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Trauma Chapter 19: Trauma & orthopaedics 265
https://t.me/med1917
Subarachnoid haemorrhage
CLINICAL PRESENTATION:
• Thunderclap headache – severe & sudden
• Vomiting & LOC
ON EXAMINATION:
• Meningism – stiff neck, photophobia, +ve Kernig’s
• Subhyaloid (intraocular) haemorrhage
• Reduced GCS (not always)
INVESTIGATIONS3:
1. Non-contrast CT: detects >95% SAH within first 24h
If CT is negative = consider lumbar puncture
→ Look for xanthochromia
→ Must be ≥12h after headache onset
2. Bloods: FBC, ESR, U&Es, glucose, LFT, clotting
MANAGEMENT3:
1. Refer to neurosurgery: investigate for cause e.g. berry aneurysms
2. Nimodipine: calcium antagonist to prevent vasospasm
3. Radiological intervention: clipping/coiling of berry aneurysms
→ maintain hydration but ensure SPB <180
→ anti-epileptic medication if seizures present
Causes of SAH:
• Berry aneurysms = 80%
• AVMs = 15%
• Intracranial malignancy
Risk factors for SAH:
• PKD, CTDs (associate with berry aneurysms)
• Uncontrolled HTN
• Anticoagulants/coagulopathies
• Alcohol/smoking
Differentials of SAH:
• Migraine
• Meningitis
• Coital headache – much briefer (30–60min)
& recurrent
• Reversible vasoconstriction syndrome
→ after decongestants
• Intracerebral bleed
• Cortical vein thrombosis
Complications of SAH:
• Death (30%)
• Rebleed (20% in first 3d)
• Hydrocephalus
• Cerebral vasospasm → ischaemia
• Hyponatraemia
3
NICE Draft Guideline (2021) Subarachnoid haemorrhage due to ruptured aneurysms [GID-NG10097]
Fig. 19.7 Diagrammatic representation
of CT head showing star-shaped SAH.
Musculoskeletal disease
DCML (dorsal column medial lemniscus)
= pain & temperature
266 Chapter 19: Trauma & orthopaedics
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266 Chapter 19: Trauma & orthopaedics Trauma
Spinal cord injury → Direct damage or 2° to pressure
Types of spinal cord injury
Classified using ASIA chart
4
Complete Incomplete
No motor or sensory function
below injury level
• Bulbocavernosus reflex still present
Some motor or sensory function below injury level
• Voluntary anal contraction or
• Palpable/visible muscle contraction or
• Perianal sensation
Acute phase conditions (resulting from spinal cord injury)
Neurogenic shock Spinal shock
Pathogenesis Loss of autonomic tone causing
haemodynamic changes
Loss of spinal reflexes causing flaccid
areflexia & paralysis
→ type of distributive shock
Symptoms Occurs if injury above T5
• Hypotension & bradycardia
Management Lasts 3d – 3w
• Vasoactive drugs & close monitoring
→ not true form of shock
Can occur with any cord injury
• Hypotension & bradycardia
• Absent reflexes (including
bulbocavernosus)
Lasts weeks to months
• Bladder & bowel management
• Monitor for respiratory difficulty
• Monitor for fever (cannot perspire
where paralysed)
Spinal cord anatomy
Descending tracts: motor tracts
→ corticospinal = voluntary movement of ipsilateral limbs
→ mainly in posterior half of spinal cord (except anterior corticospinal)
→ most decussate in brainstem = injury causes ipsilateral paralysis
Ascending tracts: sensory tracts
→ DCML = posterior half of spinal cord
→ Spinothalamic = anterior half of spinal cord
→ DCML decussates in brainstem = injury causes ipsilateral loss of fine touch, vibration &
proprioception
→ Spinothalamic decussate 2–3 levels above where they enter cord = injury causes
contralateral pain & temperature loss
Tracts to upper limbs = medial
Tracts to lower limbs = lateral
Tracts to upper limbs = lateral
Tracts to lower limbs = medial
Musculoskeletal disease
= ne touch & proprioception
spinothalamic (ST)
4
ASIA (2011) International standards for neurological classification of spinal cord injury. J Spinal
Cord Med, 34:535
Lateral
Fig. 19.8
Trauma Chapter 19: Trauma & orthopaedics 267
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Clinical syndromes
BROWN-SÉQUARD SYNDROME = hemisection of the spinal cord
• Loss of ipsilateral motor & fine touch / proprioception below level injured
• Loss of contralateral temp / pain 2–3 levels below level injured
Cause: penetrating trauma e.g. gunshot wound
CENTRAL CORD SYNDROME = injury to central grey matter of cord
• Loss of motor function in upper limbs > lower limbs (medial motor tracts
affected)
• Variable sensory loss
Cause: pre-existing cervical spondylosis (elderly) + hyperextension injury
→ causes simultaneous anterior & posterior cord compression
ANTERIOR CORD SYNDROME = injury to anterior part of cord
• Pain & temperature bilaterally affected
• Loss of motor function in lower limbs > upper limbs (lateral motor tracts
affected)
• Sparing of fine touch & proprioception (dorsal columns)
Cause:
1. Ischaemic damage via injury of anterior spinal artery
2. Burst fracture: crushed vertebral body pushed posteriorly into cord
POSTERIOR CORD SYNDROME = injury to posterior part of cord
• Fine touch & proprioception lost below damage (bilateral if both columns
affected)
• Sparing of motor function
Cause:
1. Neck hyperflexion
2. B12 deficiency
3. Posterior spinal artery infarct
Evaluation & management of spinal cord injury
5
DCML
CS
ST
Fig. 19.9 Area of spinal cord damaged in
Brown-Séquard syndrome.
