Compartment syndromes from head to toe

Zsolt J. Balogh, MD, PhD, FRACS; Nerida E. Butcher, MD

T he fixed-walled compartmentsof the human body separateand protect vital organs. Thewalls of the compartments can

be fascia/connective tissue (muscle com-partments, pericardium, and capsulatedvisceral organs) or bone and connectivetissue (brain, spinal cord, and orbit).Connective tissues with high collagencontent are less tensile than muscle orskin and key determinants of the volumeof the compartments. In broad terms,compartment syndrome is defined as thedysfunction of organs/tissues within thecompartment due to limited blood supplycaused by increased pressure within thecompartment. Without timely interven-tion, compartment syndromes cause per-manent and irreversible damage to thetissues within the compartment. In thecase of vital organs, they cause rapidphysiologic deterioration and death. Pre-vention, timely recognition, and immedi-ate intervention are the strategies of themanagement of patients with potential

compartment syndromes. The detrimen-tal effects of increased pressure in theskull (cerebral/cerebellar herniation),pleural cavity (tension pneumothoraxand massive hemothorax), and pericar-dium (pericardial tamponade) are well-described, life-threatening conditions inmedical textbooks. The basic pathophys-iology and definition of these conditionsare consistent with the ones of the com-partment syndrome, but they are not re-garded as compartment syndromes incurrent medical terminology and are notcovered in this review. Without furtherspecification, the term compartmentsyndrome refers to the extremity com-partment syndromes (ECS); in the case ofother anatomical areas, the specific bodycompartment must be defined (abdomi-nal, thoracic, etc.). Considering the crit-ical care focus, only acute compartmentsyndromes are discussed in this article,but many compartments can have sub-acute or chronic syndromes with a lessdramatic clinical picture. The aim of thisarticle is to introduce and discuss acutecompartment syndromes that are essen-tial for critical care physicians to recog-nize and manage.

General Pathophysiology

The underlying pathophysiology of allcompartment syndromes is the inade-quate perfusion and oxygenation of theorgans/tissues within the confined space

(1). Pressure in the microcirculation de-termines the adequacy of nutrient bloodflow in the capillaries, and this pressureis opposed by both venous and tissuepressures.

Although authors agree that cellularanoxia is the final common pathway, sev-eral explanations (2) have been proposedto account for the complex pathophysiol-ogy resulting in compartment syndrome.The two generally accepted theories are:1) the ischemia-reperfusion syndrome(3); and 2) the arteriovenous pressuretheory (4). Although the two theories arecomplementary and not contradictory,the most recognized explanation is thearteriovenous pressure gradient theory.

The perfusion of the intracompart-mental tissues is hindered by the eleva-tion of the interstitial fluid pressureabove the level of the pressures in thecapillaries. The interstitial pressure inloose connective tissue spaces is reportedto be subatmospheric, whereas in tightlyencased tissues, it is positive pressure�10 mm Hg (5). The capillary pressureson the arterial and the venous ends are�30 mm Hg and �10 mm Hg, respec-tively. Depending on the organs’ normalinterstitial pressure and potential for au-toregulation, the compartment pressure,which causes organ dysfunction, is be-tween 15 and 25 mm Hg. In most com-partments, pressure of �30 mm Hg crit-ically compromises organ perfusion.

From the Department of Traumatology, JohnHunter Hospital and University of Newcastle, New-castle, NSW, Australia.

The authors have not disclosed any potential con-flicts of interest.

For information regarding this article, E-mail:Zsolt.Balogh@hnehealth.nsw.gov.au

Copyright © 2010 by the Society of Critical CareMedicine and Lippincott Williams & Wilkins

DOI: 10.1097/CCM.0b013e3181ec5d09

Compartment syndrome is defined as the dysfunction of or-gans/tissues within the compartment due to limited blood supplycaused by increased pressure within the compartment. The aim ofthis article is to introduce and discuss acute compartment syn-dromes that are essential for critical care physicians to recognizeand manage. Various pathophysiological mechanisms (ischemia-reperfusion syndrome, direct trauma, localized bleeding) couldlead to increased compartmental pressure and decreased bloodflow through the intracompartmental capillaries. Although com-partment syndromes are described in virtually all body regions,the etiology, diagnosis, treatment, and prevention are best char-acterized for three key body regions (extremity, abdominal, andthoracic compartment syndromes). Compartment syndromes canbe classified as either primary (pathology/injury is within the

compartment) or secondary (no primary pathology or injury withinthe compartment), and based on the etiology (e.g., trauma, burn,sepsis). A recently described phenomenon is the “multiple” com-partment syndrome or “poly”-compartment syndrome, which isusually a complication of a severe shock and massive resuscita-tion. The prevention of compartment syndromes is based onpreemptive open management of compartments (primary syn-dromes) in high-risk patients and/or careful fluid resuscitation(both primary and secondary syndromes) to limit interstitialswelling. (Crit Care Med 2010; 38[Suppl.]:S445–S451)

