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PubMed1993

Hypoglycaemia in the diabetic child.

Hypoglycaemia is the most frequent acute complication of insulin-dependent diabetes mellitus. The clinical symptoms of insulin-induced hypoglycaemia can be grouped into those attributable to the sympathetic and adrenergic responses, e.g. tremor, pallor, palpitation, sweating, mydriasis ('hypoglycaemia awareness'), and those attributable to brain dysfunction, ranging from headache to convulsions and coma. Hypoglycaemia in diabetic children can occur at any time of the day, but nocturnal hypoglycaemia is a particular fear and worry. The frequency of mild hypoglycaemia is almost impossible to ascertain and the incidence of severe hypoglycaemia varies between 0.07 and 3.6 episodes per patient-year, though most authors report a range of 0.1-0.2 episode per patient-year. The most frequent causes of hypoglycaemia in diabetic children are deviations from treatment routine such as strenuous exercise, omission of snacks or skipped meals, and gross deviations from the prescribed times of insulin injections and recommended doses of insulin. Other predisposing factors include intensified insulin treatment, improved glycaemic control, young age, longer duration of diabetes and defective counterregulation. The available paediatric studies do not seem to support the suggestion that human insulin impairs the perception of hypoglycaemic symptoms ('hypoglycaemia unawareness') and increases the frequency of hypoglycaemic episodes, but further conclusive studies are needed. Prolonged and recurrent severe hypoglycaemia, particularly in younger children, can cause permanent neuropsychological dysfunction (e.g. learning disabilities) and permanent electroencephalographic abnormalities. Mild hypoglycaemia has also been documented to affect cognitive function, and the performance of neuropsychological tasks can remain decreased for some time (up to several hours) after full clinical recovery from hypoglycaemia. An impending hypoglycaemic attack can usually be averted by the ingestion of 20 g of rapidly absorbed carbohydrate. A severe episode can be effectively treated outside hospital with subcutaneous or intramuscular glucagon (0.5-1.0 mg) or in the hospital by an intravenous bolus of 0.2-0.5 g/kg glucose followed by a continuous glucose infusion. Patient and parent education and vigilant application of diabetes self-care principles are perhaps the most effective means of prevention, but in very young children a less strict metabolic control (higher glycosylated haemoglobin levels) may be necessary.

Child↗

PubMed1992

Endocrine emergencies. Hypoglycaemia.

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.

Emergencies↗

PubMed1995

Antecedent hypoglycaemia in non-diabetic subjects reduces the adrenaline response for 6 days but does not affect the catecholamine response to other stimuli.

1. Recent hypoglycaemia reduces the counter-regulatory and symptomatic response to the next episode of hypoglycaemia. This study was designed to determine whether antecedent hypoglycaemia (a) affected the sympathoadrenal response to other stimuli (postural change and a mathematical stress test, (b) was associated with adaptation of cognitive function and (c) if avoided for 6 days led to the restoration of the counter-regulatory response to hypoglycaemia. 2. On the morning of day 1, 10 healthy men had their response to the sympathoadrenal stimuli assessed before an episode of hypoglycaemia (2.5 mmol/l). A further hyperinsulinaemia clamp was performed for 2h (blood glucose 3.0 mmol/l or 5.0 mmol/l) in the afternoon and the assessments repeated the next day and 6 days later. Cognitive function using the four-choice reaction time test was assessed before and during the episodes of morning hypoglycaemia. The whole study was repeated 4 weeks later with the other afternoon glucose level. 3. Adrenaline levels and sweat rates were reduced (P < 0.05) on day 2 during hypoglycaemia on both occasions and had not returned to normal after 6 days. Symptom scores were lower (P < 0.05) only on day 2 after the afternoon of hypoglycaemia. The responses to the sympathoadrenal stimuli and cognitive function were unaffected by antecedent hypoglycaemia. 4. The adaptation of the counter-regulatory response to antecedent hypoglycaemia appears to be specific to hypoglycaemia. The response takes longer than 6 days but less than 4 weeks to return to normal. Antecedent hypoglycaemia does not lead to cerebral adaptation.

Adaptation, Physiological↗

PubMed2000

Comparison of one week 0900 h serum cortisol, low and standard dose synacthen tests with a 4 to 6 week insulin hypoglycaemia test after pituitary surgery in assessing HPA axis.

