Adult Hyperglycaemia

Question 1

What determines Diabetic Ketoacidosis (DKA)

Answer 1

Any patient with:
- A pre-existing history of diabetes
- BGL > 11 mmol/L, and
- Clinical features of DKA

Question 2

Clinical Features of DKA

Answer 2

• Dehydration
• Confusion
• Tachypnoea
• Polydipsia
• Polyuria
• Polyphagia
• Kassmaul’s Respirations
• Hx of Diabetes

Question 3

How many DKA pts will present with low-moderate hyperglycemia (11-29mmol/L)?

Answer 3

50%

Question 4

Determinants of Hyperosmolar Hyperglycaemic State (HSS)

Answer 4

• Pts typically older
• Have higher BGL levels (>30mmol/L)
• Usually do not present with clinical features of DKA

Question 5

Mgx of Hyperglycaemia

Answer 5

Less than adequate perfusion AND clinical features of DKA/HSS
- NS 20mL/kg titrated to pt perfusion status
- Consider antiemetic as per N/V CPG

Question 6

Mgx for Hyperglycaemia SD3

Answer 6

R+R
Position - POC/Supine
IV Access
Fluids NS 20mL/kg
Ondansetron IV 8mg/4mL
MICA up/downgrade/cancel
Extrication Wheelchair -> Stretcher
Reassess 10/60 VSS
Load Sig ? - MICA ?

Question 7

Differential Diagnosis for Hyperglycaemia

Answer 7

DKA
HHS
Dehydration
Altered Conscious State
Asthma
COPD
Stroke

Question 8

Pathophysiology of DKA

Answer 8

Insulin deficiency
↓
Glucose levels in the blood rise as insulin cannot take it into the cell
↓
The body metabolises fat which results in ketone by product
↓
Excessive ketones cause metabolic acidosis
↓
Excessive glucose exceeds the renal glucose reabsorption threshold – therefore additional glucose in the filtrate draws in water and electrolytes and leads to osmotic diuresis
↓
Resp rate is increased to blow of Co2 to buffer the metabolic acidosis, buy production of ketones continues – Kassmaul Resps
↓
Metabolic acidosis and dehydration causes cellular dysfunction
↓
SHOCK, COMA, DEATH

Question 9

Difference between T1DM and T2DM

Answer 9

Type 1:
Autoimmune destruction of Beta cells (which produce insulin) in the pancreas
↓
Insulin not produced therefore glucose unable to enter cell
↓
Leads to hyperglycaemia

Type 2:
Cells resistant to insulin or inadequate insulin production
↓
Number of insulin receptors at muscle are decreased due to long term insulin production
↓
Glucose transporters reduced

Question 10

DKA Definition

Answer 10

Acute life-threatening complication of T1DM leading to the metabolism of fats and proteins for energy – resulting in ketone production, dehydration and metabolic acidosis

Question 11

HHS Definition

Answer 11

Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose and hyperosmolarity with little or no ketosis.

Similar to DKA, however nil break down of fats, no ketone production, no kassmaul respirations. Relative insulin deficiency (however little amounts of insulin still working)

Question 12

Causes of Hyperglycaemia in the Diabetic Patient

Answer 12

• Non-compliance with insulin/diabetic medication
• Illness or infection
• Not following management plan
• Inactivity
• Using steroids/immunosuppressants

Question 13

Ondansetron Mode of Action

Answer 13

5-HT3 antagonist – exact mode of action is not fully understood. Release of serotonin (5-HT) is
thought to trigger a vomiting reflex in both the peripheral (GIT) and central nervous system.

Question 14

Ondansetron Indications

Answer 14

• Undifferentiated nausea and vomiting
• Prophylaxis where vomiting could be clinically detrimental (e.g. spinally immobilised,
  penetrating eye trauma)

Question 15

Ondansetron Contraindications

Answer 15

Apomorphine

Question 16

Ondansetron Precautions

Answer 16

1) Pregnancy 1st trimester – consult with receiving hospital
2) Congenital Long QT syndrome – ondansetron causes QT prolongation and increases the risk of Torsades de pointes in patients with a prolonged QT interval. Unlikely when administered at approved doses but avoid if the patient has a history of congenital Long QT syndrome.
3) Severe hepatic disease (e.g. cirrhosis) – limit total daily dose to a maximum of 8 mg
4) Ondansetron ODT may contain aspartame which should be avoided in patients with phenylketonuria. Ondansetron injection can be administered if appropriate

Question 17

Ondansetron Adverse Effects

Answer 17

CNS: Headache, dizziness
CV: QT prolongation (rare)
GI: Constipation
Other: Visual disturbance, including transient loss of vision (rare, associated with rapid IV administration)

Question 18

Ondansetron Significant Interactions (ApoMorphine)

Answer 18

Apomorphine (injection used in the treatment of severe Parkinson’s disease) – reports of
profound hypotension and loss of consciousness. Do not administer ondansetron to patients
currently receiving apomorphine

Question 19

Ondansetron in Pregnancy/Breastfeeding

Answer 19

Pregnancy
a) 1st trimester – consult with receiving hospital
b) 2nd and 3rd trimester – administer only if vomiting is very severe and benefits outweigh risk
- Consider IV fluid rehydration as per CPG A0701
Breastfeeding
- Considered safe

Question 20

Ondansetron Peak/Duration Time

Answer 20

Peak: 10 minutes (IV, IM); 30 minutes (oral)
Duration of action: Several hours

Question 21

Ondansetron Presentation

Answer 21

4mg ODT, 8mg/4mL Glass Ampoule

Question 22

Ondansetron Presentation

Answer 22

4mg ODT, 8mg/4mL Glass Ampoule

Question 23

Prochlorperazine Mode of Action

Answer 23

Dopamine antagonist – antiemetic effects are primarily due to D2 receptor blockade. Also acts on
other neurotransmitter systems including histaminic, cholinergic, and α-adrenergic receptors

Question 24

Prochlorperazine Indications

Answer 24

Nausea and vomiting in patient ≥ 21 years of age; specifically for
- Known allergy or C/I to ondansetron
- Vestibular nausea
Headache (irrespective of nausea/vomiting)

Question 25

Prochlorperazine Contraindications

Answer 25

• CNS depression (i.e. unconscious or severely intoxicated)
• Patients < 21 years of age. (Children and young adults are more susceptible to extrapyramidal reactions with
  prochlorperazine.)

Question 26

Prochlorperazine Precautions

Answer 26

Elderly patients - More susceptible to adverse effects

Parkinson’s disease - Can worsen symptoms of Parkinson’s disease, avoid if possible

Question 27

Prochlorperazine Adverse Effects

Answer 27

CNS: Sedation, blurred vision
CV: Postural hypotension, QT prolongation (rare)
Other: Extrapyramidal reactions

Question 28

Prochlorperazine Pregnancy/Breastfeeding

Answer 28

Pregnancy - Considered safe
High doses or prolonged use in late pregnancy may be associated with an increased risk of
withdrawal effects in the newborn

Breastfeeding - Considered safe

Question 29

Prochlorperazine Onset/Peak/Duration Times

Answer 29

Onset of action: 10-20 minutes
Duration of action: 3-4 hours

Question 30

Prochlorperazine Presentation

Answer 30

12.5 mg in 1mL glass ampoule