Pressure, Perfusion, and Compartments: Challenges for the Acute Care Surgeon

AAST 2013 MASTER SURGEON LECTURE

Pressure, perfusion, and compartments: Challenges for the acute care surgeon

Rao R. Ivatury, MD, Richmond, Virginia

would like to thank President Mackersie and the American ICP and CPP.5Y7 In an analysis of 20 patients with severe brain IAssociation for the Surgery of Trauma (AAST) for this great injury with real-time monitoring of focal cerebral blood flow privilege of giving a master surgeon lecture. It is a great honor (fCBF) and pressures, seven patients died. Five had technically and a humbling experience. adequate recordings before and as death supervened. Three patients had a pressure death (CPP decreased before fCBF decreased), and two patients had a nonpressure death (fCBF DEDICATION decreased before CPP decreased). The authors concluded that Dr. William Stahl, my mentor at the Lincoln Medical & there are pathologic processes in the injured brain that do not Mental Health Center in New York, who introduced me to the directly involve increases in ICP and decreases in CPP. These intricacies of trauma and surgical critical care and shaped my authors, in a previous study, investigated the relationship between career, passed on at the end of last year. I gratefully dedicate perfusion and fCBF in 23 patients. They noted that CPP did not this lecture to his memory. have a linear relationship with fCBF over a range of 50 mm Hg to The intricate relationships of pressure and perfusion occur 150 mm Hg in patients who survived. In those who died, four of on a regular basis in the many compartments, ubiquitously found seven showed some indication of linearity. They concluded that in in the human body. The ultimate sequelae of an acute increase in a normal brain, autoregulation of cerebral blood flow pre- pressure in these rigid compartments may range from limb loss to dominates, leading to the lack of an obvious relationship between organ failures and death. The pathophysiology, however, is perfusion pressure and flow. Interestingly, the onset of a pressure- unclear, the diagnosis is uncertain, and the treatment is often flow correlation may be an early warning of this autoregulation and delayed and incomplete.1Y3 This area is of the greatest challenge a clinical deterioration. A similar concept of looking beyond ICP to the acute care surgeon as a clinician to improve the current and CPP was proposed by a Swiss group of investigators. They management principles. This is also a fertile field for game- suggested that secondary brain injury may be better managed by changing research. This review will briefly cover some aspects multimodal brain monitoring, including brain tissue oxygen of the more relevant and important compartments. (PbtO2), cerebral microdialysis, and transcranial Doppler, to op- timize cerebral blood flow and the delivery of oxygen/energy substrate.6,7 There, evidently, is much more to be discovered in the INTRACRANIAL COMPARTMENT SYNDROME pressure-perfusion tale of the injured brain. The rigid intracranial compartment and the effects of intracranial pressure (ICP) elevation are very familiar to the trauma surgeon. Simplistically, the outcomes, both short and long term, ORBITAL COMPARTMENT SYNDROME are poor when the ICP is elevated, the cerebral perfusion pres- The orbit is another closed compartment, bound anteriorly sure (CPP) is either too low or too high. In a British study of by the eyelids and orbital septum and posteriorly by the bony 429 patients with head injury, mortality was significantly higher orbital walls. ‘‘Orbital compartment syndrome’’ with the char- with ICP greater than 20 mm Hg and CPP lower than 55 mm Hg. acteristic protrusion of the eye and the limitation of lateral gaze is Interestingly, severe disability increased even with elevated CPP of greater than 95 mm Hg. There was no difference between not so well known but can have disastrous consequences in a short time because of the occlusion of central retinal artery and mean ICP and CPP in good/moderate and severe disability the resultant ischemia of optic nerve (Fig. 1). It not only can be outcome groups.4 More recent studies are questioning whether caused by retrobulbar trauma or hemorrhage but also can occur in the prognosis of traumatic brain injury is totally dependent on patients with severe burns who are receiving massive resuscitation volumes. Of 13 patients with burns greater than 25% body From the Department of Surgery, Virginia Commonwealth University, Richmond, surface area in one burn center, 5 had intraocular pressures Virginia. greater than 30 mm Hg and required lateral canthotomy for This study was presented at the 72nd annual meeting of American Association for decompression.8 Singh et al.9 reported similar results in a group the Surgery of Trauma, September 19, 2013, in San Francisco, California. United States Patent : US 7,113,814 B2; September 26, 2006 Ward KR, Barbee of 29 patients with burns. They noted a 4.4% relative risk of the RW, Terner J, Ivatury RR, Hawkridge F: Tissue Interrogation Spectroscopy. need for orbital decompression in patients receiving more than Address for reprints: Rao R. Ivatury, MD, Department of Surgery, Virginia Com- 8 mL of fluids per body surface area of burns. In such patients, monwealth University, 1200 East Broad St, Richmond, VA 23298; email: it is imperative that ocular pressure be monitored. It is important [email protected]. to note that 60 minutes to 100 minutes of elevated intraocular DOI: 10.1097/TA.0000000000000240 pressure can result in orbital nerve ischemia and permanent J Trauma Acute Care Surg Volume 76, Number 6 1341

