Home / Clinical Knowledge / Trauma

Trauma Management

Clinical reference only. This content is intended as a study and revision aid for paramedic students. Always follow current clinical practice guidelines and your service's protocols. Drug doses and clinical criteria may vary by jurisdiction and scope of practice.

Traumatic Brain Injury

TBI is the leading cause of morbidity and mortality in trauma, and the leading cause of mortality in individuals under 45 years of age.

GCS Classification of TBI
Mild TBI
13–15
Headache, dizziness, memory problems, blurred vision
Moderate TBI
9–12
Slurred speech, confusion, repeated vomiting
Severe TBI
3–8
Seizures, coma, persistent headaches, neurological signs
Interactive GCS Severity Classifier
Eye Opening (E)
Verbal Response (V)
Motor Response (M)
Total GCS Score
—
Primary vs Secondary Brain Injury
Primary Brain Injury

The initial mechanical insult — cannot be reversed, only prevented.

  • Cerebral contusion (bruising from impact)
  • Cerebral laceration (tissue tear)
  • Intracranial haemorrhage
  • Subdural haematoma (surface vessel rupture)
  • Extradural/epidural haematoma (between dura & skull)
  • Diffuse axonal injury (DAI) — shearing of nerve fibres
Secondary Brain Injury

Ongoing physiological effects — the primary target of prehospital management.

  • Intracranial: Rising ICP, haematoma expansion, cerebral oedema
  • Extracranial: Hypoxia, hypotension, hypercarbia, acidosis
  • Reduction in cerebral perfusion pressure (CPP)
  • Progressive brain tissue displacement from expanding mass
Monroe-Kellie Doctrine

The total volume of intracranial contents must remain constant. Any increase in one component (brain, blood, or CSF) must be compensated by a decrease in another — otherwise ICP rises.

Normal ICP
7–15 mmHg. Values above 20 mmHg are considered raised and require urgent management.
Intracranial Contents
Brain
80%
Blood
10%
CSF
10%
Signs of Raised ICP & Cushing's Triad
Signs of Raised ICP
Headache · Nausea/vomiting · Restlessness, agitation, drowsiness · Slurred speech · Papilloedema · Seizures · Reduced GCS · Abnormal respiratory patterns
Cushing's Triad — Pre-herniation Sign
Hypertension (widening pulse pressure) · Bradycardia · Irregular respirations
This is the body's last-ditch response to raised ICP. Often a precursor to brain herniation and death.
CPP & MAP Calculator
Cerebral Perfusion Pressure
CPP = MAP − ICP
Mean Arterial Pressure
MAP = DBP + (SBP − DBP) ÷ 3
Interactive CPP / MAP Calculator Interactive
MAP
—
mmHg
CPP
—
mmHg
Normal MAP: 70–110 mmHg  |  Target CPP in severe TBI: ≥60 mmHg  |  Critical CPP: <50 mmHg
Management Principles
  • 1
    Recognise severe TBI — GCS ≤8, clinical signs of raised ICP, Cushing's triad
  • 2
    Airway & oxygenation — Maintain SpO₂ >95%, avoid hypoxia at all costs
  • 3
    Ventilation — Avoid hypoventilation (hypercarbia↑ICP) and hyperventilation (vasoconstriction). Target EtCO₂ 35–40 mmHg
  • 4
    Blood pressure — Avoid hypotension; maintain SBP ≥90 mmHg. Hypotension dramatically worsens outcomes
  • 5
    Treat other life-threatening injuries — haemorrhage control, tension pneumothorax
  • 6
    Transport — Most appropriate major trauma centre; pre-notify
Avoid in TBI
Hypotension · Hypoxia · Hypercarbia · Hypocarbia (aggressive hyperventilation) · Hypertension (extreme) · Hypoglycaemia

Spinal Cord Injury

The spinal cord originates at the caudal end of the medulla oblongata and ends around L1 at the conus medullaris, continuing as the cauda equina.