KEY WORDS: extremity compartment syndrome; abdominal com-partment syndrome; acute compartment syndrome; organ/tissuedysfunction; multiple compartment syndrome

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More recently, it has been recommendedthat compartment pressures be inter-preted in the context of the difference ofdiastolic or mean arterial pressure (�P �diastolic pressure � compartment pres-sure) rather than absolute pressures (6,7). This approach helps to consider thecompartment pressure in context of thearterial inflow. Once the compartment’sperfusion is compromised, a vicious cycleof hypoxia, anaerobic metabolism,edema, further pressure increase and fur-ther decrease of capillary flow takes place.This process is irreversible without inter-vention.

The increased pressure in the com-partment can be due to the increasedcontent within the fixed volume space(bleeding, edema) or due to the decreasedvolume of the compartment (externalcompression, bandage, cast), or both.Compartments can be in relative isch-emic state due to higher oxygen demand(exercise, trauma, sepsis) but peripheralvasoconstriction (vasopressor medica-tion) also can further limit their perfu-sion. This absolute or relative ischemiacan lead to massive tissue edema andconsequent compartment syndrome afterreperfusion. The symptoms of the specificcompartment syndrome are dependenton the function of the enclosed organs.Compartment syndromes, in general, canbe classified as primary (the pathology/injury is within the compartment) or sec-ondary (no primary pathology or injurywithin the compartment).

Individual Compartments

Thoracic/mediastinalcompartment syndrome

A syndrome of “tight mediastinum”after prolonged cardiac surgery was de-scribed by Riahi et al (8) in 1975. Thecondition, known as thoracic or medias-tinal compartment syndrome, has beendescribed in almost 200 reported cases ofadult and pediatric patients undergoingcardiac surgical procedures. Open chestmanagement has gained acceptance as atechnique in the management of hemo-dynamically unstable patients where car-diac compression by sternal closure is nottolerated. Early concerns to use this tech-nique were related to the potential in-creased risk of mediastinitis after pro-longed open sternotomy; however,infectious complications and sternalmorbidity have been less frequent thanfirst anticipated in the late 1970s (9–12).

Although thoracic compartment syn-drome is well known in the cardiac sur-gical literature, it is hardly mentioned inthe noncardiac surgical and trauma liter-ature (13).

Etiology. Research into cardiac func-tion after cardiac surgery has found thatrestriction of diastolic filling is the mainpoint at which compression or tamponadedevelops in the thoracic cavity. Both thepericardium and the sternum act to in-crease diastolic stiffness; however, a largerdecrease in cardiac output noted after ster-nal closure suggests that the latter mayexert a greater effect than pericardial clo-sure, particularly in patients with fluidoverload (14). The decrease in bloodpressure and the increased end-dia-stolic pressure can result in subendo-cardial ischemia, leading to a cycle ofprogressive deterioration (13). Low car-diac output can be improved by openingthe sternum (15).

Thoracic compartment syndrome isan infrequent occurrence, even in thebusiest cardiac and trauma centers. Pro-longed open sternotomy with delayedsternal closure has been illustrated asuseful after cardiac surgery in the settingof severe myocardial dysfunction, markedmyocardial edema, coagulopathy withuncontrolled bleeding, and relentless ar-rhythmias (16 –18). Patients with de-creased lung compliance, acute pulmo-nary edema, or congestive cardiac failureare also at a significant risk for a delayedsternal closure.

There are two case reports in the lit-erature describing thoracic compartmentsyndrome after noncardiac thoracic pro-cedures (13, 19).

With regard to the trauma patient,Kaplan et al (20) reported a patient with agunshot wound causing thoracic and car-diac injuries that was treated with de-layed sternal closure. This is the only casereported in the literature of thoraciccompartment syndrome with the etiologyof trauma. The lack of further data tosupport prolonged open sternotomy intrauma patients (more than anecdotal ev-idence) is due largely to the limited sur-vival of patients whose injuries are signif-icant enough to result in massive tissueedema after resuscitation from thoracictrauma. In this context, it is important tonote that thoracic compartment syn-drome can also occur after thoracotomywith packing for trauma.

