BLOOD, DCR & FLUIDS (62) Flashcards

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1
Q

INTRA-OSSEOUS BLOODS

A

IO Bloods appear Leukaemic, so:

  • cant be used for cell counts, eg WCC and Platelets
  • can be used for Hb measurement and X match
  • but are unreliable for some electrolytes
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2
Q

WHATS IN A UNIT OF FFP?

A
  • traditionally, one unit of FFP = the snap frozen plasma fraction of a single blood donation after the cells have been spun off
  • it’s typically ~250 mls and contains most of the clotting factors, but only ~1/2 the FIBRINOGEN, so Fibrinogen topups (CRYOPRECIPITATE or concentrates) are required in Massive Transfusion
  • increasingly, Plasma is being sieved off directly from donors by APHERESIS
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3
Q

WHY DO WE FREEZE (OR FREEZE DRY) PLASMA?

A
  • Freshly collected Plasma has a short storage life of 5 days at 1-6C, so most is snap frozen soon after collection for long term storage
  • Plasma can also be FREEZE DRIED (aka LYOPHILISED) to produce a a lightweight product with a long room temperature shelf life. It was widely used in WW2 but discontinued soon after as it was a pooled product with infectious concerns. It is undergoing renewed interest for austere use.

Note: the 2nd World War plasma must have been universal donor sourced from AB donors, given the lack of field cross match

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4
Q

HOW TO THAW FFP

A
  • FFP is thawed in a 37C waterbath for 20m
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5
Q

STORAGE LIFE OF THAWED FFP?

A
  • thawed FFP should be used within 6h, or stored at 1-6C for 5 days
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6
Q

WHATS IN CRYO-PRECIPITATE ?

A
  • Cryoprecipitate is a clotting factor concentrate produced by thawing a unit of FFP to just above zero degrees C, and collecting the ‘cold insoluble’ proteins that precipitate
  • it contains high levels of Fibrinogen, F8 and VWF
  • it was originally used for F8 replacement in Haemophillia, but is now mostly used for Fibrinogen replacement in coagulopathy
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7
Q

STORAGE OF CRYOPRECIPITATE

A
  • paradoxically, perhaps, CRYO is stored at room temperature and is ruined by freezing
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8
Q

WHATS IN A UNIT OF PLATELETS?

A
  • traditionally, one unit of platelets contained the pooled platelets from 4 RANDOM blood donations (ie unmatched), suspended in a small amount of plasma
  • increasingly, platelet ‘4 packs’ are being ‘APHERESED’ from SINGLE DONORS (allowing matching if desired).
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9
Q

HOW ARE PLATELETS STORED?

A
  • Traditionally, platelets can be stored at room temperature for 5 days with constant agitation, but are ruined if cooled
  • Alternatively, platelets can be Deep Frozen for long term storage if DMSO* treated first.
  • Surprisingly, the freeze/thaw process increases platelet activity, (producing thrombo-embolic concerns) although the resultant clots are less stable, possibly increasing rebleeding risk.

* Di-methyl-sulphoxide : thawed platelets smell of sulphur!

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10
Q

RBC STORAGE

A
  • traditionally, RBC can be stored for 4-6 weeks at 1-6 degrees C by adding of one of the proprietary preservatives, eg ACD or CPD, but accumulate an increasing STORAGE LESION as they age, including 2-3DPG depletion, which
    • impairs their ability to give up O2 at the tissues
    • persists for hours after transfusion
    • and is only partly reversible.
  • For this reason, RBC given in massive transfusion should be as fresh as possible, preferably <21 days
  • alternately, RBC can be suspended in Glycerol and deep frozen for many years, but take 90 minutes to thaw and de-glycerolise for use.
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11
Q

HYPOCALCAEMIA AND STORED BLOOD PRODUCTS

A
  • all 3 major blood products (RBC, FFP and PLATELETS) are ‘CITRATED’ to bind CALCIUM and prevent activation of the coagulation cascade in storage.
  • As such, hypocalcaemia can occur early in massive transfusion and Calcium administration should not be forgotten.
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12
Q

STORAGE OF FWB

A
  • FWB can be kept at room temperature for 18h only, after which it needs to be refrigerated at 1-6C, which permanently inactivates the platelets
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13
Q

WHAT ARE THE ABO, RHESUS AND MINOR BLOOD GROUPS?

