print

Soft-tissue injury: Pathophysiology, evaluation, and classification

Options
 Introduction
 Pathophysiology and biomechanics
 Pathophysiological responses in healing
 Problems of diagnosis and assessment
 Secondary damage mechanisms
 Compartment syndrome
 Systemic response to soft-tissue injury
 Emergency evaluation of soft-tissue injury
 Classification of soft-tissue injury in fractures
 Bibliography
Introduction

The effective treatment of fractures depends upon good softtissue management. Fractures with a soft-tissue injury must be considered as surgical emergencies. They need a sophisticated management protocol and an excellent grading system to achieve the goal of uncomplicated healing with complete restitution of function.

Open fractures and fractures with severe, closed soft-tissue damage are often associated with polytrauma. Life-saving treatment must always take priority and the surgeon must consider both the local injury and the whole patient. Evaluation of the fracture must determine the extent of the softtissue injury, which will be a key factor in management. The surgeon needs to be familiar with the pathophysiology of a soft-tissue injury and the timing, risks, and benefits of the different treatment options.


Pathophysiology and biomechanics

The condition of the wound after injury is determined by the following factors:

  • type of insult and area of contact (blunt, penetrating, crushed, etc);
  • force applied;
  • direction of force;
  • area(s) of body affected;
  • wound contamination;
  • general physical condition of the patient.

A combination of these factors will produce different types of wounds.


Types of wounds.

Type of forceType of injury
Sharp, pointedStab wound
BluntContusion injury, cut
Extension, twistLaceration
ShearDegloving, wound defect, avulsions, abrasion
Combination of forcesWounds from blows, impaling, bites, and gunshot
CrushingTraumatic amputation, rupture, crush injury
ThermalBurns

 


Wounds do not only differ in their shape, but also in the type of treatment required and the prognosis for healing [1]. All injuries cause bleeding and tissue destruction. This activates humoral and cellular mechanisms to stop bleeding and resist infection. The sequential healing process starts immediately after trauma and can be divided into three phases:

  • exudative or inflammatory phase;
  • proliferative phase;
  • reparative phase.

Pathophysiological responses in healing

Inflammatory phase

In the inflammatory phase, there is a massively increased interaction between leukocytes and the injured microvascular endothelium. Trauma exposes subendothelial collagen structures, leading to the aggregation of thrombocytes. These release serotonin, adrenaline, and thromboxane-A, causing vasoconstriction and producing cytokines such as platelet derived growth factor (PDGF) and transforming growth factor (TGF-β) that have a strong chemotactic and mitogenic effect on macrophages, polymorphonuclear neutrophils, lymphocytes, and fibroblasts. Vasoconstriction and thrombocyte aggregation contribute to the clotting and are an important part of the coagulation process to stop bleeding. As a side effect the damaged tissue is underperfused, leading to hypoxia and acidosis. The first cells to move from the small vessels into the damaged tissue are polymorphonuclear neutrophils (PMN) and macrophages. PMN are mobilized rapidly and produce an extremely vigorous initial response. The main function of the macrophages is the removal of necrotic tissue and microorganisms (phagocytosis and secretion of proteases) and the production and secretion of cytokines (PDGF: mitogenic and chemotactic; TNF-α: proinflammatory and angiogenic; β-FGF, EGF, PDGF, and TGF-β: mitogenic [2]).

Macrophages are responsible for the cytokine-induced early activation of immunocompetent cells, the inhibition and destruction of bacteria, and the removal of cell debris from the damaged tissue. However, the capacity of the macrophages for phagocytosis is limited. If their capacity is overloaded by an excessive amount of necrotic tissue, this will decrease the antimicrobial activities of the mononuclear phagocytes. Since these phagocytic activities are associated with superoxide production and high oxygen consumption, areas of hypoxia and avascular areas are especially threatened by infection. Thus, the pathophysiological rationale for performing radical surgical debridement of dead tissue is to support the phagocytic process of the macrophages [3, 4].

Chemotactic substances, such as kallikrein, improve vascular permeability and exudation by releasing the nanopeptide bradykinin that belongs to the α2-globulin fraction. Prostaglandins, originating from tissue debris, stimulate the release of histamine from mast cells and cause local hyperemia, which is necessary for the metabolic processes of wound healing. In addition, highly reactive oxygen and hydroxyl radicals are released during the peroxidation of membrane lipids [5], which cause a further destabilization of the cell membranes. These mechanisms result in an impairment of capillary endothelial permeability, which again promotes hypoxia and acidosis in the damaged areas. The infiltrating granulocytes and macrophages with their capacity to resist infection and to engulf cell debris and bacteria (physiological wound debridement) play a key role in the inflammatory response of traumatized tissue and therefore have a decisive effect on the subsequent reparative processes [5].


