Acute Diabetes Complication (DKA, HHS, Hypoglycaemia)

Notes

Diabetic Ketoacidosis

Definition

Ketoacidosis: A condition resulting from deficient insulin availability, leading to lipid oxidation and metabolism rather than glucose metabolism. The insulin absence results in free fatty acid (FFA) released from adipose tissue and in unregulated hepatic FFA oxidation and ketogenesis.
Type I Diabetes: Autoimmune disease where there is attack of beta cells of the pancreas leading to insulin deficiency and a requirement for exogenous insulin to prevent ketoacidosis.
Type II Diabetes: It usually consists of tissue-level insulin resistance (although exogenous insulin is often required) and rarely leads to ketoacidosis.
Kussmaul breathing: Deep, rapid respirations associated with acidosis.

Overview

Diabetic Ketoacidosis may be the presenting feature in a patient not previously recognised as having diabetes. In a patient with known diabetes, it may be precipitated by omitting insulin doses, or by the insulin. Diabetic ketoacidosis has a mortality rate of 8- to 50% in the elderly.

Clinical Presentation

Signs of dehydration
- polyuria
- polydypsia
- weight loss
GI symptoms
Hyperventilation (↑Respiratory Rate – Kussmaul breathing)
True coma – 10% of cases)

Side note

Kussmaul breathing is air hunger, rapid deep breathing a sign of metabolic acidosis. This is different to Kusmaul’s sign looks at JVP relationship with breathing.

Aetiology (5I’s) + Initial Diagnosis

Infection
Infarction
Insufficient insulin
Intercurrent illness
Inappropriate withdrawal of Insulin
Initial Diagnosis

Remember

Precipitating factors of DKA 5 I’s: Infection Ischemia Infarction Intoxication Insulin missed.

Investigations

Bloods – EUC, Glucose, bicarbonate (HCO3 – < 12 mmol/L indicates severe acidosis)
ABG – Assess severity of acidosis
Urine – Ketones, Glucose
ECG – Hypokalaemia – arrythmias
Troponin – in older patients as MI could be a trigger
Infection screen – FBC, Blood and urine culture, CRP, CXR. Although leukocytosis invariably occurs, this represents a stress response and does not necessarily indicate infection

Think

Check ABG, EUC and glucose every 4hours. Monitor ECG for hypokalaemia/hyperkalaemia. Monitor IV fluid, insulin, glucose and K+ should all be run in separate lines.

Differential Diagnosis – high blood glucose and coma

Head injury
Alcohol
Drug overdose

Diagnosis of DKA

Hyperglycemia (>11.1mmol/L)
Metabolic acidosis (pH <7.3 or
- Severity is assessed this way
Hyperketonemia
Ketonuria

Side Effects Different types ketones produced include B-Hydroxymutyrate, acetatoacetate and acetone.

Treatment

The main aim in treating DKA is to progressively improve blood pH and clear the body of excessive ketones by aggressive fluid replacement and insulin therapy.

Assess Airway, Breathing, Circulation
IV Fluids – Normal Saline 0.9% NaCL (switch to 5% dextrose with 0.45% NaCl when serum glucose reaches ~15)
Insulin – Insulin infusion until pH stabilizes
Potassium – Administration of Insulin can cause hypokalemia, potassium levels should be checked prior to insulin administration
ABG assessment – assess pH and need for bicarbonate
Monitoring
- Check ABG, EUC every 4hours.
- Check Urine Glucose and Ketone 4hourly
- Check Blood glucose hourly.
- Monitor ECG for hypokalaemia/hyperkalaemia
- Monitor GCS regularly

Remember

Hypokalaemia ECG changes include flat/inverted T-wave, ST Depression and widened QRS.

Glasgow Coma Scale
Behaviours	Response	Score
Eye response (score 1-4)	Spontaneously To Speech To Pain No response	4 3 2 1
Verbal response (score 1-5)	Orientated good Confused Inappropriate words Incomprehensible sounds No response	5 4 3 2 1
Motor response (score 1-6)	Obeys command Moves to localised pain Withdrawal from pain Decorticate Decerebrate No response	6 5 4 3 2 1
Score	Best response Coma Unresponsive (Lowest possible)	15 <8 3

Complications of DKA

Cerebral oedema
- May be caused by very rapid reduction of blood glucose, use of hypotonic fluids and/or bicarbonate
- High mortality
- Treat with mannitol, oxygen Acute respiratory distress syndrome
Thromboembolism
Disseminated intravascular coagulation (rare)
Acute circulatory failure

Hyperosmolar Hyperglycaemia

Definition

Hyperosmolar Hyperglyaecmic State is a complication of type 2 diabetes. It involves extremely high blood sugar (glucose) levels without the presence of ketones.
Type I Diabetes: Is caused by a severe endogenous insulin deficiency and a requirement for exogenous insulin to prevent ketoacidosis.
Type II Diabetes: It usually consists of tissue-level insulin resistance (although exogenous insulin is often required) and can lead to HHS, rarely leads to ketoacidosis.

Overview

Hyperosmolar Hyperglycaemia (HOH) state occurring primarily in type 2 diabetes and is characterised by marked hyperglycaemia and dehydration without ketoacidosis. The disturbance in consciousness in patients varies from drowsy to comatose. HOH is a more sinister complication than ketoacidosis with a mortality rate as high as 50%.

Diagnosis – biochemical

Hyperglycemia
Serum osmolality is high (>350 mmol/kg)
No acidosis
No ketonuria + on urine dip testing can occur with starvation and vomiting.

Serum osmolality (in mosmol/kg) can be calculated if not available from the laboratory using the following equation:

Osmolality = 2(sodium + potassium) + glucose + urea

Pathophysiology

This condition results from a combination of insulin deficiency and coun- terregulatory hormone excess. The insulin present stops ketone produc- tion but in insufficient quantities to prevent worsening hyperglycemia.

Treatment

Same as DKA, but with a few exception because patients are usually older.

IV Fluids – Normal Saline 0.45% NaCL (switch to 5% dextrose with 0.45% NaCl when serum glucose reaches ~15)
Insulin – Slow Insulin infusion until pH stabilizes
Potassium – Administration of Insulin can cause hypokalemia, potassium levels should be checked.
Antibiotics – if infection
ABG assessment – assess pH and need for bicarbonate