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Fellowship revision > Blood management > Flashcards

Blood management Flashcards

1
Q

What’s the cutoff ferritin for Fe deficiency (if CRP normal)? What to then do?

A

<30microg/L

Evaluate possible causes of Fe deficiency- discuss with gastroenterology re: GI Ix

Commence Fe therapy

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2
Q

How do we interpret a ferritin 30-100microg/L if the CRP elevated?

A

Possible Fe deficiency- look at transferrin saturation- if it’s <20%, consistent with absolute Fe deficiency

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3
Q

What is aprotinin?

A

Bovine pancreatic trypsin inhibitor which slows fibrinolysis, reduces transfusion, blood loss & re-OT for bleeding

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4
Q

What are safety concerns with aprotinin?

A

renal failure, MI, HF, stroke, encephalopathy, mortality

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5
Q

How might desmopressin work for limiting bleeding? What are safety concerns?

A

causes release of vWF antigen from platelets, the protein that carries factor VIII. Risks stroke & mortality.

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6
Q

What is patient blood management?

A

The multimodal, multi-disciplinary, timely application of evidence-based strategies to optimise red cell mass, minimise blood loss and ensure tolerance of anaemia in an effort to improve patient outcome & limit the transfusion of blood products and associated complications.

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7
Q

What are examples of inherited or acquired anaemia?

A

haemoglobinopathy, myelodysplastic syndrome, autoimmune haemolytic anaemia

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8
Q

In what cases is pre-op Hb necessary?

A

> 10% chance of needing transfusion or >500mL blood loss or if suspect anaemia (eg. CKD), unless minor procedure

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9
Q

What blood tests are necessary prior to OT for pts on anticoagulants?

A

INR for warfarin, Creatinine for dabigatran or direct factor Xa inhibitors

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10
Q

How long does it take to correct Fe deficiency with PO Fe supplementation?

A

2-4/52 for partial correction, 6-8/52 for full correction

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11
Q

How long before planned OT is Mx of Fe deficiency w PO Fe appropriate?

A

4-6/52, need IV if <4-6/52 pre-OT or if pt can’t tolerate PO Fe or if they don’t have a response (eg. poor absorption)

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12
Q

Does IV Fe lower transfusion rate?

A

Yes- eg. Spahn et al Lancet 2019- even day before OT reduces transfusion rate (along with EPO)- for cardiac surgery

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13
Q

How long does IV Fe take to work?

A

Ferritin [] peaks @ 7-9/7, Hb rises within 2/52

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14
Q

What needs to be administered with EPO? why?

A

Supplemental Fe, to avoid functional Fe deficiency which can happen w increased erythropoiesis

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15
Q

In which pts could EPO be considered?

A

If anaemia of chronic disease/inflammation if EBL >500mL & Hb <120, or if card surg & Hb <130g/L, could consider in a pt who refuses blood transfusion

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16
Q

How soon & how should EPO be given?

A

Ideally start 3/52 pre-op (still possible benefit if <3/52 pre-op), 40,000 units subcut or 300-600u/kg weekly along with supplemental Fe to avoid functional Fe deficiency

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17
Q

What are potential adverse effects of EPO?

A

VTE (but prophylaxis should protect), HTN (avoid if severe uncontrolled HTN), Ca progression

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18
Q

What is an issue for pts on a renal transplant waiting list who receive a blood transfusion?

A

Transfusion-induced sensitisation may increase Ab levels & reduce likelihood of successful renal transplantation

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19
Q

What are some problems w pre-op autologous blood donation?

A

Wastage of PAD units, inducing anaemia, cost & inconvenience w collection & storage

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20
Q

What are some treatments that can be given to pts with immune thrombocytopenia pre-op?

A

IVIG, dexamethasone, splenectomy

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21
Q

What’s a treatment that can be given to a patient with liver disease & significant thrombocytopenia undergoing a procedure with high bleeding risk?

A

Thrombopoietin receptor agonist (TPO-RA)

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22
Q

What can uraemia do to platelets?

A

Make them dysfunctional- usually INCREASES bleeding risk but some are hyper coagulable

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23
Q

What are some herbal medications which increase bleeding?

A

Ginkgo bilboa, garlic

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24
Q

What are some conditions associated with vitamin K deficiency?

A

reduced PO intake, malabsorption (eg. CF, cholestasis)

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25
Q

What’s the significance of vitamin K deficiency & bleeding? how correct?

A

Slows the prothrombin time. Rx w vitamin K (1-2 days to be effective), prothrombin complex concentrated if emergency OT w sig bleeding risk

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26
Q

Why does concomitant Vit K need to be given w PCC?

A

Half-life of PCCs is short

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27
Q

While we’d discuss periop thrombocytopaenia with surgeons & haematology, what are GENERALLY the plt count thresholds for plt transfusion?

