Hypoglycaemia in Clinical Diabetes

116 MODERATORS, MONITORING AND MANAGEMENTby relatives or friends after minimal training. Paramedics can also use it at the patient’shome or in an ambulance. The disadvantages are that it takes longer (approximately 10minutes) than intravenous glucose to restore consciousness and does not work in patientswho have deficient or absent hepatic glycogen stores (alcoholics or people with cachexia).Unfortunately, even where glucagon is available, relatives or friends may not use it. Inone study (Muhlhauser et al., 1985b), 53 of 123 episodes of severe hypoglycaemia weretreated by relatives or friends with glucagon, 30 by assisting physicians and 44 requiredhospital admission. When glucagon was available but not used, it was because those whoknew how to use it were not present (20 cases) or were too anxious to do so (24 cases).In children with diabetes, Daneman et al. (1989) found that glucagon was used in only athird of households in which it was available – presumably because relatives were eithertoo frightened or poorly educated. Another problem is the limited shelf life; Ward et al.(1990) found that nearly three-quarters of patients knew about glucagon but only 20% hada supply that was in date. Its effect is less certain if coma has been prolonged. In a studyof 100 patients brought to a hospital outpatient department, glucagon was immediatelyeffective in only 41% of patients whose mean estimated duration of coma was 50 minutes(MacCuish et al., 1970).Within five minutes the traditional dose of 50 ml of a 50% glucose (dextrose) solutionraises blood glucose from below 1 to > 12 mmol/l (Collier et al., 1987). This dose isnow considered to be too large by using too concentrated a solution, and 20% dextrosewill suffice. The main problem is the difficulty of giving an intravenous injection toan uncooperative patient who may be refusing or resisting treatment or who has to bephysically restrained to receive an intravenous injection. Extravasation of the concentratedglucose solution outside the vein causes painful phlebitis and, because of its hypertonicity,even an intravascular injection can cause phlebitis or thrombosis. It is not thereforeused much outside hospitals, and few GPs carry glass vials of dextrose for thispurpose.When a patient known to have type 1 diabetes is admitted to hospital in hypoglycaemiccoma, but fails to recover after being given intravenous glucose, other causes ofcoma such as excessive ingestion of alcohol, self-poisoning with opiates or other drugs,acute vascular events such as subarachnoid haemorrhage or stroke, head injury or otherintracranial catastrophes must be excluded. Cerebral oedema is a recognised sequel ofsevere hypoglycaemia, and urgent neuroimaging is required to establish its presence; treatment(Table 5.3) is usually in an intensive care unit as this complication has a highmortality.The most difficult decision is to know for how long to continue treatment. Patients,who have made a full recovery after being unconscious for several days, may (anecdotally)appear subsequently to have significant cognitive impairment or permanent brain damage.It is beyond the scope of this chapter to discuss the investigation and management ofhypoglycaemia in non-diabetic individuals.In conclusion, hypoglycaemia continues to be a common problem in the management ofindividuals with type 1 diabetes. The use of newer technologies of continuous glucose monitoringhas highlighted that it is almost impossible to eliminate hypoglycaemia completelywith present insulin therapy, although understanding moderating factors such as alcohol andincluding them as a component of education programmes for people with insulin-treateddiabetes may help to alleviate some of the anxiety associated with the risk of living constantlywith the threat of hypoglycaemia.