BLOOD AND
BEYOND:
TRAUMA SHOCK
RESUSCITATION AND
MASSIVE
TRANSFUSION
PROTOCOLS
DR.ANKUR SHARMA
Additional Professor
AIIMS Jodhpur
TYPES OF SHOCK
HEMORRHAGIC SHOCK NON-HEMORRHAGIC SHOCK
SEPTIC SHOCK
NEUROGENIC SHOCK
CARDIOGENIC SHOCK
OBSTRUCTIVE SHOCK
An abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation
HEMORRHAGIC SHOCK
• Severe hemorrhage carries a mortality rate of 30-40%.
• Important cause of post-resuscitation organ failure and late mortality.
• Sources of potential blood loss-
“CHEST,ABDOMEN, PELVIS, RETROPERITONEUM, EXTREMITIES and
EXTERNAL BLEEDING”
“BLOOD ON FLOOR AND FIVE
MORE”
PATHOPHYSIOLOGY
Impaired oxidative metabolism
and homeostasis
Global insult to the vascular
endothelium
Progressive cellular and organ
dysfunction
Prolonged hypoperfusion
OXYGEN DEBT
Activates coagulation and
inflammatory system
Hypoperfusion to organs resulting in inadequate cellular
waste removal
Blood loss Intravascular volume depletion
TRAUMA INDUCED COAGULOPATHY
SIGNS AND
SYMPTOMS
DIAGNOSIS
• Clinical information :Heart rate, Blood pressure, skin perfusion, and mental status.
• Arterial blood gas : pH, pO2, PCO2, oxygen saturation, and base deficit, lactate
• Elevated lactate and base deficit are late findings.
• An earlier finding is an increase in oxygen extraction, indicated by a decrease in
indicators of oxygen consumption such as mixed or central venous hemoglobin
oxygen saturation.
TREATMENT
• In the ED, priorities are to
• Restore intravascular volume to reverse or limit systemic and regional
hypoperfusion,
• Maintain oxygen-carrying capacity so that tissue oxygen delivery meets
demand,
• Limit ongoing blood loss,
• Prevent the development of coagulopathy
• Prevent Hypothermia
CIRCULATION
• Control obvious hemorrhage.
• Bleeding from external wounds in the extremities
• Controlled by direct pressure to the bleeding site
• Massive blood loss from an extremity may require a tourniquet.
• A sheet or pelvic binder : In pelvic fractures.
• Surgical or angioembolization :In internal hemorrhage.
• The priority is to stop the bleeding, not to calculate the volume of fluid lost.
PREVENT HYPOTHERMIA
• Infusing crystalloids stored in warmers or infusing through intravenous fluid
warmers.
• Blood products can only heated by passage through intravenous fluid warmers.
• External warming devices/ thermal caps/ heated respiratory gases/ heat lamps.
• Severe hypothermia extracorporeal bypass indicated.
• Preventive measures are best.
VASCULAR ACCESS AND MONITORING
• Establish adequate IV access concurrent with airway management.
• Large-bore (14- to 16-gauge in adults) peripheral lines ,two or more to be secured.
• Intraosseous lines if peripheral IV access is difficult.
• Continuous ECG heart rate monitoring, continuous pulse oximetry.
• Monitor ABG, mental status, and peripheral perfusion frequently.
• Bedside FAST and POCUS:To identify intraperitoneal bleeding, assess cardiac function
and volume status, and assist in central venous cannulation.
FLUID THERAPY
• Warmed bolus of isotonic fluid is preferred.
• 1L for adults and 20mL/kg for paediatric patients weighing less than 40kg.
• Includes any fluid given in prehospital setting.
• Assess the patient’s response to fluid resuscitation and plan for further therapeutic and
diagnostic decisions on this response.
• Persistent infusion of large volumes of fluid and blood is not a substitute for definitive
control of bleeding.
FLUID THERAPY
ISOTONIC CRYSTALLOIDS
COLLOIDS
PACKED RED BLOOD CELLS
PLASMA
PLATELETS
ISOTONIC CRYSTALLOID SOLUTIONS
Concerns about each fluid:
(1) Infusion of large volumes of either NS or RL can cause increased neutrophil activation;
(2) RL solution can increase cytokine release  Increase lactic acidosis when given in large volumes;
(3) NS can exacerbate intracellular potassium depletion  Hyperchloremic acidosis
PRBC
• Packed red blood cells
(PRBCs) are the most commonly
transfused blood product.
• If hemorrhage is definitively
controlled, do not transfuse if
the hemoglobin concentration is
>7 grams/dL.
• Typed and cross-matched blood
Type-specific blood  low-
titer O-negative blood.
• PRBCs can be stored for up to
45 days.
FFP
• A unit of FFP: 200 to 250 ml
• Contains all the coagulation
factors present in fresh blood.
• Kept frozen, FFP can be
stored for up to a year.
• When transfusing FFP,ABO
compatibility is required, Rh
compatibility is less important.
• Universal donor:AB+ and
does not require cross-
matching for emergency use.
PLATELETS
• Platelets are collected from
whole-blood donations or
from single donors using
apheresis techniques.
• Stored for up to only 5 days.
• Six units of RDP or one
apheresis-collected SDP in an
adult  will increase platelet
count up to 50,000/mm3.
Failure to respond to crystalloids
and blood administration
Search other causes
• Blunt myocardial injury
• Tension pneumothorax
• Cardiac tamponade
• Neurogenic shock
• Ongoing hemorrhage
• Hypoadrenalism
• Diabetic acidosis
• Acute fluid loss
• Acute gastric distension
• Myocardial infarction
BLADDER CATHETERISATION
• Urinary output is a prime indicator of resuscitation and patient’s response.
