fetters from health professionals on subjects connected with the practical management of diabetes or diabetes education are welcomed and should be addressed to the Editor

Brain damage following hypo- glycaemia in alcoholic diabetics Sir, Drs Khaw and Cassar (Ref I ) describe three interesting cases of brain damage following hypoglycaemia in alcoholic diabetics. A few additional comments may be of interest.

Binge drinking, in non-diabetics, is occasionally associated with strokes, even in young subjects (Ref 2). Several mech- anisms have been suggested to account for this phenomenon (Ref 2). One possibility is that platelet thrombus formation or the release of vasoconstrictors from platelets play a role. In this context, three independent findings may be relevant:

(i) Abstention (for approximately 2 weeks) in chronic alcoholics may result in thrombocytosis with hyperaggregable platelets, which release excessive amounts of the vasoconstrictor thromboxane A2 (TXA2) (Ref 3). This contrasts with the inhibitory effect of ethanol on platelet TXA2 release in normal subjects, even at relatively low blood ethanol levels (Ref 41.

(ii) Hypoglycaemia, especially in diabetics, is associated with enhanced platelet aggregation (and therefore presumably TXA2 release), raised levels of factor VIII and an increased incidence of strokes/transient ischaemic attacks (see Ref 5 for other relevant studies). In addition, acute hypokalaemia may develop during hypoglycaemia (Ref 5): this may predispose such patients to cardiac arrhythmias.

hypoglycaemia (Ref I ) but also with hypothermia (Ref 6). It is mandatory to exclude this latter possibility, especially since hypothermia may aggrevate hypoglycaemia (Ref 6), and hypoglycaemia, in turn, may aggravate hypothermia (Ref 6). In addition, cooling induces several changes which increase the risk of thrombosis (see Ref 7 for relevant studies).

In diabetics, hypoglycaemia occurs against the background of an increased risk of vascular disease, including stroke (Ref 8). There is also evidence that high insulin concentrations inhibit synthesis of prostacyclin (a vasodilator and inhibitor of platelet aggregation), in vitro (Ref 9). In addition, diabetics have significant abnormalities in the regulation of their cerebral blood flow (CBF), following inhalation of carbon dioxide, which is a powerful cerebral vasodilator in normal subjects; diabetics also have unpredictable falls in their basal CBF of up to 30% (Ref 10). Both of these abnormalities may contribute to an enhanced risk of cerebral infarction, as well as to an increase in the size of the infarct.

Finally, alcohol intoxication and hypothermia are often additional factors in hypoglycaemic diabetic and non-diabetic patients (Ref 6). It would also appear that the presence of two or more of the factors (alcohol; hypothermia; hypoglycaemia) that make up this triad may worsen the prognosis (Refs 6, 11). D P MIKHAILIDIS Senior Lecturer and Hon Senior Registrar M A BARRADAS Research Fellow J Y JEREMY Research Fellow P DANDONA Physician in charge, Diabetic Service, and Director, Metabolic Unir Metabolic Unit, Department of Chemical Pathology & Human Metabolism, Royal Free Hospital & School of Medicine, Pond Street, London, NW3 2QG.

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(iii)Alcoholic intoxication is not only associated with

References Khaw K, Cassar J. Brain damage following hypoglycaemia in alcoholic diabetics. Practical Diab, 1986; 3(1): 43.

Wilkins M R, Kendall M J. Stroke affecting young men after alcoholic binges. Br Med J, 1985; 291: 1342.

Jenkins W J, Mikhailidis D P, Barradas M A, Jeremy J Y, Dandona P. Impaired platelet function and prolonged bleeding time in chronic alcoholics. Gut, 1984; 25: A544.

Mikhailidis D P, Jeremy J Y, Barradas M A, Green N, Dandona P. Effect of ethanol on vascular prostacyclin (PG12) synthesis, platelet aggregation and platelet thromboxane release. Br Med J, 1983; 287: 1495-8.

Mikhailidis D P, Barradas M A, Hutton R A, Jeremy J Y, Sabur M, Dandona P. The effect of non-specific beta blockade on metabolic and haemostatic variables during hypoglycaemia. Diab Res, 1985; 2: 127-34.

