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Fluid management and blood transfusion Flashcards

1
Q

Describe water distribution in the body by weight

A

Water is about 60% of weight so for a 70 kg male

Intracellular 65% 28L
Extracellular 35% 14L
— Interstitial 27.5% 11L
— Plasma 7.5% 3L

TBW 100% 42L

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2
Q

In general how is total body water regulated

A

ECF as ICF follows changes in the ECF

There are no “water pumps” in the body

ECF is controlled by the movement of Na and thus water as Na is responsible for 90% of the body’s osmotic activity

Na intake (diet/IV)
Na EXTRA-Renal loss (Sweating/faeces)
Na renal excretion

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3
Q

What is transcellular fluid

A

CSF | Synovial fluid | Ocular fluid

Glandular secretions (lungs/GIT)

Bile

Total transcellular fluid is ± 2 % TBW (± 800 ml)

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4
Q

What is the equation for plasma osmolarity

A

Plasma osmolarity = 2[Na] + 2[K] + glucose + urea

Sodium and potassium are doubled to account for their conjugate anions - glucose and urea don’t have conjugate anions

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5
Q

What is the difference between molarity and osmolarity

A

Osmolarity refers to the number of osmotically active particles per litre of solution

Molarity refers to the the number of moles of solute per litre of solution i.e. the concentration

NaCl – contributes 2 osmoles
But the molarity can only represent either Na+ or Cl-

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6
Q

How is osmolality different from osmolarity

A

Osmolality is the number of dissolved osmotically active particles per unit MASS of solution

Osmolarity is the number of osmotically active particles dissolved per unit VOLUME of solution

The problem with osmolarity (vs osmolality) is that the volume of the solvent (water) changes with the addition of solute and with temperature

Osmolality is independent of changes in mass of solute and temperature.

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7
Q

Why do we use 5% dextrose for infusions instead of just infusing water

A

Water infusion would lead to acute drop in osmolarity of the fluid surrounding the red blood cells. The circulating RBCs would find themselves surrounded by a hypotonic solution, causing them to swell. RBC can only hold a certain amount of water before haemolysis occurs. For this reason 5% dextrose infusion are used

Osmolarity of 5% Dextrose is 278 mOsm/L and plasma osmolarity is normally 285 - 295 mOsm/L

Once the glucose is metabolized, it is as if free water has been infused but without the acute drop in osmolarity.

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8
Q

How does ADH work in the kidneys to increase H2O reabsorption

A
  1. Luminal wall CD is impermeable to water
  2. Basolateral wall CD has aquaporins 3 and 4 and is permeable to water
  3. ADH binds to V2 receptors in the CDs –> cAMP 2nd messenger –> aquaporin 2 being inserted into the luminal walls of the CD
  4. Water moves down Conc gradient created by the high osmolarity in the renal medulla.
  5. High osmolarity in the renal medulla is generated by active reabsorption of Na in the aLOH and DCT, counter current mechanism and urea cycling.
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9
Q

How is ECF volume controlled

A
  1. Brain
    - Hyperosmolarity (also stress and pain)
    - Hypothalamus: osmoreceptors
    - Posterior pituitary: ADH release
    - Thirst stimulated
  2. Heart
    - Baroreceptors in atria (low P) tonic firing with normal P
    - Low P –> low firing –> decreased inhibition ADH release–> increase ADH
    - RA stretch –> release ANP –> Natriuresis
    - Reduced RAP –> less ANP –> Na retention
  3. Kidneys
    - Decreased arterial filling pressure sensed by juxtaglomerular apparatus
    - Macula densa cells release renin
    - RAAS activated
    - Angiotensin 2 restores filling P in renal arterioles
    - Aldosterone increases Na retention
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10
Q

How does increased SNS tone affect renal perfusion

A
  1. Global RBF decreased

2. Redistribution of RBF to inner juxtamedullary nephrons: improved Na and water retention

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11
Q

Classify the “stress response”

A

Neurohumoral

Neural –> SNS activation
Humoral –> Glucocorticoids / Thyroid H / GH / CAT = anti-insulin hormones