• O.5mL/kg/hr in adults and 1mL/kg/hr in paediatrics.
• Less than 1yr, 2mL/kg/hr is adequate urine output.
• Inability to obtain urinary output at these levels or decreasing urinary
output with increasing specific gravity suggests inadequate resuscitation.
• Blood at meatus/ perineal hematoma indicates urethral injury.
ON REASSESSMENT, PATIENT STILL IN
SHOCK!!! WHAT NEXT???
VASOPRESSORS ARE CONTRAINDICATED
IN HEMORRHAGIC SHOCK AS IT
WORSENS TISSUE PERFUSION
VASOPRESSORS?
1.Permissive Hypotension
2.Haemostatic Resuscitation (Massive Transfusion Protocol)
3.Haemorrhage Control (Damage Control Surgery)
• Damage Control Resuscitation (DCR) is the concept of rapid haemorrhage
control through:
DAMAGE CONTROL RESUSCITATION
(DCR)
Intravascular volume deficits
 Acute coagulopathy of trauma
Preserve oxygen-carrying capacity
Prevention of dilutional coagulopathy.
Early administration of blood products in a balanced ratio 1:1:1 for units of plasma to
platelets to red blood cells helps treat -
HYPOTHERMIA ACIDOSIS
HYPOCALCEMIA
LETHAL TRIAD
COAGULOPATHY
LETHAL DIAMOND
HEMOSTATIC-HYPOTENSIVE RESUSCITATION
• Hypotensive resuscitation limits initial fluid resuscitation to an acceptable systolic blood
pressure goal until surgical control of the bleeding is obtained, usually in the operating room.
• Complete normalization of BP will raise hydrostatic pressure and can increase hemorrhage,
where raising BP could potentially “pop the clot” and reestablish active hemorrhage.
• “Controlled resuscitation” / “Balanced resuscitation” / “ Permissive hypotension”
• Used as a bridge, not as substitute.
• Hypotensive resuscitation shouldn’t be used in conditions where low SBP exacerbates end organ
hypo perfusion such as TBI/ Myocardial diseases/ Cerebral ischemia.
• Patients can not tolerate hypotensive resuscitation for prolonged time. It can lead to irreversible
damage from prolonged tissue hypoxia if adequate tissue oxygenation is not restored.
MASSIVE TRANSFUSION PROTOCOL
OBJECTIVE
MASSIVE TRANSFUSION
• Administering 10 or more units of whole blood or packed red blood cells
(PRBCs) within 24 hours.
• Ultra-massive transfusion is defined as using more than 20 units of PRBCs within
a 24- to 48-hour period.
• Massive Blood transfusion is defined as the replacement of one blood volume
within 24 hours.
• > 10 units of RBCs in 24 hrs
• > 4 units of RBCs in an hour
• Replacement of 50% blood volume in 3-4 hrs
Jennings LK, Watson S. Massive Transfusion. [Updated 2023 Oct 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499929/
WHAT IS MT PROTOCOL?
• Document/guidelines followed by a Center that should be followed by all staffs
and doctors when it is activated
• Maintain competency of staffs -Training and Drills
CONTENT OF THE PROTOCOL
• When should MTP be activated?
• What is the ratio of blood products to be transfused?
• Define a process to allow immediate availability of blood products
• Standardization of Assessment
• What is the end point of resuscitation?
• When should MTP be De - activated?
• Did we go wrong? If soWhere can we Improve?
• Quality improvement strategies
TRIGGERS FOR STARTING MTP
• Dilemma – decreased mortality versus increased morbidity
• Predicting need of MTP:
• Assessment of Blood consumption Score (ABC)
• Shock index
• Modified shock Index
• Age Shock index
• TASH Score (Trauma Associated Severity Haemorrhage)
• The TASH score has a range from
0 to 28
• somewhat complex to calculate.
• Well validated
• 1 point for each score
• Score ≥ 2 indicate the necessity to initiate MTP.
• positive predictive value of 50% to 55%
• Identifies over 95% of patients requiring a MTP but
has a negative predictive value of less than 5%.
• Over estimation is the problem
*ACQS Massive transfusion in trauma guidelines 2014
TIME IS OF THE ESSENCE
• Inform blood bank and inform your team
• A blood refrigerator within the resuscitation bay stocked with universal donor
products
• Ideally comprising a minimum of 8 units of O-negative PRBCs and 8 units of
thawed group AB or low titer anti-B group A plasma.
• Rapid availability of blood products in trauma bay
• Establish suitable intravenous (IV) or
intraosseous access
• 14 to 18 gauge IV Cannula
• Use a blood warmer
BLOOD WARMER
• Warms the blood to body temperature
• Prevents hypothermia
• Plasma and Blood can be given
• Platelets and Cryoprecipitate cannot be given through blood
warmers
• Begin Universal Blood Product transfusion instead of crystalloids
• Ratio is 1:1:1 (RBC:Plasma:Platelets)
• Blood Products should automatically be sent by blood bank in the established ratios
• Subsequent coolers should be delivered at 15 minutes interval until the MTP has
been terminated
• Goal is to keep one MTP cooler ahead for the duration of MTP activation
• When shifting patient to OT – communicate with blood bank so that they can send
the blood products there
TRANSFUSION
PROPPR TRIAL
Pragmatic RCT
680 patients
12 level 1 trauma centres in USA
2015
• Early administration of plasma, platelets, and red
blood cells in a 1:1:1 ratio compared with a 1:1:2
ratio did not result in significant differences in
mortality at 24 hours or at 30 days.
