HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Respond to This Article Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Take the CE Test Citing Articles Citing Articles via Google Scholar Google Scholar Articles by White, K. A. Articles by Ruth-Sahd, L. A. Search for Related Content PubMed PubMed Citation Articles by White, K. A. Articles by Ruth-Sahd, L. A.

Bronchiolitis Obliterans Organizing Pneumonia

Lisa A. Ruth-Sahd, a nurse educator and a winner of a Nightingale Award of Pennsylvania, is currently an associate professor at York College of Pennsylvania, York, Pa. She also works part-time as a staff nurse in the intensive care unit at Lancaster General Hospital, Lancaster, Pa. She has 23 years of experience in the emergency department and intensive care.

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.

Financial Disclosures
None reported.

This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

1. Describe the pathophysiology of bronchiolitis obliterans organizing pneumonia (BOOP)
   
2. Identify clinical manifestations of BOOP and the significant signs and symptoms that differentiate BOOP from other lung diseases
   
3. Describe nursing interventions for patients with acute respiratory illness due to BOOP
   

Corresponding author: Krista A. White, Lancaster General College of Nursing and Health Sciences, Lancaster, PA 17602 (e-mail: kawhite{at}LancasterGeneral.org).

	Definition

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
Defining BOOP requires an awareness of bronchiolitis. Bronchiolitis is a generic term used to describe a variety of inflammatory diseases that affect the bronchioles. Bronchiolitis is a common pathological change but is rarely marked enough to cause clinical signs or symptoms.^4,5 Obliterans refers to the ability of the pathological change to obliterate, eradicate, or destroy the airways. The term bronchiolitis obliterans was first used in the literature in 1901 by Lange to describe a group of patients who had submucosal and peribronchiolar fibrosis leading to obliteration of the bronchiolar lumens.^4,6 These patients did not have organizing pneumonia. Later, Epler and his colleagues^2,3,6 described BOOP as an inflammatory clinicopathological lung disease characterized by polypoid intralumenal and endobronchial connective tissue plugs. These plugs are composed of proliferating myxoid fibroblasts and myofibroblasts that fill the lumens of terminal bronchioles and extend in a continuous fashion into the alveolar ducts and alveoli, characteristics of an organizing pneumonia.

The airway plugs formed by the proliferation of connective tissue and fibroblasts may lead to a cast formation that outlines the branching of the inflamed alveolar ducts and distal airways. In BOOP the airway lumens are occluded from within, so the background architecture is generally preserved.⁴ This inflammation and the occlusive infiltrates in the bronchioles lead to restricted lung volumes and decreased vital capacity. BOOP is sometimes referred to as cryptogenic organizing pneumonia, a term that is considered more general and representative of what happens clinically, pathologically, and structurally within the lung tissue. However, the term BOOP is specific for a lesion that occurs in the distal bronchioles and alveoli simultaneously and is a popular term used throughout the world.

	Types and Causes of BOOP

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
In many instances, the cause of BOOP cannot be determined. Epler,³ the leading clinical expert on BOOP, identifies several known causes or associated diseases and classifies them according to types (Table 1). No links exist between the types of BOOP except that all the types lead to a final common clinical pathway that may be devastating if not detected promptly.

Rapidly progressive BOOP is a deadly form that can be fatal within 1 to 3 days of the onset of signs and symptoms. Patients may have an acute onset of acute respiratory distress syndrome; therefore, clinically, rapidly progressive BOOP can be indistinguishable from acute interstitial pneumonia.^2,3 Acute respiratory failure quickly results and leads to death. Early diagnosis based on histological examination of the primary BOOP lesion and initiation of corticosteroid therapy might improve survival in these patients.⁶ This form of BOOP occurs in less than 10% of patients with BOOP and occurs equally in men and women and at all ages.

Focal nodular BOOP is clinically important because distinguishing it from lung cancer is difficult.^18–21 It occurs in approximately one fourth of patients who have idiopathic BOOP.²² Although some focal nodular lesions might progress to the typical bilateral process of idiopathic BOOP, most do not, and resection results in a cure. Multiple bilateral nodular lesions may regress on their own without treatment.²⁰ Approximately 50% of patients with multiple nodular lesions (mean number of masses was 5) have pleuritic chest pain.

BOOP can occur after a variety of different types of infectious pneumonias,¹ including those caused by bacterial pathogens such as Chlamydia,²³ Legionella, and Mycoplasma pneumoniae.²⁴ Viral causes include cytomegalovirus, parainfluenza virus,²⁵ and adenovirus.²⁶ BOOP after parasitic infections such as malaria²⁷ and fungal infections, including those caused by Cryptococcus neoformans²⁸ and Pneumocystis carinii,²⁹ has also been reported. The relationship between many types of infection and the onset of BOOP is still unknown.¹

Drug-related BOOP can occur after the use of several different types of medications, including anti-inflammatory and immunosuppressive agents such as bleomycin sulfate,¹¹ gold, cyclophosphamide, penicillamine, and methotrexate; antibiotics such as sulfasalazine, sulfamethoxypyridazine, cephalosporins, and amphotericin B; anti-seizure medications such as carbamazepine⁹ and phenytoin^6,30; illicit use of cocaine; and a massive dose of L-tryptophan. Minocycline-associated BOOP³¹ has been reported in a woman who was taking this medication for acne. Other medications thought to lead to BOOP and commonly administered by critical care nurses are amiodarone,³² ticlopidine hydrochloride, and nitrofurantoin.³³