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12
Q

Describe the neurohumoral response

A

Neuro
Stress –> CNS (brainstem) –> SNS activation with PSNS inhibition

Adrenalin: Predominant beta agonist effects

  • -> Increased CO
  • -> Vasodilation in Coronary / Skeletal muscle BV

Noradrenalin: Predominant alpha agonist effects
–> VC - skin / kidney / liver / GIT

Although blood is diverted away from the kidney –> blood distribution in the kidney is shifted toward inner juxtamedullary nephrons which have long LOH and are more suited to Sodium and water retention resulting in accentuated sodium and water retention.

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13
Q

What features of the part of the nephron in the renal medulla assist with the generation of the medullary osmolar gradient?

A
  1. Differential permeability of descending and ascending limbs of LOH to water (descending) and ions (ascending)
  2. Countercurrent exchange mechanism
  3. Hair pin design of the vasa recta
  4. Urea reabsorption from inner medullary collecting duct.
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14
Q

What is diabetes insipidus vs SIADH

A

Central Diabetes insipidus (head injury)

  • Posterior pituitary fails to secrete ADH
  • Polyuria, hypvolaemia, hypernatraemia, dilute urine

Nephrogenic diabetes insipidus (Lithium toxicity)
- Insensitivity to normal levels of ADH

SIADH (Intracranial pathology vs ectopic source Small cell lung Ca)

  • Hyponatraemia (headache/nausea/confusion/seizures/coma)
  • Fluid overload (sometimes)
  • Inappropriately high urine osmolarity
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15
Q

Describe the humoral aspect of the neurohumoral response

A 
Counter-regulatory hormones:
Catecholamines
Glucocorticoids
Growth Hormone
Thyroid Hormone

Anti-insulin hormones that reduce insulin release and tissue sensitivity to preserve and increase blood glucose for use by fight or flight organs (heart/skeletal muscle/lungs and brain)

Glycogen break down initially increased
Then Gluconeogenesis accelerated

Other organs (over days become fat adapted)

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16
Q

Summarise the overall fluid and electrolyte outcome consequent to the stress response

A
  1. Maximal sodium and water retention RAAS/ADH
  2. Hypernatraemia (dilutional) - ADH
  3. Hypokalaemia - RAAS
  4. Metabolic alkalosis
  5. Decreased RBF: Renal failure
  6. Hyperglycaemia
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17
Q

Describe the redistribution of crystalloid solutions after IV administration and state the clinical relevance of this

A

1 : 3 ratio
1ml stays intravascular while 3 ml moves into ECF

This means that crystalloids are inefficient effective circulating volume expanders as 3 x the volume lost of crystalloid replacement would is required to replace the blood loss.

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18
Q

What is the goal of maintenance fluids

A

Provide sufficient water and electrolytes for a patient not taking oral fluids

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19
Q

What is the goal of fluid replacement therapy

A

Fluids should resemble fluid losses which will generally resemble ECF

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20
Q

Why should glucose containing solutions be avoided in resuscitation

A

They are usually hypotonic with minimal expansion of effective circulating volume.

Furthermore, in scenarios requiring resuscitation, the physiological response increases blood sugar levels regardless of glucose administration.

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21
Q

What is the daily requirement of the following

H2O 
Na+ 
K+ 
Ca2+ 
Mg2+ 
PO4
A 
H2O – 30 mL/kg
Na+ – 2mmol/kg
K+ – 1mmol/kg
Ca2+ – 0.1mmol/kg
Mg2+ – 0.1mmol/kg
PO4 – 0.1mmolkg

Dextrose ± 100 grams/day (Adults) to prevent ketosis

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22
Q

Whats the difference between normal saline, ringers lactate, modified ringers lactate (Plasmalyte L) and Plasmalyte B (Balsol)

A

NS: Na 154 | Cl 154 | OSM: 308
RL: Na 131 | Cl 110 | OSM: 273 | K 4 | Ca 1.8 | Lac 28
MRL: Na 131 | Cl 110 | OSM: 273 | K 4 | Ca 0 | Lac 28
Pl. B: Na 131 | Cl 98 | OSM: 273 | K 4 | Mg 1.5 | HCO3 27 (Buffered with gluconate and acetate instead of lactate) (Balsol)

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23
Q

Why should maintenance solutions only ever be given slowly and should never be given as resuscitation fluid

A

They contain up to 26 mmol/L of potassium

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24
Q

Historically, it was thought that low sodium solutions are preferred in the perioperative period in paediatrics. How has this thinking and practice changed

A

Balanced salt solutions are preferred now.