OBJECTIVE: To compare the use of 0900 h serum cortisol and both low and standard dose Synacthen tests, one week after pituitary surgery with an insulin hypoglycaemia test performed 4-6 weeks after surgery in assessing the integrity of the hypothalamic-pituitary-adrenal (HPA) axis. DESIGN: 0900 h basal serum cortisol was measured on days 6 and 7 after pituitary surgery (24 h off replacement hydrocortisone) followed by a low dose Synacthen test (1 microg intravenously) on day 6 and a standard dose Synacthen test (250 microg intramuscularly) on day 7. Three to 5 weeks later an insulin hypoglycaemia test was performed on all patients. Both low and standard dose Synacthen tests were performed on control subjects using an identical protocol. SUBJECTS: Forty-two patients (21 male, 21 female), median age 49 years (range 23-73) who had pituitary surgery (Cushing's disease excluded). One patient had undergone repeat surgery for residual tumour and was studied following each operation. Sixteen healthy normal volunteers, median age 37 years (range 21-55). MEASUREMENTS: Serum cortisol measured by radioimmunoassay. RESULTS: Two standard deviations below the mean serum cortisol (logarithmic transformation) in the normal volunteers 30 minutes after low dose Synacthen (1 microg) was 496 nmol/l and after standard dose Synacthen (250 microg) was 504 nmol/l. A normal response was therefore taken as serum cortisol > 500 nmol/l at 30 minutes in both tests (using 496 and 504 nmol/l did not alter results). 0900 h serum cortisols 1 week after surgery were > 250 nmol/l in 31 patients and 29 of these had a normal response to hypoglycaemia (peak serum cortisol > 550 nmol/l). Of the remaining two patients, one had 0900 h serum cortisol on day 6 and 7 after surgery of 405 and 441 nmol/l with a peak serum cortisol response to hypoglycaemia of 451 nmol/l; the other patient had 0900 h serum cortisols of 416 and 251 nmol/l and a peak cortisol response to hypoglycaemia of 498 nmol/l. All eight patients who had a 0900 h serum cortisol < 100 nmol/l failed a subsequent insulin hypoglycaemia test. Seven discrepancies were noted between the low dose Synacthen test and the insulin hypoglycaemia test in the 41 patients who had both tests. In six of these, a subnormal response to low dose Synacthen was followed by a normal response to hypoglycaemia. Three discrepancies were noted between the standard dose Synacthen test and the insulin hypoglycaemia test in the 40 patients who had both tests. In all three cases a normal response to Synacthen was followed by a subnormal response to hypoglycaemia. CONCLUSIONS: A 0900 h serum cortisol < 100 nmol/l (24 h off replacement hydrocortisone) indicated ACTH deficiency and need for lifelong steroid replacement. A 0900 h serum cortisol > 450 nmol/l one week after pituitary surgery is highly suggestive of a normal cortisol response to hypoglycaemia. A 0900 h serum cortisol between 250 and 450 nmol/l one week after pituitary surgery permits safe withdrawal of steroid therapy pending an insulin hypoglycaemia test 1 month after surgery. Patients with 0900 h serum cortisol between 100 and 250 nmol/l should continue replacement steroids until definitive testing. Low dose and standard dose Synacthen tests 1 week after pituitary surgery are unreliable and should not be used.

Adenoma↗

PubMed1997

Hypoglycaemia unawareness.

Hypoglycaemia unawareness, a frequent syndrome in insulin-dependent diabetes mellitus (IDDM), involves a decrease or absence of perception of specific symptoms which normally inform the subject that plasma glucose is decreasing to dangerous levels leading to neuroglycopenia. Without warning symptoms, IDDM patients are unable to take measures (e.g. eating) to prevent severe neuroglycopenia (unconsciousness). As hypoglycaemia unawareness is associated with impaired glucose counterregulation, especially reduced adrenaline responses, it can lead to severe hypoglycaemia. Various studies in animals and humans have indicated that hypoglycaemia unawareness is largely, if not entirely, secondary to increased brain glucose transport due to recurrent or chronic hypoglycaemia. In fact, meticulous prevention of hypoglycaemia largely restores the warning symptoms and adrenaline responses, at least in short-term IDDM. In long-term IDDM, recovery is less complete. Diabetologists and IDDM patients need to be familiar with hypoglycaemia unawareness and how to prevent or treat it. Intensive therapy strictly for normoglycaemia may actually increase the frequency of hypoglycaemia and hypoglycaemia unawareness. However, if intensive therapy is combined with a hypoglycaemia prevention programme, the percentage of HbA1c can be maintained below risk values for the onset or progression of complications, and the frequency of hypoglycaemia can be kept low. Under these conditions, IDDM patients can maintain the warning symptoms and adrenaline response to hypoglycaemia, ensuring a vital backup system for safe intensive therapy of IDDM.

