Vascular Injury With Fracture or Dislocation

Vascular injury with a fracture or dislocation is a limb-threatening trauma problem. The orthopaedic surgeon is often the first clinician to recognise it, because the vessel injury hides behind a dramatic fracture, a reduced dislocation or an apparently normal pulse.

Where it happens. The settings are predictable enough to check for actively:

• Knee dislocation and high-energy tibial plateau fracture, with popliteal artery risk
• Elbow fracture-dislocation or paediatric supracondylar fracture, with brachial artery risk
• Shoulder dislocation or proximal humeral fracture, especially in older patients, with axillary artery risk
• Pelvic, acetabular, femoral and tibial trauma with major haemorrhage or limb ischaemia
• Open fracture, crush, blast or ballistic injury with arterial disruption
• Iatrogenic injury during fixation, arthroplasty, deformity correction or revision surgery

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How fracture-dislocations injure vessels. Vessels are injured by stretch, compression, transection, intimal disruption, thrombosis, spasm or entrapment. A dislocation can tear the artery at the moment of injury, while a fracture spike can lacerate or tent it. Reduction may restore flow, but it can also reveal an intimal injury that later thromboses.

Tethered vessels are vulnerable. By region:

• The popliteal artery is relatively tethered at the adductor hiatus and soleus arch, so knee dislocation and plateau fracture patterns can stretch or disrupt it
• The brachial artery crosses the elbow anteriorly and is vulnerable in supracondylar fracture, elbow dislocation and distal humerus trauma
• The axillary artery is at risk in shoulder dislocation, proximal humeral fracture and traction injuries around the shoulder girdle
• The femoral and iliac vessels are at risk in pelvic, acetabular and proximal femoral trauma, especially when haemorrhage is the dominant problem

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Why a pulse can mislead. Palpable pulses may persist through collateral flow, a partial injury, resolving vasospasm, or an intimal flap that has not yet thrombosed. A normal pulse is reassuring only when it fits with a normal examination, a normal ABI/API and a low-risk mechanism.

The mechanism shifts both the probability of vascular injury and the kind of lesion to expect, and each has its own orthopaedic implication.

Classify vascular injury in terms that change treatment: by the clinical signs, by the arterial lesion and by the orthopaedic context.

The obvious case. A bleeding or pulseless limb after a major fracture or dislocation: active external bleeding or a rapidly expanding haematoma, a cold, pale or mottled distal limb, absent or asymmetric pulses, an absent Doppler signal, and severe pain, paraesthesia or motor weakness, in the setting of a major fracture-dislocation, an open wound or a crush mechanism.

The subtle case is the dangerous one. Examples include:

• A knee dislocation that has reduced before arrival
• A tibial plateau fracture with symmetric pulses but a high-risk mechanism
• A shoulder dislocation in an older patient with a small pulse difference
• An elbow fracture with a pink hand but an abnormal Doppler or a neurological deficit
• A ballistic wound near a major vessel with no hard signs
• Delayed thrombosis after an initially normal examination

Delayed presentation. A missed injury can surface later as increasing pain or swelling, a pseudoaneurysm, an arteriovenous fistula, delayed thrombosis or compartment syndrome. It can also present as claudication or reduced exercise tolerance, or as wound breakdown or failed fracture healing from poor perfusion.

Examine repeatedly, and time it. Document the findings before reduction, after reduction, after splinting or fixation, after vascular repair and during postoperative observation.

Look. Record the colour, temperature and capillary refill of the limb, any deformity or dislocation, an open wound or active bleeding, and an expanding haematoma. Look at the skin for tension, blistering or threatened areas, at the muscle for swelling and compartment tension, and at the whole patient for polytrauma or shock.

Feel. Palpate the radial, ulnar, brachial, dorsalis pedis and posterior tibial pulses as relevant, and compare both limbs. Palpate a haematoma gently so as not to provoke bleeding, and feel for a temperature gradient from proximal to distal. Assess compartment firmness, but do not rely on firmness alone.

Move, and the nerves. Document motor function by named nerves and sensation by territory, and look for deterioration after reduction or revascularisation. Remember that a neurological deficit can be vascular, nerve, compartment or fracture-related.

Not every cold or painful limb has the same cause, and the clues below tell them apart.

Algorithm

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Management turns on physiology, perfusion, fracture stability, time since ischaemia and team availability. An unstable patient (shock, uncontrolled haemorrhage, multiple trauma or a threatened airway) needs the primary survey, haemorrhage control and damage-control decision-making. An ischaemic limb (cold, pale, pulseless and painful, with an absent Doppler or motor or sensory deterioration) needs urgent vascular involvement and a reperfusion pathway, and a gross knee, ankle, elbow or shoulder deformity with threatened perfusion is reduced urgently, with neurovascular status documented before and after.

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The vein is a decision too. The artery gets the attention, but a concomitant major venous injury is a genuine decision point and a frequent omission. A divided major outflow vein (popliteal, femoral) causes venous hypertension and limb oedema, which worsens compartment syndrome and can compromise the arterial repair, because poor outflow promotes arterial thrombosis.

Repair or ligate. In the stable patient with a salvageable limb, repair a major vein by lateral suture or interposition graft; this reduces oedema and compartment risk and supports arterial patency, particularly for the popliteal vein. In the unstable or polytrauma patient, or with a difficult exposure, ligating even a major vein is a legitimate life-saving damage-control shortcut. Expect marked limb swelling: ligation mandates fasciotomy, with leg elevation and compression afterwards. Small, expendable veins are simply ligated.