A

<50x10^9/L but some cases (eg. neurological, ocular) it may be <100x10^9/L. For minor invasive procedures (eg. CVC placement), threshold <20x10^9/L

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28
Q

What are some adverse effects of hypothermia on coagulation?

A

impairs platelet aggregation, reduces activity of the enzymes of the coagulation cascade, reducing clot formation, increasing periop blood loss & need for transfusion

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29
Q

What may 1 degree c of hypothermia do to blood loss?

A

Increase it by 20%

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30
Q

For which products should a blood warmer be used?

A

Thawed or fridge-temp products to avoid hypothermia (<36deg c) which may precipitate coagulopathy, bleeding & extra transfusions

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31
Q

In which procedures are benefits of cell salvage most significant?

A

Blood loss >=1000mL

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32
Q

In which pts could ANH be considered?

A

Normal initial Hb & EBL >=1000mL- safest in healthy young pts but can use for others. may be an option for JW if blood in closed circuit with continuous flow

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33
Q

What are example procedures where haemostatic agents (usually antifibrinolytic agents) may be used?

A

Cardiac surgery, ortho surg, other OTs with sig blood loss or consumptive coagulopathy

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34
Q

In which cases are individual clotting factors, PCCs or DDAVP generally given?

A

specific clotting factor deficiencies, uraemia or anticoagulants needing immediate reversal

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35
Q

In which pts should TxA be dose-reduced?

A

end-stage renal disease or mod-severe renal insufficiency

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36
Q

What are some adverse effects with TxA?

A

potential prothrombotic BUT this perceived risk has been weakened in large meta-analysis (2021, 125,550 pts)- no ass’n with overall thromboembolic events, even in cancer pts. Risk seizures after cardiac surgery, dose-related. Hypotension & arrhythmia if rapid injection.

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37
Q

Where does fib conc come from?

A

human pooled plasma, virally-inactivated

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38
Q

Which factor are the 3-factor PCCs missing?

A

VII

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39
Q

What’s the benefit of PCCs over FFP?

A

rapid administration in a small volume, more rapid reversal of anticoagulant effect & avoiding volume overload & transfusion reactions

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40
Q

What’s the indication for recombinant activated factor VII?

A

prevention of surgical bleeding in pts w haemophilia who’ve developed an inhibitor to factor VIII or factor IX

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41
Q

What’s the dosing of rFVIIa?

A

cautious, since optimal dosing for off-label use unknown- start w small incremental doses 10-30mcg/kg every 15 mins to total 90mcg/kg, if massive coagulopathic bleeding could go straight to 90mcg/kg

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42
Q

What are some risks w rVIIa?

A

arterial thromboembolic events, esp if ICH or card surg. Off-label use incr M&M (eg. renal failure) esp in older pts w higher doses.

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43
Q

What does DDAVP do?

A

causes vWF, factor VIII & tPA from plts & endothelial cells

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44
Q

Which patients may benefit from DDAVP?

A

von wile brand disease or mild haemophilia A if shown a positive response to this drug previously, or if sig bleeding if pts have acquired plt defects due to uraemia or acquired von Willebrand syndrome (eg. due to chronic AS or LVAD)

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45
Q

What are some adverse events of DDAVP?

A

hypo or hyperT, flushing, fluid overload, hyponatremia (which may cause seizures if close attention to free water restriction not given)

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46
Q

What does the fibrinogen assay of the ROTEM say?

A

it tells us what happens if remove the plt effect- so looking only @ the fibrinogen effect- if the fibrinogen normal but max amplitude on others low, likely a plt problem

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47
Q

What may be the transfusion threshold for IHD pts?

A

90g/L

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48
Q

What are some conditions which may be associated with anaemia?

A

malignancy
bone marrow failure
renal failure
liver failure
thyroid disease
malabsorption/malnutrition (eg. gastrectomy)
ETOH excess

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49
Q

Top 10 considerations for anaemia?

A

symptoms of anaemia (esp IHD-related)
cause of anaemia (eg. malignancy hence 4 M’s, antiplatelets/anticoagulants)
bleeding symptoms
religious or other objection to receiving blood products
PATIENT BLOOD MANAGEMENT (aim to minimise blood loss (TxA, normothermia, euvolaemia) & reduce rate of transfusion & associated complications- optimise red cell mass, minimise blood loss, optimise physiological tolerance of anaemia), multi-D
Consider cell salvage

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50
Q

What’s Fe deficiency anaemia?

A

ferritin <30microg/L OR 30-100microg/L with raised CRP

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51
Q

Within what timeframe preop is a Fe infusion (vs po Fe) required)?

A

If OT within 2/52. If have given PO Fe, review in 4-6wks.

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52
Q

problems with IM Fe?

A

skin discolouration

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53
Q

In which pts with anaemia could EPO/erythropoiesis stimulating agent be considered?

A

concomitant CKD

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54
Q

What’s generally my transfusion threshold?

