Type I:

• Imagine a spiral tibial fracture where the sharp bone end pokes through the skin, creating a small < 1 cm puncture wound. The wound is clean because it came from inside-out.
• Infection rate: ~0–2%
• No contamination. Minimal soft tissue damage. Simple fracture without comminution. ^[1]

Type II:

• Larger wound ( > 1 cm), more energy transfer, more muscle damage.
• Laceration > 1 cm. Moderate contamination. Moderate soft tissue damage. Moderate comminution. ^[1]
• Infection rate: ~2–10%

Type IIIA:

• High-energy injury, significant wound ( > 10 cm usually), but the key discriminator is: adequate soft tissue coverage of the bone is possible. ^[1]
• This means local tissues (muscle, fascia) can be rearranged to cover exposed bone.
• Infection — uncommon. Amputation ~ 0%. ^[1]

Type IIIB:

• The critical distinction from IIIA: bone coverage is poor; requires soft tissue reconstruction (i.e., a flap — local rotational or free flap). ^[1]
• Extensive periosteal stripping means the bone is devascularised — high risk of non-union and infection.
• Infection rate increased. Amputation occasionally. ^[1]

Type IIIC:

• This is IIIB plus a vascular injury requiring repair. Any open fracture with a vascular injury needing repair is automatically IIIC regardless of wound size.
• Bone coverage poor + vascular injury requiring repair. Usually requires soft tissue reconstruction. Infection rate increased. Amputation sometimes. ^[1]
• Amputation rate: up to 50% in some series

This is directly from the lecture and Maksim notes ^[2]:

Why these antibiotics?

• Cefazolin covers the most common organisms in open fracture infections: Staphylococcus aureus and Streptococcus species.
• Aminoglycosides (gentamicin) are added in Type III for Gram-negative coverage — higher contamination wounds introduce soil organisms, Gram-negatives.
• Penicillin is added for farm injuries because of Clostridium perfringens risk (gas gangrene).

• Antibiotics should be given ASAP — ideally within 1 hour of injury (the "golden hour" for antibiotics in open fractures). Each hour of delay significantly increases infection risk.
• Antibiotic choice is based on Gustilo grade (see table above).
• Anti-tetanus: Check immunisation status. Give tetanus toxoid booster if last dose > 5 years ago. Give tetanus immunoglobulin (TIG) if immunisation history is incomplete or unknown.

Debridement: ^[1]

• Excise non-viable structures
• Second-look debridement – routine at day 2–3
• May apply negative pressure dressing

Why debridement is essential from first principles: Dead tissue is a culture medium for bacteria. The "zone of injury" contains tissue that is crushed, devascularised, and contaminated. If left in situ, this tissue becomes necrotic and infected, leading to osteomyelitis, sepsis, and limb loss.

How to assess tissue viability during debridement — the 4 C's of muscle viability:

1. Colour — healthy muscle is beefy red; dead muscle is dark/grey
2. Contractility — pinch or stimulate with diathermy; viable muscle contracts
3. Consistency — viable muscle is firm and elastic; dead muscle is mushy
4. Capacity to bleed — viable muscle bleeds when cut; dead muscle does not

Second-look debridement at Day 2–3: This is routine, not optional. The reason is that tissue at the margin of the zone of injury may look viable at initial surgery but declares itself as non-viable over the next 48–72 hours. Removing this tissue at second-look prevents late infection.

Irrigation ^[1]

Irrigation washes out debris and reduces bacterial load. High-volume, low-pressure irrigation is preferred. The classic teaching is "the solution to pollution is dilution." Use normal saline — typically 3–9 litres depending on grade.

Negative pressure wound dressing ^[1]

Also called VAC (Vacuum-Assisted Closure):

• Creates a sealed environment with subatmospheric pressure
• Promotes granulation tissue formation by increasing blood flow to wound edges
• Removes exudate and reduces oedema — decreases bacterial load
• Bridges the gap between initial debridement and definitive soft tissue coverage
• Applied after debridement; changed every 48–72 hours
• NOT a substitute for debridement — you must debride first

Bony treatment: External fixation ^[1]

Why external fixation for open fractures?

• Internal fixation (plates, screws, intramedullary nails) introduces metallic implants into a contaminated wound — bacteria form biofilms on metal and are extremely difficult to eradicate.
• External fixation provides fracture stability with pins placed away from the zone of injury in clean bone, connected by bars outside the limb.
• Stabilises the fracture to allow soft tissue healing, reduces pain, and prevents further soft tissue damage from bone movement.

