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Ann Thorac Surg 2000;69:266 –7
anticoagulation, not low dose anticoagulation. For enoxaparin, the proper full dose is the same dose used to treat acute deep venous thrombosis, acute non-Q-wave myocardial infarction, or unstable angina pectoris: 1 mg/kg every 12 hours. This dose should be adjusted downward only in the presence of massive obesity or renal insufficiency. If there is uncertainty about optimal dosing, the anti-Xa level can be checked and should be targeted to the therapeutic range of 0.5 to 1.0 units/mL. This report underscores that those who use low molecular weight heparins must familiarize themselves with pharmacokinetics and proper dosing. Samuel Z. Goldhaber, MD Cardiovascular Division Brigham and Women’s Hospital 75 Francis St Boston, MA 02115
Pneumothorax Necessitans Presenting as a Presternal Pneumothoracocele Sanjay P. Tripathi, MD, Malek G. Massad, MD, Vinod K. Mehta, MD, Enrico Benedetti, MD, and Alexander S. Geha, MD Division of Cardiothoracic Surgery, Department of Surgery, The University of Illinois at Chicago, Chicago, Illinois
A 31-year-old woman who is an intravenous drug abuser developed sternoclavicular joint infection with mediastinal and subcutaneous tissue abscesses that communicated through an erosion in the manubrium caused by osteomyelitis. Air entrapment from a subsequent apical pneumothorax formed a localized anterior “pneumothoracocele.” We referred to this condition as “pneumothorax necessitans,” and we suggest including it in the differential diagnosis of anterior chest wall masses. (Ann Thorac Surg 2000;69:266 –7) © 2000 by The Society of Thoracic Surgeons
L
ocalized pneumothorax presenting as an enlarging anterior presternal air pocket has not been reported previously. In this communication, we describe this condition in a 31-year-old woman with a history of intravenous drug abuse who developed a defect in the manubrium due to osteomyelitis. An extension of a localized pneumothorax through that bony defect led to the subcutaneous air pocket that we referred to as “pneumothoracocele.”
Accepted for publication May 23, 1999. Address reprint requests to Dr Massad, Division of Cardiothoracic Surgery (M/C 958), The University of Illinois at Chicago, 840 South Wood St, CSB Suite 417, Chicago, IL 60612.
© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Fig 1. A 15 ⫻ 10 cm fluctuant mass overlying the left sternoclavicular joint.
A 31-year-old woman with a history of intravenous drug abuse was admitted to a local hospital with a history of night sweats and a tender mass on the upper left parasternal chest wall of 3 weeks duration. On physical examination, her temperature was 37.5°C. She had a 10 ⫻ 8 cm firm and tender mass over the left sternoclavicular joint. Laboratory workup showed a white blood cell count (WBC) of 15,000/mm3 (85% neutrophils). A chest roentgenogram showed a soft tissue density in the anterior mediastinum. A computerized tomogram (CT scan) of the chest showed an 8 ⫻ 6 cm cystic mass in the anterior mediastinum in continuity with the soft tissue mass felt on examination with destructive changes in the manubrium and left sternoclavicular joint. The patient was started on intravenous antibiotics (pipracillin and gentamicin) and the anterior mediastinal abscess was drained percutaneously under CT guidance. Cultures of the mediastinal fluid grew Staphylococcus aureus. The patient experienced clinical improvement and left the hospital against advice; she was readmitted 2 weeks later with fever, shortness of breath, and a soft tender anterior chest wall mass. At that point her temperature was 39°C and her respiratory rate was 26 breaths/min. Her WBC was 24,000/mm3 with the differential count showing 19 bands. A chest roentgenogram showed bilateral pulmonary infiltrates and a small right pleural effusion. CT scan of the chest showed a loculated air collection in the left pleural apex and anterior mediastinum along with an air pocket in the subcutaneous tissue. An echocardiogram showed large vegetations on the tricuspid valve. With the diagnosis of pneumonia, endocarditis, and sepsis she was started on intravenous antibiotics. Sputum and blood cultures grew S aureus. After 3 weeks of intravenous antibiotics, she gradually recovered and left the hospital against advice. Two weeks later she was admitted to our hospital with fever (38°C), tachypnea, and shortness of breath. On examination, a 15 ⫻ 10 cm soft and tender mass was present overlying the left sternoclavicular joint (Fig 1). A chest roentgenogram showed a radiolucent area over the left pleural apex. A CT scan of the chest showed a loculated left apical pneumothorax communicating with a large subcutaneous air collection anterior to the ster0003-4975/00/$20.00 PII S0003-4975(99)01203-5
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abscesses that communicated through an erosion in the manubrium and caused air entrapment from a subsequent pneumothorax. The well-formed abscess cavity prevented the entrapped air from dissecting along the subcutaneous tissue planes. We suggest referring to this condition as “pneumothorax necessitans” resulting in a “pneumothoracocele” and suggest including it in the differential diagnosis of anterior chest wall masses.
