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BED-OCCUPANCY AND WAITING-LIST FIGURES
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.
1200 with the bath-water because of minor instances of misuse of the figure. Mr. Williams suggests: " A more satisfactory figure to use would be that for thenumber of patients per bed per year ’." A few minutes with a pencil and the back of an envelope would help anyone to understand that this is a good deal less efficient as a bed-use index, because it is related only to the sum of the average duration of stay and the average turnover interval (it is 365 divided by this sum) and tells you nothing of the relation between the two elements in this sum. Again, I do not believe that waiting-list figures are as much misunderstood as Mr. Williams believes. Those who are responsible for the management of the hospital services, and I mean here the consultants who are heads of the hospital departments, were not born yesterday. They know from their own experience that waiting-lists are selective; that when beds are very short the patient may not be put on the waiting-list. In some instances waiting-lists can be inflated in order to demonstrate a heavy demand for a particular facility. No-one takes the waiting-list in isolation. What is important is the change in the waiting-list in relation to other statistical indices which enable these changes to be understood. I am, of course, entirely with Mr. Williams in saying that " it is more essential than ever that figures for medical work should be accurate, comparable, and useful." I would go even farther and say that no figures should ever be collected for any work unless they are certainly going to be useful-i.e., unless very careful thought has been given to the problem of requiring the absolute minimum of data necessary for decision making. Mr. Williams is perhaps unaware of important developments that have been taking place in hospital statistics, particularly in the development of what is called hospitalactivity analysis to tailor statistics to the individual requirements of the hospital consultant. out
Even if Yates’ correction is not applied, these workers’ p value is still erroneous since X2 (uncorrected) is 3-4, 0-10> p > 0.05. " Secondly, they report that: Malarial parasites were found in 3 (12%) of 25 children with sickle-cell trait and 32 of 100 children with normal adult hxmoglobin. The difference is striking but not statistically significant (0-1>P>0-05)." The first part of the second sentence is misleading, for Monekosso and Ibiama have, in fact, shown that there was no significant difference between malaria-parasite rates in children with AA and children with AS. Lastly, they say that: Splenomegaly was seen in 6 of 26 (23%) with sickle-cell trait and in 42 of 103 (41%) with normal adult haemogloblin." No statistical analysis was given, but the X2 (Yates’ correction) is 2-1, 0-20 >p> 0-10. "
on Genetics and International Health, Department of Medicine, and the Department of Pathology, University of Chicago, Chicago, Illinois 60637, U.S.A.
Section
JAMES E. BOWMAN.
IS DEGOS’ DISEASE OF VIRAL ORIGIN? SiR,-Degos’ disease is a rare cutaneovisceral disease of unknown setiology characterised by an eruption on the skin of pathognomonic lesions with a telangiectatic margin and a porcelain white centre. Similar lesions develop in the intestinal tract or central nervous system in a high incidence of cases. Death often follows intestinal perforation and secondary peritonitis, or progressive neurological deterioration. No therapy has proved satisfactory. We describe here electronmicroscope changes in the vascular endothelium of a skin lesion from a 24-year-old White woman with Degos’ disease
BERNARD BENJAMIN.
SPLENOMEGALY AND THE SICKLE-CELL TRAIT SiR,-In the Annual Review of Genetics, 1967, Professor Suttonstated that Monekosso and Ibiama2 have found, in a malarial area of Lagos, that splenic enlargement was more prevalent in homozygous HbA/HbA children than in Hb A ihbs children. Lest the interpretation of their contribution be established in the literature and cited (as were two previous 3 papers 4 on the malarial hypothesis which were eventually corrected by Bowman and Frischer5 and Bowman 6) I should like to point out that there is no statistical basis for Monekosso and Ibiama’s2 conclusion that: " The prevalence of splenic enlargement was significantly higher in children with normal haemoglobin (genotype AA) than in those with the sickle-cell trait (genotype AS)." " Firstly, they record that: The haemoglobin genotype was determined in all the children: 100 were AA (mean age 8-8 years), 25 were AS (mean age 8-8 years), 3 were AC, and 1 was SC. The prevalence of sickle-cell trait was 20%. The AS genotype was found in 5 (11%) of 46 children with splenomegaly and in 19 (24%) of 78 children without splenomegaly. The difference is highly significant (p<0.01)." Yates’ correction for x2 is indicated in all of the ensuing analyses,’ and Bowman and Frischer, in a letter similar to this one,5 give normal-deviate formulae8 for checking the arithmetic of ;X2 calculations with 1 degree of freedom. Recalculation of the Lagos data gives a X2 of 2-6, 0-20 >P> 0-10. 1. 2. 3. 4.
