossRef] [PubMed]
- Johney EC, Pfannschmidt J, Rieker RJ, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia and a typical carcinoid tumor. J Thorac Cardiovasc Surg. 2006;131:1207-8. [CrossRef] [PubMed]
- Reyes LJ, Majó J, Perich D, et al. Neuroendocrine cell hyperplasia as an unusual form of interstitial lung disease. Respir Med. 2007 Aug;101(8):1840-3. [CrossRef] [PubMed]
- Singhania N, Liang Q, Cool C, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) in a patient with cough and dyspnea resistant to standard therapy. J Allergy Clin Immunol. 2007;119:S173. [CrossRef]
- Ge Y, Eltorky MA, Ernst RD, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Ann Diagn Pathol. 2007 Apr;11(2):122-6. [CrossRef] [PubMed]
- Davies SJ, Gosney JR, Hansell DM, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: an under-recognised spectrum of disease. Thorax. 2007 Mar;62(3):248-52. [CrossRef] [PubMed]
- Alqdah M, Jokhio S, El-zammar O. Diffuse idiopathic pulmonary neuroendocrine hyperplasia (DIPNECH). Chest 2007; 132:711S. [CrossRef]
- Warth A, Herpel E, Schmahl A, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) in association with an adenocarcinoma: a case report. J Med Case Reports. 2008;2:21. [CrossRef] [PubMed]
- Coletta EN, Voss LR, Lima MS, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia accompanied by airflow obstruction. J Bras Pneumol. 2009; 35:489-94. [CrossRef] [PubMed]
- Sanaee MS, O'Byrne PM, Nair P. Diffuse idiopathic pulmonary neuroendocrine hyperplasia, chronic eosinophilic pneumonia, and asthma. Eur Respir J. 2009; 34:1489-92. [CrossRef] [PubMed]
- Lim C, Stanford D, Young I, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: a report of two cases. Pathol Int. 2010; 60:538-41. [CrossRef] [PubMed]
- Irshad S, McLean E, Rankin S, et al. Unilateral diffuse idiopathic pulmonary neuroendocrine cell hyperplasia and multiple carcinoids treated with surgical resection. J Thorac Oncol. 2010; 5:921-3. [CrossRef] [PubMed]
- Stenzinger A, Weichert W, Hensel M, et al. Incidental postmortem diagnosis of DIPNECH in a patient with previously unexplained 'asthma bronchiale'. Pathol Res Pract. 2010 Nov 15;206(11):785-7. [CrossRef] [PubMed]
- Tippett V M, C G Wathen. Diffuse idiopathic neuroendocrine cell hyperplasia: an unusual cause of breathlessness and pulmonary nodules. BMJ Case Rep. 2010 Dec 1;2010. pii: bcr0520103006. [CrossRef] [PubMed]
- Cameron C M, Roberts F, Connell J, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: an unusual cause of cyclical ectopic adrenocorticotrophic syndrome. Br J Radiol. 2011 Jan;84(997):e14-7. [CrossRef] [PubMed]
- Nassar AA, Jaroszewski DE, Helmers RA, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: a systematic overview. Am J Respir Crit Care Med. 2011;184:8-16. [CrossRef] [PubMed]
- Falkenstern-Ge RF, Kimmich M, Friedel G, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: 7-year follow-up of a rare clinicopathologic syndrome. J Cancer Res Clin Oncol. 2011 Oct; 137(10):1495-8. [CrossRef] [PubMed]
- Gorshtein A, Gross DJ, Barak D, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia and the associated lung neuroendocrine tumors: clinical experience with a rare entity. Cancer. 2012 Feb 1;118(3):612-9. [CrossRef] [PubMed]
- Patel C, Tirukonda P, Bishop R, Mulatero C, Scarsbrook A. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) masquerading as metastatic carcinoma with multiple pulmonary deposits. Clin Imaging. 2012 Nov-Dec;36(6):833-6. [CrossRef] [PubMed]
- Montoro Zulueta FJ, Martínez Prieto M, Verdugo Cartas MI, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia with multiple synchronous carcinoid tumors. Arch Bronconeumol. 2012 Dec;48(12):472-5. [CrossRef] [PubMed]
- Walker CM, Vummidi D, Benditt JO, et al. What is DIPNECH? Clin Imaging. 2012 Sep-Oct;36(5):647-9. [CrossRef] [PubMed]
- Mireskandari M, Abdirad A, Zhang Q, et al. Association of small foci of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) with adenocarcinoma of the lung. Pathol Res Pract. 2013 Sep;209(9):578-84. [CrossRef] [PubMed]
- Dvořáčková J, Mačák J, Buzrla P. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: case report and review of literature. Cesk Patol. 2013 Apr; 49(2):99-102. [PubMed]
