525 them were negative when tested with diluted solutions of the substance. The same reaction was seen in 10 controls tested. The skin symptoms were probably due to proteolytic effects of pancreozyme and not to delayed-type allergy. Exposure to airborne enzyme powder can induce immediate hypersensitivity reactions.1-4 Our experience illustrates, as others have found, that workers occupationally exposed to proteolytic enzymes are at great risk of sensitisation and that the utmost care must be taken to prevent contact with these substances especially the powder form. Non-allergic irritating skin reactions on exposed parts of the body such as wrists and forehead were very common. They were hard to prevent even if the workers used special overalls and when the level of airborne enzyme dust was reduced by evacuation. Of the twenty employees studied by us only two had had atopic symptoms before they started work with enzymes. We cannot conclude, therefore, atopics will be at greater risk of enzyme allergy than will non-atopics.
SCLEROSING PERITONITIS AND TIMOLOL
test
Departments of Dermatology Occupational Medicine, Södersjukhuset,
and
MARGIT FORSBECK LENA EKENVALL
S-100 64 Stockholm 38, Sweden
SUCCESSFUL CARDIAC TRANSPLANT AFTER MAINTENANCE WITH INTRA-AORTIC BALLOON PUMP
SiR,-Norman et al. described a patient assisted after openheart surgery with a mechanical cardiac support system and who had a heart transplant -but subsequently died. Our group has a patient with a surviving transplanted heart who was maintained on an intra-aortic balloon pump. A 48-year-old male, was transferred to the Columbia-Presbyterian Medical Center 11 days after acute anterior-wall myocardial infarction with an acute ventricular septal defect which had developed 2 days before admission. Intra-aortic balloonpump support6 was begun for hsemodynamic instability, and cardiac catheterisation showed a high muscular ventricular septal defect with a 4:1 shunt. Open-heart surgery was done the same day, and an extensive anterolateral and apical infarction The ventricular septal defect was repaired with a left ventriculotomy through the infarct with a limited infarctectomy. A teflon patch was attached to the left ventricular side of the normal septum with reinforced mattress sutures. Buttressed teflon strips coapted the ventricular muscle to the septal patch. Weaning from cardiopulmonary bypass with the intra-aortic balloon was satisfactory, but the patient remained dependent upon full ballon-pump support. Orthotopic cardiac transplantation was done 4 days after the initial surgery with complete recovery (balloon-pump removed in the operating room) and subsequent hospital discharge. He is now fully active. Our experience’ suggests that certain patients requiring mechanical circulatory support for acute ventricular failure superimposed on chronic end-stage heart disease may be suitable candidates for cardiac transplantation. As Norman et al. indicate, there is need for improved mechanical methods to support such patients who cannot be maintained on intra-aortic balloon support. DAVID BREGMAN RONALD DRUSIN RICHARD N. EDIE Department of Surgery, WILLIAM H. DOBELLE College of Physicians and Surgeons of Columbia University, New York 10032, U.S.A.
MARK A. HARDY KEITH REEMTSMA
Twarog, F. J., Weinstein, S. F., Kon Taik Khaw, Strieder, D. J., Colten, H. R. J. Allergy clin. Immun. 1977, 59, 35. 2. Göthe, C-J., Nilzén, A., Holmgren, A., Szamosi, A., Werner, M., Wide, L. Acta allergol. 1972, 27, 63. 3. Flindt, M. L. H. Lancet, 1978, 430. 4. Pauwels, R., Devos, M., Callens, L., van der Straeten, M. ibid. 1978, 669. 5. Norman, J. C., and others. Lancet, 1978, i, 1125. 6. Bregman, D. in Current Problems in Surgery. Chicago, 1976. 7. Reemtsma, K., Drusin, R., Edie, R., Bregman, D., Dobelle, W., Hardy, J. New Eng. J. Med. 1978, 238, 670. 1.
