June 2022 Pulmonary Case of the Month: A Hard Nut to Crack

Daniel Gergen MD¹

Anne Reihman MD¹

Carolyn Welsh MD^1,2

¹Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Colorado, Aurora, Colorado USA

²Eastern Colorado Veterans Affairs Medical Center, Aurora, Colorado USA

History of Present Illness: A 54-year-old man presented to clinic with chronic cough, dyspnea on exertion, unintentional weight loss, and night sweats. Seven months before, he developed dyspnea on exertion and symptoms did not improve with inhalers. Four months prior to presentation, he was treated for presumed community-acquired pneumonia of the right lower lobe. Neither symptoms nor chest radiograph improved with multiple courses of antibiotics. In the four weeks prior to presentation his symptoms progressed to the point that he was unable to walk in his house without significant dyspnea.

Review of systems: 10-pound unintentional weight loss and six weeks of night sweats.

Past Medical History, Social History and Family History: The patient had a 15-pack-year smoking history and quit 15 years prior to presentation. He had no other past medical history, surgical history, family history, nor medications.

Physical Examination: Vital signs were normal on presentation. Physical exam showed faint wheezing and decreased breath sounds over the right posterior lung fields.

Radiography: Chest radiograph demonstrated dense opacification in the superior segment of the right lower lobe (Figure 1).

Figure 1. Initial chest radiography. A: PA view. B: Lateral view.

What are diagnostic possibilities at this time?

1. Lung abscess
2. Lung cancer
3. Foreign body with post-obstructive pneumonia
4. Tuberculosis
5. 1 and 3
6. All the above

Cite as: Gergen D, Reihman A, Welsh C. June 2022 Pulmonary Case of the Month: A Hard Nut to Crack. Southwest J Pulm Crit Care Sleep. 2022;24(6):89-92. doi: https://doi.org/10.13175/swjpccs024-22 PDF

December 2019 Pulmonary Case of the Month: A 56-Year-Old Woman with Pneumonia

Lewis J. Wesselius, MD

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ USA

History of Present Illness

A 56-year-old woman complained of 6 weeks of increasing cough and shortness of breath. She had been treated for pneumonia with antibiotics, but when she failed to improve, she was begun on prednisone. She was receiving oxygen at 4 L/min by nasal cannula at the time she was seen.

PMH, SH, and FH

Her past medical history, social history and family were unremarkable other than a previous history of silicone breast implants. She was a nonsmoker.

Physical Examination

Her physical examination showed bibasilar crackles but was otherwise unremarkable.

Radiography

Her chest x-ray is shown in Figure 1.

Figure 1. Patient’s chest x-ray taken 6 weeks after the beginning of her illness.

Which of the following should be done at this time? (Click on the correct answer to be directed to the second of seven pages)

1. Coccidioidomycosis serology
2. Sputum gram stain and culture
3. Thoracic CT scan
4. 1 and 3
5. All of the above

Cite as: Wesselius LJ. December 2019 Pulmonary case of the month: a 56-year-old woman with pneumonia. Southwest J Pulm Crit Care. 2019;19(6):149-55. doi: https://doi.org/10.13175/swjpcc067-19 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)

1. Prior chest x-rays, CT scans, pulmonary function testing and lung biopsy
2. Repeat CT scan, pulmonary function testing
3. Rheumatological serologies
4. 1 and 3
5. 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 

March 2016 Pulmonary Case of the Month

Ramachandra R. Sista, MD

Maxwell L. Smith, MD

 Lewis J. Wesselius, MD

Departments of Pulmonary Medicine and Pathology

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): Ramachandra R. Sista, 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:

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 Banner University Medical Center Tucson

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

History of Present Illness

A 74-year-old man was referred for a recently identified right pleural effusion and dyspnea on exertion.  

Past Medical History, Family History and Social History

He has a history of anemia, hypertension, and prostate cancer with a prostatectomy in 2015. He is a life-long nonsmoker and has no occupational exposures. Family history is noncontributory.

Physical Examination

He had diminished breath sounds at the right lung base and a palpable spleen. Otherwise the physical examination was unremarkable.

Laboratory

CBC: hemoglobin  8.5 g/dL, white blood count  7.7 X 109 cells/L,  platelets 357 X 109 cells/L.