- Oba H, Nishida K, Takeuchi S, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia with a central and peripheral carcinoid and multiple tumorlets: a case report emphasizing the role of neuropeptide hormones and human gonadotropin-alpha. Endocr Pathol. 2013 Dec;24(4):220-8. [CrossRef] [PubMed]
- Karnatovskaia LV, Khoor A, Mira-Avendano I. Sarcoid-like reaction in diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Am J Respir Crit Care Med. 2014 Nov 15;190(10):e62-3. [CrossRef] [PubMed]
- Al-Ayoubi AM, Ralston JS, Richardson SR, Denlinger CE. Diffuse pulmonary neuroendocrine cell hyperplasia involving the chest wall. Ann Thorac Surg. 2014 Jan;97(1):333-5. [CrossRef] [PubMed]
- Killen H. DIPNECH presenting on a background of malignant melanoma: new lung nodules are not always what they seem. BMJ Case Rep. 2014 Feb 26;2014. pii: bcr2014203667. [CrossRef] [PubMed]
- Zhou H, Ge Y, Janssen B, et al. Double lung transplantation for diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. J Bronchology Interv Pulmonol. 2014 Oct; 21(4):342-5. [CrossRef] [PubMed]
- Erdini F, Spaltro AA, Ruiu A, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) and multiple pulmonary epithelioid hemangioendothelioma (PEH): a case report. Pathologica. 2015 Mar;107(1):37-42. [PubMed]
- Abrantes C, Oliveira RC, Saraiva J, et al. Pulmonary peripheral carcinoids after diffuse idiopathic pulmonary neuroendocrine cell hyperplasia and tumorlets: report of 3 cases. Case Rep Pulmonol. 2015;2015:851046. [CrossRef] [PubMed]
- Pietrangeli V, Piciucchi S, Tomassetti S, et al. Diffuse neuroendocrine hyperplasia with obliterative bronchiolitis and usual interstitial pneumonia: an unusual "headcheese pattern" with nodules. Lung. 2015 Dec;193(6):1051-4. [CrossRef] [PubMed]
- Chauhan A, Ramirez RA. Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) and the role of somatostatin analogs: a case series. Lung. 2015 Oct;193(5):653-7. [CrossRef] [PubMed]
- Hassan WA, Udaka N, Ueda A, et al. Neoplastic lesions in CADASIL syndrome: report of an autopsied Japanese case. Int J Clin Exp Pathol. 2015 Jun 1;8(6):7533-9. [PubMed]
- Ofikwu G, Mani VR, Rajabalan A, et al. Case report: a rare case of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Case Rep Surg. 2015;2015:318175. [CrossRef] [PubMed]
- Carr LL, Chung JH, Duarte Achcar R, et al. The clinical course of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Chest. 2015 Feb;147(2):415-2. [CrossRef] [PubMed]
- Baniak NM, Wilde B, Kanthan R. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH)--An uncommon precursor of a common cancer? Pathol Res Pract. 2016 Feb;212(2):125-9. [CrossRef] [PubMed]
- Kuruva M, Shah HR, Dunn AL, et al. 111In-Pentetreotide imaging in diffuse idiopathic neuroendocrine hyperplasia of the lung. Clin Nucl Med. 2016 Mar;41(3):239-40. [CrossRef] [PubMed]
- Cansız Ersöz C, Cangır AK, Dizbay Sak S. Diffuse neuroendocrine cell hyperplasia: report of two cases. Case Rep Pathol. 2016;2016:3419725. [CrossRef] [PubMed]
- Ishizaki U, Itoh R, Matsuo Y, et al. Diffuse Idiopathic Pulmonary neuroendocrine cell hyperplasia: a case with long-term follow-up. J Thorac Imaging. 2016 Nov;31(6):W76-W79. [CrossRef] [PubMed]
- Chatterjee K, Kamimoto JJ, Dunn A, et al. A case of DIPNECH presenting as usual interstitial pneumonia. Pneumonol Alergol Pol 2016;84(3):174-7. [CrossRef] [PubMed]
- Escudero AG, Zarco ER, Arjona JC. Expression of developing neural transcription factors in diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH). Virchows Arch. 2016 Sep;469(3):357-63. [CrossRef] [PubMed]
- Trisolini R, Valentini I, Tinelli C, et al. DIPNECH: association between histopathology and clinical presentation. Lung. 2016 Apr;194(2):243-7. [CrossRef] [PubMed]
- Warren WA, Dalane SS, Warren BD, et al. Ten years of chronic cough in a 64-year-old man with multiple pulmonary nodules. Chest. 2016; 150(3):e81-e85. [CrossRef] [PubMed]
- Hsu J, Jia L, Pucar D, et al. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia and granulomatous inflammation mimicking high-grade malignancy on FDG-PET/CT. Clin Nucl Med. 2017 Jan;42(1):47-49. [CrossRef] [PubMed]
- Frölich F. Die Helle Zelle der Bronchialschleimhaut und ihre Beziehungen zum Problem der Chemoreceptoren. Frankf Z Pathol. 1949 Apr;60(3-4):517-59.
