Orthopaedics

DEFINITION AND THE TWO ROUTES TO UNION

A fracture is a break in the structural continuity of bone. But bone is unique among tissues in that it heals by REGENERATION — forming new bone identical to the original — rather than by scar. It can do this in two entirely different ways, and understanding which one you are asking for determines how you must fix the fracture. SECONDARY (indirect) healing — the natural route — proceeds through CALLUS, and it REQUIRES a small amount of movement (micromotion) at the fracture site to stimulate it. It is what happens in a plaster cast, an intramedullary nail or an external fixator. PRIMARY (direct) healing occurs only when the fragments are held in ABSOLUTE stability with anatomical apposition — as by a compression plate. Here osteons simply grow across the fracture line, and NO callus is formed at all.

THE FOUR STAGES OF SECONDARY HEALING

1. HAEMATOMA AND INFLAMMATION (0–7 days): the fracture tears blood vessels and periosteum; a haematoma forms. Inflammatory cells arrive, releasing cytokines and growth factors (BMPs, TGF-beta, VEGF) which recruit mesenchymal stem cells. The haematoma is not waste — it is the scaffold and the signalling reservoir, which is why evacuating it (or excessive surgical stripping) impairs healing. 2. SOFT CALLUS (2–3 weeks): the stem cells differentiate into chondrocytes and fibroblasts, producing a bridging mass of fibrocartilage. The fracture becomes 'sticky' — clinically it stops moving, though it will not yet bear load. 3. HARD CALLUS (6–12 weeks): the soft callus is progressively mineralised by endochondral ossification into WOVEN bone. The fracture unites; callus is now visible on X-ray. 4. REMODELLING (months to years): woven bone is slowly replaced by organised LAMELLAR bone along the lines of stress (Wolff's law), and the medullary canal is re-established. In children, remodelling is so powerful that considerable angulation may correct itself entirely — but ROTATION never remodels.

WHY THE FIXATION MUST MATCH THE BIOLOGY

The commonest conceptual error in fracture surgery is understanding why choosing 'a bit of both' — partial stability across a gap — produces NEITHER kind of healing. If a surgeon applies a plate but leaves a gap at the fracture, they have prevented the micromotion needed for callus, but have not achieved the bone-on-bone contact needed for primary healing. The result is a fracture that cannot heal by either mechanism — and it goes on to NON-UNION. Hence the AO principle: decide the strategy first. Either provide ABSOLUTE stability with anatomical reduction (interfragmentary compression — essential for articular fractures, where the joint surface must be perfect) or provide RELATIVE stability with a well-aligned but not anatomically-reduced fracture (nailing, bridge plating, external fixation — appropriate for diaphyseal and comminuted fractures), and let callus do the work.

FACTORS THAT DELAY OR PREVENT HEALING

These are best remembered by asking what a fracture needs. It needs BLOOD SUPPLY — hence the notoriously poor healing of sites with a precarious supply (the scaphoid, the femoral neck, the talus, the distal tibia); and hence the harm done by extensive periosteal stripping, open injury, irradiation and peripheral vascular disease. It needs STABILITY — excessive movement produces a fibrous union rather than bone. It needs CONTACT — a gap, or interposed soft tissue (muscle, periosteum) between the fragments, prevents bridging. It needs a healthy host — so smoking (a powerful and much-underestimated inhibitor, via vasoconstriction), diabetes, malnutrition, vitamin D deficiency, corticosteroids, NSAIDs, chemotherapy and old age all impair it. And above all it must be free of INFECTION — which is the commonest cause of non-union in an operated fracture.