ﬂuid administration, however, contributed to a tremendous cardiac dilatation so that the pericardium and the chest could not be closed without compressing the heart and causing hypotension. The chest incision had to be left open with a temporary closure, using an Esmarch bandage sutured to the skin edges. It was closed subsequently, after a few days of diuresis. Three other cases were reported in the literature after chest trauma.12

Figure 1. Orbital compartment syndrome from retro-orbital ABDOMINAL COMPARTMENT SYNDROME hemorrhage after trauma. Note the unilateral proptosis, limitation of downward gaze, and conjunctival edema The abdomen as a rigid compartment and the pathophysi- (reproduced with permission from C. Robert Bernardino, MD, ology of increased intra-abdominal pressure (IAP) were appreci- Review of Ophthalmology). Adaptations are themselves works ated and well described approximately 150 years ago. Soon protected by copyright. So in order to publish this adaptation, forgotten, the clinical challenges of intra-abdominal hypertension authorization must be obtained both from the owner of the (IAH) confronted us with the advent of abdominal packing, copyright in the original work and from the owner of copyright in the translation or adaptation. damage-control surgery, and large-volume resuscitation of massively injured patients. It is now clear that the established abdominal compartment syndrome (ACS) and the associated organ blindness. A bedside lateral canthotomy is indicated for high 13Y16 10 failure are a late stage of unrecognized, untreated IAH (Fig. 3). pressures. An excellent review was published in 2009. Judicious use of the open abdomen, IAP measurement, attention to end points of optimal resuscitation, and monitoring THORACIC AND MEDIASTINAL of organ function have become the mainstays in the manage- COMPARTMENT SYNDROME ment of the sickest patients having ‘‘damage-control’’ lapa- rotomy. Many lessons about the open abdomen have been This is well known after prolonged cardiac surgery, again learned in the last decade and, together with the advent of such the effects of excessive volume infusion, leading to cardiac dila- innovations as negative-pressure therapy, it is now possible to tation. The resulting reduction in cardiac output and sub- accrue all the benefits and minimize the complications of an endocardial ischemia cause further reduction in cardiac output, open abdomen approach.13Y16 and the vicious cycle continues.11 Any attempts at sternal closure Many concepts were refined by the World Society of causes a reduction of cardiac output and a drop in systolic blood Abdominal Compartment Syndrome (WSACS), a group of in- pressure. In these cases, leaving the sternum unclosed for a delayed ternational collaborators interested in the challenges of IAH closure after a few days is the recommended approach. On some and ACS. The society summarized the current knowledge in a occasions, the syndrome may manifest itself a few days after the monograph,13 developed consensus definitions, and made rec- primary sternal closure. Increasing peak airway pressures and ommendations for medical and surgical interventions.14 Al- increasing hemodynamic instability should suggest the diagnosis. though the WSACS was denigrated at times as redundant and This phenomenon is also seen after trauma. For example, a young aggrandizing, it was very effective in raising awareness of the patient who had a gunshot wound of the chest causing a tangential pathophysiology of IAH and ACS throughout the world, in all laceration of the heart with cardiac tamponade had a prompt specialties of medicine and across patients of all age groups. thoracotomy, relief of tamponade, and a suture of the laceration These initiatives did produce spectacular results. Routine IAP (Fig. 2). The resuscitation should have ended then. Overzealous monitoring and sagacious use of the open abdomen were shown

Figure 2. Thoracic compartment syndrome after a small, tangential gunshot wound of the heart (arrow). Overzealous resuscitation with crystalloids after pericardiotomy and relief of tamponade caused severe cardiac dilatation. The chest could not be closed without compromising hemodynamics. A temporary closure with Esmarch bandage was necessary.

1342 * 2014 Lippincott Williams & Wilkins

restored to a level greater than 60 mm Hg, irrespective of the level of IAH, an alternative to abdominal decompression as a therapeutic option.