5. 6. 7. 8.
Sutton, H. E. A. Rev. Genet. 1967, 1, 1.
Monekosso, G. L., Ibiama, A. A. Lancet, 1966, i, 1347. Allison, A. C., Clyde, D. F. Br. med. J. 1961, i, 1346. Gilles, H. M., Fletcher, K. A., Hendrickse, R. G., Lindner, R., Reddy, S., Allan, N. Lancet, 1967, i, 138. Bowman, J. E., Frischer, H. Br. med. J. 1964, i, 1378. Bowman, J. E. Lancet, 1967, i, 1158. Croxton, F. E. Elementary Statistics with Applications in Medicine and the Biological Sciences; p. 276. New York, 1959. Brownlee, K. A. Statistical Theory and Methodology in Science and Engineering; p. 121. New York, 1960.
Fig. 1-Vascular endothelium within a skin lesion of Degos’ disease, showing a degenerating endothelial cell with increased electron density. Some of the cytoplasmic inclusions are indicated by arrows, others are present in this and the adjacent endothelial cell (E). An erythrocyte (RBC) is present in the lumen (L). Reduced to two-thirds from x 11,500.
who has been observed since the first skin lesions appeared in 1964.1 This patient now has more than 300 such lesions, and light microscopy has confirmed the clinical diagnosis. Within the area of an atrophic skin lesion (fig. 1), some vascular endothelial cells were thickened and showed degenerative changes consisting of increased electron density of the cytoplasm, irregular nuclear margin, lamellar inclusions in mitochondria, and decreased amounts of poorly defined endoplasmic reticulum, ribosomes, and Golgi apparatus. In 1. Howard, R. O., Klaus, S. N., Ophthal. N. Y. 1968, 79, 262.
Savin,
R.
C., Fenton, R. H. Archs
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.
1200 with the bath-water because of minor instances of misuse of the figure. Mr. Williams suggests: " A more satisfactory figure to use would be that for thenumber of patients per bed per year ’." A few minutes with a pencil and the back of an envelope would help anyone to understand that this is a good deal less efficient as a bed-use index, because it is related only to the sum of the average duration of stay and the average turnover interval (it is 365 divided by this sum) and tells you nothing of the relation between the two elements in this sum. Again, I do not believe that waiting-list figures are as much misunderstood as Mr. Williams believes. Those who are responsible for the management of the hospital services, and I mean here the consultants who are heads of the hospital departments, were not born yesterday. They know from their own experience that waiting-lists are selective; that when beds are very short the patient may not be put on the waiting-list. In some instances waiting-lists can be inflated in order to demonstrate a heavy demand for a particular facility. No-one takes the waiting-list in isolation. What is important is the change in the waiting-list in relation to other statistical indices which enable these changes to be understood. I am, of course, entirely with Mr. Williams in saying that " it is more essential than ever that figures for medical work should be accurate, comparable, and useful." I would go even farther and say that no figures should ever be collected for any work unless they are certainly going to be useful-i.e., unless very careful thought has been given to the problem of requiring the absolute minimum of data necessary for decision making. Mr. Williams is perhaps unaware of important developments that have been taking place in hospital statistics, particularly in the development of what is called hospitalactivity analysis to tailor statistics to the individual requirements of the hospital consultant. out
Even if Yates’ correction is not applied, these workers’ p value is still erroneous since X2 (uncorrected) is 3-4, 0-10> p > 0.05. " Secondly, they report that: Malarial parasites were found in 3 (12%) of 25 children with sickle-cell trait and 32 of 100 children with normal adult hxmoglobin. The difference is striking but not statistically significant (0-1>P>0-05)." The first part of the second sentence is misleading, for Monekosso and Ibiama have, in fact, shown that there was no significant difference between malaria-parasite rates in children with AA and children with AS. Lastly, they say that: Splenomegaly was seen in 6 of 26 (23%) with sickle-cell trait and in 42 of 103 (41%) with normal adult haemogloblin." No statistical analysis was given, but the X2 (Yates’ correction) is 2-1, 0-20 >p> 0-10. "
on Genetics and International Health, Department of Medicine, and the Department of Pathology, University of Chicago, Chicago, Illinois 60637, U.S.A.
