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As discussed in Chapter 1, the primary cause of ketoacidosis is an absolute or relative insulin deficiency. Briefly, the effects of insulin deficiency and thus an increase in glucagon/insulin ratio in the portal circulation together with increases in levels of counter-regulatory hormones (catecholamines, cortisol and growth hormone) are summarised in Figure 2.1. Elevated levels of ketone bodies result from mobilisation of fatty acids from adipose tissues and their preferential b-oxidation within the hepatic mitochondria; the finite capacity of peripheral tissues to utilise ketone bodies

Insulin deficiency

Increased counterregulatory hormones

Glucagon Growth hormone Cortisol

Catecholamines t Hepatic gluconeogenesis

I Peripheral use of glucose



Osmotic diuresis

(loss of H2O, sodium, chloride, potassium, phosphate)

t Protein catabolism

T Amino acids


T NEFA release from adipose tissue








Figure 2.1 Schema of the pathophysiology of diabetic ketoacidosis. Adapted with permission from Lyen KR, Hale D, Baker L. Endocrine emergencies. In: Fleisher G, Ludwig S (Eds). Textbook of Pediatric Emergency Medicine. Baltimore, MD: Williams and Wilkins © 1983. NEFA = non-esterified fatty acids contributes to the hyperketonaemia. Most of the acidaemia in diabetic ketoacidosis is accounted for by the production and dissociation of organic ketoacids, but lactic acidosis from tissue hypoperfusion may also contribute (see Chapter 6).

The regulation of ketosis during childhood differs in some respects from that observed in adults. In normal children, circulating levels of ketone bodies are relatively high prior to puberty. The finding of intermittent ketonuria is not unusual in non-diabetic young children, particularly after an overnight fast. During puberty, as plasma insulin levels increase, fasting ketone levels tend to fall. However, in adolescents with type1 diabetes, even when blood glucose levels are maintained at 5 mmol/L overnight using an intravenous insulin infusion, there is still a substantial increase in nocturnal ketogenesis, which appears to be due mainly to excessive growth hormone secretion. This may help explain the rapid decompensation that can occur in teenagers overnight following either a short episode of vomiting or the omission of bedtime insulin. Teenage girls in particular may present with severe acidosis despite only modest elevations of blood glucose.

Children develop ketosis more rapidly than adults.

Diabetic ketoacidosis is associated with severe losses of body fluids. The water deficit is made up of varying combinations from the osmotic diuresis, vomiting, hyperventilation and, when present, pyrexia. Sodium losses are also variable, depending on the predominating route of fluid loss, the duration of polyuria and the adequacy of renal perfusion. There is always total body depletion of potassium and phosphate, even though plasma levels of these ions may be low, normal or high. There will also usually have been some attempt by the child or its parent to correct the fluid losses with increased oral consumption of fluids, which can affect the blood biochemistry at presentation. Much of the information concerning the specific fluid and electrolyte deficits in diabetic ketoacidosis has been obtained from experiments carried out in adults in the 1930s, studies that have not been repeated in children. Thus there is little direct information concerning electrolyte and fluid losses in children; this may explain some of the historical debate concerning optimal management.

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