Postoperative hypoglycaemia in small children

Six of 57 children under 4 years old became hypoglycaemic during postoperative recovery from various surgical procedures. Fluids either by mouth or intravenously did not always prevent this. Children at risk could not be predicted on the basis of age or weight-for-age. Small children should be fed as soon as practicable after operations, preferably with milk.     

Brain imaging in neonatal hypoglycaemia

Magnetic resonance imaging studies in two cases of neonatal hypoglycaemia showed cortical and white matter cerebral damage that was most obvious in the occipital lobes. Both cases showed oedema in the parieto-occipital cortex and underlying white matter in the acute phase, with profound atrophy of these regions in the chronic phase. These findings support those of pathological studies which suggest that hypoglycaemia induces cerebral damage by a mechanism separate from the effects of cerebral hypoxia-ischaemia caused by secondary seizures.     

Nesidioblastosis-associated hypoglycaemia presenting with prominent cardiac manifestations

We present a case of nesidioblastosis presenting with hyperinsulinaemic hypoglycaemia and electrocardiographic abnormalities.     

Lipolytic response during spontaneous hypoglycaemia in insulin-dependent diabetic subjects

OBJECTIVE: To gather qualitative data regarding HIV/AIDS patients' perspectives about HIV-1 protease inhibitors (PIs), and about their experiences taking and adhering to regimens containing PIs. DESIGN: Six focus groups of persons under care for HIV were conducted between September and November 1996 regarding participants' knowledge, awareness, experiences when taking, and adherence to antiretroviral regimens containing PIs. An identical discussion guide was used to facilitate all six groups. Focus group proceedings were audiotaped, transcribed, coded for themes, and analyzed qualitatively. SETTING: HIV/AIDS practices of three teaching hospitals and two community health centers. PATIENTS/PARTICIPANTS: Fifty-six patients with HIV disease: 28 men and 28 women. MEASUREMENTS AND MAIN RESULTS: Knowledge and positive impressions of PIs were prevalent among this diverse group of persons with HIV, and did not differ by race/ethnicity or gender. Most knew that these were new, potent medications for treating HIV/AIDS. Networks of persons with HIV and medical providers were the most important information sources. Those taking PIs were aware that adherence to the regimen is important, and most were using special strategies to maximize their own adherence, but expressed considerable frustration about the central role these medication regimens had assumed in their life. A subset who did not believe they would adhere to these regimens had declined treatment with them. Motivating factors for taking and adhering to these complex regimens were improving CD4 counts and viral loads and the patient-provider relationship. CONCLUSIONS: Among those with HIV/AIDS, awareness of PIs and their effectiveness is substantial, owing to the impact of informal networks and medical providers. This early positive "reputation" of PIs may enhance motivation for adherence. Those who are taking PIs invest substantial effort adhering to these complex regimens, but resent the need to make medications the focus of their lives.     

Intensified insulin therapy and the risk of severe hypoglycaemia

The objectives of the present analyses were to assess the association between HbA1c levels and severe hypoglycaemia (SH, treatment with glucose i.v. or glucagon injection) and to identify predictors of SH in a prospective multicentre trial. The study population consisted of 636 insulin-dependent diabetic patients who had participated in a structured 5-day in-patient group treatment and teaching programme for intensification of insulin therapy (ITTP) in one of 10 hospitals and who were re-examined after 1, 2, 3, and 6 years including assessment of demographic, disease and treatment related parameters, diabetes-related knowledge, behaviour, and emotional coping. At baseline, age (mean +/- SD) was 27 +/- 7 years, diabetes duration 9 +/- 7 years and HbA1c 8.3 +/- 1.9 %. During the 6-year follow-up, the mean HbA1c value improved to 7.6%, and in patients with a diabetes duration of more than 1 year at entry into the study (n = 538) the incidence of SH decreased from 0.28 cases/patient/year during the year preceding the ITTP to 0.17 cases/patient/year. The patient group was divided into decile groups according to mean follow-up HbA1c values. In each group more than 230 patient years could be analysed. Groups with mean HbA1c values of 5.7, 7.0, 7.4, 7.7 and 8.9% had comparable risks of SH (0.15-0.19 cases/patient/year). In a logistic regression analysis, mean HbA1c during follow-up, a history of SH during the year preceding the ITTP, C-peptide level, emotional coping, carrying emergency carbohydrates (as assessed at the 1-year follow-up), and age at onset of diabetes were significant independent predictors of SH. The incidence of SH between centres varied between 0.05 and 0.27 cases/patient/year. In conclusion, in the present analyses no linear or exponential relationship between HbA1c and severe hypoglycaemia could be identified by using simple group comparisons. Applying complex regression analyses, various patient-related predictors of severe hypoglycaemia were identified.     