Rheumatologic or connective tissue BOOP can occur in patients with connective tissue diseases such as lupus erythematosus,³⁴ rheumatoid arthritis,³⁵ Sjögren syndrome,³⁶ and dermatomyositis.³⁷ BOOP can also occur in patients with ankylosing spondylitis³⁸ and polymyalgia rheumatica,^39,40 and it can affect patients with immunological diseases such as immunodeficiency syndrome⁴¹ and cryoglobulinemia.⁴²

BOOP can occur in recipients of lung,⁴³ kidney,⁴⁴ bone marrow,^44,46 and stem cell transplants.⁴⁷ In lung transplantation, BOOP generally occurs up to 10 months after transplantation and is usually associated with an acute rejection reaction.^5,48,49 This type of BOOP has been reported in 10% to 28% of lung transplant recipients and is often reversible, especially if the underlying acute rejection is successfully treated. If a transplant recipient is admitted to a critical care unit within this time frame because of an acute onset of shortness of breath, BOOP should be considered as a causative factor. In these patients, the BOOP reactions should be treated aggressively.

BOOP has been described in a patient who underwent an allogeneic marrow transplantation and in another patient who received a syngeneic bone marrow transplant from his twin brother.⁴⁶ Too few reports have been published to determine whether BOOP in these patients was an incidental finding or an actual complication of bone marrow transplantation. BOOP can also occur as a late complication after transplantation of hematopoietic stem cells.⁴⁷

BOOP is an important clinical complication in patients being treated with radiotherapy for breast cancer and may occur in up to 3% of women receiving radiation therapy for breast carcinoma.^50–53 The usual signs and symptoms are fever, non-productive cough, and various degrees of shortness of breath that occur up to 12 months after completion of radiotherapy. Chest radiographs show peripheral patchy or alveolar infiltrates, often outside the radiation field.⁵⁰ In one study,⁵² patients had infiltrates outside the irradiated lung to the contralateral nonirradiated lung. The underlying mechanism of radiotherapy BOOP remains unknown. A patient’s condition may improve with the initiation of corticosteroid therapy, but relapses may occur.^50,51

Environment-related BOOP has been reported in relation to textile printing dye¹⁴; the authors of the report suggested that the cause was related to the spraying of a respirable aerosol; however, the reactive chemical agent is a mystery. Another environmental cause is Penicillium janthinellum mold dust, inhaled from a powdery dust of a growth on the top of a discarded orange juice container.⁵⁴ BOOP due to smoke inhalation has been reported in a patient with erythema nodosum who was in a house fire.⁵⁵

Miscellaneous BOOP continues to be reported in association with myelodysplastic syndrome,⁵⁶ interstitial cystitis,⁵⁷ chronic thyroiditis,⁵⁸ and disorders of the liver such as alcoholic cirrhosis⁵⁸ and primary biliary cirrhosis.⁵⁹ It has been reported in patients infected with HIV⁶⁰ and has occurred during pregnancy.⁶¹ Guzman et al⁶² described a case of BOOP in a patient who had coronary artery bypass graft surgery. In patients with inflammatory bowel disease, BOOP is an important treatable abnormality.⁶³ BOOP also can occur in patients with T-cell leukemia or lymphoma.^64,65

	Pathophysiology

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
A trigger of some kind, for example, an infectious agent, a drug, or a connective tissue disorder, stimulates the inflammatory process known as BOOP. Because BOOP is an inflammatory lung disease, the key pathophysiological findings are related to the inflammatory pathway rather than to the fibrosing pathway as in idiopathic pulmonary fibrosis. Inflammation in the walls of the alveoli and bronchioles and an increase in foamy, lipid-laden macrophages in the alveoli are significant and lead to accumulations of fibromyxoid connective tissue.⁶⁶

Histological features include clusters of mononuclear inflammatory cells that form granulation tissue and plug the distal airways and alveolar spaces. These plugs of granulation tissue may form polyps that migrate within the alveolar ducts or may be focally attached to the wall.^2,3,5 The polyps may extend in a continuous fashion from the alveoli and alveolar ducts into the terminal and distal bronchioles.^2,3,5 The Figure provides a summary the pathophysiology of BOOP.

View larger version (49K): [in this window] [in a new window]   Pathophysiology of bronchiolitis obliterans organizing pneumonia (BOOP). Thicker arrows denote the shorter time frame from the onset of rapidly progressive BOOP through the pathophysiologic sequence to the onset of clinical manifestations and respiratory failure.

	Epidemiology and Mortality

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

	Prognosis and Incidence of Relapse

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
Most patients with idiopathic BOOP fully recover after a sufficient course of corticosteroids. However, the success of this treatment depends on the presence of other comorbid conditions and associated problems such as connective tissue disorders or underlying pulmonary diseases.^1,4,67,68 Compared with treatment of BOOP alone, treatment of BOOP in patients with other disease processes is more challenging because of the multidisciplinary approach required. Furthermore, once successful treatment has been started, relapses occur in approximately one third to one half of patients. The likelihood of relapse may be linked to several factors, including completion of the recommended corticosteroid treatment regimen and the severity of hypoxemia manifested initially.^3,22,69

	Clinical Manifestations

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
Signs and Symptoms
The onset of clinical manifestations of BOOP is usually acute (1 week) to subacute (months) no matter what the causative factor; the mean time is 4 to 10 weeks. Patients commonly have weeks to months of nonspecific respiratory signs and symptoms. The clinical manifestations vary according to the type of BOOP. Typical idiopathic BOOP is characterized by a flulike illness, bilateral crackles, and patchy infiltrates on chest radiographs. The initial signs and symptoms may include fever and night sweats, malaise, non-productive cough and dyspnea, and sore throat. Anorexia and weight loss are common. Physical assessment reveals tachypnea, hypoxia, and respiratory crackles over the involved lung fields in more than 80% of patients.⁶⁸ Wheezing and hemoptysis are rare.⁶ The severity of the illness depends on the signs and symptoms.

