Glycaemic control

Question 1

What are the different mechanisms behind elevated glucose in ICU patients?

Answer 1

Increased gluconeogenesis
Insulin resistance
Catecholamines - both endogenous and exogenous
Glucose-containing preparation
Corticosteroids

Question 2

What harm can hyperglycaemia cause to ICU patients?

Answer 2

Increased mortality
Increased HAI
Associated with adverse outcomes in TBI

Question 3

What are the causes of hypoglycaemia in ICU patients?

Answer 3

Insulin admin
Severe illness e.g. sepsis
Liver failure

Question 4

What are the systemic effects of hypoglycaemia?

Answer 4

Inflammatory response
Neuroglycopenia
Cerebral vasodilatation
Autonomic dysfunction
Impaired stress response

Question 5

What did the Van den Berghe study show?

Answer 5

Van den Burghe published a single-centre RCT in 2001 which demonstrated decreased mortality in surgical ICU patients with intensive insulin therapy - keeping BM between 4.4-6.1

Question 6

What does NICE-Sugar say about glycaemic control?

Answer 6

NICE-SUGAR was a multi-centre RCT that found that tight glycaemic control in ICU was associated with:

• excess mortality
• increased hypoglycaemia

Question 7

What do the guidelines from the Society of Critical Care Medicine suggest for glycaemic control?

Answer 7

Aim to keep blood sugar below 10
Avoid hypoglycaemia
It has also been postulated that glycaemic variation may be as detrimental as hyperglycaemia itself

Question 8

What is diabetic ketoacidosis?

Answer 8

Occurs in patients with insulin deficiency

Is defined metabolically as a triad of ketonaemia, hyperglycaemia and metabolic acidosis

Question 9

What is the pathophysical response that occurs in DKa?

Answer 9

-insulin deficiency
-concurrent increase in counter-regulatory hormones e.g. glucagon and adrenaline
-decreased utilization of glucose and
-increased hepatic gluconeogenesis leading to hyperglycaemia
-glycosuria and subsequent osmotic diuresis
Increased lipolysis in liver motichrondria and subsequent production of acetoacetic acid, acetone and 3-beta-hydroxybutyrate (most abundant ketone)

Question 10

What are the most common causes of death in patients with DKA?

Answer 10

Cerebral oedema (mainly young children and adolescents)
ARDS
hypokalaemia
Co-morbidities

Question 11

What are the common precipitants for DKA?

Answer 11

New onset diabetes
Non-compliance with insulin
Admin if out of date insulin
Lipohypertrophy of injection sites and subsequent impaired absorption
Intercurrent illness e.g. infection, gastroenteritis, MI

Question 12

Which guidelines provide recommendations for the management of DKA?

Answer 12

Joint British Diabetes Societies (JBDS) Inpatient Working Group

Question 13

What are the principles of managing DKA?

Answer 13

• Restore circulating volume using IV fluids
• Suppress ketogenesis and clear ketonaemia using fluids and insulin
• Treat hyperglycaemia
• Avoid hypoglycaemia
• Replace potassium and avoid hypokalaemia
• Identify and treat precipitating factors

Question 14

What specific recommendations does the JBDS make for the management of DKA?

Answer 14

• Use of fixed rate insulin (0.1 units/kg/hr)
• Add 10% dextrose once BM < 14
• Increase insulin if ketone clearance isn’t being achieved
• Administrate 0.9% saline as resuscitation fluid (there is widespread experience and it comes mixed with K.Hartmens may be used in ICU)
• Measurement of ketones should guide management a fall of at least 0.5mmol/l/hr should be targeted
• Venous samples should be used for patient safety and comfort
• Continue long-acting insulin - reducing the risk of rebound hyperglycaemia
• Pts with markers of severity should be considered for critical care admission

Question 15

What are the markers of severity in DKA?