Brain↗

PubMedDate not supplied

Severe hypoglycaemia in 1076 adult patients with type 1 diabetes: influence of risk markers and selection.

BACKGROUND: Differences between studies in rates of severe hypoglycaemia in type 1 diabetic cohorts are common and poorly understood. The purpose of this study was to assess the frequency of severe hypoglycaemia in unselected patients treated in different secondary care centres and to evaluate the influence of risk markers, clinical setting and selection. METHODS: Cross-sectional Danish-British multicentre survey of 1076 consecutive adult patients with clinical type 1 diabetes who completed a detailed questionnaire on hypoglycaemia and related issues. Key variable was the self-reported rate of severe hypoglycaemia during the preceding year. RESULTS: The overall rate of severe hypoglycaemia in the preceding year was 1.3 episodes/patient-year and episodes were reported by 36.7% of subjects. The distribution was highly skewed with 5% of subjects accounting for 54% of all episodes. There were no significant differences between countries or centres. Reduced hypoglycaemia awareness, peripheral neuropathy and smoking were the only significant risk markers of severe hypoglycaemia in a stepwise multivariate analysis. In a subgroup selected to be similar to the Diabetes Control and Complications Trial (DCCT) cohort, the rate of severe hypoglycaemia was 0.35 episodes/patient-year and only retinopathy was a significant risk marker together with state of awareness. CONCLUSION: Severe hypoglycaemia remains a significant clinical problem in type 1 diabetes. The rate of severe hypoglycaemia and the influence of risk markers are very sensitive to selection and differences in rates between centres or studies seem to disappear after correction for differences in clinical characteristics. Smoking is a novel overall risk marker of severe hypoglycaemia.

Adult↗

PubMed2002

Traffic hypoglycaemias and accidents in patients with diabetes mellitus treated with different antidiabetic regimens.

OBJECTIVES: Insulin-treated patients with diabetes are at a higher risk than the general population in causing traffic accidents due to hypoglycaemias. Preceding investigations focused on insulin-treated patients and hypoglycaemia-induced accidents as "end-points". We studied the incidence of symptomatic hypoglycaemia and hypoglycaemia-induced accidents during driving and put it in relation to the different treatment modes of insulin therapy (Conventional Insulin Treatment = CT, Intensified Conventional Insulin Treatment = ICT, Continuous Subcutaneous Insulin Infusion = CSII) as well as to patients treated with oral hypoglycaemia-inducing agents and the two main types of diabetes mellitus. DESIGN SUBJECTS AND SETTING: We investigated 450 patients (122 treated with sulphonylureas, 151 with CT, 143 with ICT and 34 with CSII) by an anonymous questionnaire at different locations to avoid bias. A total of 176 persons had type 1 diabetes, 243 persons had type 2 diabetes, 31 subjects could not be classified. RESULTS: Symptomatic hypoglycaemias during driving were rare events with an occurrence of 0.19-8.26 (minimal and maximal mean, depending on the mode of treatment), if given as hypoglycaemias per 100 000 km on one treatment regimen, or 0.02-0.63, if given as events per year driven. Their incidence increased significantly with the degree of "strictness" between the treatment groups, except between the patients treated with ICT and CSII. Hypoglycaemia-induced accidents are rare with 0.01-0.49, if given as events per 100 000 km and 0.007-0.01, if given as events per year driven. These differences were not significant. Significant confounders influencing the traffic safety of the patients were age, duration of diabetes and concomitant antihypertensive medication. Analysing the data in accordance with the type of diabetes revealed a significantly higher rate of hypoglycaemic events in patients with type 1 diabetes. The number of hypoglycaemia-induced accidents was considerably higher in this group, but failed slightly to reach statistical significance. CONCLUSIONS: Hypoglycaemias during driving are rare events, their occurrence is significantly influenced by the treatment regimen and type of diabetes. Hypoglycaemia-induced accidents are extremely rare, presumably as a positive effect of patient education in our group.