Proliferative and reparative phases

The proliferative phase begins when fibroblasts, followed by endothelial cells, migrate into the area of the wound and proliferate there. This is stimulated by mitogenic growth factors. These cells have a series of growth factor receptors on their surfaces and, by paracrine and autocrine processes, release several cytokines and synthesize the structural proteins of the extracellular matrix (collagen). Fibronectins—proteins detached from the surface of the fibroblasts by hydrolases—facilitate the bonding of type I collagen to α1-chains. This is an important prerequisite for progressive, reparative cell proliferation.

There is a smooth transition to the reparative phase and, simultaneously, the proliferating endothelial cells form ingrowing capillaries, the typical characteristic of granulation tissue. At the end of the reparative phase, water content is reduced and the collagen initially formed is replaced by crosslinked collagen type III. Fibrosis and scarring follow. The role of the growth factors in scar formation remains unclear, but it seems that TGF-β plays a decisive role [6, 7].


Problems of diagnosis and assessment

In open soft-tissue injuries, contamination and infection of the wound have a negative effect on the healing process. In closed injuries, the degree of injury and ischemic tissue may not be apparent and this can make diagnosis and therapeutic decisions difficult [8]. Many modern imaging techniques permit qualitative assessment of closed soft-tissue injuries, but clinically useful quantitative assessment of damage is not yet available. Unfortunately, there are no diagnostic criteria that allow definitive, preoperative differentiation between reversibly (living) and irreversibly (dead) damaged tissue. Thus, clinical experience and good judgment remains essential when selecting options for treatment and prognosis. Drugs that can reduce posttraumatic microvascular dysfunction and restore disturbed microcirculation may be available in the future, and there is some experimental evidence that selective COX-2 inhibitors [9] or N-acetylcysteine may be helpful [10].


Secondary damage mechanisms
Pathophysiology of soft-tissue injury

The immune response to trauma results in a drastic increase in leukocyte-endothelial interaction and subsequent loss of endothelial integrity with increased microvascular permeability.This leads to transendothelial leakage of plasma and interstitial edema [11]. Edema may reduce the microvascular blood supply in adjacent areas and this can result in progressive necrosis of skeletal muscle in marginal areas that were not directly affected by trauma. Thus, secondary tissue loss will occur.


Compartment syndrome

Compartment syndrome is due to raised pressure in a closed fascial or osteofascial space that results in local tissue ischemia. This will compromise neuromuscular function [12–14].

 

Mechanism and local pathology


Compartment syndrome is due to a vicious circle.

In closed fractures with soft-tissue injury, the threat posed by compartment syndrome is not to be underestimated. It is triggered by an increase in intramuscular pressure within a closed osteofascial space, at a level above a critical microvascular perfusion pressure [15]. The cause may be exogenous pressure (eg, restrictive plaster casts) or endogenous, due to an increase in volume within the compartment from hemorrhage, perivascular infusions or edema from abnormal capillary permeability caused by prolonged ischemia or reperfusion. If impairment of the microcirculation from increased tissue pressure persists, severe and irreversible neuromuscular dysfunction due to hypoxia will result and lead to muscle necrosis and axonotmesis.


Originally, it was believed that the threshold for compartment syndrome was a constant intramuscular pressure > 30 mm Hg. However, it is now recognized that the key factor is the difference between the diastolic blood pressure (dBP) and the intramuscular pressure (IMP). This determines the mean muscle perfusion pressure (MPP):

Muscle perfusion
pressure
=Diastolic blood
pressure
-Intramuscular
pressure

If the muscle perfusion pressure is less than 30 mm Hg, there will be hypoxia and anaerobic cell metabolism. It is important to note that blood pressure has a direct relationship to perfusion pressure. Thus, multiply injured patients with hypotension and hypoxia are predisposed to compartment syndrome. Other injuries carrying a high risk of developing compartment syndrome include: vascular injuries with peripheral ischemia, high-energy trauma, severe soft-tissue crush, and comminuted fractures of the tibia [16]. The aim of any therapeutic procedure must be immediate compartment decompression by dermatofasciotomy to achieve reperfusion of the capillary bed.