Enhancement of alcohol-induced hypoglycaemia by H2-receptor antagonists

Male Wistar rats were kept in a hypoxia chamber (9% O2) for eight hours. Control animals breathed room air in the same chamber for a similar period of time. One week later the brains of all rats were prepared for the immunohistochemical demonstration of Mn-superoxide dismutase (Mn-SOD). In comparison with the sham-exposed controls, the hypoxia-treated animals showed an increase in the number of Mn-SOD-immunoreactive neurons in several hippocampal structures. The 72 kD heat shock protein was not found to be induced one week after a moderate hypoxia.     

Forearm substrate exchange during hyperinsulinaemic hypoglycaemia in normal man

To assess muscle substrate exchange during hypoglycaemia, 8 healthy young male subjects were studied twice during 2 h of hyperinsulinaemic euglycaemia followed by 4 h of (1) hypoglycaemia (plasma glucose < 2.8 mmol l-1), and (2) euglycaemia. Insulin was infused at a rate of 1.5 mU kg-1 min-1 throughout. When compared to euglycaemia, hypoglycaemia was associated with: (1) increment in circulating glucagon (65 +/- 8 vs 23 +/- 4 ng l-1, p < 0.05), growth hormone (19.9 +/- 3.6 vs 2.6 +/- 1.3 micrograms l-1, p < 0.05), adrenaline (410 +/- 88 vs 126 +/- 32 ng l-1, p < 0.05) and increased suppression of C-peptide (0.5 +/- 0.1 vs 1.0 +/- 0.1 micrograms l-1, p < 0.05) along with a modest lowering of insulin (103 +/- 10 vs 130 +/- 13 mU l-1, p < 0.05); (b) decrease in plasma glucose level (3.0 +/- 0.07 vs 5.0 +/- 0.12 mmol l-1, p < 0.05), forearm glucose uptake (0.21 +/- 0.09 vs 1.21 +/- 0.21 mmol l-1, p < 0.05) and requirement for exogenous glucose (5.6 +/- 1.1 vs 13.2 +/- 0.9 mg kg-1 min-1 p < 0.005) together with an impaired suppression of isotopically determined endogenous glucose production (0.34 +/- 0.5 vs -2.3 +/- 0.3 mg kg-1 min-1, p < 0.05); (3) exaggerated increase in blood lactate (1680 +/- 171 vs 1315 +/- 108 mumol l-1, p < 0.05) and a decrease in alanine (215 +/- 18 vs 262 +/- 19 mumol l-1, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma gastrin concentration related to acid secretion during insulin hypoglycaemia

The release of gastrin by insulin hypoglycaemia was studied in man before and after vagotomy. Completeness of vagotomy was judged by the gastric acid response to the same hypoglycaemia, using several criteria including one that allows for pyloric losses and duodenogastric reflux. A total of 137 tests was performed on 10 subjects. The plasma gastrin concentration was found to rise in the preoperative studies and also in the postoperative studies no matter what type of vagotomy had been performed or what criteria of completeness of vagotomy were used. We concluded that gastrin can be released in response to hypoglycaemia in the absence of the vagus nerve.     

Double blind clinical and laboratory study of hypoglycaemia with human and porcine insulin in diabetic patients reporting hypoglycaemia unawareness after transferring to human insulin

OBJECTIVES: To compare awareness of hypoglycaemia and physiological responses to hypoglycaemia with human and porcine insulin in diabetic patients who reported loss of hypoglycaemia awareness after transferring to human insulin. DESIGN: Double blind randomised crossover study of clinical experience and physiological responses during slow fall hypoglycaemic clamping with porcine and human insulin. SETTING: Clinical investigation unit of teaching hospital recruiting from diabetes clinics of five teaching hospitals and one district general hospital. SUBJECTS: 17 patients with insulin dependent diabetes mellitus of more than five years' duration who had reported altered hypoglycaemia awareness within three months of transferring to human insulin. MAIN OUTCOME MEASURES: Glycaemic control and frequency of hypoglycaemic episodes during two months' treatment with each insulin. Glucose thresholds for physiological and symptomatic responses during clamping. RESULTS: Glycaemic control did not change with either insulin. 136 hypoglycaemic episodes (eight severe) were reported with human insulin and 149 (nine severe) with porcine insulin (95% confidence interval -4 to 2.5, p = 0.63). 20 episodes of biochemical hypoglycaemia occurred with human insulin versus 18 with porcine insulin (-0.8 to 1, p = 0.78). During controlled hypoglycaemia the mean adrenaline response was 138 nmol/l/240 min for both insulins; neurohormonal responses were triggered at 3.0 (SE 0.2) versus 3.1 (0.2) mmol/l of glucose for adrenaline and 2.5 (0.1) versus 2.5 (0.1) mmol/l for subjective awareness. CONCLUSIONS: These data suggest that human insulin per se does not affect the presentation of hypoglycaemia or the neurohumoral, symptomatic, and cognitive function responses to hypoglycaemia in insulin dependent diabetic patients with a history of hypoglycaemia unawareness.     