Accidents, Traffic↗

PubMed1983

Insulin and cortisol secretion during OGTT in patients with reactive hypoglycaemia with or without clinical symptoms.

A five hour OGTT was performed on 24 women with 75 g glucose load. Seven of these were normal controls (group I). Eleven women had symptomatic reactive hypoglycaemia (group II). Six women were without clinical symptoms of reactive hypoglycaemia but had biological hypoglycaemia (group III). Biological hypoglycaemia was defined by a plasma glucose level below 2.8 mmol/l, occurring between 150 and 270 minutes during OGTT. Plasma glucose, insulin and cortisol levels were assayed every 30 minutes before and after glucose ingestion. In normal subjects and in the 6 women with asymptomatic reactive hypoglycaemia, plasma insulin and cortisol levels did not differ between both groups during the five hour OGTT. In these patients the cortisol level decreased during the OGTT. In patients with reactive hypoglycaemia with clinical symptoms, the cortisol decreased between 0 and 150 minutes, and then increased between 150 and 240 minutes from 5.9 to 19.8 +/- 1.4 micrograms/100 ml during the phase of clinical hypoglycaemia. This suggests increased plasma cortisol after reactive hypoglycaemia is a specific biological finding with clinical symptoms due to reactive hypoglycaemia; this differentiates the pathological hypoglycaemia from a transitory physiological state, both associated with biological hypoglycaemia.

Adolescent↗

PubMed1993

Frequency and morbidity of severe hypoglycaemia in insulin-treated diabetic patients.

To estimate the frequency and morbidity of insulin-induced hypoglycaemia, a retrospective survey was undertaken of the frequency of severe hypoglycaemia in 600 randomly selected patients with insulin-treated diabetes who were attending a large diabetic outpatient clinic in a teaching hospital. The resulting morbidity (hypoglycaemia-related injuries, convulsions, and road traffic accidents) was ascertained in 302 patients. One hundred and seventy-five (29.2%) of the 600 patients reported a total of 964 episodes of severe hypoglycaemia in the preceding year, giving an overall frequency for the group of 1.60 episodes patient-1year-1. The frequency of severe hypoglycaemia which was documented in 544 Type 1 (ketosis prone) diabetic patients was double that observed in a subgroup of 56 Type 2 diabetic patients who were being treated with insulin (1.70 vs 0.73 episodes patient-1year-1). In the subset of 302 patients, those who had experienced severe hypoglycaemia had greater morbidity associated with an estimated rate of injury of 0.04 injuries person-1year-1. Twenty (6.6%) patients reported a total of 37 convulsions associated with hypoglycaemia, 5 of which had occurred in the preceding year (0.02 convulsions person-1year-1). Five patients reported road traffic accidents in the preceding year which had been caused by hypoglycaemia. The only reliable predictors of severe hypoglycaemia were a history of previous severe hypoglycaemia (p < 0.001), a history of hypoglycaemia-related injury (p < 0.001) or convulsion (p < 0.001), and the duration of insulin therapy (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Accidents↗

PubMed2004

Assessment of hypoglycaemia awareness using continuous glucose monitoring.

AIMS: To investigate the possibility of assessing hypoglycaemia awareness in patients with Type 1 diabetes using continuous glucose monitoring. METHODS: Twenty patients with Type 1 diabetes were investigated. Ten patients with Type 1 diabetes and strongly impaired hypoglycaemia awareness were compared with 10 patients with intact hypoglycaemia awareness regarding quality of hypoglycaemia perception (number of undetected hypoglycaemic episodes per 24 h, glucose level < 3.3 mmol/l). Hypoglycaemia detection was assessed using the event function of the Continuous Glucose Monitoring System (CGMS; Medtronic MiniMed, Northridge, CA, USA). Patients were instructed to enter an event upon suspecting being hypoglycaemic. RESULTS: Satisfactory CGMS performance could be achieved [mean r = 0.893 between calibration measurements and CGMS data, mean absolute difference (MAD) = 20.6%], although artefacts were observable and had to be controlled. Hypoglycaemia unaware patients showed a significantly higher total number of hypoglycaemic episodes (P < 0.05), number of undetected hypoglycaemic episodes (P < 0.01), and mean glucose levels (P < 0.05). Even in aware patients, undetected hypoglycaemia was observable. No significant differences regarding occurrence of nocturnal hypoglycaemia were observable. CONCLUSIONS: The possibility of direct assessment of hypoglycaemia awareness using continuous glucose monitoring was demonstrated. Its application in clinical practice could be of use for assessing hypoglycaemia perception and evaluating the impact of treatment changes on hypoglycaemia awareness.