Clinical manifestation

A compartment is an anatomical space, bounded on all sides by bone or deep fascia, which contains one or more muscle belly. In addition, the surrounding epimysium, the skin, or a constricting dressing can create such an envelope with limiting boundaries. The relative inelasticity of the enveloping wall means that if the muscle tissue swells, the pressure in the osseofascial envelope will increase.

The diagnosis of a compartment syndrome in a conscious patient is usually made by the clinical manifestation of unrelenting ischemic muscle pain that is unrelieved by the expected amounts of analgesia. Any nerve traversing the involved compartment will become ischemic, often causing numbness and tingling in the nerve distribution. Reporting of these symptoms requires an alert, conscious and cooperative patient whose perceptions or response have not been changed by distracting injury, alcohol, or drugs.

Clinical examination will show a tense, swollen compartment; palpation will reproduce the pain and passive stretching of the digital muscles of the involved compartment will also increase the pain. This sign may be helpful, although not very specific. A sensory deficit in the nerve traversing the compartment may or may not be present. Motoric weakness is a late change. Pulses are always palpable in a compartment syndrome, because in a normotensive patient the muscle pressure rarely exceeds the systolic level. Persistent, unexplained tachycardia should also be regarded as a possible sign of compartment syndrome in the unconscious patient once other causes (eg, hypovolemia) have been excluded.


Effects of increasing compartment pressure. The tissue recovers after extensive fasciotomy.

Tissue necrosis will result when interstitial pressure is increased beyond an individual threshold for a long enough period of time. Patients who suffer an untreated or overlooked compartment syndrome will develop ischemic contracture, as described by Volkmann. This results in a contracted, nonfunctional limb. The surgeon must be aware that all limb injuries are at risk of compartment syndrome. It is most common in high-energy fractures and crush injuries but can also be seen after simple injuries and without any associated fracture. Patients on anticoagulant therapy are at high risk and young males have a higher risk of compartment syndrome, possibly because they have relatively thick and inelastic fascia. Compartment syndrome can also develop after reperfusion of an ischemic limb. This is seen in patients who have been unconscious for a number of hours (eg, drug addicts) and also after repair of arterial injuries. Therefore, most trauma patients who have an arterial repair must have prophylactic distal dermatofasciotomies.


Diagnosis

Differential diagnosis includes arterial injury and peripheral nerve injury: Absent pulses indicate arterial injury; peripheral nerve injury is the diagnosis of exclusion. A high amount of suspicion is essential if cases of compartment syndrome are not to be missed. The surgeon must be vigilant as the symptoms and signs may be minimal. Medical and nursing staff must be aware that analgesics can mask the symptoms and this can be a particular problem following surgery when patient controlled analgesia (PCA) is administered. Excessive use of the PCA should alert staff to the possibility of compartment syndrome.

Compartment syndrome can also be diagnosed by tissuepressure measurements. This is extremely helpful in situations where clinical examination is unreliable, such as in head injury or intoxicated patients. The tissue pressure is usually elevated before signs and symptoms develop and so pressure measurements can be used to diagnose an impending compartment syndrome. They can also be used to monitor patients at high risk of developing this complication following surgery. Pressure measurements can be taken by a variety of techniques. The infusion technique is simple and continuous, but may worsen the syndrome and usually has a higher pressure threshold than other methods. The wick technique uses some fine material inside the catheter to maintain the opening to allow continuous monitoring. The stick technique is usually a reliable, simple system to use but the appropriate equipment must be purchased. Over the past few years, fine-wire, intracompartment pressure transducers have become available. These are simple and reliable and allow continuous pressure monitoring in the perioperative period [17].


Management

The initial treatment should include release of all circumferential dressings and elevation of the limb to the level of the heart (to maximize tissue perfusion pressure).

  • Compartment syndrome is a surgical emergency and the treatment of choice is immediate dermatofasciotomy.
  • In trauma, percutaneous fasciotomy is not indicated since the skin, as long as it remains intact, acts as a limiting membrane and may sustain the compartment syndrome.

Compartment syndrome is most common in the lower leg. All four compartments must be released using either Mubarak’s double-incision technique [18] or the parafibular dermatofasciotomy described by Matsen [12]. The fibulectomy- fasciotomy, as popularized in the vascular surgical literature, is contraindicated for trauma patients. Even if the pressure is increased in only one or two compartments, it is mandatory to completely release all. This is true for every possible location of compartment syndrome in the upper or lower extremity.


Clinical pictures after compartment release.

a  Live muscles.

b  Death of all muscles in the compartment.


