Hyperosmolar Hyperglycaemic State (HHS) Flashcards
Hyperglycaemic hyperosmolar state (HHS) is an acute diabetic emergency that occurs in patients with …
Hyperglycaemic hyperosmolar state (HHS) is an acute diabetic emergency that occurs in patients with type 2 diabetes mellitus.
HHS occurs insidiously over several days with dehydration and metabolic disturbances that are more extreme than diabetic ketoacidosis (DKA).
It is characterised by:
Hypovolaemia
Hyperglycaemia (> 30 mmol/L)
Mild or absent ketonaemia (blood ketones < 3 mmol/L)
High osmolality (> 320 mOsm/kg)
Epidemiology
HHS
HHS is a life-threatening condition, which usually occurs in the elderly but is increasingly recognised in younger patients.
The incidence is difficult to calculate, but it estimated that HHS accounts for only 1% of diabetic hospital admissions. The average age of presentation is 60 years old and it is associated with a 15-20% mortality.
HHS is often the first the presentation of type 2 diabetes mellitus in up to 20-30% of cases.
In HHS, the relative lack of … is coupled with a rise in counter-regulatory hormones (e.g. cortisol, growth hormone, glucagon) that leads to a profound rise in glucose.
In HHS, the relative lack of insulin is coupled with a rise in counter-regulatory hormones (e.g. cortisol, growth hormone, glucagon) that leads to a profound rise in glucose.
Common precipitants of HHS include:
Infection High-dose steroids Myocardial infarction Vomiting Stroke Poor treatment concordance
Onset of HHS is usually …
Onset of HHS is usually insidious with development of increased renal water loss and dehydration over days to weeks.
Symptoms of HHS
Polydipsia Polyuria Nausea Vomiting Muscle cramps Weakness Altered mental status Seizures Coma
Signs of HHS
Dehydration (dry mucous membranes, sunken eyes, reduced capillary refill, decreased skin turgor) Hypotension Decreased urine output Decreased conscious level Coma Focal neurology signs Features of the precipitating cause
Immediate investigations to establish diagnosis of HHS:
Laboratory glucose: > 30 mmol/L Serum osmolality: > 320 mOsm/kg Ketones: Urine: 1+, trace, negative OR Blood: < 3 mmol/L
Investigations.
Hhs
The key investigations for management of HHS include a laboratory glucose, urea & electrolytes blood test, a blood gas (venous/arterial) and a blood or urinary ketone level.
Management HHS
Normalise osmolality Normalise blood glucose Replace fluid and electrolytes Prevention of arterial/venous thrombosis Prevention of complications & foot ulceration
Initial assessment hhs.
All patients should undergo a clinical assessment following an ABCDE approach.
Intravenous access (x2 large bore cannula)
Blood / urinary ketones
Capillary & plasma blood glucose
FBC, U&Es, venous blood gas, plasma osmolality
Blood cultures
Urinalysis +/- MSU, Pregnancy test (as indicated)
ECG
CXR
Urinary catheter
Additional tests as indicated by the presentation/investigations (e.g. troponin, CT head).
Severity - HHS
Patients with HHS usually represent an elderly population with multiple co-morbidities and can be extremely unwell.
Ideally, patients should be managed in a high-dependency environment (level 2 care and above). The following features are markers of severity that would definitely warrant management in a high level of care:
Osmolality > 350 mosm/kg Sodium > 160 mmol/L pH < 7.1 GCS < 12 Systolic BP < 90 mmHg Serum creatinine > 200 μmol/L Macrovascular event (.e.g MI, CVA) Severe electrolyte abnormalities (e.g. hyper/hypokalaemia)
Intravenous fluids
HHS
Patients with HHS can have a tremendous fluid deficit.
Patients with HHS can have a tremendous fluid deficit.
Due to the significant fluid deficit, the initial management requires fluid resuscitation to restore circulating volume. The initial fluid of choice is 0.9% sodium chloride (normal saline) and at least 1 litre should be given over an hour (quicker in the presence of significant hypotension).
Further fluids can be given aiming for a positive fluid balance based on hourly measurement of urine output. A proposed target is 2-3 litres positive by 6 hours. Initiation of normal saline may cause a transient rise in sodium levels, however, if the osmolality is falling appropriately this is not an indication for hypotonic saline (e.g. 0.45%). Importantly, rapid correction of the fluid deficit is not advisable as it can precipitate osmolar shifts leading to cerebral oedema (generally aim for 4 litres positive within the first 24 hour).