Diagnosis. In the poststernotomystate, massive resuscitation and acutemediastinal swelling/bleeding should

alert critical care physicians. Rising peakinspiratory pressure during thoracic wallclosure may serve as an early warningthat the patient is at risk for thoraciccompartment syndrome (20). Since therest of the symptoms—like falling cardiacoutput and worsening acidosis—are non-specific, clinical suspicion remains a cru-cial component in the diagnosis of tho-racic compartment syndrome. Thesyndrome may not develop until hoursand possibly days postclosure when ven-tilation pressure monitoring has ceased.

Treatment. Immediate decompressionof the chest and open chest managementwith delayed sternal closure is the key inthoracic compartment syndrome wherethoracic closure precipitates hemody-namic collapse. Open sternotomy in-volves leaving the sternum and subcuta-neous layer open after surgery. The skincan be left open and packed, or closeddirectly or with an interposed syntheticmaterial. Several approaches have beenillustrated in the literature (13, 20).

Maintenance of the open chest mustcontinue until the patient demonstratescorrection of the hemodynamic instabil-ity. There must be evidence of increasedcardiac output, decreased filling pres-sures, and improved lung function beforeclosure, with the average time to closurereported from 2 to 7 days (21). Aggressivediuresis to achieve this has been sug-gested; however, this may be difficult andpotentially detrimental in patients under-going acute traumatic shock resuscita-tion.

Abdominal compartmentsyndrome

Abdominal compartment syndrome(ACS) is the most frequently cited com-partment syndrome after ECS. The clin-ical consequences of elevated intra-abdominal pressure (IAP) were describedas early as the mid-19th century (22).Pediatric surgeons became aware of thecatastrophic consequences of attemptedclosure of omphaloceles, and vascularsurgeons described the problem after sur-gical management of ruptured abdominalaortic aneurysms (23, 24). Damage con-trol surgery improved the chances of sur-vival of patients with hemorrhagic shockand severe abdominal trauma. The factthat the patients survived and some of thepractices of damage control (abdominalpacking and aggressive fluid resuscita-tion) led to the emergence of the epi-demic of postinjury ACS (25). The expo-

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nential increase of scientific publicationson the topic and the regular monitoringof IAP increased the awareness of thesyndrome. During the last decade, theconsequences of intra-abdominal hyper-tension (IAH) and ACS were described bymost surgical specialties and also recog-nized as prevalent conditions amongnonsurgical intensive care unit (ICU) pa-tients.

Classification, definitions. The WorldSociety of the Abdominal CompartmentSyndrome (WSACS, founded in 2004) wasfundamental to establish consensus defi-nitions driven by a multidisciplinarygroup of experts. The WSACS recom-mends the intravesical (bladder) route forIAP measurement, and among many, itestablished the following definitions (26):

● Intra-abdominal hypertension (IAH) isdefined as IAP of �12 mm Hg withoutpathophysiology of ACS. IAH is gradedfrom I to IV based on the IAP value(grade I: 12–15 mm Hg; grade II: 16–20mm Hg; grade III: 21–25 mm Hg; gradeIV: �25 mm Hg.

● ACS is defined as a sustained IAP of�20 mm Hg that is associated withnew organ dysfunction/failure defined.

● Primary ACS is a condition associatedwith injury or disease in the abdomi-nopelvic region that frequently re-quires early surgical or interventionalradiologic intervention.

● Secondary ACS refers to conditionsthat do not originate from the abdomi-nopelvic region.

The clinically most relevant classifica-tion is to describe the acuity of the syn-drome (acute, subacute, or chronic), theetiology (e.g., postinjury, sepsis, burn, ab-dominal aortic aneurysm), and the pri-mary or secondary nature of the problem.

Etiology. The acutely increased IAP,the IAH, and the ACS can be due to avariety of abdominal and extra-abdominalfactors (Table 1) (27). Considering thesize of the abdominal cavity, its centrallocation in the body, and the number ofvital organs located within, it is not sur-prising that ACS has symptoms related toextra-abdominal organs (Table 2) (28,29). In patients with already marginalorgan function, the characteristic IAH/ACS-related organ dysfunctions tend tobe apparent at lower IAP.