• However, more patients in the 1:1:1 group
achieved hemostasis and fewer experienced death
due to exsanguination by 24 hours.
2009 -2010
PROMMTT trial
Established early plasma transfusion
THE FUTURE?
Transfusion with WB + COMP is associated with lower 24-h mortality
versus COMP and transfusion with WB is associated with a lower
volume of red blood cells transfused at both 6 and 24 h.
ADDITIONAL REQUIREMENTS FOR MTP
• Effective communication with blood banks
• Sufficient number of personnel for timely sample collection
• Dedicated Runner for the procurement of blood and blood products.
• Inclusion of surface warmers
• Switch to Laboratory point of care based transfusion once the major bleeding has been
controlled
• Ratio of blood Products should be assessed at the time of bleeding control and not at any point
of time during MTP
• Switch to cross matched blood products as soon as possible
• Continuous core temperature monitors.
• An invasive arterial blood pressure monitor.
• Adequate supply of colloid and crystalloid infusion sets.
• IV calcium preparations.
• Point-of-care testing for various bodily functions, including arterial blood gas
(ABG), hemoglobin, electrolytes, lactate, and thromboelastography (TEG).
• Rapid infusion pumps or pressure bags to expedite the fluid infusion rates.
UNIVERSAL DONORS
• patients are given O-negative blood until crossmatched PRBCs become accessible.
• For the initial phase, it is advisable to have universal thawed plasma, typically AB
plasma, readily available.
• Type A plasma with low titers of anti-B can also be a suitable choice.
• Patients should promptly receive group-specific plasma when their blood typing
is completed.
DEFINITIVE MANAGEMENT
• Should incorporate Damage control resuscitation:
• abbreviated surgical and/or endovascular interventions for hemorrhage
control and management of intra-abdominal contamination
• critical care support to correct deranged physiologic measures (hypothermia,
acidosis, coagulopathy)
• Delayed definitive surgical repair
MTP In ICU
• Patients requiring MTP should get admitted
to ICU
• ICU driven Algorithm
• Fixed ratio should be followed in ICU until
Specific laboratory data is available
• Goal Directed Therapy
THERAPEUTIC ADJUNCTS
• tranexamic acid (TXA) can mitigate coagulopathy and improve survival rates
among patients with combat injuries
• functions by blocking fibrinolysis or the breakdown of clots and is most effective
when administered within 3 hours of the trauma.
• As a result, many MTPs now incorporate TXA into their procedures.
MONITORING
• Continuous monitoring throughout the resuscitation process is important.
• The typical practice is to assess the following parameters after approximately 5
units of PRBCs have been administered:
• Complete blood count (CBC) with platelet count
• Prothrombin time (PT)
• Activated partial thromboplastin time (aPTT)
• Fibrinogen concentration
Jennings LK, Watson S. Massive Transfusion. [Updated 2023 Oct 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499929/
• Ideal monitoring involves measuring every 20 to 30 minutes
• pH, blood gases
• electrolytes, and
• metabolites such as glucose
• Lactate
• TEG assesses platelet function, clot strength, and fibrinolysis.
• Therefore, when TEG is accessible, the results obtained from the test can inform
decisions regarding the timing of additional plasma, cryoprecipitate, platelets, or
antifibrinolytics, depending on the specific TEG profile.
• The resuscitation objectives in the context of massive transfusion include:
• A mean arterial pressure (MAP) within the range of 60 to 65 mm Hg
• Hemoglobin level between 7 and 9 g/dL
• International normalized ratio (INR) below 1.5
• Fibrinogen levels within the range of 1.5 to 2 g/L
• Platelet counts above 50,000 μL
• pH between 7.35 and 7.45
• Core temperature above 35 °C
Calcium in transfusion
• Hypocalcemia on arrival is known to be associated with poor short-term
prognosis and massive blood transfusions
• Calcium decreases with transfusion due to citrate as preservative
• When administering one round of MTP (containing 6 units PRBCs), it's reasonable
to add either 1-2 gram of IV calcium chloride or 3-6 grams of IV calcium gluconate
• Measure Ionized Calcium to guide calcium administration
END POINTS of TRANSFUSION
• Who Decides?
• Trauma surgeon in conjunction with
anesthetists in OT
• Intensivist in ICU
• When?
• Clinical end points: hemodynamic stability
• Laboratory end points:
DEACTIVATING MTP
• The attending physician will call the blood bank to deactivate the MTP when
clinically appropriate.
• The blood bank staff members will record the date, time, and attending physician
name.
• Blood Bank technician will notify on-call Transfusion medicine specialist
• System to return unused blood Products
SUMMARY
Predict need for
MTP
Activate MTP Transfuse
Definitive
management
Re-assess
end point
Resuscitation
Deactivate
MTP
DO IT AS QUICKLY AS POSSIBLE
ABC score
Hemodynamic
instability
Active bleeding
communicate
ABC score
Shock Index
Modified Shock
Index
Storage in trauma
bay
Universal donors
Large IV bore
cannula
Interrosseus access
Blood warmers
Maintain ratio
Clinical end points
Laboratory end
points
Angioembolisation
OT
Correction of
coagulopathy
Hemodynamics
APTT
TEG/ROTEM
PTINR
Hb
Lactate
ABG
fibrinogen
COMPLICATIONS OF BLOOD TRANSFUSION
DEFINITION OF MASSIVE
TRANSFUSIONS:
• Transfusion of >10 PRBC units in 24hrs ( oneTBV)
• Transfusion of >4PRBC in one hour with anticipation of continues need for blood
support .