Vertebral Anatomy & Effects of SCI by Level
Cervical
C1–7
7 vertebrae
Most debilitating. Paralysis, respiratory compromise. Diaphragm affected at C3–5.
Thoracic
T1–12
12 vertebrae
Affects trunk, chest & abdomen. Respiratory distress. Paralysis less likely.
Lumbar
L1–5
5 vertebrae
Upper extremities unaffected. Weakness/paralysis in lower limbs.
Sacral
S1–5
5 fused
Upper body function intact. Partial lower limb function. Bladder/bowel affected.
Risk Factors & SCI Patterns
High-Risk Mechanisms
  • ▲RTC involving rollover or ejection
  • ▲Fall from significant height
  • ▲Diving head-first into shallow water
  • ▲Axial loading of the spine (e.g. rugby)
  • ▲Pre-existing cervical spine abnormalities
  • iCommon mechanisms: flexion & hyperextension
PatternDescription
CompleteFull transection of spinal cord. Total loss of motor/sensory below injury
Central CordHyperextension compresses cord. Arms > legs affected. Common in elderly
Anterior CordAnterior artery compromise. Loss of motor & pain/temp; proprioception intact
Brown-SéquardHemisection of cord. Ipsilateral motor loss, contralateral pain/temp loss
Clinically Significant SCI Criteria
At Least One of the Following Required
Paraplegia · Quadriplegia · Clinically significant limb weakness · Clinically significant loss of sensation
C-Spine Clinical Clearance Criteria
C-Spine Can Be Cleared if ALL Criteria Met
Normal level of alertness  ·  No tenderness at posterior midline of cervical spine  ·  No signs/symptoms of SCI  ·  No distracting pain or factors
If C-Spine Cannot Be Cleared
Apply soft cervical collar if significant posterior midline tenderness or SCI symptoms. Maintain MILS. Use head blocks, rolled towels or manual stabilisation.
Cervical Spinal Cord Neuropraxia

Temporary, reversible loss of motor/sensory function from bruising or stretching of the cervical spinal cord — without permanent damage.

  • iBurning pain, numbness, tingling in limbs
  • iWeakness or paralysis (transient)
  • iAll four limbs usually involved
  • ▲Spinal cord blood flow dependent on perfusion pressure — maintain SBP
SCI Management Principles
  • 1
    Assess for other major injuries
  • 2
    Appropriate positioning/immobilisation — neutral alignment, MILS, cervical collar if indicated
  • 3
    Keep patient warm — thermoregulation impaired below level of injury
  • 4
    IV fluid — if signs of poor perfusion
  • 5
    Consider inotropes/vasopressors — if hypotensive (neurogenic shock)
  • 6
    Antiemetic + analgesia
  • 7
    Transport to major trauma centre
Autonomic Dysreflexia

Abnormal stimulation of the autonomic nervous system in patients with chronic SCI (usually T6 or above). An overstimulation of the sympathetic nervous system below the injury causes vasoconstriction and severe hypertension, triggering a parasympathetic response above the level of injury.

Common Triggers
  • ▲Bladder distention
  • ▲Bowel distention
  • ▲Acute injury or pain
  • ▲Infection
  • ▲Labour
Signs & Symptoms
  • !Severe hypertension
  • !Headache
  • !Bradycardia
  • ▲Anxiety, sweating
  • ▲Vasodilation above injury
  • ▲Vasoconstriction below injury
Complications
  • !Cerebral haemorrhage
  • !Myocardial infarction
  • !Seizures
Management
Identify & remove trigger → Positioning → GTN SL 0.4mg → Consider fentanyl/morphine → Labetalol 10–20mg IV every 5 min → GTN IV infusion 2mg/hr if refractory
Cauda Equina Syndrome
Surgical Emergency
CES requires urgent specialist assessment and intervention. Most commonly caused by large lumbar disc prolapse at L4–L5 or L5–S1. Untreated → significant disability.
Clinical Presentation
  • !Back or leg pain
  • !Difficulty urinating
  • !Altered sensation in saddle area
  • !Altered sensation or power in both legs
  • ▲Sexual dysfunction
Back Pain Red Flags
  • !Loss of bladder or bowel control
  • !Temperature >38°C / rigors
  • !Saddle area altered sensation
  • !Thoracic pain, abdominal tenderness
  • !Pain radiating down both legs
  • ▲Unable to mobilise

Facial & Neck Trauma

Facial trauma predominantly results from RTCs, assault, falls and sports injuries. The face has significant innervation of blood vessels and nerves, making it susceptible to complex injury.

