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528 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

TABLE 19.13 Treatment of DKA and HHNS 344-346

Issue Treatment considerations
Dehydration and ● Intravenous fluid is initially given to restore intravascular volume. Isotonic fluid such as normal saline or a colloid
sodium loss solution may be used. Solutions containing sodium are used in order to replace sodium lost as a result of the osmotic
diuresis.
● Assessment of volume status is undertaken using basic clinical assessment, such as heart rate, blood pressure, urine
output (allowing for the possibility of continuing osmotically-driven diuresis), or invasive haemodynamic monitoring.
● Hypotonic solutions are added after the initial fluid resuscitation to correct the total body water deficit.
● Adequate resuscitation and rehydration reduces the effect of the counterregulatory hormones.
Insulin therapy ● A soluble insulin is usually administered via continuous infusion to allow rapid titration of dose.
● Blood glucose levels and blood chemistry should be regularly monitored.
● Care is taken to prevent too rapid a change in blood sugar level, as this will cause a rapid reduction in the
extracellular fluid osmolarity. This rapid reduction would result in fluid shift from the extracellular space to the
intracellular space, which may result in cerebral oedema.
● There is a risk of hypoglycaemia resulting from insulin therapy. Sympathetic activation accompanies a low blood
glucose level and results in sweating, tremor, tachycardia and anxiety. Reduced blood glucose levels also cause
global CNS depression and result in depression of the level of consciousness and possibly fitting. Severe
hypoglycaemia with a blood glucose level <2 mmol/L is a medical emergency and is treated with administration of
50 mL 50% glucose.
Electrolytes ● Intravenous potassium replacement will be required.
● Plasma potassium levels will fall rapidly as a result of commencement of insulin therapy and to a lesser extent with
rehydration. Insulin causes the lowering of plasma potassium by mediating the re-entry of potassium into the
intracellular compartment.
● Phosphate and magnesium replacement may be required.
DKA = diabetic ketoacidosis; HHNS = hyperglycaemic hyperosmolar non-ketotic state.

replacement, correction of acidosis (in DKA), monitoring outcomes in this group of patients. EN is the preferred
for and prevention of complications hypoglycaemia, method of nutritional support in the critically ill, although
hypokalaemia, hyperglycaemia, and fluid volume over- ensuring adequate delivery of nutrients can be challeng-
load, and patient teaching and support. 341,350,351 Assess- ing. The availability of enteral feeding guidelines is useful
ment of blood glucose levels is essential. Effectiveness of for some aspects of clinical practice although there
treatment is usually assessed by resolution of the acidosis remains little evidence to inform many of the issues, such
and the control of hyperglycaemia. Regular testing of as measurement of gastric residual volume, that concern
arterial blood gases, blood sugar and electrolytes (espe- nurses. When nutritional goals are difficult to achieve, PN
cially potassium) is vital until the blood sugar has stabi- may be used to supplement EN. Less frequently, critically
lised and the ketosis and acidosis resolves. 344 Considering ill patients may require TPN as their sole nutritional
that fewer patients are now admitted to ICU with DKA support therapy.
and HHNS, understanding the management of these
patients is vital and protocols have been developed to Critically ill patients, particularly those who have respira-
guide practice. 350,351 tory failure requiring mechanical ventilation for >48
hours and those with coagulopathy, are at increased risk
Blood ketones (beta-hydroxybutyrate) can now easily be for developing stress-related mucosal disease. Recognis-
measured using blood from a fingerprick with a bedside ing risk factors and implementing prophylactic pharma-
handheld monitor. It has been suggested that blood cotherapy is required to reduce the incidence of clinically
ketone monitoring allows for insulin titration with refer- important bleeding.
ence to ketones in addition to usual blood sugar monitor-
ing. 352 An outline of the collaborative treatment of DKA Liver dysfunction causing hepatocellular injury and death
and HHNS is presented in Table 19.13.
can occur due to direct injury or cellular stress. This can
be mediated via several avenues, such as metabolic dis-
SUMMARY turbances, ischaemia, inflammatory processes, or reactive
oxygen metabolites from drug and alcohol ingestion.
During episodes of critical illness, metabolic function can Acute failure can be acute or chronic. In Australia and
become compromised and the normal processes respon- New Zealand, high rates of hepatitis B and C predispose
sible for digestion, endocrine and liver function deterio- individuals to chronic liver dysfunction that can lead to
rate. Specifically, the gastrointestinal system can become acute hepatic decompensation. Whilst acute liver failure
hypoperfused and normal physiological processes respon- is uncommon, patients who present are often critically
sible for digestion, absorption, immunity and protection ill. In addition, liver failure causes major disturbances in
become compromised. Critical illness increases the meta- other body systems often resulting in coagulopathy, cere-
bolic demand and nutritional support that meets this bral oedema (hepatic encephalopathy), sepsis, renal
increased demand has been shown to improve clinical failure and metabolic derangement. Therapy is usually