DCML
CS
ST
Fig. 19.10 Area of spinal cord damaged in
central cord syndrome.
DCML
ST
CS
IMMEDIATE: ATLS approach
1. Triple immobilised: manual inline stabilisation, back board for transport
2. Consider intubation: if injury above C5 (potential for airway compromise)
3. Pain management
ON ADMISSION:
1. C-spine imaging: CT C-spine, X-ray spinal column
2. Prophylaxis: VTE, pressure sore prevention
3. Monitor: BP, urine output & bowel function and neuro obs
DEFINITIVE:
1. Reduce pressure / decompress cord: e.g. remove osteophytes etc.
2. Stabilise – surgical management + soft collars
3. Rehab – physio, SALT → set realistic goals with patient
5
NICE (2016) Spinal injury [NG41]
Fig. 19.11 Area of spinal cord damaged in
anterior cord syndrome.
DCML
CS
ST
Fig. 19.12 Area of spinal cord damaged in
posterior cord syndrome.
Musculoskeletal disease
268 Chapter 19: Trauma & orthopaedics Trauma
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Chest injuries
Potentially life-threatening chest injuries
Remember with ‘ATOM FC’
A Airway obstruction Symptoms:
• Stridor/gurgling
• Hoarse voice
• Surgical emphysema
Management:
1. Manoeuvres
2. Suction
3. Adjuncts
4. Intubation
T Tension pneumothorax Symptoms:
• Trachea deviates away from pneumothorax
• Breath sounds
• Hyper-resonant percussion
Management:
1. Needle thoracotomy + chest drain
O Open pneumothorax Symptoms:
• Penetrating chest wall injury (open wound)
• + Clinical signs of pneumothorax (as above)
Management:
1. Partially occlusive (3 sides sealed) dressing + chest drain
2. Surgical closure
M Massive haemothorax
Blood loss >1500ml or
>200ml/h
F Flail chest
≥2 contiguous ribs
fractured in ≥2 places
C Cardiac tamponade Symptoms:
Symptoms:
• Dull percussion
• Breath sounds
• CXR consolidation
• Haemorrhagic shock
Management:
1. Fluid/haemostatic resuscitation
2. Chest drain → chest thoracotomy if severe
Symptoms:
• Flail segment of chest wall
• Paradoxical chest movements
• Chest pain
Management:
1. Analgesia (± regional anaesthesia)
2. Close respiratory monitoring
3. ± Surgical fixation
• Beck’s triad
• Shock
Management:
1. Fluid resuscitation
2. Pericardiocentesis
1. Distended neck veins
2. Distant heart sounds
3. Decreased BP
Musculoskeletal disease
Trauma Chapter 19: Trauma & orthopaedics 269
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6
Major haemorrhage
Major haemorrhage is 50% volume blood loss in 3h (practically, we class it as
any bleeding causing HR>110 ± SBP<90)
MANAGEMENT:
Recognise blood loss &
trigger major haemorrhage protocol
Take blood samples for:
G&S, FBC, U&Es, clotting screen
If <3h from injury
Give TXA 1g bolus + 1g over 8h
NHS guidelines suggest all
hospitals have their own major
haemorrhage protocol policy
Indications for blood components:
Falling Hb: RBCs
APPT ratio >1.5: FFP
Fibrinogen <1.5: cryoprecipitate
Platelets <50 × 109: platelets
Liaise with blood bank
Order agreed ratio of components
Use O negative cells until X-match done
in a 1:1 ratio of red cells to FFP
Fig. 19.13
6
Trust Policy for blood transfusion and major haemorrhage (Queens Hospital Burton)
Musculoskeletal disease
270 Chapter 19: Trauma & orthopaedics Trauma
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Burns
Damage to tissues causing necrosis and a hypermetabolic, inflammatory
response
Pathophysiology
Local: coagulation, ischaemia & necrosis plus cytokine release → inflammatory
response (hyperaemia, erythema, oedema)