Malouf R, Brust J C M. Hypoglycaemia: causes, neurological manifestations, and outcome. .4nn Neurol, 1985; 17: 421-30.

Mikhailidis D P, Jeremy J Y, Barradas M A, Dandona P. Increases in platelet and red cell counts, blood viscosity, and arterial pressure during mild surface cooling. Br Med J, 1985; 290: 74-5.

Oppenheimer S M, Hoffbrand B I, Oswald G A, Yudkin J S. Diabetes mellitus and early mortality from stroke. Br Med J, 1985; 291: 1014-5.

Jeremy J Y, Mikhailidis D P, Dandona P. Simulating the diabetic environment modifies in vitro prostacyclin synthesis. Diabetes, 1983; 32: 217-21.

Dandona P, Woollard M L, James I M, Newbury P, Beckett A G. Instability of cerebral blood flow in insulin-dependent diabetics. Lancet, 1979; ii: 1203-6.

Critchley J A J H, Proudfoot A T, Boyd S G, Campbell I W, Gordon A. Deaths and paradoxes after intentional insulin overdose. Br Med J, 1984; 289: 225.

Advantages and costs of screenicg a - with non-mydriatic fundus camera Sir, Any method which will improve the screening of diabetics for retinopathy is highly desirable, and fundus photography is one of the options. Our own experience using this technique (Ref I ) , has shown that assessinent of 35mm slides provides results as good as retinal examination performed by experienced ophthalmologists. We believe, however, that if a non-mydriatic fundus camera is employed to screen the diabetic population then the Polaroid option may be preferable, as the photographs can be added to the notes in the same way as the results of biochemical or x-ray examinations. Over several years, any change in the retinal appearance may be readily appreciated, whereas 35mm

Practical DIABETES May/June 1986 Vol 3 No 3

Lemxsmthe€ditm! Advantages of non-mydriatic camera; Home BG monitoring in eiderly NtDDs

transparencies, i f removed from their protective folder for projection, tend to get mislaid.

The suggestion that the screening of 2,000 diabetics costs an extra f17,000, if optometrists are employed, has no basis in fact. Diabetics already attending an ophthalmology clinic or who are blind d o not need annual screening. In a recent survey of three groups of diabetics attending hospital clinics in Districts where there was no encouragement to promote screening by optometrists, 71% had attended an optometrist within the previous two years, 52% within one year and 69% were currently wearing glasses (unpublished data).

The actual cost of employing optometrists to assist in the screening of diabetics is certainly less than half the figure quoted by Waugh et a1 (Ref 2). They will at the same time detect glaucoma, another major cause of preventable blind- ness. The fundus camera involves a high initial outlay and no provision has been made by Waugh et a1 to cost the maintenance or repairs following breakdown of the apparatus. Our experience of using fundus cameras, extending over twen- ty years, shows that such costs are not negligible and certainly cannot be ignored.

Consultant Physician J C DEAN HART Consultant Ophthalmic Surgeon Frenchay Hospital Bristol, BS16 1LE

C J BURNS-COX

References (1) Burns-Cox C J, Dean Hart J C.

Screening of diabetics for retinopathy by ophthalmic opticians. Br Med J, 1985; 290: 1052-4.

(2) Waugh N R, Ellingford A, Scott S D. Screening for diabetic retinopathy: options and cost effectiveness. Practical Diabetes, 1986; 3(1): 30-1.

Home blood glucose monitoring in elderly NIDDs Sir, 1 was disappointed to read the paper by Martin B J et a1 (Jan/Feb 1986, page 37) which recommended an increased availability to elderly NIDDs of home blood glucose monitor- ing. First, I cannot envisage that this would provide the physi- cian with any more information regarding glycaemic control than could be obtained by a simple random blood sugar taken at each clinic visit. NIDDs are less prone to wide blood sugar fluctuations than are IDDs, thus allowing random sampling to be representative enough to form the basis of clinical decisions. If one wishes to exercise particular scrutiny, eg in younger NIDDs, the fasting plasma glucose would be a further refinement (Ref).

