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By Dr Reshma Gaya FRCA Consultant Anaesthetist ABH Mauritius

By Dr Reshma Gaya FRCA Consultant Anaesthetist ABH ... of storage V and VIII Use of PRC Early use of FFP/platelet/cryoppte FFP stored at < -20 Freshly thawed and stored for up to 5

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By Dr Reshma GayaFRCAConsultant AnaesthetistABHMauritius

Krug EG, Sharma GK, Lozano R: The global burden of injuries. The global burden of injuries. The global burden of injuries. The global burden of injuries.

Am J Public Health 2000, 90:90:90:90:523-526

Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage on trauma outcome:

an overview of epidemiology, clinical presentations, and therapeutic considerations.

J Trauma 2006; 60 (Suppl 6):S3–S11.

� Timely interventionTimely interventionTimely interventionTimely intervention

� Early recognition of blood lossEarly recognition of blood lossEarly recognition of blood lossEarly recognition of blood loss

� Early control of bleeding Early control of bleeding Early control of bleeding Early control of bleeding

� Early restoration of circulating volumeEarly restoration of circulating volumeEarly restoration of circulating volumeEarly restoration of circulating volume

� Judicious transfusion of fluid and blood and Judicious transfusion of fluid and blood and Judicious transfusion of fluid and blood and Judicious transfusion of fluid and blood and

blood productsblood productsblood productsblood products

Timely intervention

Time elapsed between injury and operation be minimised for patients in need of urgent surgical bleeding control (Grade 1A).

� Patients presenting with haemorrhagic shock and an identified source of bleeding should undergo immediate surgical bleeding control

� Patients presenting with haemorrhagic shock and an unidentified source of bleeding should undergo immediate further assessment as appropriate using focused sonography, computed tomography, serum lactate, and/or base deficit measurements

� ATLS guidelines: Diagnosis and management must be performed in rapid succession

� Priorities adequate ventilation/haemorhage control/tissue perfusion to vital organs

� Airway

� Breathing

�Circulation

� Baseline recordings: NIBP, ECG, Pulse oximeter

Class I Class II Class III Class IV

Blood loss (ml) Up to 750 Up tp 750 -1500

1500 - 2000 >2000ml

Blood loss % BV

Up to 15% 15-30% 30-40% >40%

Pulse Rate <100 >100 >120 >140

BP normal normal decreased decreased

RR 14-20 20-30 30-40 >35

Urine output ml/hr

>30 20 -30 5 -15 negligible

Mental status Slightly anxious

Mildly anxious Anxious and confused

Confused and lethargic

� Young people compensate well for large-volume blood loss

� Elderly people may tolerate much smaller blood losses only

� Pedestrian – motor vehicle accidents

� Multiple long bone fractures

Unilateral haemothorax 3000ml

Heamoperitoneum + abdominal distension 2000 – 5000ml

Full thickness soft tissue defect 500ml

Pelvic # 1500ml – 2000ml

Femur # 800 – 1200ml

Tibial # 350 – 650 ml

Smaller # 100 – 500 ml

� Massive transfusion: refers to a transfusion of greater than 10 units of red blood cell in 24 hours

� The replacement of a patient's total blood volume in less than 24 hours

� The acute administration of more than half the patient's estimated blood volume per hour

� Blood loss >150 ml/minute

� Control obvious haemorrhage by direct pressure

� Establish adequate IV access 2 large bore IV cannula

� Send blood for routine investigations and crossmatch

blood and blood products

� ABGs, Hb, Electrolytes, coagulation profile, platelet count

� Start fluids

� Prevent Hypothermia

� Correct Acidosis

� Prevent Coagulopathy

� Early haemodynamic effects – restore end organ

perfusion and oxygen delivery, increase blood flow

and potentiate rebleeding

� Effects on haemostasis; detrimental effects on

haemostasis, primary thrombus may be dislodged,

dilute clotting factors, reduce blood viscosity,

hypothermia unless warmed

.

For hypotensive patients with penetrating torso injuries, delay of aggressive fluid resuscitation until operative intervention improves the outcome.

598 adultsPenetrating torso injurySBP < or = 90 mmHgStd fluid resuscitation /delayed resuscitation

Maintaining a low MAP during intraoperative resuscitation in seriously ill trauma patients is safe, reduces use of blood products, and decreases the incidence of postoperative coagulopathy and the related consequence of death.

