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VANISHING LUNGS
860 associated
movement after Bell’s palsy cannot be explained by compression. This reasoning may not be generally accepted ; but in any event the place for decompression will be small, since even denervation, when it does occur, is rarely so substantial as to cause disabling spasm or associated movement.
Thus, unless we are to submit many to unnecessary operation, we need a method of identifying cases in which denervation is going to be severe. Improvements in the technique of electromyography may provide such- a method ; but meanwhile most patients will be content to let the condition take its natural course. In the very occasional case where palsy is apparently permanent and some mechanical blockage to regeneration seems possible, exploration may be useful ; but in this group it can be logically undertaken only after any chance of recovery by regeneration has been excluded by the passage of months without improvement. VANISHING LUNGS RADIOGRAPHY sometimes reveals the development, in the course of pulmonary tuberculosis, of cyst-like spaces in areas where the disease is regressing ; and this feature has been observed much more commonly since the introduction of effective chemotherapy. Rappaport1 discusses it under the piquant title " vanishing lungs." Some of these spaces are no doubt thin-walled cavities, but the consensus of opinion seems to be that most are emphysematous bullae caused by a check-valve mechanism set up by partial bronchial obstruction. This mechanism can sometimes be convincingly demonstrated at operation for the removal of large bullous cysts of lung,2 and it is almost certainly responsible for the cyst-like lesions which so commonly come and go in the course of staphylococcal pneumonia in children. Sometimes an emphysematous tension-cyst may reach such large dimensions that there appears to be nothing but air in the hemithorax ; but the lung has not really " vanished "-it is merely compressed by the cyst-and the thoracic surgeon can conjure it back again by removing the cyst and thus enabling the sound lung tissue to re-expand. If the airspaces which develop in tuberculous lungs after treatment are tension-cysts of this sort, the term " vanishing lung " is misleading; but Rappaport suggests that in some instances, perhaps the majority, it is truly descriptive. He points out that exudative tuberculous lesions may occasionally undergo spontaneous healing by actual resolution rather than by fibrosis 3; and that this process is common and much more complete when antituberculous drugs, especially isoniazid, are given-a view which appears to be amply confirmed by Dick’s4 pathological studies. Rappaport submits that there is every reason to suppose that as they clear away debris caused by the disease scavenger cells will likewise remove alveolar septa damaged by toxins, so that air-spaces will appear which may increase in size owing to normal lung traction or to secondary obstructive hyperinflation. Whatever the nature of these air-spaces, how to deal with them is an important current problem. Some take the view that since an emphysematous bulla cannot be distinguished from a thin-walled cavity the lesion should be regarded as a cavity and collapsed or resected. Others argue that since " open " healing of a cavity may follow chemotherapy that is to say, the cavity may become lined with epithelium derived from the bronchus of supply or be left with a clean fibrous lining) the lesions should be looked on as innocent unless tubercle bacilli are recovered from the respiratory secretions. Rappaport advocates resection because he believes that, even if Rappaport, I. J. Amer. med. Ass. 1955, 158, 1436. Allison, P. R. Thorax, 1947, 2, 169. Pinner, M. Pulmonary Tuberculosis in the Adult. Ill., 1945 ; p. 39. 4. Dick, J. C. Lancet, July 30, 1955, p. 216. 1. 2. 3.
Springfield,
there is
no
recrudescence of
emphysema,
once
lurking tuberculous foci,
started, is likely to extend.
the On the
other hand, a growing number of physicians are so impressed with the results of long-term chemotherapy in pulmonary tuberculosis that they are reluctant to
consider surgery until there is clear evidence that servative treatment has failed.
