Metabolic Complications of DM

Question 1

What are the major short term hyperglycaemic complications of diabetes?

Answer 1

Diabetic Ketoacidosis (DKA): Type 1
Hyperosmolar Hyperglycaemic Syndrome: Type 2

Question 2

Outline who gets DKA and the metabolic pathway underlying DKA?

Answer 2

A disorder due to the imbalance of insulin levels and counteregualtory hormones such as glucagon.

Occurs in undiagnosed type 1 diabetics and type 1 diabetics who stop taking their insulin often due to another illness.

Patients have high circulating blood glucose but due to a lack of insulin this cannot be taken up into cells.

Due to the lack of glucose in cells, ketogenic pathways are switched on.

Lipolyisis occurs and FFA’s are transported to the liver bound to albumin.

FFA’s are broken down into acetate and converted into ketoacids (acetoacetate and beta-hydroxybutyrate).

Ketoacids are then transported to skeletal muscle and the brain. Ketoacidosis occurs when the production of ketoacids is greater than the utilisation of them therefore there is an acidosis.

Question 3

Explain why there is dehydration in DKA?

Answer 3

Due to the high blood glucose there is a high osmolality therefore water will leave cells.

As vomiting occurs there will be a further loss of fluids and electrolytes.

Question 4

What are the diagnostic criteria for DKA?

Answer 4

Ketones present: more than 3mmol or 2+ on urine dip
Hyperglycaemia: greater than 11mmol
Acidosis or bicarbonate less than 15mmol

Question 5

What is the pathogenesis underlying hyperosmolar hyperglycaemic syndrome?

Answer 5

Tends to occur in more elderly T2 diabetics with an underlying illness which causes there to be a limited oral intake (usually infection).

It is characterised by severe hyperglycaemia with marked serum hyperosmolarity, without evidence of significant ketosis.

The basic underlying mechanism of HHS is a relative or absolute reduction in effective circulating insulin with a rise in counter-regulatory hormones.

Decreased renal clearance and decreased peripheral utilization of glucose lead to hyperglycemia.

Hyperglycemia and hyperosmolarity result in an osmotic diuresis and an osmotic shift of fluid to the intravascular space, resulting in further intracellular dehydration.

This diuresis also leads to loss of electrolytes, such as sodium and potassium.

Question 6

What are the symptoms of HHS?

Answer 6

Early symptoms of generalised weakness, leg cramps or visual impairment.

Nausea and vomiting but less marked than in DKA.

Later symptoms include confusion, weakness, seizures and coma in 10% of cases.

Question 7

Describe the presentation of diabetic ketoacidosis?

Answer 7

Abdominal pain.
Nausea and vomiting.
Polyuria and polydipsia.

Signs:
Kussmaul breathing.
Clinically dehydrated.
Ketone breath.

Question 8

Describe how you manage DKA and HHS?

Answer 8

ABCDE

1. Fluid replacement
2. Fixed rate insulin infusion 0.1 units/kg/hr
3. Monitor K+

If BP unstable give the 1st bag as a challenge
1L NaCL over 1hr
1L NaCL over 2hr
1L NaCL over 2hr
1L NaCL over 4hr
1L NaCL over 4hr

General rule but take care not to fluid overload your patient.

Administer K+ replacement one K+ falls below 5.5, target range should be between 4.0-5.0.
Give K+ in all bags after the 1st bag*.
Concentration should be 20-40mmol per litre.
Max rate should 10mmol/hr or 20mmol/hr if on a cardiac monitor.
Max daily K+ should be 3mmol/kg/day

Continue treatment until acidosis and ketosis has corrected.

*1st bag is going through over an hour so risk of a K+ bolus.

HHS slightly different; insulin only when Ketones>1, bm dropping <5/hour, give 0.05units/kg/hr

Question 9

What are the complications of DKA?

Answer 9

1. Hypokalaemia: May appear as a pseudo-hyperkalaemia as acidosis shifts K+ out of cells. Total body K+ will be depleted.
2. Hypoglycaemia (over treatment: once glucose is less than 14mmol add glucose to regime dextrose 10% 125ml/hr)
3. Cerebral oedema: due to the fluid shift from the intracellular space to the extracellular space

Question 10

What are counter-regulatory hormones to insulin?

Answer 10

Insulin promotes the storage of glucose.

Counter-regulatory hormones promote the production and mobilisation of glucose:

• Glucagon
• Cortisol
• Growth Hormone
• Catecholamines (adrenaline)

Question 11

Outline the response of glucagon to hypoglycaemia?

Answer 11

Glucagon promotes the production and mobilisation of glucose.

Insulin promotes the storage of glucose.

Glucagon stimulates:
Glycogenolysis (breakdown of glycogen)
Inhibits the synthesis of glycogen.
Gluconeogenesis

Question 12

Describe the causes of hypoglycaemia?

Answer 12

Pneumonic ExPLAIN

Exogenous insulin: Excess exogenous insulin. (Particularly at risk if type 1 patients do not adjust their dosing with exercise.)

Pituitary Insufficiency (produces many of the counter regulatory hormones)

Liver Failure (effects of glucagon cannot occur)

Addison’s Disease (no cortisol counteracting insulin)

Islet Cell Tumours (secreting insulin)

Non- pancreatic neoplasias (secreting IGF-1)

Question 13

Describe the symptoms of hypoglycaemia?

Answer 13

• Hunger
• Sweating
• Dizziness
• Fatigue
• Blurred vision
• Tremor
• Irritability
• Difficulty concentrating
• Confusion
• Reduced conciousness

Question 14

What is the treatment of hypoglycaemia?

Answer 14

Oral glucose followed by long acting carbohydrate.

200/300ml of 10% dextrose IV if not conscious.

IM glucagon if cannot gain IV access.