671 PNEUMOTHORAX

SIR,-Iread with interest the article by Dr Peatfield and on two cases of fatal tension pneumothorax and would like to offer an alternative explanation for the pathogenesis of this condition. My routine necropsy technique includes the measurement bilaterally, of intrapleural pressure. This is done by inserting a manometer needle between the ribs before opening the thorax. On 26 occasions in a total of 685 adult necropsies, I have demonstrated clinically unsuspected tension pneumothorax almost always accompanied by air bubbles in the loose connective tissue of the mediastinum. In 4 cases "interstitial lung emphysema" was also detected by the time-consuming technique of large nitrocellulose-embedded sections. The histological demonstration of air is inherently difficult, especially in adult lung tissues where it can be mistaken for dilated periarterial lymphatics or vesicular emphysema. In neonates, in whom the condition is more common,’ the histological picture is uncomplicated and consequently more easily recognised. In my series of 685 necropsies I was unable to demonstrate convincingly the presence of a tension pneumothorax and/or interstitial lung emphysema in cases of vesicular or bullous emphysema, no matter how severe, if they were not complicated by some secondary acute disease process such as bronchitis, heartfailure, or pulmonary embolism. In cases where a high intrapleural pressure was discovered-for example, in patients who had experienced periods of severe vomiting, coughing, or respiratory effort or who had been subjected to positive-pressure resuscitation or an explosion-it was almost always possible to find ectopic air either within the interstitial tissues of the lung or within the adjacent loose connective tissue. These findings, together with the results of experiments in rabbits2 and the work of Macklin and Macklin,3,4 point to the likelihood that almost every pneumothorax is precipitated by a too high pressure within the bronchial tree and alveoli which in turn leads to leakage of air into the periarterial tissues. The probable cause of this interstitial type of emphysema is that the marginal alveoli, bordering the vascular tree, are unequally supported by the surrounding tissues. Air finding its way into the interstitium via this route cannot return to the respiratory passages because of the valvular effect of the damaged alveoli. By continuing respiratory efforts the air is pumped further along the perivascular interstitium in the form of dissecting emphysema.5 In this way it reaches the pleura, the mediastinum, and, from there, even the subcutis and mesentery. I cannot imagine how the mediastinal and surgical emphysema of Peatfield’s second case could have happened in any other way. I find it difficult to believe in a hypothesis which implies that interstitial emphysema is secondary to, or a complication of, a pneumothorax. In my opinion a pneumothorax is usually secondary and follows the escape of air from the mediastinum, one reason being that the visceral pleura is stronger than the mediastinal pleura. Such a sequence also seems a more acceptable explanation for double-sided pneumothorax. Perhaps, in these circumstances, the term emphysema should be avoided and, in cases such as those described, the terms pulmonary, mediastinal, or cutaneous pneumatosis should be used instead. That pulmonary pneumotosis can occur in cases of vesicular or bullous emphysema complicated by bronchtis, heart-failure, or pulmonary embolism is understandable because increasing respiratory difficulties lead to even greater respiratory effort,

colleagues (Feb. 17, p. 356)

thus increasing the risk of pulmonary pneumatosis ("interstitial emphysema"). Besides the therapy described by Peatfield et al., one can also give 95% oxygen. The oxygen partially replaces the air in 1 2 3

Emery, J. L. J. clin. Path. 1955, 8, 180. Saltet, J. F. Thesis, University of Leiden, 1971. Macklin, C.C. Can. med. anat. J. 1937, 36, 414. 4. Macklin, M. T., Macklin, C. C. Medicine, 1944, 23, 281. 5. Liebow, A. A. Int. Acad. Path. Monog no. 8. Baltimore, 1968.

the lung tissues, mediastinum, and pleural space and, because oxygen is more readily absorbed by venous blood, it is possible to produce a marked improvement in the condition of some pa-

tients.6 Department of Pathology, Bleulandziekenhuis, Gouda, Netherlands

J. F. SALTET

IMMUNOHISTOLOGICAL DEMONSTRATION OF PROSTATIC ORIGIN OF MALIGNANT NEOPLASMS

SIR,-We

have used the

peroxidase-antiperoxidase

tech-

nique to localise prostate-specific acid phosphatase (P.S.A.P.) in a variety of primary and metastatic neoplasms. Our aim was to explore the histogenesis of tumours affecting the prostate gland and to demonstrate the prostatic origin of metastases in lymph-nodes, bone-marrow, and other sites. A highly specific

z

Cellular localisation of P.S.A.P. in

prostatic carcinoma. (Peroxidase-antiperoxidase, hxmatoxylin; x 400.)

antiserum

raised, in rabbits, and the peroxidaseantiperoxidase procedure was carried out on formalin-fixed, to P.S.A.P. was

paraffin-embedded routine surgical-pathology material. Of 26 cases of known primary and metastatic prostatic carcinomas, all stained positive for P.S.A.P. (see figure) whereas none of the 34 cases of proven non-prostatic primary and metastatic tumours stained positive for P. S.A.P. (see table). P.A.P. FOR PROSTATIC ACID PHOSPHATASE

preliminary data, as well as results reported by Jobsis al.,’ suggest that demonstration ofp.s.A.P. by immunoperoxidase technique is a practical, sensitive, and specific test for the prostatic origin of an otherwise unclassifiable primary or metastatic neoplasm. This may prove to be invaluable in the Our

et

P. Ann intern. Med. 1961, 54, 46. Jöbsis, A. C., DeVries, G. P., Anholt, R. R. H., Sanders, G. T. B. Cancer,

6. Bodey, C. 1.

1978, 41, 1788.

Pneumothorax.

671 PNEUMOTHORAX SIR,-Iread with interest the article by Dr Peatfield and on two cases of fatal tension pneumothorax and would like to offer an alter...
197KB Sizes 0 Downloads 0 Views