Adult↗

PubMed1985

Nocturnal hypoglycaemia in patients receiving conventional treatment with insulin.

The prevalence of nocturnal biochemical hypoglycaemia--that is, blood glucose concentrations below 3 mmol/l (55 mg/100 ml)--was evaluated in a random sample of 58 insulin dependent diabetics receiving twice daily insulin. Seventeen patients had at least one blood glucose value below 3 mmol/l (55 mg/100 ml) and five a value below 2 mmol/l (36 mg/100 ml) during the night. Both bedtime (2300) and fasting morning (0700) blood glucose concentrations were significantly lower in the group with nocturnal hypoglycaemia compared with the group without (p less than 0.00001). If the bedtime blood glucose concentration was below 6 mmol/l (108 mg/100 ml) the risk of nocturnal hypoglycaemia was 80% (95% confidence limits 51-96%). If the bedtime blood glucose concentration was above 6 mmol/l the likelihood of hypoglycaemia not occurring during the night was 88% (74-96%). The mean glycosylated haemoglobin A1c (HbA1c) concentration in the group with nocturnal biochemical hypoglycaemia (8.2 (range 5.0-12.4)%) was significantly lower than that in the group without (9.4(7.0-14.2)%) (p less than 0.02). The prevalence of nocturnal hypoglycaemia in the patients receiving twice daily insulin (29%) was compared with that in 15 patients receiving thrice daily insulin (47%) and was not found to be significantly different. The likelihood of this risk being greater with thrice daily insulin was, however, 88%. No patient with nocturnal biochemical hypoglycaemia woke up during the night with symptomatic hypoglycaemia. Nocturnal biochemical hypoglycaemia is common during twice daily treatment with insulin, and low values of HbA1c might be associated with a higher risk of such hypoglycaemia. The blood glucose concentration at bedtime is a significant predictor of nocturnal biochemical hypoglycaemia, and HbA1c values might be of help in identifying patients at risk.

Adolescent↗

PubMed1990

Unawareness of hypoglycaemia and inadequate hypoglycaemic counterregulation: no causal relation with diabetic autonomic neuropathy.

OBJECTIVE: To examine the traditional view that unawareness of hypoglycaemia and inadequate hypoglycaemic counterregulation in insulin dependent diabetes mellitus are manifestations of autonomic neuropathy. DESIGN: Perspective assessment of unawareness of hypoglycaemia and detailed assessment of autonomic neuropathy in patients with insulin dependent diabetes according to the adequacy of their hypoglycaemic counterregulation. SETTING: One routine diabetic unit in a university teaching hospital. PATIENTS: 23 Patients aged 21-52 with insulin dependent diabetes mellitus (seven with symptoms suggesting autonomic neuropathy, nine with a serious clinical problem with hypoglycaemia, and seven without symptoms of autonomic neuropathy and without problems with hypoglycaemia) and 10 controls with a similar age distribution, without a personal or family history of diabetes. MAIN OUTCOME MEASURES: Presence of autonomic neuropathy as assessed with a test of the longest sympathetic fibres (acetylcholine sweatspot test), a pupil test, and a battery of seven cardiovascular autonomic function tests; adequacy of hypoglycaemic glucose counterregulation during a 40 mU/kg/h insulin infusion test; history of unawareness of hypoglycaemia; and response of plasma pancreatic polypeptide during hypoglycaemia, which depends on an intact and responding autonomic innervation of the pancreas. RESULTS: There was little evidence of autonomic neuropathy in either the 12 diabetic patients with a history of unawareness of hypoglycaemia or the seven patients with inadequate hypoglycaemic counterregulation. By contrast, in all seven patients with clear evidence of autonomic neuropathy there was no history of unawareness of hypoglycaemia and in six out of seven there was adequate hypoglycaemic counterregulation. Unawareness of hypoglycaemia and inadequate hypoglycaemic counterregulation were significantly associated (p less than 0.01). The response of plasma pancreatic polypeptide in the diabetic patients with adequate counterregulation but without autonomic neuropathy was not significantly different from that of the controls (change in plasma pancreatic polypeptide 226.8 v 414 pmol/l). The patients with autonomic neuropathy had a negligible plasma pancreatic polypeptide response (3.7 pmol/l), but this response was also blunted in the patients with inadequate hypoglycaemic counterregulation (72.4 pmol/l) compared with that of the controls (p less than 0.05). CONCLUSIONS: Unawareness of hypoglycaemia and inadequate glucose counterregulation during hypoglycaemia are related to each other but are not due to autonomic neuropathy. The blunted plasma pancreatic polypeptide responses of the patients with inadequate hypoglycaemic counterregulation may reflect diminished autonomic activity consequent upon reduced responsiveness of a central glucoregulatory centre, rather than classical autonomic neuropathy.