EXTREMITY COMPARTMENT SYNDROME Compartment syndrome in the extremities is a particularly frequent and complex clinical entity. It can result from an increase in the contents of the many rigid compartments prevalent in the extremities. Examples include fractures, hematoma, soft tissue injury, crush syndrome, revascularization, exercise, fluid infusion, snake bite, nephrotic syndrome, myositis, and osteo- myelitis. It is also caused by a myriad of causes of reduced compartmental volume such as after burns.1Y3,20Y22 Pathophysiology Just as in other compartments, a small increase in volume Figure 3. The relationship between IAH and ACS. Intervention can have a profound effect on the intracompartmental at the stage of IAH will prevent the established ACS (reproduced pressure.1Y3,20Y23 This increase in interstitial tissue pressure, with permission from Ivatury et al.13). So in order to publish exceeding the perfusion pressure, results in a narrowed A-V this adaptation, authorization must be obtained both from gradient, capillary collapse, as well as muscle and tissue is- the owner of the copyright in the original work and from the chemia. Ischemic skeletal muscle responds by the secretion of owner of copyright in the translation or adaptation. histamine-like substances. The resultant increased vascular permeability leads to leakage of plasma, sludging of capillary to lead to improved fascial closure rates, reduced prevalence of flow, and worsening of muscle ischemia. Myocytes undergo the full-blown syndrome of ACS, and enhanced survival, while lysis; myofibrillar proteins escape into the interstitium, os- minimizing such dreaded complications as enteroatmospheric motically extract fluid, and increase the compartmental pres- fistulas.15 Furthermore, Balogh et al.16 reported that in se- sure further. Muscle ischemia worsens and perpetuates this verely injured patients, while IAH may be prevalent, ACS and vicious cycle (Fig. 5). Other scientists questioned this con- organ failures could be prevented. The prospect of eliminating cept.23 They postulate the presence of a critical closing pres- the morbid ACS is suddenly on the horizon! A more recent sure (termed the P crit), approximately 30 mm Hg, within the undertaking of WSACS, accomplished under the leadership of muscle compartments, which determines the level at which Kirkpatrick,17 is a systematic grading of all available evidence muscle blood flow decreases. This theory proposes that arte- on the subject of IAH and ACS. Along with the 2013 update of rioles require high arteriole-tissue gradient to maintain patency consensus definitions and recommendations, this is presented and conditions causing extremity compartment syndrome in a massive document on the Web. An abridged version is (ECS) cause a reduction or removal of this gradient, leading to published in Intensive Care Medicine. arteriolar collapse. Regardless of the mechanism, the effect is ischemia- induced cellular destruction and alterations in muscle cell POLYCOMPARTMENT SYNDROME It is fascinating to note that all the compartments, namely, intracranial, intrathoracic and intra-abdominal, have an interplay, in some cases leading to a polycompartment syndrome. Scalea et al.18 noted that our therapeutic efforts to increase CPP in patients with concomitant head and multisystem injury may have adverse effects on pulmonary function. This will neces- sitate efforts to improve lung function by increasing ventilator support. The result may be a further increase in IAP and ICP.In some patients, this intracranial hypertension may be resistant to all conventional interventions, until abdominal decompression is performed to reduce IAP and, secondarily, the ICP. This clinical scenario has been dubbed the polycompartment syndrome (Fig. 4). Further support for the interplay between the compartments was shown by a porcine study from Greece.19 IAH significantly reduced cerebral and spinal perfusion pressures, concomitantly increasing interleukin 6, lactate, and tu- Figure 4. Polycompartment syndrome in a patient with mor necrosis factor > in cerebrospinal fluid, suggesting the multisystem injuries with pelvic fracture and head injury. development of central nervous system ischemia. This effect Large-volume resuscitation resulted in compartment syndromes was transient and reversible when perfusion pressures were in the head, chest, abdomen, and the extremities.

* 2014 Lippincott Williams & Wilkins 1343

bedside by several techniques, including the Stryker Quick Pressure Monitor Instrument, manometric IV pump method, and the slit catheter technique. The Stryker instrument has the advantage of simplicity. Normal resting CP is approximately 8 mm Hg in adults and slightly higher (13Y16 mm Hg) in children. CP varies by location both within normal compartments and in the injured limb and with distance from the site of fracture, reasons for measuring at multiple sites within multiple compartments.32Y35

Spectroscopy Other useful diagnostic techniques for the determination of ECS include methods to detect its sequelae of tissue ischemia.36 Near-infrared spectroscopy (NIRS) is a technique to determine tissue oxygen tension by a bedside monitor both noninvasively Figure 5. Pathophysiology of ECS. and continuously.37 An inverse correlation between CP and oxygenation and a correlation between perfusion pressure Y membrane, leading to the release of myoglobin into the cir- and oxygenation were demonstrated in an animal model.38 42 culation. This rhabdomyolysis results in renal injury.21,22,24 A human model of compartment syndrome showed that both The pathophysiology of ECS following vascular occlusion tissue oxygenation and CP significantly correlated with a de- may differ slightly. Ischemia-reperfusion injury plays a dom- crease in deep peroneal conduction, cutaneous peroneal sensi- inant role. We will return to this later in the discussion of the tivity, and pain.40 NIRS was shown to be at least as good as CP role (or absence of it) of fasciotomy in vascular occlusion. monitoring for detecting developing ECS. Giannotti et al.39 published a series of case reports on patients who underwent Prevalence fasciotomy, who showed that tissue oxygenation levels in pa- Tibial fracture accounts for approximately 10% of all tients with compartment syndrome were significantly lower than cases of ECS and seems to be more common in open a matched control group with lower extremity injuries and no fractures.1Y3,22 Vascular injury is the other frequent area. compartment syndrome. The measured tissue perfusion of the Feliciano et al.25 reported that 19% of patients with vascular compartment syndrome group was also significantly lower than injury required fasciotomy for ECS. Secondary ECS describes postfasciotomy values. the syndrome developing without significant injury to the Multiple case reports have been published detailing the use of NIRS as an adjunct for continuous monitoring of lower extremity itself and is an iatrogenic phenomenon occurring in 41,42 42 massively injured patients receiving large-volume resuscitation extremity perfusion. Shuler et al. published a series of (Fig. 6). In the first series from Grady reported by Tremblay patients who underwent fasciotomies based on ICP monitor- et al.,26 10 of 11,996 patients and a mean of 3.1 extremities ing with simultaneous NIRS monitoring. All compartments developed this complication in 10 upper and 12 lower extremi- showed decreasing tissue oxygenation with decreasing perfu- ties. Mortality in the group was 70%. In their follow-up series,27 sion pressure. NIRS has also been used to characterize changes these authors presented a similar group of very severely injured in perfusion following tibial fracture in patients without com- patients who received massive resuscitation but who were partment syndrome, as compared with subjects’ contralateral carefully monitored for compartment syndrome. The incidence extremity and uninjured extremities in other controls. Of note, of renal failure and death was reduced but was still substantial a lack of posttraumatic hyperemia (15% increase in tissue at 35%. Of the 46 extremities with ECS, 7 required amputation.