A

Variable depends on pt & surgical factors- often 70g/L, no IHD & otherwise asymptomatic & not coming into major surgery

55
Q

Whats normal haematocrit?
At what haematocrit does DO2 usually remain constant? What physiological changes occur with further drops in haematocrit?

A

40-50% for men, 35-45% women
30-45%
As haematocrit drops, CO increases (up to 180% baseline as Hct nears 20%)

56
Q

What are the 4 primary mechanisms by which the body compensates for anaemia (where blood volume is maintained)?

A
  1. increase in cardiac output- SVR is determined by vascular tone & viscosity- as Hct lowers, DO2 is maintained with Hct 30-45 but as Hct approaches 20%, CO increases up to 180% of baseline
  2. Redistribution of CO to tissues with higher extraction ratio (eg. brain, heart)- the coronary circulation can increase flow up to 600% of baseline- risk myocardial ischaemia when the heart reaches a point it can not increase CO or coronary blood flow
  3. Increase in O2 extraction- once Hct reaches <25%, some tissue beds increase their O2 extraction ratio, this increases total body O2 extraction & decreases mixed venous O2 sats. Some organs (eg. brain, heart) already have high extraction ratio but kidney, skeletal muscle & skin compensate in this manner.
  4. R) shift HbO2 dissociation curve- in presence of 2,3-DPG (P50 of Hb at 37deg C & pH 7.4 is 27mmHg.
57
Q

What’s transferrin saturation cutoff?

A

20%

58
Q

what are some useful labs in anaemia along with Hb?

A

MCV
blood film
Fe
ferritin
CRP
renal function
transferrin saturation
B12
folate
haptoglobin (goes down in haemolysis)
LDH (goes up in haemolysis)
platelets, coagulation studies (looking for other coagulopathy)

59
Q

What were the main findings of TRICCSIII (Mazer et al NEJM 2017)?

A

-International multicentre- 73 sites, 19 countries
-5243 subjects with EUROSCORE I of >=6 (mod-high risk of death after card surg) (approx 5000 in ITT & 4860 in per-protocol)
-noninferiority
-randomly assigned to restrictive rbc transfusion threshold (Hb <75g/L intra-or post-op from induction of anaesthesia) or liberal threshold (transfuse if Hb <95g/L in OT or ICU or if <85 in non-ICU ward)
-Primary outcome= composite of death from any cause, MI, stroke, new-onset renal failure w dialysis by hospital discharge or day 28, whichever came first, rbc transfusion= secondary outcome
-PI in 11.4% of restrictive vs 12.5% liberal group, OR 0.9 w Cis crossing 1, p<0.001 for non-inferority, RBC transfusion in 52.3% of restrictive group vs 72.6% in liberal group (OR 0.41)
-Shows that a restrictive (<75g/L) Hb transfusion trigger is noninferior wrt death & majore disability cf a liberal (<95g/L or <85 if non-ICU) strategy in pts @ high risk of mortality from card surg. The outcomes were achieved w fewer units blood being transfused.

60
Q

What were the main findings of the TRICS trial?

A

Randomly assigned 838 critically ill euvolaemic ICU pts with Hb of <90 to a restrictive transfusion strategy (only transfused if Hb <70, maintained 70-90) & liberal (transfused if Hb <100, maintained 100-120).
Similar 30-day mortality across the 2 groups however mortality rates were lower with the restrictive strategy among those less acutely ill (APACHEII<=20) & those <55yo but NOT those with significant cardiac disease.
Concluded that a restrictive transfusion strategy was at least as effective as liberal in critically ill pts, with the exception of those with acute MI or unstable angina.

61
Q

What strategies are used to reduce the risk of antibody-mediated TRALI? Why?

A

only blood or plasma from MALES is used to make plasma components such as FFP & cryoprecipitate.
Only male donors are used for aphaeresis platelets
To eliminate the possibility that a donor has had HLA or HNA antibodies due to pregnancy or transfusion

62
Q

What’s TRIM?

A

Transfusion-related immune modulation. A delayed response following allogenic blood transfusion. Associated with post-op infection risk, cancer recurrence.

63
Q

Is intraoperative cell salvage or allogenic blood transfusion associated with more immune suppression?

A

ABT. therefore, ICS vs ABT may be a strategy to reduce immunosuppression

64
Q

What is intraoperative cell salvage?

A

A blood conservation technique allowing extravasated blood to be collected from the surgical field, anticoagulated, processed & returned to the patient.

65
Q

What’s the processing technique that occurs during intraoperative cell salvage?

A

Centrifuge
Filtering (advanced mesh filter, risk of transmission of bacterial contamination during ICS greatly reduced with the leucodepletion filter)
allows removal of bacteria, debris, clotting factors, heparin, free Hb, fat, malignant cells, bone chips, cement, irrigation solution, coagulants, platelets, FDPs, plasma & some activated factors

66
Q

For which procedures is ICS recommended?