• Replacement of >50% ofTBV with blood products in 3 hrs
• Bleeding >150ml/minute (AAGBI 2016)
WHY WE NEED MASSIVE TRANSFUSION
PROTOCOLS IN TRAUMA ?
• Hemorrhage in trauma accounts for the most common cause of the
early death.
• Coagulopathy sets in as early as 30 mins of injury – Early Trauma Iduced
coagulopathy (ETIC).
• Resuscitation phase leads to lethal triad.
• Balanced resuscitation – early administration of blood corrects the ETIC
, prevents dilution and corrects the acidosis.
WHEN TO ACTIVATE MTP
• Class 2 of hemorrhagic shock with ongoing hemorrhage/expected utilization of
more blood products.
• Class 3 & 4 of hemorrhagic shock.
• Evidence of massive hemorrhage with
1. Coagulopathy
2. MAP <60mm/hypotension
3. Electrolyte imbalance and acidosis
4.Tissue hypoxia
PREDICTING MASSIVE TRANSFUSION
TASH score – Male , Unstable pelvic fracture , Open femur fracture , FAST
positive , Pulse , SBP ,Hb , Base defict (if >16 -50% MT, >27-100 % MT)
TWH score – Unstable pelvic fracture , Open femur fracture, FAST positive ,
pulse , SBP , Hb , Base deficit , GCS
Vandromme score – Pulse , SBP <,Hb, Base defict ,INR
ABC score – FAST positive ,Pulse , SBP, Penetrating injury :>/=2 s/o MT
ALGORITHM
VISCO ELASTIC TESTS GUIDED
MANAGEMENT
• Identifies ETIC – helps to administerTranexa.
• Identifies trauma induced platelet dysfunction.
• Identifies coagulopathy due to traumatic brain injury even with minimal bleeding
• Will help to correct dilutional coagulopathy.
• TEG guided algorithm as well as ROTEM .
• VET can guide blood component therapy and dose required.
• Rapid turn around time if used as point of care device.
TEG
WHEN TO STOP
• Attaining hemostasis/ no active bleeding
• Stable vitals / temperature >35 C
• No severe base deficit
• MAP>60mmhg
• No acidosis
• Review after 24 hours/as requires clinically
1 Hb >7g/dl
2 Platelet>75,000/ul
3 PT/aPTT normal or <1.5times of normal
4 fibrinogen >100 mg/dl
COMPLICATIONS OF MASSIVE
TRANSFUSION
• Transfusion reactions – Immune and non –Immune
• Metabolic complications –Hypocalcemia,
Hypomagnesemia , Hyper/Hypokalemia ,Metabolic alkalosis
, Metabolic acidosis , Hypothermia
• Coagulopathy
• Air embolism
SOME GROUND BREAKING WORK IN
TRAUMA AND MASSIVE TRANSFUSION
1:1:1 component ratio in massive transfusion has reduced mortality from
66% to 19 % (Borgman 2007,J of trauma)
Early infusion of FFP and platelets is associated with decreased mortality –
PROMMTT trial
• Conclusions Higher plasma and platelet ratios early in resuscitation were associated with
decreased mortality in patients who received transfusions of at least 3 units of blood
products during the first 24 hours after admission.Among survivors at 24 hours, the
subsequent risk of death by day 30 was not associated with plasma or platelet ratios.
February 3, 2015
JAMA
Conclusions and Relevance Among patients with severe trauma and major bleeding,
early administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared
with a 1:1:2 ratio did not result in significant differences in mortality at 24 hours or at 30
days.
• TXA safely reduced the risk of death in bleeding trauma patients in this study. On
the basis of these results,TXA should be considered for use in bleeding trauma
patients.
SHOCK OR NOT
• SCENARIO 1:
• A 25 year old male, athlete had a h/o fall from bike presented to ED
• HR: 74/min, BP: 110/50mmhg, SpO2: 95% on RA
• Patient is confused.
YES
• Young, healthy patients may mask hypotension and tachyacrdia symptoms;
• peripheral hypoperfusion and mental status changes are key early signs of severity.
SHOCK OR NOT
• SCENARIO 2:
• A 60 year old male, hypertensive on medication, presented to ED with
h/o fall from stairs.
• HR: 64/min, BP: 110/70 mmhg, SpO2: 92% on RA.
YES
Elderly patients may not develop tachycardia due to underlying heart disease or medications such as
-adrenergic blockers.
β
SHOCK OR NOT
• SCENARIO 3:
• A 28 year old primigravida, 8 months POG, h/o trivial fall, presented to
ED.
• HR: 104/min, BP: 86/50 mmhg, SpO2: 99% on RA.
• EFAST: Negative
NO
In a pregnant trauma patient, compression of the inferior vena cava by the gravid uterus can decrease
central venous return and worsen hypotension and tachycardia in the setting of less severe
hemorrhage.
SHOCK OR NOT
• SCENARIO 4:
• A 18 year old male, with A/h/o assault, blunt injury to abdomen,
presented to ED with
• HR: 54/min, BP: 90/60 mmhg, SpO2: 94% on RA.
YES
Bradycardia or lack of tachycardia may occur in about 30% of patients with .
intra-abdominal hemorrhage from increased vagal tone in response to hemoperitoneum.
FAST : POSITIVE
THANK YOU

Trauma Shock Resuscitation and Massive Transfusion Protocols.pptx

  • 1.
    BLOOD AND BEYOND: TRAUMA SHOCK RESUSCITATIONAND MASSIVE TRANSFUSION PROTOCOLS DR.ANKUR SHARMA Additional Professor AIIMS Jodhpur
  • 2.
