1. Resuscitation and management of life-threatening injuries must take priority over any extremity problems.
2. Haemorrhage from the extremities must be controlled by direct pressure or tourniquet.
3. Use hard signs (lack of palpable pulses, continued blood loss, or expanding haematoma) to diagnose vascular injury. Do not rely on capillary return or Doppler signal to exclude vascular injury. The pink pulseless limb must be assumed to have an arterial injury until proven otherwise.
4. Devascularised limbs are a clinical emergency. If following fracture and joint reduction the limb remains devascularised, immediate surgical exploration is essential.
5. Revascularisation must take place as soon as possible and definitely within 3–4 hours as both muscle and neural tissue are especially susceptible to hypoxia.
6. Preoperative angiography is not necessary and wastes valuable time. The site of vascular injury can usually be ascertained from the mechanism of injury, fracture location and configuration, and by clinical examination. In a patient with multi-level trauma to the same limb or polytrauma who is undergoing a computed tomography (CT) scan, CT angiography may be helpful.
7. The use of vascular shunts revascularises the limb rapidly, minimising ischaemia time. Systemic anticoagulation is not necessary.
8. Once circulation is restored and an adequate reperfusion interval observed, re-evaluate the potential for limb salvage.
9. If salvage is deemed appropriate, perform skeletal fixation followed by definitive vascular repair followed by definitive soft tissue cover as required.
10. Access incisions for vascular repair must take into account the potential need for compartment decompression and definitive skeletal and soft tissue reconstruction.
12. In patients with a single patent artery (usually posterior tibial) free flaps can be anastomosed end to side if required for soft tissue reconstruction.
Open extremity fractures occur in an environment of high energy transfer. Consequently, systemic injuries should be suspected in all cases and emergency management approached in accordance with advanced trauma life support (ATLS) principles, recognising the primacy of airway management and cervical spine stabilisation, oxygenation and ventilation, and fluid resuscitation. Rarely, an open extremity fracture is associated with major haemorrhage. Importantly, control of catastrophic haemorrhage is now addressed at the first stage of the primary survey together with airway management and cervical spine stabilisation, CABCDE (Circulation (exsanguinating haemorrhage), Airway, Breathing, Circulation, Disability, Exposure). Major haemorrhage control may be achieved by applying direct pressure to the source of major bleeding, thereby maintaining such tissue perfusion as exists. In the field, the use of a tourniquet may save lives (1). If used, the time applied must be noted or written on the tourniquet to avoid unnecessarily prolonged ischaemia in the event of successful retrieval. Blind clamping of an actively bleeding vessel is potentially detrimental to vascular tissue and accompanying nerves and should be avoided (2).
Whether accompanied by major haemorrhage or not, a devascularised limb associated with an open fracture, designated ‘IIIC’ by the amended Gustilo–Anderson classification (3), is a clinical emergency requiring prompt recognition and treatment. Recognition is based on hard clinical signs, including lack of palpable pulses, continued bleeding, or an expanding haematoma (4). If possible, the quality of the pulses should be compared to the uninjured contralateral limb. Fractures or joint dislocations should be reduced as this may restore distal circulation. Pulses may be weak if the patient is hypovolaemic and this should be corrected. Assessment of pulses should not rely on the use of Doppler ultrasound and the ankle-brachial pressure index (ABPI) is associated with a substantial false negative rate (4) and inter-observer variability (5). Capillary refill time is a poor indicator of vascular compromise as pooling of blood in the limb may give the impression of slow capillary return.
The common injury patterns associated with loss of distal perfusion are:
1. Fracture of the femur with an associated wedge-shaped or butterfly fragment at a level close to Hunter’s canal where the superficial femoral artery comes closest to the posteromedial surface of the femur. These are often closed injuries.
2. Fracture dislocations of the knee.
3. Fracture dislocations of the ankle. The distal pulses often return following reduction of the dislocation and skeletal realignment.
4. Injury to all three vessels distal to the trifurcation. This vascular injury pattern is associated with severe soft tissue and bony injury; there is often non-viable muscle in multiple compartments and segmental bone loss. This patient group may be best served by expeditious amputation (Chapter 12).
