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Hyperglycæmia and Diabetes After BurnsHYPERGL YCaeMIA after burns can be of several kinds.

The early shortlived effect, which also appears after

haemorrhage, trauma, and other acute conditions, beginswithin an hour or so, and seldom lasts more than a fewhours or at most a day or twO.1-8 The transient glyco-suria which usually accompanies it was described inthese pages by GOOLDEN 9 over a hundred years ago.Hyperadrenalinaemia is believed to be the main factor,though adrenocortical steroids may play a part andthere is also evidence of extra-adrenal influence.1 3 10The utilisation of glucose may also be disturbed, forthe plasma of burned rats very quickly acquires thepower to inhibit the uptake of glucose by muscle."This body-carbohydrate response is a physiologicalreaction to acute stress. GREEN and STONER 12 regardedit as a primitive defence mechanism whereby the bodymobilises and conserves energy for recovery in the faceof increased metabolic demands from the injured area.

Sometimes hyperglycxmia after burns is pathological.Burning increases the hyperglycsemia and glycosuria ofknown diabetics; ketonuria is common, and more insulinis needed for a time.7 13 Diabetics apart, in some

patients the early hyperglycxmia persists for days or

even weeks after burning before it finally disappears.There may be ketonuria, and insulin may be needed.THOMSEN 14 found a protracted disturbance of carbo-hydrate metabolism in some injured patients, particu-larly older ones, but none became overt diabetics after-wards. This form of hyperglycxmia may be either anacute exacerbation of a mild and usually unsuspecteddiabetes mellitus or the merging of the early responseinto mild diabetes provoked by the burn. Such diabetes,sometimes called pseudodiabetes of burns, or burns-stress diabetes, can be serious and even fatal. 8 15 16 It

usually begins a week or two after extensive burning,and high blood-glucose levels, ranging from 800 to 1600mg. per 100 ml., are not uncommon. Accompanyingthe hyperglycxmia are glycosuria, polyuria, dehydra-tion, often azotasmia, a severe mental disturbance oftenculminating in coma, and an absence of ketone bodies.Dehydration can be accounted for by the osmotic diu-resis produced by the glycosuria, but surface losses offluid, including considerable evaporation from the burn,may contribute. In turn, the dehydration leads to

azotxmia. This acute diabetic state is not peculiar toburns: a similar condition with coma but without ketosis1. Slocum, M. A., Lightbody, H. D. Am. J. Physiol. 1931, 96, 35.2. Taylor, F. H. L., Levenson, S. M., Adams, M. A. New Engl. J. Med.

1944, 231, 437.3. Clark, E. J., Rossiter, R. J. Q. Jl exp. Physiol. 1944, 32, 269, 279.4. Anderson, A. B., Semeonoff, E. in Studies of Burns and Scalds; p. 166.

London, 1945.5. Keyser, J. W. Ann. Surg. 1948, 127, 605.6. Gefter, I. M., Miliuskevitch, G. F. Khirurgiya Mosk. 1949, 26, no. 4.7. Sevitt, S. Burns: Pathology and Therapeutic Applications. London,

1957.8. Bailey, B. N. Br. med. J. 1960, ii, 1783.9. Goolden, R. H. Lancet, 1854, i, 656.

10. Selye, H., Dosne, C. Proc. Soc. exp. Biol. Med. 1941, 48, 532.11. Young, M. K., Jr., Seraile, L. G., Brown, W. L. Am. J. Physiol. 1957,

191, 119.12. Green, H. N., Stoner, H. B. Br. med. Bull. 1954, 10, 38.13. Root, H. E. New Engl. J. Med. 1945, 232, 279.14. Thomsen, V. Acta med. scand. 1938, suppl. p. 91.15. Evans, E. I., Butterfield, W. J. H. Ann. Surg. 1951, 134, 588.16. Rosenberg, S. A., Brief, D. K., Kinney, J. M., Jerrera, M. G., Wilson,

R. E., Moore, F. D. New Engl. J. Med. 1965, 272, 931.

has been described in other patients.17 18 Rehydrationmay restore consciousness, indicating that dehydrationunderlies the mental disturbance (and also suggestingthat ketosis is not the full explanation of the more usualkind of diabetic coma).Why does this condition happen after burns ? The

patients described in two earlier reports 15 19 and nowthe patient studied by ROSENBERG and his colleagues 16had a high-calorie and high-carbohydrate diet (4000-6000 calories a day) to compensate for the excessivenitrogen catabolism after severe burns. BUTTERFIELD 20believed that this diet was the precipitating cause, andthat the considerable adrenocortical activity which fol-lows burning was the underlying factor. BAILEY alsoregarded the condition as adrenocortical in origin,especially since it was insulin-resistant in his patients,but he rejected high-calorie feeding as a cause, sincein one case hyperglycaemia appeared before this dietwas started. ROSENBERG calculated from his patient’surinary nitrogen that gluconeogenesis from proteincatabolism (a process mediated by adrenal steroids)could not account for the high blood-glucose and severeglycosuria (140-335 g. lost daily), and he concludedthat only the high intake of carbohydrate could explainthe loss quantitatively. Most of the carbohydrate is,nevertheless, metabolised, and this accounts for theabsence of ketone bodies. Does the pancreas play a part ?In most reported cases the hyperglycxmia has been atleast relatively resistant to insulin, particularly at firstwhen large doses have been needed. But, like BUTTER-FIELD, ROSENBERG et al. conclude that underlying thesyndrome is a partial failure of the pancreas caused byexcessive intake of carbohydrate. The pancreatic isletscan be damaged in animals by prolonged administrationof glucose, 21 22 but this observation may not be consist-ent with the relatively early onset of the diabetic stateafter burning. SEVITT 23 reported pyknosis, hyper-chromatism, and other evidence of islet-cell damage inburned patients with hyperglycoemia, and he concludedthat the diabetic state was at least partly due to earlypancreatic damage provoked by extensive burning.Mitotic figures in the islet cells suggested to SEVITTthat the damage was reversible, and this view is inaccord with the complete clinical recovery of the patientswho survive their burns. Bacterial infections such as

septicaemia and bronchopneumonia are common in

badly burned patients, and may help to provoke thediabetic state.

Evidently diabetes of burns is not yet fully under-stood. The condition needs to be recognised early,since the mortality is very high when it is untreated;and frequent ward testing for glycosuria should ensureearly diagnosis. Finally, the policy in some centres ofgiving a high carbohydrate diet to extensively burnedpatients should be reconsidered.17. Iyengar, M. O. P. Lancet, 1961, ii, 664.18. Lucas, C. P., Grant, N., Daily, W. J., Reavan, G. M. ibid. 1963, i, 75.19. Arney, G. K., Pearson, E., Sutherland, A. B. Ann. Surg. 1959, 152, 77.20. Butterfield, W. J. H. Lancet. 1955, i, 489.21. Dohan, F. C., Lukens, F. D. W. Endocrinology, 1948, 42, 244.22. Vining, K. K. J. Lab. clin. Med. 1949, 34, 1760.23. Sevitt, S. Lancet, 1955, i, 566.