Diabetic Emergencies Flashcards

1
Q

What is Diabetic Ketoacidosis?

A

T1DM not producing insulin themselves and is not injecting adequate insulin to compensate for this.

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2
Q

What are the main problems that arise with diabetic ketoacidosis?

A

ketoacidosis, dehydration and potassium imbalance.

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3
Q

What is ketoacidosis?

A

As the cells in the body have no fuel and think they are starving
-> ketogenesis
» higher glucose and ketones levels.

kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH.

The ketone acids use up the bicarbonate and the blood starts to become acidic.

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4
Q

How does dehydration occur in DKA?

A

Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine.

The glucose in the urine draws water out with it in a process called osmotic diuresis.

Polyuria->severe dehydration.

thirst centre stim -> polydypsia

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5
Q

How can a potassium imbalance arise in DKA?

A

Insulin drives potassium into cells.

Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in the urine
total body potassium is low because no potassium is stored in the cells.

When treatment with insulin starts patients can develop severe hypokalaemia (low serum potassium) very quickly and this can lead to fatal arrhythmias.

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6
Q

How does someone present with DKA?

A
Polyuria
Polydipsia
Nausea and vomiting
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered Consciousness
They may have symptoms of an underlying trigger (i.e. sepsis)
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7
Q

What is the priority for managing DKA?

A

The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis.
priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis.
followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones

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8
Q

What is the diagnostic criteria for DKA?

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

The triad of Hyperglycaemia with Glucose of 30 mmol/L (>11.1mmol/L),
Acidosis with Bicarbonate of 6 mmol/L (Bic <15mmol/L) and Ketonuria (Urine
dipstick positive for ketones ++++) are diagnostic of diabetic ketoacidosis.
Abdominal pain and Kussmaul’s Breathing/ air hunger and the smell of
ketones/ nail varnish are all important clinical signs.

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9
Q

How is DKA managed (FIG PICKE)?

A

F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)
Establish the patient on their normal subcutaneous insulin regime prior to stopping the insulin and fluid infusion.

Remember as a general rule potassium should not be infused at a rate of more than 10 mmol per hour.

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10
Q

What is hyperosmolar hyperglycaemic state?

A

it is characterised by profound hyperglycaemia (glucose >33.3 mmol/L [>600 mg/dL]), hyperosmolality (effective serum osmolality ≥320 mmol/kg [≥320 mOsm/kg]), and volume depletion in the absence of significant ketoacidosis (pH >7.3 and HCO3 >15 mmol/L [>15 mEq/L])

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11
Q

What can HHS be the first presentation of?

A

T2 diabetes (no ketacidosis)

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12
Q

How does HHS present?

A
altered mental status
polyuria
polydipsia
weight loss
weakness
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13
Q

How do you treat HHS?

A

Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated.
Give saline IV.

Potassium replacement is often required as the metabolic problems are corrected.

Insulin is given to reduce blood glucose concentration; however, as it also causes the movement of potassium into cells, serum potassium levels must be sufficiently high or dangerously low blood potassium levels may result.

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14
Q

How does hypoglycaemia present?

A

Typical symptoms are tremor, sweating, irritability, dizziness and pallor. More severe hypoglycaemia will lead to reduced consciousness, coma and death unless treated.

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15
Q

How to treat hypoglycaemia (moderate)?

A

Hypoglycaemia needs to be treated with a combination of rapid acting glucose such as lucozade and slower acting carbohydrates such as biscuits and toast for when the rapid acting glucose is used up.

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16
Q

How to treat severe hypoglycaemia?

A

Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.

17
Q

How does insulin insufficiency lead to diabetic ketoacidosis?

A

DKA occurs as a result of Insulin Deficiency and counter regulatory catabolic
hormone excess e.g. Glucagon.
Insulin deficiency results in excess mobilisation of free fatty acids from
adipose tissue which provides the substrate for ketone production from the
liver.
Ketones (β hydroxyl butyrate, acetoacetate, acetone) are excreted by the
kidneys and buffered in the blood initially but eventually this system fails and
acidosis develops.
Hyperglyceamia also occurs as the liver produces glucose from lactate and
alanine which are generated by muscle proteinolysis.
Reduced peripheral glucose utilisation associated with Insulin deficiency
exacerbates hyperglycaemia.
The osmotic diuresis produced by hyperglycaemia and ketonuria causes
hypovolaemia.

18
Q

What are possible causes of DKA other than new presentation of T1DM?

A
  • Non compliance with Insulin
  • Inappropriate alterations in Insulin
  • Infection
  • Myocardial infarction
  • Pregnancy