Laboratory Studies
Hematologic abnormalities are most prevalent in BOOP, although other serum abnormalities may also be evident (Table 2). White blood cell counts are most consistently elevated.^3,4,70 In a differential count, neutrophils may be increased to as high as 0.72 (proportion of 1.00), lymphocytes to 0.16, and monocytes to 0.12.⁷¹ Increases in eosinophils are rare.⁷⁰ In 2 case studies,⁷² 2 patients with fairly typical sequelae of pulmonary tuberculosis had BOOP, and 1 of the 2 had thrombocytosis, which occurs in approximately 20% of cases of BOOP.

	Differential Diagnosis

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
Both clinically and radiographically, BOOP mimics a variety of other pulmonary abnormalities. Clinically, fever, malaise, nonproductive cough, mild dyspnea, and weight loss of insidious onset can be due to a myriad of causes. Radiographic findings characteristic of BOOP may help in narrowing the list of possible causes to a more manageable number, but the definitive means for confirming BOOP is histological examination.^5,74 BOOP should be considered in patients with a suspected infective pulmonary disorder who do not respond to antibiotic therapy.^5,74 Table 3 provides a differential diagnosis for patients with indications suggestive of BOOP.

	Diagnostic Studies

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

The first pattern is patchy alveolar and diffuse interstitial infiltrates, usually bilaterally. These findings are consistently visualized on chest radiographs.^{1,6,68,69,71,72} In as many as 25% of patients with BOOP, the infiltrates are described as migratory, a term that implies the movement of the newly formed granulation tissue within small distal airways and alveolar ducts.^1,68,71 These migratory lesions may also spontaneously regress or vanish.⁶⁰ These opacities are often present peripherally, indicating their location just under the pleural lining and thus are termed subpleural. On computed tomography, such opacities are seen as a ground-glass pattern with peripheral orientation.^3,71,72,81 Pleural effusions and airway hyper-inflation are uncharacteristic in idiopathic BOOP.^1–4,68,74

The second radiographic finding suggestive of BOOP is multiple foci of consolidation or solitary nodular-appearing lesions.^1,74,81 In some patients with cancer, notably renal carcinoma, these lesions have been confused with pulmonary metastases, but the lesions may spontaneously regress, an unlikely occurrence in metastatic disease.⁶⁷

The third and final characteristic radiographic finding is the appearance of small linear or crescent-shaped densities surrounding the ground-glass area of attenuation. This finding is less frequent than other radiograph patterns; it occurs in approximately 20% of patients with BOOP.^1,4,74,81

High-Resolution Computed Tomography
In patients with BOOP, high-resolution computed tomography reveals ground-glass attenuation with a subpleural and peribronchial distribution.^1,3,5,66,81 The ground-glass appearance may be the result of alveolar septal inflammation and the organizing pneumonia in alveolar ducts.⁸¹ In addition, as many as 65% of patients have peripheral lower lobe consolidation.^66,71 The pattern of this peripheral consolidation is similar to that of a triangle with the base along the pleural surface and the tip of the triangle toward the mediastinum.^6,68,71 In comparison, patients with fibrotic lung disease have a classic honeycombing pattern.^4,66,69,71

Video-Assisted Thoracoscopy With Open Lung Biopsy
Although both clinical manifestations and radiological findings may suggest BOOP as a probable diagnosis, histological findings are required to confirm the diagnosis. Video-assisted thoracoscopy with open lung biopsy is the preferred method for gathering samples and making the diagnosis.^3,5,6,68,74 This open technique allows for enhanced visualization, more complete tissue sampling, and less risk of errors due to small-sized samples. Because the distal airway and alveolar lesions are migratory, the location of the areas of opacity should be confirmed via chest radiography just before the biopsy is done.¹ This sequence will ensure the most accurate tissue sampling, which will in turn help in making the most probable diagnosis. Using the open technique to obtain samples for histological examination is imperative because use of corticosteroids, the primary treatment for BOOP, is not beneficial for many of the differential diagnoses.⁸²

Though limited, bronchoalveolar lavage as a diagnostic means has been used effectively.^1,3,5,6,74 Bronchoalveolar lavage indicates that large percentages of lymphocytes, often 20% to 40% of the white blood cells in the lavage fluid, are most characteristic of BOOP. Epler⁶ notes that findings of more than 0.25 lymphocytes are suggestive of BOOP. Other cell types, such as neutrophils, eosinophils, mast cells, and plasma cells, may also be present, but in smaller amounts.⁶

Histological Studies
In confirmed cases of BOOP, the main findings on histological examination are organized granulation tissue in the distal bronchioles and organized alveolar exudates composed of interstitial infiltrates with mononuclear cells (organizing pneumonia).^1–4,81 A finding of organizing pneumonia is not diagnostic for BOOP because this type of pneumonia can occur in association with other pulmonary diseases or abnormalities.^1,2,66 Pathological examination of a tissue obtained via open lung biopsy is the best method for an accurate diagnosis. Examination of bronchoalveolar lavage fluid alone cannot be used to diagnose BOOP.