Adult↗

PubMed2005

Impact of hypoglycaemia on quality of life and productivity in type 1 and type 2 diabetes.

AIM: To characterise the impact of increasing severity and frequency of hypoglycaemia on utility, quality of life, primary care resource use and productivity (time away from normal activities) in people with both Type 1 and Type 2 diabetes. METHODS: A postal survey was sent to 3200 people with diabetes. Self-reported episodes of mild, moderate, severe and nocturnal hypoglycaemia were quantified from a list of signs and symptoms. A number of instruments were used to explore the effect of frequency and severity of hypoglycaemia on quality of life and productivity. RESULTS: There were 861 respondents for whom diabetes type was identifiable. Of these respondents, 629 (73%) experienced some form of hypoglycaemia, 516 (60%) non-exclusively experienced mild or moderate hypoglycaemia, 57 (7%) experienced severe hypoglycaemia and 191 (22%) experienced nocturnal hypoglycaemia. Quality of life and health-related utility decreased as the frequency and severity of hypoglycaemia increased. The use of primary care resources and lost productivity increased as the severity and frequency of hypoglycaemia increased. These associations were independent in multivariate analysis. CONCLUSIONS: These findings suggest hypoglycaemia impacts heavily on the well-being, productivity and quality of life of people with diabetes, and that every effort should be made to minimise hypoglycaemia while aiming for good glycaemic control.

Adolescent↗

PubMed2005

Fear and other disturbances of severe hypoglycaemia in children and adolescents with type 1 diabetes mellitus.

OBJECTIVE: To study perceived occurrence and magnitude of fear and other disturbances of severe hypoglycaemia in children and adolescents with type 1 diabetes mellitus (DM) receiving intensive treatment with active education and psychosocial support. PATIENTS AND METHODS: Out of a geographic population of 112 patients <19 years of age and their families, with a DM duration >1 year, HbA1c mean+/-SD 6.7+/-0.9 (method 1.15% below DCCT level), 74 responded to a questionnaire. Visual analogue scales, 5-graded Likert scales and open questions were used. RESULTS: Global quality of life was high, but lower among patients with severe hypoglycaemia within the last year (p = 0.0114). Worse perceived health was correlated to higher HbA1c year mean (r = 0.32, p = 0.0227). Patients and parents regard severe hypoglycaemia more as a problem (p <0.0001) and the risk of it more disturbing than mild hypoglycaemia (p <0.0001), insulin injections (p <0.0001) or blood glucose determinations (p <0.0001). The disturbance is higher during exercise, disco/party and in travel situations. Severe hypoglycaemia with unconsciousness causes more fear than severe hypoglycaemia needing assistance but without unconsciousness (p = 0.0001) or the potential late complications of DM (p = 0.0014). Severe hypoglycaemia needing assistance but without unconsciousness causes more fear than mild hypoglycaemia (p = 0.0001) and diabetic ketoacidosis (p <0.0001) but less than the potential late complications of DM (p = 0.0034). CONCLUSIONS: Severe hypoglycaemia frequently causes fear and various disturbances in spite of active education and psychosocial support. There is a potential for increased quality of life from interventions targeted at the prevention of severe hypoglycaemia. Further research and improved strategies for the prevention of severe hypoglycaemia are needed.