Diagnosis The familiar cardinal p’s of ECS, namely, pallor, pulselessness, paraesthesia, pressure, poikilothermia, and pa- ralysis are more speciﬁc than sensitive.1Y3,20Y22,28Y31 They are poor indicators of the syndrome, unless there are multiple symptoms present, especially in the appropriate clinical setting. Laboratory tests are often unhelpful. However, the relevant tests for rhabdomyolysis (Creatine phosphokinase levels, renal function, urine myoglobin levels, and urinalysis) may raise suspicion for ECS. Conventional radiographs, computed to- mographic scans, and magnetic resonance imaging studies may be indicated in selected patients with compartment syndrome of the pelvis, thigh, and so on. Figure 6. Delayed diagnosis and fasciotomy in a patient with Compartment pressure (CP) monitoring is the most secondary ECS. Note the necrotic muscle in the swollen useful test for diagnosis.28,29,32,33 This can be performed compartment.

1344 * 2014 Lippincott Williams & Wilkins

Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. J Trauma Acute Care Surg Volume 76, Number 6 Ivatury oxygenation seen in injured extremities) was felt to actually important. Matsen and Krugmire20 suggest 2 hours to 4 hours represent a compartment syndrome even if oxygenation in the of ischemia as causing functional impairment of muscles, injured leg is equivalent to that in the uninjured extremity.41 which becomes irreversible after 4 hours to 12 hours. For nerve Tissue oxygenation, as determined by NIRS, may help tissue, these critical times are 30 minutes to 45 minutes and avoid fasciotomy. In a study of patients with clinical signs of 12 hours to 24 hours. compartment syndrome after revascularization surgery for There are high-risk groups of patients and high-risk situ- lower limb ischemia, Arato´ et al.43 reported that measurement ations when critical muscle ischemia either goes undetected or of compartmental pressure and NIRS-measured tissue oxy- occurs very early. Tissue that has been previously subjected to genation could be used to determine whether fasciotomy was intervals of ischemia, patients under general anesthesia, sedated, needed. Patients with pressure less than 40 mm Hg and normal or obtunded, and those receiving postoperative epidurals after tissue oxygen saturation were treated conservatively. tibial fracture fixation are especially susceptible to an insidious Recently, resonance Raman spectroscopy, using excita- onset of critical ECS.2,3 tion by a Krypton ion laser, was tested in our institution in The importance of timeliness of fasciotomy in vascular animal models of hemorrhagic shock and resuscitation.44 injuries was investigated by Farber et al.,47 analyzing National Raman spectroscopyYderived sublingual oxygen tension Trauma Data Bank data of 612 patients who underwent (Smo2) was calculated as the ratio of the oxygenated heme fasciotomies, 543 early and 69 late (before 8 hours and after spectral peak height to the sum of the oxyhemoglobin and 8 hours of vascular repair). Patients in the early fasciotomy deoxyhemoglobin spectral peak heights. Measurements were group had lower amputation rate and shorter total hospital stay compared with central venous oxygen tension (Scvo2) as well compared with those in the late fasciotomy group. On multi- as with other indicators of oxygenation. Smo2 was significantly variable analysis, early fasciotomy was associated with a (p G 0.0001) correlated with Scvo2 (r = 0.80), lactate fourfold lower risk of amputation and 23% shorter hospital (r = j0.78), base excess (r = 0.80), and shed blood volume stay. The role of fasciotomy in crush injuries of extremities (r = j0.75). The technique was thought to show promise as a was emphasized by two recent articles from the Middle East method to noninvasively monitor tissue oxygenation. In a wars. In the first series,48 a total of 336 patients underwent subsequent study,45 the ability of resonance