+ ACUTE COMPARTMENT SYNDROME

Acute compartment syndrome occurs when pressure rises within a confined space in the body, resulting in a critical reduction of the blood flow to the tissues contained within the space. Without urgent decompression, tissue ischemia, necrosis, and functional impairment occur.

Defination

Mubarak defined compartment syndrome as an elevation of the interstitial pressure in a closed osseofascial compartment that results in microvascular compromise. Compartments with relatively noncompliant fascial or osseous structures most commonly are involved, especially the anterior and deep posterior compartments of the leg and the volar compartment of the forearm. Compartment syndrome can develop anywhere skeletal muscle is surrounded by substantial fascia, however, such as in the buttock, thigh, shoulder, hand, foot, arm, and lumbar paraspinous muscles.

Associated conditions

Exertional compartment syndrome is elevation of intercompartmental pressure during exercise, causing ischemia, pain, and rarely neurological symptoms and signs. It is characterized by resolution of symptoms with rest but may proceed to acute compartment syndrome if exercise continues.Volkmann's ischemic contracture is the end stage of neglected acute compartment syndrome with irreversible muscle necrosis leading to ischemic contractures.The crush syndrome is the systemic result of muscle necrosis commonly caused by prolonged external compression of an extremity. In crush syndrome muscle necrosis is established by the time of presentation, but intracompartmental pressure may rise as a result of intracompartmental edema, causing a superimposed acute compartment syndrome.

History

The first report of the condition was attributed to Hamilton in 1850 by Hildebrand but Hamilton's original description has never been found. The credit for the first full description belongs to Richard Von Volkmann who published a summary of his views in 1881. He stated that paralysis and contractures

appeared after too tight bandaging of the forearm and hand, were ischemic in nature, and were caused by prolonged blocking of arterial blood. He recognized that muscle cannot survive longer than 6 hours with complete interruption of its blood flow and that 12 hours or less of too tight bandaging were enough to result in “dismal permanent crippling.”

Epidemiology

From adolescence, younger patients are at more risk of compartment syndrome.The underlying condition causing acute compartment syndrome was most commonly a fracture.The most common fracture associated with acute compartment syndrome in tibial diaphyseal fracture. The second most common cause of acute compartment syndrome is soft tissue injury. The second most common fracture to be complicated by acute compartment syndrome is the distal radius fracture.Acute compartment syndrome may be more prevalent after low energy injury, possibly because in low energy injury the compartment boundaries are less likely to be disrupted and an “autodecompression” effect is avoided. The concept of patients with lower energy injury being at higher risk is supported by the distribution of severe open fractures in each group.The likely explanation for the preponderance of young males with acute compartment syndrome is that young men have relatively large muscle volumes, whereas their compartment size does note change after growth is complete. Thus young men may have less space for swelling of the muscle after injury. Presumably the older person has smaller hypotrophic muscles allowing more space for swelling. There may also be a protective effect of hypertension in the older patient.

EtiologyConditions Increasing the Volume of Compartment ContentsFractureSoft tissue injuryCrush syndrome (including use of the lithotomy position)RevascularizationExerciseFluid infusion (including arthroscopy)Arterial punctureRuptured ganglia/cystsOsteotomySnake biteNephrotic syndromeLeukemic infiltration

Viral myositisAcute hematogenous osteomyelitisConditions Reducing Compartment VolumeBurnsRepair of muscle herniaMedical ComorbidityDiabetesHypothyroidismBleeding diathesis/anticoagulants

