In this section : Diabetes and Endocrinology
Paediatric Diabetic Ketoacidosis (DKA) Guideline
Paediatric Ketone Correction Guideline
Insulin Correction Factor Table (Paediatrics)
Management of Hypoglycaemia in Children with Type 1 Diabetes
Newly diagnosed diabetic – not in DKA (Walking wounded)
Prescribing Advice on Admission – Insulin
Diabetic Retinopathy
Adrenal Insufficiency
Hyperglycaemia & Steroids
Variable Rate Insulin Infusion
In-patient Hyperglycaemia Management
Hyperthyroidism
Newer Antidiabetic Drugs
Hypoglycaemia
Diabetic Ketoacidosis
Switching from VRII
Insulin Pumps
Diabetes Mellitus
The Diabetic Foot
Subcutaneous Insulin
Diabetes and Acute Coronary Syndrome
Hyperosmolar Hyperglycaemic State
Hyperosmolar Hyperglycaemic State
Last updated 15th September 2023
Introduction
- This is the metabolic emergency characteristic of type 2 diabetes
- HHS is characterised by severe hyperglycaemia without significant ketosis or acidosis, dehydration and effective osmolality >320mosmol/kg
- Usually affects the elderly, many of whom have previously undiagnosed diabetes.
- Commonly triggered by thiazide diuretics and intercurrent illness.
- Presenting features include dehydration and impairment of consciousness, with stupor leading ultimately to coma. The presence of neurological impairment is a key feature of Hyperosmolar Hypergylcaemia state.
- Mortality is higher than for DKA at around 20%
- Glucose in HHS frequently exceeds 56 mmol/L and neurological compromise is present in more than 50%
Beginner’s Guide to and Significance of Osmolarity
- Normal effective plasma osmolarity is 280-300mOsm/kg.
- Effective Posm (in mosmol/kg) is the portion of total osmolality that is generated by sodium salts and glucose (and, if present, mannitol or sucrose). Effective osmoles do not penetrate most cell membranes and can cause movement of water across membranes to achieve osmolal equilibrium. Effective Posm does not include “ineffective” osmoles, such as urea, because urea is rapidly permeable across most cell membranes and its accumulation does not induce major water shifts between the intracellular spaces (including the brain) and the extracellular water space
- Together these ions exert a ‘pressure’ which causes water to move across cell membranes from weaker to stronger solutions until the concentration of solutes are equal on both sides.
- Effective Posm = [2 x Na (mmol/L)] + glucose (mmol/L) if serum osmolality is calculated in the lab then Effective Posm = Measured osm – urea (mmol/L)
- Impairment of consciousness is directly related to severity of hyperosmolarity
Differences Between DKA and HHS – Presentation
Differences Between DKA and HHS – Treatment
- The fall in BG should be no more than 5 mmol/L/hr so as to reduce risk of cerebral oedema. Patients are usually sensitive to insulin – so start infusion at 3u/hr
- Aim to give 3-6 litres IV fluid by 12 hours and the remaining replacement of estimated fluid losses within next 12 hours.
- Use IV 0.9% saline to restore circulating volume and reverse dehydration. Only switch to 0.45% saline if osmolality is not declining despite adequate fluid. An initial rise in sodium is expected and is not itself an indication for hypotonic fluids. The rate of fall of sodium should not exceed 10 mmol/L in 24 hours.
- Significant risk of thromboembolic complications – so Rx LMWH