- Barnes PJ. Pharmacology of airway smooth muscle. Am J Respir Crit Care Med. 1998 Nov;158(5 Pt 3):S123-32. [CrossRef] [PubMed]
- Lach E, Haddad EB, Gies JP. Contractile effect of bombesin on guinea pig lung in vitro: involvement of gastrin-releasing peptide-preferring receptors. Am J Physiol. 1993 Jan; 264(1 Pt 1):L80-6. [PubMed]
- Campanha RB, Matos C, Nogueira F. DIPNECH (diffuse idiopathic pulmonary neuroendocrine cell hyperplasia): a rare syndrome or undiagnosed? J Pulm Respir Med 2015;5:4. [CrossRef]
- Aubry MC, Thomas CF Jr, Jett JR, et al. Significance of multiple carcinoid tumors and tumorlets in surgical lung specimens: analysis of 28 patients. Chest. 2007 Jun;131(6):1635-43. [CrossRef] [PubMed]
Cite as: Yamin HS, Hawarri F, Labib M, Massad E, Haddad H. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia in a patient with multiple pulmonary nodules: case report and literature review. Southwest J Pulm Crit Care. 2017;15(6):282-93. doi: https://doi.org/10.13175/swjcc139-17 PDF
November 2017 Pulmonary Case of the Month
Lewis J. Wesselius, MD
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
A 67-year-old man developed a right neck mass and underwent a right radical neck dissection. It was initially thought to be a high-grade sarcomatoid cancer, but after review was determined to be metastatic melanoma.
Past Medical History, Social History and Family History
He had no significant past medical or family history. He was a nonsmoker.
Physical Examination
His initial physical examination showed a right neck mass but was otherwise unremarkable. No abnormal skin lesions were identified.
PET/CT Scan
A positron emission tomography/computed tomography (PET/CT) scan showed increase uptake in the neck (Figure 1A) but his chest showed no increased uptake (Figure 1B).
Figure 1. Panel A: PET/CT scan showing increased tracer uptake in the right neck (arrow). Panel B: No abnormal tracer uptake is seen within the chest.
Which of the following is/are true? (Click on the correct answer to proceed to the second of four pages)
- Bronchoscopy should be performed to search for bronchial melanoma
- Radiation and oncology consultation should be obtained
- The pathologic diagnosis is likely wrong since no primary melanoma can be identified
- 1 and 3
- All of the above
Cite as: Wesselius LJ. November 2017 pulmonary case of the month. Southwest J Pulm Crit Care. 2017;15(5):181-7. doi: https://doi.org/10.13175/swjpcc117-17 PDF
June 2017 Pulmonary Case of the Month
Robert Horsley, MD
Lewis J. Wesselius, MD
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ USA
History of Present Illness
A 61-year-old woman presented to the emergency department for 3 days of fevers up to 102º F, malaise, and progressive shortness of breath. Her symptoms started immediately after he last naltrexone injection for alcohol use disorder.
Past Medical History, Social History and Family History
- Alcohol use disorder
- Treated with monthly naltrexone injections, received 3 doses total, and gabapentin
- No other previous medical issues
- Nonsmoker
Physical Examination
- Vital signs: Pulse 100, BP 108/90, respiratory rate 34, SpO2 93% 10L non-rebreathing mask
- Cyanotic on room air
- Lungs clear
Radiography
A portable chest x-ray was performed in the emergency department (Figure 1).
