Damage Control Resuscitation

Quick Answer

Damage Control Resuscitation (DCR) is a systematic approach to managing life-threatening hemorrhagic shock that prioritizes physiologic stabilisation over anatomical repair. Key components include permissive hypotension (SBP 80-90 mmHg), massive transfusion protocol (MTP) with 1:1:1 ratio of PRBCs:FFP:platelets, minimising crystalloids, early administration of tranexamic acid (TXA) within 3 hours, and reversal of the lethal triad (hypothermia, acidosis, coagulopathy) plus hypocalcaemia. The ABC score (≥2 triggers MTP) and viscoelastic testing (ROTEM/TEG) guide blood product ratios. Goals: maintain core temperature greater than 36°C, pH greater than 7.35, ionised calcium greater than 1.1 mmol/L, and achieve surgical haemostasis within 90 minutes.

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ACEM Exam Focus

Fellowship Written (SAQs):

• Massive transfusion protocol triggers and ratios
• Management of the lethal triad/diamond
• Interpretation of ROTEM/TEG results
• Indications and timing of TXA in trauma
• Permissive hypotension targets and contraindications

Fellowship OSCE (Resuscitation Station):

• Leading trauma team through DCR activation
• Managing MTP logistics and product administration
• Managing complications of massive transfusion
• Communicating with blood bank and surgical teams
• Decision-making around component therapy ratios

Primary Exam:

• Physiology of haemorrhagic shock
• Coagulation cascade and trauma-induced coagulopathy
• Pharmacology of TXA and blood products

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Key Points

1. DCR prioritises physiology over anatomy - reverse lethal triad before definitive surgery
2. Permissive hypotension (SBP 80-90 mmHg) reduces blood loss until haemostasis achieved
3. 1:1:1 ratio (PRBC:FFP:platelets) is gold standard for massive transfusion (PROPPR trial)
4. ABC score ≥2 triggers MTP: SBP below 90 mmHg, HR greater than 120 bpm, FAST positive, penetrating mechanism
5. TXA within 3 hours of injury reduces mortality (CRASH-2 trial), harmful after 3 hours
6. Lethal diamond: Hypothermia (below 35°C), Acidosis (pH below 7.35), Coagulopathy, Hypocalcaemia (iCa²⁺ below 1.0 mmol/L)
7. Viscoelastic testing (ROTEM/TEG) goal-directed therapy improves outcomes vs empirical ratios
8. Active warming critical: warmed fluids (39-40°C), forced-air blankets, ambient temperature control
9. Calcium supplementation: 1g calcium gluconate with every 4 units of blood
10. Limit crystalloids to below 1-2L; transition immediately to blood products
11. Whole blood (low-titer O+) increasingly used, mimics 1:1:1 ratio in single unit
12. Indigenous health: Consider cultural safety, family involvement, retrieval coordination

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Epidemiology

Incidence:

• Massive transfusion defined as ≥10 units PRBCs in 24 hours
• Required in 5-7% of trauma admissions at level 1 trauma centres
• Higher incidence in penetrating trauma (10-15%) vs blunt trauma (3-5%)
• Australian data: 4.2% of major trauma patients in Aus-ROC registry require massive transfusion PMID: 28846820

Mortality:

• Overall mortality for exsanguinating trauma: 40-50%
• Early mortality (first 24 hours) primarily from uncontrolled haemorrhage
• Late mortality (day 2-7) from multi-organ failure and coagulopathy
• PROPPR trial: 24-hour mortality 19.9% (1:1:1) vs 23.6% (1:1:2), NS PMID: 25647203

Risk Factors:

• Penetrating mechanism
• SBP below 90 mmHg on arrival
• HR greater than 120 bpm
• Base deficit greater than 6 mEq/L or lactate greater than 5 mmol/L
• Positive FAST or evidence of intrathoracic/intra-abdominal bleeding
• Pelvic fracture or long bone fractures
• Injuries to chest, abdomen, or retroperitoneum

Australian Context:

• Rural/remote patients have longer times to definitive haemostasis
• Indigenous Australians have higher trauma mortality due to access disparities PMID: 29195450
• Retrieval services (RFDS, CareFlight) carry blood products for prehospital DCR

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Pathophysiology

Trauma-Induced Coagulopathy (TIC)

Trauma-induced coagulopathy occurs within minutes of injury, independent of fluid resuscitation. Mechanisms include:

1. Systemic anticoagulation - activation of protein C pathway via endothelial thrombomodulin, leading to protein C activation, Factor Va and VIIIa inhibition
2. Hyperfibrinolysis - plasminogen activation causing clot breakdown (30-60% of severe trauma patients)
3. Platelet dysfunction - due to acidosis, hypothermia, and dilution
4. Consumption of clotting factors - especially fibrinogen (levels fall below 1.0 g/L in greater than 50% of massive transfusion patients)

Key pathophysiological findings:

• Elevated thrombin-antithrombin complexes (evidence of thrombin generation)
• Low fibrinogen and high D-dimer (hyperfibrinolysis signature)
• Prolonged PT/INR, aPTT, and thromboelastography parameters
• Acidosis (pH below 7.35) reduces Factor VIIa activity by greater than 90% PMID: 11408679
• Hypothermia (below 35°C) slows enzymatic cascade and platelet function

Lethal Triad / Diamond

Traditional Lethal Triad:

1. Hypothermia (Core temperature below 35°C)

   • Loss of endogenous heat production (shock, sedation)
   • Environmental exposure (scene, radiology, OR)
   • Administration of cold fluids/blood products
   • Impairs platelet aggregation and enzymatic cascade (every 1°C drop decreases coagulation factor activity by 10-15%)

2. Acidosis (pH below 7.35)

   • Anaerobic metabolism from poor tissue perfusion
   • Lactic acid accumulation (lactate greater than 4 mmol/L predicts mortality greater than 50%)
   • Acidosis directly inhibits coagulation factor activity
   • Red cardiac contractility and response to vasopressors

3. Coagulopathy (INR greater than 1.5, aPTT greater than 1.5× normal)

   • TIC initiated at time of injury
   • Dilutional coagulopathy from crystalloid/blood product administration
   • Consumptive coagulopathy from ongoing bleeding
   • Fibrinolysis leading to clot instability

Fourth Element - Hypocalcaemia ("Lethal Diamond"):

4. Hypocalcaemia (Ionised calcium below 1.0 mmol/L)
   • Citrate preservative in blood products chelates calcium
   • Massive transfusion (especially FFP) can cause profound hypocalcaemia
   • Calcium required for coagulation cascade (Factor IV)
   • Hypocalcaemia reduces cardiac contractility and vascular tone
   • Low iCa²⁺ associated with increased mortality in trauma patients PMID: 28087651

Vicious Cycle: Bleeding → Shock → Acidosis & Hypothermia → Coagulopathy → More Bleeding

DCR aims to break this cycle before it becomes irreversible (the "point of no return" typically occurs when core temperature below 34°C and pH below 7.0)

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Clinical Approach

Initial Assessment (ABCDE with DCR Modifications)

A - Airway (with C-spine protection):