    TYPES OF SHOCK HEMORRHAGICSHOCK NON-HEMORRHAGIC SHOCK SEPTIC SHOCK NEUROGENIC SHOCK CARDIOGENIC SHOCK OBSTRUCTIVE SHOCK An abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation
  • 3.
    HEMORRHAGIC SHOCK • Severehemorrhage carries a mortality rate of 30-40%. • Important cause of post-resuscitation organ failure and late mortality. • Sources of potential blood loss- “CHEST,ABDOMEN, PELVIS, RETROPERITONEUM, EXTREMITIES and EXTERNAL BLEEDING” “BLOOD ON FLOOR AND FIVE MORE”
  • 4.
    PATHOPHYSIOLOGY Impaired oxidative metabolism andhomeostasis Global insult to the vascular endothelium Progressive cellular and organ dysfunction Prolonged hypoperfusion OXYGEN DEBT Activates coagulation and inflammatory system Hypoperfusion to organs resulting in inadequate cellular waste removal Blood loss Intravascular volume depletion
  • 5.
  • 6.
  • 7.
    DIAGNOSIS • Clinical information:Heart rate, Blood pressure, skin perfusion, and mental status. • Arterial blood gas : pH, pO2, PCO2, oxygen saturation, and base deficit, lactate • Elevated lactate and base deficit are late findings. • An earlier finding is an increase in oxygen extraction, indicated by a decrease in indicators of oxygen consumption such as mixed or central venous hemoglobin oxygen saturation.
  • 8.
    TREATMENT • In theED, priorities are to • Restore intravascular volume to reverse or limit systemic and regional hypoperfusion, • Maintain oxygen-carrying capacity so that tissue oxygen delivery meets demand, • Limit ongoing blood loss, • Prevent the development of coagulopathy • Prevent Hypothermia
  • 9.
    CIRCULATION • Control obvioushemorrhage. • Bleeding from external wounds in the extremities • Controlled by direct pressure to the bleeding site • Massive blood loss from an extremity may require a tourniquet. • A sheet or pelvic binder : In pelvic fractures. • Surgical or angioembolization :In internal hemorrhage. • The priority is to stop the bleeding, not to calculate the volume of fluid lost.
  • 10.
    PREVENT HYPOTHERMIA • Infusingcrystalloids stored in warmers or infusing through intravenous fluid warmers. • Blood products can only heated by passage through intravenous fluid warmers. • External warming devices/ thermal caps/ heated respiratory gases/ heat lamps. • Severe hypothermia extracorporeal bypass indicated. • Preventive measures are best.
  • 11.
    VASCULAR ACCESS ANDMONITORING • Establish adequate IV access concurrent with airway management. • Large-bore (14- to 16-gauge in adults) peripheral lines ,two or more to be secured. • Intraosseous lines if peripheral IV access is difficult. • Continuous ECG heart rate monitoring, continuous pulse oximetry. • Monitor ABG, mental status, and peripheral perfusion frequently. • Bedside FAST and POCUS:To identify intraperitoneal bleeding, assess cardiac function and volume status, and assist in central venous cannulation.
  • 12.
    FLUID THERAPY • Warmedbolus of isotonic fluid is preferred. • 1L for adults and 20mL/kg for paediatric patients weighing less than 40kg. • Includes any fluid given in prehospital setting. • Assess the patient’s response to fluid resuscitation and plan for further therapeutic and diagnostic decisions on this response. • Persistent infusion of large volumes of fluid and blood is not a substitute for definitive control of bleeding.
  • 14.
  • 15.
    ISOTONIC CRYSTALLOID SOLUTIONS Concernsabout each fluid: (1) Infusion of large volumes of either NS or RL can cause increased neutrophil activation; (2) RL solution can increase cytokine release  Increase lactic acidosis when given in large volumes; (3) NS can exacerbate intracellular potassium depletion  Hyperchloremic acidosis
  • 16.
    PRBC • Packed redblood cells (PRBCs) are the most commonly transfused blood product. • If hemorrhage is definitively controlled, do not transfuse if the hemoglobin concentration is >7 grams/dL. • Typed and cross-matched blood Type-specific blood  low- titer O-negative blood. • PRBCs can be stored for up to 45 days. FFP • A unit of FFP: 200 to 250 ml • Contains all the coagulation factors present in fresh blood. • Kept frozen, FFP can be stored for up to a year. • When transfusing FFP,ABO compatibility is required, Rh compatibility is less important. • Universal donor:AB+ and does not require cross- matching for emergency use. PLATELETS • Platelets are collected from whole-blood donations or from single donors using apheresis techniques. • Stored for up to only 5 days. • Six units of RDP or one apheresis-collected SDP in an adult  will increase platelet count up to 50,000/mm3.
  • 17.
    Failure to respondto crystalloids and blood administration Search other causes • Blunt myocardial injury • Tension pneumothorax • Cardiac tamponade • Neurogenic shock • Ongoing hemorrhage • Hypoadrenalism • Diabetic acidosis • Acute fluid loss • Acute gastric distension • Myocardial infarction
  • 18.
    BLADDER CATHETERISATION • Urinaryoutput is a prime indicator of resuscitation and patient’s response. • O.5mL/kg/hr in adults and 1mL/kg/hr in paediatrics. • Less than 1yr, 2mL/kg/hr is adequate urine output. • Inability to obtain urinary output at these levels or decreasing urinary output with increasing specific gravity suggests inadequate resuscitation. • Blood at meatus/ perineal hematoma indicates urethral injury.
  • 19.