A
  • A patient’s blood may be classified or ‘typed’ according to the presence or absence of a variety of antigens on the Red Cell surface.
  • Incompatibility between RBCSAg and plasma antibodies, eg after transfusion, can cause cell lysis
  • The most important RBCSAg are the A and B antigens, because the reciprocal plasma antibodies are always expressed, irrespective of prior transfusion
  • The patient’s blood type is classified
    • ‘A’ if A antigens are present
    • ‘B’ if B are
    • ‘AB’ if both are
    • and ‘O’ if neither are.
  • Similarly, blood may be further subtyped according to the presence or absence of a host of other ‘minor’ antigens, including RHESUS, KELL etc.
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14
Q

CROSS MATCHING BLOOD - RBC

A
  • it is essential to ensure that the recipient plasma does not contain antibodies which can attack cell surface antigens on the donor RBC.
  • Antibodies to the A&B antigens are most important, given their universal expression, then Rhesus, then the minor groups
  • the first test for compatibility is the ‘TYPE AND SCREEN’:
    • the ABO TYPE of the recipients Red cells is determined (and thus by reciprocity whether A or B antibodies will be present in their plasma)
    • then their plasma is SCREENED for a standard battery of minor group antibodies.
  • These 2 steps determine which antibodies are present in the recipient, and allows identification of potentially compatible donor units.
  • secondly, the selected donor unit is CROSS MATCHED by physically mixing it with the recipient plasma, to check it doesn’t clot or Lyse.
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15
Q

CROSS-MATCHING BLOOD : FFP

A
  • whilst Donor FFP contains no RBCSAg, and hence is not at risk of attack by antibodies in the recipient plasma, it may contain sufficient Antibodies of its own to launch an attack on the recipient RBC.
  • hence FFP should be ABO matched, or Universal Donor AB FFP used*.
  • If unavailable, A is the next safest choice.

* Dave Roxby says Rh compatibility is not important

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16
Q

CROSS-MATCHING BLOOD: PLATELETS

A
  • whilst platelets do not have RBCSAg, and hence are not at risk of lysis by recipient antibodies, they do contain some plasma which could theoretically mount an attack on the recipient red cells, but these reactions are generally minor and the traditional platelet ‘4 PACK’ is a POOLED RANDOM DONOR product so it cant be matched anyway
  • APHERESIS PLATELETS are single donor, so can be matched if desired, but most platelets are still given unmatched in trauma
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17
Q

WHO IS THE UNIVERSAL DONOR FOR RBC, PLASMA AND WHOLE BLOOD?

A
  • UNIVERSAL DONOR RBC come from O- donors, because they have no A, B or Rhesus (D) RBCSAg, hence cannot be attacked by the reciprocal antibodies
  • conversely, Universal donor Plasma is AB*, as it comes from donors with both A and B antigens on their RBC, hence neither of the reciprocal Antibodies are expressed in their plasma
  • NOTE: these 2 reciprocal requirements mean that, strictly speaking, THERE IS NO UNIVERSAL DONOR FOR FWB, although in practice, RBC compatibility is much more important than plasma compatibility, and O Neg FWB can usually be safely given, particularly if sourced from donors known to naturally produce low Anti-A and Anti-B antibody titres.

* not, as is often stated, AB+: Rh compatibility is unimportant with plasma

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18
Q

HOW TO CROSS MATCH FRESH WHOLE BLOOD

A

tba

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19
Q

WHAT WARMERS AND FILTERS SHOULD BE USED TO GIVE BLOOD PRODUCTS?

