HHS Flashcards
What does HHS stand for
Hyperosmolar Hyperglycaemic State (HHS)
HHS is a medical emergency that occurs in patients with what type of diabetes mellitus
Type 2 diabetes mellitus
HHS is charactersied by?
Characterised by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis
What is the onset of HHS like
Occurs insidiously over several days to weeks
Features get worse as there is more renal water loss and higher levels of hyperglycaemia
What is the mortality associated with HHS
High mortality (5-15%)
Describe the pathophysiology of HHS
The relative lack of insulin (not enough to produce ketones) is coupled with a rise in counter-regulatory hormones leading to a profound rise in glucose (hyperglycaemia)
Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium.
This is because the proximal tubules within the kidneys only have a certain capacity for reabsorption of glucose thus when this limit is reached the remaining glucose pass through causing diuresis
This severe volume depletion results in profound dehydration and reduced circulating volume – hyperosmolarity and hyperglycaemia
The hyperosmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood – which increases the risk of arterial and venous thrombosis e.g. DVT
HHS is characterised by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis.
What happens in the body to cause the hyperglycaemia
The relative lack of insulin (not enough to produce ketones) is coupled with a rise in counter-regulatory hormones leading to a profound rise in glucose (hyperglycaemia)
HHS is characterised by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis.
What happens in the body to cause the hyperosmolality and volume depletion
HHS is characterised by hyperglycaemia
The hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium.
This is because the proximal tubules within the kidneys only have a certain capacity for reabsorption of glucose thus when this limit is reached the remaining glucose pass through causing diuresis
This severe volume depletion results in profound dehydration and reduced circulating volume – hyperosmolarity and hyperglycaemia
The hyperosmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood – which increases the risk of arterial and venous thrombosis e.g. DVT, PE
Why are patients with HHS at a high risk of developing thrombosis
Patients with HHS have a hyperviscosity of their blood - due to the hyperosmolarity
Name the precipitants of HHS
New diagnosis of type 2 diabetes
Poor treatment concordance in T2DM
Infection
High dose steroids
MI
Vomiting
Stroke
Describe the onset of clinical features for HHS
The onset of features is usually insidious, developing over days to weeks as there is an increase in renal water loss and higher levels of hyperglycaemia
Name some of the early features of HHS
Polyuria
Polydipsia
Nausea
Dehydration e.g. dry mucous membranes, sunken eyes, reduced capillary refill, decreased skin turgor
Weight loss
Hypotension
Decreased urine output
Name some of the late features of HHS
Altered mental status
Seizures
Shock
Coma
How is HHS diagnosed
Diagnosed based on the presence of characteristic features:
- Severe hyperglycaemia (glucose >30 mmol/L)
- Hyperosmolality (serum osmolality > 320 mOsm/Kg)
- Absence of acidosis
- Mild/absent ketogenesis (urine: 1+ or trace; blood < 3 mmol/L)
These should be taken in context with the clinical state of the patient e.g. dehydrated
HHS vs DKA
Both are characterised by hyperglycaemia Unlike DKA, the hyperglycaemia in HHS is not accompanied by significant acidosis (pH > 7.3; Bicarb > 15 mmol/L) or ketosis (ketones > 3mmol/L)
This is because in HHS, the presence of endogenous insulin production is sufficient to “switch off” ketone production preventing the ketoacidosis
What are the key investigations for HHS
- Blood glucose
- Blood ketones
- VBG
- Serum osmolarity
- U+Es
- Urine ketone
- Serum osmolarity test
Name some extra bedside tests that can aid in HHS
ECG – to look for cardiac precipitants of HHS e.g. MI
Urinalysis – signs of UTI
Name some extra bloods test that can aid in HHS
Cardiac enzymes – if you suspect MI as a precipitant
LFTs – screen for hepatic precipitants
CRP – screen for infective precipitants
Name some extra imaging test that can aid in HHS
CXR – screen for infective precipitants and heart failure
What is the initial management of HHS
- ABCDE approach
- Fluid replacement - with normal saline (0.9% sodium chloride) with at least 1L within the 1st hour
- Aim to replace 50% of estimated fluid loss within 12 hours and the remainder in the following 12 hours – however be wary in patients with co-morbidities e.g. heart failure
- Typical fluid losses are 100-220 mL/Kg
If you are giving fluid replacement what must you remember always to do
To have an accurate fluid balance chart (requires catheter to monitor urine output)
Why is fixed rate IV insulin not used in all patients with HHS
Fluid replacement alone will result in a gradual decline of blood glucose and osmolarity
Most patients with HHS are insulin sensitive thus administration of insulin can result in a rapid decline of serum glucose and thus osmolarity
In what group of patients should fixed rate IV insulin be used to manage HHS
In patients with significant ketoanaemia or ketonuria start fixed rate IV insulin infusion at a rate of 0.05 units/Kg/hours
Why should IV fluids always started before insulin
Insulin before fluids can cause cardiovascular collapse
Patients with HHs are at higher risk of developing thrombosis due to their blood hyperviscosity.
How is this managed
Patients are given VTE prophylaxis, usually low molecular weight heparin e.g. apixaban
Given TEDs (Thrombo-Embolus Deterrent Stockings)
Name some complications of HHS
MI
Thrombotic complications
Cerebral oedema