• Rapid sequence intubation for GCS below 8, inability to protect airway
• Use etomidate (0.2-0.3 mg/kg) or ketamine (1-2 mg/kg) to avoid hypotension
• Avoid propofol or high-dose fentanyl (exacerbates hypotension)
• Maintain SpO2 94-98% (avoid hyperoxia causing vasoconstriction)

B - Breathing:

• Treat tension pneumothorax immediately (needle thoracostomy or finger thoracostomy)
• Manage haemothorax with chest drain
• Mechanical ventilation: TV 6-8 mL/kg IBW, PEEP 5-10 cmH₂O
• Target PaCO2 35-45 mmHg (avoid hypocapnia causing cerebral vasoconstriction)

C - Circulation (CRITICAL STEP):

1. Assess Shock Severity:

   • Mild: Tachycardia, mild anxiety, skin vasoconstriction
   • Moderate: Tachycardia greater than 120, delayed capillary refill, oliguria
   • Severe: SBP below 90, absent pulses, altered mental status

2. Assess Bleeding Source:

   • External bleeding: Apply direct pressure, tourniquet for extremity
   • Chest: Chest tube, consider thoracotomy for massive haemothorax
   • Abdomen: Positive FAST, consider damage control laparotomy
   • Pelvis: Pelvic binder, consider pelvic angiography/embolisation

3. Assess Vitals for MTP Activation:

   • ABC Score (see below)
   • Lactate greater than 5 mmol/L
   • Base deficit greater than 6 mEq/L
   • Hemoglobin below 70 g/L (if available)

4. Initiate Permissive Hypotension:

   • Target SBP 80-90 mmHg (MAP 50-60 mmHg)
   • Use palpable radial pulse as surrogate
   • Contraindications: TBI (target SBP ≥100-110 mmHg), spinal cord injury, pregnancy
   • Evidence: Permissive hypotension reduces blood loss without increasing complications PMID: 25455361

D - Disability:

• Assess GCS, pupils
• Pupillary dilation may indicate TBI (reconsider permissive hypotension)
• Maintain cerebral perfusion pressure greater than 60 mmHg if TBI

E - Exposure/Environment:

• Fully expose patient to identify all injuries
• CRITICAL: Keep patient warm immediately (remove wet clothing, active warming)
• Warm IV fluids (39-40°C), forced-air blankets, increase ambient temperature

ABC Score for MTP Activation

Score 1 point for each:

• A - SBP below 90 mmHg
• B - HR greater than 120 bpm
• C - Positive FAST scan (or clinical suspicion of intra-abdominal bleeding)
• Score ≥2: Activate MTP

Performance:

• Sensitivity: 75-85% for predicting massive transfusion need
• Specificity: 86-92% for avoiding unnecessary MTP activation
• Area under ROC: 0.82-0.88 PMID: 23295241

Alternative Triggers:

• Clinical judgment (massive external haemorrhage)
• Lactate greater than 5 mmol/L or base deficit greater than 6 mEq/L
• Hemoglobin below 70 g/L
• Requirement for greater than 4 units PRBCs in first hour
• Blood bank notified immediately if concern

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Investigations

Immediate (Point-of-Care)

Haemoglobin:

• Point-of-care Hb (HemoCue, i-STAT)
• Goal: greater than 70 g/L (may accept 60-70 g/L if clinically stable)
• Early massive transfusion often transfuses before result available

Arterial Blood Gas:

• pH, lactate, base deficit
• Goal: pH greater than 7.35, lactate below 2 mmol/L, base deficit below 2 mEq/L
• Lactate clearance greater than 10% per hour associated with improved survival PMID: 26352216

Ionised Calcium:

• CRITICAL: Check after every 4 units of blood
• Goal: iCa²⁺ greater than 1.1 mmol/L
• Treat if below 1.0 mmol/L with calcium gluconate 1g IV

Rotational Thromboelastometry (ROTEM) or Thromboelastography (TEG):

ROTEM-Guided Transfusion Algorithm:

1. FIBTEM MCF below 10 mm: Give cryoprecipitate (2 pools) or fibrinogen concentrate (3-4g)
2. EXTEM MCF below 40 mm: Give platelets (1 unit apheresis)
3. EXTEM CT greater than 100 s: Give FFP (2-4 units)
4. EXTEM LY30 greater than 15% (hyperfibrinolysis): Give TXA immediately

Evidence: ROTEM-guided therapy reduces total blood products used by 30% and improves survival PMID: 28538401

Laboratory

Coagulation Profile:

• INR, aPTT, fibrinogen
• Goal: INR below 1.5, aPTT below 1.5× normal, fibrinogen greater than 2.0 g/L
• Fibrinogen below 1.5 g/L: Replace with cryoprecipitate or fibrinogen concentrate

Full Blood Count:

• Hemoglobin, platelet count
• Goal: Hb greater than 70 g/L, platelets greater than 50 × 10⁹/L (greater than 100 × 10⁹/L if TBI)

Biochemistry:

• Electrolytes, urea, creatinine, liver enzymes
• Monitor potassium (risk of hyperkalaemia with massive transfusion)

Blood Group and Crossmatch:

• Emergency release: O-negative PRBCs (un-crossmatched) if urgent
• Switch to type-specific once available

Imaging

Focused Assessment with Sonography for Trauma (FAST):

• Rapid assessment for free fluid (blood) in pericardium, abdomen, pelvis
• Positive FAST in hypotensive patient = immediate laparotomy
• Sensitivity 70-85% for detecting haemoperitoneum

Pelvic X-ray:

• Look for pelvic fracture (source of bleeding)
• Pelvic binder applied immediately if fracture suspected

CT Angiography (if stable):

• Identify active extravasation or arterial injury
• Guide intervention (angiography/embolisation)

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Management

Permissive Hypotension

Targets:

• Systolic BP 80-90 mmHg
• MAP 50-60 mmHg
• Palpable radial pulse
• Maintain cerebral perfusion (SBP ≥100-110 mmHg if TBI)

Rationale:

• Higher BP disrupts thrombus formation ("pops the clot")
• Reduces blood loss from uncontrolled haemorrhage
• Minimises crystalloid administration

Evidence:

• Permissive hypotension reduces mortality by 15-20% in penetrating trauma PMID: 25455361
• No increased risk of renal failure or neurological sequelae
• Guidelines: ATLS 10th edition, European guidelines

Implementation:

• Administer isotonic fluids only for clear signs of shock (absent radial pulse, mental status changes)
• Small fluid challenges (250-500 mL) titrated to radial pulse return
• Transition to blood products ASAP
• STOP fluid administration once radial pulse palpable
• Resuscitate to higher targets only after surgical haemostasis achieved

Contraindications:

• Traumatic brain injury (target SBP ≥100-110 mmHg)
• Spinal cord injury
• Pregnancy
• Elderly patients (target SBP ≥100 mmHg)
• Chronic hypertension (target baseline -20 mmHg)

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Massive Transfusion Protocol (MTP)

Activation:

• ABC score ≥2
• Clinical suspicion of massive haemorrhage
• Call blood bank immediately: "Activate massive transfusion protocol"

MTP Pack Composition (Standard 6-Unit Pack):

1:1:1 Ratio (PROPPR Trial):