A
  • cold blood products (RBC and (thawed) FFP) should be given via 37 degree warming devices, but PLATELETS are stored at room temperature so warming is less important, and indeed is generally avoided due to (unfounded) concerns it damages them
  • all blood products should be given through 200 micron filters* to remove larger clots, AND platelets should only be given thru virgin filters that have not had other blood products through them, or risks activation of the platelets in the filter, clogging it
  • some advocate using finer 40 micron filters to remove micro clots and reduce TRALI, but these clog quickly & evidence of benefit is weak

* these are found in standard giving sets

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20
Q

INR: ORIGINAL USE AND NR

A
  • the INR was initially developed to monitor Warfarinisation
  • it tests ONLY the INITIATION PHASE of the coagulation cascade.
    • N = 0.8-1.2
    • DVT Rx = 2-3
    • Valve prophylaxis = 3-4
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21
Q

APTT: ORIGINAL USE AND NORMAL & THERAPEUTIC RANGES

A
  • the APTT tests Heparinisation
    • Normal = 26-40 s
    • Heparinised = 50-80 s
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22
Q

WHAT IS HEPARIN? & BASIC DOSING

A
  • Heparin is a naturally occurring anticoagulant found in the Mast cells of all animals*
  • it enhances the activity of ANTI-THROMBIN III, an endogenous THROMBIN (Factor 2) inhibitor.
  • Dose:
    • LD 5000u IV, then 1000u/hr vs APTT
  • PERIOPERATIVELY: T1/2 = 1h, stop 4h preop

* but originally isolated from canine liver, hence Hepar-in

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23
Q

WHAT ARE the LMW HEPARINS?

A
  • NATURAL HEPARIN consists of a spectrum of molecules of different sizes.
  • Heparin preparations containing only the LOW MOLECULAR WEIGHT (LMW) fractions have the following advantages
    1. can be given BD S/C instead of requiring IV infusion
    2. do not require APTT monitoring
    3. have less risk of bleeding
    4. less risk of HITS
  • but, are less reversible by PROTAMINE
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24
Q

WHAT IS PROTAMINE?

A
  • PROTAMINE is a Heparin binding and inactivating protein, originally derived from salmon spermatozoa, but now synthetic
  • DOSE:
    • 1mg of Protamine neutralises 100u of Heparin (or 1 x 50mg Amp neutralises 5000u)
    • Give very slow IV as it causes Anaphylactoid reactions
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25
Q

WHAT ARE ACTs ?

A
  • The ACT, or ACTIVATED CLOTTING TIME, is a point of care test for high level Heparinisation, using Diatomaceous earth to ‘activate’ clotting
    • N = 80 - 140s
    • High level heparinisation = 480+
26
Q

WARFARIN : action and reversal

A
  • Warfarin acts as an anticoagulant by inhibiting the production of (but not the activity of) the VITAMIN K DEPENDENT ‘TV Factors’ (2,7,9,10) by blocking the intracellular recycling of oxidised Vitamin K, producing a Vitamin K deficiency.
  • Turnover of the TV factors is rapid, so onset of WARFARIN is swift (1-2 days) and duration is long (4-5 days) given Warfarin’s half life of over 24h.
  • WARFARIN REVERSAL: you can reverse Warfarin
    • in a WEEK by stopping it, waiting 4-5/7 for it to wear off and 1-2/7 for new factors to be made
    • in a DAY by giving Vitamin K (Konakion) 10 mg IV/IM
    • IMMEDIATELY by giving FFP 4u +/- Prothrombinex 50u/kg
27
Q

WHATS PROTHROMBINEX? & BASIC DOSING

A
  • PROTHROMBINEX = Human freeze dried F27*910
  • it’s used for WARFARIN reversal
  • DOSE:
    • 50u/kg IV, (max 6x 500u amps)
    • works immediately

* PTX does contain some F7, although some overseas ‘Prothrombin Complex Concentrates’ do not

28
Q

COULD PROTHROMBINEX BE USED FOR FACTOR REPLACEMENT IN CONSUMPTIVE COAGULOPATHY?

A
  • PROTHROMBINEX contains 2,7,9,10, so it could potentially be used to replace these factors in consumptive coagulopathy
  • but it doesnt contain FIBRINOGEN, which is *the* critical factor for clot formation, and depletes fastest.
29
Q

How do ASPIRIN, NSAIDS AND PLAVIX inhibit platelet aggregation?