SiR,-Mr Baxter-Smith and colleagues (July 15, p. 149) de-
patient with a perforation of the jejunum and peritonitis who had been receiving timolol (’Blocadren’) for 18 months immediately before hospital admission scribe a fibrinous
and emergency surgery for acute small-bowel obstruction. In the opening paragraph they imply that timolol is more cardioselective than practolol. In fact, practolol is relatively cardioselective while timolol, like propranolol, is not. In my opinion, no objective evidence is presented which indicates that this is a case of sclerosing peritonitis of the type seen with practolol. In cases of sclerosing peritonitis associated with practolol the patients presenting with subacute or chronic small-bowel obstruction almost always had involvement of organs other than the peritoneum,’2 and in no case was bowel perforation present. Contrary to what Mr Baxter-Smith and his colleagues say, the parietal peritoneum and other abdominal viscera are not often spared from the sclerotic process.1-3 In their case only the visceral peritoneum was affected. I agree that the histology of the adhesions, as presented, is not like that seen in the practolol syndrome; it is more characteristic of secondary peritonitis. Absent in this case are the characteristic findings of the sclerosis associated with practolol (i.e., relatively avascular, dense, laminated fibrous tissue composed of collagen bundles and focal, perivascular, mononuclear cell infiltrates in the adipose tissue1 4. The 48 h duration of obstructive symptoms is probably too short for the development of organising fibrinous peritonitis; however, peritonitis can result from ischsemic and/or ulcerative lesions of the gut per se without perforation. S6 The duration of the ulcerative process in the jejunum was likely to have been longer than 48 h and could have been accompanied by a slow leak of jejunal contents producing chemical peritonitis. Certainly without this protective peritoneal reaction, the gut perforation would have presented as an acute surgical abdomen. There are similarities between this case and that reported by Kennedy and Ducrow.7 In their case, a patient with chronic gastric-ulcer disease and angina pectoris was treated with oxprenolol for only 4 months. 4 years later, during surgery for a rectal neoplasm, extensive fibrinous peritonitis was found which affected all the abdominal organs. The short treatment period with oxprenolol is not consistent with the practolol experience and suggests that this patient may have had a peritoneal reaction to her ulcer disease or rectal neoplasm and conceivably an undetected small perforation at either site. Meyboom9 has pointed out that idiopathic fibrosing peritonitis was described as early as 1942, long before any beta-adrenergic blocking agent was introduced. The lesion of the jejunum in Baxter-Smith’s case, the astiology of which is not apparent, raises questions concerning other medications the patient was receiving, such as enteric-coated potassium chloride tablets, one of the newer wax matrix formulations of this salt, or a diuretic with potassium included. Simple ulceration of the small bowel was a rare disease,9 until about 1963 when enteric-coated potassium-chloride tablets were introduced. 10 Furthermore, small-bowel ulcers with necrotising angiitis are usually multiple and associated with a collagen disease which may not be diagnosed until necropsy.11
1. Marshall, A. J., and others. Q. Il Med. 1977, 46, 135. 2. Thompson, R. P. H., Jackson, B. T. Br. med. J. 1977, i, 1393. 3. Kristensen, K., and others. Lancet, 1975, i, 741. 4. Nicholls, J. T. Ann. clin Res. 1976, 8, 229. 5. Horn, R. C. in Pathology (edited by W. A. D. Anderson); p. 1140, St. Louis, 1971. 6. Lee, F. D. in Muir’s Textbook of Pathology (edited by W. A. D. Anderson); 7. 8. 9. 10. 11.
p. 596, Chicago, 1976. Kennedy, S. C., Ducrow, M. Br. med. J. 1977, i, 1598. Meyboom, R. H. B. Lancet, 1975, i, 334. Watson, M. R. Archs Surg. 1963, 87, 600. Baker, D. R., and others. J. Am. med. Ass. 1964, 190, 586. Finkbiner, R. B., Decker, J. P. New Engl. J. Med. 1963, 268, 14.
SCLEROSING PERITONITIS AND TIMOLOL
test
Departments of Dermatology Occupational Medicine, Södersjukhuset,
and
MARGIT FORSBECK LENA EKENVALL
S-100 64 Stockholm 38, Sweden
SUCCESSFUL CARDIAC TRANSPLANT AFTER MAINTENANCE WITH INTRA-AORTIC BALLOON PUMP
SiR,-Norman et al. described a patient assisted after openheart surgery with a mechanical cardiac support system and who had a heart transplant -but subsequently died. Our group has a patient with a surviving transplanted heart who was maintained on an intra-aortic balloon pump. A 48-year-old male, was transferred to the Columbia-Presbyterian Medical Center 11 days after acute anterior-wall myocardial infarction with an acute ventricular septal defect which had developed 2 days before admission. Intra-aortic balloonpump support6 was begun for hsemodynamic instability, and cardiac catheterisation showed a high muscular ventricular septal defect with a 4:1 shunt. Open-heart surgery was done the same day, and an extensive anterolateral and apical infarction The ventricular septal defect was repaired with a left ventriculotomy through the infarct with a limited infarctectomy. A teflon patch was attached to the left ventricular side of the normal septum with reinforced mattress sutures. Buttressed teflon strips coapted the ventricular muscle to the septal patch. Weaning from cardiopulmonary bypass with the intra-aortic balloon was satisfactory, but the patient remained dependent upon full ballon-pump support. Orthotopic cardiac transplantation was done 4 days after the initial surgery with complete recovery (balloon-pump removed in the operating room) and subsequent hospital discharge. He is now fully active. Our experience’ suggests that certain patients requiring mechanical circulatory support for acute ventricular failure superimposed on chronic end-stage heart disease may be suitable candidates for cardiac transplantation. As Norman et al. indicate, there is need for improved mechanical methods to support such patients who cannot be maintained on intra-aortic balloon support. DAVID BREGMAN RONALD DRUSIN RICHARD N. EDIE Department of Surgery, WILLIAM H. DOBELLE College of Physicians and Surgeons of Columbia University, New York 10032, U.S.A.
