LOCAL INSULIN FOR DIABETIC GANGRENE

1199 LOCAL INSULIN FOR DIABETIC GANGRENE SIR,-Gangrene of the lower extremities is common in diabetics. 22-3% of all the diabetic patients admitted to the New England Deaconess Hospital from October, 1962, until October, 1963, had foot lesions.1 These lesions heal with difficulty, and in 11-66% of cases amputation is necessary.2 Hitherto the treatment of these patients has been based on strict dietetic control, parenteral insulin, antibiotics, local irrigation with such substances as hydrogen peroxide and potassium 4permanganate, and5 if these fail the affected part is removed.3 In 1966 Paul introduced a new therapeutic method by using soluble insulin locally on the infected wound of a diabetic patient, obtaining a dramatic response within four days. We report here the use of soluble insulin in two diabetic patients with infectious gangrene of the lower extremities, resistant to the commonly used treatments. Case1 A 66-year-old man was admitted on Jan. 1, 1967, with an ulcer on the anterior aspect of the right leg, which he had had since November, 1966. His diabetes had been discovered in 1963 and 3 years before admission he had been treated for phthisis. He had not taken any antidiabetic medication for the last two months before admission. His general condition was fair, blood-pressure (B.P.) 140/90 mm. Hg, temperature 98-8°F (37-1°C). Eyes: conjunctivas congested, with bilateral pterygia. Heart: apex palpable in sixth intercostal space on midclavicular lines. His ulcer, on the lower third of the anterior aspect of the right leg, was covered by a foul-smelling purulent secretion and surrounded by a violet halo. The posterior-tibial and dorsalis-pedis pulses were decreased bilaterally, and there was diminution of sensation to pin-prick on both lower extremities. Urine: traces of albumin and glucose. Blood-sugar: 290 mg. per 100 ml., hxmoglobin 12.3 mg. per 100 ml., haematocrit 41% white blood-cells 6000 per c.mm. (polymorphs 65%, lymphocytes 30%, eosinophils 4%, band forms 1%), erythrocyte-sedimentation (E.S.R.) 94 mm. in the lst hour. The patient was placed on a 1500-calorie diet (carbohydrate 150 g., protein 80 g., fat 65 g.), and given benzylpenicillin intramuscularly, 1 megaunit q.q.h. The ulcer was irrigated with 0-1% permanganate solution of potassium t.i.d. He was given 30 i.u. of isophane insulin daily. On Feb. 9, 1967, he was switched to procaine penicillin, 800,000 I.u. 12-hourly. His fasting blood-sugar levels remained between 69 and 160 mg. per 100 ml. during most of his hospital stay. On April 12, 1967, the ulcer remained about the same. On that day the use of compresses (twice daily) soaked with 20 I.U. of soluble insulin was started. On April 14, 1967, the penicillin was discontinued. Soon after the local use of soluble insulin was begun, the ulcer showed a striking tendency to heal, and on May 8, 1967, it was almost completely healed. Case 2 A 20-year-old woman, a known diabetic for 1 year, was admitted on March 3, 1967, with infection of the right foot. 15 days before she had removed a corn from her right foot. After this the foot had begun to swell, and she had developed a necrotic ulcer accompanied by fever. Her temperature was normal, pulse-rate 96 per minute, B.P. 100/60, and her teeth Her general condition was good. She had an area were poor. of infection and necrosis on the dorsal aspect of the right foot. Blood-sugar 270 mg. per 100 ml., urine glucose 4+, haemoglobin 14-2 g. per 100 ml., hasmatocrit 46%, white blood-cells 6450 (polymorphs 63%, lymphocytes 35%, eosinophils 1%, monocytes 1 %), E.S.R. 68 mm. in the 1st hour, serum creatinine 1-8 mg. per 100 ml., liver-function tests normal. The patient was placed on a 1400-calorie diet and received soluble insulin according to Benedict’s tests on urine collected before meals. Later she was switched to 60 i.u. of isophane 1. 2.

