HYPERGLYCAEMIC

HYPEROSMOLAR STATE
■ Hyperglycaemic hyperosmolar state (HHS) is characterised by
severe hyperglycaemia (> 30 mmol/L (600 mg/
di)),hyperosmolality (serum osmolality > 320 mOsm/ kg), and
dehydration in the absence of significant hyperketonaemia (<3
mmol/L) or acidosis (pH > 7.3, bicarbonate > 15 mmol/L). It was
previously referred to as hyperosmolar non-ketotic(HONK) coma
but, as in DKA, coma is not invariable.
■ there si glycosuria, leading to an osmotic diuresis, with loss of
water, sodium, potassium and other electrolytes. However, in
MHS, hyperglycaemia usually develops over a longer period (a
few days to weeks), causing more profound hyperglycaemia and
dehydration (fluid loss may be 10-22 litres in a person weighing
100 kg). The reason that patients with HHS do not develop
significant ketoacidosis is unclear, although it has been
speculated that insulin levels may be too low to stimulate
glucose uptake in insutin-sensitive tissues, but still sufficient to
prevent lipolysis and subsequent ketogenesis. Amixed picture of
HHS and DKA can occur.
■ Although typically occurring in the elderly, HHS is increasingly seen in younger
adults. Common precipitating factors include infection, myocardial infarction,
cerebrovascular events or drug therapy (e.g. corticosteroids). Poor prognostic
signs include hypothermia, hypotension (systolic blood pressure <90 mmHg)

■ tachy- or bradycardia, severe hyperatraemia (sodium > 160 mmol/L), serum

osmolality >360 m05m/kg, and the presence of other serious
comorbidities. Mortality rates are higher than in DKA - up to 20%
■ The principles of therapy. The aims are to normalise osmolality, replace
fluid and electrolyte losses, and normalise bloodglucose, at the same time
preventing complications such as arterial or venous thrombosis, cerebral
oedema and central pontine demyelinosis Comorbidities also need to be
taken intoaccount; for example, rapid fluid replacement may precipitate
cardiac failure in patients with coronary artery disease.Historically,
management of HHS has followed DKA guidelines, but increasing
recognition of the differences between HHS andDKA has led to new
approaches in HHS. In particular, rapidshifts in osmolality should be
avoided through more measuredfluid replacement regimens that are
guided by serialcalculations of serum osmolality. Akey recommendation is
that 0.9% sodium chloride solution alone is used for initialtreatment, and
that insulin is introduced only when the rate of fall in blood glucose has
plateaued
■ If osmolality cannot be measured frequently, osmolarity can be calculated as
follows and used as a surrogate (based on plasma values in mmol/L): Plasma
osmolarity 2Na glucose urea =+++ [][] [] The normal value is 280-290 mmol/L
andconsciousness si impaired when it si high (> 340 mmol/L), as commonly
occurs in HHS