Pancoast Syndrome: An Unusual Complication of Pulmonary Infection by Staphylococcus aureus Karen J. Gallagher, MB, ChB, Robert R. Jeffrey, FRCS, Keith M. Kerr, MRCPath, and Malcolm M. Steven, FRCP Department of Medicine, Raigmore Hospital, Inverness; and Departments of Cardiothoracic Surgery and Pathology, Aberdeen Royal Infirmary, Aberdeen, Scotland, United Kingdom

Pancoast syndrome, which comprises a lower brachial plexus lesion and Horner’s syndrome, usually results from local invasion beyond the confines of the lung by an apical lung carcinoma. Other causes are rare. We report the unusual occurrence of a case of Pancoast syndrome caused by a destructive sclerosing fibrosis after pulmo- nary Staphylococcus aureus infection.

(Ann Thoruc Surg 1992;53:9034)

41-year-old woman was admitted to the Ortho- A paedic Out-Patient Department in Inverness giving a 3-day history of acute onset of interscapular and neck pain with marked restriction of neck movement. There was no history of trauma and the patient was a non- smoker with right side dominance. On examination, the neck was rigid with tenderness over the lower cervical and upper thoracic vertebrae and the right trapezius. Neck movement was limited due to muscle spasm but right shoulder movement was full. There was weakness (grade I11 to IV) of the intrinsic muscles of her right hand, but no other neurological deficit was noted.

Over the next 2 days the pain progressed to radiate down the medial border of the right arm with paresthesia in the right hand. Writing and gripping had become difficult. Outpatient treatment comprising analgesics, nonsteroidal antiinflammatory drugs (diclofenac sodium), and a cervical collar was commenced for a presumed diagnosis of prolapsed cervical disc. Two weeks later, the neck pain was now more severe and was exacerbated by movement. The neurological deficits persisted, and in addition she had a small right pupil which was nonreac- tive to light.

Laboratory investigations revealed a raised erythrocyte sedimentation rate on three consecutive occasions (80 to 110 mm in the first hour), but other hematological indices were normal. Serum electrophoresis and tests for antinu- clear antibodies, rheumatoid factor, and Bence-Jones pro- tein were all negative, and she remained afebrile.

A chest radiograph (Fig 1) revealed a right apical opacity, confirmed by computed tomography as a right apical lung mass extending into the root of the neck.

Accepted for publication Sep 11, 1991.

Address reprint requests to Mr Jeffrey, Department of Cardiothoracic Surgery, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, AB9 228, Scotland. UK.

Isotope bone scan showed radionuclide uptake in the first thoracic vertebra and first right rib. Sputum cultures were negative. Although a nonsmoker, the patient was sus- pected of having an apical bronchogenic carcinoma, but percutaneous fine-needle aspiration biopsy under radio- logical screening produced inflammatory cells only, pre- dominantly neutrophil polymorphs. There was no evi- dence of malignancy. The patient was transferred to the Thoracic Surgical Unit at Aberdeen Royal Infirmary where a repeat fine-needle aspiration again showed inflamma- tory cells only.

Exploration through a high parascapular thoracotomy revealed an intense fibrotic reaction confined to the apical segment of the right upper lobe with extrapleural fibrosis and an extrapleural abscess cavity. Culture of tissue revealed a profuse growth of Staphylococcus uureus. Histo- logical examination showed an intense extrapleural fi- brotic reaction with cellular and focally hyalinizing fibro- connective tissue obliterating the pleural space, replacing chest wall skeletal muscle and extending septally and interstitially into the apical segment of the right upper lobe. Centrally but outside the lung was an acute abscess cavity. There was no evidence of malignancy.

Treatment was commenced with intravenous fluclox- acillin subsequently followed by 2 weeks of oral medica- tion with the same antibiotic. She made a good recovery from operation and at review, 6 months later, the only residual neurological deficits were reduced reflexes in the right arm and a right pupil smaller than the left but reactive to light. A repeat computed tomogram of the chest showed right apical pleural thickening and a small air-filled cavity at the lung apex. There was no evidence of rib destruction or recurrence of the mass lesion.

Comment Henry Pancoast, a radiologist in Philadelphia, first de- scribed the syndrome that bears his name in 1932 [l]. It comprised pain in the axilla and arm, weakness of the intrinsic hand musculature, and ipsilateral Horner’s syn- drome with radiological evidence of an apical lung lesion with rib erosion. The most common cause of Pancoast syndrome is bronchogenic carcinoma; nonmalignant causes, although rare, are recognized. Pulmonary tuber- culosis [2] and hydatid cysts [3] at the thoracic outlet have been reported to produce the syndrome, and fungal infection by Allescheriu boydii in immunosuppressed pa- tients has been implicated [4]. Our patient had previously

0 1992 by The Society of Thoracic Surgeons 0003-4975/92/$5.00

904 CASE REPORT GALLAGHER ET AL NONNEOPLASTIC PANCOAST SYNDROME

Ann Thorac Surg 1992;53:90M

there was some similarity between the fibrous reaction seen here and that seen in cases of fibrosing mediastinitid pulmonary hyalinizing granuloma [5]. These conditions are thought to be related to previous tuberculous or Histoplasma infection [6] and are known to be progressive, causing tissue destruction. Their pathogenesis is not known but may be related to an atypical immunological response. It seems possible that this case may represent an example of a progressive fibrosing reaction, possibly sharing similar pathogenesis with the above conditions, on this occasion precipitated by infection with Staphylococ- cus aureus.

This case report illustrates a rare but treatable cause of Pancoast syndrome. It highlights that fibrosing reactions at the apex of the lung may cause Pancoast syndrome and reemphasizes the importance of tissue diagnosis in all suspected malignant conditions.

References Fig 1 . Chest radiograph showing mass at apex of right lung.

been well with no evidence of any of these infections. Nonetheless, they illustrate that inflammatory lesions at the lung apex may cause progressive local damage suffi- cient to result in Pancoast syndrome.

The anatomical site of the lesion and the profuse growth of Staphylococcus aureus from the pus found at operation in our patient implied pulmonary infection by this organism, yet her clinical course was quite unlike a staphylococcal pneumonia. At presentation there was neither history nor clinical evidence suggesting a site of sepsis other than the right lung apex. Histopathologically

1. Pancoast HK. Superior pulmonary sulcus tumour. Tumour characterised by pain, Horner’s syndrome, destruction of bone and atrophy of hand muscles. JAMA 1932;99:1391-6.

2. Paulson DL. Superior sulcus tumours: results of combined therapy. N Y State J Med 1971;71:2050-7.

3. Stathatos C, Kontaxis NA, Zafiracopoulos P. Pancoast’s syn- drome due to hydatid cyst of thoracic outlet. J Thorac Cardio- vasc Surg 1969;58:764-8.

4. Winston DJ, Jordon MC, Rhodes J. Allescheria boydii infections in the immunosuppressed host. Am J Med 1977;63:8300-5.

5. Katzenstein A-L, A’skin FB. Surgical pathology of non- neoplastic lung disease. Philadelphia: W.B. Saunders, 1990:

6. Engleman P, Leibnow AA, Gmelich J, et al. Pulmonary hyalinising granuloma. Am Rev Respir Dis 1977;115:997-1008.

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