Supportive care in ICU

Question 1

Summarise the choice of agent and dosing of prophylactic anticoagulation in the ICU for weight and renal function.

Answer 1

GFR > 30
- < 50 kg –> 30mg enoxaparin daily
- 50 - 120 kg –> 40 mg enoxaparin daily
- > 120 kg –> 0.25 mg/kg enoxaparin 12 hourly (or 30 mg bd)

GFR < 30
- < 50 kg –> heparin 5000 IU 12 hourly
- 50 - 120 kg –> heparin 5000 IU 8 hourly
- > 120 kg (monitor anti Xa levels - blue top tube)

Question 2

In which patients should anti-Xa levels be monitored?

Answer 2

1. Unusual weight
2. Pregnancy
3. Borderline renal function

Question 3

What does a light blue top phlebotomy blood sample tube contain and how does this prevent coagulation of blood in the tube

Answer 3

2.7 mls of 3.2% Sodium Citrate

It sequesters Calcium from blood preventing coagulation

Question 4

When should an anti-Xa level be tested (i.e. after how many doses of anticoagulant) and what is the target level for antiquate prophylactic anticoagulation

Answer 4

IT should be sampled 4 hours after the 3rd dose and the target level is 0.3 - 0.5 IU/ml

Question 5

List the non-pharmacological measures of GI prophylaxis in the ICU

Answer 5

1. Stop aspirin if not indicated
2. No NSAIDS in ICU
3. Enteral nutrition preferable whenever possible

Question 6

In which ICU patients is GI prophylaxis indicated

Answer 6

GSH guidelines
- “Pantoprazole 40mg IV if not on full feeds”

EMCRIT
- Intubated patients
- Non-intubated patients with numerous risk factors
–> Coagulopathy
–> Shock
–> Prior GI bleed
–> Steroid therapy (dose equivalent > 60mg pred daily)
–> COVID patients on dexamethasone

Question 7

What are the benefits of PPI over H2 receptor antagonists?

Answer 7

1. PPI greater efficacy
2. PPI lower risk of delirium
3. C.Difficile/Pneumonia concern recently debunked by SUP-ICU trial

Question 8

What is ICU haemoglobin drift?

Answer 8

ICU patients experience gradual Hb decrease
1. Suppression haematopoiesis by critical illness
2. Phlebotomy - seriel lab Ix
3. Subclinical GI loss from minor GI stress ulceration

Question 9

Describe your initial evaluation and investigation of acutely falling Hb

Answer 9

Cause: Likely bleeding or haemolysis
(unlikely synthesis issue: Retic/Iron/B12 Ix - waste of resources)

For bleeding and haemolysis look for cause of bleeding with imaging investigations (endoscopy/ultrasound/CT angio etc). Repeat FBC and do LDH to exclude haemolysis.

Question 10

Describe the blood transfusion targets

Answer 10

Post-CABG patients with active IHD:
–> Transfuse if Hb < 8mg/dL

Everyone else:
–> Transfuse if Hb < 7 mg/dL

Question 11

Why should blood be transfused one unit at a time?

Question 12

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 12

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 13

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 13

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 14

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 14

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 15

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 15

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 16

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 16

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 17

rr

Answer 17

rr

Question 18

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 18

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 18

rr

Answer 18

rr

Question 19

rr

Answer 19

rr

Question 20

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 20

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 22

rr

Answer 22

rr

Question 23

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 23

Heparin
- Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney)

Enoxaparin
- Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin.
- 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 24

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 24

Heparin - Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney) Enoxaparin - Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin. - 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 25

Differentiate the mechanism of action of heparin and enoxaparin

Answer 25

Heparin - Binds antithrombin III receptor --> conformational change --> increasing the receptors availability to its normal ligands: Factor Xa and thrombin. This leads to increased activity of antithrombin ---> anticoagulant effect. Enoxaparin - Binds antithrombin III receptor --> conformational change --> increasing the receptors availability to its normal ligands: Factor Xa (BUT NOT thrombin). This leads to increased activity of antithrombin ---> anticoagulant effect.