Stress response leads to a water retentive state (and possibly hyponatraemia) –> Solutions resembling ECF should preferably be used in the first 24 hours postoperatively.

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25
Q

Why are dextrose concentrations of 5% used rather than 10%

A

5% provides 50 g of dextrose per 1 L bag of maintenance fluid. 2 - 3 bags over a 24 hour period will provide just enough glucose to prevent ketosis and starvation state.

10% solutions are hypertonic

  • -> damage veins into which they are infused
  • -> Potentially cause hyperglycaemia
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26
Q 
Compare the contents of the following solutions
D5W
General Maintenance Solution
Maintelyte
Paediatric Maintenance Solution
Neonatelyte
A

D5W: Na 0 | Cl 0 | OSM: 253 | K 0 | Dex 5%
GMS: Na 26 | Cl 52 | OSM: 382 | K 26 | Dex 5%
Maint: Na 35 | Cl 65 | OSM: 683 | K 25 | Mg 2.5 | Dex 10%
PMS: Na 35 | Cl 47 | OSM: 372 | K 12 | Dex 5%
Neo: Na 20 | Cl 15 | OSM: 638 | K 15 | Dex 10% | Lac 20 | Ca 2.5 | Mg 0.5 | PO4 37.5

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27
Q

What is the fundamental difference between D5W and GMS

A

D5W has no electrolytes and is hypotonic

GMS attempts to cover all daily requirements for water, electrolytes and glucose

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28
Q

What is the fundamental difference between GMS and Maintelyte

A

GMS is 5% dex

Maintelyte is 10% dex, more sodium and has Mg

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29
Q

What is the fundamental difference between GMS and Paediatric Maintenance Solution

A

PMS has less potassium and more sodium

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30
Q

What is the fundamental differnce between PMS and neonatalyte

A

PMS is 5% dex

Neonatalyte is 10% dex, has less sodium and Mg/Ca/Lac/PO4

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31
Q

Replacement fluids should resemble ECF as this is most commonly the type of fluid that is lost.

Outline some situations when a different strategy for fluid replacement should be adopted

A
  1. Diabetes insipidus
    - water loss > Na loss
    - Rx measure Urine and plasma electrolytes and reduce Na: Water ratio of replacement fluid
  2. Intestinal losses
    - K loss - supplement K
    - HCO3 loss (upper intestinal fistulae)
  3. Gastric losses
    - Cl - loss –
    - K loss
    - Rx: 0.9% NaCl + K replacement
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32
Q

How many liters of intraoperative 0.9% NaCL can cause acidosis due to chloride load?

A

2L

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33
Q

What are the suggested harmful effects of hyperchloraemic metabolic acidosis

A

Clinical Significance yet to be determined

  1. Cl induced VC
  2. AbN coagulation
  3. Renal dysfunction
  4. Delirium

No human data to suggest decreased survival

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34
Q

When is the slight hypotonic property of ringers lactate possibly probelmatic

A

In patient’s at risk for cerebral oedema - head injury or when the BBB is disrupted.

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35
Q

Why can ringers lactate and blood transfusion not be transfused via the same administration set

A

The calcium in Ringers lactate (1.8 - 2.5 mmol/L) is sufficient to coagulate stored blood in the giving set.