Raman spectros- 643 fasciotomies. The majority were to the lower leg (49%) and copy to monitor tissue hemoglobin oxygenation (RRS-StO2) forearm (23%). Patients who underwent a fasciotomy revision during hemorrhage was studied and compared with conven- had higher rates of muscle excision and mortality compared tional invasive mixed venous (SmvO2) and central venous with those who did not receive a revision. Patients who (ScvO2) hemoglobin oxygen saturation and NIRS tissue he- underwent fasciotomy after evacuation had higher rates of moglobin oxygenation (NIRS-StO2). The following receiver muscle excision (25% vs. 11%), amputation (31% vs. 15%), operating characteristic areas under the curve were obtained: and mortality (19% vs. 5%) compared with patients who re- SmvO2 (1.0), ScvO2 (0.994), RRS-StO2 (0.972), and NIRS- ceived their fasciotomies in the combat theater, suggesting that StO2 (0.611). RRS-StO2 seemed to have significantly better revisions and delayed fasciotomies result in increased com- ability to predict shock based on elevated lactate levels when plications and mortality. The army, of course, went into a compared with NIRS-StO2. Future investigations should focus correction mode and did an education program designed to on the ability of RRC-StO2 to diagnose critical muscle is- improve surgeon knowledge. Subsequent analysis49 showed chemia from evolving ECS. Continuous monitoring of StO2 that this resulted in higher fasciotomy rates, reduced revisions, and CP with careful serial clinical examination in high-risk and improved survival. clinical situations must be studied in the future to allow early In the civilian setting, conditions obviously are much diagnosis of ECS. more favorable than the battlefield, and timely fasciotomy may be expected to be the rule rather than the exception. Several series, however, document the opposite. Feliciano et al.25 Timely Fasciotomy reported in 1988 on 125 fasciotomies (25 upper and 100 lower). Unfortunately, none of these methods tell us (yet) what Nineteen percent of lower extremity fasciotomies for vascular the critical CP is, which requires compartmental decompres- injuries were not performed at the primary operation, and 75% sion, while all agree that early diagnosis for a prompt of amputations were from delayed or incomplete fasciotomies. fasciotomy is important. The indication for fasciotomy was In a review of 81 popliteal artery injuries (39 arterial and also an area clouded with lack of clarity. Some investigators 42 combined), Fainzilber et al.50 performed primary fasciotomy recommend the so-called Delta P (diastolic blood pressure j on 53% of their patients. Of the 35 patients who did not have a compartmental pressure) with a critical range of 10 mm Hg to primary fasciotomy, 6 required an amputation. In a retrospective 30 mm Hg.33Y35 Others use an absolute threshold of 30 mm Hg. review, Abouezzi et al.51 noted two amputations for extensive Mubarak and Hargens46 argue for the consideration of the total popliteal vascular injury despite primary fasciotomy. One am- clinical picture: they recommend fasciotomy in patients who putation was the result of a delayed fasciotomy and failure of are normotensive with positive clinical findings and CP greater vascular repair. The overall amputation rate for popliteal injuries than 30 mm Hg, when the duration of increased pressure is was 9%. They also observed that four of nine patients who had unknown or thought to be longer than 8 hours, in those who are neurologic deficit in the extremity also had failure of vascular uncooperative or unconscious with a CP greater than 30 mm repair and delayed fasciotomy. Another multicenter civilian se- Hg, and those with low blood pressure and a CP greater than ries from Canada52 documented significant delays in diagnosis 20 mm Hg. The timeliness of fasciotomy obviously is terribly and treatment in both traumatic and nontraumatic cases of ECS.

