Endo - Diabetic Emergencies

Question 1

What is DKA

Answer 1

Life threatening metabolic complication of DMTriad of: Ketonaemia Hyperglycaemia Acidaemia

Question 2

Pathophys of DKA

Answer 2

Relative or absolute insulin deficiency…Increased glucagon, cortisol and catecholamines—> lipolysis, free fatty acid production and ketogenesis
Ketoacids (3-b-hydroxybutyrate, acetone, acetoacetate) —> acidosis
Hyprglycaemia —> increased hepatic gluconeugenesis/glycolysis

Question 3

Why is there fluid depletion in DKA

Answer 3

Hyperglycaemia —> osmotic diuresis
Vomiting
Reduced oral intake (low GCS)

Question 4

Causes of DKA

Answer 4

Intercurrent infection
Not talking meds
MI
Surgery

Question 5

Features of DKA

Answer 5

Thirst
Polyuriea
N/VAbdo pain
Dehydration
Ketotic smell
Kussmaul breathing
Confusion and coma

Question 6

Diagnosis of DKA

Answer 6

Capillariy glucose > 11 mmol/L
Ketonaenmia > 3mmol/l OR 2+ urine dip
Venous bicarb < 15mmol/L OR pH<7.3

Question 7

Commonest cause of death in DKA

Answer 7

Cerebral oedema (worse in children/young adults)

Question 8

In DKA, when would you consider admission to HDU/ITU

Answer 8

Ketones>6
Bicarb < 5
pH<7.1
Low K < 3.5
GCS < 12SpO2 < 92%
Systolic BP < 90
HR <60 or > 100
Anion gap >16

Question 9

Treatment goals in DKA

Answer 9

Decrease ketones by 0.5mmol/l per hour
Increase bicarb by 3mmol/l per hour
Decreased Cap BM by 3mmol/l per hour
Maintain K

Question 10

What are the broad headings of treatment in DKA

Answer 10

ABCDE and treat etc…Fluid and electrolyte management
Insulin and metabolic correction
Treat the cause
Supportive care

Question 11

Describe the fluid and electrolyte tx

Answer 11

AIm to restore volume and clear ketones, and correct imbalances
Saline is fluid of choice
Give 500ml bolus if BP<90
Further fluids over 1-4 hours depending on policy
When potasssium less than 5.5, supplement with K

Question 12

Insuline therapy

Answer 12

Fixed rate infusion - 0.1 unit/kg/hr
DO NOT BOLUS
Continue long acting insulin
Regular venous bloods and urine/blood ketones
If they hypo - 10% glucose

Question 13

Supportive care

Answer 13

VTE prophylaxis - mechanical/pharma
Stress ulcer
Enteral feed

Question 14

How does management differ in kids

Answer 14

Markedly increased risk of cerebral oedema
Bolus fluid in shocked patietns
Work out fluid requirements and deficit and replace
Maintenannce fluid needs are lower
Delay insulin for 1 hour

Question 15

What is HHS

Answer 15

Hyperglycaemic hyperosmolar state
Severe hyperglycaemia with fluid depletion
No/mild ketosis
Found in elderly with type II DM

Question 16

Mortality of HHS

Answer 16

15-30%
Much higher than DKA

Question 17

Features of HHS

Answer 17

Hypovolaemia — Significant losses (100-220ml/kg)
Hyperglycaemia (MARKED>30) Without ketone
Without acidosis
Serum hyperosmolarity >320mosmol/kg

Question 18

Goals of treatment HHS

Answer 18

Treat underlying cause
Normalise osmolality (2xNa + glucose +urea)
Replace losses 0. 9% saline +/- potassium 0. 45% if osmolality not falling
Replace K is <5.5
Normalise BM
Prevent complications

Question 19

Targets for treatment HHS

Answer 19

K 4.0 to 5.5
Na reduces by <10mmol/l in 24 hours
Glucose fall by 5mmol/L per hour

Question 20

How do you achieve Glucose normalisation in HHS

Answer 20

Fluid should do it
If glucose stops falling —> insulin fixed at 0.05units/kg/hour

Question 21

When to admit HHS to ITU

Answer 21

Osm>350
Na > 160
pH < 7.1
High or low K
GCS < 12
SpO2 < 92%
HR <60 or > 100
U/O less than 0.5ml/kg/hr
Creatinine > 200 umoll
Hypothermia
MI, Stroke or comorbidity

Question 22

What are the pharmacological treatment options of DM?

Answer 22

Insulin and non-insulin

Insulin
- peptide hormone produced by the β-cells in the pancreas
- Insulin causes the insertion of the GLUT4 transporter in the cell membranes of muscle and fat tissues
- also induces anabolic state - glycogen and fat synthesis and inhibits lysis
- Short acting, intermittent or longacting

Non insulin

Sulphonylureas - gliclazide. increase in peripheral insulin concentration by binding on the sulphonylurea receptor in the pancreatic β-cell.

Intestinal alpha-glucosidase inhibitors- Acarbose

Sodium-glucose linked transporter inhibitors (SGLT-2 inhibitors). dapagliflozin - prevent glucose reabsorption from the proximal convoluted tubules

Biguanides - Metformin - decrease glucose absoption, increase insulin receptor expression

Thiazolidinediones - pioglitazone - increase the sensitivity of naturally released insulin

Incretin mimetics/GLP-1 analogues e.g exenatide. - early saiety, improves insulin secretion

The gliptins/dipeptidyl peptase-4 inhibitors (DPP4 inhibitors). sitagliptin