Common Facial Fractures
FractureKey FeaturesClinical Tips
Mandibular Most common facial fracture 3 questions: Normal bite? Lip/chin numbness? Pain opening jaw?
Maxillary (Le Fort) Midface fractures I–III; can involve airway High risk of airway compromise; C-spine consideration
Zygoma (Cheekbone) Flattening of cheek, periorbital swelling Assess for visual changes and periorbital haematoma
Nasal Bone Most common facial bone fractured Epistaxis control, assess for septal haematoma
TMJ Dislocation Jaw locked open, deviation of jaw Cannot close mouth; significant pain
Hyphema
Blood in the anterior chamber of the eye following blunt facial trauma. Eye may appear red or have visible blood layer. Transport upright if possible, avoid Valsalva manoeuvres.
Facial Trauma Management Principles
  • 1
    Airway — priority; facial trauma can rapidly compromise the airway
  • 2
    Oxygenation & ventilation
  • 3
    C-spine consideration — significant facial trauma implies high-energy mechanism
  • 4
    Haemorrhage control
  • 5
    IV fluid & analgesia
Neck Trauma Assessment — TWELVE
T
Tracheal Deviation
Shift away from midline may indicate tension pneumothorax or haematoma
W
Wounds
Penetrating or open wounds to the neck; assess zone of injury
E
External Markings
Bruising, ligature marks, abrasions indicative of mechanism
L
Laryngeal Disruption
Hoarseness, stridor, crepitus or deformity over larynx
V
Venous Distention
Raised JVP — may indicate cardiac tamponade or tension pneumothorax
E
Emphysema (Surgical)
Subcutaneous crepitus suggesting air tracking from airway or lung injury
Strangulation & Hanging Assessment

Complete primary and secondary surveys. Obtain history where possible. Symptoms can evolve — patient may appear well initially.

Assess For
  • !Dyspnoea / orthopnoea
  • !Stridor / hoarseness
  • !Haemoptysis
  • ▲Progression of symptoms
Management
  • iMaintain patent airway
  • iAdequate oxygenation & ventilation
  • iHaemorrhage control
  • iC-spine consideration
  • iCall for backup, frequent reassessment

Thoracic Trauma

RTCs account for over 70% of blunt chest trauma. Thoracic injuries can be immediately life-threatening and require rapid identification and intervention.