* 2014 Lippincott Williams & Wilkins 1345

A decade later, a report53 from, arguably, the most distin- distinguished Blaisdell,56 AAST past president, who was guished trauma center in the country identified 83 cases of com- called the father of modern trauma care: ‘‘The question is, partment syndrome over 7 years. Six percent had amputations, and what factor is responsible for the increased compartmental 8% died, after predominantly orthopedic injuries. Eight percent pressure?Whentherehasbeentraumatoacompartmentand had considerable morbidity from repeated debridement of dead the cause of increased compartment pressure is hemorrhage muscle due to delayed fasciotomy. Of note, none had pressure either into muscle or into a compartmental space, then few monitoring. Another 7% had iatrogenic transection of superfi- could argue the rationale for fasciotomy. When a limb has cial peroneal nerve during the performance of fasciotomy. The been revascularized after many hours of ischemia, the reason authors concluded that compartment syndrome remained a sig- for the swelling is not quite so clearI I contend that we still nificant diagnostic and management challenge with great mor- do not have a clear understanding of the reason for the high bidity in terms of limb loss and neurologic outcome. They compartment pressures nor do we have the precise point at proposed a key pathway with a multidisciplinary approach for which fasciotomy will be more beneficial than harmful.’’ In a optimal outcome in these patients. Figure 7 is based on their more recent communication elucidating the pathophysiology recommendation. of skeletal muscle ischemia and reperfusion, Blaisdell57 ex- Such honest reports of suboptimal therapy of ECS, pounds on the relative merits of fasciotomy versus anti- presented from distinguished institutions without adornment coagulation in the ischemic extremity. ‘‘Only in this region will or embellishment, are not frequent in the surgical literature. therapy be of any benefit, whether fasciotomy to prevent pres- An accurate estimation of avoidable amputations and dys- sure occlusion of the microcirculation, or anticoagulation to functional limbs may, hence, be an unattainable goal. Personal prevent further microvascular thrombosisI In instances in experience and privileged communications from around the which the process involves the bulk of the lower extremity, country, however, substantiate delays in fasciotomy and the amputation rather than attempts at revascularization may be the tragedy of limb amputations and organ failures in both or- most prudent course to prevent the toxic product in the ischemic thopedic and vascular cases. limb from entering the systemic circulation.’’ For vascular injuries in high-risk patients (those with Despite these hazy areas, many other issues have clarity. prolonged ischemia time, significant preoperative hypotension, At a critical pressure, perfusion goes down. This happens at associated crush injury, combined arterial and venous injury, or much lower pressures and to a greater extent by previous shock the need for a major venous ligation in the lower limb), an early and resuscitation. A vicious cycle of ischemia and end-organ fasciotomy is recommended before arterial exploration.54 The damage is set in motion to culminate in ECS. We do not role of fasciotomy in cases of ECS caused by vascular occlu- have a reliable test to diagnose ECS: clinical signs are late, and sion is even less clear.55Y57 If ECS is diagnosed late, fasciotomy compartmental pressures and muscle oxygenation are useful is of no benefit. In fact, fasciotomy probably is contraindicated but not specific. The result is a delayed diagnosis and treat- after the third or fourth day following the onset of the syn- ment of ECS. Inevitably, the outcomes are poor, including drome. When fasciotomy is performed late, severe infection neurodeficits, muscle necrosis, organ failures, death, and am- usually develops in the necrotic muscle. However, if the ne- putations. Limb loss comes at a great cost to the unfortunate crotic muscle is left alone and the compartment is not opened, it patient. The projected lifetime health care cost for the patients can heal with scar tissue. This may result in a more functional who had undergone amputation had been noted to be three extremity with fewer complications.55 times higher than when treated with reconstruction ($509,275 This notion of delayed fasciotomy causing more harm and $163,282, respectively).58 than good was supported by this 1989 editorial from the The goal of the acute care surgeon, therefore, should be first to prevent ECS by avoiding secondary syndromes. Ag- gressive crystalloid overloading or ‘‘fluid-creep’’59 should be avoided, since that seems to be the common denominator for many compartment syndromes. The next goal should be to pursue methods to diagnose compartment syndrome at its onset, so that compartmental decompression can be timely and reap the maximum benefit. Fasciotomy must be technically exquisite with long incisions and decompression of all four compartments in the leg. Iatrogenic nerve injury must be avoided. It is perhaps time to borrow the graph (Fig. 3) from the story of ACS: define and emphasize the stage of compartmental hypertension, and pursue its diagnosis and treatment (Fig. 8) to eliminate progression of pathology to the established ECS and Figure 7. Suggested Practice Management Guidelines for ECS. the potential for the loss of limbs, organs, and life. CS, compartment syndrome; PE, physical examination; GCS, In summary, the field of pressure, perfusion, and com- Glasgow Coma Scale score; CP, compartmental pressure; StO2, muscle tissue oxygen saturation. Modified from Kashuk et al.53 partments has many gaps in knowledge. The current state of So in order to publish this adaptation, authorization must our management is tentative, with huge implications for patient be obtained both from the owner of the copyright in the safety. It is time to accept our imperfection, rise to the chal- original work and from the owner of copyright in the translation lenge, and generate innovative concepts in basic as well as or adaptation. clinical research. The acute care surgeon should intervene