Figure 1. AP chest radiograph taken in the emergency department.
A thoracic CT scan was performed (Figure 2).
Figure 2. Representative images from thoracic CT in lung windows.
Laboratory
- CBC showed a white blood cell count of 12,000 cells/mcL.
- The differential showed a left shift.
- Lactate was 5.2 mmol/L
Which of the following is (are) true? (Click on the correct answer to proceed to the second of five pages)
- A lactate level of 5.2 can be a normal finding in a critically ill patient
- Her symptoms are likely an allergic reaction to naltrexone
- The most likely diagnosis is an atypical pneumonia
- 1 and 3
- All of the above
Cite as: Horsley R, Wesselius LJ. June 2107 pulmonary case of the month. Southwest J Pulm Crit Care. 2017;14(6):255-61. doi: https://doi.org/10.13175/swjpcc063-17 PDF
April 2016 Pulmonary Case of the Month
Lewis J. Wesselius, MD
Rodrigo Cartin-Ceba, MD
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, 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): Lewis J. Wesselius, MD. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity.
Learning Objectives:
As a result of this activity I will be better able to:
- Correctly interpret and identify clinical practices supported by the highest quality available evidence.
- Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
- Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
- 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 Banner University Medical Center Tucson
Current Approval Period: January 1, 2015-December 31, 2016
Financial Support Received: None
History of Present Illness
The patient is a 75-year-old woman who presented with a chest mass incidentally found on chest x-ray. She was asymptomatic
Past Medical History, Social History and Family History
She has no significant past medical history and has never smoked. Family history is noncontributory.
Physical Examination
Physical examination was unremarkable.
Radiography
A thoracic CT scan was performed (Figure 1).
Figure 1. Representative thoracic CT scan in soft tissue windows showing a mass (arrow).
Which of the following are possible causes of the mass? (Click on the correct answer to proceed to the second of four panels)
Cite as: Wesselius LJ, Cartin-Ceba R. April 2016 pulmonary case of the month. Southwest J Pulm Crit Care. 2016 Apr;12(4):126-9. doi: http://dx.doi.org/10.13175/swjpcc032-16 PDF
December 2015 Pulmonary Case of the Month
Zachary M. Berg, MD
Kashif Yaqub, MD
Brian Wojek, MD
Khang Tran, MD
Karen L. Swanson, DO
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ
History of Present Illness
The patient is a 70-year-old man with a history of a chronic dry cough for 5 years, who presented to the emergency department with worsening cough and shortness of breath.
Two weeks prior to symptom onset, was on trip in the United Kingdom, he developed gastroenteritis which spontaneously resolved.
Past Medical History, Social History, and Family History
- Old healed TB scar with positive PPD at 17 years of age prior to joining Air Force. No treatment given and patient was asymptomatic from a pulmonary point of view since then.
- Squamous cell carcinoma of the skin on the scalp, status post excision complicated by osteomyelitis, status post surgical graft from hip with prolonged course of IV antibiotics in 2010.
- Fractured left clavicle, status post repair 20 years ago.
- Hay fever.
- Hyperlipidemia.
- Squamous cell carcinoma removed from left arm.
- Varicose veins, lower extremity.
- Married. Retired police officer. Does not smoke.
- Family history is noncontributory
Physical Examination
- General: In moderate respiratory distress.
- Vitals: SpO2 on room air of 65%, 94% on high flow oxygen. Blood pressure 124/84, afebrile
- Lungs: Fine bibasilar crackles posteriorly.
- Heart: Regular rhythm without murmur.
- The remainder of the physical examination was normal.
Laboratory Evaluation
- CBC: unremarkable except white blood cell count 20.5 x 103 cells/ɥL, neutrophil predominant
- BNP: 366 pg/mL
- Mycobacterium Quantiferon: Positive
- Mycoplasma IgM: Positive at 1.18 U/L
Radiography
Initial chest x-ray is shown in Figure 1.
Figure 1. Initial chest x-ray.