Pratt, T. C. Med. Clins. N. Am. 1965, 49, 987. Collens, W. S., Vlahos, E., Dobkin, G. B., Neumann, E., Rakow, R.; Altman, M., Siegman, F. J. Am. med. Ass. 1962, 181, 692. 3. Wheelock, F. C. New Engl. J. Med. 1961, 264, 316. 4. Hoar, C. S. ibid. 1962, 266, 440. 5. Paul, T. N. Lancet, 1966, ii, 574.

insulin.

She was given benzylpenicillin 2 megaunits q.q.h., terramycin 500 mg. 6-hourly, and trypsin (’Parenzyme’) 2 ml. 12-hourly, intramuscularly, and nitrofurazone (’ Furacin’) locally. On this regimen her fasting blood-sugar levels ranged between 220 and 85 mg. per 100 ml. On April 4, 1967, the use of soluble insulin locally was begun, and soon thereafter the ulcer showed a striking tendency to heal; after 13 days of this treatment the middle of the ulcer was occupied by clean granular tissue, and on May 10, 1967, the ulcer was completely healed. It is well known that diabetic patients develop anatomical changes of the small vessels (diabetic microangiopathy) which

make conservative treatment of the ischaemic lesions of the lower extremities difficult, because the collateral circulation is affected.The metabolic compensation resulting from treatment by diet and with parenteral insulin is evaluated by the blood-sugar values, assuming that the sugar concentration in the affected area is the same. However, it is possible that because of the microangiopathy the insulin does not reach the infected tissues. Thus it is possible to have a normal bloodsugar level with a raised concentration of sugar in the affected tissues, which would cause cellular dehydration and consequent decreased resistance to infections.7 The local application of soluble insulin would notionally enhance the glucose transport inside the cells, producing a local metabolic compensation which, together with the systemic metabolic compensation, would lead, we think, to the rapid healing of diabetic ulceronecrotic lesions. JOSE ENRIQUE LOPEZ Carabobo University Medical School, BENITO MENA. Valencia, Venezuela.

BED-OCCUPANCY AND WAITING-LIST FIGURES SIR,ņThe point of view of Mr. Williams (May 11, p. 1029) is not representative of the point of view of those hospital consultants with whom I come into contact and who are trying to manage their departments on a rational basis-i.e., on the basis of some proper measurement of their management

experience. In the first place, anyone who understands the arithmetic of the bed-occupancy rate knows that algebraically it is identical with the ratio of the average duration of stay to the total interval between admissions to a bed. This last interval is the sum of the average duration of stay and the turnover interval so that a bed-occupancy rate of 100% would indicate a turnover interval of zero. No-one in their right senses could imagine a worse state of medical inefficiency than a zero turnover interval. Quite apart from the pressure on the medical staff and the possible injury to the patient, the burden on the nursing staff would be intolerable. No-one that I know of has ever indicated that a bed-occupancy rate of 100% indicates a high state of efficiency. If one thinks of a turnover interval of not less than 1 day with an average duration of stay in a general hospital of, say, 12 days, then the optimum occupancy-rate would be not much more than 90%; in fact one normally talks of something like 85% as reasonable. I do not think that the time at which the bed state is fixed is important in relation to the meaning of the index, but it is very important in relation to the accuracy of the figure. This is why hospitals are encouraged to make their count at the quietest time of the day-i.e., the time at which movements are minimal. If hospitals use their good sense in this way a lot of the difficulties referred to by Mr. Williams will be avoided. It would not be right to try to run the hospitals only on the basis of bed-occupancy figures. Medical efficiency and other humanitarian interests demand that other factors should be brought into account. But beds are costly and form a very large part of hospital resources. It is essential in the interests of good management to have some index of bed utilisation, and it would be silly to throw the baby G., Huhselman, B., Seidler, I., Stotter, G. Medna Alemana, 1960, 1, 638. 7. Williams, R. H. Text-book of Endocrinology; p. 694. Philadelphia, 6. Engenhart,

1962.