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Intensive Care > Supportive care in ICU > Flashcards

Supportive care in ICU Flashcards

1
Q

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

A

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)

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2
Q

In which patients should anti-Xa levels be monitored?

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

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

A

2.7 mls of 3.2% Sodium Citrate

It sequesters Calcium from blood preventing coagulation

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4
Q

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

A

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

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5
Q

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

A
  1. Stop aspirin if not indicated
  2. No NSAIDS in ICU
  3. Enteral nutrition preferable whenever possible
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6
Q

In which ICU patients is GI prophylaxis indicated

A

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

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7
Q

What are the benefits of PPI over H2 receptor antagonists?

A
  1. PPI greater efficacy
  2. PPI lower risk of delirium
  3. C.Difficile/Pneumonia concern recently debunked by SUP-ICU trial
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8
Q

What is ICU haemoglobin drift?

A

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

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9
Q

Describe your initial evaluation and investigation of acutely falling Hb

A

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.

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10
Q

Describe the blood transfusion targets

A

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

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

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11
Q

Why should blood be transfused one unit at a time?

A
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12
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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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13
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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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14
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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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15
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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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16
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

17
Q

rr

A

rr

18
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

18
Q

rr

A

rr

19
Q

rr

A

rr

20
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

21
Q
A
22
Q

rr

A

rr

23
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

24
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

25
Q

Differentiate the mechanism of action of heparin and enoxaparin

A

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.

26
Q

Compare the adverse effects of heparin versus enoxaparin

A

Heparin
- Bleeding (higher risk than clexane)
- Heparin Induced Thrombocytopaenia (HIT)

  • osteopaenia
  • mineralocorticoid deficiency
  • Alopecia
  • LFT derangement

Enoxaparin
- Much lower risk of HIT

27
Q

ICU blood glucose targets

A

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

28
Q

List the benefits of enteral vs parenteral nutrition

A
  1. Maintains gut integrity (prevent bacterial translocation into bloodstream)
  2. Prevent ileus
  3. Reduce stress ulcers
  4. Prevent malnutrition
  5. Avoid starvation ketoacidosis
29
Q

What are the legitimate contraindications to enteral feeds

A
  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./

30
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

30
Q

Differentiate the mechanism of action of heparin and enoxaparin

A

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.

30
Q

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

A
  1. Gastroparesis ± vomiting
  2. Prolonged NG feeds (more comfortable)
    –> e.g. hepatic encaphalopathy/TBI - when it is NB to maintain gut access after extubation.
31
Q

Compare the adverse effects of heparin versus enoxaparin

A

Heparin
- Bleeding (higher risk than clexane)
- Heparin Induced Thrombocytopaenia (HIT)

  • osteopaenia
  • mineralocorticoid deficiency
  • Alopecia
  • LFT derangement

Enoxaparin
- Much lower risk of HIT

32
Q

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

A

It cannot be used to empty the stomach before extubation

33
Q

Differentiate the mechanism of action of heparin and enoxaparin

A

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.

33
Q

Differentiate the metabolism of enoxaparin and unfractionated heparin

A

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.

34
Q
A
34
Q

Compare the adverse effects of heparin versus enoxaparin

A

Heparin
- Bleeding (higher risk than clexane)
- Heparin Induced Thrombocytopaenia (HIT)

  • osteopaenia
  • mineralocorticoid deficiency
  • Alopecia
  • LFT derangement

Enoxaparin
- Much lower risk of HIT

Intensive Care (22 decks)

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