Auditory information processing during acute insulin-induced hypoglycaemia in non-diabetic human subjects

Acute insulin-induced hypoglycaemia impairs performance on tests of general mental ability in humans. It is recognized that different brain functions vary in their sensitivity to neuroglycopenia, but little is known about the effects of neuroglycopenia on specific brain processes. The effect of controlled hypoglycaemia on two aspects of auditory information processing (auditory temporal processing and simple auditory processing) was examined in a homogeneous group of 20 healthy non-diabetic human subjects. Auditory temporal processing (temporal order discrimination) and simple auditory processing (pitch discrimination, single-tone duration and single-tone loudness discrimination) tests were part of the Test of Basic Auditory Capabilities (TBAC). Two tests of general cognitive performance (Digit Symbol Substitution and Trail Making B) were included to provide a measure of general brain functioning during hypoglycaemia. Hypoglycaemia lead to a significant deterioration in auditory temporal processing (P < 0.01), and a deterioration in one of three tasks of simple auditory processing (discrimination of single-tone loudness, P < 0.05). Significant disruptions also occurred in both tests of general brain functioning. These results are congruent with other studies in human subjects, showing a disruptive effect of hypoglycaemia on visual information processing when examined under conditions of limited perceptual time, and they provide further evidence of the importance of sensory processing speed in basic perceptual and cognitive functions. The disruptive effect of moderate insulin-induced hypoglycaemia on auditory perception may have implications for insulin-treated diabetic humans exposed to this metabolic stress, because of the importance of hearing in everyday life.     

Case report. Computed tomography of the brain in severe hypoglycaemia

Computed tomographic (CT) findings in a case of extreme hypoglycaemia induced by an overdose of chlorpropamide are described. Brain lesions tend to be preferentially localized along the boundary zones ("watersheds") between the territories of the main cerebral arteries. In our case, generalized brain damage occurred during severe hypoglycaemic coma. Neuropathological changes in this condition have been the subject of previous studies in experimental animals. Computed tomography allows follow-up studies of the human brain damaged by hypoglycaemic coma. Abnormalities revealed by CT probably represent reparative tissue reactions that indirectly reflect the extent of neuronal destruction.     

Prevention and treatment of hypoglycaemia unawareness in type 1 diabetes mellitus

Unawareness of hypoglycaemia (reduced ability/failure to recognize hypoglycaemia symptoms at the physiological threshold of 3.0 mmol/l) occurs frequently in type 1 diabetes mellitus, and patients are then at risk for severe hypoglycaemia. Unawareness of hypoglycaemia is the result of earlier frequent episodes of hypoglycaemia (iatrogenic). Likewise, a history of hypoglycaemia induces unawareness, while meticulous prevention of hypoglycaemia can reverse hypoglycaemia unawareness. Therefore, it is essential that insulin therapy regimens for type 1 diabetes mellitus be designed not only to maintain near-normoglycaemia, but also to minimize hypoglycaemia. Such a goal is feasible as long as (1) a rational plan of insulin therapy is adopted, including appropriate use of the short-acting insulin analogue lispro, (2) blood glucose is properly monitored, (3) blood glucose targets are individualized, and (4) education programs are widely implemented.     

Prognosis of infants of diabetic mothers in relation to neonatal hypoglycaemia

A prospective follow-up study was conducted to determine whether neonatal hypoglycaemia in infants of diabetic mothers affects subsequent neurological and intellectual performance. 37 such infants (25 hypoglycaemic and 12 non-hypoglycaemic) were examined for physical, neurological and developmental performance at an average age of 4 1/2 years. 11 children were abnormal, with generalised retardation and neurological abnormalities, or delays in particular areas of development; three children were possibly abnormal; and 23 children were normal. Abnormality at follow-up could not be related to neonatal blood glucose level, to the duration of hypoglycaemia or to any other measurement made in the neonatal period, nor to any factor relating to the maternal diabetes. Compared with the normal children, the abnormal group had slightly small head-circumferences at birth relative to their gestational age, but a follow-up there was no difference in head size. At follow-up the children of diabetic mothers tended to be shorter than average. The poor prognosis of the infants in this study was not due to brain damage caused by neonatal hypoglycaemia.