Systemic response to soft-tissue injury
Systemic effects of soft-tissue injury. PMN = polymorphonuclear neutrophil granulocytes.

Severe soft-tissue injury results in local microvascular and cellular damage and can also lead to a marked systemic inflammatory response due to the release of proinflammatory cytokines (TNF-α, IL-1, IL-6, IL-10). These affect vascular endothelia in various organs, resulting in margination, migration and activation of polymorphonuclear neutrophils, increased capillary permeability, interstitial edema and an inflammatory response. The systemic inflammatory response syndrome (SIRS) results in damage to various organs—multiple organ dysfunction syndrome (MODS). The damage is not only to organs such as the lungs (ARDS), liver, gastrointestinal tract, kidneys, myocardium, and central nervous system, but also affects the entire immune system: Sepsis remains the most common cause of death in these patients [19–21]. Thus, the pathophysiological changes in damaged tissue after soft-tissue trauma are the product of a vicious circle.


Emergency evaluation of soft-tissue injury

Case history

To determine the appropriate choice and timing of treatment, the surgeon needs to know when, where, and how the injury occurred. For instance, prolonged entrapment in a car suggests the possibility of a compartment syndrome, and barnyard accidents have a high risk of infection. Most important of all is the knowledge of the amount and direction of force or energy causing the injury. This determines both the extent of the injury and the necessary steps in treatment. The greater the force, the more serious the damage and sequelae will be.


Vascular status

It is mandatory to determine the vascular status of all injured limbs. The peripheral pulses, temperature and capillary refill must be checked and compared with the uninjured side. Although the absence of a palpable pulse is an important pointer to potential vascular damage, the presence of a pulse or good capillary refill does not necessarily guarantee an intact vascular supply. Doppler examination of the injured and unharmed extremity may be helpful for screening and the ankle-brachial index (ABI) is also useful [22]. In all cases of doubt or where the case history, the physical examination, or the radiographic fracture pattern suggests vascular damage, the opinion of a vascular surgeon must be obtained urgently. Management strategies include urgent angiography in the vascular radiology suite, immediate on-table angiography or direct w of the injured vessel. The method chosen will depend upon local facilities and protocols.


Neurological status

Neurological assessment can be difficult in unconscious patients with multiple injuries. However, examination of the reflexes and the response to strong, painful stimuli give some indication of major deficits. These examinations have to be performed repeatedly because the confirmation of a major nerve deficit can be decisive in the choice between salvage versus amputation in severely injured extremities.


Soft-tissue conditions

Soft-tissue injuries in closed fractures are less obvious than in open fractures, but still have enormous importance. Their evaluation can be much more difficult than open fractures and their severity is easily underestimated. Simple abrasions represent an injury of the physiological skin barrier and can allow the development of deep infection. If this occurs, it is usually more challenging and difficult to manage than a simple perforation of the skin.

In open fractures, the wound is covered by a sterile dressing at the site of the accident and this should not be removed before the patient is in the operating room. Only there, and under sterile conditions, the full extent of the soft-tissue damage is assessed. (Some authors allow one removal for a photograph to facilitate planning.)

The degree of wound contamination is important and influences the course and outcome of the injury. Foreign bodies and dirt particles give useful information about the level of contamination and help the surgeon with grading these injuries. High-velocity shotgun wounds and farming accidents are considered as severely contaminated.

After formal surgical skin preparation, with washout of dirt and debris, the traumatic wound is excised and, if necessary, extended. Gentle manipulation and inspection give best information about the condition of the bone and the extent of softtissue damage. The surgical debridement becomes a diagnostic exercise as skin edges, subcutaneous fat, muscles, and fascial elements are checked for viability and bleeding. The definitive assessment of a soft-tissue injury requires an experienced surgeon because it determines the treatment protocol as well as the choice of implant for fracture fixation.

Compartment syndrome is seen most frequently in the lower leg but can also occur in the forearm, buttock, thigh, hand, and foot. Compartment syndromes may occur at any time during the first few days after trauma or surgery.


Assessment of the fracture

At the time of debridement, careful inspection of bone fragments, their relationship to the soft-tissue envelope and blood supply, as well as the information obtained from x-rays, help to optimize assessment of the damage. The radiographic fracture pattern provides indirect information about the softtissue injury, and can show foreign bodies, dirt, soft-tissue density, or entrapped air around and/or distal to the fracture site.


Management algorithm

The following figure shows a flow chart of considerations and actions required in the management of fractures with concomitant softtissue damage.