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36
Q

NS or RL for renal failure with hyperkalaemia and why

A

Ringers Lactate is preferred

RL - despite containing potassium - the quantities are minimal and have minimal biochemical impact

NS - Causes acidosis and will increase the K significantly

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37
Q

NS / RL /Balsol for DKA

A

NS (NO: acidosis –> deranged K)

RL (NO: if patients on metformin: impaired lactate metabolism)

Balsol: Yes –> No lactate (acetate and gluconate used as buffers - also contains HCO3)

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38
Q

How much crystalloid on the day of surgery has been shown to be beneficial and what benefits are cited

A
  1. 5L/24 hours on the day of surgery
  2. Improved postop lung function
  3. Improved exercise capacity
  4. Reduced stress home response
    - less nausea
    - less thirst
    - less fatigue
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39
Q

What is the problem with excessive crystalloid therapy

A
  1. Positive fluid balance in ICU - independent RF for mortality
  2. In trauma: supranormal haemodynamic resuscitation with large volumes of crystalloid (13.5 L on average)
    - -> Abdominal Compartment Syndrome
    - -> Multiple Organ Failure
    - -> Mortality
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40
Q

Summarise the advantages and disadvantages of colloids

A

Advantages
1. Better effective circulating volume expansion than crystalloids

Disadvantages

  1. Do not resuscitate ECF –> diminished renal function
  2. Allergic risk (all)
  3. Coagulation interference
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41
Q

Why is human albumin not used

A

Higher cost
No evidence that it is superior to synthetic colloids
(for the treatment of both hypovolaemia and hypoalbuminaemia)

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42
Q

What are examples and the pros and cons of the gelatins how are they made

A

Examples: Gelofusine | Haemaccel
Synthesis: gelatin derived from bovine material

Pros
1. Least effect on coagulation

Cons

  1. Short acting (1 hour) –> quickly excreted by kidneys
  2. Highest risk of allergy
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43
Q

What are examples and the pros and cons of the dextrans and how are they made

A

Examples: Macrodex | Rheomacrodex
Synthesis: Sucrose

Pros

  1. Last longer
  2. Good rheological properties (good flow)

Cons

  1. Bind vWF and Factor VIII and impair coagulation the most approximate effect of SC LMWH
  2. Interfere with cross matching techniques
  3. Significant allergy risk
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44
Q

What are examples and the pros and cons of the Hydroxyethyl Starches (HES) how are they made

A

Examples: Voluven | Volulyte
Synthesis: Potatoes or Maize starch

Pros

  1. Last longer (6 hours)
  2. Beneficial effect to vascular endothelium

Cons

  1. Less Impaired coagulation vs dextrans (higher MW the worse –> Medium MW used preferably because of this)
  2. Renal impairment (without crystalloid adminsitration)
  3. Avoid in sepsis
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45
Q

Is there clear evidence of survival benefit with use of colloids

A

None BUT data suggesting that crystalloid overload may be harmful should be kept in mind

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46
Q

What is fluid optimization

A

The use of beat to beat dynamic measures (SVV and PPV) to guide appropriate fluid therapy

  • -> instead of ‘chasing’ urine volume
  • -> urine production is deranged in the perioperative period due to the stress response and less accurately aligns with the patient’s fluid status

Also valid options:

  • U/S IVC collapsibility
  • Straight leg raise test
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47
Q

Describe an ideal colloid

A

in vivo MW of 70 kDa (small) and suspended in a balanced salt solution.

48
Q

Which infections is whole blood donations screened for

A

HIV 1 and 2
Hep B and C
Syphilis

49
Q

What is the volume per unit of whole blood

A

550 mL

50
Q

What is the haematocrit of whole blood

A

35%

51
Q

What is the preservative used for whole blood

A

CPD - A (Citrate, Phosphate, dextrose , adenine)

52
Q

What is the shelf life for whole blood

A

35 days at 4 deg C

53
Q

What are specific indications for whole blood administration

A
  1. Massive haemorrhage with possibility of recurrence
  2. Rx of established hypovolaemic shock
  3. Blood replacement after burns
54
Q

How is red cell concentrate made

A

Removal of plasma from whole blood

–> plasma can then be used to prepare FFP’s and clotting factors

55
Q

What is red cell concentrate suspended in?

