Hemoptysis Due to Migration of a Fractured Kirschner Wire

Hemoptysis Due to Migration of a Fractured Kirschner Wire

described had class IV CF mutations, which are associated with pancreatic sufficiency and intermediate tissue levels of CF transmembrane conductance r...

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described had class IV CF mutations, which are associated with pancreatic sufficiency and intermediate tissue levels of CF transmembrane conductance regulator (CFTR).7. As opposed to classic pancreatic-insufficient CF, persons with class IV and class V mutations do not have extensive fibrotic replacement of the pancreas and usually retain both exocrine and endocrine function. It is only in this group of pancreatic-sufficient individuals, however, that idiopathic acute pancreatitis has been described.7,8 This suggests that while class IV and class V CF mutations do not reduce CFTR levels enough to cause pancreatic insufficiency, they may reduce CFTR levels enough to cause injury or make the pancreas more susceptible to injury. Close observation is warranted in the future to determine if persons with class IV and class V CF mutations and pancreatic sufficiency are at increased risk for minocycline-induced pancreatitis.

References 1 Cystic Fibrosis Foundation Patient Registry, annual data report 1998. Bethesda, MD: Cystic Fibrosis Foundation, 1999 2 Kurlandsky LE, Fader RC. In vitro activity of minocycline against respiratory pathogens from patients with cystic fibrosis. Pediatr Pulmonol 2000; 29:210 –212 3 Somech R, Arav-Boger R, Assia A, et al. Complications of minocycline therapy for acne vulgaris: case reports and review of the literature. Pediatr Dermatol 1999; 16:469 – 472 4 Chiu AM, Chuenkongkaew WL, Cornblath WT, et al. Minocycline treatment and pseudotumor cerebri syndrome. Am J Ophthalmol 1998; 126:116 –121 5 Teitelbaum JE, Perez-Atayde AR, Cohen M, et al. Minocycline-related autoimmune hepatitis: case series and literature review. Arch Pediatr Adolesc Med 1998; 152:1132–1136 6 Patterson PR. Minocycline in the antibiotic regimen of cystic fibrosis patients: weight gain and clinical improvement. Clin Pediatr (Phila) 1977; 16:60 – 63 7 Cohn JA, Friedman KJ, Noone PG, et al. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med 1998; 339:653– 658 8 Sharer N, Schwarz M, Malone G, et al. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis. N Engl J Med 1998; 339:645– 652

has many causes. Migration and erosion of H emoptysis hardware into the chest have very rarely been associated with hemoptysis. We report an unusual case of hemoptysis due to penetration of the trachea by a fractured migrating Kirschner wire.

Case Report A 50-year-old man presented to the emergency department with the complaint of hemoptysis and left shoulder pain. The hemoptysis consisted of blood without mucus and was associated with a “tickling” sensation in the throat. The left shoulder pain began 4 months prior to admission and was exacerbated by movement of the left arm. The patient’s only medications were ibuprofen and aspirin, which had recently been started for shoulder pain. The patient exercised daily, including punching a punching bag as part of his exercise routine. The patient’s medical history was significant for a third-degree separation of the acromioclavicular joint in January of 1995 after a fall. Open reduction and internal fixation with placement of two Kirschner wires were performed. These were removed 3 months later. Five months after the initial injury, the patient reinjured the acromioclavicular joint and required a second open reduction with internal fixation surgery. Two new Kirschner wires were placed to secure the acromioclavicular joint. The two Kirschner wires were cut short and bent at the distal end. The patient then became unemployed, was unavailable for follow-up, and did not have the wires removed. On physical examination, the patient appeared younger than his stated age. His cardiac, pulmonary, and abdominal examinations were unremarkable. A chest radiograph and chest CT scan were then obtained (Fig 1, 2). The chest radiograph showed two Kirschner wires that had fractured into four pieces, with one wire fragment migrating to the trachea and the second migrating to the left supraclavicular soft-tissue space. The chest CT scan demonstrated the presence of a wire fragment that had migrated through the thyroid tissue and into the trachea. The wire fragment traversed the tracheal airway with penetration of both sides of the trachea. The patient then underwent open surgical removal of the transtracheal wire fragment. A future surgery is planned for removal of the remaining wire fragments. In retrospective examination, a shoulder radiograph obtained 1 month prior to admission demonstrated partial migration of the two fractured wires within the right hemithorax.