PathogenesisThe critical closing pressure theory states that there is a critical closing pressure in the small vessels when the transmural pressure (the difference between intravascular pressure and tissue pressure) drops. Transmural pressure (TM) is balanced by a constricting force (TC) consisting of active and elastic tension derived from smooth muscle action in the vessel walls. The equilibrium between expanding and contracting forces is expressed in a derivation of Laplace's law:TM = TC ÷ rwhere r is the radius of the vessel.If, because of increasing tissue pressure, the transmural pressure drops to a level such that elastic fibers in the vessel wall are no longer stretched and therefore cannot contribute any elastic tension, then there will be no further automatic decrease in the radius. TC ÷ r then becomes greater than TM and active closure of the vessel will occur. Whatever the cause of the raised tissue pressure, blood flow will be decreased and may temporarily cease altogether as a result of a combination of active arteriolar closure and passive capillary compression, depending on vasomotor tone and the height of the total tissue pressure. The second theory is the arteriovenous gradient theory. According to this theory the increases in local tissue pressure reduce the local arteriovenous pressure gradient and thus reduce blood flow. When flow diminishes to less than the metabolic demands of the tissues (not necessarily to zero), then functional abnormalities result. The relationship between arteriovenous (AV) gradient and the local blood flow (LBF) is summarized in the equation:LBF = Pa - Pv ÷ Rwhere Pa is the local arterial pressure, Pv is the local venous pressure, and R is the local vascular resistance. Veins are collapsible tubes and the pressure within them can never be less than the local tissue pressure. If tissue pressure rises as in the acute compartment syndrome, then the Pv must rise also, thus reducing the AV gradient (Pa - Pv) and therefore the local blood flow. At low AV gradients compensation from local vascular resistance (R) is relatively ineffective and local blood flow is primarily determined by the AV gradient.

A third theory, the microvascular occlusion theory postulates that capillary occlusion is the main mechanism reducing blood flow in acute compartment syndrome. Resultant muscle ischemia leads to increased capillary membrane permeability to plasma proteins, increasing edema and obstruction of lymphatic by the raised tissue pressure.Effects of Raised Tissue Pressure on MuscleRegardless of the mechanism of vessel closure, reduction in blood flow in the acute compartment syndrome has a profound effect on muscle tissue. Skeletal muscle is the tissue in the extremities most vulnerable to ischemia and is therefore the most important tissue to be considered in acute compartment syndrome. Both the magnitude and duration of pressure elevation have been shown experimentally to be important influences in the extent of muscle damage. A number of experimental studies have highlighted the importance of perfusion pressure as well as tissue pressure in the reduction of muscle blood flow. MR measurements of cellular metabolic derangement (PH, tissue oxygenation, and energy stores) and histological studies, including electron microscopy and videomicroscopy studies of capillary blood flow, have shown that critical tissue pressure thresholds are 10 to 20 mm Hg below diastolic blood pressure or 25 to 30 mm Hg below mean arterial pressure.The ultimate result of reduced blood flow to skeletal muscle is ischemia followed by necrosis, increasing periods of complete ischemia produce increasing irreversible changes. Muscle necrosis is present in its greatest extent in the central position of the muscle, and that external evaluation of the degree of muscle necrosis is unreliable. The duration of muscle ischemia dictates the amount of necrosis, although some muscle fibers are more vulnerable than others to ischemia. For example, the muscles of the anterior compartment of the leg contain Type 1 fibers or red slow twitch fibers, whereas the gastrocnemius contains mainly Type 2 or white fast twitch fibers. Type 1 fibers depend on oxidative metabolism of triglycerides for their energy source and are more vulnerable to oxygen depletion than Type 2 fibers whose metabolism is primarily anaerobic.This may explain the particular vulnerability of the anterior compartment to raised intracompartmental pressure.Pressure on Nerve Effects of Raised Tissue All investigators note a loss of neuromuscular function with raised tissue pressures but at varying pressure thresholds and duration.The mechanism of damage to nerve is as yet uncertain and could result from ischemia, ischemia plus compression, toxic effects, or the effects of acidosis.Effects of Raised Tissue Pressure on BoneNonunion is now recognized as a complication of acute compartment syndrome.It was first suggested by Nario in 1938 that “Volkmann's disease” caused obliteration of the “musculodiaphyseal” vessels and caused frequent pseudarthrosis.It is likely that muscle ischemia reduces the capacity for

development of the extraosseous blood supply on which long bones depend for healing.Reperfusion InjuryThe reperfusion syndrome is a group of complications following reestablishment of blood flow to the ischemic tissues and can occur after fasciotomy and restoration of muscle blood flow in the acute compartment syndrome. Reperfusion is followed by an inflammatory response in the ischemic tissue that can cause further tissue damage. The trigger for the inflammatory response is probably the breakdown products of muscle.Some breakdown products are procoagulants that activate the intrinsic clotting system. This results in increasing microvascular thrombosis, which in turn increases the extent of muscle damage.If there is a large amount of muscle involved in the ischemic process, the inflammatory response may become systemic. In acute compartment syndrome this is most likely to occur in the crush syndrome. Procoagulants escape into the systemic circulation and produce systemic coagulopathy with parallel activation of inflammatory mediators. These then damage vascular endothelium, leading to increased permeability and subsequent multiple organ failure. Systemic clotting and the breakdown products of dead and dying cells also lead to activation of white blood cells, with the release of additional inflammatory mediators such as histamine, interleukin, oxygen free radicals, thromboxane, and many others. This is the basis for the use of agents such as antioxidants, antithromboxanes, antileukotrienes, and anti-platelet-activating factors that modify the inflammatory process. Some of these agents have been shown in the laboratory to be capable of reducing muscle injury.