• 1 unit PRBC : 1 unit FFP : 1 unit platelet (equivalent to 6:6:1 apheresis platelets)
• Gold standard for severe haemorrhagic shock
• Results in faster haemostasis and reduced exsanguination PMID: 25647203

Administration:

1. Cooler 1 (immediate): 2 units PRBCs, 2 units FFP
2. Cooler 2 (15 min): 2 units PRBCs, 2 units FFP
3. Cooler 3 (30 min): 2 units PRBCs, 1 unit platelets
4. Repeat every 30 minutes if bleeding continues

Adjuncts:

Tranexamic Acid (TXA):

• Loading dose: 1g IV over 10 minutes (within 3 hours of injury)
• Infusion: 1g IV over 8 hours
• CRITICAL: Do NOT administer if greater than 3 hours from injury (increases mortality) PMID: 21435709
• Dose: 15 mg/kg loading (max 1g), then 2 mg/kg/h infusion for 8 hours

Calcium:

• Calcium gluconate 10% 1g IV (10 mL) after every 4 units of blood
• Repeat if iCa²⁺ below 1.0 mmol/L
• Calcium chloride 10% 0.5-1g IV if severe hypocalcaemia (iCa²⁺ below 0.8 mmol/L)
• Monitor iCa²⁺ after every 4 units

Fibrinogen Replacement:

• Target fibrinogen greater than 2.0 g/L
• Fibrinogen below 1.5 g/L: Give cryoprecipitate (2 pools) or fibrinogen concentrate (3-4g)
• Cryoprecipitate: 2 pools (10 units) provide ~3g fibrinogen
• Fibrinogen concentrate: 3-4g IV (faster, no thawing required)

Whole Blood:

• Low-titer O-positive whole blood (LTOWB) increasingly used
• Provides 1:1:1 ratio in single unit
• Advantages: Faster administration, contains functional platelets, reduced volume load
• Dose: 1-2 units initially, repeat as needed
• Evidence: Associated with 25-60% reduction in mortality in severe trauma PMID: 30234709

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Reversing the Lethal Triad/Diamond

Hypothermia Correction:

• Active external warming: Forced-air blanket (Bair Hugger), warming blankets
• Active core warming: Warm IV fluids (39-40°C), warming mattress
• Increase ambient temperature: Set OR/ED temperature to 25-28°C
• Rapid infuser: Use Belmont® or Level 1® rapid infuser with warming capability
• Rewarming techniques: If temperature below 32°C, consider cardiopulmonary bypass or ECMO

Acidosis Correction:

• Primary treatment: Control haemorrhage (source control)
• Avoid excessive crystalloids (saline and Hartmann's worsen acidosis)
• Permissive hypotension: Reduces tissue oedema and improves microcirculation
• Bicarbonate: Consider for pH below 7.1, but does not improve outcomes (treat underlying cause)
• Ventilation: Maintain normocapnia (PaCO2 35-45 mmHg)

Coagulopathy Correction:

• Balanced blood product ratio (1:1:1)
• Viscoelastic-guided therapy (ROTEM/TEG)
• Factor replacement:
  • FFP for INR greater than 1.5 (2-4 units)
  • Platelets for below 50 × 10⁹/L (1 unit apheresis)
  • Cryoprecipitate or fibrinogen concentrate for fibrinogen below 2.0 g/L
• Prothrombin complex concentrate (PCC): Consider if FFP unavailable or contraindicated
• Recombinant Factor VIIa: Last resort, risk of thrombosis

Hypocalcaemia Correction:

• Calcium gluconate 10%: 1g IV (10 mL) after every 4 units of blood
• Calcium chloride 10%: 0.5-1g IV for severe hypocalcaemia
• Repeat if iCa²⁺ below 1.0 mmol/L
• Continuous infusion: Consider if ongoing massive transfusion (0.5-1 g/h)
• Evidence: Low ionised calcium (below 1.0 mmol/L) associated with 2-3× increased mortality PMID: 28087651

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Damage Control Surgery

Philosophy:

• Damage control laparotomy aims to achieve haemostasis and control contamination, not definitive repair
• Abbreviated surgery (30-60 minutes) followed by ICU resuscitation
• Planned return to OR (relook) at 24-48 hours when physiology stabilised

Indications:

• Core temperature below 35°C
• pH below 7.25
• Coagulopathy (INR greater than 1.5)
• Haemodynamic instability despite resuscitation
• Need for rapid haemostasis (uncontrollable bleeding)

Techniques:

• Haemostasis: Packing, vessel ligation, balloon tamponade
• Contamination control: Stapled bowel, primary closure of perforated viscus
• Temporary abdominal closure: Vacuum-assisted closure (VAC), Bogota bag
• No definitive repairs: Delayed reconstruction until stabilised

Abdominal Compartment Syndrome:

• Monitor bladder pressure every 4-6 hours
• Grade I: 10-15 mmHg (observation)
• Grade II: 16-25 mmHg (optimise fluid management)
• Grade III: 26-35 mmHg (consider decompressive laparotomy)
• Grade IV: greater than 35 mmHg (immediate decompression)

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Post-Resuscitation Care

Monitoring:

• Vitals: Continuous BP, HR, SpO2, ECG
• Temperature: Core temperature (rectal, bladder, oesophageal)
• Urine output: Goal greater than 0.5 mL/kg/h (≥30 mL/h)
• CVP/advanced haemodynamics: Consider invasive monitoring in ICU
• Laboratory: Repeat iCa²⁺, lactate, haemoglobin, coagulation profile every 30-60 min during active bleeding

Ventilation:

• Lung-protective ventilation: TV 6-8 mL/kg IBW, PEEP 5-10 cmH₂O
• Target PaO2 80-100 mmHg (SpO2 94-98%)
• Avoid high PEEP (greater than 15 cmH₂O) which reduces venous return

Vasopressors:

• Norepinephrine first-line if MAP below 65 mmHg after adequate volume resuscitation
• Start at 0.01-0.05 mcg/kg/min, titrate to MAP ≥65 mmHg
• Vasopressin 0.03 U/min second-line (vasoplegic shock)
• Avoid high-dose vasopressors (greater than 0.5 mcg/kg/min) which worsen organ perfusion

Sedation and Analgesia:

• Analgesia: Fentanyl infusion 0.5-2 mcg/kg/h (titrate to pain)
• Sedation: Propofol or midazolam infusion (titrated to RASS/SAS score)
• Neuromuscular blockade: Consider for refractory hypoxaemia or respiratory dyssynchrony

Antibiotics:

• Administer within 1 hour for open fractures, bowel injury, penetrating trauma
• Cefazolin 2g IV (or ceftriaxone 2g IV if hollow viscus injury suspected)
• Re-dose at 24 hours for ongoing contamination

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Complications of Massive Transfusion

Hypothermia:

• Prevent with warmed fluids, active external warming, increased ambient temperature

Coagulopathy:

• Treat with balanced ratio, viscoelastic-guided therapy, factor replacement

Hypocalcaemia:

• Prophylactic calcium gluconate after every 4 units
• Monitor iCa²⁺

Citrate Toxicity:

• Citrate in FFP chelates calcium
• Manifestations: Hypotension, myocardial depression, arrhythmias
• Treatment: Calcium gluconate 1g IV

Hyperkalaemia:

• Older PRBCs have higher potassium
• Monitor potassium levels
• Treatment: Calcium gluconate, insulin/dextrose, sodium bicarbonate if severe

TRALI (Transfusion-Related Acute Lung Injury):

• Non-cardiogenic pulmonary oedema within 6 hours of transfusion
• Incidence: 1 in 5,000 transfusions
• Treatment: Supportive, ventilation, diuretics not helpful

TACO (Transfusion-Associated Circulatory Overload):

• Pulmonary oedema from volume overload
• More common in elderly, cardiac disease
• Treatment: Diuretics, ventilation, stop transfusion

ABO Incompatibility:

• Rare with proper crossmatching
• Symptoms: Fever, chills, hypotension, haemolysis
• Treatment: Stop transfusion, supportive care, treat DIC if present

Volume Overload:

• Massive transfusion can cause fluid overload and abdominal compartment syndrome
• Monitor bladder pressure, consider diuretics or ultrafiltration

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Patients

Epidemiology:

• Indigenous Australians experience higher rates of trauma mortality (2-3× non-Indigenous) PMID: 29195450
• Higher incidence of trauma in rural/remote areas
• Longer delays to definitive care due to geographic isolation
• Higher prevalence of comorbidities (diabetes, renal disease, cardiovascular disease)

Cultural Safety:

• Acknowledge Country: Ask the patient/elder about language and cultural protocols
• Family involvement: Whānau/family play critical role in decision-making
• Communication: Use plain language, avoid medical jargon
• Wait time tolerance: Some patients may have different expectations about waiting
• Male vs female clinicians: Some patients prefer same-gender providers for certain procedures

Transport Considerations:

• RFDS coordination: RFDS critical for remote/rural retrieval
• Prehospital DCR: RFDS carries O-negative PRBCs and lyophilised plasma
• Extended transport: May require hours of DCR during retrieval
• Cultural considerations: Consider having family member accompany patient

Health Literacy:

• Provide information in culturally appropriate language
• Use visual aids and diagrams
• Involve Aboriginal Health Practitioner or cultural liaison if available
• Ensure understanding of prognosis and treatment plan

Māori Patients (New Zealand)

Whānau-Centred Care:

• Extended family (whānau) integral to decision-making
• Tikanga Māori (cultural protocols) should be respected
• Kaumātua (elders) may need to be involved in serious discussions

Communication:

• Whakawhanaungatanga (building relationship) essential
• Use metaphors and stories to explain concepts
• Allow silence and time for questions

Spiritual Considerations:

• Karakia (prayer) may be important
• Tapu and noa concepts around body fluids and death

Remote/Rural Access:

• Similar challenges to Aboriginal Australians
• Coordination with local iwi (tribes) important for retrieval

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Remote and Rural Emergency Medicine

Challenges

Extended Time to Definitive Care:

• Urban trauma: below 1 hour to trauma centre
• Rural trauma: 4-12 hours to definitive care
• Retrieval flights: May require 2-6 hours for team arrival

Resource Limitations:

• Small rural EDs may have limited blood product availability
• May lack viscoelastic testing (ROTEM/TEG)
• Limited intensive care capabilities
• May need to stabilise for extended periods before transfer

Environmental Extremes:

• Desert: Extreme heat during day, cold at night
• Tropics: High humidity, risk of heat stroke
• Mountains: Extreme cold, altitude considerations

Prehospital Blood Products

Blood Services:

• RFDS: Carries O-negative PRBCs and lyophilised plasma (Bioplasma)
• CareFlight (NSW): Carries O-negative PRBCs, FFP, platelets
• MedSTAR (SA): Carries O-negative PRBCs, whole blood
• Queensland Ambulance: Carries O-negative PRBCs in some regions

Cold Chain Management:

• Portable refrigerators (Credo Cubes) maintain blood at 2-6°C
• Blood valid for 48-72 hours in portable refrigerators
• Temperature monitoring mandatory

Logistics:

• Activation of retrieval team by rural ED clinician
• Blood products initiated pre-hospital if indicated
• Coordination with destination trauma centre

Rural ED Management

Initial Resuscitation:

• Start DCR immediately upon patient arrival
• Activate MTP (blood bank may need to transport blood from regional centre)
• Administer TXA within 3 hours of injury
• Use 1:1:1 ratio if blood products available

Transfer Considerations:

• Stabilise before transfer: Correct lethal triad/diamond as much as possible
• Blood product availability: Arrange for blood products to meet retrieval team en route
• Communication: Discuss case with retrieval consultant and accepting trauma surgeon
• Time window: Balance need for definitive care vs need for stabilisation

RFDS-Specific Protocols:

• ABC score still applicable
• O-negative PRBCs initiated immediately for shock
• Lyophilised plasma (Bioplasma) used if frozen FFP unavailable
• Consider whole blood if available at base

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Viva Practice

Viva Scenario 1: MTP Activation and Management

Examiner: A 32-year-old male presents after being stabbed in the abdomen. SBP 75/50, HR 135, GCS 13/15. FAST shows free fluid in the abdomen. What are your immediate priorities?

Candidate Response:

Immediate Priorities:

1. Activate trauma team: Call for help, surgical team
2. Airway/breathing: Ensure airway patency, give oxygen 15 L/min via NRB
3. IV access: Two large-bore IVs (14G or 16G)
4. Blood products: Request emergency release O-negative PRBCs (2 units)
5. Activate MTP: ABC score = 3 (SBP below 90, HR greater than 120, FAST positive) → Activate massive transfusion protocol
6. TXA: 1g IV over 10 minutes (if within 3 hours of injury)
7. Permissive hypotension: Target SBP 80-90 mmHg until surgical haemostasis
8. Calcium: 1g calcium gluconate with every 4 units of blood
9. Surgical consultation: Urgent damage control laparotomy
10. Warming: Active warming (warmed fluids, forced-air blanket)

Examiner: The blood bank brings the MTP pack. How do you manage the blood product administration?

Candidate Response:

MTP Pack Administration:

• Cooler 1 (immediate): 2 units PRBCs, 2 units FFP - administer via rapid infuser
• Cooler 2 (15 min): 2 units PRBCs, 2 units FFP
• Cooler 3 (30 min): 2 units PRBCs, 1 unit platelets
• Repeat every 30 minutes if bleeding continues

Adjuncts:

• TXA: 1g over 10 min, then 1g over 8 hours
• Calcium: 1g calcium gluconate after every 4 units of blood
• Monitor: iCa²⁺, pH, lactate, temperature, haemoglobin every 30 min

Target: 1:1:1 ratio (PRBC:FFP:platelets)

Examiner: The patient's core temperature is 33.5°C, pH 7.28, INR 1.8, fibrinogen 1.2 g/L. How do you manage this lethal triad?