Question 26

Compare the adverse effects of heparin versus enoxaparin

Answer 26

Heparin - Bleeding (higher risk than clexane) - Heparin Induced Thrombocytopaenia (HIT) - osteopaenia - mineralocorticoid deficiency - Alopecia - LFT derangement Enoxaparin - Much lower risk of HIT

Question 27

ICU blood glucose targets

Answer 27

Are arbitrary but AVOID hypoglycaemia ! - HbA1C < 7% HGT: 8 - 12 - HbA1C > 7 % HGT: 10 - 14

Question 28

List the benefits of enteral vs parenteral nutrition

Answer 28

1. Maintains gut integrity (prevent bacterial translocation into bloodstream) 2. Prevent ileus 3. Reduce stress ulcers 4. Prevent malnutrition 5. Avoid starvation ketoacidosis

Question 29

What are the legitimate contraindications to enteral feeds

Answer 29

1. GI catastrophe - Obstruction / perforation / mesenteric ischaemia / major UGIB (NB pancreatitis is not a C/I to enteral feeds) No evidence for bowel sounds. waste of time to listen./

Question 30

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 30

Heparin - Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney) Enoxaparin - Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin. - 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 30

Differentiate the mechanism of action of heparin and enoxaparin

Answer 30

Heparin - Binds antithrombin III receptor --> conformational change --> increasing the receptors availability to its normal ligands: Factor Xa and thrombin. This leads to increased activity of antithrombin ---> anticoagulant effect. Enoxaparin - Binds antithrombin III receptor --> conformational change --> increasing the receptors availability to its normal ligands: Factor Xa (BUT NOT thrombin). This leads to increased activity of antithrombin ---> anticoagulant effect.

Question 30

When should a post-pyloric small bore soft feeding tube indicated?

Answer 30

1. Gastroparesis ± vomiting 2. Prolonged NG feeds (more comfortable) --> e.g. hepatic encaphalopathy/TBI - when it is NB to maintain gut access after extubation.

Question 31

Compare the adverse effects of heparin versus enoxaparin

Answer 31

Heparin - Bleeding (higher risk than clexane) - Heparin Induced Thrombocytopaenia (HIT) - osteopaenia - mineralocorticoid deficiency - Alopecia - LFT derangement Enoxaparin - Much lower risk of HIT

Question 32

What is the downside of a post-pyloric small bore soft feeding tube

Answer 32

It cannot be used to empty the stomach before extubation

Question 33

Differentiate the mechanism of action of heparin and enoxaparin

Answer 33

Heparin - Binds antithrombin III receptor --> conformational change --> increasing the receptors availability to its normal ligands: Factor Xa and thrombin. This leads to increased activity of antithrombin ---> anticoagulant effect. Enoxaparin - Binds antithrombin III receptor --> conformational change --> increasing the receptors availability to its normal ligands: Factor Xa (BUT NOT thrombin). This leads to increased activity of antithrombin ---> anticoagulant effect.

Question 33

Differentiate the metabolism of enoxaparin and unfractionated heparin

Answer 33

Heparin - Sequestered into reticuloendothelial cells, gradually degraded into inactive metabolites (these are then cleared by the kidney) Enoxaparin - Metabolised in liver via desulfation and depolymerization to lower molecular weight fragments which are less potent than enoxaparin. - 40% of active and inactive fragments are excreted renally which is why this drug is not suited to patients with GFR < 30.

Question 34

Compare the adverse effects of heparin versus enoxaparin

Answer 34

Heparin - Bleeding (higher risk than clexane) - Heparin Induced Thrombocytopaenia (HIT) - osteopaenia - mineralocorticoid deficiency - Alopecia - LFT derangement Enoxaparin - Much lower risk of HIT