con-
TRAUMA AND ADRENAL HEMORRHAGE " SINCE Roux and Yersin1 described haemorrhagic in diphtheria, adrenals congestion " of the guineapig’s adrenal haemorrhage has usually been ascribed to a toxic-infectious process ; the clearest example is the Waterhouse - Friderichsen syndrome, due to meningococcal infection. Adrenal haemorrhage has been found in association with many different disorders, ranging from acute alcoholic poisoning2 to ulcerative colitis treated with corticotrophin 3 ; but accounts of it are still so few 4as to warrant detailed reports of individual cases. of adrenal is not A macroscopic diagnosis haemorrhage always borne out by detailed histological examination.5 The series of 17 cases of post-traumatic adrenal apoplexy reported by Sevitt6 is therefore of great clinical interest. Sevitt found these 17 cases in 60 necropsies of patients. who had met with various accidents. The haemorrhage was bilateral in 5, and unilateral (mostly on the right side) in 12 ; and in some cases haemorrhage into the adrenal was associated with haemorrhage or bruising of the periadrenal tissues. Histologically central haemorrhage had destroyed the medullary tissue ; necrosis of the cortical tissue, probably the result of ischaemia, was also seen. Thrombosis of the adrenal veins, described by several workers,7-9 was found in only 1 case; but small tears, fissures, or ruptures of the walls of the venules were present in 12 out of 17 h8emorrhagi& glands. Sevitt suggests that these result from temporary compression of the gland. Traumatic haemorrhage of the adrenals might be judged to be uncommon from the scanty references to it in ,
published work, particularly if, as Gruenwald5 insists, the not uncommon adrenal haemorrhage of the newborn is no longer to be ascribed to trauma. Some textbooks of pathology 1011 do not mention adrenal haemorrhage at all. Martland 12 merely states that massive haemorrhage into one or both glands can be seen after blunt-force compression injuries to the abdomen or lower part of the chest. Adrenal haemorrhage might be expected to be fairly common in air-raid casualties ; but, although this. lesion has occasionally been found in laboratory animals. exposed to blast and in an air-raid victims recent accounts of observations in the 1939-45 war 14 15 do not mention the lesion ; nor has adrenal haemorrhage been seen in the victims of the recent Comet disasters,16 It would therefore seem that such haemorrhage is produced by trauma of a particular type (presumably rather localised), leading to rupture of medullary vessels; the high proportion of unilateral adrenal lesions associated with ipsilateral injuries to the chest or abdomen in 1. Roux, E., Yersin, A. Ann. Inst. Pasteur, 1888, 2, 629. 2. Santo, E. Frankfurt. Z. Path. 1941, 55, 115. 3. Wilson, D. A., Roth, D. J. A ner. med. Ass. 1953, 152, 230. 4. Mackenzie, D. H. J. Path. Bact. 1955, 69, 333. 5. Gruenwald, P. Arch. Path. (Lab. Med.), 1955, 60, 150. 6. Sevitt, S. J. clin. Path. 1955, 8, 185. 7. Snelling, Ch. E., Erb, I. H. J. Pediat. 1935, 6, 22. 8. Hall, E. M., Hemken, L. Arch. intern. Med. 1936, 58, 448. 9. Keele, D. V. K., Keele, K. D. K. Brit. med. J. 1942, ii, 687. 10. Anderson, W. A. Pathology. London, 1953. 11. Moritz, A. R. Pathology of Trauma. London, 1954. 12. Martland, H. S. Arch. Path. (Lab. Med.), 1944, 37, 147. 13. Zuckerman, S. Proc. R. Soc. Med. 1941, 34, 171. 14. Benzinger, Th. In German Aviation Medicine, World War II; vol. 2. Department of U.S. Air Force, Washington. 15. Schubert, W. Virchows Arch. 1952, 321, 295. 16. Armstrong, J. A., Fryer, D. J., Stewart, W. K., Whittingham, H. Lancet, 1955, i, 1135.
movement after Bell’s palsy cannot be explained by compression. This reasoning may not be generally accepted ; but in any event the place for decompression will be small, since even denervation, when it does occur, is rarely so substantial as to cause disabling spasm or associated movement.
Thus, unless we are to submit many to unnecessary operation, we need a method of identifying cases in which denervation is going to be severe. Improvements in the technique of electromyography may provide such- a method ; but meanwhile most patients will be content to let the condition take its natural course. In the very occasional case where palsy is apparently permanent and some mechanical blockage to regeneration seems possible, exploration may be useful ; but in this group it can be logically undertaken only after any chance of recovery by regeneration has been excluded by the passage of months without improvement. VANISHING LUNGS RADIOGRAPHY sometimes reveals the development, in the course of pulmonary tuberculosis, of cyst-like spaces in areas where the disease is regressing ; and this feature has been observed much more commonly since the introduction of effective chemotherapy. Rappaport1 discusses it under the piquant title " vanishing lungs." Some of these spaces are no doubt thin-walled cavities, but the consensus of opinion seems to be that most are emphysematous bullae caused by a check-valve mechanism set up by partial bronchial obstruction. This mechanism can sometimes be convincingly demonstrated at operation for the removal of large bullous cysts of lung,2 and it is almost certainly responsible for the cyst-like lesions which so commonly come and go in the course of staphylococcal pneumonia in children. Sometimes an emphysematous tension-cyst may reach such large dimensions that there appears to be nothing but air in the hemithorax ; but the lung has not really " vanished "-it is merely compressed by the cyst-and the thoracic surgeon can conjure it back again by removing the cyst and thus enabling the sound lung tissue to re-expand. If the airspaces which develop in tuberculous lungs after treatment are tension-cysts of this sort, the term " vanishing lung " is misleading; but Rappaport suggests that in some instances, perhaps the majority, it is truly descriptive. He points out that exudative tuberculous lesions may occasionally undergo spontaneous healing by actual resolution rather than by fibrosis 3; and that this process is common and much more complete when antituberculous drugs, especially isoniazid, are given-a view which appears to be amply confirmed by Dick’s4 pathological studies. Rappaport submits that there is every reason to suppose that as they clear away debris caused by the disease scavenger cells will likewise remove alveolar septa damaged by toxins, so that air-spaces will appear which may increase in size owing to normal lung traction or to secondary obstructive hyperinflation. Whatever the nature of these air-spaces, how to deal with them is an important current problem. Some take the view that since an emphysematous bulla cannot be distinguished from a thin-walled cavity the lesion should be regarded as a cavity and collapsed or resected. Others argue that since " open " healing of a cavity may follow chemotherapy that is to say, the cavity may become lined with epithelium derived from the bronchus of supply or be left with a clean fibrous lining) the lesions should be looked on as innocent unless tubercle bacilli are recovered from the respiratory secretions. Rappaport advocates resection because he believes that, even if Rappaport, I. J. Amer. med. Ass. 1955, 158, 1436. Allison, P. R. Thorax, 1947, 2, 169. Pinner, M. Pulmonary Tuberculosis in the Adult. Ill., 1945 ; p. 39. 4. Dick, J. C. Lancet, July 30, 1955, p. 216. 1. 2. 3.