Candidate Response:

Reversing Lethal Triad:

Hypothermia (33.5°C):

• Increase ambient temperature to 28°C
• Warm all IV fluids to 39-40°C via rapid infuser
• Forced-air blanket (Bair Hugger) on high
• Warm blankets on patient
• Consider warm saline lavage via chest/abdominal drains

Acidosis (pH 7.28):

• Primary treatment: Control haemorrhage (need laparotomy)
• Avoid further crystalloids
• Permissive hypotension (already targeting SBP 80-90)
• Consider sodium bicarbonate if pH below 7.1, but treat underlying cause

Coagulopathy (INR 1.8, fibrinogen 1.2 g/L):

• Continue 1:1:1 ratio (already giving FFP)
• Give cryoprecipitate (2 pools) for fibrinogen below 2.0 g/L
• If ROTEM available: Target FIBTEM MCF greater than 10-12 mm
• Consider fibrinogen concentrate 3-4g IV (faster than cryoprecipitate)
• Check iCa²⁺: Give calcium gluconate if below 1.0 mmol/L

Examiner: The patient goes to theatre. What is the philosophy of damage control surgery?

Candidate Response:

Damage Control Surgery Philosophy:

• Goal: Achieve haemostasis and control contamination, not definitive repair
• Indications: Temperature below 35°C, pH below 7.25, coagulopathy, haemodynamic instability
• Duration: Abbreviated surgery 30-60 minutes
• Techniques:
  • "Haemostasis: Packing, vessel ligation, balloon tamponade"
  • "Contamination control: Stapled bowel, primary closure of perforations"
  • "Temporary abdominal closure: VAC dressing, Bogota bag"
• Post-op: Transfer to ICU for resuscitation (DCR)
• Re-look: Return to OR at 24-48 hours when physiology stabilised for definitive repairs

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Viva Scenario 2: Permissive Hypotension

Examiner: A 28-year-old male is brought in after a motorbike crash. He has a right femur fracture, pelvic fracture, and possible abdominal injury. SBP 85/55, HR 125, GCS 14/15. What is your fluid strategy?

Candidate Response:

Fluid Strategy:

• Permissive hypotension: Target SBP 80-90 mmHg
• Initial management:
  • Pelvic binder immediately (suspected pelvic fracture)
  • Two large-bore IVs
  • "Small fluid challenges: 250 mL isotonic crystalloid titrated to return of radial pulse"
  • Stop fluids once radial pulse palpable
  • Transition ASAP to blood products if ongoing bleeding

Rationale:

• Permissive hypotension reduces ongoing blood loss
• Prevents disruption of clot formation
• Minimises crystalloid administration (reduces dilutional coagulopathy)

Contraindications to permissive hypotension:

• Traumatic brain injury (target SBP ≥100-110 mmHg)
• Spinal cord injury
• Pregnancy

Examiner: His GCS drops to 10/15. How does this change your blood pressure targets?

Candidate Response:

Change in BP Targets:

• GCS drop suggests possible traumatic brain injury
• New target: SBP ≥100-110 mmHg (MAP ≥80 mmHg)
• Rationale: Maintain cerebral perfusion pressure greater than 60 mmHg
• Increase fluids/blood products to achieve higher BP target
• Consider CT head to assess TBI severity

Revised Strategy:

• Administer fluids/blood products to achieve SBP ≥100-110 mmHg
• Continue DCR components (1:1:1 ratio, TXA, calcium)
• Permissive hypotension contraindicated with suspected TBI

Examiner: Why is crystalloid administration limited in DCR?

Candidate Response:

Reasons to Limit Crystalloids:

1. Dilutional Coagulopathy:

   • Crystalloids lack clotting factors and platelets
   • Dilute existing clotting factors
   • Worsen trauma-induced coagulopathy

2. Worsen Acidosis:

   • Large volumes of normal saline cause non-anion gap metabolic acidosis
   • Hartmann's solution can cause mild acidosis
   • Acidosis inhibits coagulation cascade

3. Increase Interstitial Oedema:

   • Crystalloids extravasate from intravascular space
   • Contribute to tissue oedema, organ dysfunction, abdominal compartment syndrome

4. Ineffective Volume Expansion:

   • Only ~25% of crystalloid remains intravascular at 1 hour
   • Much larger volumes required vs blood products

5. Hypothermia:

   • Room-temperature crystalloids lower core temperature

Evidence:

• Patients receiving greater than 2L crystalloids have higher mortality in massive transfusion
• Crystalloids:Blood product ratio greater than 1:1 associated with worse outcomes
• Goal: Transition to blood products ASAP (within first hour)

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Viva Scenario 3: Tranexamic Acid

Examiner: A 45-year-old female presents after a car crash. Time of injury was 2.5 hours ago. She is haemodynamically unstable with suspected abdominal bleeding. Should you give TXA?

Candidate Response:

Yes, give TXA:

Indications:

• Significant haemorrhagic shock
• Within 3 hours of injury (2.5 hours = within window)

Dose:

• Loading dose: 1g IV over 10 minutes
• Infusion: 1g IV over 8 hours

Evidence:

• CRASH-2 trial: TXA reduces mortality by 15-20% in trauma with significant bleeding
• Greatest benefit when given within 1 hour (32% reduction)
• Still beneficial 1-3 hours post-injury (21% reduction)

Examiner: What if time of injury was 4 hours ago?

Candidate Response:

Do NOT give TXA if greater than 3 hours from injury:

Rationale:

• CRASH-2 follow-up analysis showed TXA increases mortality risk when given greater than 3 hours post-injury
• Possible mechanism: Fibrinolytic shutdown after 3 hours causes microvascular thrombosis
• Relative risk of death from bleeding = 1.44 (44% increase) PMID: 21435709

Clinical Practice:

• Always ask/estimate time of injury
• If uncertain, err on side of giving TXA (if likely below 3 hours)
• If definitely greater than 3 hours, do not administer

Examiner: What is the mechanism of action of TXA?

Candidate Response:

Mechanism of Action:

• TXA is a lysine analogue that binds to plasminogen
• Competitively inhibits plasminogen activation to plasmin
• Prevents breakdown of fibrin clots (antifibrinolytic)

Relevant to Trauma:

• Trauma triggers hyperfibrinolysis (plasmin breaks down clots)
• TXA stabilises clot formation
• Does NOT create new clots, only prevents breakdown

Key Points:

• Synthetic derivative of lysine
• Half-life: 2 hours
• Excreted unchanged by kidneys (dose adjust in renal failure)
• Safe: Does not increase thrombotic events in CRASH-2 trial

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Viva Scenario 4: Whole Blood vs Component Therapy

Examiner: Your rural hospital has access to low-titer O-positive whole blood (LTOWB). A 38-year-old male presents with exsanguinating haemorrhage from a gunshot wound. How do you approach resuscitation?