What is the best next step in the patient's evaluation? (Click on the correct answer to proceed to the second of five panels)
- Begin erythromycin or doxycycline for Mycoplasma pneumonia
- Begin heparin for presumptive pulmonary embolism
- Thoracic CT scan
- 1 and 3
- All of the above
Cite as: Berg ZM, Yaqub K, Wojek B, Tran K, Swanson KL. December 2015 pulmonary case of the month. Southwest J Pulm Crit Care. 2015;11(6):240-5. doi: http://dx.doi.org/10.13175/swjpcc146-15 PDF
Pulmonary Hantavirus Syndrome: Case Report and Brief Review
Charles J. VanHook, MD
Britt Warner, PA
Angela Taylor, MD
Longmont United Hospital
Longmont, Colorado
A 31-year-old white man presented to the emergency department complaining of fever, headache, mild confusion, and muscle aches. Approximately three days earlier he had developed non-quantified fever and diffuse muscle aches and pains. He was employed as a feedlot worker. He had visited an urgent care center one day earlier and had been advised to increase his oral fluid intake and to use non-steroidal anti-inflammatory agents as needed. Upon arrival to the emergency department he was found to have a temperature of 103.6º Fahrenheit, blood pressure of 125/72 mm Hg, respiratory rate of 40 breaths per minute, and room-air oxygen saturation of 84% by pulse oximetry. Auscultation of the chest disclosed diffuse rales. Heart sounds were rapid and regular. Abdominal exam was benign. There was no skin rash. Central nervous exam demonstrated agitation and confusion, but was otherwise non-focal. Laboratory examination revealed a white blood count of 11.7 K/uL, hemoglobin of 21.5 g/DL, hematocrit of 66.8%, platelet count of 73 K/uL, partial thromboplastin time of 36 seconds, lactic acid of 2.4 mm/L, and procalcitonin of 43 ng/mL. Chest radiograph disclosed extensive bilateral infiltrates (Figure 1).
Figure 1. Chest x-ray showing bilateral infiltrates
The patient precipitously declined, with severe respiratory distress, and was emergently intubated. Despite aggressive measures, including mechanical ventilation with an FIO2 of 1.0 and PEEP of 18 cm H2O, vigorous intravenous intravenous fluid resuscitation with normal saline, and pressor support with intravenous norepinephrine and vasopressin, the patient developed refractory hypoxemia. This was followed by a bradycardic arrest and death 2 hours after presentation. Serology sent at the time of admission later returned as IgM positive for hantavirus, with subsequent testing positive for Sin Nombre IgM.
Hantaviruses are RNA viruses of the family Bunyaviridae that are transmitted to humans by contact with the saliva, urine, or feces of infected rodents, which serve as persistently infected hosts (1). Patients who work in proximity to rodents, such as animal trappers, farmers, and forestry workers are at highest risk for infection. In the Western Hemisphere, there are approximately 200 cases per year of Hantavirus Pulmonary Syndrome (HPS), which was first identified in the Four Corners area of the Southwestern United States in 1993 (2). In the United States, HPS is most commonly caused by the Sin Nombre subfamily of hantavirus. A two-week incubation period precedes a 3-6 day prodromal period during which fever and myalgia are prominent features. The cardiopulmonary phase of HPS follows, with the development of acute non-cardiogenic pulmonary edema and multi-organ dysfunction. Typical laboratory abnormalities are leukocytosis and thrombocytopenia. Elevations in hematocrit and partial thromboplastin time are strong predictors of mortality, which approaches 40%. Definitive diagnosis depends on the serologic identification of IgM antibody to hantavirus using ELISA technology. Immunochromatographic technology may allow for same day diagnosis (3). Treatment is supportive, and varies with the severity of disease. It may include volume resuscitation, ventilatory support, and renal replacement therapy. There is no established anti-viral therapy for Hantavirus infection, although ribavirin is often used in Asia. Corticosteroids have also been used sporadically with some success, but their use remains controversial (3).
Although Hantavirus remains a rare disease, prodromal symptoms in a patient with associated epidemiologic risk factors should heighten clinical suspicion.
References
- Lednicky JA. Hantavirus: A short review. Arch Pathol Lab Med. 2003;127:30-35. [PubMed]
- Duchin JS, Koster FT, Peters CJ, Simpson GL, Tempest B, Zaki S, Ksiazek TG, Rollin PE, Nichol S, Umland E, Moolenaar RL, Reef SE, Nolte KB, Gallaher MM, Butler JC, Breiman RF. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. N England J Med 1994;330:949-55 [CrossRef] [PubMed]
- Bi Z, Formenty P, Roth C Hantavirus infection: A review and global update. J Infect Developing Countries. 2008;2(1):3-23. [CrossRef] [PubMed]
Cite as: VanHook CJ, Warner B, Taylor A. Pulmonary hantavirus syndrome: case report and brief review. Southwest J Pulm Crit Care. 2015;11(3):121-3. doi: http://dx.doi.org/10.13175/swjpcc122-15 PDF
September 2015 Pulmonary Case of the Month: Holy Smoke
Samir Sultan, DO
David M. Baratz, MD
Banner University Medical Center Phoenix
Phoenix, AZ
History of Present Illness
A 43-year-old woman presents to the office for second opinion of her dyspnea. She has very mild dyspnea with exertion which she notices when she cannot keep up with people going up stairs. She also has a "smoker’s cough".