    ON REASSESSMENT, PATIENTSTILL IN SHOCK!!! WHAT NEXT??? VASOPRESSORS ARE CONTRAINDICATED IN HEMORRHAGIC SHOCK AS IT WORSENS TISSUE PERFUSION VASOPRESSORS?
  • 20.
    1.Permissive Hypotension 2.Haemostatic Resuscitation(Massive Transfusion Protocol) 3.Haemorrhage Control (Damage Control Surgery) • Damage Control Resuscitation (DCR) is the concept of rapid haemorrhage control through: DAMAGE CONTROL RESUSCITATION (DCR)
  • 21.
    Intravascular volume deficits Acute coagulopathy of trauma Preserve oxygen-carrying capacity Prevention of dilutional coagulopathy. Early administration of blood products in a balanced ratio 1:1:1 for units of plasma to platelets to red blood cells helps treat -
  • 22.
  • 23.
    HEMOSTATIC-HYPOTENSIVE RESUSCITATION • Hypotensiveresuscitation limits initial fluid resuscitation to an acceptable systolic blood pressure goal until surgical control of the bleeding is obtained, usually in the operating room. • Complete normalization of BP will raise hydrostatic pressure and can increase hemorrhage, where raising BP could potentially “pop the clot” and reestablish active hemorrhage. • “Controlled resuscitation” / “Balanced resuscitation” / “ Permissive hypotension” • Used as a bridge, not as substitute. • Hypotensive resuscitation shouldn’t be used in conditions where low SBP exacerbates end organ hypo perfusion such as TBI/ Myocardial diseases/ Cerebral ischemia. • Patients can not tolerate hypotensive resuscitation for prolonged time. It can lead to irreversible damage from prolonged tissue hypoxia if adequate tissue oxygenation is not restored.
  • 24.
  • 25.
    MASSIVE TRANSFUSION • Administering10 or more units of whole blood or packed red blood cells (PRBCs) within 24 hours. • Ultra-massive transfusion is defined as using more than 20 units of PRBCs within a 24- to 48-hour period. • Massive Blood transfusion is defined as the replacement of one blood volume within 24 hours. • > 10 units of RBCs in 24 hrs • > 4 units of RBCs in an hour • Replacement of 50% blood volume in 3-4 hrs Jennings LK, Watson S. Massive Transfusion. [Updated 2023 Oct 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499929/
  • 28.
    WHAT IS MTPROTOCOL? • Document/guidelines followed by a Center that should be followed by all staffs and doctors when it is activated • Maintain competency of staffs -Training and Drills
  • 29.
    CONTENT OF THEPROTOCOL • When should MTP be activated? • What is the ratio of blood products to be transfused? • Define a process to allow immediate availability of blood products • Standardization of Assessment • What is the end point of resuscitation? • When should MTP be De - activated? • Did we go wrong? If soWhere can we Improve? • Quality improvement strategies
  • 30.
    TRIGGERS FOR STARTINGMTP • Dilemma – decreased mortality versus increased morbidity • Predicting need of MTP: • Assessment of Blood consumption Score (ABC) • Shock index • Modified shock Index • Age Shock index • TASH Score (Trauma Associated Severity Haemorrhage)
  • 31.
    • The TASHscore has a range from 0 to 28 • somewhat complex to calculate.
  • 32.
    • Well validated •1 point for each score • Score ≥ 2 indicate the necessity to initiate MTP. • positive predictive value of 50% to 55% • Identifies over 95% of patients requiring a MTP but has a negative predictive value of less than 5%. • Over estimation is the problem *ACQS Massive transfusion in trauma guidelines 2014
  • 36.
    TIME IS OFTHE ESSENCE • Inform blood bank and inform your team • A blood refrigerator within the resuscitation bay stocked with universal donor products • Ideally comprising a minimum of 8 units of O-negative PRBCs and 8 units of thawed group AB or low titer anti-B group A plasma. • Rapid availability of blood products in trauma bay
  • 37.
    • Establish suitableintravenous (IV) or intraosseous access • 14 to 18 gauge IV Cannula • Use a blood warmer
  • 38.
    BLOOD WARMER • Warmsthe blood to body temperature • Prevents hypothermia • Plasma and Blood can be given • Platelets and Cryoprecipitate cannot be given through blood warmers
  • 39.
    • Begin UniversalBlood Product transfusion instead of crystalloids • Ratio is 1:1:1 (RBC:Plasma:Platelets) • Blood Products should automatically be sent by blood bank in the established ratios • Subsequent coolers should be delivered at 15 minutes interval until the MTP has been terminated • Goal is to keep one MTP cooler ahead for the duration of MTP activation • When shifting patient to OT – communicate with blood bank so that they can send the blood products there TRANSFUSION
  • 40.
    PROPPR TRIAL Pragmatic RCT 680patients 12 level 1 trauma centres in USA 2015 • Early administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared with a 1:1:2 ratio did not result in significant differences in mortality at 24 hours or at 30 days. • However, more patients in the 1:1:1 group achieved hemostasis and fewer experienced death due to exsanguination by 24 hours. 2009 -2010 PROMMTT trial Established early plasma transfusion
  • 41.
    THE FUTURE? Transfusion withWB + COMP is associated with lower 24-h mortality versus COMP and transfusion with WB is associated with a lower volume of red blood cells transfused at both 6 and 24 h.
  • 42.
    ADDITIONAL REQUIREMENTS FORMTP • Effective communication with blood banks • Sufficient number of personnel for timely sample collection • Dedicated Runner for the procurement of blood and blood products. • Inclusion of surface warmers • Switch to Laboratory point of care based transfusion once the major bleeding has been controlled • Ratio of blood Products should be assessed at the time of bleeding control and not at any point of time during MTP
  • 43.