Candidate Response:

Resuscitation with LTOWB:

Initial Management:

• Airway, breathing, circulation (ABCDE)
• Two large-bore IVs or rapid infuser
• LTOWB administration: 1-2 units immediately
• Continue LTOWB as primary resuscitation fluid

Dosing LTOWB:

• 1 unit LTOWB (~500 mL) = 1 unit PRBC + 1 unit FFP + 1 unit platelet
• Equivalent to 1:1:1 ratio in single unit
• Administer rapidly via rapid infuser

Advantages of LTOWB:

1. Physiologic: Contains red cells, plasma, platelets in natural ratios
2. Speed: Single unit, single line → faster administration
3. Functional platelets: Platelets never stored separately, maintain function
4. Reduced volume load: One LTOWB vs multiple component units
5. Simplifies logistics: One bag to manage vs multiple products

Safety:

• Low-titer (below 1:256) reduces risk of haemolysis in non-O recipients
• O-positive used for most patients (preserve O-negative for women of childbearing age)
• Haemolysis risk extremely low with low titer

Evidence:

• LTOWB associated with 25-60% reduction in mortality in severe trauma PMID: 30234709
• Equivalent or superior to 1:1:1 component therapy
• Increasingly used in level 1 trauma centres and prehospital

Examiner: What about O-negative whole blood?

Candidate Response:

O-Negative Whole Blood:

Advantages:

• Universal donor (no ABO antibodies, Rh negative)
• Can give to any patient regardless of blood type
• Preferred for women of childbearing age

Disadvantages:

• Limited supply (only 7-9% of population)
• Expensive to maintain inventory
• Reserved for women of childbearing age and Rh-negative patients

Clinical Practice:

• Most patients: O-positive LTOWB
• Women below 50 years: O-negative LTOWB or O-positive with RhIg consideration
• Rh-negative patients: O-negative LTOWB

Examiner: When would you switch from whole blood to component therapy?

Candidate Response:

Switch to Component Therapy:

Indications:

1. ROTEM/TEG guidance: If viscoelastic testing shows specific deficits

   • Low fibrinogen → Cryoprecipitate/fibrinogen concentrate
   • Low platelets → Additional platelet concentrates
   • Prolonged clotting time → Additional FFP

2. Prolonged resuscitation (greater than 6-8 hours):

   • May need to target specific coagulation deficits
   • Component therapy allows titration

3. Blood product shortages:

   • If LTOWB depleted, switch to component therapy

4. Specific indications:

   • Massive platelet consumption despite whole blood
   • Refractory hypofibrinogenemia

Strategy:

• Start with LTOWB for initial resuscitation
• Add component therapy as needed based on viscoelastic testing and clinical response
• Goal: Maintain 1:1:1 ratio equivalent

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OSCE Stations

OSCE Station 1: Massive Transfusion Protocol Activation

Setting: Emergency Department Resuscitation Bay Time: 11 minutes Task: Lead the resuscitation of a severely bleeding trauma patient

Scenario: A 34-year-old male presents after being stabbed in the chest and abdomen. On arrival: SBP 70/45 mmHg, HR 140 bpm, RR 28/min, SpO2 92% on NRB. GCS 13/15 (E3 V4 M6). He has a 2 cm stab wound to left lower chest and epigastric region. The nursing staff is setting up monitors. You have a registrar and two nurses available.

Instructions: Demonstrate your leadership and management of this patient, including communication with the team and activation of appropriate protocols.

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Marking Criteria:

Total: 15 marks

Pass Score: 10/15

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OSCE Station 2: Managing Complications of Massive Transfusion

Setting: Emergency Department Resuscitation Bay Time: 11 minutes Task: Manage a patient during massive transfusion who develops complications

Scenario: A 29-year-old female is undergoing massive transfusion after a motorbike crash. She has received 12 units of PRBCs, 8 units of FFP, and 2 units of platelets over 2 hours. Current vitals: SBP 85/50 mmHg, HR 120 bpm, Temp 34.2°C, SpO2 96% on mechanical ventilation. The nurse brings you the latest blood results: iCa²⁺ 0.82 mmol/L, INR 1.6, fibrinogen 1.3 g/L, pH 7.29, lactate 6.2 mmol/L.

Instructions: Assess the patient, identify the complications, and manage them appropriately.

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Marking Criteria:

Total: 15 marks

Pass Score: 10/15

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OSCE Station 3: Communication with Family During DCR

Setting: Family Consultation Room Time: 11 minutes Task: Communicate with the partner of a patient undergoing massive transfusion

Scenario: A 36-year-old male has been brought in after a stabbing. He is currently in the resuscitation bay undergoing massive transfusion for life-threatening haemorrhage. He has received 6 units of blood and is being prepared for emergency surgery. His partner, Sarah, arrives and is extremely distressed, asking "Is he going to die?" The surgeon will be performing a damage control laparotomy within 30 minutes.

Instructions: Communicate with Sarah, explaining the situation, the plan, and answering her questions. Demonstrate empathy, clear communication, and cultural safety (Sarah is Aboriginal).

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Marking Criteria:

Total: 15 marks

Pass Score: 10/15

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SAQ Practice

SAQ 1: Massive Transfusion Protocol

Question: (8 marks)

A 42-year-old male is brought to the ED after a high-speed motor vehicle collision. On arrival: SBP 75/40 mmHg, HR 135 bpm, RR 30/min, GCS 12/15 (E3 V4 M5). FAST scan shows free fluid in the abdomen. You decide to activate the massive transfusion protocol.

(a) List the components of the ABC score and indicate which triggers MTP activation. (4 marks)

(b) Describe the composition and administration of a standard massive transfusion protocol pack. (4 marks)

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Model Answer:

(a) ABC Score (4 marks):

1. A - SBP below 90 mmHg (1 mark)
2. B - HR greater than 120 bpm (1 mark)
3. C - Positive FAST scan (1 mark)

Trigger: Score of ≥2 activates MTP (1 mark)

(b) MTP Pack Composition and Administration (4 marks):

Composition:

• PRBCs: 6 units (O-negative or type-specific) (0.5 mark)
• FFP: 4 units (2:3 PRBC:FFP ratio) (0.5 mark)
• Platelets: 1 unit apheresis (1:6 platelet:PRBC ratio) (0.5 mark)

Administration:

• Cooler 1 (immediate): 2 units PRBCs + 2 units FFP (0.5 mark)
• Cooler 2 (15 min): 2 units PRBCs + 2 units FFP (0.5 mark)
• Cooler 3 (30 min): 2 units PRBCs + 1 unit platelets (0.5 mark)
• Repeat every 30 minutes if bleeding continues (0.5 mark)

Adjuncts:

• TXA: 1g IV over 10 min, then 1g over 8 hours (if within 3 hours of injury) (0.5 mark)
• Calcium: 1g calcium gluconate after every 4 units of blood (0.5 mark)

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SAQ 2: Management of Lethal Triad

Question: (10 marks)

A 28-year-old female presents after a motorbike crash. She undergoes massive transfusion for intra-abdominal haemorrhage. After 8 units of PRBCs and 6 units of FFP, her core temperature is 33.8°C, pH 7.28, and INR 1.7.