Radiography

A chest X-ray showed a right pleural effusion. Representative images from the CT scan are shown in Figure 1.

Figure 1. Representative images from the CT scan.

Which of the following is the most likely diagnosis? (Click on the correct answer to proceed to the second of five panels)

1. Empyema
2. Lung cancer
3. Tuberculosis
4. Usual interstitial pneumonia
5. Valley fever (coccidioidomycosis)

Cite as: Sista RR, Smith ML, Wesselius LJ. March 2016 pulmonary case of the month. Southwest J Pulm Crit Care. 2016;12(3):74-80. doi: http://dx.doi.org/10.13175/swjpcc020-16 PDF

Why Chronic Constipation May be Harmful to Your Lungs: A Case Report and Review of Lipoid Pneumonia and Mycobacterium fortuitum Leading to Acute Respiratory Failure and Septic Shock

Sandra Till, DO

Manoj Mathew, MD 

Da-Wei Liao, MD

Christina Ramirez, MD 

Banner University Medical Center

Phoenix, AZ

Case Report

A 43 year-old female with a past medical history of right-sided hemiparesis secondary to motor vehicle accident 17 years prior presented a two week history of cough, fever and right-sided pleuritic chest pain. Her baseline status included using a wheelchair, living alone at home and working as a teacher.

On admission she had a temperature of 39.6º C, was tachycardia and hypotensive requiring vasopressors. Labs were remarkable for a white count of 25,000 cells/mcL. Chest x-ray showed right-sided infiltrate and pleural effusion (Figure 1).

Figure 1. Chest x-ray on presentation.

Bronchoscopy and thoracentesis was performed upon admission. The pleural fluid wasexudative with a glucose of 78 and no suggestion of loculations on chest x-ray or ultrasound. The patient was started on therapy for community-acquired pneumonia.

On day 4 after admission, the patient had increasing sinus tachycardia, hypotension and was worsening despite being on antimicrobial therapy. A CT angiogram of the chest was performed (Figure 2).

Figure 2. Initial CT scan on day 4 of admission. Panel A: axial view showing pneumonia and right pleural effusion. Panel B: coronal view.

CT angiogram was negative for pulmonary embolism and a percutaneous chest tube was placed on day 4 for drainage of pleural effusion due to development of loculations. On day 7, the pleural fluid from initial thoracentesis grew acid-fast bacteria identified as Mycobacterium fortuitum.

Bronchoscopy was performed on day 8 and there was no endobronchial obstruction.

Bronchoscopic alveolar lavage cultures grew Mycobacterium fortuitum. She had no history of bronchiectasis, skin infection, or immunoglobulin deficiency. Treatment with amikacin and levofloxacin was initiated based on susceptibilities.

The pleural chest tube was removed on day 14 (Figure 3). At this time the patient was transferred to a skilled nursing facility.

Figure 3. CT scan on day 13 prior to chest tube removal. Panel A: axial view. Panel B: coronal view.

The patient continued antibiotic treatment for Mycobacterium fortuitum with amikacin and levofloxacin, however, serial sputum cultures remained positive. On day 25, in the skilled nursing facility, the patient developed respiratory failure due to increased right effusion and worsening pneumonia. She was transferred to our facility were she was intubated and a new right-sided chest tube was placed. After placement of chest tube and drainage the right lung did not expand. Decompensation was felt to be related to the inadequate evacuation of the empyema with plans to solely continue antimicrobial therapies by the outside facility.

Figure 4. CT scan on day 30 showing trapped lung. Panel A: axial view. Panel B: coronal view. 

Repeat pleural fluid cultures and BAL once again grew Mycobacterium fortuitum. She was taken for decortication and right middle and lower lobe resection by thoracic surgery. Due to extensive disease the patient required right thoracotomy, decortication, parietal pleurectomy, right middle lobectomy, and wedge resection of a right lower lobe lung abscess.

The lung pathology is shown below and was consistent with lipoid pneumonia (Figure 5).

Figure 5. Panels A & B: CD 163 stains showing lipid present within histiocytes. Panels C & D: histology demonstrating severe lipoid pneumonia. Panels E & F: Granulomatous inflammation with giant cells. Panel G: pleura. Panel H: abscess.

There were no mycobacteria cultured on the lung biopsy. There were areas of both acute and chronic fibrosis noted on pathology report along with areas of acute interstitial pneumonitis and granulomatous inflammation.