1346 * 2014 Lippincott Williams & Wilkins

14. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Z, Leppa¨niemi A, Olvera C, Ivatury R, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med. 2006;32(11):1722Y1732. 15. Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med. 2010;38(2):402Y407. 16. Balogh ZJ, Martin A, van Wessem KP, King KL, Mackay P, Havill K. Mission to eliminate post injury abdominal compartment syndrome. Arch Surg. 2011;146(8):938Y943 17. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, Duchesne J, Bjorck M, Leppaniemi A, Ejike JC, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39(7):1190Y1206. 18. Scalea TM, Bochicchio GV,Habashi N, McCunn M, Shih D, McQuillan K, Figure 8. Suggested graph for the prevention of ECS by an Aarabi B. Increased intra-abdominal, intrathoracic, and intracranial pres- intervention at the stage of compartmental hypertension. sure after severe brain injury: multiplecompartment syndrome. J Trauma. 2007;62(3):647Y656. 19. Marinis JA, Argyra E, Lykoudis P,Brestas P,Theodoraki K, Polymeneas G, timely and competently in compartment syndromes, paying Boviatsis E, Voros D. Ischemia as a possible effect of increased intra- attention and worrying constantly about the diagnosis. abdominal pressure on central nervous system cytokines, lactate and perfusion pressures. Crit Care. 2010;14:R31. DISCLOSURE 20. Matsen FR, Krugmire RB. Compartmental syndromes. Surg Gynecol Y The author declares no conflict of interest. Obstet. 1978;147:943 949. 21. Shadgan B, Menon M, Sanders D, Berry G, Martin C Jr, Duffy P, Stephen D, O’Brien PJ. Current thinking about acute compartment syndrome of the Y REFERENCES lower extremity. Can J Surg. 2010;53(5):329 334. 22. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syn- 1. Balogh Z, Butcher NE. Compartment syndromes from head to toe. Crit drome. Who is at risk? J Bone Joint Surg Br. 2000;82(2):200Y203. Care Med. 2010;38(Suppl):S445YS451. 23. Shrier I, Magder S. Pressure-flow relationships in in vitro model of 2. Taylor RM, Sullivan MP, Mehta S. Acute compartment syndrome: Y obtaining diagnosis, providing treatment, and minimizing medicolegal compartment syndrome. Appl Physiol (1985). 1995;79(1):214 221. risk. Curr Rev Musculoskelet Med. 2012;5(3):206Y213. 24. Wall CJ, Lynch J, Harris IA, Richardson MD, Brand C, Lowe AJ, Sugrue 3. Mabvuure NT, Malahias M, Hindocha S, Khan W, Juma A. Acute com- M. Clinical practice guidelines for the management of acute limb com- Y partment syndrome of the limbs: current concepts and management. Open partment syndrome following trauma. ANZ J Surg. 2010;80(3):151 156. Orthop J. 2012;6:535Y543. 25. Feliciano DV,Cruse PA,Spjut-Patrinely V,Burch JM, Mattox KL. Fasciotomy 4. Balestreri M, Czosnyka M, Hutchinson P,Steiner LA, Hiler M, Smielewski after trauma to the extremities. Am J Surg. 1988;156(6):533Y536. P, Pickard JD. Impact of intracranial pressure and cerebral perfusion 26. Tremblay LN, Feliciano DV, Rozycki GS. Secondary extremity compart- pressure on severe disability and mortality after head injury. Neurocrit ment syndrome. J Trauma. 2002;53(5):833Y837. Care. 2006;4(1):8Y13. 27. Goaley TJ Jr, Wyrzykowski AD, MacLeod JB, Wise KB, Dente CJ, 5. Chovanes G, Richards RM. Pressure is only part of the story in traumatic Salomone JP,Nicholas JM, Vercruysse GA, Ingram WL, Rozycki GS, et al. brain injured patients; focal cerebral blood flow goes to zero in some Can secondary extremity compartment syndrome be diagnosed earlier? Am patients with adequate cerebral perfusion pressure. Surg Neurol Int. J Surg. 2007;194(6):724Y726. 2012;3:12. 28. Shadgan B, Menon M, O’Brien PJ, Reid WD. Diagnostic techniques in acute 6. Chovanes GI, Richards RM. The predominance of metabolic regulation of compartment syndrome of the leg. JOrthopTrauma. 2008;22(8):581Y587. cerebral blood flow and the lack of ‘‘Classic’’ autoregulation curves in the 29. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. Y viable brain. J Emerg Med. 2013;44(5):1039 1044. J Bone Joint Surg Br. 2003;85(5):625Y632. 7. Jan Bouzat P, Sala N, Payen JF, Oddo M. Beyond intracranial pressure: 30. Shuler FD, Dietz MJ. Physicians’ ability to manually detect isolated ele- optimization of cerebral blood flow, oxygen, and substrate delivery after vations in leg intracompartmental pressure. J Bone Joint Surg Am. 2010; traumatic brain injury. Ann Intensive Care. 2013 Jul 10;3(1):23. 92(2):361Y367. 8. Sullivan SR, Ahmadi AJ, Singh CN, Sires BS, Engrav LH, Gibran NS, 31. Ulmer T. The clinical diagnosis of compartment syndrome of the lower Heimbach DM, Klein MB. Elevated orbital pressure: another untoward effect of massive resuscitation after burn injury. J Trauma. 2006;60:72Y76. leg: are clinical findings predictive of the disorder? JOrthopTrauma. 2002; 16(8):572Y577. 9. Singh CN, Klein MB, Sullivan SR, Sires BS, Hutter CM, Rice K, Jian- Amadi A. Orbital compartment syndrome in burn patients. Ophthal Plast 32. Mubarak SJ, Hargens AR, Owen CA, Garetto LP, Akeson WH. The wick Reconstr Surg. 2008;24(2):102Y106. catheter technique for measurement of intramuscular pressure. A new Y 10. Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D. research and clinical tool. J Bone Joint Surg Am. 1976;58(7):1016 1020. Orbital compartment syndrome: the ophthalmic surgical emergency. Surv 33. Whitesides TE, Haney TC, Morimoto K, Harada H. Tissue pressure Ophthalmol. 2009;54(4):441Y449. measurements as a determinant for the need of fasciotomy. Clin Orthop 11. Riahi M, Tomatis LA, Schlosser RJ, Bertolozzi E, Johnston DW. Cardiac Relat Res. 1975;113:43Y51. compression due to closure of the median sternotomy in open heart sur- 34. McQueen MM, Court-Brown CM. Compartment monitoring in tibial gery. Chest. 1975;67(1):113Y114. fractures. The pressure threshold for decompression. J Bone Joint Surg Br. 12. Kaplan LJ, Trooskin SZ, Santora TA. Thoracic compartment syndrome. 1996;78(1):99Y104. J Trauma. 1996;40(2):291Y293. 35. Nelson JA. Compartment pressure measurements have poor specificity for 13. Ivatury R, Cheatham M, Malbrain M, Sugrue M eds. Abdominal Com- compartment syndrome in the traumatized limb. J Emerg Med. 2013;44 partment Syndrome. Georgetown: Landes Bioscience; 2006. (5):1039Y1044.