• Fracture healing is REGENERATION, not scar. SECONDARY (indirect) healing goes through CALLUS and REQUIRES micromotion (cast, nail, external fixator). PRIMARY (direct) healing needs ABSOLUTE stability with anatomical apposition (compression plate) and forms NO callus.
• Four stages: HAEMATOMA and inflammation (days) → SOFT (fibrocartilaginous) CALLUS (2–3 weeks) → HARD (woven bone) CALLUS (6–12 weeks) → REMODELLING into lamellar bone (months–years, along the lines of stress — Wolff's law).
• The fixation must MATCH the biology — a plate across a GAP prevents callus without allowing primary healing, and is a classic cause of NON-UNION. Choose absolute stability (articular fractures) OR relative stability (diaphyseal, comminuted).
• Factors impairing healing: poor BLOOD SUPPLY (scaphoid, femoral neck, talus, distal tibia; periosteal stripping, open injury, irradiation), excessive MOTION, a GAP or interposed soft tissue, INFECTION (the commonest cause in an operated fracture), SMOKING, diabetes, malnutrition, vitamin D deficiency, steroids, NSAIDs, and old age.
• In CHILDREN healing is fast and remodelling is powerful — significant ANGULATION may correct spontaneously, but ROTATION NEVER remodels and must be corrected.

WHY AN OPEN FRACTURE IS A DIFFERENT DISEASE

An open fracture is one in which the fracture haematoma communicates with the outside world — whether or not bone is visible. That single fact transforms the injury. It means that the fracture is CONTAMINATED (not merely 'infected' — yet), that the soft-tissue envelope which supplies the bone with blood has been damaged, and that the energy of the injury was high. Consequently the priorities change entirely: the risk of deep infection, osteomyelitis and non-union rises dramatically, and the eventual outcome depends far more on the state of the SOFT TISSUES than on the fracture pattern. A perfectly-fixed fracture in a dead or infected limb is worthless.

GUSTILO-ANDERSON CLASSIFICATION

TYPE I — a clean wound under 1 cm, usually an inside-out puncture; minimal soft-tissue damage; simple fracture. TYPE II — a wound of 1–10 cm with moderate soft-tissue damage and moderate contamination. TYPE III — extensive soft-tissue damage, high energy, gross contamination, or a segmental/severely comminuted fracture (any farmyard injury, gunshot or crush is at least type III, whatever the wound size). Type III is subdivided: IIIA — adequate soft tissue remains to COVER the bone; IIIB — there is a periosteal stripping and the bone cannot be covered, so a FLAP is needed; IIIC — there is an ARTERIAL injury requiring repair for limb survival. A crucial practical point: the grade can only be assigned reliably AFTER surgical debridement — the skin wound systematically UNDERSTATES the underlying damage, and 'the wound is small' is a treacherous reassurance.

THE MANAGEMENT SEQUENCE

In the emergency department: ATLS first (an open fracture is rarely the thing that kills). Then — give intravenous ANTIBIOTICS WITHIN ONE HOUR (this is the single most important intervention and is far more time-critical than the surgery); give TETANUS prophylaxis; photograph the wound once; remove gross contamination and cover with a saline-soaked sterile dressing (and do NOT keep uncovering it to look); splint the limb; and assess and document the NEUROVASCULAR status. Antibiotics: a first- or second-generation cephalosporin, with an aminoglycoside for type III and penicillin where clostridial contamination is likely (soil, farmyard). In theatre: the definitive step is a thorough, systematic DEBRIDEMENT — excising all devitalised tissue and foreign material, extending the wound, and lavaging copiously. Then stabilise the fracture (an external fixator or nail, according to the injury), and plan early soft-tissue COVER — ideally within 72 hours, since delayed cover markedly increases infection.

WHY THE '6-HOUR RULE' HAS BEEN RELAXED

A dogma that has been revised is understanding why the traditional insistence on debridement within 6 hours is no longer supported — while the antibiotic rule has, if anything, been tightened. Modern evidence shows that the QUALITY of the debridement and the timeliness of ANTIBIOTICS and SOFT-TISSUE COVER predict infection far better than the hour at which the operation began. A hasty debridement at 3 a.m. by a tired junior team is worse than a meticulous one at 8 a.m. by a senior surgeon with the right equipment. Hence current practice: antibiotics within the hour; urgent (but not necessarily immediate) debridement by an experienced team, ideally within 12–24 hours; and early definitive cover. The exceptions that still demand immediate surgery are: gross contamination, a devascularised limb (IIIC), or compartment syndrome.