A

Small volume of nutrient fluid called:

SAGM (Saline, Adenosine, Glucose, Mannitol)

56
Q

Does RCC contain citrate

A

Yes, smaller amounts than whole blood

57
Q

What is the volume of a unit of RCC

A

300 ml

58
Q

What is the haematocrit of RCC

A

60%

59
Q

What is the shelf life of RCC

A

42 days at 4 deg C

60
Q

How much does RCC increase the patient Hb

A

4 ml/kg raises HB by 1 g/dl (adults)

So 70 kg male:
1 bag RCC - 300 ml –> should raise Hb by 1 g/dl

61
Q

What does co-administration of furosemide during a blood transfusion require

A

Evaluation of fluid status

62
Q

What is the indication for FFP

A

To replace deficient clotting factors in patients who also need plasma volume support

63
Q

What are the risks of administering FFPs

A

Higher risk of TRALI

Many of the same risks as blood transfusion

64
Q

Is FFP equivalent to plasma in terms of clotting factors

A

No. It has less, and specifically, it is relatively low in thrombin. FDP and cryoprecipitate contain more thrombin

65
Q

What is the difference between FFPs and cryoprecipitate and how is it made

A

Cryoprecipitate is processed FFP made by skimming off the clotting factors it contains (akin to taking the cream from the top of the glass of milk fresh from the cow)
- Provides high concentration of clotting factors at low volume

66
Q

Compare the volume of FFP to cryoprecipitate

A

FFP - 300 ml

Cryoprecipitate - 10 - 20 ml

67
Q

Cryoprecipitate is concentrated coagulation factors, what is the down side

A

It is expensive

- Lifesaving in DIC and massive blood loss

68
Q

When are platelets administered and why are there such limited indications

A

Extremely expensive resource

Indications

  1. TEG - indicates platelets abnormal plt function
  2. Known severe thrombocytopaenia
  3. As part of massive transfusion protocol
69
Q

How are platelets stored

A

At room temp (20 - 24 deg C)
With gentle agitation
For max 5 days

70
Q

How long until POOLED platelets expire

A

After platelets are pooled they expire after 4 hours

71
Q

What does group and screen mean

A

Blood group determined
Specimen is screened for antibodies

BUT blood will still need to be cross matched

72
Q

Describe the degrees of urgency for ordering blood

A
  1. Routine
    - Complete cross match done
    - Specify time blood required
  2. ASAP
    - Complete cross match done
    - Ready 30min - 1 hr of specimen arriving at blood bank
  3. STAT
    - Incomplete cross match done
    - Group specific blood issued within 5 mins
    - higher risks of reactions as full screening for antibodies is not done
73
Q

What is the most common cause for a transfusion reaction?

A

Clerical error when collecting the blood sample

74
Q

Describe the actions to be taken prior to transfusion of blood

A
  1. Check the form and products independently against patient demographics
  2. Check that group is compatible and expiry date
75
Q

What temperature is blood stored at prior to infusion

A

2 - 10 deg C

76
Q

What temperature should blood not be warmed above and why

A

37 deg C –> haemolysis if higher which may provoke a transfusion reaction

Never rewarm

77
Q

What is the maximum time for a blood transfusion

A

6 hours

78
Q

How is the patient monitored for a transfusion reaction

A

Vitals, LOC, well being and verbal inquiry

79
Q

Why should stoppered empty blood bags be returned to the blood bank

A

The pilot tube contains residual blood that is used for investigation of the transfused blood in the event of a patient reaction

80
Q

Which study suggested a restrictive policy with regard to blood transfusion and how did this study alter the Hb trigger to initiate a blood transfusion

A

TRICC ( Transfusion in Critical Care)

  • Transfusion trigger of 7 g/dl (instead of 9 g/dl)
  • Significantly improved survival
81
Q

What is the trigger and target for blood transfusion and what are the exceptions

A

Trigger 7 g/dl
Target 9 g/dl

Exceptions: IHD and elderly

82
Q

Classify and describe complications of blood transfusions

A

IMMUNE reactions

Haemolytic

  • Early (ABO)
  • Late (Rhesus)