ACS can be caused by many pathologicconditions but the high-risk patients al-

ways have some abdominal mass effect(fluid, blood, packs, intraluminal con-tents, tumor) and/or requirement formassive fluid resuscitation (traumaticshock, septic shock, ischemia-reperfusioninjury, burns). With regard to the patientwith burns, they are a specifically highrisk of secondary ACS due to the commonsituation of free fluid accumulation aftermassive burn resuscitation. Consideringthe multitude of etiologies, most ICU pa-tients have at least one risk factor todevelop ACS (30).

Diagnosis. The measurement of theIAP is essential for the monitoring of thehigh-risk patients, as the clinical exami-nation has been repeatedly shown to beinaccurate to detect ACS and to estimateIAP (31, 32). The accepted method tomeasure IAP is via the urinary catheter,using the bladder as a conduit of theabdomen (“bladder pressure” and “uri-nary bladder pressure/UBP” are fre-quently used synonyms of IAP). Kron etal (24) originally described the technique,and today numerous modifications existin the literature. The measurement canbe performed with a “homemade” kit of aFoley catheter, a three-way stopcock, anda pressure transducer connected to thebedside monitor, but several proprietarydevices are also available. The main prin-ciples are to use a closed system, fixedreference point (midaxillary line), stan-dard instillation volume (�25 mL), andstandardized recording (respiratoryphase, body position). Most ICUs practicean initial screening among patients whohave at least one risk factor, and later,2–8 hourly monitoring in high-risk pa-tients or in patients with initially abnor-mal measurements.

The normal IAP is considered �10mm Hg among nonlaparotomy, non-trauma hospitalized patients (33). Post-laparotomy patients and morbidly obesepatients have a higher baseline IAP value.Traumatic shock patients requiring hem-orrhage control and resuscitation typi-cally have grade II–III IAH during thefirst 24 hrs of resuscitation (34). The ef-fect of this transient IAH on the outcomeis largely unknown. After damage controlsurgery (both trauma and emergencygeneral surgery) and during shock resus-citation (regardless of the etiology), fre-quent monitoring is recommended. Inshocked multiple trauma patients, ACScan develop within 6 hrs of ICU admis-sion, presenting with oliguria, increasedairway pressures, inability to oxygenate,and no response to preload driven resus-

Table 1. Frequent causes of abdominal compartment syndrome

Primary Secondary

Ascites Whole-body ischemia/reperfusion injuryAbdominal trauma Hemorrhagic shockDamage control laparotomy Septic shockRuptured abdominal aortic aneurysm Major burnsAbdominal aortic cross-clampingIntestinal obstructionIleusSevere constipationMajor abdominal surgeryAbdominal sepsisLarge abdominal tumors

(especially ovarian)PancreatitisLiver transplantation

Table 2. Organ dysfunctions caused by increased intra-abdominal pressure

Organ/Body Part Symptoms/Signs

Brain Increased intracranial pressureLungs Increased airway pressures, decreased compliance, poor oxygenation,

CO2 retentionChest Increased intrathoracic pressure, elevated diaphragmsHeart/circulation Elevated filling pressures, decreased cardiac output, increased systemic

vascular resistanceVisceral organs Decreased intestinal pH, intolerance of enteral nutrition, bowel edema,

compromised intestinal barrier function, ileusKidneys Decreased urine output, decreased glomerular filtration rateLower extremities Venous congestion, edema, increased risk for deep vein thrombosis

and extremity compartment syndromes

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citation. When the abdominal compart-ment is already on the steep phase of itspressure-volume curve, a decrease incompliance and even small increases involume can lead to sharp elevationsin IAP. In most critically ill patients, con-tinuous IAP monitoring is recommendedvia the irrigation port of the previouslyinserted three-way catheter (35). The di-agnosis of ACS is confirmed if the dete-riorated organ functions improve afterthe IAP is decreased by either operative ornonoperative means.

Based on a retrospective study,Cheatham et al (7) have recommendedabdominal perfusion pressure (abdominalperfusion pressure � mean arterial pres-sure � IAP) as a potentially superior andmore physiology-oriented definition ofIAH and ACS. Abdominal perfusion pres-sure was recommended to be kept at �60mm Hg; however, this therapeutic goalremains to be proven by higher-level ev-idence.