    • Switch tocross matched blood products as soon as possible • Continuous core temperature monitors. • An invasive arterial blood pressure monitor. • Adequate supply of colloid and crystalloid infusion sets. • IV calcium preparations. • Point-of-care testing for various bodily functions, including arterial blood gas (ABG), hemoglobin, electrolytes, lactate, and thromboelastography (TEG). • Rapid infusion pumps or pressure bags to expedite the fluid infusion rates.
  • 44.
    UNIVERSAL DONORS • patientsare given O-negative blood until crossmatched PRBCs become accessible. • For the initial phase, it is advisable to have universal thawed plasma, typically AB plasma, readily available. • Type A plasma with low titers of anti-B can also be a suitable choice. • Patients should promptly receive group-specific plasma when their blood typing is completed.
  • 45.
    DEFINITIVE MANAGEMENT • Shouldincorporate Damage control resuscitation: • abbreviated surgical and/or endovascular interventions for hemorrhage control and management of intra-abdominal contamination • critical care support to correct deranged physiologic measures (hypothermia, acidosis, coagulopathy) • Delayed definitive surgical repair
  • 46.
    MTP In ICU •Patients requiring MTP should get admitted to ICU • ICU driven Algorithm • Fixed ratio should be followed in ICU until Specific laboratory data is available • Goal Directed Therapy
  • 47.
    THERAPEUTIC ADJUNCTS • tranexamicacid (TXA) can mitigate coagulopathy and improve survival rates among patients with combat injuries • functions by blocking fibrinolysis or the breakdown of clots and is most effective when administered within 3 hours of the trauma. • As a result, many MTPs now incorporate TXA into their procedures.
  • 48.
    MONITORING • Continuous monitoringthroughout the resuscitation process is important. • The typical practice is to assess the following parameters after approximately 5 units of PRBCs have been administered: • Complete blood count (CBC) with platelet count • Prothrombin time (PT) • Activated partial thromboplastin time (aPTT) • Fibrinogen concentration Jennings LK, Watson S. Massive Transfusion. [Updated 2023 Oct 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499929/
  • 49.
    • Ideal monitoringinvolves measuring every 20 to 30 minutes • pH, blood gases • electrolytes, and • metabolites such as glucose • Lactate • TEG assesses platelet function, clot strength, and fibrinolysis. • Therefore, when TEG is accessible, the results obtained from the test can inform decisions regarding the timing of additional plasma, cryoprecipitate, platelets, or antifibrinolytics, depending on the specific TEG profile.
  • 50.
    • The resuscitationobjectives in the context of massive transfusion include: • A mean arterial pressure (MAP) within the range of 60 to 65 mm Hg • Hemoglobin level between 7 and 9 g/dL • International normalized ratio (INR) below 1.5 • Fibrinogen levels within the range of 1.5 to 2 g/L • Platelet counts above 50,000 μL • pH between 7.35 and 7.45 • Core temperature above 35 °C
  • 51.
    Calcium in transfusion •Hypocalcemia on arrival is known to be associated with poor short-term prognosis and massive blood transfusions • Calcium decreases with transfusion due to citrate as preservative • When administering one round of MTP (containing 6 units PRBCs), it's reasonable to add either 1-2 gram of IV calcium chloride or 3-6 grams of IV calcium gluconate • Measure Ionized Calcium to guide calcium administration
  • 52.
    END POINTS ofTRANSFUSION • Who Decides? • Trauma surgeon in conjunction with anesthetists in OT • Intensivist in ICU • When? • Clinical end points: hemodynamic stability • Laboratory end points:
  • 54.
    DEACTIVATING MTP • Theattending physician will call the blood bank to deactivate the MTP when clinically appropriate. • The blood bank staff members will record the date, time, and attending physician name. • Blood Bank technician will notify on-call Transfusion medicine specialist • System to return unused blood Products
  • 55.
    SUMMARY Predict need for MTP ActivateMTP Transfuse Definitive management Re-assess end point Resuscitation Deactivate MTP DO IT AS QUICKLY AS POSSIBLE ABC score Hemodynamic instability Active bleeding communicate ABC score Shock Index Modified Shock Index Storage in trauma bay Universal donors Large IV bore cannula Interrosseus access Blood warmers Maintain ratio Clinical end points Laboratory end points Angioembolisation OT Correction of coagulopathy Hemodynamics APTT TEG/ROTEM PTINR Hb Lactate ABG fibrinogen
  • 56.
  • 58.
    DEFINITION OF MASSIVE TRANSFUSIONS: •Transfusion of >10 PRBC units in 24hrs ( oneTBV) • Transfusion of >4PRBC in one hour with anticipation of continues need for blood support . • Replacement of >50% ofTBV with blood products in 3 hrs • Bleeding >150ml/minute (AAGBI 2016)
  • 59.
    WHY WE NEEDMASSIVE TRANSFUSION PROTOCOLS IN TRAUMA ? • Hemorrhage in trauma accounts for the most common cause of the early death. • Coagulopathy sets in as early as 30 mins of injury – Early Trauma Iduced coagulopathy (ETIC). • Resuscitation phase leads to lethal triad. • Balanced resuscitation – early administration of blood corrects the ETIC , prevents dilution and corrects the acidosis.
  • 60.
    WHEN TO ACTIVATEMTP • Class 2 of hemorrhagic shock with ongoing hemorrhage/expected utilization of more blood products. • Class 3 & 4 of hemorrhagic shock. • Evidence of massive hemorrhage with 1. Coagulopathy 2. MAP <60mm/hypotension 3. Electrolyte imbalance and acidosis 4.Tissue hypoxia
  • 61.
