Overview
The outcome of fracture treatment depends on soft-tissue management. The energy needed to break a bone also injures the adjacent soft tissue, creating a zone of injury around the fracture. Girdlestone compared bone to a plant whose roots are in the soft tissue. Life-saving treatment always comes first, and the surgeon must consider both the local injury and the patient as a whole. (AO)
This guide covers pathophysiology, assessment, compartment syndrome and the main classification systems (Gustilo–Anderson, Tscherne, AO soft-tissue grading). (AO)
Pathophysiology
Determinants of the wound: type of injury and area of contact (blunt, penetrating, crush, ballistic), magnitude and direction of force, body region and the patient's general condition. Wound types include contusion, laceration, abrasion, avulsion, crush injuries, high-velocity and ballistic wounds, and burns. (AO)
Healing phases: inflammation, proliferation and regeneration (remodeling), beginning immediately after injury. Growth factors such as PDGF, TGF, VEGF, IGF and EGF released by platelet activation drive cell migration, proliferation, angiogenesis and matrix formation. TGF-beta appears to play a key role in scar formation. (AO)
Inflammatory phase: vasoconstriction and platelet aggregation, then neutrophils and macrophages remove necrotic tissue and microorganisms. Macrophage phagocytic capacity is limited. If it is overloaded by necrotic tissue, antimicrobial activity falls. Hypoxic and avascular areas are especially threatened by infection and biofilm. This is the pathophysiologic reason for radical surgical debridement of dead tissue. (AO)
Proliferation and repair: fibroblasts and then endothelial cells migrate into the wound, forming granulation tissue and collagen. Fibrosis and scarring follow. (AO)
Secondary injury: the immune response increases leukocyte–endothelial interaction and microvascular permeability, causing transendothelial plasma leak and interstitial edema. Edema can reduce microvascular perfusion of neighboring regions and cause progressive necrosis of muscle or skin that was not directly injured. (AO)
Systemic response: severe injury can cause a systemic inflammatory response (TNF-alpha, IL-1, IL-6, IL-10) leading to SIRS, ARDS, multiple organ dysfunction and sepsis, which is the most common cause of death in these patients. (AO)
Assessment
History
Know when, where and how the injury happened. Prolonged entrapment suggests compartment syndrome. Farm injuries carry high infection risk. Ballistic injuries have a hidden zone of injury due to velocity and cavitation. The magnitude and direction of the force determine the extent of injury and the steps needed in treatment. (AO)
Skin and muscle
Closed fractures hide soft-tissue injury, which is easy to underestimate. Simple abrasions are a breach of the skin barrier and can lead to deep infection.
Closed degloving (closed avulsion): shear force separates skin from the underlying fascia without an external wound. The space fills with serous fluid or hematoma and dermal blood supply is at risk. The dermis is denervated, so a numb, "slippery" area on palpation aids diagnosis. Treatment is early drainage and compressive dressing. In some cases a permanent dressing is left and gradually withdrawn to act as an in situ skin graft, with close monitoring for necrosis. A degloving with a skin tear is an open degloving, and with an associated fracture it is treated as an open fracture. Intradermal collections are at risk of contamination and can be a source of deep infection (the Morel-Lavallée lesion in pelvic and acetabular fractures is an example).