Widespread: fluid loss – hypovolaemia → distributive shock → systemic
dysregulation (e.g. AKI, hypothermia, immunosuppression, ARDS, infection)
Shock occurs when:
• >15% SA involved (>10% in children)
• if 50–70% SA involved = can be lethal
Investigations
• O2 sats, ABG
• Serum electrolytes (K+ & Na+)
• U&Es & creatinine (for AKI)
• FBC, serum protein, albumin
If inhalation: CXR, carboxyhaemoglobin levels
Categories of burns
Thermal: (most common)
• Direct contact with hot object / flame (burns), or liquids/vapour (scalds)
• Damage depends on temperature, duration of exposure, thickness of skin
Electrical:
• Entry and exit burns visible superficially but consider damage along internal
path as well e.g. vessel thrombus & rhabdomyolysis (leading to AKI)
• Severity depends on voltage and duration
Chemical: immediate, copious irrigation with water
• Difficult to remove source and often cause continuing damage
• Damage depends on substance (alkali worse than acid), concentration and
exposure duration
Cold (frostbite):
• Freezing of water within tissues
Irradiation:
• Due to UV exposure (e.g. sunburn)
Other types of burn:
1. Inhalation: facial burns, hoarseness, stridor, soot in mouth/nose, airway oedema and
obstruction
→ Consider inhaled toxic gases e.g. CO
→ 100% O2 & consider intubation if airway swelling
2. Circumferential: full thickness burns around extremities causing restrictive eschar
(necrotic tissue)
→ Results in compartment syndrome and acute limb ischaemia (check colour, temp,
neurovascular status of limb)
→ Need escharotomy to release restriction
Musculoskeletal disease
Complications
Early Late
• Hypovolaemia & shock ( BP, UO) → AKI
• Wound sepsis
→ S. pyogenes in 1st week
→ Pseudomonas afterwards
• Compar tment syndrome / acute limb
ischaemia in circumferential burns
• Infection (± sepsis)
• DIC
• ARDS
• Curling’s gastric ulcer (needs PPI prophylaxis)
• Hypermetabolic state (5–7d later)
→ Needs nutrition
→ ± Anabolic steroids ± beta-blockers
Trauma Chapter 19: Trauma & orthopaedics 271
Subcutaneous
Subcutaneous
Subcutaneous
Back = 18%
https://t.me/med1917
Assessing burn severity
7
1. DEPTH
Degree Thickness Characteristics Appearance
1st Superficial: epidermis
2nd 2a Superficial partial: upper dermis
2b Deep partial: lower dermis
3rd Full thickness: subcutaneous tissue
→ Pain, erythema, swelling
→ Blanches
→ Pain, erythema, vesicles/blisters
→ Blanches
→ Minimal pain, mottled, vesicles/blisters
→ Non-blanching
→ No pain, white, necrosis
→ Non-blanching
Heals with dense scar tissue (needs graft)
Fig. 19.14
Epidermis
Dermis
Epidermis
Dermis
Epidermis
Dermis
4th Most severe: full thickness that may involve tendons, muscles, bones
2. SURFACE AREA
• Lund & Browder charts8:
determine % body SA affected
• Can estimate % SA with rule of 9s
(palm of hand = approx 1%)
Segment % SA in adult
Head 9%
9%
Trunk 36% (4 × 9%)
Arms 18% (2 × 9%)
Thighs 18% (2 × 9%)
Lower legs and feet 18% (2 × 9%)
Genital region 1%
Management
1. ATLS protocol – primary & secondary survey + burn cooling (cool water)
2. IV fluid resuscitation: if burns >15% body SA (>10% in children)
• Parkland formula: used to calculate volume of Hartmann’s needed in first 24h
3. Analgesia: IV morphine
4. Burn care:
1st & 2nd degree: irrigation, topical moisturisers/antiseptics, dressings
3rd & 4th degree: early debridement of necrotic tissue, topical ABX, skin grafts
5. Good nutrition
Systemic ABX: if systemic infection
9%
18%
9%
9% 9%
Fig. 19.15 Rule of 9s.