Past Medical History, Family History, Social History
Her past medical history, family history and social history are unremarkable other than she smokes 1 ppd for the past 20 years and had a "collapsed lung" about 15 years ago.
Physical Examination
Her physical examination was unremarkable except for a small scar on her right chest.
Radiography
A chest x-ray (Figure 1) was performed.
Figure 1. PA (Panel A) and lateral (panel B) chest radiography.
Which of the following are true regarding the chest x-ray? (Click on the correct answer to proceed to the second of five panels)
- The chest -ray shows a widened mediastinum
- The chest x-ray is normal
- The chest x-ray shows a diffuse reticulonodular infiltrate
- The chest x-ray shows bilateral hilar adenopathy
- The chest x-ray shows small bilateral pleural effusions
Cite as: Sultan S, Baratz DM. September 2015 puilmonary case of the month: holy smoke. Southwest J Pulm Crit Care. 2015;11(3):90-6. doi: http://dx.doi.org/10.13175/swjpcc112-15 PDF
April 2015 Pulmonary Case of the Month: Get Down
Michael Pham, MD
Karen Swanson, DO
Department of Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ
History of Present Illness
A 59 year old woman was admitted with hypercapnic respiratory failure and an altered mental state. She had progressive “breathing issues” for the last year and was increasingly error prone with decreased mental acuity at the end of her work shift for the last 6 months. She was on oxygen at 2 L by nasal cannula at home and has had several admissions over the last 3 months for hypercapnic respiratory failure.
Past Medical History
Obstructive sleep apnea with continuous positive airway pressure (CPAP) intolerance, type 2 diabetes mellitus, and fibromyalgia. She is a life-long nonsmoker.
Physical Examination
Vital signs: T 36.9º C, P 116 beats/min, R 42 breaths/min, BP 134/80 mm Hg, SpO2 93% on room air.
General: She appeared very short of breath.
Neck: No jugular venous distention.
Lungs: Clear anteriorly.
Heart: RR with a tachycardia.
Abdomen: no organomegaly or masses.
Neurologic:
- +3-to-4 of 5 strength upper and lower extremities
- Difficulty holding upright posture
- Decreased sensation in lower extremities
- R > L lower extremity gastrocnemial fasciculations
- Hand asterixis/tremor bilaterally
- Decreased DTRs diffusely
Laboratory
ABG's: pH 7.3 / CO2 82 / pO2 77. Following 4 hours CPAP: pH 7.4 / CO2 68 / pO2 80
Basic metabolic panel: Na+ 138 | Cl- 86 | Creatinine 0.4
K+ 4.8 | TCO2 44 | BUN 13
Ca++ 4.9 / PO4- 4.1 / Mg++ 1.9
Complete blood count: WBC 11.9 cells/mm3, Hemoglobin 10.8 g/dL
Liver function tests, ammonia and lactate were all normal.
Radiography
Admission chest x-ray is shown in Figure 1.
Figure 1. Admission chest x-ray.
Which of the following is/are true regarding the chest x-ray? (Click on the correct answer to proceed to the second of four panels)
- Elevated right hemidiaphragm
- Right pleural effusion
- Volume loss in the right hemithorax
- 1 and 3
- All of the above
Reference as: Pham M, Swanson K. April 2015 pulmonary case of the month: get down. Southwest J Pulm Crit Care. 2015;10(4):152-8. doi: http://dx.doi.org/10.13175/swjpcc040-15 PDF
January 2015 Pulmonary Case of the Month: More Red Wine, Every Time
Uzair Ghori, MD (UGhori@salud.unm.edu)
Shozab Ahmed, MD (Sahmed@salud.unm.edu)
University of New Mexico
Albuquerque, New Mexico
History of Present Illness
A 41-year-old man travelling from Texas to Las Vegas, Nevada presents to the Emergency Room in Albuquerque, New Mexico with petechial rash, photophobia and headache of 2 weeks duration. The patient complains of general malaise, arthralgia, trouble sleeping, shortness of breath associated with cough and intermittent bilateral lower extremity swelling of 3 weeks duration.
