Hyperosmolar Hyperglycaemic State

OVERVIEW

• Hyperosmolar hyperglycaemic state (HHS) = Hyperosmotic Hyperglycaemic Syndrome (HHS)
• three times less frequent than DKA
• deaths often due to co-morbid conditions (MI)
• higher mortality rate than DKA
• part of a continuum with DKA, with insulin resistance predominant over insulin deficiency

PATHOPHYSIOLOGY

• triggers: infection, MI, surgery, omission of normal medications
• decreased insulin or resistance -> decreased glucose utilisation in skeletal muscle, increased fat and muscle breakdown
  -> increased hepatic gluconeogenesis
  -> increase in glucagon, cortisol, catecholamines
  -> increased BSL
  -> glycosuria + osmotic diuresis
  -> just enough insulin to prevent lipolysis and ketone production

HISTORY

• polydipsia
• polyuria
• weight loss
• weakness
• slow onset
• progressive dehydration
• coma
• causes: MI, infection, diuretics, CVA, PE

RISK FACTORS

• elderly
• type II DM
• mental obtundation/dementia
• physical impairment limiting access to H2O
• renal dysfunction
• inappropriate diuretic use
• steroids
• beta-blockers
• phenytoin

EXAMINATION

• CVS – tachycardia, decreased skin turgor, sunken eyes, dry mouth
• RESP – tachypnoea
• CNS – drowsy, delirium, coma, focal or generalised seizures, visual changes, hemiparesis

INVESTIGATIONS

• very high osmolarity (> 320mosmol/kg)
• very high glucose
• little or no ketonuria (beta-hydroxybutyrate)
• hyponatraemia (or pseudohyponatraemia -> hyperglycaemia draws water out of cells) or hypernatraemia
• hypokalaemia
• hypomagnesaemia
• normal anion gap
• ABG: pH normally > 7.3 (metabolic acidosis is not severe)
• normal level of ketones
• renal dysfunction commonly present

Diagnostic Criteria

• serum osmolarity > 320mosmol/L
• serum glucose > 33mmol/L
• profound dehydration (elevated urea:creatinine ratio)
• no ketoacidosis

Investigations for cause

• CXR: chest infection
• compliance with medication
• ECG + TNT: MI
• FBC
• CRP
• blood cultures
• urine

MANAGEMENT

Goals

(1) correct dehydration (often 6-9 L of H2O loss)
(2) provide insulin
(3) replace electrolytes
(4) correct metabolic acidosis

Resuscitation

A – may require intubation if coma and not protecting airway
B – mechanical ventilation can minimise WOB and manage possible metabolic acidosis
C – resuscitate with isotonic fluid until patient has a normal heart rate and BP (see below for H2O replacement) or can use colloids.

Treatment

Specific

(1) Calculate corrected Na+

• if hypernatraemic, the corrected Na+ = measured Na+ + glucose/3
• monitor this as Na+ changes for glucose

(2) Calculate H2O deficit

• H2O deficit = 0.6 x premorbid weight x (1 – 140/corrected Na+)

(3) Fluid management in first 24 hours

• maintenance as D5W at standard rate
• if hypernatraemic: replace half the H2O deficit over 24 hours using ½ normal saline.

(4) Monitor Na+ closely – should not change more than 10mmol in 24 hours

(5) Replace other electrolytes as required

• K+ (often require aggressive replacement – 10-20mmol/hr, make sure not anuric)
• Mg2+
• PO43
• Ca2+

(6) Fluid management in second 24 hours

• when glucose < 15mmol/L -> use D5W @ 100-250mL/hr AND saline
• keep Na+ between 140-150mmol/L
• the metabolic acidosis rarely requires specific treatment as responds to volume expansion and insulin therapy.

General

• insulin at 0.05 U/kg/h
• do not allow blood glucose to drop by more than 3 mmol/L/h
• once glucose <15mmol/L and corrected Na+ 10% dextrose
• thromboprophylaxis (SCD’s, clexane, TEDS) -> high risk of VTE
• diagnose cause and treat: infection, compliance, MI, CVA

Disposition

• needs management in ICU
• endocrine/general medical referral
• family informed

Complication Management

• delirium -> coma
• cerebral oedema (prevent by resuscitation with isotonic fluid and slow correction of glucose)
• seizures (focal and generalized)
• severe dehydration and shock
• renal failure
• thrombotic complications: VTE, stroke, AMI
• intercurrent events: sepsis, MI, aspiration
• occlusive events: focal CNS signs, chorea, DIC, leg ischaemia, rhabdomyolysis
• fluid overload and congestive heart failure
• metabolic derangement: hypokalaemia, hypophosphataemia, hypomagnesaemia, hypoglycaemia, hyperchloraemia with NAGMA