Hyperosmolar Hyperglycaemic State (HHS) Flashcards

1
Q

Hyperglycaemic hyperosmolar state (HHS) is an acute diabetic emergency that occurs in patients with …

A

Hyperglycaemic hyperosmolar state (HHS) is an acute diabetic emergency that occurs in patients with type 2 diabetes mellitus.

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2
Q

HHS occurs insidiously over several days with dehydration and metabolic disturbances that are more extreme than diabetic ketoacidosis (DKA).

It is characterised by:

A

Hypovolaemia
Hyperglycaemia (> 30 mmol/L)
Mild or absent ketonaemia (blood ketones < 3 mmol/L)
High osmolality (> 320 mOsm/kg)

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3
Q

Epidemiology

HHS

A

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.

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4
Q

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.

A

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.

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5
Q

Common precipitants of HHS include:

A
Infection
High-dose steroids
Myocardial infarction
Vomiting
Stroke
Poor treatment concordance
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6
Q

Onset of HHS is usually …

A

Onset of HHS is usually insidious with development of increased renal water loss and dehydration over days to weeks.

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7
Q

Symptoms of HHS

A
Polydipsia
Polyuria
Nausea
Vomiting
Muscle cramps
Weakness
Altered mental status
Seizures
Coma
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8
Q

Signs of HHS

A
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
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9
Q

Immediate investigations to establish diagnosis of HHS:

A
Laboratory glucose: > 30 mmol/L
Serum osmolality: > 320 mOsm/kg
Ketones:
Urine: 1+, trace, negative OR
Blood: < 3 mmol/L
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10
Q

Investigations.

Hhs

A

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.

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11
Q

Management HHS

A
Normalise osmolality
Normalise blood glucose
Replace fluid and electrolytes
Prevention of arterial/venous thrombosis
Prevention of complications & foot ulceration
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12
Q

Initial assessment hhs.

A

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).

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13
Q

Severity - HHS

A

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)
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14
Q

Intravenous fluids

HHS

A

Patients with HHS can have a tremendous fluid deficit.

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15
Q

Patients with HHS can have a tremendous fluid deficit.

A

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).

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16
Q

Insulin therapy

HHS

A

The use of insulin in HHS should be led by a specialist or senior clinician with experience of HHS management.

17
Q

Electrolyte replacement

HHS

A

Electrolytes including sodium, potassium, phosphate and magnesium should be monitored regularly (4 hourly minimum) and replaced as necessary.

18
Q

Monitoring and replacing potassium is particularly important if insulin is started. This is because insulin drives potassium intracellularly leading to a low plasma concentration that could cause dangerous arrhythmias.

As a general rule for potassium:

A

Serum K+ > 5.5 mmol/L: Nil potassium replacement
Serum K+ 3.5-5.5 mmol/L: 40 mmol potassium replacement
Serum K+ < 3.5 mmol/L: Senior review for more invasive potassium replacement

19
Q

Patients with HHS should be on cardiac monitoring and assessed at regular intervals.

A

Every hour, blood glucose, urea & electrolytes and a laboratory or calculated plasma osmolality should be completed for the first 6 hours. If there is a satisfactory fall in osmolality by 3-8 mOsm/kg/hr and glucose by 5 mmol/L/hr, then blood taking can be reduced to 2 hourly. At all times, an accurate fluid balance should be completed with the urine output documented hourly.

As there is improvement in clinical and biochemical parameters, monitoring can be reduced to 4 hourly and then 12 hourly. At all times, it is important to assess for any complications of HHS (e.g. stroke, DVT, cerebral oedema) and manage any underlying precipitant (e.g. infection, MI).

20
Q

There are two main metabolic treatment targets that should be achieved during the management of HHS.

A

Plasma osmolality: falling by 3-8 mOsm/kg/hr

Blood glucose/l falling by at least 5 mmol/L/hr

21
Q

Continuing care

HHS

A

The specialist diabetic team should always be informed regarding a presentation of HHS. Ideally, they should assess the patient within 24 hours.

22
Q

It is imperative that patients with HHS are started on …

A

It is imperative that patients with HHS are started on prophylactic LMWH during admission as they are high risk for thrombotic complications. They should also have a regular foot assessment to look for any ulcerations and encouraged to mobilise early with removal of the catheter when clinically appropriate.

23
Q

HHS is an acute, life-threatening diabetic emergency that is associated with a number of complications related to both the disease process and treatment.

A

Myocardial infarction: The hypovolaemia, hyperviscosity and severe state of illness places strain on the heart, often in patients with pre-existing coronary disease, increasing the risk of myocardial infarction.
Thrombotic complications: The hyperviscosity state and hypovolaemia predisposes patients to clots that may manifest as DVT, PE or stroke. In the absence of contra-indications patients are commenced on prophylactic LMWH to reduce this risk.
Cerebral oedema: This may occur from rapid correction of hyperglycaemia with a resulting rapid drop in plasma osmolarity and cerebral oedema, manifesting with headache, reduced GCS and untreated eventually death.