• An open fracture communicates with the exterior — so it is CONTAMINATED, the soft-tissue envelope (and hence the blood supply) is damaged, and the energy was high. The outcome depends more on the SOFT TISSUES than on the bone.
• GUSTILO-ANDERSON: I — wound <1 cm, clean; II — 1–10 cm, moderate damage; III — extensive damage/high energy/gross contamination (IIIA — bone can be COVERED; IIIB — needs a FLAP; IIIC — ARTERIAL injury needing repair). Grade only AFTER debridement — the skin wound UNDERSTATES the damage.
• IV ANTIBIOTICS WITHIN ONE HOUR — the single most important intervention. Plus TETANUS prophylaxis, photograph once, remove gross contamination, cover with a saline-soaked dressing (do not keep uncovering it), splint, and document the NEUROVASCULAR status.
• In theatre: thorough systematic DEBRIDEMENT (excise ALL devitalised tissue, extend the wound, copious lavage) → fracture STABILISATION → early soft-tissue COVER (ideally within 72 hours — delayed cover markedly increases infection).
• The old '6-hour rule' is relaxed — the QUALITY of debridement and the timeliness of antibiotics and cover matter more than the hour of surgery. But immediate surgery is still needed for gross contamination, a devascularised limb (IIIC) or COMPARTMENT SYNDROME. Complications: infection, osteomyelitis, non-union, and — in a grossly contaminated wound — GAS GANGRENE and TETANUS.

THE MECHANISM — A VICIOUS CYCLE IN A CLOSED BOX

A muscle compartment is bounded by inelastic FASCIA — so it is, in effect, a closed box of fixed volume. Anything that increases the contents (bleeding, oedema after fracture or reperfusion, a crush injury, a burn) or decreases the volume (a tight cast, a bandage, prolonged limb compression) raises the INTRACOMPARTMENTAL PRESSURE. Once that pressure exceeds the pressure in the capillaries and small veins (which is low), venous outflow ceases — so blood continues to arrive but cannot leave. Congestion worsens the oedema, which raises the pressure further, which worsens the congestion: a self-amplifying VICIOUS CYCLE. The result is tissue ISCHAEMIA — and irreversible muscle and nerve NECROSIS begins within 4 to 6 HOURS.

WHY THE PULSE IS THE MOST DANGEROUS SIGN OF ALL

The single fact that most often costs a patient their limb is understanding why the PULSES REMAIN PRESENT in compartment syndrome — and why waiting for them to disappear is a catastrophic error. The compartment pressure needed to occlude the capillaries and veins is far LOWER than systolic arterial pressure. So for the pressure to abolish the distal pulse, it would have to exceed systolic pressure entirely — which almost never happens before the limb is already dead. Hence: a NORMAL pulse, a warm foot and a normal capillary refill DO NOT EXCLUDE compartment syndrome — they are entirely compatible with muscle that is dying at that moment. The classic 'five Ps' (pain, pallor, paraesthesiae, paralysis, pulselessness) are a dangerously misleading teaching, because four of them are LATE. The diagnosis rests on the FIRST P.

THE SIGNS THAT MATTER — AND THE DIAGNOSIS

PAIN OUT OF PROPORTION to the injury — severe, escalating, and requiring increasing doses of analgesia (a patient whose opioid requirement is climbing is sounding an alarm) — is the earliest and most important sign. PAIN ON PASSIVE STRETCH of the muscles in the compartment (e.g. passive extension of the toes in an anterior leg compartment syndrome) is the most SENSITIVE sign. Then: a tense, swollen, woody compartment; and paraesthesiae in the distribution of the nerve traversing it (an early sign of nerve ischaemia). Paralysis and pulselessness are pre-terminal. It is a CLINICAL diagnosis. Compartment pressure monitoring is useful chiefly in the unconscious, the child, or the patient with a nerve block or spinal anaesthesia — who cannot report pain (and in whom the diagnosis is therefore most often missed): a DELTA PRESSURE (diastolic BP minus compartment pressure) below 30 mmHg indicates decompression.