A
  • both Aspirin and NSAIDs NON-SPECIFICALLY inhibit platelet aggregation by blocking the enzyme CYCLO-OXYGENASE (COX), which has many functions, including the production of THROMBOXANE A2, a powerful platelet aggregator.
  • Aspirin inhibits Platelet function permanently, so should be stopped 5 days before surgery, whereas NSAIDs cause a reversible inhibition which recovers after 2 days
  • PLAVIX blocks platelet aggregation by specifically targetting the platelet P2Y12 receptor, so it doesnt have the wide ranging NSAID side effects*, but, like Aspirin, the effect is irreversible, so it should also be stopped 5 days before surgery

* gastric, renal, pulmonary etc

30
Q

COX Selective NSAIDs

A
  • The enzyme CYCLO-OXYGENASE comes in at least 2 variants, COX-1 & COX-2
  • for a time, COX2 selective NSAIDS like Celecoxib were marketed as having fewer GIT s/e, but many have now been withdrawn, due to higher CVS death rates, ? Due to a having lesser anti-platelet effects than the non selective NSAIDS
31
Q

WHATS TIROFIBAN?

A
  • TIROFIBAN (aka TIRO-TAIPAN) is a new class of antiplatelet drug derived from the venom of the SAW SCALED VIPER
  • ACTION : it inhibits platelet GLYCOPROTEIN 2a/3b receptors
  • BENEFITS:
    • can be given IV
    • short t1/2 : N function returns after 6h
32
Q

WHAT are PERSANTIN AND ASASANTIN?

A
  • these are both antiplatelet agents containing the active ingredient DIPYRIDAMOLE, which impairs platelet aggregation by affecting intracellular cAMP
  • both should be stopped 2/7 preop, except for Asasantin, which also contains Aspirin…so should be stopped 5/7 prior (As-asantin - As-pirin)
33
Q

NOVO-7 and the coagulopathy of trauma

A
  • Severe trauma patients often develop a resistant coagulopathy due to the combined effects of CONSUMPTION, DILUTION, ACIDOSIS & COLD. This can cause diffuse ongoing bleeding even after surgical haemostasis and aggressive DCR
  • NOVO-7 (rF7a) has been promoted as an ‘injury site specific’ pro-coagulant on the basis that it is only activated when exposed to TISSUE FACTOR at sites of vascular injury, where it activates F9 & F10
  • USE AT FMC?
    • unproven
    • address usual MASSIVE TRANSFUSION goals first, particularly ACIDOSIS & COLD
    • then consider asking lab about NOVO-7, 90 mcgkg slow IV 2/24
34
Q

WHAT IS PROTEIN C?

A
  • PROTEIN C, aka Factor 14, is an important endogenous anticoagulant
  • it is implicated in the causation of ACUTE TRAUMATIC COAGULOPATHY
  • conversely, HEREDITARY PROTEIN C DEFICIENCY produces thrombophillia
35
Q

WHAT IS ACUTE TRAUMATIC COAGULOPATHY?

A
  • ATC = the early onset coagulopathy seen in ~30% of severe trauma patients, well before the usual causes of consumption, dilution, acidosis and cold could be responsible.
  • The cause is thought to be a combination of:
    1. early overactivity of the fibrinolytic system (which is activated whenever clotting is - to confine the clot to the site of injury)
    2. auto anticoagulation via the PROTEIN C pathway, triggered by factors released from under perfused endothelium.
  • the mechanism is complex, but the take home point is that treating this form of coagulopathy with factor replacement alone is ineffective, and restoration of perfusion is also reqd.
36
Q

WHY MAY IT BE THAT ‘ALL POLITICS ARE LOCAL’ IN ACUTE TRAUMATIC COAGULOPATHY?

A
  • whereas auto-anticoagulation in severe trauma makes little sense at the whole body level, it does make sense at the local level if it is viewed as a response to the individual cells assuming they have lost their perfusion due to a clot upstream in their supply vessel, rather than whole body hypovolaemia
37
Q

HOW DOES HAEMATOCRIT INFLUENCE PLATELET FUNCTION?

