Hyperosmolar Hyperglycaemic State / HONK

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

acute stressor/triggers:
- infection – half of patients (common sources include pneumonia, urinary tract)
- Pancreatitis, trauma, heat exposure
- MI
- Insulin nonadherence or inadequate dosing
- Surgery
- Medication changes (glucocorticoid, thiazides, phenytoin, beta-blockers, anti-calcineurin immunosuppressives, HIV protease inhibitors, antipsychotics)
increases levels of cortisol and catecholamines –>
- decreased insulin sensitivity
- decreased insulin
-> decreased glucose utilisation in skeletal muscle, increased fat and muscle breakdown
has enough insulin to prevent ketoacidosis/ketone production
but not enough insulin to control hyperglycemia

increased hepatic gluconeogenesis
increase in glucagon, cortisol, catecholamines
increased BSL
glycosuria + osmotic diuresis –> loss of water
Patients fail to compensate adequately for water loss by increasing oral water intake (e.g., due to baseline debility, bed-bound status, or a relatively insensitive central drive to maintain normal tonicity).
Over a period of several days, uncontrolled water loss leads to a hypertonic state. This may lead to altered mental status (which exacerbates the patient’s inability to drink an adequate amount of water)

HISTORY

RISK FACTORS

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
ABG:
- pH normally > 7.3 (metabolic acidosis is not severe)
- normal anion gap
Beta-hydroxybutyrate level (most precise way to quantify the presence and severity of ketoacidosis)
normal level of ketones
renal dysfunction commonly present

Diagnostic Criteria

Investigations for cause

MANAGEMENT

HHS is a deranged state which develops gradually over days to weeks.
However, these patients generally adapt to their new state and often tolerate it relatively well.
As a general rule of thumb, if an abnormal state develops gradually then it may be treated gradually.
The primary risk of treating HHS is overly aggressive therapy, which may cause dangerous swings in electrolyte levels and osmolality.
When in doubt, the safest approach to HHS is generally to correct abnormalities slowly.
Goals
- correct dehydration (often 6-9 L of H2O loss)
- provide insulin
- replace electrolytes
- 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

Calculate corrected Na+
- if hypernatraemic, the corrected Na+ = measured Na+ + glucose/3
- monitor this as Na+ changes for glucose
Calculate H2O deficit
- H2O deficit = 0.6 x premorbid weight x (1 – 140/corrected Na+)
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.
Monitor Na+ closely – should not change more than 10mmol in 24 hours
Replace other electrolytes as required
- K+ (often require aggressive replacement – 10-20mmol/hr, make sure not anuric)
- Mg2+ – Magnesium should be aggressively repleted.magnesium level on the high end will tend to prevent Torsade de Pointes if the potassium level falls.
- PO4 – Phosphate should be repleted as necessary
- Ca2+
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.