Treatment. The treatment of ACS en-tails the resolution of the underlyingproblem simultaneously with measuresto decrease IAP. The authors believe thatmedical methods to decrease IAP (diuret-ics, skeletal muscle paralysis, motilityagents, gastric and colonic decompres-sion) can have a role in less acutely de-veloping IAH, especially without surgicalcauses (36). In the acute setting, espe-cially postinjury, ACS deteriorates the al-ready critically ill patient’s physiology toorgan failure within hours. This fulmi-nant process prevents the opportunity toreassess and titrate medical treatment be-fore the condition becomes irreversible.Thus, in the acute ACS, abdominal de-compression is recommended. In cases ofprimary ACS, this means usually abdom-inal reexploration in the operating roomfor continued bleeding or for major septicsource. In secondary ACS, decompressivelaparotomy can be performed at the bed-side as a lifesaving measure, because nofurther surgical intervention is necessarywithin the abdomen (37).

There are promising preliminary re-ports on percutaneous drainage of theintraperitoneal fluid (especially in burns)and subcutaneous linea alba fasciotomy(pancreatitis) (38–40). However, thesetechniques always require careful reas-sessment of the potential need for formaldecompression (full midline laparotomy).The limitation of percutaneous decom-pression is the fact that, apart from burnsinjury, secondary ACS is rarely caused byfree intraperitoneal fluid alone and with-

out associated significant bowel edema.Although the subcutaneous linea alba de-compression could prevent two potentialmorbid consequences of the open lapa-rotomy (peritonitis, fistula formation), itsdecompressive effect may not be suffi-cient in all cases. It is important to em-phasize that the previously recommendedfluid boluses to overcome the IAH-relatedorgan dysfunctions are usually inefficientand can lead to full-blown ACS (41).

Some early reports (42) described sud-den circulatory collapse in cases that de-compressed late, but in general after ab-dominal decompression, there is aprompt improvement in blood pressure,filling pressures, vascular resistance, ox-ygenation, and airway pressures. Al-though these improvements show the ef-fectiveness of decompression, they areunfortunately not necessarily associatedwith better outcomes. Survivors respondwith consistently improved cardiac out-put and urine output (34).

Prevention. Outcomes of ACS are pooreven with timely decompression becausethe maintenance of an open abdomen isalso a condition with significant morbid-ity and mortality. For this reason, pri-mary prevention is the most rational ap-proach. To date, postinjury ACS is thebest characterized form of the syndromewith statistically validated predictors(34). Primary ACS can be predicted by thedamage control physiology and manage-ment pattern (rapid transport to the op-erating room, hypothermia, acidosis, hy-potension and massive transfusion).Primary postinjury ACS is largely pre-ventable with the liberal use of open ab-domen and limiting the number of lapa-rotomy packs left in the abdominalcavity. It is important to emphasize thatACS can also develop in the open abdo-men (recurrent ACS).

Secondary ACS is always associatedwith shock and massive resuscitation, re-gardless of the etiology (trauma, sepsis,burn). Aside from the commonality of noabdominal surgery, independent predic-tors for the development of secondaryACS include: metabolic acidosis, admin-istration of �7 L of crystalloid over thefirst 6 hrs and lengthy pre-ICU diagnos-tics. The prevention of secondary ACSrelies on timely elimination of the causeof shock and avoidance of uncontrolled re-suscitation with repeated crystalloid bo-luses. The importance of understanding thequality and magnitude of fluid resuscita-tion is further emphasized by the fact thatshock resuscitation aimed at supranormaloxygen goals has been found to result inmore ACS and organ failure than resusci-tation aimed at normal oxygen deliverygoals and the use of significantly less crys-talloid infusions (43).

Skeletal muscle compartments

Etiology and risk factors. Any condi-tion that increases the content or reducesthe volume of a compartment can pro-duce a compartment syndrome (Table 3).ECS most often develops in the context ofsignificant trauma, commonly long-bonefractures; however, it may also developfrom both minor trauma and nontrau-matic causes, such as exertion (44, 45).

