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Pancoast's syndrome results from bronchogenic carcinoma in the superior pulmonary sulcus. The classic syndrome includes pain in the shoulder, arm, and hand in the distribution of C8 and T1 nerve roots, weakness and atrophy of the hand muscles, Horner's syndrome, and first rib erosion secondary to Pancoast's tumor in the superior thoracic inlet. Anatomically, the superior pulmonary sulcus is the area on the superior surface of the lung traversed by the subclavian vessels and encircled by the first rib and spine (Fig. 67-1). It also may be described as the thoracic outlet or thoracic inlet. The treatment of choice has been preoperative irradiation (3000 rads over 2–3 weeks) followed by surgical en bloc resection of the lung, chest wall, lower brachial plexus, and vertebrae at a 1-month interval. This effects approximately a 35% 5-year survival with N0 stage I patients. In recent years, chemoinduction therapy in combination with this protocol has markedly improved survival.

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Figure 67-1.
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Defining anatomy of the superior pulmonary sulcus.

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Edward Hare in 1838 described a patient with pain and numbness in the area of his left ulnar nerve with Horner's syndrome associated with a tumor in the left side of his neck. Henry K. Pancoast, a radiologist, in 1924 described the clinical radiographic findings of four patients with pain in the upper extremity, Horner's syndrome, and erosion of the first rib and vertebra secondary to cancer in the superior pulmonary sulcus. He presented seven patients in 1932, from which resulted the eponym Pancoast's tumor and Pancoast's syndrome. He localized the lesions to tumors in the thoracic outlet or inlet. He coined the term superior pulmonary sulcus tumor rather than apical chest tumor but mistakenly felt that these tumors came from the embryonic cell rest of the fifth branchial cleft. Tobias recognized that these tumors produced a “painful apical costovertebral syndrome” and were secondary to cancers of pulmonary origin. Pancoast's syndrome may be produced by both benign and malignant lesions but most frequently is secondary to carcinomas of bronchogenic origin.

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In the early 1950s, these tumors were considered unresectable and were treated primarily by irradiation therapy only. Few patients survived. Midway through the irradiation therapy of one patient in 1951, the patient became extremely ill, and irradiation was stopped. Dr. Robert Shaw (my senior partner) elected to resect the lesion because the patient's pain was still severe. This was done empirically approximately 4 weeks after the 3000 rads had been delivered over a 2–3 week period. The patient subsequently became pain-free and lived 15 years thereafter without evidence of disease, expiring from another cause. This successful outcome caused our group to treat several other patients in similar fashion with 3 000 rads to the tumor and mediastinal lymph nodes over a period of 2–3 weeks, followed by a waiting period of 2–4 weeks. This delay allows time for the ...

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