TREATMENT — AND THE CONSEQUENCE OF DELAY

This is a surgical emergency measured in hours. Immediately: remove all constricting dressings and SPLIT THE CAST DOWN TO SKIN (a split cast that is not opened through the padding does nothing); place the limb at heart level (NOT elevated — elevation reduces the arterial inflow pressure and worsens the ischaemia); give oxygen and analgesia; and correct hypotension. Then: urgent, complete FASCIOTOMY of ALL compartments — through long incisions (a two-incision, four-compartment fasciotomy in the leg), left OPEN and dressed, with delayed closure or skin grafting. If diagnosed and decompressed in time, function is preserved. If missed, the dead muscle is replaced by fibrous tissue which contracts — producing VOLKMANN'S ISCHAEMIC CONTRACTURE (a fixed, useless, clawed limb) — and the myoglobin released causes RHABDOMYOLYSIS with acute kidney injury and hyperkalaemia.

WHY A NERVE BLOCK CAN COST A LIMB

A modern and increasingly important danger is understanding why regional anaesthesia — a nerve block or an epidural — given for pain relief after a fracture, may MASK the one sign that would have saved the limb. The entire diagnosis of compartment syndrome rests on PAIN: pain out of proportion, escalating pain, and pain on passive stretch. A patient with an effective regional block feels nothing — so the alarm never sounds. The surgeon and nurses, seeing a comfortable patient, are reassured; the analgesic requirement does not climb; and the muscle dies silently. Numerous cases of missed compartment syndrome have followed exactly this course. Hence: regional blocks must be used with great caution — or avoided — in high-risk injuries (tibial fractures, crush injuries, forearm fractures in children, vascular injury and reperfusion), and where they are used, the limb must be monitored with COMPARTMENT PRESSURE measurement rather than relying on symptoms. The same applies to the unconscious, the intubated, the intoxicated and the very young child — all of whom cannot report pain, and in all of whom the diagnosis is most often missed.

WHY IT ALSO OCCURS WITHOUT A FRACTURE

A further point that catches the unwary is understanding why compartment syndrome does NOT require a fracture at all — and is therefore easily missed in patients who have not been to theatre. It can be caused by anything that raises the compartment contents or reduces its volume. Hence it occurs after a CRUSH injury (even without fracture); after prolonged limb COMPRESSION — the classic case being a patient found unconscious after an overdose, having lain on their own limb for hours; after REPERFUSION following a vascular injury or arterial repair (the reperfused muscle swells dramatically); after a BURN (a circumferential eschar acts exactly like a tight cast, and needs ESCHAROTOMY); after intense EXERCISE (chronic exertional compartment syndrome); after a snake bite; after intravenous EXTRAVASATION; after intramuscular bleeding in a HAEMOPHILIAC or a patient on anticoagulants; and — iatrogenically — from a TIGHT CAST or bandage. In every one of these, the same rule applies: escalating pain and pain on passive stretch mean compartment syndrome until proved otherwise.

• Compartment syndrome: raised pressure within a closed fascial compartment → venous outflow ceases → a self-amplifying VICIOUS CYCLE of congestion and oedema → ischaemia. Irreversible muscle and nerve necrosis begins in 4–6 HOURS.
• THE PULSES REMAIN PRESENT — compartment pressure rarely exceeds SYSTOLIC pressure. A normal pulse, warm foot and normal capillary refill DO NOT EXCLUDE IT. Do NOT wait for the 'five Ps' — four of them are LATE.
• The signs that matter: PAIN OUT OF PROPORTION (earliest — an escalating analgesic requirement is an alarm) and PAIN ON PASSIVE STRETCH (most sensitive); a tense, woody compartment; paraesthesiae. It is a CLINICAL diagnosis.
• Measure the pressure in those who CANNOT report pain (the unconscious, the child, and — crucially — the patient with a nerve block or epidural): decompress if the DELTA PRESSURE (diastolic BP − compartment pressure) is <30 mmHg.
• TREAT IMMEDIATELY: remove all dressings and SPLIT THE CAST DOWN TO SKIN; keep the limb AT HEART LEVEL (do NOT elevate); then urgent, complete FASCIOTOMY of ALL compartments, left OPEN. Missed → VOLKMANN'S ISCHAEMIC CONTRACTURE, and RHABDOMYOLYSIS with acute kidney injury and hyperkalaemia.