Answer 15

Blood ketones > 6
Serum bicarb < 5
Venous or arterial pH < 7.0
Potassium < 3.5 on admission
GCS < 12
SaO2 < 92% RA
Hr < 60 or > 100
Anion gap > 16

Question 16

At what point do patient with DKA get switched back to sc insluin?

Answer 16

Pt should be tolerating oral diet and fluids
Blood ketones < 0.6
pH > 7.3
Involve diabetes team in the transition
S/C regimes should be restarted with meals and the IV insulin stopped 30-60mins later

Question 17

When should phosphate be replaced in DKA?

Answer 17

There is no evidence that it improves outcome and should be reserved for those with respiratory or skeletal muscle weakness

Question 18

Why should you not use bicarb in DKA?

Answer 18

There is evidence that it may be associated with CSF acidosis and is implicated in cerebral oedema in children

Question 19

Describe sodium correction in hyperglycaemia

Answer 19

• The osmotic effect of plasma glucose draws water into the intravascular compartment, diluting ions, most significantly sodium
• Correction of sodium concentration for hyperglycaemia more accurately reflects sodium and allows sodium to be trackes as hyperglycaemia resolves
• Tracking or corrected sodium is particularly important in children and adolescents who are at greater risk of cerebral oedema - it’s the fall in the corrected sodium that it the primary precipitant of cerebral oedema

Question 20

How do you calculate corrected sodium in the context of hyperglycaemia?

Answer 20

Measured Na x (0.3 x (plasma glucose-5.5))

Question 21

Who does hyperosmolar hyperglycaemia normally affect?

Answer 21

Tends to be older patients
However can be younger patient with the changing demographic of T2DM
Normally a/w T2DM

Question 22

What are the characteristic features on hyperosmolar hyperglycaemia?

Answer 22

No standard diagnostic definition
Characterised by:
-marker hyperglycaemia
- BM > 30 in the absence of significant hyperketonaemia (<3.0) or significant metabolic acidosis and a bircarb > 15
- Serum osmolality > 320

Question 23

What is the pathophysiology of HHS?

Answer 23

Unclear
Degree of insulin deficiency but not sufficient to cause marked ketosis
Osmotic diuresis does however lead to profound dehydration and electrolyte disturbance

Question 24

What complications are typically a/w HHS?

Answer 24

Vascular complications such as arterial/venous thrombosis and foot ulceration
Complications of fluid/electrolyte shifts e.g. cerebral oedema (less common)

Question 25

How is HHS managed?

Answer 25

Recommendations made by JBDS Inpatient Working Group
Goals are the replace fluid and electrolytes, normalise osmolality and blood glucose while preventing potential complications
Treat underlying causes e.g. MI

Question 26

What recommendations do JBDS make for the fluid management in patients with HHS?

Answer 26

• Use 0.9% saline
• 50% of estimated fluid deficit should be replaced in the first 12 hours
• Blood glucose should fall at a max rate of 5mmol/hr
• Sodium nay rise but should only be a concern if the osmolality is not falling and BM not adequately falling
• Monitor and replace potassium

Question 27

What recommendations do JBDS make for insulin treatment in pts with HHS?

Answer 27

• Insulin should only be strated in the initial phase if ketosis is present, otherwise BM should fall with fluid admin
• When BM stops falling with fluids then consider insulin
• Start a fixed rate of 0.05 units/kg/hr to target BM 10-15

Question 28

Discuss anticoagluation in patients with HHS

Answer 28

Unless contra-indicated prophylactic LMWH should be administeres
High risk patients may need 3 months of treatment
There is no robust evidence for treatment dose LMWH

Question 29

In which patients with HHS should you consider ICU care?

Answer 29

Osmolality > 350
Na > 160
Venous pH < 7.1
K < 3.5 or > 6 on presentation
GCS < 12
Sats < 92% on RA
SBP < 90
Hr < 60 or >100
U/O < 0.5ml/kg/hr
Serum creatinine > 200
Hypothermia
Acute macrovascular event
Significant co-morbidities