Management algorithm for the treatment of fractures with a concomitant soft-tissue injury (modified according to Waydhas and Nast-Kolb).


Classification of soft-tissue injury in fractures

A classification of the soft-tissue injury should consider all essential factors and guide treatment. It effectively decreases complications by preventing avoidable treatment errors and should be of some prognostic value. There is also the possibility to monitor and compare standardized treatment protocols. The most commonly used classifications were devised by Gustilo and Anderson [23, 24] and by Tscherne [25].


Gustilo classification of open fractures

Gustilo and Anderson developed their classification on the basis of a retrospective and prospective analysis of 1,025 open fractures. They initially described three types, but clinical application led Gustilo, Mendoza, and Williams to extend and subdivide the classification of the severe (type III) injuries into subgroups A, B, and C.

  • Type I: These are fractures with a clean wound of less than 1 cm in size with little or no contamination. The wound results from an inside-out perforation by one of the fracture ends. The fracture pattern is simple (eg, spiral or short oblique fractures).
  • Type II: Skin laceration is longer than 1 cm but the surrounding tissues have minor or no signs of contusion. There is no dead muscle present and the fracture instability is moderate to severe.
  • Type III: There is extensive soft-tissue damage, frequently with compromised vascularity with or without severe wound contamination. The fracture pattern is complex with marked fracture instability.

Because of the many different factors occurring in this group, Gustilo proposed three subtypes.

  • Type IIIA: It usually results from an high-energy trauma. There is still adequate soft-tissue coverage of the fractured bone, despite extensive soft-tissue laceration or flaps (similar to AO classification IO 2).
  • Type IIIB: There is extensive soft-tissue loss with periosteal stripping and bone exposure. These injuries are usually associated with massive contamination (similar to AO classification IO 3).
  • Type IIIC: This is associated with any open fracture associated with arterial injury requiring repair. It is independent of the fracture type (similar to AO classification IO 4)

Tscherne classification of open soft-tissue injuries

In Tscherne’s classification, soft-tissue injuries are grouped into four categories according to severity. The fracture is labeled as open or closed by an “O” or a “C”.

  • Open fracture grade I (Fr. O 1): The skin is lacerated by a bone fragment from the inside. There is no or minimal contusion of the skin, and these simple fractures are the result of indirect trauma (type A1 and A2 fractures according to the AO classification).
  • Open fracture grade II (Fr. O 2): There is a skin laceration with a circumferential skin or soft-tissue contusion and moderate contamination. All open fractures resulting from direct trauma (AO classification type A3, type B and type C) are included in this group.
  • Open fracture grade III (Fr. O 3): There is extensive softtissue damage, often with an additional major vessel and/ or nerve injury. Every open fracture that is accompanied by ischemia and severe bone comminution belongs in this group. Farming accidents, high-velocity gunshot wounds, and compartment syndrome are included because of their high risk of infection.
  • Open fracture grade IV (Fr. O 4): These are subtotal and total amputations. Subtotal amputations are defined by the Replantation Committee of the International Society for Reconstructive Surgery as a “separation of all important anatomical structures, especially the major vessels, with total ischemia”. The remaining soft-tissue bridge may not exceed 1/4 of the circumference of the limb.

Cases requiring revascularization can be classified as grade III or IV open.


Tscherne classification of closed fractures

  • Closed fracture grade 0 (Fr. C 0): There is no or minor soft-tissue injury with a simple fracture from indirect trauma. A typical example is the spiral fracture of the tibia in a skiing injury.
  • Closed fracture grade I (Fr. C 1): There is superficial abrasion or skin contusion, simple or medium severe fracture types. A typical injury is the pronation-external rotation fracture dislocation of the ankle joint: The soft-tissue damage occurs through fragment pressure at the medial malleolus.
  • Closed fracture grade II (Fr. C 2): There are deep contaminated abrasions and localized skin or muscle contusions resulting from direct trauma. The imminent compartment syndrome also belongs to this group. The injury results in transverse or complex fracture patterns. A typical example is the segmental fracture of the tibia from a direct blow by a car fender.
  • Closed fracture grade III (Fr. C 3): There is extensive skin contusion, destruction of muscle or subcutaneous tissue avulsion (closed degloving). Manifest compartment syndrome and vascular injuries are included. The fracture types are complex.

Hanover fracture scale

Tscherne developed a soft-tissue classification because he realized that closed injuries were frequently underestimated. From this original classification evolved the much more elaborate Hanover fracture scale.