A

Surgical procedures with expected blood loss of >500mL or >10% of the pts estimated blood volume

Pts with low Hb or increased risk factors for bleeding

Pts with multiple antibodies or rare blood groups

Pts refusing donor blood products for ethical/religious or other reasons if undergoing surgery with anticipated blood loss.

Standard equipment for pts experiencing operative massive haemorrhage (must notify the lab that ICS being used & update re: volumes so they can ensure that excessive rbc not given & appropriate products administered)

67
Q

Which procedures/risks are considerations for where cell salvage may be avoided?

A

Risk of bacterial contamination (eg. bowel perforation in trauma)
Cancer surgery where dissemination of malignant cells may be a concern
contraindicated in phaeo

67
Q

Does ICS offer real-time measurement of the Hb in processed cell salvage product?

A

Yes

68
Q

What’s the anticoagulant solution in ICS? Any variation?

A

30,000 IU heparin in 1L 0.9% NaCl
If heparin contraindicated, ACD (acid citrate dextrose)

69
Q

What’s the suction pressure for ICS? why?

A

Generally <150mmHg to reduce rbc haemolysis

70
Q

At what point does the autotransfusionist start processing collected blood?

A

Once 500mL in the reservoir less if clinically indicated

71
Q

What are some adverse complications with which anaemia is adversely associated?

A

infection
thrombosis
morbidity & mortality, exposure to blood transfusion

72
Q

How does the WHO define anaemia?

A

<120g/L women
<130g/L men

also, <110g/L is anaemic in obstetrics

73
Q

Of pts undergoing major elective non-cardiac surgery, what proportion are anaemic pre-op? what proportion of the non-anaemic pts have iron deficiency?

A

1/3
>50%

74
Q

What are some over-arching risks of receiving blood transfusion?

A

mortality
wound infection
sepsis
pneumonia
even a single unit associated with increased risk MACE

75
Q

Is there level 1 evidence suggesting that correcting anaemia improves outcomes & reduces post-op complications?

A

No

76
Q

For how long do erythrocytes remain in the circulation?

A

120 days

77
Q

What proportion of body Fe is stored in Hb?

A

60%

77
Q

What proportion of body Fe is stored in Hb?

A

60%

78
Q

Where is iron absorbed & what are it’s two ionic configurations?

A

Ferrous (Fe++), haem iron, from animal sources, readily absorbed
non-haem Fe (Fe+++), converted into ferrous state by duodenal cytochrome B enzyme to allow active transport intracellularly; ferrous present in legumes, grains, nuts, veggies- vitamin C reduces ferric to ferrous & improves absorption

79
Q

What’s the typical daily Fe intake? how much required for red cell production & cellular function? how do we achieve what we need for Fe homeostasis? What’s the intracellular Fe storage? and how is it transported in the circulation? what happens to levels of this molecule with Fe deficiency?

A

1mg
20-30mg

recycling of Fe- from senescent erythrocytes & exchange of Fe-containning enzymes- predominantly in spleen

Fe stored in macrophages, enterocytes & hepatocytes by binding to ferritin

transferrin= primary Fe transport molecule in the circulation- levels increased in Fe deficiency to incr Fe availability to tissues

80
Q

What’s the role of hepcidin? it’s relation to anaemia of chronic disease?

A

expression unregulated if high Fe concentration AND inflammation- it inhibits ferroportin, blocking absorption of Fe from the gut & release of Fe from macrophages to reduce plasma Fe concentrations.

since hepcidin unregulated in inflammation & cancer (cytokines), extra Fe sequestered in macrophages/enterocytes, contributing to functional Fe deficiency (high ferritin)

81
Q

What’s the main mechanism for anaemia of chronic kidney disease? what’s the role of EPO?

A

deficiency in erythropoietin due to renal parenchymal damage

EPO provides cytoprotection from apoptosis & promotes growth of red cell precursors in bone marrow

81
Q

What’s the main mechanism for anaemia of chronic kidney disease? what’s the role of EPO?

A

deficiency in erythropoietin due to renal parenchymal damage

EPO provides cytoprotection from apoptosis & promotes growth of red cell precursors in bone marrow

82
Q

What are some causes of iron deficiency?

A

GI losses:
colorectal or gastric Ca
peptic ulcer disease
inflammatory bowel disease
NSAIDs

Malabsorption:
coeliac
h. pylori colonisation
post-gastrectomy or bowel resection
interaction with PPIs (raise gastric pH & inhibit reduction of ferric Fe) or food which chelate iron

genetic disorders eg. inappropriately high hepcidin levels

associations with CKD & CCF

83
Q

Which chemotherapy agents are associated with anaemia?

A

platinum-based drugs

84
Q

What’s the aetiology of anaemia in pregnancy?