9%
9%
Burns first aid:
Cool water 20min + cling film
Indications for referral9:
• >15% of total body SA
• Deep dermal burns >5% body SA
• Full thickness burns
• Hands, face, feet, genitalia
• Circumferential injury
• Associated inhalation injury
• Chemical or electrical injuries
• Extremes of age
• Suspected non-accidental injury
Parkland formula:
= 4 × total % SA × weight
(give ½ in first 8h, then ½ in next 16h)
NB: new guidelines suggest only 2 × SA ×
weight due to risks of fluid overload
Skin grafts:
• Within 5d
• Must be infection-free
• Autograft = best option
• Cover donor site with dressing
7
McCaughey P, McAllister S (2016) Initial assessment and management of burns. BMJ, 352:h5583
8
Lund C, Browder NC (1944) The estimation of areas of burns. Surg Gynecol Obstet, 79:352
9
NICE (2020) CKS – Burns and scalds, Scenario: First aid and initial management
Musculoskeletal disease
272 Chapter 19: Trauma & orthopaedics Fractures
Spiral Oblique Transverse ComminutedWedge
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General fracture principles
Classication of fractures
OPEN FRACTURES → Gustilo–Anderson classification
Type I Type II Type IIIa Type IIIb Type IIIc
• Skin wound <1cm
• Clean
• Simple fracture pattern
Low impact Moderate impact High impact
Sutures often enough IV ABX, irrigation & surgical debridement
• Skin wound ≥1cm
• Moderate soft tissue damage
• Minimal comminution
Extensive soft tissue damage
(still adequate cover)
Or multi-fragmented/segmental
Or crush / farm injur y
Or massively contaminated
Management
Reconstruction (or temporary external fixation or amputation)
Increasing risk of infection, non-union & amputation
Type IIIa + inadequate
soft tissue cover
(needs flap)
Type IIIa + vascular
injury
(needs repair)
CLOSED FRACTURES → Oestern–Tscherne classification
Grade 0 Grade 1 Grade 2 Grade 3
• Minimal soft tissue damage
• Simple fracture pattern
• Superficial abrasion/contusion
• Mild fracture pattern
Indirect injury Direct injury
• Deep abrasion
• Skin/muscle contusion
• Severe fracture pattern
• Extensive skin contusion
• Severe damage to muscle
• Compartment syndrome
Describing fractures
1. Demographics – name, age, date, anatomical markers, projection
2. Anatomical site – name, side, bone & joint → proximal, middle, distal or
diaphysis, epiphysis, metaphysis
3. Intra- or extra-articular
4. Fracture configuration – oblique, spiral, wedge etc.
5. Displacement – how distal fragment has moved relative to proximal AND
proportion of surfaces in contact (e.g. 50%)
6. Angulation – describe in degrees & whether varus or valgus → need 2 views
7. Shortening & rotation
8. Open/closed → associated soft tissue injury & neurovascular status
TIP: start with describing the most obvious abnormality
Exam tip:
Always ask for a 2nd view when given an X-ray
Musculoskeletal diseaseMusculoskeletal disease
two or more
fragments
Fig. 19.16 Fracture configurations.