Many problems in the treatment of complex fractures are due to high-velocity injury patterns causing severe soft-tissue damage. The above mentioned and most frequently used classifications have shown limitations for these types of injuries. Brumback [26] has shown that there is only a moderate interobserver reliability in classifying open fractures using the Gustilo and Anderson classification. For these reasons, Tscherne and Oestern [25] developed the Hanover fracture Scale (HFS) from an analysis of approximately 1,000 open fractures from 1980 to 1989 and this has been further updated and validated [27, 28].


Hanover fracture scale with correlation of the fracture scale score to Tscherne’s classification of open and closed fractures.

 

A Fracture typePoints C Ischemia/compartment syndromePoints
Type A1 No0
Type B2 Incomplete10
Type C4 Complete 
Bone loss     < 4 hours15
   < 2 cm1    4-8 hours20
   > 2 cm2    > 8 hours25
B soft tissuesPoints D NervesPoints
Skin (wound, contusion)  Palmar/plantar sensations 
   No0    Yes0
   < 1/4 circumference1    No8
   1/4-1/22 Finger/toe motion 
   1/2-3/43    Yes0
   > 3/44    No8
Skin defect (loss)  
   No0 E ContaminationPoints
   < 1/4 circumference1 Foreign bodies 
   1/4-1/22    None0
   1/2-3/43    Single1
   > 3/44    Multiple2
Deep soft tissues (muscle, tendon,
ligaments, joint capsule) 
    Massive10
   No0 F Bacteriological smearPoints
   < 1/4 circumference1 Aerobe 1 germ2
   1/4-1/22 Aerobe > 1 germ3
   1/2-3/43 Anaerobe2
   > 3/46 Aerobe/anaerobe4
Amputation  G Onset of treatmentPoints
   No0 (Only if soft-tissue score > 2) 
   Subtotal/total guillotine20 6-12 hours1
   Subtotal/total crush30 > 12 hours3
     
     
ClassificationTotal A-B ClassificationTotal C-G
Fr. O 12-3 points Fr. C 01-3 points
Fr. O 24-19 points Fr. C 14-6 points
Fr. O 320-69 points Fr. C 27-12 points
Fr. O 4> 70 points Fr. C 3> 12 points

The scale considers every detail of the injury to the involved extremity and forms a checklist. The fracture type (according to the Müller AO Classification), skin condition, underlying soft tissues, vascularity, neurological status, level of contamination, presence or absence of compartment syndrome, time interval between injury and treatment, and the overall severity of the injury are summed to provide the total score. Bone loss represents bone fragments that have been lost at the site of the accident. The longest axis of the missing piece of bone is measured and graded either as smaller or greater than 2 cm.

For the evaluation of soft tissues, the score provides three different categories:

  • size of the skin wound;
  • area of skin loss;
  • damage to deep soft tissues such as muscles and tendons.

Due to different diameters and thickness at different levels in the involved extremity, the extent of soft-tissue damage is related to the volume of the soft-tissue envelope. The three different categories of soft-tissue damage allow evaluation of both superficial and deep injury. The category Amputation evaluates the mechanism of injury and the possibility of replantation. An exact evaluation of the neurological status is often difficult at the time of admission but monitoring of reflexes allows a gross estimation of possible neurological damage. This can be important in the process of deciding for or against limb salvage. At the time of admission, a bacteriological evaluation may not yet be available. However, bacterial contamination is still a part of the score to remind the treating surgeons to take it into account. The overall score guides general patient management and local treatment. Some of the category scores (eg, bone score or soft-tissue score) are valuable for treatment decisions and estimation of possible complications [29].


The AO soft-tissue grading system

Because of the limitations of the existing classification systems, including moderate interobserver reliability and the grading of many different injuries into the same subgroup, AO developed a more detailed and precise grading system for fractures with soft-tissue damage. This grading system identifies injuries to the different anatomical structures and assigns them to different severity groups. The skin (integument), muscles and tendons, and the neurovascular system are the targeted anatomical structures; the fracture is classified according to the AO classification of fractures. The grading of the skin lesion is done separately for open or closed fractures: The letters “O” and “C” designate these two categories. Each is divided into 5 severity groups. Thus, IC 1 represents the injury of the integument in a closed fracture. The digit “1” indicates the least severe injury. IC 5 has the most severe soft-tissue damage.