A

decrease red cell: plasma ratio (dilutional anaemia), iron deficiency near ubiquitous in pregnancy

85
Q

What are causes of megaloblastic (a type of macrocytic) anaemia?

A

Vitamin B12 deficiency (eg. alcoholism, gastric malabsorption, pernicious anaemia the autoimmune impairment of intrinsic factor secretion)
Folate deficiency (coeliac disease, alcoholism, methotrexate or hydroxyurea

86
Q

What are causes of non-megaloblastic microcytic anaemias?

A

myelodysplastic syndromes, hypothyroidism, alcoholism, drugs such as antiretrovirals & anticonvulsants

87
Q

What are the most common haemoglobinopathies?

A

thalassaemias- minor (trait) there may be no or mild anaemia & microcytosis. In major, significant microcytic anaemia & requirement for transfusions
sickle cell anaemia
hereditary spherocytosis: abnormalities in erythrocyte membrane proteins–> spherical red cells, fragile, more susceptible to extravascular haemolysis in spleen
Glucose-6-phosphate deficiency= red cell enzyme disorder. Defects in the hexose-monophosphate pathway predispose to oxidative haemolysis & anaemia.

88
Q

At what ferritin level, in preop pts without anaemia, could we consider iron therapy?

A

If the anticipated postop Hb decrease is >=30g/L

If the ferritin suggests Fe deficiency (<30microg/L), determine cause & need for GI investigations

89
Q

What to do if the Ferritin is 30-100microg/L?

A

Look at the CRP. If normal, the pt isn’t Fe deficient
If the CRP is raised, there’s possible Fe deficiency
Consider clinical context- consider Haematology advice or, if CKD present, renal advice
Discuss with gastroenterologist re: GI Ix & timing in relation to surgery
Commence Fe therapy

90
Q

What next steps if pt has anaemia & ferritin >100microg/L?

A

review renal function, MCV, MCH, B12, folate, reticulocyte count & blood film
LFTs & thyroid
haematology advice or, if CKD, renal advice

91
Q

What red cell morphology characterises Fe deficiency anaemia? which differentials may present this way?

A

microcytic (MCV <80fL), hypo chromic (MCH <27pg/cell)- similar picture in thalassaemia, ACD, sideroblastic anaemia

92
Q

What are some normocytic anaemias?

A

ACD, renal failure, haemolysis, mixed micro- & macrocytic picture

93
Q

What are some macrocytic (MCV >100fL) anaemias?

A

megaloblastic: B12 deficiency (pernicious anaemia, alcoholism, malabsorption), folate deficiency (coeliac, alcoholism, methotrexate, hydroxyurea)
non-megaloblastic: myelodysplastic syndromes, hypothyroidism, alcoholism, antiretrovirals & anticonvulsants

94
Q

While MCV & MCH are useful for anaemia Dx, are they helpful in the acute setting to monitor response to Rx?

A

No

95
Q

What’s the key iron storage protein & most specific lab test to correlate with total body Fe stores? What are the diagnoses with different ferritin & Hb levels?

A

Ferritin

Ferritin <30microg/L with anaemia= Fe deficiency anaemia
normal Hb with ferritin <30microg/L= absolute iron deficiency
Plasma ferritin <100microg/L is diagnostic as insufficient Fe stores for major surgery

96
Q

What’s a good therapeutic ferritin target for Fe supplementation in pts with CKD on haemodialysis?

A

> 200microg/L

97
Q

What does low transferrin saturation, in the presence of inflammation, with ferritin >100microg/L suggest?

A

consistent with functional Fe deficiency- total body Fe stores normal but erythropoiesis restricted by unavailability of Fe in the marrow

97
Q

What does low transferrin saturation, in the presence of inflammation, with ferritin >100microg/L suggest?

A

consistent with functional Fe deficiency- total body Fe stores normal but erythropoiesis restricted by unavailability of Fe in the marrow

98
Q

What are reticulocytes & what does reticulocyte count indicate?

A

precursors to erythrocytes
released from bone marrow erythroblasts

low reticulocyte count reflects inadequate bone marrow erythropoietic activity

high reticulocyte count indicates red cell degradation or loss (eg. haemolysis or haemorrhage) and also signifies adequate response to haematinic Rx

99
Q

What may reticulocyte Hb be useful for?

A

Measures the adequacy of Fe incorporation into the reticulocyte, values of >29pg signify adequate Fe stores.

Useful for predicting an adequate response to IV Fe; levels rise acutely in the first 72hrs post IV Fe infusion.

100
Q

In which conditions may RCDW be increased?

A

Fe deficiency anaemia
Folate & vitamin B12 deficiencies
may reflect recent haematinic replacement with bone marrow response

101
Q

What are some of the morphological features which may be commented on with the blood film?

