Major Trauma in the Elderly

• Prehospital triage tools rely on mechanism and physiology, both of which are less reliable in older patients:
• Serious injury can result from low-energy mechanisms
• Classical signs of shock may be absent or masked (beta-blockers, pacemakers, pre-existing hypertension)
• Cognitive impairment makes history and baseline GCS difficult to establish
• As a result, many are taken to a trauma unit without a pre-alert, delaying CT and specialist care
• A lower threshold for suspecting major injury is needed

• SBP ≤110 mmHg
• Heart rate ≥100 bpm
• Fall with GCS ≤12
• Taking anticoagulants
• Comorbidities: liver disease, renal failure, heart failure, COPD

• Changes:
• Reduced chest wall and lung compliance; weaker respiratory muscles
• Reduced FEV₁, FVC and inspiratory reserve volume
• FRC unchanged, but closing volume rises and encroaches on FRC, especially supine
• Reduced upper airway tone and cough reflex


• Significance in trauma:
• Increased V/Q mismatch: faster desaturation, particularly supine and at induction
• Poor airway clearance: atelectasis, hypoxia and pneumonia, especially with rib fractures
• Opioid-sparing and regional analgesia, physiotherapy and early mobilisation are key

• Changes:
• Reduced baroreceptor responsiveness and myocardial sensitivity to catecholamines
• Stiff, hypertrophied left ventricle with greater reliance on atrial contraction
• Reduced arterial compliance (raised afterload); hypertension is common
• Atrial dilatation and fewer pacemaker cells: AF and other arrhythmias


• Significance in trauma:
• Attenuated tachycardia gives falsely reassuring heart rate
• BP maintained by raised SVR and may be deceptively normal: risk of occult hypoperfusion
• Reduced ability to compensate for blood loss
• Arrhythmias can precipitate heart failure and ischaemia
• Avoiding hypotension is key to maintaining organ perfusion

• Cerebral atrophy, cerebrovascular disease, dementia and cognitive impairment
• Impaired autoregulation: greater susceptibility to ischaemia with hypotension
• Atrophy allows a larger intracranial haemorrhage before ICP rises, so TBI presents late (e.g. subdural haematoma after a 'minor' fall)
• Delirium is common; rehabilitation is harder

• Fewer and smaller nephrons; renal blood flow falls by about 10% per decade after 30
• Impaired autoregulation: high risk of AKI with hypovolaemia
• Reduced clearance of renally excreted drugs; creatinine may overestimate function (low muscle mass), so consider creatinine clearance
• Avoid or limit NSAIDs

• Malnutrition and sarcopenia are common; low albumin forms part of frailty assessment
• Impaired thermoregulation: more prone to hypothermia

• High prevalence of anticoagulant and antiplatelet use
• The incidence of major haemorrhage after trauma doubles after the age of 65

• Osteoporosis: fractures from low-energy mechanisms; low threshold for suspecting fracture
• Reduced muscle mass and thin skin: care with manual handling and pressure areas
• Cervical spondylosis and stenosis: central cord syndrome is increasing with an ageing population

• Reduced cardiac output and smaller central compartment means higher peak plasma concentration after a bolus, but a slower arm-brain time, so it is easy to give too much before the effect is seen
• Reduced total body water and lean mass but increased fat: smaller volume of distribution for hydrophilic drugs but prolonged action of lipophilic drugs
• Reduced albumin so higher free fraction of protein-bound drugs
• Reduced hepatic blood flow and renal clearance mean prolonged duration of action and risk of accumulation

• Increased brain sensitivity to anaesthetic agents, opioids and benzodiazepines
• Blunted sympathetic and baroreceptor responses lead to exaggerated hypotension with vasodilating agents
• In trauma, hypovolaemia compounds all of these and it is very easy to 'over-anaesthetise' the shocked older patient

• Have a high index of suspicion for intracranial injury with any external sign of head trauma or subtle change from baseline
• Management focuses on preventing secondary brain injury and rapid diagnosis

• Established protocols are needed for rapid reversal if bleeding is suspected
• Warfarin: PCC for immediate reversal plus vitamin K to prevent rebound
• DOACs: local protocol with haematology input

• In TBI, TXA within 3 hours reduced mortality in mild to moderate TBI (GCS 9-15) (CRASH-3)
• NICE recommends a 2 g IV bolus within 2 hours of injury, before imaging, for patients ≥16 years with moderate or severe TBI

• High risk in an unfasted older patient outside theatre: should be performed by a senior anaesthetist at the direction of the trauma team leader
• Resuscitate before you intubate: two wide-bore cannulae and blood products available or running
• Ketamine is ideal (cardiovascular stability, negligible effect on ICP); propofol lowers SVR and CPP and should be avoided
• Presume cervical spine injury; consider MILS
• Use an RSI checklist and videolaryngoscopy as the primary technique; anticipate difficulty

• 'Hard' indications:
1. Airway failure (actual or impending)
2. Ventilatory failure (hypoxia, profound hypercapnia)
3. Unconsciousness (GCS ≤8)


• 'Soft' indications, which may warrant a team risk-benefit discussion in older patients:
4. Unmanageable (combative with TBI)
5. Predicted decompensation
6. Humanitarian need

• Standardised regimens reduce cognitive load with doses adjusted for age, injury, cardiovascular stability and frailty (CFS):

Adapted from Major trauma in the elderly: unique challenges and considerations (BJA Education, 2025)

• Principles are the same: maximise oxygen delivery, limit blood loss, prevent and treat coagulopathy, and achieve early haemorrhage control (see major haemorrhage)
• Aim to do the minimum needed for stability in the ED before expedited transfer to theatre or IR


• Considerations:
• Permissive hypotension is potentially harmful and relatively contraindicated (impaired autoregulation, cerebral and coronary disease)
• Only consider it for high-pressure, high-volume uncontrolled arterial bleeding


• Hypoperfusion may be more difficult to recognise and non-haemodynamic signs (base deficit, lactate, UO, cap. refill, altered mentation, tachypnoea) may be more sensitive


• Higher risk of TACO so consider using lower volumes where possible e.g. fibrinogen concentrate over cryoprecipitate

• Safe induction, ongoing resuscitation and prevention of the lethal triad remain the priorities
• Invasive monitoring must not delay knife-to-skin as an arterial line can be sited after surgery starts
• Titrate depth of anaesthesia carefully
• After haemostasis, consider a 'dilate and fill' strategy e.g. small fentanyl boluses (1µg/kg) to offset catecholamine-induced vasoconstriction, followed by volume, repeated until hypoperfusion resolves
• Endpoints are the same but resuscitation may take longer


• Consider higher targets for Hb (100g/L) and platelets (100)

• Prognosis is difficult and requires an individualised approach: baseline function, comorbidity, injury and frailty
• Distinguish chronological age from physiological age
• Outcomes are worse with liver disease, renal disease and cancer
• Early comprehensive geriatric assessment: pain, infection, delirium, psychological wellbeing, medication optimisation

• Decisions to withhold treatment must not be based on age or anticipated quality of life alone
• Consider the individual prognosis, any advance directive and the family's understanding of the patient's wishes
• Where benefit is uncertain, a time-limited trial of treatment can be considered
• A palliative approach may be considered with catastrophic injury, disabling injury with poor anticipated quality of life, significant frailty with likely death within 12 months, or another life-limiting illness
• Early involvement of palliative care, care of the elderly and trauma rehabilitation specialists improves outcomes, reduces in-hospital mortality and length of stay, avoids unnecessary surgery and improves communication with families
• See the ICM trauma page for ICU admission decisions