A
  • falling haematocrits impair platelet function independently of Platelet numbers, possibly because RBC supply the ADP which powers them
  • as such, target haematocrits in trauma may be higher than that required for Oxygen transport alone
38
Q

WHAT IS HAEMOSTATIC RESUSCITATION?

A
  • Haemostatic Resuscitation is another name for ‘Damage Control Resuscitation’ (DCR): the strategy of giving RBC, FFP and PLATELETS in the 1:1:1 ratio from the outset, aiming to preserve the clotting ability and oxygen carrying capacity of the blood during massive transfusion
39
Q

WHAT IS 1:1:1:1 TRANSFUSION?

A
  • this is the DCR strategy that recognises that even if RBC + FFP + Plates are given in the 1:1:1 ratio from the outset, the pt will still likely end up FIBRINOGEN deficient, requiring the addition of a 4th component, (CRYO, concentrate etc)
40
Q

DOES 1:1:1 TRANFUSION EQUATE TO GIVING WHOLE BLOOD?

A
  • No, even if plasma and platelets are started at the same time as the RBC*, due to diluents etc, the fluid administered comprises at best, a 65% strength solution with respect to RBC, Coag factor concentrations & PLATELETS

* which is unlikely, given their different storage requirements

41
Q

FFP vs PURIFIED CLOTTING FACTOR CONCENTRATES

A
  • whereas Australia and the US generally use FFP for ‘broadspectrum’ replacement of clotting factors in coagulopathy, EUROPE increasingly prefers purified single factor concentrates (esp FIBRINOGEN), which have several advantages:
    • long room temperature storage life (freeze dried)
    • its pure Fibrinogen, so no need to cross match
    • lower volumes required to repair coagulation, with less TRALI etc
42
Q

WHATS IN FIBRINOGEN CONCENTRATE?

A
  • like PROTHROMBINEX, FIBRINOGEN concentrate is a pooled, freeze dried, human product, with suitable processing to address the attendant infective concerns
  • Modern preparations are sourced by apheresis and contain purified Fibrinogen only, hence do not require crossmatch.
  • Typical initial dosage is 6 amps.
43
Q

HIGH DOSE VASOPRESSIN IN TRAUMA

A
  • High dose Vasopressin (10u IV 5/60 x3) has recently been claimed to have a survival benefit in uncontrolled hemorrhage by
  • boosting BP (whilst) diverting blood *away* from the injury (!?)
44
Q

WHAT CENTRAL VENOUS SpO2 SHOULD BE TARGETTED IN TRAUMA?

A
  • aim for >70%: less indicates inadequate tissue perfusion
45
Q

WHY CRYSTALLOIDS ARE BAD IN TRAUMA

A
  1. they don’t carry O2 per se, but rely on increased VR allowing increased CO
  2. they contribute to dilution
  3. they can exacerbate Acidosis, due to
    • their acidic pH (NS & CSL are both 4-6)
    • The HYPERCHLORAEMIC METABOLIC ACIDOSIS OF NS
  4. not being colloids, they leak out of circulation rapidly thru the INJURED ENDOTHELIUM OF TRAUMA
46
Q

WHAT IS THE ROLE OF COLLOID and CRYSTALLOID IN MASSIVE TRANSFUSION?

A

minimal if any !: the best resuscitation fluid is

  1. FWB
  2. if unavailable (usually), the next choice is RBC, FFP and Platelets in the 1:1:1 (+1) ratio from the outset
  3. if unavailable, the 3rd choice is COLLOID, with 3rd gen HES best, and
  4. CRYSTALLOID is the final option, with HARTS better than NS due HYPERCHLORAEMIC METABOLIC ACIDOSIS
47
Q

WHAT IS THE HYPERCHLORAEMIC METABOLIC ACIDOSIS OF NS?

A
  • NS is ‘hyperchloraemic’ compared to normal ECF viz:
    • ECF contains Na 140 mmol/l and Cl 100, but
    • NS = Na 145 & Cl 145
  • When NaCl dissociates in water viz
    • NaCl + H2O > NaOH + HCl,

the higher than normal Cl content means you make more HCl

48
Q

WHAT ARE COLLOIDS ?