Life-Threatening Thoracic Injuries
Tension Pneumothorax
  • One-way valve effect — air accumulates
  • Dyspnoea, tachycardia, hypotension
  • ↓ breath sounds, distended neck veins
  • Emergency needle decompression
Open Pneumothorax
  • Sucking chest wound
  • Air enters pleural space through wound
  • Apply HyFin Vent chest seal (vented)
  • Monitor for tension development
Massive Haemothorax
  • >1500mL blood in pleural space
  • Haemodynamic compromise
  • ↓ breath sounds, dull percussion
  • IV access, fluid/blood products, urgent surgery
Flail Chest
  • ≥3 consecutive ribs fractured in ≥2 places
  • Paradoxical chest wall movement
  • Respiratory compromise, atelectasis, pneumonia
  • Analgesia, ventilatory support
Cardiac Tamponade
  • Blood in pericardium restricts CO
  • Beck's Triad: ↑JVP, muffled HS, ↓BP
  • Usually penetrating trauma
  • Urgent pericardiocentesis / surgery
Airway Disruption
  • Rare but rapidly fatal
  • Haemoptysis, subcutaneous emphysema
  • Stridor, dyspnoea, cyanosis
  • Immediate airway management
Pneumothorax — Open vs Tension
Simple / Open Pneumothorax
  • Air in pleural space, no pressure buildup
  • Dyspnoea, chest pain, reduced A/E
  • Subcutaneous emphysema
  • Vented chest seal — allows air out, not in
  • Monitor for tension conversion
Tension Pneumothorax
  • One-way valve → increasing pleural pressure
  • Cardiovascular collapse (↓CO)
  • Tracheal deviation (late sign)
  • Distended neck veins
  • Emergency chest decompression required
Emergency Chest Decompression
Needle Thoracostomy / Finger Thoracostomy (CCP)
Procedural
Indications
Traumatic cardiac arrest (with torso involvement) · Suspected tension pneumothorax
Insertion Sites
2nd intercostal space, mid-clavicular line (anterior) · 4th/5th intercostal space, mid-axillary line
Technique
Insert cannula over superior border of rib (avoid neurovascular bundle below rib). Release hiss of air confirms tension pneumothorax.
Contraindications
Obvious non-survivable injury in traumatic cardiac arrest · Patient <50kg (~14 years old)
Rib Fractures — Special Considerations
Elderly Patients — Significantly Higher Risk
19% mortality when >4 ribs are fractured in older patients. Associated pneumonia rate of 27%. Each additional rib fracture increases mortality and pneumonia risk. Analgesia is critical to allow effective breathing and coughing.
Flail Chest Definition
≥3 ribs
Fractured in ≥2 consecutive places producing a free-floating segment with paradoxical movement
Haemopneumothorax
Blood + Air
Accumulation of both blood and air in the pleural space; combines haematoma and pneumothorax management

Abdominal & Pelvic Trauma

Missed blunt abdominal trauma is a major cause of preventable death. The pelvis is highly vascular — pelvic fractures can accommodate massive concealed haemorrhage.

Key Clinical Signs in Abdominal Assessment
Kehr's Sign
Shoulder Tip Pain
Acute pain at the tip of the shoulder. Sign of ruptured spleen — diaphragmatic irritation from blood
Cullen's Sign
Periumbilical Bruising
Bruising around the umbilicus. Sign of retroperitoneal haemorrhage (e.g. ruptured abdominal aorta, pancreatitis)
Grey Turner's Sign
Flank Bruising
Bruising of the flank areas. Sign of retroperitoneal haemorrhage — takes time to develop, may not be present acutely
Physical Examination Checklist
Assess For
  • !Seatbelt sign (bruising pattern)
  • !Rebound tenderness
  • !Hypotension
  • ▲Abdominal distension
  • ▲Abdominal guarding
  • iConcomitant femur fracture (distracting)
Management Principles
  • 1
    History, MOI, thorough examination (flanks & back)
  • 2
    Consider CCP/HARU backup (blood products, FAST)
  • 3
    Pelvic binder if indicated, IV access
  • 4
    Analgesia, antiemetic, TXA if indicated
  • 5
    Temperature management
Pelvic Trauma
Concealed Haemorrhage Risk
The pelvis can accommodate 3–4 litres of blood without sufficient tamponade. Significant association with massive haemorrhage. Usually requires extreme force — RTC, crush, fall from height. In elderly, consider even minor falls.
Young-Burgess TypeMechanismStabilityHaemorrhage Risk
LC I–IIILateral compressionVariableLow to moderate
APC I–IIIAnteroposterior compression (open book)UnstableHigh
VSVertical shear (fall)Very unstableVery high
CMCombined mechanismVery unstableVery high
Pelvic Binder Indications
MOI suggestive of pelvic fracture PLUS any of: HR >100 or SBP <90 · GCS <13 · Abnormal clinical assessment of pelvis suggestive of fracture · Distracting injury
Genitourinary Trauma
Kidney Injury
50%
Kidneys account for 50% of all GU trauma. Majority caused by blunt force. Flank pain, haematuria, bruising over costovertebral angle.
Male GU Trauma
Sport / Assault
Highly sensory-rich area. Risk of haemorrhage, psychological impact. Testicular trauma can be associated with blast injury.
Female GU Trauma
Variable MOI
Pelvic injury, sexual assault, straddle-type mechanism, childbirth. Bladder/urethral injuries common with pelvic fractures.