Fractures account for approximately75% of all ECS. Although the condition ismore frequent in closed fractures, limbswith open fractures can also developcompartment syndrome because theopen wound does not necessarily result inadequate decompression of all compart-ments (1, 46). Comminuted, displacedfractures (large area for potential bleed-ing, high energy transfer) of the proximaltibial shaft and proximal forearm (more

Table 3. Causes of extremity compartment syndrome

Increased Content of Compartment Reduced Volume of Compartment

Fracture-related swelling, bleeding Direct compression by fracture fragmentsVascular injury, bleedingHemorrhage into compartment Constriction via casts, dressings, clothing

Bleeding diathesisAnticoagulation Constriction via surgical closure of fasciaBleeding disorders

Increased vascular permeability Constrictive pressure via burns escharBurns, shockVenomous bites Obtunded/sedated patients positional pressure

EdemaPostischemic reperfusionUnusual exertion Excessive traction of fracturesDecreased serum osmolarityExtravasation of intravenous fluids

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muscle bulk and thick, nontensile fascia)are the most dangerous patterns. In thepediatric population, supracondylar hu-merus fractures are frequent causes ofexcessive swelling, but in these fracturesdirect arterial and nerve injury/compro-mise often dominate lead the clinical pic-ture. The involvement of the foot, thigh,and gluteal region is also now well rec-ognized, in particular, in multiple traumapatients (47–49).

Closed fracture reduction theoreti-cally decreases the blood loss into thecompartment and the ongoing traumati-zation of the soft tissues, but tight cir-cumferential bandages or casts can fur-ther compromise the limb. Operativefracture fixation, especially intramedul-lary reaming/nailing and prolonged tour-niquet use, may also cause increases incompartment pressures. McQueen et al(50) showed that pressures during in-tramedullary nailing of the tibia peakedduring the procedure but fell again overthe next 36 hrs. The risk of compartmentsyndrome also increases in proportion tothe length of the procedure.

Thermal injuries, in particular, full-thickness burns, cause secondary tissueconstriction, eschar, edema, and largefluid shifts associated with major burnsadding to extra volume pressure. The ob-tunded patient with prolonged limb com-pression, either during surgery or post-operative sedation, is at particular risk fordevelopment of a extremity compartmentsyndrome, which may go unnoticed. Pro-longed positioning of a limb, especially intraction or lithotomy position can alsoplace compartments at risk, in particular,if there is ongoing bleeding related toinjury (51). Victims of penetrating ex-tremity trauma can also develop a com-partment syndrome (52).

Diagnosis. The diagnosis of compart-ment syndrome depends on close atten-tion to clinical history and symptoms.Multiple studies have shown that, on itsown, clinical examination is insufficientto accurately assess compartment pres-sures and to differentiate between gener-alized swelling and a tight compartment.Compartment pressure monitoring isnow an established method of managingat-risk patients; however, there is a lackof consensus on which patients are indi-cated for monitoring and the thresholdpressures that should be used to guidefasciotomy. In terms of the role of in-creasing creatine kinase levels, myoglo-binuria, or rhabdomyolysis, these arenonspecific signs of muscle necrosis and,

thus, are late signs of untreated irrevers-ible compartment syndrome. Althoughcreatine kinase is helpful for monitoringongoing muscle necrosis, it is probablynot specific enough to diagnose ECS.

Clinical signs. The diagnosis of com-partment syndrome in alert patients re-lies on clinical suspicion. The classic 5 P’s(pain, pallor, pulselessness, paresthesias,paralysis), associated with arterial insuf-ficiency, are often mistakenly describedas signs of compartment syndrome (53).Of the five classic signs, only pain andperhaps paresthesia are associated withreversible compartment syndrome. Anynerve running through the involved com-partment will become ischemic, often re-sulting in sensory deficit in the nervedistribution. Pulselessness and paralysisare late signs and the result of extremepressures invariably associated with lossof function. The most important sign toemphasize is pain out of proportion toinjury and pain felt on passive stretchingof the muscles within the compartment.These symptoms are hard to differentiatefrom the acute fracture-related pain butcompartment syndrome pain is typicallya dull pressure (ischemic pain), whichdoes not respond to pain relief. In sum-mary, in a conscious patient, whose per-ception or response is not changed bydistracting injury, alcohol, or drugs, thediagnosis of a compartment syndrome isusually made by the clinical manifesta-tion of unrelenting ischemic pain thatfails to respond to the expected amount ofanalgesia. Later, pain may become amuch less reliable indicator of significantpressure elevation after muscle necrosishas occurred.

It is important to highlight that, al-though capillary refill may be slowed, pal-pable pulses are always present in ACS un-less there is an associated arterial injury.Pressure within the compartment (assum-ing the patient is normotensive) is unlikelyto increase sufficiently to totally obstructthe systolic pressure in the major arterytraversing the compartment (54).

