HHS Flashcards

1
Q

What does HHS stand for

A

Hyperosmolar Hyperglycaemic State (HHS)

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2
Q

HHS is a medical emergency that occurs in patients with what type of diabetes mellitus

A

Type 2 diabetes mellitus

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3
Q

HHS is charactersied by?

A

Characterised by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis

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4
Q

What is the onset of HHS like

A

Occurs insidiously over several days to weeks

Features get worse as there is more renal water loss and higher levels of hyperglycaemia

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5
Q

What is the mortality associated with HHS

A

High mortality (5-15%)

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6
Q

Describe the pathophysiology of HHS

A

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

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7
Q

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

A

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)

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8
Q

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

A

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

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9
Q

Why are patients with HHS at a high risk of developing thrombosis

A

Patients with HHS have a hyperviscosity of their blood - due to the hyperosmolarity

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10
Q

Name the precipitants of HHS

A

New diagnosis of type 2 diabetes

Poor treatment concordance in T2DM

Infection

High dose steroids

MI

Vomiting

Stroke

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11
Q

Describe the onset of clinical features for HHS

A

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

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12
Q

Name some of the early features of HHS

A

Polyuria

Polydipsia

Nausea

Dehydration e.g. dry mucous membranes, sunken eyes, reduced capillary refill, decreased skin turgor

Weight loss

Hypotension

Decreased urine output

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13
Q

Name some of the late features of HHS

A

Altered mental status

Seizures

Shock

Coma

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14
Q

How is HHS diagnosed

A

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

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15
Q

HHS vs DKA

A

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

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16
Q

What are the key investigations for HHS

A
  • Blood glucose
  • Blood ketones
  • VBG
  • Serum osmolarity
  • U+Es
  • Urine ketone
  • Serum osmolarity test
17
Q

Name some extra bedside tests that can aid in HHS

A

ECG – to look for cardiac precipitants of HHS e.g. MI

Urinalysis – signs of UTI

18
Q

Name some extra bloods test that can aid in HHS

A

Cardiac enzymes – if you suspect MI as a precipitant

LFTs – screen for hepatic precipitants

CRP – screen for infective precipitants

19
Q

Name some extra imaging test that can aid in HHS

A

CXR – screen for infective precipitants and heart failure

20
Q

What is the initial management of HHS

A
  • 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
21
Q

If you are giving fluid replacement what must you remember always to do

A

To have an accurate fluid balance chart (requires catheter to monitor urine output)

22
Q

Why is fixed rate IV insulin not used in all patients with HHS

A

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

23
Q

In what group of patients should fixed rate IV insulin be used to manage HHS

A

In patients with significant ketoanaemia or ketonuria start fixed rate IV insulin infusion at a rate of 0.05 units/Kg/hours

24
Q

Why should IV fluids always started before insulin

A

Insulin before fluids can cause cardiovascular collapse

25
Q

Patients with HHs are at higher risk of developing thrombosis due to their blood hyperviscosity.

How is this managed

A

Patients are given VTE prophylaxis, usually low molecular weight heparin e.g. apixaban

Given TEDs (Thrombo-Embolus Deterrent Stockings)

26
Q

Name some complications of HHS

A

MI

Thrombotic complications

Cerebral oedema