Adolescent↗

PubMed2002

Abnormalities of the electrocardiogram during hypoglycaemia: the cause of the dead in bed syndrome?

We have previously demonstrated that experimental hypoglycaemia in adults with type 1 diabetes causes an abnormal electrocardiogram (ECG), with increases in QT interval and dispersion. These abnormalities in cardiac repolarisation indicate a risk of ventricular tachycardia and sudden death in other conditions, including ischemic heart disease and congenital long QT syndrome. We have hypothesised that they could contribute to the dead in bed syndrome--the recently described sudden unexpected death in young people with type 1 diabetes--which occurs around three times more frequently than in those without diabetes. It is clearly impossible to explore the causes of a rare and fatal complication by direct observation. We have therefore explored the pathophysiology in a series of experimental studies involving non-diabetic subjects and surrogate endpoints. These have demonstrated that abnormal cardiac repolarisation occurs consistently during insulin-induced hypoglycaemia and that either potassium infusion or beta-blockade prevents increased QT dispersion but only partially prevents QT lengthening. The sympathoadrenal discharge induced by hypoglycaemia alters cardiac repolarisation by both direct and indirect (by reducing extracellular potassium) mechanisms. Other factors that might contribute to the clinical risk of cardiac arrhythmias during nocturnal hypoglycaemia include autonomic neuropathy. This is associated with prolonged QT interval in the non-hypoglycaemic state and has been proposed as a cause of sudden death in those affected. We have examined cardiac repolarisation during clamped hypoglycaemia in patients with type 1 diabetes, with and without autonomic neuropathy. Our data demonstrate lengthening of QTc (QT interval corrected for heart rate) during hypoglycaemia in all groups with no significant differences between the groups, suggesting that autonomic dysfunction does not contribute to hypoglycaemia-induced QTc lengthening in type 1 diabetes. Our hypothesis would be strengthened by demonstrating similar changes during clinical hypoglycaemia. We have recently completed studies in prepubescent children and adults that show modest but significant changes in QTc during nocturnal hypoglycaemia in both populations. We have also demonstrated that pre-treatment with beta-blocking agents prevents abnormal cardiac repolarisation during experimental hypoglycaemia. This has identified a possible treatment if we can identify patients at high risk. Further work is necessary to determine whether we can reliably identify patients who could be at special risk during hypoglycaemia and who might benefit from protection with agents such as beta-blockers. Sudden death in young people with diabetes is, thankfully, rare. However its consequences are so devastating that an excess risk of 3 to 4 times the non-diabetic population seems sufficient to warrant further investigation of the mechanisms that may cause it.

Adult↗

PubMed2001

Activity of angiotensin-converting enzyme and risk of severe hypoglycaemia in type 1 diabetes mellitus.

BACKGROUND: The insertion (I) allele of the angiotensin-converting-enzyme (ACE) gene occurs at increased frequency in endurance athletes. This association suggests that low ACE activity is favourable for performance in conditions with limited substrate availability. Such conditions occur in endurance athletes during competition and in diabetic patients during insulin-induced hypoglycaemia. Patients rely on preserved functional capacity to recognise hypoglycaemic episodes and avoid progression by self-treatment. We studied whether ACE activity is related to the risk of severe hypoglycaemia in type 1 diabetes. METHODS: Consecutive adult outpatients with type 1 diabetes, untreated with ACE inhibitors or angiotensin-II-receptor antagonists (n=207) reported their experience of mild and severe hypoglycaemia during the previous 1 year and 2 years. The patients were further characterised by diabetes history, degree of hypoglycaemia awareness, measurement of C-peptide, haemoglobin A(1c), and serum ACE concentrations, and determination of ACE genotype. FINDINGS: Patients with the DD genotype had a relative risk of severe hypoglycaemia in the preceding 2 years of 3.2 (95% CI 1.4-7.4) compared with those who had the II genotype. There was a significant relation between serum ACE activity and the rate of severe hypoglycaemia (relative risk per 10 U/L increment 1.4 [1.2-1.6]), corresponding to a 3.5 times higher risk for patients in the highest quartile than for those in the lowest quartile. Multiple regression analysis showed that the effect of the ACE genotype was explained by its influence on serum ACE activity and that the only other significant determinants of the risk of severe hypoglycaemia were the degree of hypoglycaemia awareness, b-cell function, and duration of diabetes of more than 20 years. INTERPRETATION: ACE activity is a clinically significant marker of the risk of severe hypoglycaemia in patients with type 1 diabetes, especially in those with impaired defence against hypoglycaemia. These findings need to be confirmed in prospective studies.