Non-hemolytic

  • Fever
  • Urticaria
  • Purpura
  • TRALI
  • Anaphylaxis
  • Immune supression
  • Graft vs Host disease

NON- IMMUNE reactions

Infectious

  • Viral
  • Parasitic
  • Bacterial
  • Prions

Massive Blood Transfusion

  • Hypothermia
  • Hyperkalaemia
  • Hypocalcaemia
  • Citrate toxicity
  • DIC
  • Acid-base disturbance
  • Fluid overload
83
Q

Define a transfusion reaction

A

Any potentially adverse sign or symptom that occurs after the start of a transfusion of blood or blood product

84
Q

Summarise the classification of transfusion reactions

A

IMMUNE

  • Hemolytic
  • Non-hemolytic

NON-IMMUNE

  • Infection
  • Massive blood transfusion
85
Q

Describe the clinical presentation of ABO incompatibility

A

Symptoms (Sick patient with SNS activation)

  • Anxiety and restlessness
  • Nausea and vomiting
  • Back/flank/precordial pain
  • Itching
  • Cold and clammy
Signs
Any abnormal autonomic finding
Hburia/oliguria/anuria
Jaundice
Coma 
Death
86
Q

Describe the management of a patient with suspected ABO incompatibility transfusion reaction

A 
STOP transfusion
Call for help
Declare situation
ABCDE
- Vasopressor/inotropes as needed
- Antihistamines/Steroids
- Fluids (maintain adequate renal perfusion)

Labs

  • FBC for Hb / UE for renal failure and K/ Clotting profile for DIC
  • Inform blood bank promptly (legal requirement)
  • Send all units / post transfusion specimens/ urine sample / reaction form
87
Q

What should be sent to blood bank post transfusion reaction

A
  1. Call them and tell them promptly
  2. All units transfused
  3. Post transfusion specimens (clotted and EDTA)
  4. Urine sample
  5. Complete untoward reaction form
88
Q

What is the definition of a Massive Blood Transfusion and what is haemostatic resuscitation

A
  1. More than 10 units in an adult
  2. Replacement of entire blood volume < 24 hours
  3. Replacement of > 50% blood volume within 3 hours
  4. Rate of blood loss > 150 ml/min

Haemostatic resuscitation
- Delivering RBCs and blood components in a fixed ratio - 1:1:1

89
Q

What is the evidence to suggest that blood transfusions suppress immunity

A
  1. Kidney transplant patients - longer kidney survival
  2. Reduced 5 year survival in cancer patients
  3. Increase incidence of sepsis
90
Q

What are the consequences of giving massive transfusion

A
  1. Risks of giving a single transfusion are multiplied
    - infection
    - Incompatibility
  2. Multiple physiological consequences of giving a large amount of stored blood
91
Q

What happens to platelets and clotting factors after massive blood transfusion

A

Diluted

92
Q

What happens to pH after massive blood transfusion

A

Initially lactic acidosis (stored RBC’s)

Later metabolic alkalosis as liver converts citrate to HCO3

93
Q

Is the P50 for the OHDC shifted for the transfused cells and why

A

Significantly reduced 2.3 DPG levels and LEFT shifted P50 OHDC

94
Q

What effect does massive blood transfusion have on body temperature

A

Hypothermia –> left shifted OHDC and coagulopathy

95
Q

Discuss potassium after massive blood transfusion

A

Initial increase (RBCS lose 1 mmol K per day of storage)

Later: When RBC recover –> rapid uptake of K –> hypokalaemia

96
Q

What is the effect of citrate in the massive blood transfusion.
What is the stored blood concentration of ionized calcium?