Ballistics & Blast Injury

Explosive blasts and ballistic injury present unique multi-system trauma. Scene safety and the TECC framework are fundamental to the prehospital response.

Mechanisms of Blast Injury
Primary
Pressure Wave (Barotrauma)
Affects gas-filled organs: blast lung (pulmonary barotrauma, haemorrhage into alveoli, V/Q mismatch), tympanic membrane rupture, bowel perforation. Silent killer — no external signs.
Secondary
Flying Debris & Shrapnel
Most common cause of death in blast injuries. Penetrating trauma that mimics GSW. Fragments can be propelled at high velocity in multiple directions.
Tertiary
Body Displacement (Blunt Trauma)
Body thrown by blast wind. Mainly orthopaedic injuries — fractures, TBI. Spinal injuries common. Injuries similar to fall from height or MVC.
Quaternary
Burns, Inhalation & Crush
Thermal burns, inhalation injuries, toxic/chemical exposure, dust and environmental contaminants, crush injury from structural collapse.
Quinary
Systemic / Delayed Effects
Immunosuppression, hyper-inflammatory state, chronic pain. Contamination with bacteria, radiation or chemical agents from "dirty bombs".
Blast Lung Injury — High Mortality
Pulmonary barotrauma · Haemorrhage into alveoli · Oedema & interstitial fluid · V/Q mismatch. Careful IPPV — hyperventilation and high pressures worsen outcome. Traumatic amputation of any limb is a marker for multi-system injury.
Ballistic Injury
Low Velocity (<300m/s)
  • Handguns, pistols, shotguns
  • Injury mainly along wound track
  • Less cavitation
  • Shotguns: pellet dispersion, rapid deceleration
High Velocity (>300m/s)
  • Military assault rifles, hunting rifles
  • Significant cavitation effect
  • Yaw and tumble increase tissue interaction
  • Fragmentation creates multiple wound tracks
Key Principle: Kinetic Energy
KE = ½mv² — velocity has a greater effect than mass on tissue destruction. Yaw (wobble) and tumble increase interaction with tissue, causing cavitation even at moderate velocities.
Initial Assessment — Blast & Ballistic ABCDE
  • A
    Airway — assume spinal injury; facial/neck burns may compromise airway rapidly
  • B
    Breathing — blast lung, tension pneumothorax risk; careful IPPV
  • C
    Circulation — catastrophic haemorrhage control first (tourniquet, wound packing); hypovolaemic shock
  • D
    Disability — TBI can occur without external signs in blast injury
  • E
    Exposure — full exposure, secondary survey; suspect delayed bowel injury
Scene Safety & TECC Zones
Hot Zone: Direct threat — self-aid only · Warm Zone: Indirect threat — tactical care · Cold Zone: No threat — evacuation care. Never enter an unsafe scene. PPE, secondary device awareness. Escape — Hide — Tell if armed offender situation develops unexpectedly.

Trauma in Special Groups

Paediatric, geriatric, and obstetric patients have unique anatomical and physiological characteristics that alter their response to trauma and require modified management.