Springfield,
there is
no
recrudescence of
emphysema,
once
lurking tuberculous foci,
started, is likely to extend.
the On the
other hand, a growing number of physicians are so impressed with the results of long-term chemotherapy in pulmonary tuberculosis that they are reluctant to
consider surgery until there is clear evidence that servative treatment has failed.
con-
TRAUMA AND ADRENAL HEMORRHAGE " SINCE Roux and Yersin1 described haemorrhagic in diphtheria, adrenals congestion " of the guineapig’s adrenal haemorrhage has usually been ascribed to a toxic-infectious process ; the clearest example is the Waterhouse - Friderichsen syndrome, due to meningococcal infection. Adrenal haemorrhage has been found in association with many different disorders, ranging from acute alcoholic poisoning2 to ulcerative colitis treated with corticotrophin 3 ; but accounts of it are still so few 4as to warrant detailed reports of individual cases. of adrenal is not A macroscopic diagnosis haemorrhage always borne out by detailed histological examination.5 The series of 17 cases of post-traumatic adrenal apoplexy reported by Sevitt6 is therefore of great clinical interest. Sevitt found these 17 cases in 60 necropsies of patients. who had met with various accidents. The haemorrhage was bilateral in 5, and unilateral (mostly on the right side) in 12 ; and in some cases haemorrhage into the adrenal was associated with haemorrhage or bruising of the periadrenal tissues. Histologically central haemorrhage had destroyed the medullary tissue ; necrosis of the cortical tissue, probably the result of ischaemia, was also seen. Thrombosis of the adrenal veins, described by several workers,7-9 was found in only 1 case; but small tears, fissures, or ruptures of the walls of the venules were present in 12 out of 17 h8emorrhagi& glands. Sevitt suggests that these result from temporary compression of the gland. Traumatic haemorrhage of the adrenals might be judged to be uncommon from the scanty references to it in ,
published work, particularly if, as Gruenwald5 insists, the not uncommon adrenal haemorrhage of the newborn is no longer to be ascribed to trauma. Some textbooks of pathology 1011 do not mention adrenal haemorrhage at all. Martland 12 merely states that massive haemorrhage into one or both glands can be seen after blunt-force compression injuries to the abdomen or lower part of the chest. Adrenal haemorrhage might be expected to be fairly common in air-raid casualties ; but, although this. lesion has occasionally been found in laboratory animals. exposed to blast and in an air-raid victims recent accounts of observations in the 1939-45 war 14 15 do not mention the lesion ; nor has adrenal haemorrhage been seen in the victims of the recent Comet disasters,16 It would therefore seem that such haemorrhage is produced by trauma of a particular type (presumably rather localised), leading to rupture of medullary vessels; the high proportion of unilateral adrenal lesions associated with ipsilateral injuries to the chest or abdomen in 1. Roux, E., Yersin, A. Ann. Inst. Pasteur, 1888, 2, 629. 2. Santo, E. Frankfurt. Z. Path. 1941, 55, 115. 3. Wilson, D. A., Roth, D. J. A ner. med. Ass. 1953, 152, 230. 4. Mackenzie, D. H. J. Path. Bact. 1955, 69, 333. 5. Gruenwald, P. Arch. Path. (Lab. Med.), 1955, 60, 150. 6. Sevitt, S. J. clin. Path. 1955, 8, 185. 7. Snelling, Ch. E., Erb, I. H. J. Pediat. 1935, 6, 22. 8. Hall, E. M., Hemken, L. Arch. intern. Med. 1936, 58, 448. 9. Keele, D. V. K., Keele, K. D. K. Brit. med. J. 1942, ii, 687. 10. Anderson, W. A. Pathology. London, 1953. 11. Moritz, A. R. Pathology of Trauma. London, 1954. 12. Martland, H. S. Arch. Path. (Lab. Med.), 1944, 37, 147. 13. Zuckerman, S. Proc. R. Soc. Med. 1941, 34, 171. 14. Benzinger, Th. In German Aviation Medicine, World War II; vol. 2. Department of U.S. Air Force, Washington. 15. Schubert, W. Virchows Arch. 1952, 321, 295. 16. Armstrong, J. A., Fryer, D. J., Stewart, W. K., Whittingham, H. Lancet, 1955, i, 1135.