A

COLLOIDS are IV fluids consisting of a balanced salt solution to which large molecules have been added to produce a ‘COLLOID OSMOTIC PRESSURE’ to resist loss of water from the vascular space

COLLOIDS INCLUDE: Albumins, Gelatins, Dextrans and Starches

  • ALBUMINS: include 4% NSA, which contains human albumin, so is expensive & an infect risk
  • GELATINS: include Haemaccel or Gelofusine, which contain proteins from rendered animal tissues, so are an infection and anaphylaxis risk
  • DEXTRANS: include Dextran 40 or 70, (where the number relates to MW), containing synthetic polysaccharides
  • STARCHES: eg Voluven 6%, contain synthetic Hydroxy-Ethyl -STARCHES (HES)

Overall, the 3rd generation HES eg Voluven are probably the best colloids in trauma

49
Q

HYPERTONIC SALINE AS A VOLUME EXPANDING RESUSCITATION FLUID

A
  • NORMAL SALINE = a 0.9% NaCl solution
  • HYPERTONIC (7.5%) SALINE has been promoted as a ‘Volume expanding’ resuscitation fluid on the basis that it’s Hypertonic nature draws water into the vascular space But if this is true, it must also be true that:
    1. it dehydrates the source tissues (this is how it reduces brain swelling)
    2. not being a colloid, the Na and Cl molecules (and water) leak swiftly out again, particularly if there is endothelial dysfunction (as there is in trauma)
50
Q

ROLE OF LACTATE IN METABOLISM?

A
  • LACTATE is the end product of the ANAEROBIC metabolism of Glucose for energy.
  • This pathway is less efficient than regular aerobic metabolism, but remains a useful stopgap during tissue hypoxia
  • low level production is normal, with the resultant Lactate re-oxidized back to glucose in the liver
  • Raised lactate levels, >4mmol/l, usually indicate ongoing tissue hypoxia, although there are specific metabolic causes, eg METFORMIN
51
Q

WHAT IS BASE EXCESS?

A
  • BASE EXCESS is a measure of the METABOLIC COMPONENT of an acid-base disorder, being defined as the amount of H+ you would need to add to a sample to return it’s pH to 7.40, given you had already eliminated any RESPIRATORY COMPONENT by returning the pCO2 to 40mmHg
  • in a METABOLIC ALKALOSIS, there is an excess of HCO3-, or a +BE
  • in a METABOLIC ACIDOSIS, there is a deficiency of HCO3-, or a -BE
  • BE is N +/- 2mmol/l, and > -6 = a metabolic acidosis
52
Q

TRANEXAMIC ACID IN TRAUMA

A
  • TXA is a Fibrinolysis inhibitor which reduces clot breakdown by blocking the activation of PLASMINOGEN to PLASMIN by TPA.
  • the CRASH2 Trial showed a ‘significant’ survival benefit if given early* in major trauma, with overall mortality falling from 16 to 14.5%, and haemorrhagic mortality from 5.7 to 4.9%
  • DOSE
    • 1g IV over 10/60
    • then again over 8/24 (in 50mls NS at 6mls/h) but not into a blood or HES line

* best given within 1h, and harmful after 3

53
Q

TNK: ACTION AND USAGE?

A

TNK = TENECTEPLASE, a synthetic TPA used for clot lysis in MI

  • ACTION : like endogenous TPA, TNK activates PLASMINOGEN to PLASMIN, causing clot lysis
  • METHOD:
    • check for C/I
      • existing coagulopathy
      • recent bleeding
      • intracranial timebomb, eg AVM, tumour
      • severe HT
    • give TNK, 0.5mg/kg slow IV push
    • repeat administration is probably safe as its much less allergenic than STK
54
Q

VASCULAR PUNCTURE AFTER TNK?