Which first. When both are injured, many surgeons restore arterial inflow first, by shunt or repair, to limit ischaemia, and then address the vein.

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Each region has its own vessel at risk and its own checks, and these are the patterns to look for actively.

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When it happens. Compartment syndrome can occur before repair, after reduction, after vascular repair, after shunting or during resuscitation, and it can occur despite restored pulses.

Do not wait for late findings. Paralysis, pulselessness and pallor are late, and should not be the trigger for fasciotomy. The early pattern that matters is escalating pain, pain on passive stretch, an increasing analgesic requirement, paraesthesia and tense compartments.

Part of the operation. When the risk is high, fasciotomy belongs to the vascular-injury operation rather than following it as an afterthought. The indications include:

• Established compartment syndrome
• Prolonged ischaemia
• Reperfusion after arterial repair
• Combined arterial and venous injury
• High-energy fracture, crush or open injury
• Tense compartments or an unreliable examination
• Need for major resuscitation

Prophylactic fasciotomy. It is considered when the risk of missing compartment syndrome is higher than the morbidity of fasciotomy. This is common after prolonged ischaemia, reperfusion, combined fracture and vascular injury, crush injury or an unreliable examination.

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Documentation. Record, with times:

• Time of injury and estimated ischaemia duration
• Time of reduction, shunt and repair
• Pulse, Doppler and ABI/API findings
• Compartment findings and analgesic requirement
• The reason for fasciotomy, or the reason for observation

The warm-ischaemia clock. Restoring flow to a long-ischaemic limb is not purely good news: the systemic reperfusion load can be lethal. Skeletal muscle tolerates roughly six hours of warm ischaemia before irreversible necrosis, and beyond this, reperfusion washes the products of dead muscle into the circulation.

Reperfusion syndrome. Historically the "myonephropathic-metabolic syndrome": the sudden release of potassium, myoglobin, hydrogen ions and lactate causes hyperkalaemia (arrhythmia or arrest), myoglobinuric acute kidney injury and metabolic acidosis. The hit can come the moment the clamp or shunt is released.

Anticipate it. Warn anaesthesia before reperfusion. Give aggressive IV fluids, monitor and treat hyperkalaemia, monitor creatine kinase and renal function, and maintain a brisk urine output, with consideration of urinary alkalinisation. Correct acidosis, and perform fasciotomy to relieve the muscle oedema.

The complications to anticipate, with why each occurs and how to prevent or answer it.

Active surveillance. Postoperative care is active surveillance rather than routine observation. Monitor:

• Neurovascular status, hourly or by protocol initially
• The Doppler signal, documented
• Compartments and analgesic requirement
• Wounds and fasciotomy dressings
• The graft or repair, according to the vascular plan
• Renal and metabolic function after crush or reperfusion

Immobilisation and fixation. External fixator pin sites must not compromise vascular access or planned flaps, and splints should not compress the repair or the compartments. The timing of definitive fixation depends on physiology, perfusion, soft tissues and infection risk, and the location of the vascular graft affects the surgical approach and reoperation planning.

Rehabilitation. Recovery depends on nerve, muscle, bone and soft tissue, and a perfused limb may still be weak, painful or functionally limited. The early goals are protection of the repair, oedema control, joint motion where safe, wound care and realistic patient counselling.

Outcome depends less on the vessel alone than on the whole limb. The prognostic factors are:

• Warm ischaemia time
• Blunt versus penetrating mechanism
• Popliteal or multi-level tibial vessel injury
• Associated fracture-dislocation or open fracture
• Nerve injury
• Muscle viability
• Need for fasciotomy
• Infection and soft-tissue cover
• Patient physiology and rehabilitation capacity

Extremity vascular injury complicates roughly 1 to 3 percent of major limb trauma in civilian series, rising sharply in penetrating and military cohorts. The popliteal and superficial femoral arteries dominate lower-limb injury, and the brachial artery dominates the upper limb. Outcomes are driven less by the artery and more by ischaemia time, mechanism (blunt worse than penetrating) and associated musculoskeletal and nerve injury.

Side-by-side guidance

Registry and large-cohort data (multicentre civilian shunt series and the PROOVIT vascular-injury registry) consistently show that severely injured shunted limbs achieve salvage rates comparable to or better than non-shunted limbs despite greater injury severity, and that blunt mechanism, popliteal location and pulseless presentation predict eventual amputation.

High- versus limited-resource practice

In high-resource trauma networks, definitive CTA, vascular surgery, interventional radiology, intensive care and orthoplastic reconstruction are available in one centre, allowing single-stage vessel-and-bone management. In limited-resource or pre-transfer settings, the priorities are haemorrhage control, reduction of limb-threatening dislocations, documented serial neurovascular checks, early senior consultation and transfer planning. A temporary intravascular shunt plus a spanning external fixator is a powerful damage-control combination that restores perfusion and stabilises the skeleton while definitive vascular and orthopaedic reconstruction is arranged or the patient is transferred.

Several questions in this field have no single right answer and are common viva ground.

• PubMed: EAST lower-extremity arterial trauma guideline
• PubMed: CTA effectively evaluates extremity vascular trauma
• PubMed: imaging vascular trauma systematic review
• PubMed: physical examination and occult arterial injury follow-up
• PubMed: ABI and ultrasonography systematic review
• PubMed: temporary shunts systematic review
• PubMed: combined orthopaedic and vascular trauma shunting
• PubMed: civilian lower-extremity arterial trauma outcomes