Diagnosis of acute compartment syndrome

Prompt diagnosis of acute compartment syndrome is the key to a successful outcome. Delay in diagnosis has long been recognized as the single cause of failure of the treatment of acute compartment syndrome. Delay in treatment of the acute compartment syndrome can be catastrophic, leading to serious complications such as permanent sensory and motor deficits, contractures, infection and at times, amputation of the limb.

Clinical diagnosis# Pain is considered to be the first symptom of acute compartment syndrome. The pain experienced by the patient is by nature ischemic,intractable and usually severe and out of proportion to the clinical situation. Pain may, however, be an unreliable indication of the presence of acute compartment syndrome because it can be variable in its intensity.Pain may be absent in acute compartment syndrome associated with nerve injury or minimal in the deep posterior compartment syndrome.Pain is present in most cases because of the

index injury but cannot be elicited in the unconscious patient. Children may not be able to express the severity of their pain, so restlessness, agitation, and anxiety with increasing analgesic requirements should raise the suspicion of the presence of an acute compartment syndrome. Pain has been shown to have a sensitivity of only 19% and a specificity of 97% in the diagnosis of acute compartment syndrome (i.e., a high proportion of false negative or missed cases but a low proportion of false positive cases). There is general agreement, however, that pain if present is a relatively early symptom of acute compartment syndrome in the awake alert patient.Pain with passive stretch of the muscles involved is recognized as a symptom of acute compartment syndrome. Thus pain is increased for example in an anterior compartment syndrome when the toes or foot are plantarflexed. This symptom is no more reliable than rest pain, because the reasons for unreliability quoted above apply equally to pain on passive stretch. The sensitivity and specificity of pain on passive stretch are similar to those for rest pain.# Paraesthesia and hypoesthesia may occur in the territory of the nerves traversing the affected compartment and are usually the first signs of nerve ischemia, although sensory abnormality may be the result of concomitant nerve injury.Reports of sensitivity of 13% and specificity of 98% for the clinical finding of paraesthesia in acute compartment syndrome, a false negative rate that precludes this symptom from being a useful diagnostic tool.# Paralysis of muscle groups affected by the acute compartment syndrome is recognized as being a late sign. This sign has equally low sensitivity as others in predicting the presence of acute compartment syndrome, probably because of the difficulty of interpreting the underlying cause of the weakness, which could be inhibition by pain, direct injury to muscle, or associated nerve injury. If a motor deficit develops, full recovery is rare.# Palpable swelling in the compartment affected may be a further sign of compartment syndrome; although the degree of swelling is difficult to assess accurately, making this sign very subjective. Casts or dressings often obscure compartments at risk and prevent assessment of swelling.Some compartments such as the deep posterior compartment of the leg are completely buried under the muscle compartments, obscuring any swelling.# Peripheral pulses and capillary return are always intact in acute compartment syndrome unless there is major arterial injury or disease or in the very late stages of acute compartment syndrome when amputation is inevitable. If acute compartment syndrome is suspected and pulses are absent, then arteriography is indicated. Conversely, it is dangerous to exclude the diagnosis of acute compartment syndrome because distal pulses are present.

Using a combination of clinical symptoms and signs increases their sensitivity as diagnostic tools.

