Supportive care in ICU Flashcards
Summarise the choice of agent and dosing of prophylactic anticoagulation in the ICU for weight and renal function.
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)
In which patients should anti-Xa levels be monitored?
- Unusual weight
- Pregnancy
- Borderline renal function
What does a light blue top phlebotomy blood sample tube contain and how does this prevent coagulation of blood in the tube
2.7 mls of 3.2% Sodium Citrate
It sequesters Calcium from blood preventing coagulation
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
IT should be sampled 4 hours after the 3rd dose and the target level is 0.3 - 0.5 IU/ml
List the non-pharmacological measures of GI prophylaxis in the ICU
- Stop aspirin if not indicated
- No NSAIDS in ICU
- Enteral nutrition preferable whenever possible
In which ICU patients is GI prophylaxis indicated
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
What are the benefits of PPI over H2 receptor antagonists?
- PPI greater efficacy
- PPI lower risk of delirium
- C.Difficile/Pneumonia concern recently debunked by SUP-ICU trial
What is ICU haemoglobin drift?
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
Describe your initial evaluation and investigation of acutely falling Hb
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.
Describe the blood transfusion targets
Post-CABG patients with active IHD:
–> Transfuse if Hb < 8mg/dL
Everyone else:
–> Transfuse if Hb < 7 mg/dL
Why should blood be transfused one unit at a time?
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
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Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
rr
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rr
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Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
rr
rr
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the mechanism of action of heparin and enoxaparin
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.
Compare the adverse effects of heparin versus enoxaparin
Heparin
- Bleeding (higher risk than clexane)
- Heparin Induced Thrombocytopaenia (HIT)
- osteopaenia
- mineralocorticoid deficiency
- Alopecia
- LFT derangement
Enoxaparin
- Much lower risk of HIT
ICU blood glucose targets
Are arbitrary but AVOID hypoglycaemia !
- HbA1C < 7% HGT: 8 - 12
- HbA1C > 7 % HGT: 10 - 14
List the benefits of enteral vs parenteral nutrition
- Maintains gut integrity (prevent bacterial translocation into bloodstream)
- Prevent ileus
- Reduce stress ulcers
- Prevent malnutrition
- Avoid starvation ketoacidosis
What are the legitimate contraindications to enteral feeds
- 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./
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Differentiate the mechanism of action of heparin and enoxaparin
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.
When should a post-pyloric small bore soft feeding tube indicated?
- Gastroparesis ± vomiting
- Prolonged NG feeds (more comfortable)
–> e.g. hepatic encaphalopathy/TBI - when it is NB to maintain gut access after extubation.
Compare the adverse effects of heparin versus enoxaparin
Heparin
- Bleeding (higher risk than clexane)
- Heparin Induced Thrombocytopaenia (HIT)
- osteopaenia
- mineralocorticoid deficiency
- Alopecia
- LFT derangement
Enoxaparin
- Much lower risk of HIT
What is the downside of a post-pyloric small bore soft feeding tube
It cannot be used to empty the stomach before extubation
Differentiate the mechanism of action of heparin and enoxaparin
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.
Differentiate the metabolism of enoxaparin and unfractionated heparin
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.
Compare the adverse effects of heparin versus enoxaparin
Heparin
- Bleeding (higher risk than clexane)
- Heparin Induced Thrombocytopaenia (HIT)
- osteopaenia
- mineralocorticoid deficiency
- Alopecia
- LFT derangement
Enoxaparin
- Much lower risk of HIT