Paediatric Trauma
Key Anatomical & Physiological Differences
  • iRTC is the most common MOI
  • !TBI is the most common cause of mortality
  • ▲Fontanelles susceptible in young children (open until ~18 months)
  • ▲Small airways — high O₂ consumption, more susceptible to obstruction
  • iBlood volume higher per kg; stroke volume fixed — compensation via ↑HR
  • !Hypotension is a late sign — compensatory mechanisms are effective until decompensation
Paediatric ABCDE
  • A
    Airway — large head, short neck, large occiput; neutral/sniffing position
  • B
    Breathing — respiratory rate is the most sensitive vital sign
  • C
    Circulation — weight-based fluid dosing (20mL/kg bolus)
  • D
    Disability — AVPU/paediatric GCS; blood glucose
  • E
    Exposure — prevent hypothermia; proportionally large BSA
Geriatric Trauma — Physiological Changes
SystemAge-Related ChangesClinical Implications
Neurological Brain atrophy (shrinks); increased comorbidities More vulnerable to TBI; subdural haematoma from minor trauma; delirium common
Cardiovascular ↓ stroke volume & contractility; ↑ BP; degeneration of conduction system Cannot increase HR to compensate; fixed cardiac output; mask tachycardia response
Respiratory Rib calcification; ↓ respiratory muscle efficiency; senile emphysema; ↑ residual volume Poor tolerance of rib fractures; aspiration risk; difficult to wean ventilation
Renal ↓ functional units; ↓ renal blood flow; ↓ GFR Drug toxicity risk; fluid overload; delayed excretion of medications
Musculoskeletal ↓ muscle mass; joint immobility; osteoporosis Fractures from minor MOI; NOFF; Colles' fracture from simple falls
Pharmacological Polypharmacy; altered pharmacokinetics/dynamics Anticoagulants → haemorrhage risk; beta-blockers → masked tachycardia; opioid sensitivity ↑
Neck of Femur Fracture (NOFF)
Leading cause of morbidity in Australians >65yo. 25% die within 1 year. Mechanism: low energy fall. Signs: hip/groin pain, unable to weight bear, abduction, shortening & external rotation of leg.
Head Injury + Anticoagulants
Determine all anticoagulant medications (warfarin, NOACs, aspirin). High risk of intracranial haemorrhage even from minor head injury. Low threshold for CT and urgent ED assessment.
Obstetric Trauma

RTC, domestic violence and falls are the most common mechanisms. Goal is to maintain uteroplacental perfusion and foetal oxygenation.

Physiological Changes
  • i↑ cardiac output & blood volume
  • i↑ HR, ↓ BP (supine hypotension)
  • ▲Upper airway oedema → difficult airway
  • ▲↓ residual capacity → desaturates quickly
Shock Considerations
  • ▲Supine hypotensive syndrome (IVC compression)
  • !Can lose significant volume before haemodynamic signs
  • !Foetal distress may occur before maternal signs
Avoid
  • !Hypoxia
  • !Hypotension
  • !Acidosis
  • !Hypothermia
  • !Supine position — left lateral tilt
Frailty & Elder Abuse
Atypical Presentations in Elderly
  • ▲No pain with ACS
  • ▲Delirium as first sign of infection
  • ▲Dyspnoea without known cause
  • ▲Painless acute abdomen
Timed Up & Go (TUG) Test

Stand from chair → walk 3m → return. >12 seconds indicates high fall risk. Assesses mobility and balance.

Elder Abuse Red Flags
  • !Injuries inconsistent with stated mechanism
  • !Unexplained bruising in various stages of healing
  • !Fearful or withdrawn behaviour
  • !Signs of neglect (malnutrition, poor hygiene)
  • ▲Risk factors: cognitive impairment, psychiatric illness, frailty, social isolation

Trauma Pharmacology

Key drugs used in prehospital trauma management. Use the filter below to sort by indication.