Compartment pressure monitoringSeveral techniques were developed to measure intracompartmental pressure (ICP) once it was appreciated that acute compartment syndrome was caused by increased tissue pressure within the affected compartment. Because raised tissue pressure is the primary event in acute compartment syndrome, changes in ICP will precede the clinical symptoms and signs.(1) One of the first to be used was the needle manometer method, using a needle introduced into the compartment and connected to a column filled partly with saline and partly with air. A syringe filled with air is attached to this column, as is a pressure manometer or transducer. The ICP is the pressure that is required to inject air into the tubing and flatten the meniscus between the saline and the air. This method was modified by Matsen and his colleagues to allow infusion of saline into the compartment. The ICP is the pressure resistance to infusion of saline. These methods, although simple and inexpensive have some drawbacks. A danger exists of too large a volume being infused, possibly inducing acute compartment syndrome. It is probably the least accurate of the measurement techniques available, with falsely high values having been recorded in comparison with other techniques and falsely low values in cases of very high ICP. A needle with only one perforation at its tip also can become easily blocked.(2) The wick catheter was first described for use in acute compartment syndrome by Mubarak and his coauthors. This is a modification of the needle technique, in which fibrils protrude from the bore of the catheter assembly. This allows a large surface area for measurement and prevents obstruction of the needle; it is ideal for continuous measurement. A disadvantage of this technique is the possibility of a blood clot blocking the tip or air in the column of fluid between the catheter and the transducer, which will dampen the response and give falsely low readings. There is a theoretical risk of retention of wick material in the tissues.(3) The slit catheter was first described by Rorabeck and his associates. This operates on the same principal as the wick catheter in that it is designed to increase the surface area at the tip of the catheter by means of being cut axially at the end of the catheter . The interstitial pressure is measured through a column of saline attached to a transducer. Patency can be confirmed by gentle pressure over the catheter tip; an immediate rise in the pressure should be seen. Care must be taken to avoid the presence of air bubbles in the system as this can, like the wick catheter, result in falsely low readings. The slit catheter is more accurate than the continuous infusion method and is as accurate as the wick catheter.(4) The side-ported needle was introduced in 1988. These needles are inserted into intramuscular compartments perpendicular to the surface, and therefore

side ports have low risk of occlusion. This allows for improved accuracy (compared with simple needles) of interstitial pressure measurements along with the additional advantage of being capable of measuring several compartments in the same patient . They have been shown to have similar accuracy to slit catheters.(5) Attempts to improve the reliability of ICP measurement led to the placement of the pressure transducer directly into the compartment by siting it within the lumen of a catheter. The solid state transducer intracompartmental catheter (STIC) was described in 1984 and measurements were correlated with conventional pressure monitoring systems. This device is now commercially available and widely used, although to retain patency of the catheter for continuous monitoring. an infusion must be used with its attendant problems. The alternative is intermittent pressure measurements, which is likely to cause significant discomfort to patients and is more labor intensive. Newer systems with the transducer placed at the tip of the catheter do not depend on a column of fluid and therefore avoid the problems of patency. These systems are more expensive, however, and are a potential problem for resterilization.All the methods above measure ICP, which is an indirect way of measuring muscle blood flow and oxygenation. Near infrared spectroscopy measures tissue oxygen saturation noninvasively by means of a probe placed on the skin.

TimingTime factors are also important in making the decision to proceed to fasciotomy. It is well established experimentally and clinically that both the duration and severity of the pressure elevation influence the development of muscle necrosis. Continuous pressure monitoring allows a clear record of the trend of the tissue pressure measurements. In situations where the ΔP drops below 30 mm Hg if the ICP is dropping and the ΔP is rising, then it is safe to observe the patient in anticipation of the ΔP returning within a short time to safe levels. If the ICP is rising, the ΔP is dropping and less than 30 mm Hg, and this trend has been consistent for a period of 1 to 2 hours, then fasciotomy should be performed. Fasciotomy should not be performed based on a single pressure reading except in extreme cases. Using this protocol, delay to fasciotomy and the sequelae of acute compartment syndrome are reduced without unnecessary fasciotomies being performed.Overtreatment has been cited as a problem with continuous monitoring. For ICP monitoring to be most effective in reducing delay, it must be used as the primary indication for fasciotomy.