Both animal and human studies indicate that administration of large amounts of intravenous crystalloids prior to controlling bleeding is associated with

� cardiac dysfunction, � abdominal compartment syndrome, � harmful inflammation, � acute respiratory distress syndrome, � multiple organ dysfunction syndrome and� increased deaths

� Check radial pulse, do not rush with fluids

� Impaired mental status, give fluids until mental

status improves

� Severe HI ; Aim CPP >80, liberal with fluids until BP

improves

� Tolerate SBP 90,

� Avoid dextrose containing solutions

� R/lactate – Hypotonic

� Colloid – avoid large volume/risk of coagulopathy

Fluid should not be administered to trauma victims before haemorrhage control if a radial pulse can be felt. Judicious aliquots of 250 ml should be titrated for other patients.

� Essential component of trauma

� Fundamental concept military in origin

Early bleeding control be achieved by

◦ direct surgical bleeding controldirect surgical bleeding controldirect surgical bleeding controldirect surgical bleeding control

◦ the use of local haemostatic proceduresthe use of local haemostatic proceduresthe use of local haemostatic proceduresthe use of local haemostatic procedures

Resuscitative, abbreviated surgery

� control of hemorrhage and contamination

� definitive repairs deferred.

ICU:

� active rewarming,

� correction of coagulopathy

� correction of acidosis

Definitive surgical management

Rotondo MF, Schwab CW, McGonigal MD, Phillips GR, 3rd, Fruchterman TM, Kauder DR, et al. ‘Damage control’: An approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35:375–82

� Establish adequate IV access 2 large bore IV cannula

� Send blood for routine investigations and crossmatch blood and blood products

ABGs, Hb, Electrolytes, coagulation profile, platelet count

� Start fluids – N/saline: permissive hypotension

� Prevent Hypothermia

� Correct Acidosis

� Prevent Coagulopathy

� Hypothermia

� Acidosis

� Coagulopathy

� Defined as the triad of death in exsanguinating patient

Traumatic Haemorrhage

Irreversible shock

death

DCR/surgery

Transfusion of blood products MOF

Tissue hypoxia

Acidosis

Coagulopathy

Hypothermia

Dilutional of coagulational

factors

� Hypothermia, defined as a core body temperature of less than 35°C

� A mortality of 100% has been reported in trauma patients whose body temperature fell below 32C, regardless of severity of injury, degree of hypotension, or fluid replacement.

� Gubler KD, Gentilello LM, Hassantash SA, Maier RV. The impact ofhypothermia on dilutional coagulopathy. J Trauma. 1994;36:847–51.

Impairs platelet function

Impairs thrombin formation

Increases fibrinolysis

� Restoration and maintenance of normothermia

� Ambient: thermoneutral zone 28

� Remove wet clothing

� Use of fluid warming devices

� Covering the patient to avoid additional heat loss,

� Forced air warming,

� (in extreme cases) extracorporeal re-warming

devices

� Acidosis is a result of tissue hypoperfusion and subsequent switch from aerobic to anaerobic respiration

� Causes adverse effects on cardiac function

� Causes impairment of oxygen utilization and coagulation dysfunction

� Dunn EL, Moore EE, Breslich DJ, Galloway WB. Acidosis-induced coagulopathy. Surg Forum. 1979;30:471–3.

� Manger WM, Nahas GG, Hassam D, Habif DV, Papper EM. Effect of pH control and increased O2 delivery on the course of hemorrhagic shock. Ann Surg. 1962;156:503–10.

Decreases global clotting factor enzyme activity

� Replete intravascular volume

� Maximize oxygen delivery

Abnormal coagulation status is associated with a five fold increase

in mortality

Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma 2003;54:

This study shows for the first time that tissue injury and hypoperfusion followed by the activation of the anticoagulation thrombomodulin protein C pathway plays the central role in the pathogenesis of acute traumatic coagulopathy.

� Consumption and dilutional of platelets and coagulation factors

� Hypothermia and acidosis affects platelet function

� There is a 98% probability of developing life-threatening coagulopathy

� if the Injury Severity Score is >25 (a method for describing patients with multiple injuries)

� systolic blood pressure < 70 mmHg� pH < 7.1

Jama 2006: 60:S1-S2 Early massive trauma transfusion: state of the art. John B Holcomb, MD, FACS and John Hess MD, MPH, FACP, FAAAAS 1:1:1

Early use of RBC + plasma+ platelets offers best chance of limiting coagulopathy

Still awaiting results of prospective, randomized, clinical trials:

PROMMTT - PRospective, Observational, Multi-center Massive Transfusion sTudy

Prospective, randomized trial

Evaluate transfusion of stored whole blood and pooled platelets during transfusion therapy. [ Time Frame: First 24 hours after ED admission ] [ Designated as safety issue: No ]

A) Compare its ability to reduce transfusion requirements as compared to component therapy (packed red blood cells, fresh frozen plasma, and platelet units)

B) Compare overall mortality as compared to component therapy

C) Compare incidence of multiple organ failure as compared to component therapy D) Compare the impact of age of blood products on clinical outcomes.