DEFINITIONS — AND WHY THEY MATTER

DELAYED UNION: the fracture is taking LONGER than expected to unite, but healing is still progressing — there is callus, and the process is simply slow. NON-UNION: healing has STOPPED. The fracture will not unite without intervention — defined clinically as a fracture that has shown no progression towards healing on serial X-rays over three months, or has not united by nine months (though the concept matters more than the arbitrary time). MALUNION: the fracture HAS united — but in an unacceptable position: angulated, rotated, shortened or displaced. The distinction is not academic: delayed union may need only patience and protected weight-bearing; non-union needs an operation; and malunion needs a corrective osteotomy.

THE TWO TYPES OF NON-UNION — AND WHY THEY NEED OPPOSITE TREATMENTS

A key concept is understanding why non-unions must be divided by their BIOLOGY — because the treatment is entirely different. HYPERTROPHIC ('elephant's foot') non-union: the X-ray shows abundant, exuberant callus at the fracture ends, but a persisting gap or lucent line. The biology is EXCELLENT — the bone is trying hard to heal; the problem is purely MECHANICAL: there is too much MOVEMENT. Hence the treatment is STABILITY alone — rigid internal fixation (plate or nail), often without any need for bone graft, and it will unite. ATROPHIC non-union: the X-ray shows NO callus at all; the bone ends are thin, pointed, sclerotic and osteopenic. Here the biology has FAILED — there is inadequate blood supply and no osteogenic response. Hence the treatment must supply BIOLOGY: freshen the bone ends, and add BONE GRAFT (an autologous cancellous graft from the iliac crest remains the gold standard — it is osteogenic, osteoinductive and osteoconductive), together with stable fixation.

CAUSES OF NON-UNION

Think of what a fracture needs, and what may have been withheld. MECHANICAL: excessive movement (inadequate immobilisation), or — paradoxically — a GAP or distraction (over-traction, an unreduced fracture, a plate holding the fragments apart), and soft-tissue INTERPOSITION between the fragments. BIOLOGICAL: a poor blood supply (either inherent to the site — scaphoid, femoral neck, talus, distal tibia — or destroyed by the injury or by excessive surgical stripping); a segmental fracture; bone LOSS; and irradiation. INFECTION: the commonest cause of non-union in an operated fracture, and it must be actively excluded in every case (an 'infected non-union' will not heal until the infection is eradicated). PATIENT FACTORS: SMOKING (a powerful and often decisive factor), diabetes, malnutrition, vitamin D deficiency, corticosteroids, NSAIDs, chemotherapy and old age.

MALUNION — AND THE CHILD'S EXCEPTION

Malunion causes problems in proportion to its plane and its site. It produces deformity, limb-length discrepancy, altered gait, and — most importantly — abnormal loading of the adjacent JOINTS, leading to secondary OSTEOARTHRITIS (a malunited tibial fracture with residual varus will destroy the knee over 20 years). It is treated, when symptomatic, by a corrective OSTEOTOMY. The great exception is the CHILD: the immense remodelling potential of a growing bone will correct considerable ANGULATION — particularly if the child is young, the deformity is near a rapidly-growing physis, and it lies in the PLANE OF MOVEMENT of the adjacent joint. But ROTATIONAL deformity NEVER remodels, and must always be corrected at the time of reduction.

WHY INFECTION MUST BE EXCLUDED IN EVERY NON-UNION

A rule that prevents repeated surgical failure is understanding why every non-union — particularly one following an operation — must be treated as INFECTED until proved otherwise. Infection is the commonest cause of non-union in an operated fracture, and a low-grade, indolent, 'quiet' infection may produce no fever, no discharge, no redness and normal inflammatory markers — nothing but a fracture that will not heal. And this matters absolutely, because an infected non-union will NEVER unite while the infection persists: bone grafting it, or applying a bigger plate, simply provides a fresh surface for BIOFILM and guarantees failure — the patient endures a second operation, and a third, each doomed. Hence, before any reconstructive surgery: take a careful history (a wound that was slow to heal, a course of antibiotics, a discharging sinus); check the CRP and ESR; and — the definitive step — obtain MULTIPLE DEEP TISSUE SAMPLES at surgery for culture (a superficial swab is worthless and misleading). If infection is confirmed, the sequence becomes: remove all implants and dead bone, debride thoroughly, insert an antibiotic-impregnated spacer, give prolonged targeted antibiotics — and only then reconstruct.