References
Fig 2. CT scan of the chest shows a loculated left apical pneumothorax communicating with a large subcutaneous air collection anterior to the sternum. Erosions within the manubrium are suggestive of osteomyelitis.
num with erosions within the manubrium suggestive of osteomyelitis (Fig 2). The mass grew substantially over the next 2 days after her admission. Due to the rapidly increasing size of the presternal air pocket and the suspicion of a communication with the left pleura and lung, the patient was taken to the operating room. With video-assisted thoracoscopy, left upper pleural adhesions were encountered and released. An apical bleb was identified extending through a defect in the manubrium into the anterior presternal air pocket. The apical bleb was stapled and divided with electrocautery thereby deflating the subcutaneous air collection. The defect in the manubrium became evident at that point. Punch biopsies of the edges of the manubrial defect were sent for cultures, all of which turned out negative. A left pleural apical chest tube was inserted. The postoperative course was uneventful and the patient was discharged home. An HIV test obtained during her latest hospitalization was negative.
Comment Inflammatory conditions involving the sternoclavicular joint occur in patients with rheumatoid and degenerative arthritis, ankylosing spondylitis, and septic arthritis [1]. Septic arthritis of the sternoclavicular joint is an infrequently seen infection, the diagnosis of which may be missed until the patient presents with a complication [2– 4]. Pyarthrosis, and osteomyelitis with associated cutaneous abscesses, have been described previously [1]. The majority of sternoclavicular joint infections are caused by gram-positive organisms, particularly S aureus and group B Streptococcus. In uncomplicated cases, management consists of intravenous antibiotics and drainage of any potential abscess or collection. The patient described in this report had a loculated apical pneumothorax that communicated with the subcutaneous tissue through a defect in the manubrium probably due to osteomyelitis. In this patient, sternoclavicular joint sepsis led to mediastinal and subcutaneous © 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
1. Asnis DS, Dhaliwal GS. Bilateral sternoclavicular joint septic arthritis presenting as cutaneous abscesses. Clin Infect Dis 1994;19:964– 6. 2. Boll KL, Jusik AG. Sternal osteomyelitis in drug addicts. J Bone Joint Surg 1990;72:328–9. 3. Alexander PW, Shin MS. CT manifestations of sternoclavicular pyarthrosis in patients with intravenous drug abuse. J Comput Assist Tomogr 1990;14:104– 6. 4. Chen WS, Wan YL, Lui CC, Lee TY, Wang KC. Extrapleural abscess secondary to infection of the sternoclavicular joint. Report of two cases. J Bone Joint Surg Am 1993;75:1835–9.
Bifid Sternum: Neonatal Surgical Treatment Marcello Do`mini, MD, Massimo Cupaioli, MD, Fabio Rossi, MD, Ahmad Fakhro, MD, Antonio Aquino, MD, and Pierluigi Lelli Chiesa, MD Department of Pediatric Surgery, Policlinico Sant’ Orsola, University of Bologna, Bologna, and Department of Pediatric Surgery, University “G. D’Annunzio” of Chieti, Pescara, Italy
The sternal cleft is a rare congenital anomaly resulting from a fusion failure of the sternum, generally observed at birth and asymptomatic. Surgery is indicated to protect the heart and major vessels from trauma, to improve respiratory dynamics, and for aesthetic reasons. We observed 2 neonates for a superior and medial thoracic mass. The defect involved the upper two thirds of the sternum. The surgical operation for both patients consisted in the primary closure of the defect. (Ann Thorac Surg 2000;69:267–9) © 2000 by The Society of Thoracic Surgeons
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ongenital anomalies of the sternum comprise a broad spectrum of deformities that is difficult to classify. Reviewing the world literature, Shamberger and Welch [1] in 1990 divided them into four groups: cervical ectopia cordis, thoracic ectopia cordis, thoracoabdominal ectopia cordis, and cleft sternum. There is a great differAccepted for publication May 24, 1999. Address reprint requests to Dr Do`mini, Department of Pediatric Surgery, University of Bologna, Policlinico Sant’ Orsola, Via S. Domenico 11, 40124 Bologna, Italy; e-mail:
[email protected].
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