� No data focusing on patient outcomes, which compare component therapy with whole blood in rapidly bleeding trauma patients.

� Military setting

� 246 massively transfused

(≥10 U of RBCs in 24 h)

� Trauma patients

� Significant reduction in

mortality 65% reduced to

approximately 20%;

� Similar data of improved

survival with plasma:RBC

ratios approaching 1:1 in the

civilian setting has also been

reported.

Practice guidelines for blood component therapy: a report by theAmerican Society of Anesthesiologists Task Force on BloodComponent Therapy. Anesthesiology 1996; 84: 732–47

COAGULATION COAGULATION COAGULATION COAGULATION PARAMETERPARAMETERPARAMETERPARAMETER

RECOMMENDED THARAPYRECOMMENDED THARAPYRECOMMENDED THARAPYRECOMMENDED THARAPY

PT >1.5 FFP/PTC

APTT > 1.5 FFP

FIBRINOGEN < 1. 0g/l CRYOPRECIPITATE

Platelet < 50× 10⁹/l PLATELETS

� Establish adequate IV access 2 large bore IV cannula

� Estimate blood loss and ongoing losses

� Send blood for routine investigations and crossmatch blood and blood products, ratio 1:1

� ABGs, Hb, Electrolytes, coagulation profile, platelet count

� Start fluids – permissive hypotension

� Prevent Hypothermia

� Correct Acidosis

� Prevent Coagulopathy

Contents Contents Contents Contents Time to Time to Time to Time to

prepareprepareprepareprepare

Problems Problems Problems Problems Actions Actions Actions Actions

Type O - NEG No major

antigens

5 mins Rare / low

reserves in

Blood bank

For extreme emergencies

Type O - POS Avoid in

female child

bearing age

Type specific

blood

ABO RhD

matched

10 mins Switch promptly to type specific

Full crossmatch 45 mins

WHOLE BLOODWHOLE BLOODWHOLE BLOODWHOLE BLOOD RBC COMPONENTSRBC COMPONENTSRBC COMPONENTSRBC COMPONENTS

Fresh: 500ml

Haematocrit 45%

MODERN CONCEPT335 mlHCT 55%

OPTIMISES USE OF RESOURCES

AVOIDS HARMFUL EFFECTS BY SURPLUS CONSTITUENTS

CONTAINS 200 ML PLASMA/CLOTTING

FACTORS

Factor activity 100%

Platelets 250 000/mcl

Refrigerated blood – platelet nonviable

Clotting factors V and VIII

NO COAGULATION FACTORS/PLATELETS+50 ml platelets - 55

+ FFP 275 ml

Hct 29%/86% coag factors activity

LOW pH THAT DECREASES WITH STORAGE AND INCREASES ACID LOAD

CONTRIBUTES TO COAGULOPATHY

EXCESS CITRATE IN FFP

� “No clinical evidence of

haemorrhagic diatheses appeared in any of these young men despite large volumes of transfused

blood”

� End of WW I – Use of fresh blood� Blood blanking� WW II – use of freeze dried plasma (source of

transmissible jaundice� 1945 - Whole blood� 10 years later – fractionation techniques� Excessive crystalloid administration� Concept of whole blood in massive

transfusion� Balanced resuscitation practice

� Under extreme and austere circumstances, Under extreme and austere circumstances, Under extreme and austere circumstances, Under extreme and austere circumstances, the risk:benefit ratio of whole blood the risk:benefit ratio of whole blood the risk:benefit ratio of whole blood the risk:benefit ratio of whole blood transfusion favors its use. transfusion favors its use. transfusion favors its use. transfusion favors its use.