During post-operative phase the patient confirmed that she was drinking mineral oil chronically for treatment of constipation. Repeat sputum cultures 7 days post operatively were negative for Mycobacterium fortuitum. She continued to improve with treatment of Mycobacterium fortuitum and postoperative cultures remained negative. She was able to liberate from the ventilator and returned home at after a prolonged course of rehabilitation.

Lipoid Pneumonia and Associated Mycobacterial Infection

The association between acid-fast bacteria and lipoid pneumonia was first reported in 1925 and since case reports have been noted. In 1953, a case report and literature review documented six cases of “saprophytic” mycobacteria was noted in conjunction with lipoid pneumonia. It was observed at this time that the fatty environment of lipoid pneumonia might assist with the growth of mycobacterium (1). Since then, intermittent case reports have been published reporting lipoid pneumonia with atypical mycobacteria.

There are two main categories of lipoid pneumonia, endogenous and exogenous. The endogenous form is also known as cholesterol pneumonia or golden pneumonia. It is associated with lysis of lung tissue distal to obstruction due to malignancy, fat storage disease such as Neiman-Pick or Gaucher's, medications and therapies including chemotherapeutic agents, amiodarone and radiation therapy. Pulmonary alveolar proteinosis has also been reported in idiopathic cases with granulomatosis with polyangiitis and connective tissue diseases (2-4). In polarized light microscopy after staining with sulfuric and acetic acid, the sample reveals cholesterol crystals, which is diagnostic of endogenous lipoid pneumonia (3).

Exogenous lipoid pneumonia occurs when external substances enter the lungs due to inhalation or aspiration (3). Cases have been reported from mineral oil, paraffin use, oil based nasal drops, total parenteral nutrition, mineral oil nose drops, black fat tobacco smoking, milk, and liquid hydrocarbons used by flame blowers (2-6). The pulmonary reaction to each substance varies. For example, mineral oils are fairly inert and less likely to produce alveolar inflammation, where milk fats are hydrolyzed by lung lipases leading to a significant inflammatory response (2).

The clinical presentation and appearance of lipoid pneumonia is variable from consolidation to effusion to nodule. Nodules from lipids may have elevated standardized uptake value (SUV) on positron emission tomography (PET) scan. The BAL from lipoid pneumonia may demonstrate lipid laden foamy macrophages (2). Mineral oil granuloma (paraffinoma) also can present as a spiculated mass mimicking malignancy.

Mineral oil is notorious for causing lipoid pneumonia by aspiration for several reasons. First, it floats on the column of undigested material in the esophagus so it is first to be aspirated (5); secondly, it impairs phagocytosis at the alveolar level; and lastly, it inhibits the cough reflex and motor function of ciliated mucosa (7).

The impairment of phagocytosis associated with lipoid pneumonia is thought to be a contributing factor in why atypical mycobacterium strives in the lipid rich environment of lipoid pneumonia (5,6). Malnutrition is also thought to be a component of risk as it due to impairment in cell mediated immunity (6). Lipid acts as mechanical protection for the mycobacteria favoring tissue necrosis facilitating secondary infection. Also it is thought that lipids may activate the cell walls of the atypical mycobacteria leading to increased virulence of the mycolic acids within the wall of the bacteria (8).

Mycobacterium fortuitum rarely causes pulmonary disease unless associated with lipoid pneumonia. This is often related to gastroesophageal disease and chronic vomiting and aspiration of contents. It is typically associated with skin and soft tissue infections and is a rapid growing mycobacterium and most frequently found in water and soil (2,8,9)

This case demonstrates an atypical presentation of lipoid pneumonia and Mycobacterium fortuitum infection leading to septic shock and ventilator failure. Although the association of lipoid pneumonia and mycobacterial infections is well documented, the rapid and acute decline in this patient’s clinical status is unusual. This can be attributed to incomplete drainage of the initial empyema prior to transfer to the skilled nursing facility.

The etiology of the lipoid pneumonia was chronic aspiration of mineral oil producing an ideal environment for growth of Mycobacterium fortuitum. The absence of bronchiectasis, immunoglobin deficiency, skin infections should prompt further evaluation for abnormal lung architecture serving as a nidus for Mycobacterium fortuitum Infection. In our case, failure to improve is attributed to a persistent nidus for infection. We advocate resection of diseased lung segments of lipoid pneumonia to facilitate successful treatment of Mycobacterium fortuitum. In conclusion, if a patient has lipoid pneumonia with signs of clinical infection, the possibility of rapidly growing mycobacterium such as M. fortuitum should be considered.