WHY SMOKING IS THE FACTOR WORTH ACTING ON

Among the many host factors that impair union, understanding why SMOKING deserves particular emphasis is worthwhile, because it is the one that is both powerful and modifiable. Nicotine causes peripheral VASOCONSTRICTION, reducing the blood supply to the fracture at the very moment it is most needed; carbon monoxide reduces the oxygen-carrying capacity of the blood; and smoking impairs osteoblast function and the inflammatory and angiogenic responses on which callus depends. The effect is not trivial: smokers have significantly higher rates of DELAYED UNION and NON-UNION, take substantially longer to heal, have higher rates of INFECTION and wound problems, and have poorer outcomes after fusion and after arthroplasty. The message is a practical one, and it is one that patients can act on: stopping smoking — even at the time of the injury — measurably improves the chance of union. The other modifiable factors worth attending to are NUTRITION (protein, calcium, VITAMIN D — which is very commonly deficient in India and should be checked and replaced), glycaemic control in diabetes, and avoidance of NSAIDs and corticosteroids where possible.

• DELAYED UNION: slower than expected, but still progressing. NON-UNION: healing has STOPPED (no progression on serial X-rays over 3 months; not united by ~9 months). MALUNION: united, but in an unacceptable position (angulated, rotated, shortened).
• HYPERTROPHIC non-union ('elephant's foot' — abundant callus with a persistent gap): the BIOLOGY is fine; the problem is MOTION → treat with rigid STABILITY (plate/nail); bone graft is often unnecessary.
• ATROPHIC non-union (NO callus; thin, sclerotic, pointed bone ends): the BIOLOGY has failed → treat by freshening the ends and adding BONE GRAFT (autologous iliac crest cancellous graft is the gold standard — osteogenic, osteoinductive and osteoconductive) with stable fixation.
• Causes: MECHANICAL (excessive motion; a GAP or distraction; soft-tissue interposition), BIOLOGICAL (poor blood supply — scaphoid, femoral neck, talus, distal tibia; segmental fracture; bone loss; excessive stripping), INFECTION (the commonest cause in an operated fracture — always exclude it), and PATIENT factors (SMOKING, diabetes, malnutrition, steroids, NSAIDs).
• MALUNION causes deformity, limb-length discrepancy and — crucially — abnormal joint loading and secondary OSTEOARTHRITIS; treat by corrective OSTEOTOMY. In a CHILD, ANGULATION remodels remarkably well (especially near a growing physis and in the plane of joint movement) — but ROTATION NEVER REMODELS.

THE THREE PRINCIPLES — AND WHY THE THIRD IS THE ONE FORGOTTEN

The management of any fracture rests on three principles, best stated as REDUCE — HOLD — REHABILITATE. The first two receive all the attention; the third determines the result. A fracture that has healed perfectly in a limb that is stiff, wasted and painful is a FAILURE. The purpose of treatment is not a beautiful radiograph but a functioning limb — and function is lost to the complications of immobility (joint stiffness, muscle atrophy, adhesions, osteopenia, complex regional pain syndrome) far more often than to the fracture itself. Hence: rehabilitation begins on DAY ONE, not when the cast comes off — with elevation, active movement of every joint that is not immobilised, isometric exercises within the cast, and early functional use.

