Abstract
1. Details are given of sixty-three consecutive cases with a history of pleural effusion seen at an orthopaedic hospital.
2. Twenty-four of these were post-primary effusions occurring before the onset of symptoms of the orthopaedic lesion. The bone and joint lesions ultimately developing in this group of patients were widely scattered throughout the skeleton.
3. Three others were secondary to adult-type pulmonary lesions.
4. Thirty-six patients had a pleural effusion after the beginning of their orthopaedic tuberculous history. Seven were certainly secondary to operative intervention, six in the thorax near the parietal pleura (costotransversectomy or antero-lateral decompression of the cord) and one from a haematogenous dissemination after fusion of a hip joint.
5. The remainder of this group with pleural effusion during the history of their orthopaedic tuberculous disease numbered twenty-nine. Of these, twenty-five suffered from disease of the thoracic spine; in two more details are defective. Only two definitely had neither pulmonary nor thoracic spinal disease; their lesions were in the lumbar spine.
The conclusion is drawn that the overwhelmingly common cause of pleural effusion in patients with orthopaedic tuberculosis who have normal lungs and have not recently suffered spinal decompression is transpleural infection from thoracic spinal disease and that the sequence is by no means rare. It had occurred in approximately one in six of 145 patients with thoracic Pott's disease seen during this investigation.
6. Details are given of a group of cases with thoracic paravertebral abscess tracking laterally. When the abscess is well clear of the spine and spinal ligaments it may project forwards and radiologically it may appear in the antero-posterior chest film as a shadow in the middle of one or other lung field rather than as a shadow obviously connected with the central paravertebral abscess. Aspiration will yield pus from this posterior extra-pleural abscess extension.
7. The belief that Pott's disease most commonly follows direct spread from caseous paraaortic glands secondary to tuberculous pleurisy is discussed. It is concluded that the evidence is insufficient for so sweeping a statement.