Definitive histological findings in BOOP are as follows:

• Diffuse distal airway inflammation and fibromyxoid, polypoid plugs made up of fibroblastic connective tissue are present. Located in the distal airways, alveolar ducts, and alveoli, these plugs are both newly formed^1–3,5,17 and have a large amount of vascularization, a characteristic that becomes vital for the effectiveness of treatment.³
  
• Large interstitial and alveolar infiltrates that contain mononuclear cells and "foamy" macrophages are present.^5,6,17,71,74 Foamy macrophages are lipid-laden⁶⁶ because often the phagocytosed materials are of lipoid origin and the debris inside the macrophages gives the cells the appearance of bubbling foam.
  
• Patchy involvement of pulmonary parenchyma with preservation of background lung architecture is present.^1–4,17 This architecture is preserved because BOOP occurs intraluminally within the pulmonary tree. In idiopathic BOOP, histological examinations generally reveal no microorganisms.^2,17,72
  

Table 4 gives common values for pulmonary functions tests in patients with BOOP.

	Treatment and Nursing Considerations

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

Because BOOP is generally a noninfective infiltrative lung disease, anti-infective agents are not routinely part of the treatment regimen.^3,5,17,72 Overwhelmingly, the mainstay treatment for BOOP is an extensive course of oral prednisone; most patients improve markedly after the initial 48 hours to 1 week of therapy.^1,4,5 If a patient does improve within this time frame, a physician must be alerted because other diagnostic tests may be necessary. The recommended dosing of prednisone is 0.75 to 1 mg/kg per day for 3 months, then 40 mg/d for 3 months, and finally tapering to 20 mg/d or 20 mg every other day for 6 months, for a total treatment time of approximately 1 year.^{1,3,5,17,66,68,71,72,74} Monitoring for untoward effects of steroid therapy such as gastrointestinal bleeding, hyperglycemia, fluid retention, depression, personality changes, psychosis, and restlessness is a priority of care. In addition, the risk for concomitant infections is increased because long-term corticosteroid therapy is immunosuppressive.⁵

Several schools of thought exist about the mechanism by which corticosteroids work in BOOP. The fibrous buds of newly formed connective tissue in distal airways and alveolar spaces are highly vascular, a characteristic that may allow the anti-inflammatory steroid to better attack these lesions. The specifics of how corticosteroids work in the disappearance of fibrous intra-alveolar buds, diffuse peripheral subpleural peribronchial opacities, and extensive inflammatory changes continue to perplex clinicians. Most likely fibroblasts are a key component in the formation of the buds and also play a vital role in the buds’ degradation. Degradation of the fibrous polypoid matrix requires certain enzymes. These enzymes, produced by fibroblasts and leukocytes in the intra-alveolar areas, facilitate the breakdown and resolution of the polyps or buds previously created by the fibroblasts and leukocytes. This enzymatic action may account for those patients who appear to recover spontaneously without exogenous treatment.¹ Successful resolution of clinical and radiographic findings associated with BOOP by treatment with corticosteroids has been well documented despite the unknown pharmacodynamics of the medications.

Although corticosteroids are the preferred treatment for BOOP, other medications have also been effective. Macrolides such as clarithromycin 250 mg twice daily for 2 months and then 250 mg/d for an additional 1 month can result in resolution of BOOP.¹⁷ Members of the macrolide class of anti-infective agents decrease the influx of polymorphonuclear cells in the lungs and slow the production of cytokines, which promote the inflammatory cascade.¹⁷ Erythromycin is also effective in patients with BOOP.^1–3 Cytotoxic drugs such as cyclophosphamide and azathioprine have been used in BOOP patients who had only minimal improvement in signs and symptoms and radiographic findings with usual corticosteroid treatments.^4,69,74 Inhaled triamcinolone has been used as an adjunct treatment.³ The success of drug therapy is indicated by the decrease in pulmonary signs and symptoms and the return of the results of pulmonary function tests to normal.

Vigilant pulmonary assessment and hygiene coupled with close collaboration with the pulmonary department are necessary to ensure adequate oxygenation and perfusion, which are key to improving outcomes in patients with BOOP. The critical care nurse must assess daily chest radiographs to detect the resolution of the intra-alveolar findings after corticosteroid therapy is implemented. In addition, the nurse must assess findings on pulse oximetry and analysis of arterial blood gases and observe for subtle indications of hypoxemia. Both the maintenance of proper oxygen delivery and the proper positioning of patients facilitate oxygenation, thus enhancing patients’ recovery.

Additionally, the critical care nurse must educate both patients and their families about diagnostic tests and the use and potential complications of long-term steroid therapy. Because patients have procedures such as bronchoscopy with bronchoalveolar lavage, open lung biopsy, and high-resolution computed tomography, the nurse must provide clear instructions in order to alleviate anxiety. A large array of side effects associated with use of corticosteroids may occur because patients with BOOP are often treated for long periods. Therefore, teaching about the medication must be extensive. For patients with BOOP, excellence in both the art and skill of critical care nursing is imperative to ensure the best possible outcomes. Table 5 is a plan of care for patients with BOOP.