Ext fix or IM nail ^[1]

• The lecture shows that in some cases, primary intramedullary nailing may be considered (especially for open femoral shaft fractures). ^[1]
• Open femoral shaft fractures — IM nailing is often done primarily even in open fractures because the femur has a good soft tissue envelope (quadriceps) and the reaming provides additional stability. ^[1]
• However, for open tibial fractures (especially IIIB/IIIC), external fixation remains the initial choice with conversion to IM nail later after soft tissue healing.

Open femoral shaft fracture ^[1]

Femoral shaft fractures deserve special mention:

• High energy required to break the femur in young adults
• Significant blood loss (~1–1.5L per femoral shaft fracture)
• Early stabilisation (IM nail or external fixation) reduces ARDS, fat embolism, and mortality in polytrauma patients ("damage control orthopaedics")

Major joint dislocations can kink, stretch, or rupture the vessels and nerves crossing that joint. Every minute of delay increases ischaemic time and risk of permanent neurovascular damage.

25/male traffic accident. Sustains an open posterolateral dislocation of his left knee. No other injuries. No pulses in ER – cool foot. What to do? ^[1]

Answer: Immediate closed reduction of the knee dislocation.

Why? Knee dislocation is one of the most dangerous joint dislocations because the popliteal artery is tethered above (at the adductor hiatus) and below (at the soleal arch), so it cannot move out of the way during dislocation. Up to 30–50% of knee dislocations have an associated popliteal artery injury.

A cool, pulseless foot = acute limb ischaemia. The limb is under threat. You must reduce immediately to un-kink the artery. If you waste time getting advanced imaging before reducing, you risk irreversible ischaemia and amputation.

Steps:

1. Immediate reduction — usually closed reduction in A&E under sedation
2. Reassess pulses post-reduction

Pulses come back with reduction postoperatively. ^[1]

If pulses return → the artery was kinked but not ruptured. Good sign. If pulses do NOT return → suspect arterial tear/thrombosis → urgent angiography or CT angiography → vascular surgery for repair.

How to maintain reduction ^[1]

• External fixation or a bridging external fixator across the knee joint
• Maintains alignment, prevents re-dislocation
• Allows access to the wound for soft tissue management
• Definitive ligament reconstruction is delayed (months later) until soft tissue and vascular status are stable

Associated injuries with knee dislocation:

• Popliteal artery injury (~30–50%)
• Common peroneal nerve palsy (~25–35%) — foot drop
• Multiple ligament injury (ACL + PCL + at least one collateral) — by definition, knee dislocation requires disruption of at least 3 of the 4 major ligaments
• Meniscal tears

• Mechanisms of high-energy trauma (RTA, falls from height)
• ATLS principles — primary survey, resuscitation
• "Life before limb" — address life-threatening injuries before musculoskeletal

• Definitive fixation strategies after initial external fixation
• Soft tissue reconstruction — flaps (local and free)
• Complications: infection, non-union, compartment syndrome

• Confirmed the Gustilo-Anderson classification details and antibiotic regimens
• Complications of trauma: compartment syndrome, fat embolism, DVT/PE, crush syndrome

• Trauma imaging: standard trauma series (CXR AP, pelvis AP, lateral C-spine)
• CT is best modality for organ/vascular injury
• Pelvic fractures associated with high energy, vascular injury → angiographic embolisation

• Acute limb ischaemia: 6Ps (Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold)
• Fractures/dislocations → arterial stretching → intimal tear → thrombus formation

1. Classify this open fracture — Given a clinical vignette, determine Gustilo-Anderson grade. The discriminator is always IIIA vs IIIB (soft tissue coverage) and IIIC (vascular injury).
2. What antibiotics do you give for a Type III open fracture? — 1st gen cephalosporin + aminoglycoside.
3. What are the 3 components of open fracture management? — Antibiotics/tetanus, debridement, external fixation.
4. Knee dislocation with absent pulses — what do you do? — Immediate reduction, reassess pulses, angiography if pulses don't return.
5. Factors in the amputation vs salvage decision — Bone/soft tissue damage, ischaemia, age, shock/life-threatening conditions, nerve damage.

Question stem: "A 28-year-old man is trapped under rubbles from waist down after an earthquake. When he is found by the rescue team, he has already been trapped for around six hours. He is alert and only complains of pain in the lower limbs. No open wounds are noted."

