A 66-year-old man is referred to a pulmonologist for progressive shortness of breath that has lasted for the past 3 months. His symptoms began shortly after discharge from a prolonged hospital stay for a logging accident in which he sustained multiple rib fractures and a left hip fracture. At that time, the patient had an extended stay in the intensive care unit and was on mechanical ventilatory support for 21 days. A tracheostomy had not been performed. On a post-hospitalization follow-up with his primary care provider, the patient reported shortness of breath, and wheezing had been noted during the physical examination. A trial of oral glucocorticoids and levalbuterol inhalation therapy was prescribed; however, the symptoms persisted and failed to respond to the therapy.
When seen by the pulmonologist, the patient states that he experiences shortness of breath even when he is at rest and loses his breath completely with mild exertion such as climbing a few stairs. He denies orthopnea, paroxysmal nocturnal dyspnea, and lower extremity edema. He also denies experiencing any chest pain, cough, fevers, weight loss, or night sweats. He has a history of cigarette smoking and degenerative joint disease. He takes acetaminophen/hydrocodone as needed for pain, but otherwise, he does not take any regular medications.
On physical examination, the patient is a well-developed and well-nourished man in no apparent distress. He is afebrile with a regular heart rate of 80 beats/min, a respiratory rate of 14 breaths/min, and a blood pressure of 102/64 mm Hg. High-pitched breath sounds are detected throughout all lung fields during both inspiration and expiration. The remainder of the patient's physical examination, including the head and neck and cardiac examination, is unremarkable.
Spirometry is obtained (see Image 1); {mosimage}patient flow-volume is loop shown as the solid blue line; a normal flow-volume loop is shown as the interrupted black line), with subsequent imaging by computed tomography (CT) of the neck (see Image 2).{mosimage}
What is the cause of the patient's wheezing?
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{mosimage}HINT
The high-pitched breath sounds were loudest over the central airway.
Authors:
Girendra Hoskere, MD,
Fellow, Division of Pulmonary Diseases
and Critical Care Medicine,
James H. Quillen College of Medicine,
East Tennessee State University
Thomas M. Roy, MD,
Chief of the Division of Pulmonary Diseases
and Critical Care Medicine and Professor of Medicine Department of Internal Medicine,
James H. Quillen College of Medicine,
East Tennessee State University
Rob Keith, MD,
Fellow, Division of Pulmonary Diseases
and Critical Care Medicine,
James H. Quillen College of Medicine,
East Tennessee State University
Ryland P. Byrd, Jr, MD,
Chief of Pulmonary Medicine,
Medical Director of Respiratory Therapy,
Quillen Mountain Home Veterans
Affairs Medical Center,
Professor, Department of Internal Medicine,
Division of Pulmonary Diseases
and Critical Care Medicine,
James H. Quillen College of Medicine,
East Tennessee State University
eMedicine Editors:
Erik D. Schraga, MD,
Department of Emergency Medicine,
Kaiser Permanente,
Santa Clara Medical Center, Calif
Rick G. Kulkarni, MD,
Assistant Professor,
Yale School of Medicine,
Section of Emergency Medicine,
Department of Surgery,
Attending Physician,
Medical Director,
Department of Emergency Services,
Yale-New Haven Hospital, Conn
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ANSWER
Tracheal stenosis in adults is most commonly caused by trauma but can also be caused by various medical conditions. Internal trauma to the trachea can result from prolonged endotracheal intubation, tracheotomy, surgery, irradiation, or endotracheal burns, while external trauma to the trachea can result from blunt or penetrating neck trauma. Groups of medical conditions responsible for tracheal stenoses include chronic inflammatory diseases (amyloidosis, sarcoidosis, relapsing polychondritis), benign neoplasms (respiratory papillomatosis), malignant neoplasms (primary tracheal, secondary invasion, metastatic), and collagen vascular diseases (tracheopathia osteoplastica, Wegener granulomatosis).
Upper airway (or large airway) obstructions, which include tracheal obstruction, can be separated into 3 categories based on the characteristic abnormality observed on the flow-volume loop: variable extrathoracic obstructions, variable intrathoracic obstructions, and fixed obstructions (which can be either intrathoracic or extrathoracic). Variable extrathoracic obstructions typically show flattening of the inspiratory portion of the flow-volume graph (the portion of the curve below the horizontal line). Some conditions that can cause variable extrathoracic obstruction include vocal cord paralysis, anaphylaxis, and angioedema. A flattening of only the expiratory portion of the flow-volume graph (the portion of the curve above the horizontal line) results from variable intrathoracic obstruction. Tracheomalacia, tracheal tumors located between the sternal notch and carina, and Wegener granulomatosis are all examples of conditions that can cause variable intrathoracic tracheal obstruction. A fixed large airway obstruction affects both portions of the flow-volume loop (as in this case) and can result from disorders intrinsic (extrathoracic) to the trachea, such as tracheal stenosis, or from extrinsic compression of the trachea (intrathoracic) resulting from neck masses or structural lesions of the mediastinum (eg, thyroid goiter and mediastinal lymphadenopathy).
Unrelated to upper airway obstructions, conditions such as asthma, chronic bronchitis, bronchiectasis, and emphysema all affect the smaller airways, resulting in a concave, scooped appearance of the expiratory phase of the flow-volume loop.
Prolonged translaryngeal intubation has been known to carry multiple risks, including oral or laryngotracheal injury, postextubation upper airway obstruction, and ventilator-associated pneumonia. Patients that are likely to require extended ventilatory support may benefit from early tracheotomy to avoid these complications; however, tracheotomy carries separate risks, including stomal infection, pneumothorax, subcutaneous emphysema, tracheomalacia, and the formation of granulation tissue. Nevertheless, a review comparing translaryngeal intubation and tracheotomy suggests that several end-points, including time spent in the intensive care unit and in the hospital as well as time on mechanical ventilation, are all reduced by early tracheotomy.6
The patient in this case underwent successful removal of his tracheal lesions via laser therapy. On examination, the histopathologic specimens revealed only granulation tissue. Injury to the trachea by a prolonged indwelling endotracheal tube during the patient’s previous hospital admission was thought to have resulted in the formation of granulation tissue and the resultant critical stenosis of his airway.
As an aside for further discussion, this case also illustrates the importance of spirometry expressed as a flow-volume loop in the evaluation of patients with dyspnea. Office-based spirometry machines are relatively inexpensive and easy to operate. While the measurement of airflow is a valuable tool for following patients with asthma and chronic obstructive pulmonary disease, the flow-volume loop also offers the advantage of identifying patients with large airway obstruction. In this case, without the information available from the measurement of the flow-volume graph, the urgency of the patient’s clinical situation may indeed have gone unrecognized.
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References:
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Baughman RP, Loudon RG. Stridor: differentiation from asthma or upper airway noise. Am Rev Respir Dis. Jun 1989; 139(6):1407-9. [MEDLINE 2729750]
Pellegrino R, Viegi G, Brusasco V et al. Interpretive strategies for lung function tests. Eur Resp J. Nov 2005; 26(5):948-68. [MEDLINE 16264058]
Gamsu G, Borson DB, Webb WR, Cunningham JH. Structure and function in tracheal stenosis. Am Rev Respir Dis. Mar 1980; 121(3):519-31. [MEDLINE 7416582]
Clum SR, Rumbak MJ. Mobilizing the patient in the intensive care unit: the role of early tracheotomy. Critl Care Clin. Jan 2007; 23(1): 71-9. [MEDLINE 17307117]