Tranexamic Acid (TXA)
Antifibrinolytic Agent
S4
1g
Loading IV
1g
Maintenance
Route & Administration
IV infusion: 1g in 100mL over 10 min. Second 1g over 8 hours in-hospital.
Indication
Traumatic haemorrhage — reduce mortality from haemorrhagic shock
Critical Timing Window
Must be given within 3 hours of injury. After 3 hours, TXA may increase mortality.
Mechanism of Action
Inhibits fibrinolysis by blocking plasminogen activation, preventing clot breakdown and reducing haemorrhage.
Contraindications
Thromboembolic disease · Known allergy · Isolated head injury without haemorrhage (use with caution) · >3 hours post-injury
Morphine Sulfate
Opioid Analgesic
S8
0.1mg/kg
IV/IM
2.5–5mg
IV Titrate
Indication
Moderate to severe pain in trauma. Second-line to fentanyl for acute pain. Also used in autonomic dysreflexia management.
Onset / Duration
IV onset: 5 min · Duration: 4–6 hours
Cautions in Trauma
TBI — may mask neurological signs. Hypotension risk. Elderly patients highly sensitive — reduce dose. Respiratory depression.
Mechanism of Action
Binds to µ-opioid receptors in CNS, producing analgesia, sedation and anxiolysis. Reduces sympathetic response.
Contraindications
Known hypersensitivity · Significant respiratory depression · Unmanaged hypotension · MAOIs within 14 days
Fentanyl
Synthetic Opioid Analgesic
S8
1–2mcg/kg
IV/IM
25–50mcg
IV Titrate
Indication
First-line opioid for acute trauma pain. Patella/ankle dislocation. Fractures. Procedural analgesia.
Onset / Duration
IV onset: 1–2 min · Duration: 30–60 min. Faster and shorter than morphine.
Advantages in Trauma
Rapid onset. Less histamine release than morphine. Less haemodynamic compromise. Preferred in head injury.
Mechanism of Action
Highly potent µ-opioid receptor agonist. ~100× more potent than morphine. Lipophilic — rapid CNS penetration.
Contraindications
Known hypersensitivity · Significant respiratory depression · Chest wall rigidity risk with rapid high-dose administration
Methoxyflurane (Penthrox)
Volatile Inhalational Analgesic
S4
3mL
Inhaled
Max 6mL
Per Day
Indication
Moderate to severe acute pain. Fractures, dislocations (patella, ankle), wound care. Ideal first-line while IV access being established.
Administration
Patient-controlled inhalation via Penthrox inhaler. Onset within 6–10 breaths. Duration ~25–30 min per 3mL.
Advantages
Non-invasive. Rapid onset. Patient-controlled. Does not affect haemodynamics significantly. No IV required.
Mechanism of Action
Mechanism not fully understood — produces analgesia via CNS depression at sub-anaesthetic concentrations.
Contraindications
Known hypersensitivity · Altered LOC · Unable to self-administer · Renal/hepatic impairment (repeated use) · Personal or family history of malignant hyperthermia
Ondansetron
5-HT₃ Receptor Antagonist — Antiemetic
S4
4mg
IV / IM / ODT
8mg
Max Dose
Indication
Nausea and vomiting in trauma. Post-opioid nausea. TBI patients — vomiting elevates ICP. SCI patients prone to nausea.
Routes
IV (push over 2–5 min) · IM · ODT (orally disintegrating tablet — useful in conscious patients)
Onset
IV: 1–3 min · ODT: 15–30 min
Mechanism of Action
Selectively blocks 5-HT₃ receptors in the chemoreceptor trigger zone (CTZ) and vagal afferents, suppressing nausea and vomiting.
Contraindications
Known hypersensitivity · QT prolongation risk (caution with concurrent medications) · Congenital long QT syndrome
IV Fluids in Trauma
FluidTypePrimary Use in TraumaKey Points
Normal Saline (0.9% NaCl) Crystalloid Isotonic Volume replacement, drug dilution Large volumes cause hyperchloraemic acidosis. Limit in TBI.
Hartmann's Solution Crystalloid Balanced isotonic Preferred crystalloid in trauma More physiological than normal saline. Less risk of acidosis. Preferred for SCI, abdominal trauma.
Packed Red Blood Cells (pRBC) Blood Product Colloid Major haemorrhage — carries O₂ Available at CCP/HARU level. 1:1:1 ratio with FFP/platelets in massive transfusion.
Fresh Frozen Plasma (FFP) Blood Product Colloid Coagulopathy in major haemorrhage Contains all clotting factors. Part of damage control resuscitation. Given 1:1 with pRBC.
Permissive Hypotension in Haemorrhagic Shock
In penetrating trauma without TBI, target SBP ~80–90 mmHg rather than full normalisation. Excessive crystalloid worsens coagulopathy, dilutes clotting factors, and displaces clot. Prioritise haemorrhage control over aggressive fluid resuscitation.