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meters being common in clinical practice. An impor- pathological consequences of extreme dehydration.
tant consideration with formal blood testing is the poten- Unlike DKA, where there is insufficient insulin, in HHNS
tial drop in glucose concentration of up to 6% within the insulin excretion is maintained, so lipolysis and keto-
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first hour after the blood is taken, highlighting the acidosis do not feature. Although DKA and HHNS are
importance of ensuring blood specimens are delivered to considered separate entities, DKA and HHNS may coexist
the laboratory in a timely fashion and priority is given to in about a third of cases, especially among older
sample testing. patients. 342 Additionally, DKA is increasingly being iden-
tified in patients with type 2 diabetes. 343
Point-of-care testing of blood glucose is common in criti-
cal care setting. Research examining the measurement of PATHOPHYSIOLOGY
blood glucose using these devices is conflicting with
some studies reporting good performance of devices The metabolic profile seen in DKA is similar to that seen
while others report that the devices are unsatisfactory. A in the fasting state, with substrate utilisation shifting
problematic aspect of evaluating point-of-care devices is from glucose to fat in insulin-sensitive tissues (fat, liver,
the failure of many of these to conform 332 with quality muscles). The brain is insulin-insensitive, and requires a
guidelines for conducting and reporting glucose monitor continuous supply of glucose to support metabolism
evaluation studies. 333,334 even in a fasting state or DKA. 344
It is clear that hyperglycaemia should be avoided, however, Inadequate production (or administration) of insulin to
the inconsistencies in published studies mean that an meet metabolic need (or a rise in metabolic demand
agreed specified target for blood glucose in the critically resulting from the stress of infection, trauma or surgery,
323
ill patient population is difficult to achieve. The optimal for instance) is associated with a rise in the secretion of
target blood glucose level is unknown and may differ the counterregulatory hormones glucagon, the catechol-
depending on the patient’s clinical presentation. 335 Rec- amines and cortisol. 344 The effects of the counterregula-
ommendations for patients with sepsis suggest that blood tory hormones are presented in Box 19.1.
glucose levels be kept lower than 180 mg/dL with a goal Hyperglycaemia results from increased gluconeogenesis
blood glucose approximating 150 mg/dL. 336 (glucose production from precursors other than carbo-
hydrates, e.g. amino acids), the conversion of glycogen
INCIDENCE OF DIABETES stores to glucose (glycogenolysis) and the reduced uptake
IN AUSTRALASIA of glucose resulting from insulin deficiency. 344 Free fatty
acids (FFAs) and glycerol are produced by the break-
Diabetes is known to cause substantial morbidity and down of triglycerides that results from increased cate-
mortality in Australia. The prevalence of diabetes in Aus- cholamine secretion. 344 Metabolism of FFA results in
tralia is rising and follows a global trend. 337 Reasons for accumulation of ketone bodies or ketoacids (acetone,
this include an increase in the rates of obesity, physical beta-hydroxybutyrate, acetoacetate). 344 These compensa-
inactivity, the ageing population, better detection of dia- tory mechanisms are ultimately responsible for the patho-
betes and longer survival of affected individuals. 338,339 In logical effects seen in DKA (see Table 19.12). The
2004–05, the prevalence of diagnosed diabetes among pathophysiology of DKA is illustrated in Figure 19.3.
Australians was 3.6%. 337 The rate of diabetes generally
increased with age for both males and females, although NURSING PRACTICE
declining slightly for both sexes at age 75 years and over. Management of HHNS is similar to that for DKA, and
Males had higher rates of diabetes than females at ages includes respiratory support, fluid replacement,
45–54 years, 65–74 years and 75 years and over, and insulin treatment to turn off ketogenesis and the
ranged from 0.8% vs 0.7% (0–44 years) to 16.3% vs accompanying metabolic derangement, electrolyte
11.7% (65–74 years). New Zealand is experiencing a dia-
betes epidemic that has the biggest impact in the Māori
and Pacific ethnic groups. The incidence of diabetes was
forecast to nearly double by 2011, and to be accompanied BOX 19.1 Effects of counterregulatory
by a rise in mortality. 340 hormones in DKA 345,346

DIABETIC KETOACIDOSIS ● Catecholamines:
● Promote lipolysis, resulting in the production of FFA and
Diabetic ketoacidosis (DKA) is a metabolic derangement glycerol; FFA and glycerol used as precursors for
resulting from a relative or absolute insulin deficiency, gluconeogenesis
characterised by hyperglycaemia (>11.1 mmol/L), meta- ● Glucagon:
bolic acidosis (pH <7.3) and ketosis (raised blood ketone ● Stimulates gluconeogenesis
bodies or ketonuria). It is usually precipitated, in insulin- ● Cortisol:
and non-insulin-dependent diabetics, by infection or the ● Promotes lipolysis
omission (or inadequate dosing) of insulin. It may also ● Promotes protein breakdown and release of amino acids
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be the cause of the first presentation in new-onset diabe- ● Promotes hepatic gluconeogenesis
tes. Hyperglycaemic hyperosmolar non-ketotic state
(HHNS) is seen more often in older patients with type 2 DKA = diabetic ketoacidosis; FFA = free fatty acids
diabetes, and is characterised by hyperglycaemia and the