There are no randomised controlled trials linking diagnostic strategy with patient outcomes (4). Rather, the published data report the relative sensitivities and specificities of the various diagnostic strategies (CT angiography, Doppler ABPI <0.90) and clinical examination to a control (usually invasive angiography). In this instance sensitivity is more important than specificity as the consequences of a false negative are likely to be more severe than those of a false positive (unnecessary intervention). Whilst CT angiography exhibited 100% sensitivity and specificity, an error of interpretation was noted in two cases. Importantly, the time required for an additional visit to the CT suite for angiography was considered to add an unacceptable delay. However, many patients with open fractures will have an early trauma CT scan and National Institute for Health and Care Excellence (NICE) guidelines suggest this should include a whole-body scanogram. This allows both the need for directed angiography and fracture imaging to be assessed and then images acquired at that first visit in a time-efficient manner. Whilst direct evidence is absent, indirect evidence favours reliance on hard signs (lack of pulses, expanding haematoma, continued bleeding) for making a prompt clinical diagnosis and avoiding time-consuming diagnostic tests that may alter the balance of ischaemic time on outcomes (4). All centres receiving these patients should have protocols in place for emergency referral for vascular assessment and reconstruction in collaboration with the orthopaedic team. Nevertheless, some injuries will not be salvageable. Where the patient is unconscious and a primary amputation must be performed in order to preserve life, the decision should be made by two consultants (2). One of the most difficult dilemmas is preparing an acutely injured conscious patient for the possibility of amputation. Patients must be made aware, as sensitively but unequivocally as possible, and consent obtained at primary exploration if necessary. If surgical exploration reveals the limb to be unsalvageable, the patient can be scheduled for delayed primary amputation following appropriate counselling and consent (4). The delayed primary amputation should be performed within 72 hours of injury and the decision to proceed down this route should be based on multidisciplinary assessment involving an orthopaedic surgeon, plastic surgeon, vascular specialist, rehabilitation specialist, the patient, and their family members or carers (4).
Physiological and preclinical studies reveal that muscle damage is present at 3 hours ischaemia time and is near complete, and irreversible, at 6 hours (6). The experimental data are corroborated by clinical series. In a series of 17 patients, all those with an ischaemic time of greater than 6 hours required amputation eventually whilst all limbs with an ischaemic time of less than 5 hours were salvaged (7). A meta-analysis of over 100 fractures with vascular injuries found that there was steep fall in limb salvage rate if the ischaemia time extended beyond 4 hours (8).
Popularised in 1971 (9), vascular shunts are used to establish flow to the devascularised limb prior to staged orthopaedic and vascular reconstruction (8, 9, 10, 11). The surgical sequence of shunt rescue of the devascularised limb includes establishing proximal and distal control, intravascular lavage using heparinised saline (with Fogarty balloon catheterisation to re-establish flow if necessary), and the insertion of a shunt of a similar diameter to the traumatised vessel for a distance of 15–20 mm, which is then secured (12). Shunting has been shown to reduce complications, repeat operations, amputation rate, and duration of inpatient stay in a cohort of patients with blunt popliteal artery injuries and distal ischaemia (7). Shunting improves limb salvage where a major vascular injury is associated with high energy fractures (13,14). Shunting is well tolerated for vascular trauma in combat, avoiding the need for definitive revascularisation in austere environments (15). As well as revascularising the distal extremity, shunts minimise ongoing blood loss, combating the lethal triad of acidosis, coagulopathy, and hypothermia in the injured patient (11,12).
To avoid complicating the subsequent reconstruction of an associated open fracture, access incisions to enable shunting should be planned with the reconstruction in mind and preferably with the reconstructive surgeon present. Injuries to the popliteal vessels are best accessed via a curvilinear incision in the popliteal fossa that provides direct access above and below the site of vascular injury (16).
After shunting, the patient is stabilised and the limb is assessed with a view to salvage. Following skeletal stabilisation definitive vascular repair can be performed expeditiously using a reversed vein graft (17). Forearm veins are often superior to the saphenous vein as they can be harvested by a second team, tend to be the appropriate diameter, and are not as muscular as the saphenous and, hence, are less prone to spasm. The revascularised limb is at high risk of developing compartment syndrome and there should be a low threshold for decompression of all four compartments of the leg (Chapter 11).
Proximal venous injuries, including the femoral and popliteal, should be repaired at the same time as the arterial injuries. Whilst the collateral venous system may suffice in the short term, over time the poor venous return leads to the development of post-phlebitic changes (18). Proximal venous repairs are associated with high patency rates, with only venous repairs distal to the popliteal vein suffering from early thrombosis (18).