A

Citrate toxicity
- Prevents coagulation of blood by chelating calcium
- Stored blood Ca concentration < 0.1 mmol/L (normal is 1 mmol/L)
Therefore –> massive transfusion may lower calcium

However, citrate is rapidly metabolized, and hence this is rarely a problem unless during a MASSIVE transfusion or with liver dysfunction

Citrate metabolism –> metabolic alkalosis –> shifts P50 OHDC to the left

97
Q

What is the effect of the mild hemolysis that has taken place in stored blood

A

Free Hb –> may cause renal impairment

98
Q

Why are filters used on administration sets

A

To reduce the possibility of microemboli

Microemboli are cellular-fibrin aggregates

99
Q

Describe your approach to the initiation of the massive transfusion protocol

A
  1. Recognise need and Declare situation to the team
  2. Advise surgical/anaesthetic consultant and get help if needed
  3. Ensure large bore, high capacity IV access, Ensure patient warming and other resuscitation fluids as appropriate.
  4. Tranexamic acid 1g IV over 10 mins
  5. Take blood for: FBC, CEUG, INR, Cross match
  6. Call blood bank - request STAT not ASAP:
    - 6 U RCC
    - 6 U FFP
    - 1 unit pooled plts
    - 10 U (1000IU) cryoprecipitate
  7. Repeat as needed
  8. Before transfer to ICU
    - FBC, INR & PTT, Fibrinogen levels
  9. Repeat Tranexamic acid 1 g in 200 ml over 8 hours
  10. Dont forget to document times
100
Q

What are the targets for a massive blood transfusion

A

Hb > 8 g/dl
Plts > 75 x 10^9/L
Fibrinogen > 1.0 g/l
INR & PTT < 1.5 x mean

101
Q

Which filter should be used for platelet transfusion

A

The specific one provided by the blood bank (standard blood filters will trap platelets)

102
Q

What is random donor pooled platelets

A

Platelets from 5 individual donations pooled together to produce one unit of platelet concentrate

103
Q

How much should platelets increased after a standard adult dose of pooled platelets

A

20 - 40x 10^9 /L (but lower in splenomegaly/DIC/Sepsis

104
Q

Should single donor apheresis platelets be ordered for massive transfusions

A

NO. These are indicated for patients on long term platelet replacement therapy

105
Q

What coagulation factors does cryoprecipitate contain and how is cryoprecipitate administered

A 
vWF               100IU
Factor 8         100 IU
Factor 13       
Fibrinogen     200mg
Administration: standard blood-giving IV admin set
Administered in pools of 10 units
106
Q

How much does 10 Units of cryoprecipitate increase fibrinogen and what is the target for patient plasma fibrinogen

A

10 units of cryoprecipitate
Contains ± 200mg fibrinogen
Increases plasma fibrinogen 50 - 100 mg/dL
Target fibrinogen > 1 g/dl

107
Q

How is cryoprecipitate prepared

A

Repeated thawing of FFP between 1 deg C and 6 deg C and recovering the precipitate

108
Q

Compared to FFP, what does cryoprecipitate contain

A

It contains most of 8, 13, fibrinogen, fibronectin and vWF from the FFP

109
Q

How long can cryoprecipitate be stored for

A

12 months at -25 deg C or below

110
Q

How long after thawing should cryoprecipitate be used?

A

Within 6 hours (maintain at 20 - 24 deg C)

111
Q

How long does fibrinogen last

A

3 - 5 days

112
Q

What are the Pros and Cons of FFP

A

Pros

  1. Replaces coagulation factors
  2. Has 400 mg fibrinogen
  3. Volume expander (maintains oncotic pressure)
  4. Acts as a buffer (improves AB status)

Cons

  1. Increased incidence TRALI
  2. Increased incidence of Multi-organ failure
113
Q

Why are concerns over increased incidence of TRALI with FFPs unfounded

A

Mortality for patients who require massive transfusion 30 - 60%

TRALI occurs 1 in 5000 - 10 000

  • Rx - ventilation ± 24 hours
  • Mortality 6 - 9 %
114
Q

What is the cost of a massive transfusion in RSA public sector

A

30 000 ZAR

115
Q

What is the name of the study supporting Tranexamic acid in surgical/trauma patients and what did this study find

A

CRASH 2 study suggested a 15% reduction in overall mortality with administration of tranexamic acid

116
Q

What is the mechanism of action of Tranexamic acid

A

Antifibrinolytic

- Binds to plasminogen and prevents activation to plasmin.

DA (50 decks)

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