Ketoacidosis

Question 1

Pathogenesis (3) factors

Answer 1

ketogenesis, dehydration, acidosis

Question 2

Ketogenesis

Answer 2

↓ insulin → ↑ stress hormones and ↑ glucagon → ↓ glucose utilisation + ↑ fat β-oxidation ↑ fatty acids → ↑ ATP + generation of ketone bodies.

Question 3

Dehydration

Answer 3

↓ insulin → ↓ glucose utilisation + ↑ gluconeogenesis → severe hyperglycaemia → osmotic diuresis → dehydration Also, ↑ ketones → vomiting

Question 4

Acidosis

Answer 4

Kussmaul breathing, confusion

Dehydration → renal perfusion -> AKI

Hyperkalaemia - palpitations, chest pain, muscle weakness

Question 5

Precipitants

Answer 5

Infection / stress ± stopping insulin New T1DM

Question 6

Presentation

Answer 6

Abdo pain + vomiting Gradual drowsiness Sighing “Kussmaul” hyperventilation Dehydration Ketotic breath

Question 7

Diagnosis (3)

Answer 7

Acidosis (↑AG): pH <7.3 (± HCO3 <15mM) Hyperglycaemia: ≥11.1mM (or known DM) Ketonaemia: ≥3mM (≥2+ on dipstix)

Question 8

Complications of treatment

Answer 8

Cerebral oedema: excess fluid administration Commonest cause of mortality Aspiration pneumonia Hypokalaemia Hypophosphataemia → resp and skeletal muscle weakness Thromboembolism

Question 9

Management - GRIP

Answer 9

Gastric aspiration Rehydrate Insulin infusion Potassium replacement

Question 10

Investigations (6)

Answer 10

ABC

Urine: ketones and glucose,

MCS Cap glucose and ketones

VBG: acidosis + ↑K

Bloods: U+E, FBC, glucose, cultures

CXR: evidence of infection

ECG

Question 11

Management STEP 1 after investigations

Answer 11

0.9% NS infusion via large bore cannula SBP<90 → 1L stat + more until SBP >90

SBP>90 → 1L over 1h Then: 1L over next 2h, 1L/2h, 1L/4h, 1L/4h, 1L/6h

Switch to 10% dex 1L/8h when glucose <14mM

Start Potassium Replacement in 2nd Bag of Fluids

>5.5mM → Nil

3.5-5.5mM → 40mmol/L

<3.5mM → consult senior for review

Question 12

STEP 2 - insulin infusion

Answer 12

Start continuous fixed rate IVII via an infusion pump. 50units human soluble insulin (Actrapid®, Humulin S®) made up to 50ml with 0.9% sodium chloride solution. Ideally this should be provided as a ready-made infusion

Actrapid 0.1u/kg/h IVI (i.e. 7units/hr if weight is 70kg) (6u if no wt., max 15u)

Question 13

STEP 3 - assessment (2)

Answer 13

Hx + full examination Investigations: capillary, urine, blood, imaging

Question 14

STEP 4 - additional measures (5)

Answer 14

Urinary catheter (aim: 0.5ml/kg/hr)

NGT if vomiting or ↓GCS

Thromboprophylaxis ̄c LMWH

Refer to Specialist Diabetes Team

Find and treat precipitating factors

Question 15

STEP 5 - monitoring (3) And aims (4)

Answer 15

Hrly capillary glucose and ketones

VBG @ 60min, 2h and then 2hrly

Plasma electrolytes 4hrly Aims ↓ ketones by ≥0.5mM/h or ↑HCO3 by ≥3mM/h

↓ plasma glucose by ≥3mM/h

Maintain K in normal range

Avoid hypoglycaemia

Question 16

STEP 6 - resolution

Answer 16

Ketones <0.3mM + venous pH>7.3 (HCO3 >18mM) Transfer to sliding scale if not eating Transfer to SC insulin when eating and drinking

Question 17

STEP 7 - transfer to SC insulin

Answer 17

When biochemically resolved and eating Start long-acting insulin the night before Give short-acting insulin before breakfast Stop IVI 30min after short actin

Question 18

STEP 8 - patient education

Answer 18

ID precipitating factors and provide action plan Provision of ketone meter ̄c education on use.

Question 19

Hyponatraemia in DKA

Answer 19

Hyponatraemia is the norm Osmolar compensation for hyperglycaemia ↑/Normal Na indicates severe dehydration

Question 20

Once glucose is normalised = what insulin should be avoided

Answer 20

Avoid rapid ↓ in insulin once glucose normalised Glucose decreases faster than ketones and insulin is necessary to get rid of them.

Question 21

What happens to amylase

Answer 21

Amylase is often ↑ (up to 10x)

Question 22

Why do you get refractory metabolic acidosis post treatment

Answer 22

Excretion of ketones → loss of potential bicarbonate → hyperchloraemic metabolic acidosis after Rx

Question 23

Why is it a pseudo hyperkalaemia

Answer 23

Correct acidosis, osmolarity -> correct hyper K+

Huge potassium loss secondary to polyuria

Loss of fluid activates aldosterone leading to increased K+ secretion