• (a) Apart from pain control, what treatment will you start during the extrication process? (1 mark)
• (b) Name four important signs of a limb-threatening injury when you examine the limbs after extrication. (4 marks)
• (c) If a crush syndrome is suspected after extrication, what finding in your urine test will suggest the diagnosis? (1 mark)
• (d) If the patient goes into cardiac arrest five minutes after extrication, what is the likely cause? (1 mark) What drug will you give to try to treat the cause? (1 mark)
• (e) The patient has a diagnosis of acute renal failure after admission to the hospital. What can be done to prevent this in the prehospital phase? (2 marks)

Correct answers:

• (a) IV fluid resuscitation (aggressive normal saline infusion — 1–1.5L/hour) — to dilute myoglobin, prevent renal tubular obstruction, maintain renal perfusion.
• (b) Signs of limb-threatening injury: Pain out of proportion / pain on passive stretch (compartment syndrome); pulselessness; pallor; paralysis; paraesthesia; cool limb; tensely swollen compartments.
• (c) Myoglobinuria — urine dipstick positive for blood but no RBCs on microscopy (myoglobin cross-reacts with haemoglobin on dipstick). Dark brown/cola-coloured urine.
• (d) Hyperkalaemia (from massive release of potassium from crushed muscle cells upon reperfusion). Drug: IV calcium gluconate (10 mL of 10% — cardioprotective, stabilises myocardium) + insulin-dextrose, sodium bicarbonate.
• (e) Aggressive IV fluids before and during extrication + alkalinisation of urine with sodium bicarbonate (prevents myoglobin precipitation in renal tubules).

Relevance to this lecture: This question tests the consequences of high-energy crush injury to limbs, which overlaps with open fracture/high energy trauma principles — ischaemia time, neurovascular compromise, and the concept that soft tissue injury is the critical component.

Question stem: "A 40-year-old motorcyclist sustained injury to his pelvis in a road traffic accident. Despite resuscitation in the emergency room, the blood pressure remained unstable at 80/42 mmHg. Anteroposterior X-ray of the pelvis taken at the emergency room showed pelvic fracture. Which of the following is the MOST APPROPRIATE next step?"

Options:

• A. Arterial embolisation
• B. External fixation
• C. Open exploration and ligation of bleeding vessel
• D. Urgent computed tomography scan of the pelvis

Correct answer: B. External fixation

Rationale: In a haemodynamically unstable patient with a pelvic fracture, the immediate priority is to reduce pelvic volume to tamponade bleeding. A pelvic binder (applied in A&E) or external fixation achieves this. Arterial embolisation (A) may be needed later but requires haemodynamic stability to transfer to the angiography suite. CT (D) is for stable patients. Open exploration (C) is a last resort — the source is usually venous/cancellous bone bleeding, not a discrete arterial bleeder you can tie off.

Connection to lecture: This directly tests principles of high-energy trauma management — external fixation as the bony stabilisation method and the concept that stabilising bone reduces soft tissue/vascular damage.

Question stem: "A 40-year-old man sustained a whiplash injury in a car crash. Which of the following findings suggests a high risk of respiratory compromise?"

Options:

• A. Bilateral hand numbness and clumsiness
• B. Loss of cervical lordosis
• C. Raised diaphragm on chest radiograph
• D. Systemic hypotension and bradycardia

Correct answer: C. Raised diaphragm on chest radiograph

Rationale: A raised hemidiaphragm indicates phrenic nerve palsy (C3–C5). In cervical spine trauma, injury at C3–C5 can cause diaphragmatic paralysis → respiratory compromise. Bilateral hand numbness/clumsiness (A) suggests myelopathy but at a lower level (C8-T1). Loss of lordosis (B) is non-specific. Hypotension/bradycardia (D) = neurogenic shock, which is circulatory not primarily respiratory.

Question stem: "A 45-year-old man fractured his right 4th metacarpal. The fracture was managed with a brace. Now it is 4 weeks after the injury. He feels significant reduction in pain. What would be seen if we could obtain a microscopic view of the fracture site?"

Correct answer: D. Soft callus

Rationale: At 4 weeks, the fracture is in the reparative/soft callus phase (cartilaginous callus being formed by chondrocytes, bridging the fracture gap). Hard callus (woven bone replacing cartilage) occurs later around 6–12 weeks. Haematoma (B) is the initial phase (days 1–7). Bone resorption (A) occurs later in remodelling.