Fractures Chapter 19: Trauma & orthopaedics 273
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Fracture healing
1. Primary healing: occurs if fragments can be reduced so no fracture gap via
compression across the fracture
= needs absolute stability → important for fracture at joint line to enable
a perfect healing position
2. Secondary healing: occurs if fracture gap with some, controlled, motion
between fragments (e.g. using plates/nails)
= needs relative stability → if fracture fixed too rigidly no movement at all =
won’t allow callus formation
Week 1:
Haematoma & inflammation
Haematoma converted to
granulation tissue by
infiltrating cells
Week 1–4:
Soft callus
Deposition of collagen &
fibrocartilage converts
granulation tissue to soft callus
Month 1–4:
Hard callus
Calcified soft callus resorbed
Osteoblasts lay down matrix
to form woven bone
FACTORS AFFECTING FRACTURE HEALING:
Local Systemic
Soft tissue trauma Smoking, diabetes, PVD
Neurovascular injury Nutrition
Bone loss Age
Immobilisation Previous irradiation
Infection/tumour Drugs (persistent NSAIDs)
Interposition of soft tissues Hormones
Bone type & site Associated head injury
Healing at different sites:
3 weeks: metacarpals
6 weeks: clavicle, radius,
fibula
10 weeks: humerus
16 weeks: femur, tibia
COMPLICATIONS OF BONE FRACTURES:
Immediate (when broken) Acute (during treatment) Long-term
• Severe haemorrhage & shock
• Injury to surrounding organs
• Injury to surrounding nerves/vessels**
• Skin loss/damage
• Infection – debridement & ABX
• Fat embolism syndrome**
• Crush syndrome**
• Compartment syndrome**
Immobilisation:
• DVT & PE – give LMWH/aspirin
• Renal calculi / urinary retention
• Chest infections – esp. elderly
• Pressure sores & muscle wasting
• Non-union/mal-union
• Joint stiffness & contracture
• Osteoarthritis (if joint damage)
• Regional pain syndrome**
• Heterotrophic ossification
• Avascular necrosis
▶ head of femur
▶ lunate
▶ body talus
▶ proximal scaphoid
Year 1–2:
Remodelling
Conversion to lamellar bone
& medullary canal reforms
Delayed union: fracture not healed within
double the average healing time for that patient
Non-union: fracture not healed after double
the average healing time for that patient or no
evidence of progression on serial X-rays
→ Hypertrophic non-union e.g. not sufficiently
stabilised
→ Atrophic non-union e.g. insufficient blood
supply
**See below for more on
these complications
NEUROLOGICAL DAMAGE ASSOCIATED WITH COMMON FRACTURES
Fracture/dislocation Nerve injury
Shoulder dislocation Axillary nerve
Humeral shaft Radial nerve
Supracondylar humerus Anterior interosseus / median
Monteggia fracture Posterior interosseus / radial
Distal radius Median nerve
Posterior hip dislocation Sciatic nerve
Knee dislocation Common peroneal nerve
Musculoskeletal disease
274 Chapter 19: Trauma & orthopaedics Fractures
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Fracture complications
COMPARTMENT SYNDROME:
Aetiology: muscle swells in restricted fascial compartment → occludes arterial &
venous flow → ischaemia → necrosis
Causes: follows trauma, fracture, tight casts/dressings, IV infusion
Signs:
• Out of proportion pain despite analgesia (unremitting throbbing that
develops hours after injury)
• Pain on passive flexion/extension of fingers/toes of affected limb
Investigations: assess for swelling, neurovascular status of limb*, passive
Compartment pressure diagnostic if:
>30mmHg or
<30mmHg difference from diastolic BP
stretch tests
Diagnosis: measure compartment pressure
Management: surgical emergency
1. Elevate limb, remove dressings / split casts open
2. Prompt fasciotomy
*Present pulse does not r/o this Dx
CRUSH SYNDROME:
Aetiology: systemic symptoms resulting from toxins released from crushed
muscle tissues
Causes: traumatic rhabdomyolysis or prolonged fixed position
Signs: muscle pains, vomiting, confusion
• Hypovolaemic shock
• AKI
• Hyperkalaemia
• DIC
• Raised CK
• Metabolic acidosis
Management: ABCDE
1. Treat metabolic abnormalities & catheterise (IV fluids or dialysis)
2. Crushed limbs may need amputation
Calf & forearm = most common locations
FAT EMBOLISM SYNDROME:
Aetiology: lipid emboli circulate to lung capillaries → lodge & cause
inflammatory response
Causes: 1–3d after long bone fracture → rare!
Signs:
• Major: petechial rash, confusion, respiratory distress (ground glass CXR)
• Minor: fever, tachycardia, oligo-/anuria
• Haematological: thrombocytopenia, anaemia
Prevention: early fixation & immobilisation of fractures
Management: supportive & Tx of organ dysfunction
Musculoskeletal disease
COMPLEX REGIONAL PAIN SYNDROME (CRPS):
Aetiology: dysregulation of central & autonomic nervous system → worsens
with time
Signs:
• Allodynia/hyperalgesia (increased pain sensitivity)
• Swelling & skin changes (warmth, erythema & sweating)
• Motor dysfunction (weakness, tremor, ROM)
Management: self-limiting but can take up to 2y → may need regional
nerve blocks
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