Contents
- Overview
- Primary Survey and Immediate Threats
- Haemostatic Resuscitation
- Damage Control Surgery
- Secondary Survey
- Specific Injury Patterns
- ICU Management
- Viva Questions
Overview
Major trauma is defined as injury with an Injury Severity Score (ISS) >15. In the UK, major trauma centres (MTCs) manage approximately 50,000 major trauma cases per year, with 30-day mortality of approximately 5–10%. The trimodal distribution of trauma deaths — immediate (at scene), early (minutes to hours, haemorrhage/airway), and late (days to weeks, MOF/sepsis) — informs the systematic approach. Modern trauma care aims to prevent early deaths from haemorrhage and late deaths through ICU optimisation.
Primary Survey and Immediate Threats
The ATLS (Advanced Trauma Life Support) framework provides a structured approach to simultaneous identification and treatment of immediately life-threatening injuries.
ABCDE
Modern major trauma teaching inserts massive haemorrhage control before airway —
A — Airway with cervical spine protection: Assess patency. Unconscious patients require definitive airway (ETT). Manual inline stabilisation (MILS) during laryngoscopy. Video laryngoscopy preferred in anticipated difficult airway (facial trauma, blood/vomit in airway, cervical spine immobilisation).
B — Breathing: Assess bilateral chest movement, air entry, SpO2. Immediate threats:
- Tension pneumothorax: needle decompression → chest drain
- Open pneumothorax: three-sided occlusive dressing → chest drain
- Massive haemothorax: large-bore chest drain
- Flail chest: adequate ventilation, consider intubation
C — Circulation: Assess for haemorrhagic shock. Activate massive transfusion protocol if appropriate. IV/IO access. Haemorrhage control (see below).
Signs of haemorrhagic shock (ATLS classification):
- Class I: <750 mL, minimal signs
- Class II: 750–1500 mL, tachycardia, anxiety
- Class III: 1500–2000 mL, tachycardia, hypotension, altered mental status
- Class IV: >2000 mL, life-threatening
Cardiac tamponade: suspect with penetrating chest trauma, distended neck veins, muffled heart sounds (Beck's triad). Haemodynamic instability, elevated JVP. Emergency pericardiocentesis or resuscitative thoracotomy.
D — Disability: AVPU or GCS. Pupils. Blood glucose. GCS ≤8 — intubate for airway protection.
E — Exposure: Fully expose and examine. Prevent hypothermia — active warming blankets, warm IV fluids, warm the environment.
Haemostatic Resuscitation
Uncontrolled haemorrhage accounts for approximately 30–40% of trauma deaths, and most preventable trauma deaths. The "lethal triad" of hypothermia, acidosis, and coagulopathy perpetuates haemorrhage — each element worsens the others and impairs clot formation.
Principles
Permissive hypotension (hypotensive resuscitation): Target systolic BP of 80–90 mmHg (MAP 50–65 mmHg) until surgical haemostasis is achieved, to avoid disrupting forming clots and diluting coagulation factors. Exception: TBI — maintain MAP ≥80 mmHg to ensure cerebral perfusion pressure.
Balanced blood product resuscitation: Red cells, FFP, and platelets in a 1:1:1 ratio (or equivalent). This mirrors whole blood and avoids dilutional coagulopathy from crystalloid. The PROPPR trial (Holcomb et al., JAMA 2015) demonstrated improved 24-hour and 30-day survival with a 1:1:1 vs 1:1:2 ratio.
Minimise crystalloid: Large volumes of crystalloid worsen coagulopathy, hypothermia, and abdominal compartment syndrome. Restrict to <500 mL as initial bridge before blood products.
Tranexamic acid: CRASH-2 trial demonstrated that TXA 1 g IV within 3 hours of injury (followed by 1 g over 8 hours) reduces mortality from haemorrhage. Benefit is greatest within the first hour. TXA is now standard of care in trauma haemorrhage.
Point-of-care coagulation monitoring: TEG/ROTEM allows rapid, goal-directed blood product replacement, reducing overall blood product use and guiding fibrinogen replacement. The ITACTIC trial found no mortality benefit from ROTEM-guided vs standard laboratory-guided resuscitation, but ROTEM-guided management reduced transfusion volumes.