	Case Study

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

On admission to the hospital, he continued to be short of breath, with respirations of 40/min and a resting oxygen saturation of 88%. Supplemental inhaled oxygen was administered via a facial mask. Other vital signs were blood pressure 150/90 mm Hg, heart rate 110/min, and body temperature 38.5°C. Crackles were heard bilaterally in both lungs. Laboratory findings included erythrocyte sedimentation rate 76 mm/h, white blood cell count 13.2 x 10⁹/L, level of C-reactive protein 119 mg/L, and serum albumin level 32 g/L. Other than indications of hyperglycemia and abnormal results in renal function tests, all other laboratory findings were normal. Cultures of the blood, sputum, and urine were negative for microorganisms.

Because of the findings on the chest radiograph, high-resolution computed tomography of the chest was performed. The scan showed bilateral patchy, ground-glass opacities with a triangular area of consolidation with the base along the pleural surface of the lung posteriorly. Later the next day, bronchoscopy with a bronchoalveolar lavage was performed; on the basis of the results, pneumonia was ruled out. At that time, Mr Frank was being treated with oral prednisone 60 mg/d.

Despite treatment, the lung problems continued, and therefore on the seventh day of his admission, he agreed to undergo an open lung biopsy via video-assisted thoracoscopy. Tissue samples taken from 2 anterior lung sites and 1 posterior lung site showed evidence of BOOP. Pathological examination of the biopsy specimens revealed myxoid fibroblastic tissue, foamy macrophages, and lymphocytes and eosinophils in the alveolar spaces. Of note, plugging of the distal bronchioles and alveolar spaces with organized inflammatory exudates was also evident. Cultures and stains of the biopsy specimens were negative for organisms.

Mr Frank sought a second opinion from a large teaching hospital; the diagnosis of BOOP was confirmed. He was given intravenous methylprednisolone at a dose of 80 mg every 8 hours for 5 days and then prednisone 150 mg once a day. The dosage was gradually decreased, and at the time of discharge, 3 weeks after admission, he was taking 60 mg/d. After he was discharged from the hospital, he continued treatment with supplemental oxygen at home. During the next 12 months, the dosage of prednisone was gradually decreased, and treatment with the drug was stopped when the BOOP was completely resolved.

	Conclusion

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
BOOP is an inflammation of the distal small airways (bronchioles) and surrounding alveolar lung tissue. This inflammation can affect a small region of the lung or the entire lung. Critical care nurses should consider the possibility of BOOP when caring for a patient with suspected pneumonia and respiratory failure who does not respond to conventional antibiotic therapy. As vital members of the healthcare team, critical care nurses acting as patients’ advocates will improve patients’ outcomes by providing high-quality comprehensive care appropriate for patients with BOOP. Early diagnosis and treatment with steroids is essential in reducing complications and mortality. Actions by critical care nurses are imperative to minimize pulmonary residual effects and maintain a high quality of life in BOOP patients.

	Additional Information

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 
For additional information on BOOP, visit the following Web sites:

• http://www.epler.com/boop1.html,
  
• http://www.emedicine.com/radio/topic117.htm, and
  
• http://www.pneumotox.com.
  

	Acknowledgments

 
Thank-you to "Kerry Frank" for allowing us to share his story so that others may learn and benefit from his experiences. The insignificant characteristics of the case study have been altered to comply with the regulations of the federal Health Information Portability and Accountability Act and maintain patient confidentiality. The patient’s name has been changed. An enormous thank-you to Gary R. Epler, MD, the internationally known expert and father of BOOP, for his review and mentoring during the preparation of the manuscript. Without his assistance, this article would not have been completed.

	References

Top Definition Types and Causes of... Pathophysiology Epidemiology and Mortality Prognosis and Incidence of... Clinical Manifestations Differential Diagnosis Diagnostic Studies Treatment and Nursing... Case Study Conclusion Additional Information References

 