References

1. Gibson JB. Infection of the lungs by saprophytic mycobacteria in achalasia of the cardia, with report of a fatal case showing lipoid pneumonia due to milk. J Pathol Bacteriol. 1953;65(1):239-51. [CrossRef] [PubMed]
2. Hasan A, Swamy T. Nocardia and Mycobacterium fortuitum infection in a case of lipoid pneumonia. Respiratory Medicine CME 2011: 75-78. [CrossRef]
3. Betancourt SL, Martinez-Jimenez S, Rossi SE, Truong MT, Carrillo J, Erasmus JJ. Lipoid pneumonia: spectrum of clinical and radiologic manifestations. AJR Am J Roentgenol. 2010;194(1):103-9. [CrossRef] [PubMed]
4. Harris K, Chalhoub M, Maroun R, Abi-Fadel F, Zhao F. Lipoid pneumonia: a challenging diagnosis. Heart Lung. 2011;40(6):580-4. [CrossRef] [PubMed]
5. Hughes RL, Freilich RA, Bytell DE, Craig RM, Moran JM. Clinical conference in pulmonary disease. Aspiration and occult esophageal disorders. Chest. 1981;80(4):489-95. [CrossRef] [PubMed]
6. Tranovich VL, Buesching WJ, Becker WJ. Pathologic quiz case. Chronic pneumonia after gastrectomy. Pathologic diagnosis: chronic aspiration lipoid pneumonia with Mycobacterium abscessus. Arch Pathol Lab Med. 2001;125(7):976-8. [PubMed]
7. Jouannic I, Desrues B, Léna H, Quinquenel ML, Donnio PY, Delaval P. Exogenous lipoid pneumonia complicated by Mycobacterium fortuitum and Aspergillus fumigatus infections. Eur Respir J. 1996;9(1):172-4. [Pubmed]
8. Couto SS, Artacho CA. Mycobacterium fortuitum pneumonia in a cat and the role of lipid in the pathogenesis of atypical mycobacterial infections. Vet Pathol. 2007;44(4):543-6. [CrossRef] [PubMed]
9. Vadakekalam J, Ward MJ. Mycobacterium fortuitum lung abscess treated with ciprofloxacin. Thorax. 1991;46(10):737-8. [CrossRef] [PubMed] 

Cite as: Till S, Mathew M, Liao D-W, Ramirez C. Why chronic constipation may be harmful to your lungs: a case report and review of lipoid pneumonia and mycobacterium fortuitum leading to acute respiratory failure and septic shock. Southwest J Pulm Crit Care. 2015;11(4):193-9. doi: http://dx.doi.org/10.13175/swjpcc118-15 PDF 

Giant Cell Myocarditis: A Case Report and Review of the Literature

Nathan Spence, MD

Karen Niehaus, MD

Leonardo Macias, MD

Bart Cox, MD

University of New Mexico Hospital

Albuquerque, New Mexico, United States

Introduction 

First described by Saltykow in 1905 (1), Giant cell myocarditis (GCM) is a rare but highly lethal disease. Until the 1980s the diagnosis of GCM was determined at autopsy (2). It often affects young patients (mean age of 42.6 + 12.7 years),  and appears to occur in men and women equally. The occurrence of GCM in minority patients has not been previously described (3). The most common presenting symptom is heart failure (75%), though ventricular tachycardia (14%), chest pain with ECG findings of acute myocardial infarction (6%) and complete heart block (5%) may also occur. Treatment often involves an immunosuppressive regimen as a bridge to heart transplantation. The prevalence of GCM is known primarily from autopsy studies (i.e., 0.051% in India, 0.007% in England,  and 0.023% in Japan) (4-6). In the largest GCM observational study yet published, the rate of death or cardiac transplantation was 89 percent, with a median survival of 5.5 months from the onset of symptoms to the time of death or transplantation (3). Few cases with the successful treatment of GCM have been reported (7). Here we describe a case of GCM in a Hispanic female, the first to our knowledge, in which immediate diagnosis and initiation of an immunosuppressive regimen led to a favorable hospital course, whereby she was clinically stabilized and able to be transferred for transplant evaluation.