Massive Transfusion Protocol (MTP)
Pre-defined pathways activate at the first sign of major haemorrhage, ensuring rapid delivery of blood products in predetermined ratios. MTPs include activation criteria, pack composition (e.g., 6 RBC : 6 FFP : 1 platelet pool : 2 cryoprecipitate pools), communication pathways with blood bank, and escalation triggers.
Fibrinogen: Falls first and most steeply in major haemorrhage. Target ≥1.5–2.0 g/L. Replace with cryoprecipitate or fibrinogen concentrate.
Damage Control Surgery
Damage control surgery (DCS) refers to an abbreviated surgical approach prioritising haemorrhage control and contamination control over definitive anatomical repair, allowing resuscitation in the ICU before definitive repair.
Indications
- Haemodynamically unstable patients requiring surgical haemorrhage control
- Physiological exhaustion: hypothermia <35°C, pH <7.2, base deficit >15, coagulopathy (PT/APTT >1.5× normal)
- Anticipated need for prolonged definitive repair in a deteriorating patient
Phases
DCS 1 — Emergency surgery: Laparotomy (or thoracotomy) for haemorrhage control (packing, vascular ligation, shunting) and contamination control (bowel stapling, not anastomosis). Abdomen left open — temporary abdominal closure (TAC) with VAC.
DCS 2 — ICU resuscitation: Warming, correction of coagulopathy, haemodynamic stabilisation, organ support.
DCS 3 — Definitive repair: Return to theatre (typically 24–72 hours) for bowel anastomosis, abdominal closure, and reconstruction.
Resuscitative Thoracotomy
Indicated for traumatic cardiac arrest with a witnessed cardiac arrest following penetrating chest trauma, or as a last resort in severe blunt trauma. Performed in the emergency department or operating theatre. Aims to relieve tamponade, control haemorrhage, and perform open cardiac massage. Survival rates are low except for penetrating cardiac injury.
Secondary Survey
A head-to-toe systematic examination performed after the primary survey and initial resuscitation, seeking injuries not immediately life-threatening. Includes:
- Head: lacerations, skull fractures, GCS re-assessment
- Cervical spine: tenderness, immobilisation decisions (Canadian C-spine or NEXUS criteria)
- Chest: rib fractures, pneumothorax, haemothorax, aortic injury
- Abdomen: peritonism, FAST ultrasound findings, CT imaging
- Pelvis: ring disruption (springing), perineal injury
- Extremities: fractures, vascular injuries, compartment syndrome
- Neurological: GCS trends, focal deficits
- Back: log roll, spine tenderness
FAST ultrasound (Focused Assessment with Sonography in Trauma): assesses for free fluid in hepatorenal recess (Morrison's pouch), splenorenal space, pelvis, and pericardium. Rapid, bedside, non-invasive.
Specific Injury Patterns
Traumatic brain injury: See dedicated ICU management — avoid hypoxia, hypotension, hypercarbia, hyperthermia, hyperglycaemia.
Pelvic fractures: Major bleeding source (up to 3–4 L internal haemorrhage). Pelvic binder/TPOD first. Definitive management: pre-peritoneal packing or angioembolisation for arterial bleeding; external fixation for fracture stabilisation.
Spinal cord injury: Full spinal precautions until cleared. Neurogenic shock (bradycardia + hypotension) from disruption of sympathetic outflow below T6. Managed with IV fluids and vasopressors (noradrenaline).
Aortic injury: Traumatic aortic injury (blunt deceleration — RTA, fall from height). TEVAR is now the standard of care for traumatic thoracic aortic injury; open repair in complex anatomy or contrast allergy.
Extremity vascular injury: Hard signs of vascular injury (pulsatile haemorrhage, expanding haematoma, absent distal pulses, signs of limb ischaemia) require urgent surgical exploration or endovascular intervention.
ICU Management
Immediate Priorities
- Continuing haemorrhage control and blood product resuscitation
- Warming to normothermia — active warming blankets, warm humidified ventilator gases, warm IV fluids
- Correction of coagulopathy — guided by TEG/ROTEM and product ratios
- Lung-protective ventilation in ARDS (which develops in approximately 25% of major trauma patients, particularly with massive transfusion)
Ongoing ICU Care
Analgesia and sedation: Multimodal analgesia — paracetamol, NSAIDs (caution in renal impairment and coagulopathy), ketamine, regional blocks (thoracic epidural, rib blocks for chest injuries). Minimise opioids.
Infection prevention: Major trauma patients are immunosuppressed. Wound care, VAC dressings for open fractures, early closure of contaminated wounds, antibiotic prophylaxis guidelines.