Section
JAMES E. BOWMAN.
IS DEGOS’ DISEASE OF VIRAL ORIGIN? SiR,-Degos’ disease is a rare cutaneovisceral disease of unknown setiology characterised by an eruption on the skin of pathognomonic lesions with a telangiectatic margin and a porcelain white centre. Similar lesions develop in the intestinal tract or central nervous system in a high incidence of cases. Death often follows intestinal perforation and secondary peritonitis, or progressive neurological deterioration. No therapy has proved satisfactory. We describe here electronmicroscope changes in the vascular endothelium of a skin lesion from a 24-year-old White woman with Degos’ disease
BERNARD BENJAMIN.
SPLENOMEGALY AND THE SICKLE-CELL TRAIT SiR,-In the Annual Review of Genetics, 1967, Professor Suttonstated that Monekosso and Ibiama2 have found, in a malarial area of Lagos, that splenic enlargement was more prevalent in homozygous HbA/HbA children than in Hb A ihbs children. Lest the interpretation of their contribution be established in the literature and cited (as were two previous 3 papers 4 on the malarial hypothesis which were eventually corrected by Bowman and Frischer5 and Bowman 6) I should like to point out that there is no statistical basis for Monekosso and Ibiama’s2 conclusion that: " The prevalence of splenic enlargement was significantly higher in children with normal haemoglobin (genotype AA) than in those with the sickle-cell trait (genotype AS)." " Firstly, they record that: The haemoglobin genotype was determined in all the children: 100 were AA (mean age 8-8 years), 25 were AS (mean age 8-8 years), 3 were AC, and 1 was SC. The prevalence of sickle-cell trait was 20%. The AS genotype was found in 5 (11%) of 46 children with splenomegaly and in 19 (24%) of 78 children without splenomegaly. The difference is highly significant (p<0.01)." Yates’ correction for x2 is indicated in all of the ensuing analyses,’ and Bowman and Frischer, in a letter similar to this one,5 give normal-deviate formulae8 for checking the arithmetic of ;X2 calculations with 1 degree of freedom. Recalculation of the Lagos data gives a X2 of 2-6, 0-20 >P> 0-10. 1. 2. 3. 4.
5. 6. 7. 8.
Sutton, H. E. A. Rev. Genet. 1967, 1, 1.
Monekosso, G. L., Ibiama, A. A. Lancet, 1966, i, 1347. Allison, A. C., Clyde, D. F. Br. med. J. 1961, i, 1346. Gilles, H. M., Fletcher, K. A., Hendrickse, R. G., Lindner, R., Reddy, S., Allan, N. Lancet, 1967, i, 138. Bowman, J. E., Frischer, H. Br. med. J. 1964, i, 1378. Bowman, J. E. Lancet, 1967, i, 1158. Croxton, F. E. Elementary Statistics with Applications in Medicine and the Biological Sciences; p. 276. New York, 1959. Brownlee, K. A. Statistical Theory and Methodology in Science and Engineering; p. 121. New York, 1960.
Fig. 1-Vascular endothelium within a skin lesion of Degos’ disease, showing a degenerating endothelial cell with increased electron density. Some of the cytoplasmic inclusions are indicated by arrows, others are present in this and the adjacent endothelial cell (E). An erythrocyte (RBC) is present in the lumen (L). Reduced to two-thirds from x 11,500.
who has been observed since the first skin lesions appeared in 1964.1 This patient now has more than 300 such lesions, and light microscopy has confirmed the clinical diagnosis. Within the area of an atrophic skin lesion (fig. 1), some vascular endothelial cells were thickened and showed degenerative changes consisting of increased electron density of the cytoplasm, irregular nuclear margin, lamellar inclusions in mitochondria, and decreased amounts of poorly defined endoplasmic reticulum, ribosomes, and Golgi apparatus. In 1. Howard, R. O., Klaus, S. N., Ophthal. N. Y. 1968, 79, 262.
Savin,
R.
C., Fenton, R. H. Archs