    PREDICTING MASSIVE TRANSFUSION TASHscore – Male , Unstable pelvic fracture , Open femur fracture , FAST positive , Pulse , SBP ,Hb , Base defict (if >16 -50% MT, >27-100 % MT) TWH score – Unstable pelvic fracture , Open femur fracture, FAST positive , pulse , SBP , Hb , Base deficit , GCS Vandromme score – Pulse , SBP <,Hb, Base defict ,INR ABC score – FAST positive ,Pulse , SBP, Penetrating injury :>/=2 s/o MT
  • 62.
  • 63.
    VISCO ELASTIC TESTSGUIDED MANAGEMENT • Identifies ETIC – helps to administerTranexa. • Identifies trauma induced platelet dysfunction. • Identifies coagulopathy due to traumatic brain injury even with minimal bleeding • Will help to correct dilutional coagulopathy. • TEG guided algorithm as well as ROTEM . • VET can guide blood component therapy and dose required. • Rapid turn around time if used as point of care device.
  • 64.
  • 65.
    WHEN TO STOP •Attaining hemostasis/ no active bleeding • Stable vitals / temperature >35 C • No severe base deficit • MAP>60mmhg • No acidosis • Review after 24 hours/as requires clinically 1 Hb >7g/dl 2 Platelet>75,000/ul 3 PT/aPTT normal or <1.5times of normal 4 fibrinogen >100 mg/dl
  • 66.
    COMPLICATIONS OF MASSIVE TRANSFUSION •Transfusion reactions – Immune and non –Immune • Metabolic complications –Hypocalcemia, Hypomagnesemia , Hyper/Hypokalemia ,Metabolic alkalosis , Metabolic acidosis , Hypothermia • Coagulopathy • Air embolism
  • 67.
    SOME GROUND BREAKINGWORK IN TRAUMA AND MASSIVE TRANSFUSION 1:1:1 component ratio in massive transfusion has reduced mortality from 66% to 19 % (Borgman 2007,J of trauma) Early infusion of FFP and platelets is associated with decreased mortality – PROMMTT trial
  • 68.
    • Conclusions Higherplasma and platelet ratios early in resuscitation were associated with decreased mortality in patients who received transfusions of at least 3 units of blood products during the first 24 hours after admission.Among survivors at 24 hours, the subsequent risk of death by day 30 was not associated with plasma or platelet ratios.
  • 69.
    February 3, 2015 JAMA Conclusionsand Relevance Among patients with severe trauma and major bleeding, early administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared with a 1:1:2 ratio did not result in significant differences in mortality at 24 hours or at 30 days.
  • 70.
    • TXA safelyreduced the risk of death in bleeding trauma patients in this study. On the basis of these results,TXA should be considered for use in bleeding trauma patients.
  • 71.
    SHOCK OR NOT •SCENARIO 1: • A 25 year old male, athlete had a h/o fall from bike presented to ED • HR: 74/min, BP: 110/50mmhg, SpO2: 95% on RA • Patient is confused. YES • Young, healthy patients may mask hypotension and tachyacrdia symptoms; • peripheral hypoperfusion and mental status changes are key early signs of severity.
  • 72.
    SHOCK OR NOT •SCENARIO 2: • A 60 year old male, hypertensive on medication, presented to ED with h/o fall from stairs. • HR: 64/min, BP: 110/70 mmhg, SpO2: 92% on RA. YES Elderly patients may not develop tachycardia due to underlying heart disease or medications such as -adrenergic blockers. β
  • 73.
    SHOCK OR NOT •SCENARIO 3: • A 28 year old primigravida, 8 months POG, h/o trivial fall, presented to ED. • HR: 104/min, BP: 86/50 mmhg, SpO2: 99% on RA. • EFAST: Negative NO In a pregnant trauma patient, compression of the inferior vena cava by the gravid uterus can decrease central venous return and worsen hypotension and tachycardia in the setting of less severe hemorrhage.
  • 74.
    SHOCK OR NOT •SCENARIO 4: • A 18 year old male, with A/h/o assault, blunt injury to abdomen, presented to ED with • HR: 54/min, BP: 90/60 mmhg, SpO2: 94% on RA. YES Bradycardia or lack of tachycardia may occur in about 30% of patients with . intra-abdominal hemorrhage from increased vagal tone in response to hemoperitoneum. FAST : POSITIVE
  • 75.

Editor's Notes

  • #6 (Bradycardia may develop preterminally
  • #7 Measurement of end-tidal CO2 and serum lactate can add useful diagnostic information. Etco2 decreases in shock
  • #16  Stored red blood cells can lose deformability (storage lesion), limiting their ability to pass normally through capillary beds or even resulting in capillary plugging. The oxygen dissociation curve is altered by loss of 2,3-diphosphoglycerate in the erythrocytes of stored PRBCs, impeding the off-loading of oxygen at the tissue level. Despite these changes, no consistent harm has been identified with
  • #58 AAGBI : Association of Anesthetists of Great Britain and Ireland
  • #61 Trauma Associated Severe hemorrhage (TASH) Toronto Western Hospital Score The Assessment of Blood Consumption score
  • #64 Rotem: rotational thromboelastometry
  • #70 The Pragmatic Randomized Optimal Platelets and Plasma Ratios (PROPPR) 
  • #71 CRASH 2 and CRASH 3 trial - effect on tranexamic acid in reducing the mortality in ETIC and TBI respectively