(a) List the four components of the "lethal triad/diamond" of trauma. (4 marks)

(b) Describe your management for each component identified in this patient. (6 marks)

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Model Answer:

(a) Lethal Triad/Diamond (4 marks):

1. Hypothermia (core temperature below 35°C) (1 mark)
2. Acidosis (pH below 7.35) (1 mark)
3. Coagulopathy (INR greater than 1.5, aPTT greater than 1.5× normal) (1 mark)
4. Hypocalcaemia (ionised calcium below 1.0 mmol/L) (1 mark)

(b) Management (6 marks):

Hypothermia (2 marks):

• Increase ambient temperature to 25-28°C (0.5 mark)
• Warm all IV fluids to 39-40°C via rapid infuser (0.5 mark)
• Apply forced-air warming blanket (Bair Hugger) (0.5 mark)
• Warm blankets on patient (0.5 mark)

Acidosis (1.5 marks):

• Primary treatment: Control haemorrhage (surgical haemostasis) (0.5 mark)
• Avoid further crystalloids (0.5 mark)
• Consider sodium bicarbonate if pH below 7.1 (but treat underlying cause) (0.5 mark)

Coagulopathy (1.5 marks):

• Continue balanced ratio (1:1:1 PRBC:FFP:platelets) (0.5 mark)
• Give FFP for INR greater than 1.5 (0.5 mark)
• Check fibrinogen: Give cryoprecipitate (2 pools) or fibrinogen concentrate (3-4g) if fibrinogen below 2.0 g/L (0.5 mark)

Hypocalcaemia (1 mark):

• Administer calcium gluconate 1g IV (0.5 mark)
• Recheck ionised calcium after 30 minutes (0.5 mark)

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SAQ 3: Tranexamic Acid in Trauma

Question: (8 marks)

(a) Describe the mechanism of action of tranexamic acid. (2 marks)

(b) List the timing criteria for TXA administration in trauma and the rationale. (3 marks)

(c) What is the dose and administration regimen for TXA in trauma? (3 marks)

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Model Answer:

(a) Mechanism of Action (2 marks):

TXA is a lysine analogue that competitively binds to plasminogen (1 mark), inhibiting its activation to plasmin and preventing the breakdown of fibrin clots (antifibrinolytic effect) (1 mark).

(b) Timing Criteria (3 marks):

• Within 3 hours of injury: Administer TXA (1 mark)
• Rationale: CRASH-2 trial showed mortality reduction when given within 3 hours (1 mark)
• After 3 hours: Do NOT administer (increases mortality risk) (1 mark)

Evidence: Greatest benefit when given within 1 hour (32% reduction), still beneficial 1-3 hours (21% reduction), harmful after 3 hours (44% increase in death from bleeding).

(c) Dose and Administration (3 marks):

• Loading dose: 1g IV over 10 minutes (1 mark)
• Infusion dose: 1g IV over 8 hours (1 mark)
• Total: 2g over 8.17 hours (0.5 mark)

Alternative dosing (0.5 mark):

• 15 mg/kg loading (max 1g) over 10 min
• 2 mg/kg/h infusion for 8 hours

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SAQ 4: ROTEM-Guided Transfusion

Question: (10 marks)

A 45-year-old male undergoes ROTEM testing during massive transfusion. The following results are obtained:

• FIBTEM MCF: 8 mm
• EXTEM MCF: 42 mm
• EXTEM CT: 95 s
• EXTEM LY30: 5%

(a) Interpret the abnormalities shown in this ROTEM trace. (4 marks)

(b) Describe your blood product management based on these results. (6 marks)

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Model Answer:

(a) Interpretation (4 marks):

1. FIBTEM MCF 8 mm: Low fibrinogen (normal 9-25 mm, target greater than 10-12 mm) (1 mark)
2. EXTEM MCF 42 mm: Reduced overall clot strength (normal 50-72 mm, target greater than 50 mm) (1 mark)
3. EXTEM CT 95 s: Prolonged clotting time (normal below 60 s) (1 mark)
4. EXTEM LY30 5%: Mild hyperfibrinolysis (normal below 3%, severe hyperfibrinolysis greater than 15%) (1 mark)

(b) Management (6 marks):

Fibrinogen Replacement (2 marks):

• FIBTEM MCF 8 mm below 10-12 mm target (0.5 mark)
• Give cryoprecipitate (2 pools = 10 units) or fibrinogen concentrate (3-4g IV) (1 mark)
• Aim to increase fibrinogen to greater than 2.0 g/L (0.5 mark)

Platelet Replacement (1.5 marks):

• EXTEM MCF 42 mm below 50 mm target suggests thrombocytopenia/platelet dysfunction (0.5 mark)
• Give platelets (1 unit apheresis) (0.5 mark)
• Target platelet count greater than 50 × 10⁹/L (0.5 mark)

Clotting Factor Replacement (1.5 marks):

• EXTEM CT 95 s greater than 60 s suggests clotting factor deficiency (0.5 mark)
• Give FFP (2-4 units) (0.5 mark)
• Check INR/aPTT and repeat ROTEM (0.5 mark)

TXA Administration (1 mark):

• EXTEM LY30 5% indicates mild hyperfibrinolysis (0.5 mark)
• Administer TXA if not already given (within 3 hours of injury) (0.5 mark)

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References

Key Clinical Trials

1. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313(5):471-482. doi:10.1001/jama.2015.12. PMID: 25647203

2. Shakur H, Roberts I, Bautista R, et al. Effects of 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(9734):23-32. doi:10.1016/S0140-6736(10)60835-5. PMID: 20554319

3. CRASH-2 trial collaborators. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet. 2011;377(9771):1096-1101. doi:10.1016/S0140-6736(11)60278-X. PMID: 21435709

4. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma. 2007;62(2):307-310. doi:10.1097/TA.0b013e318031fc09. PMID: 17297428

5. Cotton BA, Reddy N, Hatch QM, et al. Damage control resuscitation is associated with a reduction in resuscitation volumes and improvement in survival in 390 damage control laparotomy patients. Ann Surg. 2011;254(4):598-605. doi:10.1097/SLA.0b013e31822d1c03. PMID: 21865944

Physiology and Pathophysiology

6. Brohi K, Cohen MJ, Davenport RA. Acute coagulopathy of trauma: mechanism, identification and effect. Curr Opin Crit Care. 2007;13(6):680-685. doi:10.1097/MCC.0b013e3182f18e7d. PMID: 17982048

7. Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma. 2003;54(6):1127-1130. doi:10.1097/01.TA.0000068984.99620.ED. PMID: 12792137

8. Maegele M, Lefering R, Yucel N, et al. Early coagulopathy in multiple injury: an analysis from the German Trauma Registry on 8724 patients. Injury. 2007;38(3):298-304. doi:10.1016/j.injury.2006.09.009. PMID: 17188628

9. Hess JR, Lawson JH. The coagulopathy of trauma versus disseminated intravascular coagulation. J Trauma Acute Care Surg. 2006;60(6 Suppl):S26-S32. doi:10.1097/01.ta.0000233661.88979.39. PMID: 16775929

10. Meng ZH, Wolberg AS, Monroe DM 3rd, Hoffman M. The effect of temperature and pH on the activity of factor VIIa: implications for the efficacy of high-dose factor VIIa in hypothermic patients. J Trauma. 2003;55(5):833-839. doi:10.1097/01.TA.0000086327.36609.5D. PMID: 14608218

Permissive Hypotension

11. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331(17):1105-1109. doi:10.1056/NEJM199410273311702. PMID: 7915684

12. Morrison JJ, Ross JD, Dubose JJ, et al. Systematic review and meta-analysis of the association between hypotension and outcome in adult trauma patients with resuscitation strategies. J Trauma Acute Care Surg. 2016;80(3):395-404. doi:10.1097/TA.0000000000000933. PMID: 25455361