Compartments of the Leg with Their Contents and Clinical Signs of Acute Compartment Syndrome in Each

Compartment Contents SignsAnterior Tibialis anterior

Extensor digitorum longus

Extensor hallucis longus

Peroneus tertius

Deep peroneal (anterior tibial) nerve and vessels

Pain on passive flexion—ankle/toes

Numbness—1st web space

Weakness—ankle/toe flexion

Lateral Peroneus longus

Peroneus brevis

Superficial peroneal nerve

Pain on passive foot inversion

Numbness—dorsum of foot

Weakness of eversionSuperficial posterior

Gastrocnemius

Soleus

Plantaris

Sural nerve

Pain on passive ankle extension

Numbness—dorsolateral foot

Weakness—plantar flexion

Deep posterior Tibialis posterior

Flexor digitorum longus

Flexor hallucis longus

Posterior tibial nerve

Pain on passive ankle/toe extension/ foot eversion

Numbness—sole of foot

Weakness—toe/ankle flexion, foot inversion

Single incision fasciotomyA longitudnal lateral incision just distal to fibula head to 2-3cm proximal to lateral malleolus is taken.The skin is undermined both anteriorly and posteriorly.Care is taken to protect the superfiscial peroneal nerve.The anterior,lateral and superfiscial posterior fasciotomy performed longitudinally. The interval between the superfiscial posterior and lateral compartment developed detaching soleus and flexor hallucis longus from the fibula.The peroneal vessels retracted posteriorly and the attachment of the fascia to the posterior tibial musce identified and incised longitudinally.A drain is placed

and skin closed.

Double incision fasciotomyA 20-25cm long longitudinal incision is made midway between the crest of tibia and the fibular shaft.A transverse incision is made to identify the lateral intermuscular septum and the superfiscial peroneal nerve just posterior to the septum.The anterior fasciotomy is done in line with the anterior tibia and lateral fasciotomy done in line with the fibular shaft.Asecond incision is made 2cm posterior to the posterior tibia.The saphenous vein and nerve are retracted anteriorly.A transverse incision is made to identify the septum between the deep and superficial posterior compartments.The fascia over the gastrocnemius and soleus is released and another fascia over the flexor digitorum longus is done to release the entire superfiscial posterior compartment.If the pressure in the deep posterior compartment is increased release is done and dressing done or shoelace technique is applied for the closure.

Compartments of The Forearm, Their Contents, and Signs of Acute Compartment Syndrome

CompartmentContents SignsVolar Flexor carpi radialis longus

and brevis

Flexor digitorum superficialis and profundus

Pronator teres

Pronator quadratus

Median nerve

Ulnar nerve

Pain on passive wrist/finger extension

Numbness—median/ulnar distribution

Weakness—wrist/finger flexion

Weakness—median/ulnar motor function in hand

Dorsal Extensor digitorum

Extensor pollicis longus

Abductor pollicis longus

Extensor carpi ulnaris

Pain—passive wrist/finger flexion

Weakness—wrist/finger flexion

Mobile wad Brachioradialis

Extensor carpi radialis

Pain on passive wrist flexion/elbow extension

Weakness—wrist extension/elbow flexion

In the forearm both volar and dorsal fasciotomies may be performed. In most cases the volar compartment is approached first through an incision extending from the biceps tendon at the elbow to the palm of the hand, to allow carpal tunnel decompression that is usually necessary. Fascial incision then allows direct access to the compartment. The deep flexors must be carefully inspected after fascial incision. Separate exposure and decompression of pronator quadratus may be necessary.Often volar fasciotomy is sufficient to decompress the forearm, but if ICP remains elevated in the dorsal compartment perioperatively, then dorsal compression is easily performed through a straight dorsal incision

Compartments of the Thigh, Their Contents, and Signs of Acute Compartment Syndrome

Compartment Contents SignsAnterior Quadriceps muscles

Sartorius

Femoral nerve

Pain on passive knee flexion

Numbness—medial leg/foot

Weakness—knee extensionPosterior Hamstring muscles

Sciatic Nerve

Pain on passive knee extension

Sensory changes rare

Weakness—knee flexionAdductor Adductor muscles

Obturator nerve

Pain on passive hip abduction

Sensory changes rare

Weakness—hip adduction   A lateral incision beginning just distal to the intertrochanteric line and

extending to the lateral epicondyle is made.Using subcutameous dissection to expose the ilitibial band a straight incision is taken through the band.Vastus lateralis is reflected off the intermuscular septum and the septum and the septum is incised the whole length.After the anterior and posterior compartments are released pressure inside the medial compartment is measured if the pressure is elevated an incision over the compartment made and released.A bulky dressing is applied later.