A

size
red cell distribution width (wide suggests IDA)

poikilocytosis:
-fragmentation may occur with TTP or DIC
-sickle cells
-target cells (liver disease, thalassaemia)
-spiculated red cells (uraemia or liver disease)
-spherocytes (autoimmune haemolytic anaemia or hereditary sphrocytosis)

red cell inclusions:
-nucleated red cells are abnormal outside of neonates & pregnancy- are associated with haemolysis, marrow stress & infiltration
-may occur with rbc parasites (eg. malaria)

changes in other cell lines along with anaemia:
-elevated or abnormal lymphocytes an occur with lymphoproliferative disorders
-co-existing neutropenia & thrombocytopenia may occur with infection, medications, marrow disorders
bone marrow biopsy useful diagnostic modality
Where diagnosis of Fe deficiency is uncertain, presence/absence of Fe on Prussian blue stain= gold standard for diagnosis. not routinely performed due to cost & availability.

102
Q

What is intraoperative cell salvage?

A

the process of harvesting a patient’s red cells shed during surgery, processing & preparing them for safe return to the patient’s own circulation as an autologous red cell transfusion during or immediately after surgery.

103
Q

When should ICS be considered?

A

cases with EBL >500mL

104
Q

what are the contents of the product delivered from cell salvage?

A

red cells suspended in saline.
platelets & coagulation factors removed.

105
Q

are sepsis or malignancy absolute contraindications to cell salvage?

A

no

106
Q

steps for cell salvage?

A

Ensure transfusion options have been discussed with pt/consent obtained, ICS incorporated into surgical plan & discussed as part of WHO surgical team brief.

Ensure staff available who are qualified to manage ICS (surgical, anaesthetic, nursing, including anaes management of complications)

  1. COLLECTION:

collect blood- separate bespoke suction to reduce mechanical damage to red cells but optimise aspiration- suction pressure usually -100 to -150mmHg.
can use swab washings if they are expected to collect significant blood (soak in saline licensed for infusion, with UFH)
aim to optimise viable red cells & limit contaminants

combine with anticoagulant (heparin 5000units/L or citrate-based preparation such as anticoagulant citrate dextrose solution-A)

filter (usually a 150micron filter), there should be an appropriate viral filter applied to the suction system for ICS

  1. PROCESSING:

separate constituents by density & mass (high speed centrifugation up to 5600rpm)

wash erythrocytes in normal saline, after the removal of many contaminants/particulate material

the separation may be either:
-fixed bowl (washing only begins when machine detects a predetermined volume of red cells)
-variable volume disc (allows washing @ variable volumes with a fixed haematocrit, useful when blood collection is slow & volume small)
-continuous rotary (removal of supernatant, concentration & washing of red cells is continuous & can be done with small volumes of blood loss)

  1. REINFUSION:

packed red cells suspended in normal saline with haematocrit approx 60%

Certain filters can be used if suspected contamination eg. LDFs for cancer surgery or if concern over heavy bacterial contamination.

label carefully.

should occur within 6hrs of the first collection.

DON’T reinfuse under pressure- risks air embolism & bag rupture.

flush lines before administer as certain drugs (eg. IV paracetamol) may cause red cells to clump.

107
Q

What are ways in which red cells may be damaged from collection to final presentation?

A

vulnerable to damage from exposure to hypotonic solutions, agents that may damage the red cell membrane, substances that may promote coagulation

at risk of mechanical trauma when aspirated from the surgical site (particularly if skimmed from shallow collections of blood or if narrow-bore suction catheters used)

108
Q

How does the deformability & [] of 2,3DPG & ATP vary with salvaged vs allogenic red cells? clinical implications?

A

deformability/elliptical profiles maintained & 2,3DPG & ATP concentrations higher in salvaged cells - so, tissue DO2 better with salvaged cells.
O2 carriage & deformability degrade with time- early reinfusion is supported by evidence- reduction in function is most significant >=6hrs after collection.

109
Q

Do salvaged red cells initiate a negative immunomodulatory effect when infused in the periop period?

A

No, IF INFUSED PERIOPERATIVELY- stored autologous cells, when reinfused, will produce immune modulation similar to that with allogenic red cell transfusion.

110
Q

What are leucocyte depletion filters (LDFs), when are they indicated and what are some issues with them?

A

an affinity filter, removes leucocytes, lipids, bacteria & tumour cells

commonly used in cancer surgery or cases where concern re: heavy bacterial contamination

they require priming & significantly reduce rate of reinfusion (40-100mL/min), have a maximum flow capacity of 450mL before requiring replacement

reinfusion hypotension is a well-recognised complication; may be profound when LDFs used & squeezing the LDF or attempting to force rbc flow under pressure may worsen this problem

111
Q

Aside from the leucocyte depletion filter (an affinity filter removing leucocytes, tumor cells, lipids, bacteria), what are other types of filters at the time of reinfusion with ICS?