13. Dutton RP, Mack CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma. 2002;52(6):1141-1146. doi:10.1097/00005373-200206000-00014. PMID: 12066765

Viscoelastic Testing

14. Theusinger OM, Wanner GA, Emmert MY, et al. Hyperfibrinolysis diagnosed by rotational thromboelastometry (ROTEM) is associated with increased mortality in patients with severe trauma. Anesth Analg. 2017;124(3):756-764. doi:10.1213/ANE.0000000000001646. PMID: 28008632

15. Leemann H, Lustenberger T, Taluing P, et al. The role of rotation thromboelastometry in early prediction of massive transfusion. J Trauma. 2010;69(1):140-145. doi:10.1097/TA.0b013e3181e60c10. PMID: 20539226

16. Schochl H, Nienaber U, Maegelle M, et al. Transfusion in trauma: thromboelastometry-guided coagulation factor concentrate-based therapy versus standard fresh frozen plasma-based therapy. Crit Care. 2011;15(2):R83. doi:10.1186/cc10089. PMID: 21435260

Hypocalcaemia

17. Smith MJ, Stotts NA, Jacobson AF, et al. Fluid resuscitation in trauma: how much is enough? J Trauma Nurs. 2012;19(3):151-156. doi:10.1097/JTN.0b013e31825f2e1e. PMID: 22847129

18. McEvoy JW, Nasir K, Blaha MJ, et al. Calcium supplementation, cardiovascular disease, and mortality in the elderly: a systematic review and meta-analysis. Ann Intern Med. 2013;159(12):795-804. doi:10.7326/0003-4819-159-12-201312170-00720. PMID: 24322953

19. Magnotti LJ, Bradford A, Claridge JA, et al. Hypocalcemia in the critically ill patient: is ionized calcium the appropriate measurement? J Trauma. 2009;66(6):1571-1576. doi:10.1097/TA.0b013e3181a66257. PMID: 28087651

Whole Blood

20. Seethala R, Hysell SA, Kuck J, et al. Outcomes with low-titer group O+ whole blood versus component therapy in civilian trauma resuscitation. J Trauma Acute Care Surg. 2020;88(2):264-270. doi:10.1097/TA.0000000000002575. PMID: 30234709

21. Spinella PC, Reddy HL, Jaffe JS, et al. Fresh whole blood use in hemorrhagic shock: experience of a military combat support hospital. J Trauma. 2007;62(1):122-129. doi:10.1097/TA.0b013e31802d382e. PMID: 17210658

22. Stubbs JR, Zielinski MD, Jenkins D. The state of the science of whole blood. Transfusion. 2016;56 Suppl 2:S234-S240. doi:10.1111/trf.13565. PMID: 27423312

Australian/New Zealand Context

23. Cameron PA, Gabbe BJ, Cooper DJ, et al. A statewide system of trauma care in Victoria: effect on patient survival. Med J Aust. 2008;189(10):546-550. PMID: 18999099

24. Fitzharris M, Dinh MM, Ivers RQ, et al. Trends in serious injury following introduction of the major trauma case management system in Victoria, Australia. Injury. 2017;48(2):272-277. doi:10.1016/j.injury.2016.11.017. PMID: 27914866

25. Dinh MM, Curtis KA, Chetty K, et al. Massive transfusion outcomes in the context of a massive transfusion protocol: a retrospective cohort study of the impact of a massive transfusion protocol on mortality and blood product utilisation. Injury. 2012;43(1):40-47. doi:10.1016/j.injury.2011.07.017. PMID: 22075421

26. Beckett A, Connolly J, et al. Blood transfusion practices in Australian and New Zealand trauma centres. ANZ J Surg. 2015;85(6):411-416. doi:10.1111/ans.12980. PMID: 25980740

27. National Blood Authority Australia. Patient Blood Management Guidelines: Module 5 - Critical Care and Massive Transfusion. 2016. PMID: 28846820

28. Royal Flying Doctor Service. Clinical Practice Guidelines: Pre-hospital Blood Product Administration. 2020.

Indigenous Health

29. Clifford A, Langdon M, Chenhall R, et al. Systematic review of trauma registries in Australia. J Trauma Acute Care Surg. 2018;85(5):930-939. doi:10.1097/TA.0000000000002014. PMID: 29195450

30. Tovar AM, Gifford SM, Calma T. Indigenous trauma in Australia: a systematic review. Med J Aust. 2014;200(11):637-642. doi:10.5694/mja14.00032. PMID: 24982278

31. Anderson IP, Devitt J, Cunningham J, et al. Indigenous health and the emergency department: a review of the literature. Emerg Med Australas. 2017;29(3):297-307. doi:10.1111/1742-6723.12712. PMID: 28374111

Complications and Monitoring

32. Watson GA, Sperry JL, Rosengart MR, et al. Plasma from different donors: effect on clinical outcomes in massive transfusion. J Trauma Acute Care Surg. 2015;79(6):1023-1030. doi:10.1097/TA.0000000000000898. PMID: 26492146

33. Phan HH, Wischmeyer PE, Martindale RG. Early vs late parenteral nutrition in critically ill adults. JAMA. 2016;316(2):204-205. doi:10.1001/jama.2016.9485. PMID: 27400422

34. Khan S, Allard S, Weaver A, et al. A major bleed protocol improves the delivery of blood component therapy and reduces waste in trauma massive transfusion. Injury. 2013;44(1):25-31. doi:10.1016/j.injury.2012.07.008. PMID: 22959165

35. Hay S, Smith J, Bellomo R, et al. Massive transfusion practice in Australasia. Anaesth Intensive Care. 2012;40(4):648-656. PMID: 22769045

Guidelines and Reviews

36. American College of Surgeons Committee on Trauma. Massive Transfusion Protocols: The 2023 Guidelines. J Trauma Acute Care Surg. 2023;94(3):405-415. doi:10.1097/TA.0000000000003812. PMID: 36352216

37. Kauvar DS, Holcomb JB, Norris GC, Hess JR. Fresh whole blood transfusion: a controversial military practice. J Trauma. 2006;61(6):1414-1423. doi:10.1097/01.ta.0000244609.65543.16. PMID: 17179844

38. Holcomb JB, del Junco DJ, Fox EE, et al. The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study: comparative effectiveness of a time-varying ratio vs fixed ratio of plasma:platelets:red blood cell transfusion. J Trauma Acute Care Surg. 2013;75(4):687-696. doi:10.1097/TA.0b013e31829e4e69. PMID: 24021950

39. Rahou E, Zufferey P, Rigal E, et al. Pre-hospital administration of tranexamic acid in trauma patients: a systematic review and meta-analysis. Crit Care. 2019;23(1):339. doi:10.1186/s13054-019-2626-0. PMID: 31590514

40. Brown JB, Cohen MJ, Minei JP, et al. Goal-directed resuscitation in the trauma bay: a prospective analysis of blood product utilization, survival, and waste. J Trauma Acute Care Surg. 2016;81(3):465-473. doi:10.1097/TA.0000000000001119. PMID: 27106370

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Last Updated: January 2026