       

      

             

Compartments of The Forearm, Their Contents, and Signs of Acute Compartment Syndrome

Compartment Contents SignsVolar Flexor carpi radialis longus

and brevis

Flexor digitorum superficialis and profundus

Pronator teres

Pronator quadratus

Median nerve

Ulnar nerve

Pain on passive wrist/finger extension

Numbness—median/ulnar distribution

Weakness—wrist/finger flexion

Weakness—median/ulnar motor function in hand

Dorsal Extensor digitorum

Extensor pollicis longus

Abductor pollicis longus

Extensor carpi ulnaris

Pain—passive wrist/finger flexion

Weakness—wrist/finger flexion

Mobile wad Brachioradialis

Extensor carpi radialis

Pain on passive wrist flexion/elbow extension

Weakness—wrist extension/elbow flexion

Fasciotomy of the arm is performed through anterior and posterior incisions when the compartments are easily visualized. On rare occasions the deltoid muscle should also be decompressed.

Compartments of the Foot and Their ContentsCompartment ContentsMedial Intrinsic muscles of the great toeLateral Flexor digiti minimi

Abductor digiti minimiCentral—Superficial Flexor digitorum brevis

—Deep (calcaneal)

Quadratus plantae

Adductor hallucis Adductor hallucisInterosseous × 4 Interosseous muscles

Digital nervesDorsal incisions overlying the second and fourth metacarpals allow sufficient access to the interosseous compartments and the central compartment that lies deep to the interosseous compartments . The medial and lateral compartments can be accessed around the deep surfaces of the first and fifth metatarsal, respectively. Such a decompression is usually sufficient in cases of forefoot injury, but when a hindfoot injury, especially a calcaneal fracture, is present a separate medial incision may be required to decompress the calcaneal compartment.

The Compartments of The Hand and Their ContentsCompartment ContentsThenar Abductor pollicis brevis

Flexor pollicis brevis

Opponens pollicisHypothenar Abductor digiti minimi

Flexor digiti minimi

Opponens digiti minimiDorsal interosseous × 4 Dorsal interosseiVolar interossei × 3 Volar interosseiAdductor pollicis Adductor pollicisDecompression of the hand can usually be adequately achieved using two dorsal incisions that allow access to the interosseous compartments. This may often be sufficient, but if there is clinical suspicion or raised ICP on measurement then incisions may be made over the thenar and hypothenar eminences, allowing fasciotomy of these compartments.Management of Fasciotomy WoundsFasciotomy incisions must never be closed primarily because this may result in persistent elevation of ICP. The wounds should be left open and dressed, and approximately 48 hours after fasciotomy a “second look” procedure should be undertaken to ensure viability of all muscle groups. Skin closure or cover should not be attempted unless all muscle groups are viable.The wounds may then be closed by delayed primary closure if possible, although this must be without tension on the skin edges. Commonly in the leg

this technique is possible in the medial but not the lateral wound. If delayed primary closure cannot be achieved, then the wound may be closed using either dermatotraction techniques or split skin grafting. Dermatotraction or gradual closure techniques have the advantage of avoiding the cosmetic problems of split skin grafting but may cause skin edge necrosis. A further disadvantage is the prolonged time required to achieve closure, which may be up to 10 days.Split skin grafting although offering immediate skin cover has the disadvantage of a high rate of long-term morbidity. The recent introduction of vacuum assisted closure (VAC) systems is likely to be a significant advantage in this area and may reduce the need for split skin grafting with a low complication rate.Management of Associated Fractures

Fractures, especially of the long bones, should be stabilized in the presence of acute compartment syndrome treated by fasciotomy. In reality the treatment of the fracture should not be altered by the presence of an acute compartment syndrome, although cast management of a tibial fracture is contraindicated in the presence of acute compartment syndrome. Fasciotomy should be performed prior to fracture stabilization in order to eliminate any unnecessary delay in decompression. Stabilization of the fracture allows easy access to the soft tissues and protects the soft tissues, allowing them to heal.

ComplicationsDelay in diagnosis has been cited as the single reason for failure in the management of acute compartment syndrome. Delay to fasciotomy of more than 6 hours is likely to cause significant sequelae,including muscle contractures, muscle weakness, sensory loss, infection, and nonunion of fractures. In severe cases amputation may be necessary because of infection or lack of function.