Discussion

Hemoptysis Due to Migration of a Fractured Kirschner Wire* Guy T. Foster, MD; Kota G. Chetty, MD, FCCP; Kees Mahutte, MD, PhD, FCCP; Janet B. Kim, MD; and Scott A. Sasse, MD, FCCP

We report a rare complication related to the insertion of Kirschner wires for stabilization of an acromioclavicular separation. Five years after placement of the Kirschner wires, the patient presented with hemoptysis. On review of chest radiographs, a fractured wire was found to have migrated from the acromioclavicular joint, through the hemithorax and into the trachea. (CHEST 2001; 119:1285–1286) Key words: hemoptysis; Kirschner wire

Migration of orthopedic pins within the chest is a rare but known complication.1 Migration of a 2.5-cm-long Kirschner wire from a patient’s wrist to the right ventricle resulting in pericardial tamponade has been reported.2 In a similar occurrence, a Kirschner wire migrated from a patient’s left hand to the heart, 31 months after initial placement, producing cardiac arrhythmias.3 Migration of shoulder pins to the pleural space has been reported several times in the past. Lyons and Rockwood4 *From the Department of Pulmonary and Critical Care Medicine, Long Beach Veterans Affairs Medical Center, Long Beach, CA. Manuscript received July 12, 2000; revision accepted September 14, 2000. Correspondence to: Scott A. Sasse MD, FCCP, Department of Pulmonary and Critical Care Medicine, Long Beach Veterans Affairs Medical Center, 5901 East 7th St, Long Beach, CA 90822; e-mail: [email protected] CHEST / 119 / 4 / APRIL, 2001

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Figure 2. CT scan of the thorax revealing transtracheal and thyroid penetration of migrating wire.

Figure 1. Chest radiograph demonstrating transtracheal penetration of first fractured wire (arrows) and supraclavicular migration of second fractured wire.

described pin migration in 37 patients. Eight cases were fatal. The mechanism for pin migration was proposed to be movement through the intravascular space, as pins were retrieved from the ascending aorta, subclavian veins, and heart in 17 cases. Migration to the lung parenchyma was recognized in eight cases. In one instance, a pin was lodged partially in both lungs. In 10 cases, pins migrated to both the mediastinum and lungs. Finally, one shoulder pin migrated to the right orbit. Grauthoff and Klammer5 also described pin migration from the shoulder to the subclavian artery, aorta, and lung. The reason for wire migration in our patient is unclear. We can hypothesize that the wire fracture and subsequent migration may have occurred due to repetitive shoulder movement, resulting from the patient’s exercise as a boxer. Anatomically, it would have been difficult for this pin to migrate via the intravascular space (subclavian artery or vein) and ultimately penetrate the thyroid and trachea. Alternative mechanisms proposed for shoulder pin migration include respiratory excursion, gravitational forces, electrolysis, or muscular activity.4

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Although the migration of a shoulder pin to the lung is not a novel occurrence, migration of a fractured pin, penetrating both sides of the trachea with resulting hemoptysis, has not been previously reported. Hemoptysis in our case was most likely due to irritation of the tracheal lining by the wire fragment. The slow rate of hemoptysis makes it unlikely that an arterial vessel was involved. A prior report6 of pin migration to the trachea exists. Interestingly, this patient also reported a “tickle” in his throat, which was followed shortly thereafter by expectoration of the pin.6

References 1 Shaffer BS, Tibone JE. Arthroscopic shoulder instability surgery: complications. Clin Sports Med 1999; 18:737–767 2 Goodsett JR, Pahl AC, Glaspy JN, et al. Kirschner wire embolization to the heart: an unusual cause of pericardial tamponade. Chest 1999; 115:291–293 3 Haapaniemi TA, Hermansson US. Cardiac arrhythmia caused by a Kirschner wire inside the heart: an unusual complication of finger osteosynthesis. J Hand Surg [Br] 1997; 22:402– 404 4 Lyons FA, Rockwood CA Jr. Migration of pins used in operations of the shoulder. J Bone Joint Surg Am 1990; 72:1262–1267 5 Grauthoff VH, Klammer HL. Complications due to migration of a Kirschner wire from the clavicle. Fortschr Geb Rontgenstr Nuklearmed 1978; 128:591–594 6 Kremens V, Glauser F. Unusual sequela following pinning of medial clavicular fracture. AJR Am J Roentgenol 1956; 76:1066 –1069

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