A high index of suspicion for associated nerve injury is essential, especially in an unconscious patient. When a sharp nerve transection is encountered it should be ideally repaired at the same operation to avoid subsequent surgical exploration in the vicinity of the vascular repair and the accompanying scar tissue surrounding it (19). For larger nerves, knowledge of nerve topography and intraoperative fascicle stimulation are helpful to achieve anatomical approximation. If the nerve is sharply transected but with segmental loss, a interposition nerve graft is necessary (19). If, as is commonly the case, the nerve has suffered blunt trauma and/or when a primary repair is not possible, any directly observed or clinically inferred nerve injury must be documented along with any anatomic details that might facilitate safe delayed exploration and repair. A period of observation supplemented with nerve conduction studies and electromyography may be necessary to evaluate recovery when considering delayed exploration (19).
Both muscle and nerve are highly sensitive to hypoxia, with histological evidence of tissue necrosis and reperfusion injury with 4 hours of warm ischaemia (6, 20, 21, 22). If the extremity was crushed, ischaemic effects may occur more quickly (23). Initially, muscle and nerve meet the ischaemic challenge by anaerobic respiration, incurring an oxygen debt. When saturated, this compromises membrane integrity and cellular homeostasis, which results in endothelial oedema leading to microcirculatory collapse and the ‘no-reflow’ phenomenon (6). Following restoration of microcirculatory flow, cell membrane peroxidation by superoxide free radicals results in the ischaemia–reperfusion injury, producing a systemic inflammatory response that may be life-threatening (24, 25, 26). Hence, surgeons must work closely with their anaesthetist colleagues to mitigate the adverse physiological consequences of delayed limb reperfusion.
The prevalence of an occult vascular injury in lower extremity trauma is high, with one study noting that a third of injuries classified as Gustilo–Anderson grade IIIB had only one patent artery distal to the trifurcation (27). When planning soft tissue reconstruction, preoperative CT angiography may be useful, although this should be used with caution as it does not yield information about flow rate within the vessel or the status of the venae commitans. A review of patients with open fractures necessitating free flap coverage found that functional outcomes were significantly worse in the group with vascular injury compared with those with normal vasculature on angiography (28). A prospective randomised trial showed that repair of an occult vascular injury led to faster fracture union and lower infection rate (27). If the posterior tibial artery is injured, reconstruction should be considered. There is no contraindication to using a single patent artery as a recipient for end-to-side anastomosis for free tissue transfer with planning for a vascular reconstruction in place in case there are problems with the end-to-side anastomosis.
A systematic review and meta-analysis of the factors predictive of secondary amputation following lower extremity vascular trauma found that among a total of 3187 vascular repairs, an associated major soft tissue injury (OR 5.80), compartment syndrome (OR 5.11), multiple vessel trauma (OR 4.85), ischaemia exceeding 6 hours (OR 4.40), or an associated fracture (OR 4.30) were the factors most predictive of secondary amputation (29). A study of the United States National Trauma Databank revealed that of 1395 popliteal artery injuries, independent predictors of amputation included an associated fracture (OR 2.40), major soft tissue injury (OR 1.90), or nerve injury (OR 1.70) (30). In the largest individual study included in the meta-analysis (550 patients with 641 lower limb arterial injuries), failed attempted revascularisation (a factor not evaluated by the aforementioned studies) was found to be the single largest predictor of secondary amputation (OR 16.70) (31). In a retrospective analysis of 58 patients with severe open tibial fractures requiring free tissue transfer, long-term limb function, assessed using the Enneking score, was significantly worse in the cohort of 18 with radiological evidence of a preoperative vascular injury (28). Correspondingly, a randomised controlled trial of 157 Gustilo–Anderson IIIA and IIIB fractures of the tibial shaft reported that repairing occult vascular injury reduced chronic swelling and atrophic skin changes, and improved power and range of movement of the ankle (27).
The devascularised limb is a clinical emergency and optimal outcomes rely on prompt identification and surgical exploration should adequate fracture reduction not result in restoration of circulation. CT angiography adds unnecessary delay if performed as a stand-alone diagnostic test. Angiography can be usefully be obtained as part of a necessary whole body trauma CT. The site of injury can be deduced usually from the three common fracture or dislocation patterns that produce vascular interruption. Prompt revascularisation is achieved by the use of shunts. Limb viability and suitability for limb salvage can then be assessed prior to skeletal stabilisation and definitive vascular reconstruction. Injuries to major veins at the level of the popliteal fossa or proximally should also be repaired. A low threshold for compartment decompression is advised. In addition to failed revascularisation, concomitant major soft tissue injuries, prolonged ischaemic time, and compartment syndrome are associated with eventual amputation.
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