PMH, SH & FH
The patient was prescribed lisinopril and metformin for hypertension and diabetes mellitus, respectively. He admitted occasional drinking, smoking a variable quantity for 30 years but currently not smoking. He denied any illicit drug use.
Physical Exam
Vitals: Heart Rate-92, Blood Pressure-116/45 mm Hg, Respiratory Rate-44 breaths/min, Temperature- 37.2ºC, SpO2-98% on non-rebreather mask.
General: His mental status was not altered.
HEENT: No papilledema was appreciated on eye exam.
Neck: JVP not appreciated.
Lungs: he had diminished breath sounds bilaterally on auscultation.
Heart: His heart had a regular rate and rhythm with no murmurs rubs or gallops.
Abdomen: No abdominal distention or lower extremity edema appreciated.
Skin: A petechial rash was noted most prominently in the lower extremities.
Based on the initial presentation the most appropriate investigations would be? (Click on the correct answer to proceed to the 2nd of 6 panels)
- CBC, CT head, echocardiogram, blood cultures, metabolic panel, inflammatory markers
- CBC, UA, lumbar puncture, chest x-ray, inflammatory markers, metabolic panel
- Echocardiogram, CBC, UA, venous blood gases, bronchoscopy, CT head
- Stress test, CXR, inflammatory markers, lumbar puncture, ultrasound abdomen, metabolic panel
- UA, lumbar Puncture, bronchoscopy, echocardiogram, CT head, inflammatory markers
Reference as: Ghori U, Ahmed S. January 2015 pulmonary case of the month: more red wine, every time. Southwest J Pulm Crit Care. 2015;10(1):1-7. doi: http://dx.doi.org/10.13175/swjpcc155-14 PDF
November 2014 Pulmonary Case of the Month: BAL Eosinophilia
Salma Imran Patel, MD, MPH
Lewis J. Wesselius, MD
Laszlo T. Vaszar, MD
Departments of Internal Medicine and Pulmonary Medicine
Mayo Clinic Arizona
Scottsdale, AZ
History of Present Illness
A 62 year-old- was admitted to the hospital for 2 weeks of worsening cough, yellowish sputum production, shortness of breath and pleuritic chest pain. The patient has had asthma since the 1970s and presently uses salmeterol/fluticasone and albuterol as a rescue inhaler. He was intubated once four years ago, and has had a total of three hospitalizations for his asthma and 15 courses of prednisone. He is sensitive to cold/hot air, all animals, aspirin and acetaminophen.
PMH, FH, SH
In addition to the asthma, he has a history of type 2 diabetes mellitus, hypertension, gastroesophageal reflux disease, and chronic abdominal pain.
Physical Examination
Vital signs: T 36.6º C, HR 98, BP129/69, RR 20 and SPO2 96% on 2 L of oxygen by nasal cannula. He was mildly distressed and coughing. His pulmonary exam showed diffuse inspiratory and expiratory wheezes. The remainder of his exam was unremarkable.
Laboratory
Significant findings on laboratory evaluation include an elevated white blood cell count of 13,400 cells/ɥL, an elevated absolute eosinophil count of 2,820 eosinophils/ɥL, an elevated glucose of 131 mg/dL, and a low sodium of 120 mEq/L.
Imaging
A thoracic CT scan was performed (Figure 1).
Figure 1. Representative images in lung windows from thoracic CT scan.
Which of the following best describes the CT scan? (click on the correct answer to proceed to the next panel)
- Cavitary changes in both apices
- Central consolidation
- Fibrotic changes at the bases
- Peripheral opacities
- Normal
Reference as: Palel SI, Wesselius LJ, Vasczar LT. November 2014 pulmonary case of the month: BAL eosinophilia. Southwest J Pulm Crit Care. 2014;9(5):251-6. doi: http://dx.doi.org/10.13175/swjpcc136-14 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
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.
PMH, FH, SH
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.
Radiography
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)
- Bronchoscopy with bronchoalveolar lavage
- Bronchoscopy with transbronchial biopsy
- Needle biopsy
- Thoracentesis
- 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: http://dx.doi.org/10.13175/swjpcc098-14 PDF