Second, the cost to the NHS of a general acceptance of these recommendations would be prohibitive. The annual cost of chemical strips for capillary blood glucose testing at a 730-bed teaching hospital in Sheffield is f35,000. This would dramatically increase if NIDDs were routinely included, since numerically they represent the greater proportion of the clinic population. Finally, I d o not feel that glycaemic control should have the same priority in the elderly population as in the younger age group. I cannot imagine what benefits to the patients the authors had in mind when they included those with poor vision (including one blind) in this study.

DR J F McCANN Research Registrar University of Sheffield, Academic Division of Medicine, Clinical Sciences Centre, Northern General Hospital, Shef- field, S5 7AU

Practical DIABETES May/June 1986 Vol 3 No 3

Reference Holman R R, Turner R C. The basat plasma glucose: a simple relevant index of maturity onset diabetes. Clin Endocrinology, 1980; 14: 279-86. Dr Martin and co-authors comment: I n response to Dr. McCann’s comments, most elderly NIDDs receiving oral hypoglyaemic agents attend diabetic clinics no more than three or four times per year. If there is any assessment of control between visits, this is usually based on intermittent urine testing, despite the recognised inadequacies of this technique, particularly in the elderly who tend to have a raised renal threshold fo r glucose. As Dr McCann states, decisions on treatment are usually based on a single random plasma glucose at clinic visits. While we would accept that NIDDs are less prone to wide plasma glucose fluctuations, there is nevertheless some variation during the 24 hours, particularly in those patients receiving shorter-acting sulphonylureas commonly prescribed in the elderly. Those attending morning clinics will have a random plasma glucose sample taken one to two hours after taking medication, the time of maximum action of dosage regimen. A five-point blood sugar profile, as we described, gives a clearer picture of the adequacy of glycaemic control over the 24 hours and gives a clearer indication a f potential hypoglycaemia, particularly if multiple dosage is used. Hypoglycaemia, induced by sulphonylurea therapy, is often missed (Ref 1) and the elderly are particularly at risk by under-reporting hypoglycaemic events. The impaired memory and mild confusion of hypoglycaemia are often mistaken fo r ?common senility” in the elderly, and the mortality rate from sulphonylurea-induced hypoglycaemia may exceed that for insulin (Ref 2).

The cost of the scheme, as described in our paper using capillary blood glucose testing strips, was 70 pence per profile. Since these were carried out at fortnightly intervals. the average cost was 5 pence per patient per dax not excessive in terms of the potential cost to the NHS of inadequate treatment. Once adequate and safe control is achieved, the frequency of profiles can be reduced, eg one profile prior to each clinic visit, leading to further cost reduction. Contrary to the scenario as seems to have been envisaged by Dr McCann, the daily monitoring applied to younger insulin-dependent diabetics was never contemplated in the elderly. Furthermore, our study was a modification of the usual home blood glucose monitoring practice, in that recordings were taken by the patient but interpreted by the doctor the following day. It demonstrated that such a procedure is feasible and could be very useful in poorly- controlled elderly NIDDs. Elderly NIDDs may have the disease for many years and are at similar risk of severe microvascular complications as young diabetics. Indeed, these complications may develop more quickly in the elderly than in the young (Ref 3). As current evidence suggests that improved control may prevent, or slow, progression of complications, adequate treatment is justified (Ref 4). Clearlx glycaemic control of elderly NIDDs does not merit the close scrutiny and individual attention afforded to juvenile and pregnant IDDs, but that is no excuse for offering second-rate management and denying the benefits of modern technology where appropriate.

References Turkington R W. Archives of Int Med, 1977; 137: 1082-3. Nelson R L. Hypoglycaemic disorders (edited Service F J). Boston, Massachusetts, G K Hall, 1983: 97. Caird F I, Pirie A, Ramsell T G. Diabetes and the eye. Oxford, Blackwell Scientific, 1969; 230. Tchobroutsky G. Handbook of diabetes mellitus (edited Brownlee M). Chichester, John Wiley & Sons, 1980; 5: 3-39.

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