Measurement. Since 1975 compart-ment pressure monitoring has been ad-vocated for early diagnosis of compart-ment syndrome (55, 56). There is,however, no consensus about the clinicalindications for monitoring compartmentpressures or about the threshold value fordiagnosis and treatment. A single normalcompartment pressure reading, whichmay be performed early in the course of

the disease, does not rule out a compart-ment syndrome; thus, serial or continu-ous measurements can be important inhigh-risk patients, especially in condi-tions where clinical examination is unre-liable. The normal pressure of a tissuecompartment falls between 0 and 8mm Hg, with symptoms and signs ofcompartment syndrome developing withpressures above approximately 20mm Hg. However, the pressure necessaryfor permanent damage varies. McQueenand Court-Brown (57) performed a pro-spective cohort study of continuous mon-itoring of the anterior compartment pres-sure in 116 diaphyseal tibia fracturepatients. Forty-three percent and 23%patients had compartment pressures of�30 mm Hg and 40 mm Hg, respectively.The authors decompressed only thosewho had a � pressure (diastolic bloodpressure � compartment pressure) of�30 mm Hg. This strategy resulted inonly three fasciotomies but prevented 50unnecessary decompressions. No patientshad missed compartment syndrome. Thisstudy highlights the need to consider thegeneral condition of the individual pa-tients and questions the need for exten-sive monitoring, especially in awake ori-ented patients.

Compartment pressures can be mea-sured with proprietary handheld devicesor with a simple ICU pressure transducerset-up connected to the bedside or oper-ating room monitor. Pressures should bemeasured in all compartments of thelimb by inserting a needle, which is con-nected to the pressure measuring device.The manometer needs to be zeroed at thelevel of the measured compartment.

Treatment. The treatment of an ECSis dermatofasciotomy (fasciotomy). Sub-cutaneous fasciotomy is not recom-mended in trauma/critical care scenarios.Fasciotomy is performed preferably in theoperating room but, in critically ill pa-tients, it should not be delayed because oflack of operating room access or a pa-tient’s general condition. Apart from itstherapeutic role, fasciotomy may also bepreventive in situations that are known tobe high risk for compartment syndrome.In this case, avoiding the procedure car-ries a higher risk than managing thecomplications of the fasciotomy itself.These scenarios include major (proximal)reimplantation, arterial repair with longischemic time, and combined arterial andvenous repair on the ipsilateral limb.

Prevention. Prehospital atraumaticsplinting and timely reduction (open or

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closed), followed by stabilization, can pre-vent compartment syndrome in low-riskinjury patterns. The avoidance of tightbandages, splints, and casts is mandatory.Some of the patients (entrapment, diffi-cult extraction, long prehospital time,and prolonged compression to the com-partments) may present with full-blowncompartment syndrome where these pre-ventive measures are no longer feasible.In high-risk situations (typical injury pat-terns, inability to reexamine the patientclinically owing to head injury or intoxi-cation), preventive fasciotomy must beconsidered. The fasciotomy woundsthemselves require planned reassessmentand gradual skin closure or skin grafting.The secondary limb compartment syn-dromes can be prevented by careful shockresuscitation (hemorrhagic, burn, andseptic) without crystalloid overload, withsimultaneous monitoring of the compart-ment pressures.

Polycompartment syndrome

More recently, the “multiple” com-partment syndrome or “poly”-compart-ment syndrome was described as a resultof a futile attempt to optimize criticaltrauma patients’ circulation with pre-load-driven resuscitation with crystalloidsolutions. The authors described a vi-cious cycle of increasing intracranialpressure, intrathoracic pressure, and IAPsecondary to fluid therapy to optimizecerebral perfusion and the aggressiveventilatory management to treat acutelung injury (58). Simultaneously, otherresearchers (59) described the potential“interactions” among different compart-ments. We believe most of these compli-cations, including the secondary ECS, areresults of the previously described “saltywater vicious cycle” of futile crystalloidloading.

CONCLUSIONS

Compartment syndromes are seriouslimb, organ, or life-threatening conditions.Clinicians need to be familiar with theiretiology and the frequently elusive presen-tation (especially secondary compartmentsyndrome) in critically ill patients. Preven-tion of compartment syndrome with pre-emptive open management of compart-ments (primary syndromes) in high-riskpatients and/or careful resuscitation (bothprimary and secondary syndromes) is therecommended approach.

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