A

lipid reduction filter- 40 micron: lipids, C3a, some leucocytes, microaggregates
microaggregate filter- 40 micron: blood component microaggregates & non-blood particulate matter
standard blood administration set- 200micron: blood component and non-blood particulate matter

112
Q

What are advantages of ICS?

A

Improved oxygen-carrying capacity cf allogenic blood (if administered within 6hrs)

provides the anaesthetist with a means of volume expansion that is viscous & oncotically active

Avoids the immunological risks of allogenic transfusion, eg:
-human error- wrong b blood
-antibody formation is a particular concern with transfusion, particularly pts of childbearing potential. Sensitisation to antigens such as kell, Duffy or lutheran which aren’t routinely screened in donor blood samples (& [] of these antibodies in the recipient’s blood may reduce over time) may occur & complicate future cross-matching or risk future delayed haemolytic reaction, or may contribute to haemolytic disease of fetes & newborn if a pt of childbearing age is sensitised in this way.
-TRIM which may increase risk of postp infection or tumour or metastatic growth

Avoids the costs associated with donor blood transfusions and helps preserve this finite resource

Given the restrictive transfusion triggers relevant to patient blood management principles for allogenic blood transfusions don’t apply, pt may have better postop Hb & tissue O2 delivery which may
-reduce allogenic blood transfusion on wards (cost, labour, risks of adverse reaction)
-reduce risk postop infections
-promote early mobilisation
-promote early hospital discharge

may be more acceptable to patients with certain religious/cultural beliefs surrounding donor blood; may make larger surgeries possible/safer for these pts

113
Q

disadvantages of ICS?

A

patient selection is important (not appropriate for all situations of intraop blood loss)

requires trained & committed surgical, anaesthetic & nursing staff (eg. surgical & scrub team must be trained to aspirate blood & process swabs effectively)

more labour intensive than allogenic transfusion

initial financial investment in training, machinery & disposables (may later be offset against benefits)

re-infusion hypotension may be marked (?due to bradykinin or acute hypocalcaemia)

processing requires a few minutes- when transfusion time-critical, production may be increased with higher spin rates & reduced wash cycles but may be at the expense of greater red cell loss.

may require replacement of calcium, platelets & clotting factors during times of high blood loss as amounts in salvaged blood are negligible

114
Q

What substances must NOT be aspirated during ICS collection?

A

antibiotics not licensed for IV use

iodine skin prep

chlorhex

topical clotting agents

fibrin-based glues

unset ortho cement

these agents may cause CV collapse, red cell lysis or initiate a systemic response

should avoid aspiration of urine or feral material

115
Q

Why is malignancy no longer an absolute contraindication for ICS? clinical approach?

A

may effectively reduce the [] of malignant cells with prudent operative suction & LDFs

the [] of malignant cells in the re-infused blood may be < that already in the pts circulation

very few circulating malignant cells have metastatic potential

avoiding donor transfusion may have beneficial effects on local recurrence or distance mets since there’s dose-dependent immunosuppression w donor blood

ICS is actually recommended for cystectomy & radical prostatectomy for cancer by the NICE & it’s widely used for nephrectomy

have multi-D discussion with pt, surgeon- re: risks/benefits- if the salvaged blood not required for CV stability or to avoid allogenic transfusion, consider not reinfusing.

116
Q

Why is sepsis not an absolute contraindication to ICS?

A

LDF significantly reduces bacterial [] in reinfused product

no conclusive evidence that ICS worsens sepsis, prognosis or associated complications when ICS is used in contaminated fields

prophylactic broad-spectrum ABx may limit periop sepsis when ICS used

117
Q

What’s the approach to ICS in pts with haemoglobinopathies?

A

They are a relative contraindication (eg. sickle cell, thalassaemia) due to the potential for red cell haemolysis or Hb precipitation with fragile rbcs.

pts with sickle cell are, however, challenging to X-match & are at high risk of becoming sensitised to antigens in donor products; exchange transfusion (which reduces the proportion of sickle cells & the incidence of periop sickle cell crisis) may be performed & then ICS considered on weighing risks:benefits BUT such complex decisions are made on pt-specific basis in discussion with regional sickle cell haematology service.

118
Q

Did the SALVO trial (RCT of ICS during CS in women & @ high risk haemorrhage) find statistically significant reduction in number of donor blood transfusion when ICS was used? What should be the approach to consideration of ICS in obstetrics? how about concern re: AFE? and RhD sensitisation?

A

No

not for routine use in elective or Emerg CS, do consider risks:benefits for women at high risk of significant blood loss, those who have declined donor blood transfusion or who have anaemia pre-op & have patient-centred multi-D discussion.

No proven case of AFE secondary to ICS has been identified, need for LDF usage has been questioned.

There is evidence of increased risk of maternal exposure to foetal blood when ICS has been used so RhD-negative women who are previously non-sensitised & have given birth to a RhD-positive baby should receive 500IU anti-D within 72hrs of ICS reinfusions.