Fracture blisters arise from epidermal separation after significant acute swelling. Clear (sterile) blisters are managed with edema control. Blood-filled blisters indicate deeper tissue damage and potential delay in healing. (AO)
Open fractures: after thorough ED irrigation, cover with a moist sterile dressing and leave it until the operating room. Full assessment is possible only there under sterile conditions. Photographs help communication. Repeated exposure of the wound significantly raises infection rates. Contamination (foreign bodies, dirt) should be assessed: high-velocity gunshot, blast and farm injuries are considered severely contaminated. Skin edges, subcutaneous fat, muscle and fascia are checked for viability and bleeding, so surgical debridement is itself a diagnostic step. (AO)
Vascular status
Document peripheral pulses, temperature and capillary refill against the uninjured side. A palpable pulse or good refill does not guarantee an intact vascular supply. Doppler examination and ankle–brachial index help. When examination or fracture pattern suggests vascular injury, get an urgent vascular surgery opinion. Options are emergency angiography, on-table angiography or direct exposure. (AO)
Neurologic status
Assess repeatedly. In unconscious polytrauma patients, check reflexes and responses to strong stimuli. Confirmed major nerve deficit can be decisive in salvage vs amputation decisions in severe limb injuries. (AO)
Fracture pattern
Radiographs give indirect information on soft-tissue injury: foreign bodies, dirt, trapped gas and soft-tissue density. The fracture pattern reflects force absorbed by bone and equivalent force transmitted to soft tissue. During debridement, inspect fragments and their relationship with the soft-tissue sleeve and blood supply. (AO)
Compartment Syndrome
Definition and sites. Raised pressure in a closed fascial or osteofascial space causes local ischemia, neuromuscular compromise, muscle necrosis, infection and possible amputation. Most common in the lower leg, but also in the forearm, thigh, buttock, hand and foot, at any time in the first days after injury or surgery. (AO)
Pathophysiology. Perfusion is determined by muscle perfusion pressure (diastolic blood pressure minus intramuscular pressure). A difference below 30 mmHg leads to hypoxia and anaerobic metabolism. Hypotensive polytrauma patients are therefore predisposed. The older fixed threshold of 30 mmHg intramuscular pressure has been replaced by this delta-pressure approach (Heppenstall's criterion was within 20 mmHg of diastolic pressure). Untreated compartment syndrome leads to ischemic contracture (Volkmann).
Risk factors. Vascular injuries with ischemia and reperfusion, high-energy trauma, severe crush injury, complex tibial fractures, anticoagulant therapy, thick inflexible fascia in young men, and reperfusion after arterial repair. Prophylactic distal dermatofasciotomy is advised in trauma patients undergoing arterial repair or reconstruction. (AO)
Diagnosis. In an alert patient, it is clinical: persistent ischemic muscle pain out of proportion to the injury and not relieved by expected analgesia, pain on palpation and on passive stretch of the muscles, a tense swollen compartment, and paresthesia or numbness in the nerve distribution. Motor weakness is a late sign. Pulses are usually still palpable. In unconscious patients, unexplained tachycardia or high lactate (after excluding other causes) may be a sign. Analgesics, PCA overuse and nerve injury may mask or alter symptoms. (AO)
Pressure measurement helps when examination is unreliable (head injury, intoxication) and for monitoring. Accuracy depends on calibration, catheter tip position, needle depth and limb position. Anterior and lateral compartments are easy to measure, but deep posterior compartment measurement is unreliable and the tibialis posterior compartment is often underassessed. Methods: infusion, wick, stick (a simple, usually reliable system needing dedicated equipment), and thin-wire transducer-tipped catheters allowing continuous monitoring. If compartment syndrome is suspected it must be actively excluded. If this is not possible, urgent clinical review with a low threshold for decompression is mandatory. (AO)
Management.
Remove all circumferential dressings and elevate the limb to heart level.
Emergency fasciotomy is the treatment. Percutaneous fasciotomy is not indicated in trauma, because intact skin acts as a constricting membrane.
In the leg, release all four compartments, using the Mubarak double-incision technique or the parafibular dermatofasciotomy of Matsen et al. Fibulectomy–fasciotomy is contraindicated in trauma. Release all four compartments even if only one or two have raised pressure. The same principle applies to all upper- and lower-limb sites.
The compartment volume must increase to allow for swelling. A fasciotomy that increases limb diameter by 2 cm gives about a 44% increase in volume and a major pressure drop.
Delayed closure techniques are many, and partial-thickness skin grafts are often needed for tension-free closure. The British Orthopaedic Association BOAST 10 guideline is helpful. (AO)
Classification of Soft-Tissue Injury with Fractures (AO)
Classification should be easily communicated, guide treatment, anticipate problems and allow comparison. All systems have reliability limits. Interobserver reliability for the Gustilo classification was only moderate.