� Fresh whole blood may, at times, be Fresh whole blood may, at times, be Fresh whole blood may, at times, be Fresh whole blood may, at times, be advantageous even when conventional advantageous even when conventional advantageous even when conventional advantageous even when conventional component therapy is availablecomponent therapy is availablecomponent therapy is availablecomponent therapy is available

prepareActions

Warm FRESH BLOOD RedPlatelets)coagulation factorsPlasma proteins

1 hour

not easily

available

red cellCoagulopathythrombocytopenia

Refrigerated blood Factors decrease after 21days of storage V and VIII

Use of PRC

Early use of FFP/platelet/cryoppte

FFP stored at < -20

Freshly thawed and stored for up to 5 days

275 thawedFactor activity 80%

20 minutes to

thaw

10 – 15 ml/kg4FFP

Increases coagulation factors to 30%10-30% required for haemostasis

Platelets if <75 –1001 pack/10kg

I unit – 50 ml increases count by 5 – 10,000/micl. Keep platelet count > 100

Cryoprecipitate1-1.5 packs/10 kg

Indicated if fibrinogen level <1g/L

Impaired O2 release from Hb

2,3 DPG, hypothermia Warm blood, maintain normothermia Core temp 36 – 37

Hypothermia Warm blood, warm room,, convective warming.humidify gases

Citrate toxicity Decreased ionised calcium

CaCl2 = 20 mg/kg

Hyperkalaemia ECG monitor, CaCl2/glucose/insulin/HCO3

Haemolytic transfusion reaction

1:40000 due to error Check and recheck donor unit

Infection Hep B 1:82000HIV 1:4.7 millionHep C 1:3.1 millionBacterial contamination from platelet transfusion 1:10 000, 1: 100000 in red cell transfusion

Immunomodulatory effects

Proinflammaotry effects -MOF

Lower transfusion trigger. Third-generation leukocyte filters.

Older RBC products

� 14 days Increased morbidity and mortalityWeinberg JA, McGwin GJ, Marques MB, Cherry SAI, Reiff

DA, Kerby JD, Rue LWI. Transfusions in the less

severely injured: does age of transfused blood affect

outcomes? J Trauma 2008;65:794–8

� Reduce recipient exposures to donors

� Reduce TRALI

� Risk of thrombocytopenia

� Warm fresh blood: finding donors/risk of virus transmission

The overall mortality of these patients is high

(57%).

Malone DL, Dunne J, Tracy JK, et al. Blood transfusion, independent of shock severity, is associated with worse outcome in trauma. J Trauma 2003;

54:898–907

Limited commodityExpensive commodityRisks/benefits – benefits of transfusion outweighs risks associated with use

Tranfusion requirements based on

� Patients physiologic needs

� Oxygen demand/consumption

� Improved mental status, CRT, Vital signs: HR, BP – non specific

� Full blood examination: Hb level inaccurate, delays in obtaining results 45 –60 mins

� Coagulation status including serum fibrinogen level

� Coagulation tests are determined in plasma rather than whole blood

� no information is available on platelet function

� a standard temperature of 37.8C rather than the patient’s temperature

� Mixed venous oxygen saturation (SvO2) is a sensitive indicator of the adequacy of whole-body tissue oxygenation.

� Mixed venous and central venous O2 saturation

(normally SvO2 >70%).

� Acid-base status including serum base deficit > -3 mmol/l

� Lactate >2 mmol - poor oxygenation, poor perfusion or circulatory failure

� Hb 7- 9 g/dl

� Platelet > 50 > 100 in TBI

� TXA to be used in bleeding trauma patients

� Tranexamic acid 1g over 10 mins + infusion of 1g over 8 hrs/placebo

CRASH-2 trial collaborators; Shakur H, Roberts I, Bautista R, et al. Effectsof tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376:23–32.

� Tranexamic acid (TXA) is an antifibrinolytic

� Inhibits both plasminogen activation and plasmin activity

� Preventing clot breakdown

� Does not promote new clot formation

� Avoid delayed transfer to theatre

� ABC

� Control obvious haemorrhage by direct pressure

� Establish adequate IV access 2 large bore IV cannula

� Estimate blood loss and ongoing losses

� Send blood for routine investigations and crossmatch blood and blood products, ratio 1:1:1, 6prc/6ffp/6platelet

� ABGs, Hb, Electrolytes, coagulation profile, platelet count, lactate, SvO2

� Start fluids – permissive hypotension

� Prevent Hypothermia

� Correct Acidosis

� Prevent Coagulopathy

Thrombelastography (TEG)

Rotation thrombelastometry (ROTEM)

The viscoelastic properties of the developing clot in whole blood

� Return of whole blood

� Freshly drawn platelets

� Small volume

� Ambient temperature storage

� Immediate availability

� Disease free