1. Cordier JF. Organising pneumonia. Thorax. 2000;55:318–328.[Free Full Text]
2. Epler GR, Colby TV, McLoud TC, Carrington CB, Gaensler EA. Bronchiolitis obliterans organizing pneumonia. N Engl J Med. 1985;312:152–158.[Abstract]
3. Epler GR. Bronchiolitis obliterans organizing pneumonia. Arch Intern Med. 2001;161:158–164.[Abstract/Free Full Text]
4. Ryu JH, Myers JL, Swensen SJ. Bronchiolar disorders. Am J Respir Crit Care Med. 2003;168:1277–1292.[Abstract/Free Full Text]
5. Moore SL. Bronchiolitis obliterans organizing pneumonia: a late complication of stem cell transplantation. Clin J Oncol Nurs. 2003; 7:659–662.[Medline]
6. Epler GR. Bronchiolitis obliterans organizing pneumonia: definition and clinical features. Chest. 1992;102(1 suppl):2S–6S.[Medline]
7. Bauwens AM, van de Graaf EA, van Ginkel, WGJ, van Kessel DA, Otten HG. Pre-transplant soluble CD30 is associated with bronchiolitis obliterans syndrome after lung transplantation. J Heart Lung Transplant. 2006;25:416–419.[Medline]
8. Kreiss K, Goumaa A, Kullman G, Fedan K, Simoes EJ, Enright PL. Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med. 2002;347:330–338.[Abstract/Free Full Text]
9. Banka R, Ward MJ. Bronchiolitis obliterans and organizing pneumonia caused by carbamazepine and mimicking community acquired pneumonia. Postgrad Med J. 2002;78:621–622.[Abstract/Free Full Text]
10. Swinburn CR, Jackson GJ, Cobden I, Ashcroft T, Morritt GN, Corris PA. Bronchiolitis obliterans organising pneumonia in a patient with ulcerative colitis. Thorax. 1988;43:735–736.[Abstract]
11. Rossi S, Erasmas JJ, McAdams HP, Sporn TA, Goodman PC. Pulmonary drug toxicity: radiologic and pathologic manifestations. Radiographics. 2000;20:1245–1259.[Abstract/Free Full Text]
12. Camus P, Lombard JN, Perrichon M, et al. Bronchiolitis obliterans organising pneumonia in patients taking acebutolol or amiodarone. Thorax. 1989;44:711–715.[Abstract]
13. Faller M, Quiox E, Popin E, et al. Migratory pulmonary infiltrates in a patient treated with sotalol. Eur Respir J. 1997;10:2159–2162.[Abstract]
14. Camus P, Nemery B. A novel cause for bronchiolitis obliterans organizing pneumonia: exposure to paint aerosols in textile workshops. Eur Respir J. 1998;11:259–262.[Medline]
15. Przepiorka D, Abu-Elmagd K, Huaringa A, et al. Bronchiolitis obliterans organizing pneumonia in a BMT patient receiving FK506. Bone Marrow Transplant. 1993;11:502.[Medline]
16. Patel A, Ryu JH, Reed CE. Hypersensitivity pneumonitis: current concepts and future questions. J Allergy Clin Immunol. 2001;108: 661–670.[Medline]
17. Stover DE, Mangino D. Macrolides: a treatment alternative for bronchiolitis obliterans organizing pneumonia? Chest. 2005;128: 3611–3617.[Medline]
18. Murphy J, Schnyder P, Herold C, Flower C. Bronchiolitis obliterans organizing pneumonia simulating bronchial carcinoma. Eur Radiol. 1998;8:1165–1169.[Medline]
19. Yang DG, Kim KD, Shin DH, Choe KO, Kim SK, Lee WY. Idiopathic bronchiolitis obliterans with organizing pneumonia presenting with spontaneous hydropneumothorax and solitary pulmonary nodule. Respirology. 1999;4:267–270.[Medline]
20. Akira M, Yamamoto S, Sakatani M. Bronchiolitis obliterans organizing pneumonia manifesting as multiple large nodules or masses. AJR Am J Roentgenol. 1998;170:291–295.[Abstract/Free Full Text]
21. Orseck MJ, Player KC, Woollen CD, Kelley H, White PF. Bronchiolitis obliterans organizing pneumonia mimicking multiple pulmonary metastases. Am Surg. 2000;66:11–13.[Medline]
22. Cordier JF, Loire R, Brune J. Idiopathic bronchiolitis obliterans organizing pneumonia: definition of characteristic clinical profiles in a series of 16 patients. Chest. 1989;96:999–1004.[Medline]
23. Diehl JL, Gisselbrecht M, Meyer G, Israel-Biet D, Sors H. Bronchiolitis obliterans organizing pneumonia associated with chlamydial infection. Eur Respir J. 1996;9:1320–1322.[Abstract]
24. Llibre JM, Urban A, Garcia E, Carrasco MA, Murcia C. Bronchiolitis obliterans organizing pneumonia associated with acute Mycoplasma pneumoniae infection. Clin Infect Dis. 1997;25:1340–1342.[Medline]
25. Peramaki E, Salmi I, Kava T, Romppanen T, Hakkarainen T. Unilateral bronchiolitis obliterans organizing pneumonia and bronchoalveolar lavage neutrophilia in a patient with parainfluenza 3 virus infection. Respir Med. 1991;85:159–161.[Medline]
26. Jeon JS, Yi Ha, Ki Sy, et al. A case of bronchiolitis obliterans organizing pneumonia associated with adenovirus. Korean J Intern Med. 1997;12:70–74.[Medline]
27. Yale SH, Adlakha A, Sebo TJ, Ryu JH. Bronchiolitis obliterans organizing pneumonia caused by Plasmodium vivax malaria. Chest. 1993;104:1294–1296.[Medline]