Gustilo–Anderson (open fractures)
Type I: wound under 1 cm, clean, little or no contamination, inside-out perforation by a bone end, simple fracture pattern.
Type II: wound over 1 cm with little contusion of surrounding tissue, no dead muscle, moderate to severe fracture instability.
Type III: extensive soft-tissue damage with or without severe contamination, often with threatened vascularity, a comminuted fracture and marked instability.
IIIA: adequate soft-tissue cover of bone despite extensive laceration or flaps (typically high energy).
IIIB: extensive soft-tissue loss with periosteal stripping and exposed bone. Needs soft-tissue cover and may be highly contaminated.
IIIC: any open fracture with an arterial injury needing repair, regardless of fracture type.
Tscherne
Open fractures: Fr. O 1 (skin pierced from inside, little or no contusion), O 2 (skin laceration with surrounding contusion and moderate contamination, including all direct-trauma open fractures), O 3 (extensive soft-tissue damage, often major vessel and/or nerve injury, ischemia, severe comminution, and including farm injuries, high-velocity gunshot wounds and compartment syndrome), O 4 (subtotal and total amputations).
Closed fractures: Fr. C 0 (indirect trauma, little or no soft-tissue injury), C 1 (superficial abrasion or contusion, simple to moderate fracture), C 2 (deep contaminated abrasions, localized skin or muscle contusion, impending compartment syndrome, transverse or complex fractures), C 3 (extensive skin contusion, muscle destruction or subcutaneous avulsion, compartment syndrome and vascular injuries).
Pigmented skin can make closed soft-tissue assessment more difficult. (AO)
AO soft-tissue grading system
Grades four structures separately, in addition to the AO/OTA fracture code:
Skin: closed (IC 1 to IC 5) or open (IO 1 to IO 5). IC 1 no visible skin lesion; IC 2 contusion without laceration; IC 3 circumscribed degloving; IC 4 extensive closed degloving; IC 5 necrosis from contusion. IO 1 skin breakage from inside out; IO 2 breakage from outside, under 5 cm, contused edges; IO 3 over 5 cm, increased contusion, devitalized edges; IO 4 considerable full-thickness contusion, abrasion, extensive open degloving, skin loss; IO 5 extensive degloving.
Muscle and tendon (MT 1 to MT 5): MT 1 no muscle injury; MT 2 circumscribed muscle damage in a single compartment; MT 3 significant damage in two compartments; MT 4 muscle defect, tendon laceration, extensive muscle contusion; MT 5 compartment syndrome, crush syndrome with a wide zone of injury.
Neurovascular (NV 1 to NV 5): NV 1 none; NV 2 isolated nerve injury; NV 3 localized vascular injury; NV 4 extensive segmental vascular injury; NV 5 combined neurovascular injury, subtotal or total amputation.
Example: a simple closed spiral mid-shaft tibial fracture from skiing is 42-A1.2/IC1-MT1-NV1. An open, complex, segmental tibial fracture with an open wound over 5 cm, muscle defect, tendon tear and peroneal artery injury is 42-C2.3/IO4-MT4-NV3.
Muscle and tendon injury and neurovascular involvement have high prognostic value, and neurovascular involvement always signals the most severe injuries (Gustilo IIIB and IIIC), with a high complication rate. (AO)
Wound care tools such as silver nanocrystalline dressings and negative pressure therapy should be known. The LEAP findings challenged dogma on timing of debridement and primary vs secondary closure, but recommendations must be tempered by local logistics and patient and surgeon profile. (AO)
Complications
Deep infection, delayed bone healing and nonunion when soft-tissue injury is underestimated. (AO)
Compartment syndrome with muscle necrosis, contracture and amputation if missed. (AO)
Progressive skin or muscle necrosis from secondary injury, and infection of unrecognized closed degloving collections. (AO)
References
Bernstein B. Soft-tissue injury: pathophysiology, assessment and classification (Chapter 1.5). In: Buckley RE, Moran CG, Apivatthakakul T, eds. AO Principles of Fracture Management. 3rd ed. Thieme; 2017 (Turkish edition: AO Kırık Tedavisinin Prensipleri).