AO soft-tissue classification: closed skin lesions (IC).
IC 1No skin lesion
IC 2No skin laceration, but contusion
IC 3Circumscribed degloving
IC 4Extensive, closed degloving
IC5Necrosis from contusion
  
AO soft-tissue classification: open skin lesions (IO).
IO 1Skin breakage from inside out
IO 2Skin breakage from outside in < 5 cm, contused edges
IO 3Skin breakage from outside in > 5 cm, increased contusion, devitalized edges
IO 4Considerable, full-thickness contusion, abrasion, extensive open degloving, skin loss
IO5Extensive degloving

AO soft-tissue classification: no skin lesion (IC 1).


 

 


AO soft-tissue classification: no skin laceration, but contusion (IC 2).


 

 


AO soft-tissue classification: circumscribed degloving (IC 3).


 

 


AO soft-tissue classification: extensive, closed degloving (IC 4).


 

 


AO soft-tissue classification: necrosis from contusion (IC 5).


 

 


AO soft-tissue classification: skin breakage from inside out (IO 1).


 

 


AO soft-tissue classification: skin breakage from outside in < 5 cm, contused edges (IO 2).


 

 


AO soft-tissue classification: skin breakage from outside in > 5 cm, increased contusion, devitalized edges (IO 3).


 

 


AO soft-tissue classification: considerable, full-thickness contusion, abrasion, extensive open degloving, skin loss (IO 4).


 

 


AO soft-tissue classification: extensive degloving (IO 5).


 

Although there may be considerable damage to a muscle envelope, there is rarely an injury to tendons except in severe injuries (Tab 1.6-5). The involvement of the neurovascular system (Tab 1.6-6) always indicates a most severe injury of the kind represented by the Gustilo types IIIB and IIIC and has a high complication rate. Muscle and tendon injuries as well as neurovascular injuries are of high prognostic value for the fate of the extremity.


AO soft-tissue classification: muscle and tendon lesions (MT).


AO soft-tissue classification: nerve and vessel lesions (NV).


This system allows a comprehensive description of the entire injury complex. The numbers and letters are useful for computerization, audit, and research. In everyday clinical practice it is the use of accurately defined, descriptive terms that aid good decision making and communication. For example, a simple, closed spiral tibial midshaft fracture from skiing with no injury of skin, muscles, tendons, nerves, or vessels is graded: 42-A1.2/IC1-MT1-NV1.

In contrast, the previous figures in the section "IO 5 extensive degloving" show a Monteggia type elbow dislocation fracture with extensive muscle and tendon injury but no neurovascular damage. This will be graded as 22-B1/IO5- MT4-NV1. The figures in section "IO 4 considerable, full-thickness contusion, abrasion, extensive open degloving, skin loss" illustrate an open, complex, segmental tibial shaft fracture with an open wound greater than 5 cm, muscle defect, and tendon laceration. There is no nerve injury but an injury of the peroneal artery. This injury will be graded as 42-C2.3/IO4-MT4-NV3.


Usage of classification systems

Higher grades of the Gustilo classification of open fractures and of the Tscherne classification of closed fractures are most challenging from the therapeutic point of view. These injuries have the highest complication rates and can cause severe disability of the patient. We should keep in mind that classification systems have several objectives, namely to

  • facilitate communication;
  • assist decision making;
  • identify treatment options;
  • anticipate problems;
  • suggest treatment method;
  • predict the outcome;
  • enable comparison with similar cases;
  • assist documentation and audit.

Conclusion

The effective treatment of fractures depends upon good management of the soft tissues. The surgeon must carefully evaluate the injury by systematically examining each structure that could be damaged: the skin, subcutaneous tissue, muscle and tendons, nerves, vessels, and bones. The possibility of compartment syndrome should always be considered and it must be recognized that closed injuries may be associated with as much soft-tissue damage as open injuries. Careful evaluation will allow the surgeon to classify the fracture using one of the comprehensive grading systems such as the AO system or the Hanover fracture scale. This will guide decision making, allow clear communication, and give an indication of potential complications and outcome.


Bibliography

[1] Levin SL (1995) Personality of soft tissue injury. Techniques Orthop; 10:65–73.

[2] Steenfos HH (1994) Growth factors and wound healing. Scand J Plast Reconstr Surg Hand Surg; 28(4):95–105.

[3] Dorow C, Markgraf E (1997) [Therapy of soft tissue injuries— biological strategies]. Zentralbl Chir; 122(11):962–969.

[4] LeVan TAL, Levin SL (1995) Principles of soft tissue handling. Techniques Orthop; 10: 94–104.

