Hypoglycaemia prevention

The plasma ketone body level increases rapidly in starvation in pregnancy, which is important in preventing hypoglycaemia in the mother and thus maintaining a supply of glucose for the developing foetus (Chapter 19). 

The IGFBPs probably fulfil several biological functions in addition to preventing hypoglycaemia. They likely protect the mitogen (e.g. from proteolysis) in the blood, and appear to significantly increase the IGF s plasma half-life. They also probably modulate IGF function locally at the surface of IGF-sensitive cells. 

Exercise is an essential yet neglected aspect of treatment for type 2 diabetes especially in its early stages where insulin resistance may predominate. Accumulation of at least 30 0 minutes of moderate physical activity on most days of the week is recommended. For type 1 diabetes the emphasis must be on adjusting the therapeutic regimen to allow safe sports participation to prevent precipitation of ketoacidosis or hypoglycaemia. Extra care is required in cases with known complications like proliferative retinopathy, nephropathy, foot ulcers and cardiac or peripheral vascular disease. 

Ford-Adams ME, Murphy NP, Moore EJ, Edge JA, Ong KL, Watts AP, Acerini CL, Dunger DB. Insulin lispro a potential role in preventing nocturnal hypoglycaemia in young children with diabetes mellitus. Diabetic Med 2003 20 656-60. 

Chelliah A, Burge MR. Hypoglycaemia in elderly patients with diabetes mellitus causes and strategies for prevention. Drugs Aging 2004 21 511-30. 

Insulin is metabolised within the liver to ensure that its effects are not prolonged, thereby preventing a potentially dangerous hypoglycaemia. 

Treatment consists of prevention or elimination of hypoglycaemia. In newborns and infants, this can be achieved by the continuous application of formula diets, if required via nasogastric tube feeding. The administration of allopurinol may also be advisable. A starch diet (e.g. uncooked com starch) is then used to ensure that glucose is released and resorbed slowly in the intestinal tract. (173, 177) After puberty, the course of disease is usually less pronounced. In the long term, espiecially in adenoma-related complications, liver transplantation may be indicated. (185)... 

It is important to prevent nocturnal hypoglycaemia, not only to protect brain function, but also to prevent insulin resistance. This may easily result in exaggerated hyperglycaemia and initiate the vicious circle -hypoglycaemia, hyperglycaemia, increase in insulin dose and risk of subsequent hypoglycaemia (Bolli and Perriello, 1990). The mechanism, frequency and even the existence of the Somogyi phenomenon, however, are all still controversial. 

Insulin-induced hypoglycaemia decreases luteinizing hormone (LH) secretion (Koivisto and Felig, 1978). The effect is prevented by the intravenous infusion of glucose, suggesting that neuroglycopenia and not a direct action of insulin is the cause of reduced LH secretion (Koivisto and Felig, 1978). 

Treatment of a person poisoned by ricin involves alimentary canal decontamination procedures so as to prevent absorption of the toxin. These include the use of syrup of ipecac to induce vomiting, activated charcoal to adsorb the toxin and cathartics to accelerate expulsion. Where a suspected poisoning has occurred but the patient remains asymptomatic, alimentary canal decontamination should still be undertaken and hospital observation for at least six hours after suspected poisoning should take place. The patient should be told to return immediately if symptoms begin. Where more severe poisoning has occurred treatment with intravenous fluids, monitoring for haemolysis and hypoglycaemia, supportive care and the possibility of hypovolaemia should be considered. 

Iatrogenic hypoglycaemia and hypokalaemia are common and preventable, provided there is access to rapid analysis of glucose and potassium and -not less important - a competent and experienced medical team. Another frequent comphcation is recurrence of DKA or unnecessary protraction of the course, typically due to insufficient insulin therapy. Thrombotic events are also not uncommon although more often in HH than DKA. 

Hawdon, J.M., Ward Platt, M.P., Aynsley-Green, A. ( 99A)Arch Dis. Child 70, 59-64. Prevention and management of neonatal hypoglycaemia. 

Inhibition of these reactions prevents hepatic glucose production resulting in hypoglycaemia. 

Figure 26.6 GSD I, von Gierke s disease. GSD I (autosomal recessive) is caused by hepatic glucose 6-phosphatase deficiency so the liver loses its ability to prevent hypoglycaemia. Neonatal hypoglycaemia can be severe and glycogen is stored in excess in the liver and kidney. Other features that are a consequence of accumulation of glucose 6-phosphate are hyperlactataemia, hyperlipidaemia, hyperuricaemia and gout.

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