A

The fibrinolytic TENECTEPLASE remains active for ‘a few hours’ after administration, so:

  • vascular puncture should be avoided where possible during this time
  • or compressible sites chosen when essential
55
Q

THE LETHAL TRIAD =

A
  1. HYPOTHERMIA (<34C)
    • ACIDOSIS (<7.1)
  2. = COAGULOPATHY
56
Q

INR & APTT vs TEG & ROTEM?

A
  • The APTT & INR were developed to monitor therapeutic anticoagulation with Heparin and Warfarin respectively
  • They test the INITIATION phase of the COAGULATION CASCADE only, not the whole pathway, and not platelet function or fibrinolysis. This, plus their >30m turnaround times*, limit their utility in bleeding trauma patients
  • In contrast, ‘VISCO-ELASTIC’ tests, like the THROMBO-ELASTOGRAM (TEG) and ROTATIONAL THROMBO-ELASTOMETRY (ROTEM) measure the totality** of the clotting system by using a moving wire or rotating cup to detect actual clot formation, strength & lysis, thus better assess clotting function in trauma patients
  • a strip graph is produced, and a variety of parameters read off, including
    • time to first clot (R or Reaction)
    • speed of clot buildup (K)
    • clot strength
    • or an overall COAGULATION INDEX or CI

* vs 10m the ROTEM

** although both heat the sample to 37C, masking any effect of hypothermia

57
Q

IDENTIFYING FIBRINOLYSIS AS A CAUSE OF COAGULOPATHY

A
  • successful clot production involves 3 discrete processes
    • formation of a PLATELET plug
    • stabilisation of the platelet plug by FIBRIN formed via the Coagulation Cascade
    • (control of) FIBRINOLYSIS
  • if excessive Fibrinolysis is contributing to Coagulopathy, this can be detected by the shape of the strip graph in the TEG, or by finding Fibrin Degradation Products, such as D-DIMER in circulation, and may motivate the use of Fibrinolysis inhibitors such as TXA
58
Q

WHAT ARE DABIGATRAN, RIVAROXABAN & APIXABAN?

A
  • DABIGATRAN (PRADAXA), RIVAROXABAN (XARELTO) & APIXABAN are all NOACs: ‘NON VITAMIN K ORAL ANTICOAGULANTS’ used as alternatives to Warfarin.
  • They act by directly inhibiting coagulation factor activity (not production) so onset and offset is faster than Warfarin, but they cannot be immediately reversed with replacement products like FFP or PROTHROMBINEX. Indeed even removal by dialysis is problematic as they are highly protein bound, although real world exp suggests they cause little trouble in trauma
  • FEATURES:
    • Predictable Therapeutic effect, so monitoring is not reqd, but if APTT is N, clotting is N
    • Elim is Renal with a T1/2 of 12h, so stop 2/7 preop, or 4/7 if major or CRF
    • hold 24h before spinal/epid
59
Q

ATLS RECOMMENDED FLUID CHALLENGE FOR HYPOTENSIVE TRAUMA PATIENTS

A
  • 1-2L (or 20ml/kg) of warm CRYSTALLOID! - repeated x2 eeeek*!

*but this may have made sense years ago, when trauma pts were seen later, having survived smaller bleeds, and where dehydration (from Starling driven shifts) rather than active bleeding, was the main issue

60
Q

ATLS HAEMORRHAGE CLASSES 1-4

A
  1. CLASS 1 = MINOR = <15%, causing, at most, minor tachycardia
  2. CLASS 2 = MODERATE = 15-30%, with moderate tachycardia and narrow pulse pressure
  3. CLASS 3 = MAJOR = 30-40%, with major tachycardia, hypotension & confusion
  4. CLASS 4 = CRITICAL = >40% = moribund
61
Q

ATLS CLASSIFICATION OF RESPONSE TO FLUID CHALLENGE?

A
  • RAPID RESPONDERS (= controlled bleeds)
  • TRANSIENT RESPONDERS (= ongoing bleeds)
  • NON RESPONDERS (= massive ongoing bleeds)
62
Q

DDAVP FOR PLATELET DYSFUNCTION

A
  • in addition to boosting F8 activity, DDAVP also enhances Platelet function and so may be beneficial in patients on ASPIRIN or other antiplatelet drugs