Case

A 56-year-old Hispanic female with a past medical history significant only for hypertension presented to our emergency department for evaluation of a non-productive cough over the last 3 days, which was associated with a headache, runny nose, myalgias, nausea, vomiting, chest pain, increased dyspnea on exertion, and lower extremity edema. On initial evaluation, heart rate was 86, blood pressure was 131/84, temperature was 37.4 degrees Celsius, oxygen saturation 96% on room air. Physical exam revealed a patient in moderate distress, a pericardial friction rub, clear lungs, and trace lower extremity edema. Laboratory testing revealed a leukocytosis of 12,800/mm³ (normal < 10,600/mm³), troponin I of 3.020 ng/mL (normal < 0.06 ng/mL), N-Terminal-Pro-BNP of 9,775 pg/mL (normal < 125 pg/mL), elevated ESR of 43 mm/hr (normal < 15mm/hr), elevated CRP of 3.6mg/dL (normal < 1 mg/dL), and a mild eosinophilia of 6% (normal < 5%).  Respiratory viral panel was negative. Chest X-Ray revealed a globular cardiac silhouette without definite evidence of congestion. Twelve-lead electrocardiogram revealed normal sinus rhythm with a new left bundle branch block. Cardiac catheterization revealed no significant coronary stenosis, with a left ventricular end diastolic pressure (LVEDP) of 22 mmHg. Upon admission to the floor, diuresis and titration of guideline based medications for dilated cardiomyopathy were begun, but were promptly discontinued due to development of hypotension. Transthoracic echocardiography (TTE) displayed severe hypokinesis of the basal inferoseptum and inferior wall of the left ventricle. Estimated ejection fraction was 35%, with mild to moderate mitral regurgitation. Blood pressure stabilized on day 2 of admission. Cardiac MR (CMR) with gadolinium was ordered, which did not show definite myocardial delayed enhancement (i.e., no evidence of infarction, myocarditis. See Figure 1).

Figure 1 Cardiac Magnetic Resonance Imaging. (A) Two chamber delayed post-gadolinium inversion recovery view. (B) Two chamber delayed post-gadolinium phase sensitive inversion recovery view.

On day 3 of hospitalization, the patient suddenly developed complete heart block, became hypotensive and confused. As a result, a temporary venous pacemaker (TVP) was placed, and endomyocardial biopsy (EMB) was performed. Five specimens were obtained. Pulmonary capillary wedge pressure was measured at 32 mmHg, with a Fick cardiac output 3.01 L/min and cardiac index of 1.77 L/min/m². Due to persistent hypotension in the cath lab, a dopamine drip was begun, a Swan-Ganz catheter was placed, and the patient was transferred to the Medical Intensive Care Unit for further hemodynamic monitoring and treatment. That afternoon, GCM was diagnosed by pathology (see Figure 2).

Figure 2 Pathology. (A) Infiltration of cardiac muscle tissue by an inflammatory infiltrate. (B) Massive myocyte necrosis with giant cells among the inflammatory infiltrate. (C) Rare eosinophils are seen among the inflammatory infiltrate. (D) Giant cell among the inflammatory infiltrate.

An immunosuppressive regimen of corticosteroids, azathioprine,  and cyclosporine was promptly initiated. Thereafter, over the course of 3 days, clinical symptoms  and hemodynamics improved significantly. TVP was removed, inotropic support was weaned off, and ACE inhibitor and diuretics were titrated. Beta-blockers were withheld out of concern for recent complete heart block and use of inotropic support. On hospital day 10, the patient was transferred, in stable condition, to be evaluated for heart transplantation, and/or mechanical circulatory support. At the outside center, she had an ICD placed for primary prevention, was maintained on the three drug immunosuppression regimen, continued to do well clinically, and was listed for transplant.