Nutritional support: Begin early enteral nutrition (within 24–48 hours). Trauma is a hypermetabolic state; nutritional targets are elevated.
VTE prophylaxis: TED stockings and IPC from admission; pharmacological prophylaxis (LMWH) when haemorrhage risk allows (typically 24–72 hours after definitive haemostasis).
Rehabilitation: Begin early physiotherapy — prevents ICU-acquired weakness and delirium. Splinting for joint injuries prevents contractures.
Damage Control Resuscitation to Damage Control Orthopaedics
The "damage control orthopaedics" (DCO) philosophy mirrors DCS for long bone fractures: temporary external fixation of femoral and tibial fractures in unstable patients, converting to definitive intramedullary nailing after physiological recovery (usually 3–7 days). Early definitive fixation in physiologically exhausted patients increases ARDS and MOF risk from the "second hit" of surgery.
Viva Questions
What is the lethal triad in major trauma and how does haemostatic resuscitation address it?
The lethal triad consists of hypothermia, acidosis, and coagulopathy — three processes that are mutually reinforcing and, together, make haemorrhage progressively less controllable. Hypothermia impairs clotting enzyme activity and platelet function (enzymes require their optimal temperature range for activation). Acidosis (from tissue hypoperfusion and lactate accumulation) further impairs coagulation enzyme function and reduces myocardial contractility. Coagulopathy arises from consumption of clotting factors, dilution with crystalloid, and the direct effects of temperature and pH on haemostasis. Haemostatic resuscitation directly targets the lethal triad. Balanced blood product replacement in a 1:1:1 ratio provides coagulation factors (via FFP), fibrinogen (via cryoprecipitate), and platelets alongside red cells, avoiding the dilutional coagulopathy of crystalloid-based resuscitation. Active warming prevents and reverses hypothermia. Tranexamic acid inhibits fibrinolysis. Permissive hypotension avoids the acidosis and dilution caused by excessive crystalloid while maintaining minimal perfusion pressure. The physiological targets are normalisation of base deficit, restoration of coagulation parameters on TEG/ROTEM, and achieving normothermia.
What is the CRASH-2 trial and what did it establish about tranexamic acid in trauma?
The CRASH-2 trial (Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage 2, Lancet 2010) was a multinational, randomised, placebo-controlled trial of over 20,000 trauma patients with significant haemorrhage or a risk of significant haemorrhage. Patients were randomised to tranexamic acid (TXA) 1 g IV over 10 minutes, followed by 1 g IV over 8 hours, or placebo. TXA significantly reduced all-cause mortality (14.5% vs 16%; RR 0.91) and death from haemorrhage (4.9% vs 5.7%). The benefit was greatest in patients treated within 1 hour of injury and was still significant when treated within 3 hours. Critically, treatment after 3 hours was associated with a trend towards increased risk of death from haemorrhage, probably because late TXA interferes with physiological fibrinolytic resolution of established clots. TXA is now standard of care in major trauma haemorrhage when given within 3 hours of injury, and is recommended by NICE major trauma guidance and ATLS-style trauma protocols. The mechanism is inhibition of plasminogen to plasmin conversion, preventing fibrinolysis and clot breakdown.
What is damage control surgery and when is it appropriate?
Damage control surgery (DCS) is an abbreviated operative strategy for haemodynamically unstable trauma patients in whom a full definitive repair would exceed their physiological reserve and risk death on the table. Rather than attempting complete anatomical reconstruction — which may take hours in a patient who cannot tolerate prolonged general anaesthesia and major blood loss — DCS achieves the minimum necessary to control haemorrhage and contamination. This typically involves abdominal packing, stapling bowel without anastomosis, ligation or temporary shunting of vascular injuries, and closure of the abdomen with temporary abdominal closure. The patient is then transferred to the ICU for resuscitation — correction of coagulopathy, warming, restoration of haemodynamics — before return to theatre for definitive repair at 24–72 hours. DCS is appropriate when any element of the lethal triad is present (temperature <35°C, pH <7.2, base deficit >15, coagulopathy), when the operation is already prolonged beyond 90 minutes with ongoing instability, when extensive bowel contamination requires staged approach, or as part of a pre-planned strategy for complex injuries. The philosophical shift from "fix everything now" to "save life first, repair later" has been associated with improved outcomes for the most physiologically compromised trauma patients.