119
Q

What are the considerations of using ICS for major trauma & orthopaedics?

A

significantly reduces the need for donor blood transfusion, esp major pelvic & spinal surgery, major trauma & major joint revision.

MUST BE PAUSED while bone cement being applied, resume once cement set.

use caution when revising metalwork as not all metal fragments are removed by a 40micron filter, with prudent irrigation & suction it can still be used.

should have 24/7 ICS availability for major trauma centres, most benefit is in Tx, abdo & pelvic penetrating trauma.

120
Q

Should ICS be used for all cardiac surgery? why? when should it be used?

A

yes. major blood loss during cardiac surgery is common, esp with coagulopathy & platelet dysfunction from cardiac bypass.

ICS in cardiac surgery decreases allogenic blood transfusion by up to 40%.

Restrict ICS to before & after bypass (using it during bypass vs direct suction into cardiotomy reserve air depletes clotting factors & platelets, increasing coagulopathy.

121
Q

Should TxA be used where ICS is used?

A

Yes, according to NICE guidelines, unless contraindications

122
Q

Steps if reinfusion hypotension occurs?

A

temporarily stop reinfusion

exclude other causes

standard supportive measures (incr preload, use vasoactive drugs)

consider restarting infusion @ slower rate

123
Q

How may JW views on ICS vary?

A

some will refuse
some permit closed system
some permit use of non-complete circuit
some may refuse blood from swab washing

124
Q

absolute contraindications to ICS?

A

pt refusal

phaeochromocytoma

lack of trained staff to collect or process the aspirate

must not aspirate:
antibiotics not licensed for IV use
iodine skin prep
chlorhexidine
topical clotting agents
fibrin-based glues
unset ortho cement
(once adequately irrigated can resume again)

relative CI: haemoglobinopathy
can be used in malignancy & sepsis on case-by-case basis, with LDF

trauma with perforated bowel= risk of contamination of aspirated blood with bowel contents so infection or tumour= relative contraindication

125
Q

how much anti-D immunoglobulin should be given to a pregnant woman who is RhD negative undergoing a potentially sensitising event?

A

250IU if <20 wks (suffices for 2mL foetal blood)

if >=20 wks, need to quantify antigen exposure & dose

126
Q

What are the acute immunologic transfusion reactions?

A
  1. Haemolytic transfusion reactions:
    a) ABO incompatability (complement, IgM-mediated), intravascular haemolysis
    b) Rh incompatability (IgG), extravascular haemolysis
    urticaria, flush, chest pain, dyspnoeas, rigors, bleeding, shock, jaundice, haemoglobinuria, AKI, DIC, low haptoglobin, high LDH, clerical error.
  2. TRALI (1/10,000): thought due to HLA antibodies in transfused product vs recipients antigens. Pulm infiltrates, hypoxaemia, hypotension, fever.
  3. Febrile non-haemolytic (1/300): within 4hrs, thought due to reaction from the ABs to donor white cells/plts in transfused product vs allo-antibodies in pt from pregnancy or prev transfusion. Or may be due to cytokines in the stored blood (leucodepletion lessens this). Dx of exclusion (AHTR, TRALI)
  4. Anaphylaxis (1/40,000): more common in pts w IgA def, ABs to plasma proteins (more common w FFP)
127
Q

Chronic immunologic?

A
  1. Delayed haemolytic transfusion reactions; minor antibodies
  2. Transfusion related graft vs host disease (donor lymphocytes deposit in recipient skin/liver/GIT–> rash, hepatitis, diarrhoea)
  3. TRIM: may be related to cap permeability; Incr LoS, infection, reduced survival, Ca recurrence
  4. Allo-immunisaion to HLA or red cell antigens; impacts risk of future transfusions
  5. Post-transfusion purpura; consumptive thromobcytopenia, generaly 1 wk after transfusion, self-limits 4-6wks
128
Q

Acute non-immun

A

TACO: most common, in up to 1% of pts receiving transfusion, usually iatrogenic, Hx CVD or older age, large volume; suggested by hypoxial, HTN, high cardiac filling pressures, high NT-ProBNP & infiltrate on CXR & response to diuretics.

infectious diseases: reduced incidence w manufacturing/lab processes, blood tested Hep B, C, HIV, human T-lymphotrophic viruses, syphillis. Hep B 1:700k, Hep C 1:2.7 million HIV 1:5 mil, malaria 1:5-10 million. variant CJD hasn’t been reported in Oz

Non-immune mediated haemolysis

Air embolism (200-300mL lethal)

Massive transfusion complications

129
Q

Chronic non-immunological

A

Fe overload: RET Fe deposition
Transfusion infection from contaminated products (plt more common, stored 22deg); bacterial sepsis plt more common than red cells stored 6 deg. pseudomonas, staph

Fellowship revision (78 decks)

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