Hyperglycaemic states

 

Diabetic ketoacidosis (DKA)

Nonketotic hyperosmolar hyperglycaemic states (HHS) / Hyperosmolar nonketoacidosis (HONK)

 

DKA

 

A state of relative or absolute insulin deficiency

Hyperglycaemia

Hyperketonaemia

Acid producing metabolic derangements

Dehydration

Ketonuria

Hypokalaemia

Hyponatraemia

 

Requires 2 things

Ketosis

Acidosis (pH < 7.3)

 

Causes

Almost always caused by type 1 diabetes mellitus

1. Stress of intercurrent illness or infection (UTI most common form of infection)

2. Disruption to insulin therapy

3. Presentation for stabilisation

4. Other stressful events, trauma, surgery, medical illness, complicated pregnancy

Insulin should never be stopped

Omit insulin only when patient can not receive carbohydrates for whatever reason

Often younger patients

 

Signs and symptoms

Polyuria

Polydipsia

Nocturia

Dehydration

Decreased skin turgor

Tackycardia

Hypotension

Tackypnoea

 

Generalised weakness and fatigue

Breath smells of acetone

 

Hyperventilation (Kussmaul)

Abdominal pain and vomiting

Coma

Nausea

Dry skin

Confusion

Peripheral vasodilation

Hypothermia

Cerebral oedema

 

Investigations

 

Urine

Ketones, glucose, cultures (UTI is a common cause)

 

Imaging

CXR (exclude chest infection as a cause)

 

Bloods

FBC

U and Es (especially potassium) at baseline, 1, 2, 3, 6 12, 24 hours

Cultures

Bicarbonate

ABGs

 

Management

 

Airway, secure

Breathing, give oxygen

Circulation, give fluids and potassium, ECG

Drugs, insulin

 

 

Correct dehydration

 

0.9 % saline probably with 20-40 mmol KCl

Probably 1L stat, 1L over 1 hour, 1L over 2 hours, 1L over 4 hours, 1L over 4 hours.

Start 5% dextrose when glucose = 15 mmol L, 1L over 8 hours

Monitor urine volumes closely

NG

CVP

 

 

Soluble insulin sliding scale

 

50 units in 50 mls of saline IV for titration

Glucose Soluble insulin

0 - 4 0.5 units / per hour

4 - 8 1 unit / per hour

8 - 12 2 units / hour

12 - 16 3 units / hour

> 16 4 units / hour

Start 5% dextrose when glucose = 12 mmol L

More insulin may be required during acute infection

Aim for a reduction of 3 6 mmol / L per hour

Half life of intravenous insulin is 2.5 minutes

Go back to normal glycaemic management when patient can eat and drink normally

 

 

Potassium

 

Acidosis causes extracellular migration of potassium; therefore total body levels may be very low. This means serum potassium may fall precipitously once treatment is started.

 

< 3.5 mmol/L give 40 mmol added potassium / L

3.5 5 mmol/L give 20 mmol/L

> 5 mmol/L give no added potassium

Maximum infusion rate of 20 mmol/hr

 

Consider LMWH until mobile again, (dehydration makes blood thicker)

 

 

Pathogenesis

 

Ketone bodies

Acetone and 2 organic acids

Produced from the breakdown of proteins and fats as emergency fuel substrates

Some are produced by the liver in normal physiology but amounts greatly increase in the absence of carbohydrates.

 

In the absence of insulin counter-regulatory hormones such as glucagons, adrenaline and growth hormone enhance triglyceride breakdown into free fatty acids. They also enhance gluconeogenesis leading to hyperglycaemia.

 

Illness causes release of stress hormones which stimulate lipolysis, producing plenty of fatty acids for hepatic ketogenesis

 

Hydrogen ions enter cells and displace potassium ions which are then excreted in the urine or lost in vomiting

 

In DKA there is uncontrolled catabolism associated with insulin deficiency

Insulin inhibits hepatic ketogenesis

 

Pathogenesis (continued)

 

 

 

Increased serum glucose Ketones

 

 

Hyperglycaemia and glucosuria Acidosis

 

 

Osmotic diuresis Vomiting

 

 

 

Fluid and electrolyte depletion (Na+ and K+ are depleted)

 

 

Renal hypoperfusion

 

 

Impaired excretion of ketones and hydrogen ions

 

 

Ketonaemia and acidosis

 

 

 

 

HHS

 

Often older type 2 diabetics

Insidious onset, weeks rather than days

 

 

Signs and symptoms

 

Dehydration

Possible coma

No acidosis

Very high glucose (>35 mmol L) therefore very hyperosmotic blood

 

 

Management

 

Correct dehydration slowly

0.45 or 0.9 % saline over 48 hours

Probably 1 unit of insulin per hour

As VTE is a risk give LMWH