MARK A. HARDY KEITH REEMTSMA
Twarog, F. J., Weinstein, S. F., Kon Taik Khaw, Strieder, D. J., Colten, H. R. J. Allergy clin. Immun. 1977, 59, 35. 2. Göthe, C-J., Nilzén, A., Holmgren, A., Szamosi, A., Werner, M., Wide, L. Acta allergol. 1972, 27, 63. 3. Flindt, M. L. H. Lancet, 1978, 430. 4. Pauwels, R., Devos, M., Callens, L., van der Straeten, M. ibid. 1978, 669. 5. Norman, J. C., and others. Lancet, 1978, i, 1125. 6. Bregman, D. in Current Problems in Surgery. Chicago, 1976. 7. Reemtsma, K., Drusin, R., Edie, R., Bregman, D., Dobelle, W., Hardy, J. New Eng. J. Med. 1978, 238, 670. 1.
SiR,-Mr Baxter-Smith and colleagues (July 15, p. 149) de-
patient with a perforation of the jejunum and peritonitis who had been receiving timolol (’Blocadren’) for 18 months immediately before hospital admission scribe a fibrinous
and emergency surgery for acute small-bowel obstruction. In the opening paragraph they imply that timolol is more cardioselective than practolol. In fact, practolol is relatively cardioselective while timolol, like propranolol, is not. In my opinion, no objective evidence is presented which indicates that this is a case of sclerosing peritonitis of the type seen with practolol. In cases of sclerosing peritonitis associated with practolol the patients presenting with subacute or chronic small-bowel obstruction almost always had involvement of organs other than the peritoneum,’2 and in no case was bowel perforation present. Contrary to what Mr Baxter-Smith and his colleagues say, the parietal peritoneum and other abdominal viscera are not often spared from the sclerotic process.1-3 In their case only the visceral peritoneum was affected. I agree that the histology of the adhesions, as presented, is not like that seen in the practolol syndrome; it is more characteristic of secondary peritonitis. Absent in this case are the characteristic findings of the sclerosis associated with practolol (i.e., relatively avascular, dense, laminated fibrous tissue composed of collagen bundles and focal, perivascular, mononuclear cell infiltrates in the adipose tissue1 4. The 48 h duration of obstructive symptoms is probably too short for the development of organising fibrinous peritonitis; however, peritonitis can result from ischsemic and/or ulcerative lesions of the gut per se without perforation. S6 The duration of the ulcerative process in the jejunum was likely to have been longer than 48 h and could have been accompanied by a slow leak of jejunal contents producing chemical peritonitis. Certainly without this protective peritoneal reaction, the gut perforation would have presented as an acute surgical abdomen. There are similarities between this case and that reported by Kennedy and Ducrow.7 In their case, a patient with chronic gastric-ulcer disease and angina pectoris was treated with oxprenolol for only 4 months. 4 years later, during surgery for a rectal neoplasm, extensive fibrinous peritonitis was found which affected all the abdominal organs. The short treatment period with oxprenolol is not consistent with the practolol experience and suggests that this patient may have had a peritoneal reaction to her ulcer disease or rectal neoplasm and conceivably an undetected small perforation at either site. Meyboom9 has pointed out that idiopathic fibrosing peritonitis was described as early as 1942, long before any beta-adrenergic blocking agent was introduced. The lesion of the jejunum in Baxter-Smith’s case, the astiology of which is not apparent, raises questions concerning other medications the patient was receiving, such as enteric-coated potassium chloride tablets, one of the newer wax matrix formulations of this salt, or a diuretic with potassium included. Simple ulceration of the small bowel was a rare disease,9 until about 1963 when enteric-coated potassium-chloride tablets were introduced. 10 Furthermore, small-bowel ulcers with necrotising angiitis are usually multiple and associated with a collagen disease which may not be diagnosed until necropsy.11
1. Marshall, A. J., and others. Q. Il Med. 1977, 46, 135. 2. Thompson, R. P. H., Jackson, B. T. Br. med. J. 1977, i, 1393. 3. Kristensen, K., and others. Lancet, 1975, i, 741. 4. Nicholls, J. T. Ann. clin Res. 1976, 8, 229. 5. Horn, R. C. in Pathology (edited by W. A. D. Anderson); p. 1140, St. Louis, 1971. 6. Lee, F. D. in Muir’s Textbook of Pathology (edited by W. A. D. Anderson); 7. 8. 9. 10. 11.
p. 596, Chicago, 1976. Kennedy, S. C., Ducrow, M. Br. med. J. 1977, i, 1598. Meyboom, R. H. B. Lancet, 1975, i, 334. Watson, M. R. Archs Surg. 1963, 87, 600. Baker, D. R., and others. J. Am. med. Ass. 1964, 190, 586. Finkbiner, R. B., Decker, J. P. New Engl. J. Med. 1963, 268, 14.