REDUCTION

Reduction restores alignment (length, angulation, rotation) — and, in an ARTICULAR fracture, the anatomy of the joint surface, which must be restored ANATOMICALLY, since any step or gap in the cartilage will cause post-traumatic osteoarthritis. In a diaphyseal fracture, by contrast, perfect anatomical reduction is unnecessary — restoring LENGTH, AXIS and ROTATION is sufficient, and callus will do the rest. Reduction may be CLOSED (by traction and manipulation — reversing the mechanism of injury; requiring adequate analgesia or anaesthesia and muscle relaxation) or OPEN (indicated when closed reduction fails or cannot be held, when there is soft-tissue interposition, for displaced ARTICULAR fractures, for avulsion fractures where the muscle pulls the fragment away, and when there is an associated vascular injury — remembered as 'NO CAST': Non-union, Open fracture, Compromised neurovascular status, Articular, intra-articular Salter-Harris III/IV, Trauma — polytrauma).

HOLDING THE REDUCTION

The reduction must be maintained until union — and the method chosen must match the fracture and the biology one is aiming for. NON-OPERATIVE: a plaster cast or functional brace (cheap, non-invasive; but the joints above and below are immobilised, causing stiffness; and there is a risk of compartment syndrome and pressure sores — hence the rule that a limb in a fresh cast is watched, and a painful cast is SPLIT); TRACTION (skin or skeletal — now used chiefly as a temporary measure, or where surgery is unavailable). OPERATIVE: INTRAMEDULLARY NAILING (a load-SHARING device; ideal for diaphyseal fractures of the femur and tibia; preserves the periosteal blood supply; allows early weight-bearing; gives RELATIVE stability and heals by callus); PLATE AND SCREWS (a load-BEARING device; gives ABSOLUTE stability with compression — the choice for articular fractures and the forearm, where anatomical restoration is essential); EXTERNAL FIXATION (for open fractures, gross contamination, damage control in polytrauma, and infected non-unions); and K-WIRES (for small fragments and paediatric fractures).

DAMAGE CONTROL ORTHOPAEDICS

A concept of great importance in the multiply-injured patient is understanding why definitive fixation of every fracture at the first operation may KILL a patient who could have survived. A severely injured patient has already sustained a large inflammatory insult ('the first hit'). A long, bloody, definitive operation constitutes a 'SECOND HIT' — which can tip them into a systemic inflammatory response, ARDS and multi-organ failure. Hence DAMAGE CONTROL ORTHOPAEDICS: in the physiologically unstable patient, perform only the minimum needed to control haemorrhage and stabilise the skeleton — typically rapid EXTERNAL FIXATION — then resuscitate in intensive care, and return for definitive fixation days later once the patient is physiologically restored. Conversely, the stable patient benefits from early total care.

• The three principles: REDUCE — HOLD — REHABILITATE. The purpose is a FUNCTIONING LIMB, not a beautiful X-ray. Rehabilitation begins on DAY ONE (elevation, active movement of all free joints, isometric exercises) — stiffness and wasting cause more disability than the fracture.
• REDUCTION restores length, axis and rotation. ARTICULAR fractures need ANATOMICAL reduction (any step causes post-traumatic OA); DIAPHYSEAL fractures need only length, axis and rotation. Indications for OPEN reduction — 'NO CAST': Non-union, Open fracture, Compromised neurovascular status, Articular (and Salter-Harris III/IV), Soft-tissue interposition, polyTrauma; also failed closed reduction and avulsion fractures.
• HOLD: CAST/brace (cheap, but causes stiffness; risk of compartment syndrome — SPLIT a painful cast); TRACTION (temporary); INTRAMEDULLARY NAIL (load-SHARING; diaphyseal femur/tibia; relative stability → callus; early weight-bearing); PLATE (load-BEARING; ABSOLUTE stability; for ARTICULAR fractures and the forearm); EXTERNAL FIXATOR (open fractures, contamination, damage control, infected non-union); K-WIRES.
• DAMAGE CONTROL ORTHOPAEDICS: in the physiologically unstable polytrauma patient, do the MINIMUM (rapid EXTERNAL FIXATION) — a long definitive operation is a 'second hit' that can precipitate ARDS and multi-organ failure. Resuscitate, then fix definitively days later. The stable patient benefits from EARLY TOTAL CARE.
• Throughout: ATLS first (life before limb), adequate ANALGESIA, splint before transfer, document the NEUROVASCULAR status BEFORE and AFTER any manipulation, and give thromboprophylaxis.