28. Carey CF, Mueller L, Fotopoulos CL, Dall L. Bronchiolitis obliterans-organizing pneumonia associated with Cryptococcus neoformans infection [letter]. Rev Infect Dis. 1991;13:1253–1254.[Medline]
29. Kleindienst R, Fend F, Prior C, Margreiter R, Vogel W. Bronchiolitis obliterans organizing pneumonia associated with Pneumocystis carinii infection in a liver transplant patient receiving tacrolimus. Clin Transplant. 1999;13:65–67.[Medline]
30. Angle P, Thomas P, Chiu B, Freedman J. Bronchiolitis obliterans organizing pneumonia and cold agglutinin disease associated with phenytoin hypersensitivity syndrome. Chest. 1997;112:1697–1699.[Medline]
31. Piperno D, Donne C, Loire R, Cordier JF. Bronchiolitis obliterans organizing pneumonia associated with minocycline therapy: a possible cause. Eur Respir J. 1995;8:1018–1020.[Abstract]
32. Conte SCS, Pagan V, Murer B. Bronchiolitis obliterans organizing pneumonia secondary to amiodarone. Arch Chest Dis. 1997;52:24–26.
33. Cameron RJ, Kolbe J, Wilsher ML, Lambie N. Bronchiolitis obliterans organising pneumonia associated with the use of nitrofurantoin. Thorax. 2000;55:249–251.[Abstract/Free Full Text]
34. Martinez FJ, Lynch JP. Connective tissue disease related bronchiolitis obliterans organizing pneumonia. In: Epler GR, ed. Diseases of the Bronchioles. New York, NY: Raven Press; 1994:347–366.
35. Ippolito JA, Palmer L, Spector S, Kane PB, Gorevic PD. Bronchiolitis obliterans organizing pneumonia and rheumatoid arthritis. Semin Arthritis Rheum. 1993;23:70–78.[Medline]
36. Imasaki T, Yoshi A, Tanaka S, Ogura T, Ishikawa A, Takahashi T. Polymyositis and Sjögren’s syndrome associated with bronchiolitis obliterans organizing pneumonia. Intern Med. 1996;35:231–235.[Medline]
37. Knoell KA, Hook M, Grice DP, Hendrix JD. Dermatomyositis associated with bronchiolitis obliterans organizing pneumonia (BOOP). J Am Acad Dermatol. 1999;40:328–330.[Medline]
38. Turner JF, Enzenauer RJ. Bronchiolitis obliterans and organizing pneumonia associated with ankylosing spondylitis. Arthritis Rheum. 1994;37:1557–1559.[Medline]
39. Epler GR, Mark EJ. A 65-year-old woman with bilateral pulmonary infiltrates. N Engl J Med. 1986;314:1627–1635.[Medline]
40. Stey C, Truninger K, Marti D, Vogt P, Medici TC. Bronchiolitis obliterans organizing pneumonia associated with polymyalgia rheumatica. Eur Respir J. 1999;13:926–929.[Abstract]
41. Kaufman J, Komorowski R. Bronchiolitis obliterans organizing pneumonia in common variable immunodeficiency syndrome. Chest. 1991;100:552–553.[Medline]
42. Zackrison LH, Katz P. Bronchiolitis obliterans organizing pneumonia associated with essential mixed cryoglobulinemia. Arthritis Rheum. 1993;36:1627–1630.[Medline]
43. Chaparro C, Chamberlain D, Maurer J, Winton T, Dehoyos A, Kesten S. Bronchiolitis obliterans organizing pneumonia (BOOP) in lung transplant recipients. Chest. 1996;110:1150–1154.[Medline]
44. Verberckmoes R, Verbeken E, Verschakelen J, Vanrenterghem Y. BOOP after renal transplantation. Nephrol Dial Transplant. 1996;11:1862–1863.[Free Full Text]
45. Gerhardt SG, McDyer JF, Girgis RE, Conte JV, Yang SC, Orens JB. Maintenance azithromycin therapy for bronchiolitis obliterans syndrome: results of a pilot study. Am J Respir Crit Care Med. 2003;168:121–125.[Abstract/Free Full Text]
46. Baron FA, Hermanne JP, Dowlati A, et al. Bronchiolitis obliterans organizing pneumonia and ulcerative colitis after allergenic bone marrow transplantation. Bone Marrow Transplant. 1998;21:951–954.[Medline]
47. Kanda Y, Takahashi T, Imai Y, et al. Bronchiolitis obliterans organizing pneumonia after syngeneic bone marrow transplantation for acute lymphoblastic leukemia. Bone Marrow Transplant. 1997;19:1251–1253.[Medline]
48. Egan JJ. Obliterative bronchiolitis after lung transplantation: a repetitive multiple injury airway disease. Am J Respir Crit Care Med. 2004;170:931–932.[Free Full Text]
49. Estenne M, Hertz MI. Bronchiolitis obliterans after human lung transplantation. Am J Respir Crit Care Med. 2002;166:440–444.[Free Full Text]
50. Van Laar JM, Holscher HC, van Krieken JHJM, Stolk J. Bronchiolitis obliterans organizing pneumonia after adjuvant radiotherapy for breast carcinoma. Respir Med. 1997;91:241–244.[Medline]
51. Crestani B, Valeyre D, Roden S, Wallaert B, Dalphin JC, Cordier JF. Bronchiolitis obliterans organizing pneumonia syndrome primed by radiation therapy to the breast. Am J Respir Crit Care Med. 1998;158:1929–1935.[Abstract/Free Full Text]
52. Arbetter KR, Prakash UBS, Tazelaar HD, Douglas WW. Radiation-induced pneumonitis in the "nonirradiated" lung. Mayo Clin Proc. 1999;74:27–36.[Medline]