Adult↗

PubMed1993

Hypoglycaemia in the adult.

Hypoglycaemia is a relatively common cause for referral of patients to the accident and emergency departments of hospitals but most of it is iatrogenic. Occasionally, however, hypoglycaemia is due to any one of up to a hundred different disorders. In some, hypoglycaemia is the cause of intermittent neuroglycopenic symptoms that lead to their referral to medical outpatients for investigation. Only the most important are discussed here. Hyperinsulinism due to abnormal beta-cell function is an uncommon but important cause of spontaneous hypoglycaemia. The diagnosis is suspected from the history of episodes of altered consciousness confirmed by demonstrating raised plasma insulin, C-peptide and proinsulin levels in peripheral blood in the presence of hypoglycaemia. Differentiation of the various causes of endogenous hyperinsulinism before surgery is difficult if not impossible and the low predictive value of most of the localizing techniques that are available makes them an additional and unnecessary cost, producing little clinical benefit. Hypoglycaemia caused by non-islet cell tumours (NICTH) is seemingly rarer than hyperinsulinism from insulinoma and tends to occur in older patients. The clinical features are similar to those of hyperinsulinism but laboratory investigation reveals appropriately depressed plasma insulin, C-peptide and proinsulin levels in the presence of hypoglycaemia. The plasma IGF-II:IGF-I ratio is characteristically high and the concentration of the E-domain of proIGF-II is raised. Autoimmune hypoglycaemia is more common in some countries than others and is most often due to autoantibodies to insulin (AIS). It may also be caused by autoantibodies to the insulin receptor and possibly to autoantibodies that are stimulatory to pancreatic beta-cells. Contrary to popular belief, idiopathic reactive hypoglycaemia is rare and only one of the possible causes of the postprandial syndrome. It is characterized by a low blood glucose concentration in blood collected during a spontaneous symptomatic episode but not at other times. Its cause is unknown. Other causes of hypoglycaemia include endocrinopathies of various kinds; sepsis including malaria; congestive cardiac failure; hepatic and renal insufficiencies; diverse inborn errors of metabolism; and exogenous toxins, of which alcohol is probably the commonest.

Adult↗

PubMed2000

Factors associated with nocturnal hypoglycaemia among patients with type 2 diabetes new to insulin therapy: experience with insulin lispro.

AIM: To identify factors associated with nocturnal hypoglycaemia in patients with type 2 diabetes who were new (< 2 months therapy) to insulin therapy. METHODS: A randomised, multicentre, 12-month parallel open-label study compared the clinical safety and efficacy of insulin lispro with regular human insulin. A cohort of North American patients completed a health-related quality of life (HRQOL) questionnaire which included questions related to the Health Beliefs Model (HBM). Measurements of hypoglycaemia rate and short-and long-term glucose control assessed clinical safety and efficacy. Three hundred and sixty-five type 2 diabetic patients were enrolled in the study, and 195 North American patients completed the HRQOL questionnaire. RESULTS: After adjustment for demographic and psychological factors, the study population demonstrated lower nocturnal hypoglycaemia risk with insulin lispro. Higher nocturnal hypoglycaemia risk was associated with reduced body mass index (b.m.i.), lower age, and basal ultralente insulin therapy. The associated hypoglycaemia risk was lower with increased alcohol consumption. Patients who completed the HRQOL survey demonstrated higher risk for nocturnal hypoglycaemia if they: (1) had more troublesome hyperglycaemia symptoms in the week before starting insulin; (2) were more confident in their ability to control their diabetes; or (3) thought that diabetes control did not offer a clear health benefit. Nocturnal hypoglycaemia risk was inversely associated with fear of hypoglycaemia. CONCLUSIONS: Type 2 diabetic patients new to insulin therapy demonstrated lower risk of nocturnal hypoglycaemia with insulin lispro. Practitioners should consider patient characteristics and psychological factors that may predispose type 2 diabetes patients to nocturnal hypoglycaemia when initiating insulin therapy.

Aged↗