[5] van der Vusse GJ, van Bilsen M, Reneman RS (1994) Ischemia and reperfusion induced alterations in membrane phospholipids: an overview. Ann N Y Acad Sci; 723:1–14.

[6] Schmid P, Itin P, Cherry G, et al (1998) Enhanced expression of transforming growth factor-beta type I and type II receptors in wound granulation tissue and hypertrophic scar. Am J Pathol; 152(2):485–493.

[7] Wu L, Siddiqui A, Morris DE, et al (1997) Transforming growth factor beta 3 (TGF beta 3) accelerates wound healing without alteration of scar prominence. Histologic and competitive reversetranscription- polymerase chain reaction studies. Arch Surg; 132(7):753–760.

[8] Levin SL, Condit DP (1996) Combined injuries—soft tissue management. Clin Orthop Relat Res; (327):172–181.

[9] Gierer P, Mittlmeier T, Bordel R, et al (2005) Selective cyclooxygenase-2 inhibition reverses microcirculatory and inflammatory sequelae of closed soft-tissue trauma in an animal model. J Bone Joint Surg Am; 87(1):153–160.

[10] Schaser KD, Bail HJ, Schewior L, et al (2005) Acute effects of N-acetylcysteine on skeletal muscle microcirculation following closed soft tissue trauma in rats. J Orthop Res; 23(1):231–241.

[11] Mittlmeier T, Schaser K, Kroppenstedt S, et al (1997) Microvascular response to closed soft tissue injury. Trans Orthop Res Soc; 44:317.

[12] Matsen FA, Winquist RA, Krugmire RB Jr (1980) Diagnosis and management of compartmental syndromes. J Bone Joint Surg Am; 62(2):286–291.

[13] Tscherne H (1983) [Wound management of fractures with soft-tissue damage.] Kinderchir; 38:34–39.

[14] Shrier I, Magder S (1995) Pressure-flow relationships in in vitro model of compartment syndrome. J Appl Physiol; 79(1):214–221.

[15] Heppenstall RB (1997) Compartment syndrome: Pathophysiology, diagnosis, and treatment. Techniques Orthop; 12:92–108.

[16] Blick SS, Brumback RJ, Poka A, et al (1986) Compartment syndrome in open tibial fractures. J Bone Joint Surg Am; 68(9):1348–1353.

[17] Willy C, Gerngross H, Sterk J (1999) Measurement of intracompartmental pressure with use of a new electronic transducertipped catheter system. J Bone Joint Surg Am; 81(2):158–168.

[18] Mubarak SJ, Owen CA (1977) Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am; 59(2):184–187.

[19] Gullo A, Berlot G (1996) Ingredients of organ dysfunction or failure. World J Surg; 20(4):430–436.

[20] Kirkpatrick CJ, Bittinger F, Klein CL, et al (1996) The role of the microcirculation in multiple organ dysfunction syndrome (MODS): a review and perspective. Virchows Arch; 427(5):461–476.

[21] Smail N, Messiah A, Edouard A, et al (1995) Role of systemic inflammatory response syndrome and infection in the occurrence of early multiple organ dysfunction syndrome following severe trauma. Intensive Care Med; 21(10):813–816.

[22] Mills WJ, Barei DP, McNair P (2004) The value of the anklebrachial index for diagnosing arterial injury after knee dislocation: a prospective study. J Trauma; 56(6):1261–1265.

[23] Gustilo RB, Anderson JT (1976) Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg Am; 58(4):453–458.

[24] Gustilo RB, Mendoza RM, Williams DN (1984) Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma; 24(8):742–746.

[25] Tscherne H, Oestern HJ (1982) A new classification of soft-tissue damage in open and closed fractures. Unfallheilkunde; 85(3):111–115.

[26] Brumback RJ, Jones AL (1994) Interobserver agreement in the classification of open fractures of the tibia. The results of a survey of two hundred and forty-fi ve orthopaedic surgeons. J Bone and Joint Am; 76(8):1162–1166.

[27] Südkamp N, Haas NP, Flory PJ, et al (1989) [Criteria for amputation, reconstruction and replantation of extremities in multiple trauma patients.] Chirurg; 60(11):774–781.

[28] Südkamp N, Haas N, Tscherne H, et al (2001) Criteria for amputation, reconstruction and replantation of extremities in multiple trauma patients. Chirurg; 72:312–318

[29] Südkamp NP, Barbey N, Veuskens A, et al (1993) The incidence of osteitis in open fractures: an analysis of 948 open fractures (a review of the Hannover experience). J Orthop Trauma;  7(5):473–482.