Hyperosmolar hyperglycaemic state

Emergency

Table of Contents

Introduction

Progressive hyperglycaemia and hyperosmolarity in a debilitated patient with poorly controlled or undiagnosed Type 2 DM, limited access to water and a precipitating medical event
Mortality significantly higher than DKA
Pathophysiology
- 1) Insulin resistance or deficiency, or both
- 2) Increased hepatic gluconeogenesis and glycogenolysis
- 3) Osmotic diuresis and dehydration followed by impaired renal excretion of glucose due to AKI
If water demand is not met following osmotic diuresis (i.e. bedbound NH patient), profound volume depletion occurs
May have total body water deficit of 20-25% of TBW (8-12L in 70kg patient)
Absence of ketoacidosis thought to be due to remnant insulin release of at least 10% of usual (only need 10% of usual insulin activity to inhibit lipolysis and subsequent ketoacidosis)

Typically present with ALOC or altered vital signs over weeks
Pneumonia and UTI make up 30-50% of precipitants
Non-compliance with glycaemic medication also common
Cocaine may increase counter-regulatory hormone release and precipitate HHS also
Associated symptoms
- Usually unable to self-care who get their own water. Thus usually old with comorbidities.
Predisposing drugs
- Diuretics, beta-blockers, lithium, mannitol, chlorpromazine, cimetidine, glucocorticoids, neuroleptics, phenytoin, CCB

Predisposing conditions

Clinical features

No precise definition but characterised by:
- BSL >30
- Serum osmolality >320
- Hypovolaemia
- Ketones <3 or <2+
- pH >7.30 or bicarb >15
Above is fairly arbitrary as metabolic acidosis (often lactic) and moderate ketonaemia are not uncommon
- Important to recognise this entity as may have starvation ketosis, azotaemia and lactic acidosis in addition
Typical deficits
- Free water 100-220mL/kg (much greater)
- Sodium 5-13mmol/kg (similar)
- Potassium 4-6mmol/kg (similar)

Severe HHS

Investigations

BSL, ECG, VBG, ketones
FBC, UEC, LFT, Lipase, CK, TFT, Troponin (if indicated), Coags
Specific Ix for underlying precipitants
Corrected Na is crucial as hyperglycaemia may obscure true Na
- If corrected Na >145; highly specific for profound volume loss
- If corrected Na normal or low = more moderate volume loss likely
- Measured Na + (Glucose -5 / 3)

Correct hypovolaemia
- Renal insufficiency and CCF are both common and make this process more complicated
Identify and treat precipitants
Correct electrolyte abnormalities
Gradually correct hyperglycaemia and hyperosmolality
Frequent monitoring

Fluids

Replace 50% of fluid deficit over initial 12 hours and the rest over the next 24 hours if possible
Start with N/S 15-20mL/kg/hr for first hour then 4-14mL/kg/hr afterwards depending on comorbidities
- = 1.4L over first hour then 700mL/hr afterwards
Fall in serum osmolality is a marker of response to treatment
Only change to 0.45% N/S if sodium AND glucose are not reducing (i.e. no response to treatment)
Target maximum drop in Na of 10mmol/24 hours

Electrolytes

Withold insulin until K >3.5
Those with initial hypokalaemia are most at risk of dysrhythmias
Once UO has begun, 10-20mmol/hr will be required
- K <4.0-5.5 – 10mmol/hr
- K 3.5-4.0 – 20mmol/hr
- K <3.5 – 4 – 40mmol/hr via CVL
Monitor K and Phos
Insulin initiated if K > 3.5 at 0.05IU/kg/hr (Cameron) to maximum 3 Units
- Aim for drop in glucose of 5mmol/hr and serum osmolarity of 3mOsm/kg/hr
- Reduce insulin infusion rate once glucose 15-18mmol/K and target 10-15mmol/L until serum osmolality < 315
Complete normalisation takes 48-72 hours

Last Updated on December 4, 2024 by Andrew Crofton