53. Majori M, Poletti V, Curti A, Corradi M, Falcone F, Pesci A. Bronchoalveolar lavage in bronchiolitis obliterans organizing pneumonia primed by radiation therapy to the breast. J Allergy Clin Immunol. 2000;105: 239–244.[Medline]
54. Bates C, Read RC, Morice AH. A malicious mould. Lancet. 1997;349:1598.[Medline]
55. Srivastava S, Haddad R, Kleinman G, Manthous CA. Erythema nodosum after smoke inhalation-induced bronchiolitis obliterans organizing pneumonia. Crit Care Med. 1999; 27:1214–1216.[Medline]
56. Tenholder MF, Becker GL, Cervoni MI. The myelodysplastic syndrome in a patient with relapsing bronchiolitis obliterans organizing pneumonia. Chest. 1992;102:1895–1897.[Medline]
57. Mana F, Mets T, Vincken W, Sennesael J, Vanwaeyenbergh J, Goossens A. The association of bronchiolitis obliterans organizing pneumonia, systemic lupus erythematosus and Hunner’s cystitis. Chest. 1993;104:642–644.[Medline]
58. Yamamoto M, Ina Y, Kitaichi M, Harasawa M, Tamura M. Clinical features of BOOP in Japan. Chest. 1992;102(1 suppl):21S–25S.[Medline]
59. Spiteri MA, Klenerman P, Sheppard MN, Padley S, Clark TJK, Newman-Taylor A. Seasonal cryptogenic organising pneumonia with biochemical cholestasis: a new clinical entity. Lancet. 1992;340:281–284.[Medline]
60. Sanito NJ, Morley TF, Condoluci DV. Bronchiolitis obliterans organizing pneumonia in an AIDS patient. Eur Respir J. 1995;8:1021–1024.[Abstract]
61. Ghidini A, Mariani E, Patregnani C, Marinetti E. Bronchiolitis obliterans organizing pneumonia in pregnancy. Obstet Gynecol. 1999;94:843.[Free Full Text]
62. Guzman EJ, Smith AJ, Tietjen PA. Bronchiolitis obliterans organizing pneumonia after coronary artery bypass graft surgery. J Thorac Cardiovasc Surg. 2000;119:382–383.[Free Full Text]
63. Camus P, Piard F, Ashcroft T, Gal AA, Colby TV. The lung in inflammatory bowel disease. Medicine (Baltimore). 1993;72:151–183.[Medline]
64. Vaiman E, Odeh M, Attias D, Ben-Arie Y, Oliven A. T-cell chronic lymphocytic leukemia with pulmonary involvement and relapsing BOOP. Eur Respir J. 1999;14:471–474.[Abstract]
65. Matsuo K, Tada S, Kataoka M, et al. Bronchiolitis obliterans organizing pneumonia (BOOP) in a case of smouldering adult T-cell leukaemia. Respirology. 2000;5:81–85.[Medline]
66. Arakawa H, Yasuyuki K, Hiroshi N, et al. Bronchiolitis obliterans with organizing pneumonia versus chronic eosinophilic pneumonia: high-resolution CT findings in 81 patients. AJR Am J Roentgenol. 2001;176: 1053–1058.[Abstract/Free Full Text]
67. Chander K, Feldman L, Mahajan R. Spontaneous regression of lung metastases: possible BOOP connection? Chest. 1999;115: 601–602.[Medline]
68. MacLaughlin LH, King MA. Radiological case of the month. Appl Radiol. August 2000;29:32–34.
69. McKee CM, Epler GR. How to differentiate between acute fulminant BOOP and AIP. J Respir Dis. 2002;23:459–466.
70. Mohan K, Sayer R, Acharya L. Lessons to be learned: a case study approach. Bronchiolitis obliterans organising pneumonia: a reversible cause of respiratory failure. J R Soc Health. 2004;124:188–190.[Medline]
71. Kroegel C, Reibig A, Hengst U, Mock B, Hafner D, Grahmann PR. Bilateral symmetrical upper lobe opacities: an unusual presentation of bronchiolitis obliterans organizing pneumonia. Chest. 2000;118: 863–865.[Medline]
72. Heller I, Biner S, Isakov A, et al. TB or not TB: cavitary bronchiolitis obliterans organizing pneumonia mimicking pulmonary tuberculosis. Chest. 2001;120:674–678.[Medline]
73. Pagana KD, Pagana TJ. Mosby’s Manual of Diagnostic and Laboratory Tests. 3rd ed. St Louis, MO: Mosby Elsevier; 2006:172–173, 199–201, 455–549.
74. Heffner JE. What caused respiratory failure in this 42-year-old man with a persistent cough and mild dyspnea? J Crit Illness. 2001;16:487–492.
75. Ryu JH, Colby TV, Hartman TE. Idiopathic pulmonary fibrosis: current concepts. Mayo Clin Proc. 1998;73:1085–1101.[Medline]
76. Ryu JH, Myers JL, Capizzi SA, Douglas WW, Vassallo R, Decker PA. Desquamative interstitial pneumonia and respiratory bronchiolitis-associated interstitial lung disease. Chest. 2005;127:178–184.[Medline]
77. Johnson JL, Hirsch CS. Aspiration pneumonia: recognizing and managing a potentially growing disorder. Postgrad Med. 2003;113:99–112.[Medline]
78. Williams VG. Tuberculosis: clinical features, diagnosis and management. Nurs Stand. February 8–14, 2006;20:49–53.[Medline]
79. Kane C, Galanes S. Adult respiratory distress syndrome. Crit Care Nurs Q. 2004;27:325–335.[Medline]
80. Ravenel J, Irshad A. Wegener granulomatosis, thoracic. Available at: http://www.emedicine.com/RADIO/topic743.htm. Accessed March 2, 2007.
81. Ujita M, Renzoni EA, Veeraraghavan S, Wells AU, Hansell DM. Organizing pneumonia: perilobular pattern at thin-section CT. Radiology. 2004;232:757–761.[Abstract/Free Full Text]