Discussion

Several autoimmune disorders have been associated with GCM, which include inflammatory bowel disease, thyroiditis, and thymoma (8). Our patient did not have a history of autoimmune disease, and the laboratory tests to detect such during her hospitalization were negative. Evidence suggests that GCM is an autoimmune disorder dependent on CD4-positive T lymphocytes and anti-myosin autoantibodies (8). Early diagnosis leading to appropriate treatment, as in our case, appears to be imperative for a favorable clinical outcome. Treatment with a combination of immunosuppressives has been shown to improve survival, compared with those not receiving immunosuppressive regimens (12.3 months vs. 3.0 months, p=0.001) (3). If patients live long enough to receive heart transplantation, longer term survival is possible. For that reason, it is a Class I (level of evidence B) guideline recommendation to perform EMB in the setting of unexplained, new-onset heart failure of < 2 weeks' duration associated with a normal sized or dilated left ventricle in addition to hemodynamic compromise (9). The sensitivity of EMB for GCM is 80% to 85% in subjects who subsequently die or undergo heart transplantation (2). Therefore, in the appropriate clinical setting, EMB may drastically alter treatment and provide important prognostic information. The pathological hallmark of GCM is the presence of multinucleated giant cells and a lymphocytic inflammatory infiltrate, associated with myocyte necrosis (10-12). CMR may display delayed myocardial enhancement to support the diagnosis of myocarditis, though a non-diagnostic study, as in our case, does not rule it out.   

We encountered, to our knowledge, the first case of GCM in a patient of Hispanic ethnicity, who presented with the classic associated symptoms of heart failure, hemodynamic collapse, and complete heart block, and whose clinical course was favorably improved by early diagnosis and initiation of an immunosuppressive regimen. CMR did not identify myocarditis. However, this case illustrates the importance of including GCM in the differential diagnosis when a patient presents with suggestive clinical features and is not responding to current evidence based treatment for acute decompensated heart failure.

References

1. Saltykow S. Uber Diffuse Myokarditis. Virchows Archiv fur Pathologische Anatomie. 1905;182:1-39. [CrossRef]
2. Shields RC, Tazelaar HD, Berry GJ, Cooper LT. The role of right ventricular endomyocardial biopsy for idiopathic giant cell myocarditis. J Card Fail. 2002;8:74-88. [CrossRef] [PubMed] 
3. Cooper LT, Berry GJ, Shabetai R. Idiopathic giant-cell myocarditis - natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators. N Engl J Med. 1997;336:1860-6.[CrossRef] [PubMed]
4. Vaideeswar P, Cooper L. Giant cell myocarditis: clinical and pathological disease characteristics in an indian population. Cardiovasc Pathol. 2013;22:70-4. [CrossRef] [PubMed]  
5. Whitehead R. Isolated myocarditis. Brit Heart J 1965;27:220-30. [CrossRef] [PubMed]
6. Okada R, Wakafuji S. Myocarditis in autopsy. Heart Vessels 1985; Suppl 1:23-9. [CrossRef]
7. Desjardins V, Pelletier G, Leung TK, Waters D. Successful treatment of severe heart failure caused by idiopathic giant cell myocarditis. Can J Cardiol. 1992;8:788-92. [PubMed] 
8. Cooper L, ElAmm C. Giant Cell Myocarditis: Diagnosis and treatment. Herz. 2012;37:632-6. [CrossRef] [PubMed] 
9. Cooper LT, Baughman KL, Feldman AM, et al. The role of endomyocardial biopsy in the management of cardiovascular disease. A scientific statement from the American heart association, the American college of cardiology, and the European society of cardiology. J Am Coll Cardiol. 2007;50(19):1914-31. [CrossRef] [PubMed] 
10. Davies M, Pomerance A, Teare R. Idiopathic giant cell myocarditis - a distinctive clinico-pathological entity. Br Heart J. 1975;37:192-5. [CrossRef] [PubMed] 
11. Davidoff R, Palacios I, Southern J, Fallon JT, Newell J, Dec GW. Giant cell versus lymphocytic myocarditis. A comparison of their clinical features and long-term outcomes. Circulation. 1991;83:953-61. [CrossRef] [PubMed] 
12. Ren H, Poston RS Jr, Hruban RH, Baumgartner WA, Baughman KL, Hutchins GM. Long survival with giant cell myocarditis. Mod Pathol. 1993;6:402-7. [PubMed] 

Reference as: Spence N, Niehaus K, Macias L, Cox B. Giant cell myocarditis: a case report and review of the literature. Southwest J Pulm Crit Care. 2014;8(4):247-51. doi: http://dx.doi.org/10.13175/swjpcc052-14 PDF