* 2014 Lippincott Williams & Wilkins 1347

36. Bariteau JT, Beutel BG, Kamal R, Hayda R, Born C. The use of near- vascular injury is associated with decreased risk of adverse limb outcomes: a infrared spectrometry for the diagnosis of lower-extremity compartment review of the National Trauma Data Bank. Injury. 2012;43(9):1486Y1491. syndrome. Orthopedics. 2011 Mar 11;34(3):178. 48. Ritenour AE, Dorlac WC, Fang R, Woods T, Jenkins DH, Flaherty SF, 37. Arbabi S, Brundate SI, Gentilello LM. Near-infrared spectroscopy: a po- Wade CE, Holcomb JB. Complications after fasciotomy revision and delayed tential method for continuous, transcutaneous monitoring for compartmental compartment release in combat patients. JTrauma. 2008;64(Suppl 2): syndrome in critically injured patients. J Trauma. 1999;47:829Y833. S153YS161. 38. Mancini DM, La Manca J, Donchez L, Henson D, Levine S. Validation of 49. Kragh JF Jr, San Antonio J, Simmons JW, Mace JE, Stinner DJ, White CE, near-infrared spectroscopy in humans. JApplPhysiol. 1994;77:2740Y2747. Fang R, Aden JK, Hsu JR, Eastridge BJ, et al. Compartment syndrome 39. Giannotti G, Cohn SM, Brown M, et al. Utility of near-infrared spec- performance improvement project is associated with increased combat troscopy in the diagnosis of lower extremity compartment syndrome. J casualty survival. J Trauma Acute Care Surg. 2013;74(1):259Y263. Trauma. 2000;48:396Y399. 50. Fainzilber T, Roy-Shapira G, Wall MJ Jr, Mattox KL. Predictors of am- 40. Gentilello LM, Sanzone A, Wang L, Liu PY, Robinson L. Near-infrared putation for popliteal artery injuries. Am J Surg. 1995;170:568Y571. spectroscopy versus compartment pressure for the diagnosis of lower 51. Abouezzi Z, Nassoura Z, Ivatury RR, Porter JM, Stahl WM. A critical extremity compartmental syndrome using electromyography-determined reappraisal of indications for fasciotomy after extremity vascular trauma. measurements of neuromuscular function. J Trauma. 2001;51:1Y8. Arch Surg. 1998;133(5):547Y5515. 41. Shuler MS, Reisman WM, Whitesides TE, et al. Near-infrared spectroscopy 52. Vaillancourt C, Shrier I, Falk M, Rossignol M, Vernec A, Somogyi D. in lower extremity trauma. J Bone Joint Surg Am. 2009;91:1360Y1368. Quantifying delays in the recognition and management of acute com- 42. Shuler MS, Reisman WM, Kinsey TL, Whitesides TE Jr, Hammerberg partment syndrome. CJEM. 2001;3:26Y30. EM, Davila MG, Moore TJ. Correlation between muscle oxygenation and 53. Kashuk JL, Moore EE, Pinski S, Johnson JL, Moore JB, Morgan S, compartment pressures in acute compartment syndrome of the leg. J Bone Cothren CC, Smith W. Lower extremity compartment syndrome in the Joint Surg Am. 2010;92:863Y870. acute care surgery paradigm: safety lessons learned. Patient Saf Surg. 43. Arato´ E, Ku¨rthy M, Sı´nay L, Kasza G, Menyhei G, Masoud S, Bertalan A, 2009;3(1):11. Verza´r Z, Kolla´r L, Roth E, et al. Pathology and diagnostic options of lower 54. Percival TJ, White JM, Ricci MA. Compartment syndrome in the setting of limb compartment syndrome. Clin Hemorheol Microcirc. 2009;41(1):1Y8. vascular injury. Perspect Vasc Surg Endovasc Ther. 2011;23(2):119Y124. 44. Ward KR, Torres Filho I, Barbee RW, Torres L, Tiba MH, Reynolds PS, 55. Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome: Pittman RN, Ivatury RR, Terner J. Resonance Raman spectroscopy: a new course after delayed fasciotomy. J Trauma. 1996;40(3):342Y344. technology for tissue oxygenation monitoring. Crit Care Med. 2006;34(3): 56. Blaisdell FW. Is there a reason for controversy regarding fasciotomy? 792Y799. J Vasc Surg. 1989;9(6):828. 45. Tiba MH, Draucker GT, Barbee RW, Terner J, Filho IT, Romfh P, 57. Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the Vakhshoori D, Ward KR. Tissue oxygenation monitoring using resonance reperfusion syndrome: a review. Cardiovasc Surg. 2002;10:620Y630. Raman spectroscopy during hemorrhage. J Trauma Acute Care Surg. 58. MacKenzie EJ, Jones AS, Bosse MJ, Castillo RC, Pollak AN, Webb LX, 2014;76(2):402Y408. Swiontkowski MF, Kellam JF, Smith DG, Sanders RW, et al. Health-care 46. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin costs associated with amputation or reconstruction of a limb-threatening North Am. 1983;63(3):539Y565. injury. J Bone Joint Surg Am. 2007;89(8):1685Y1692. 47. Farber A, Tan TW, Hamburg NM, Kalish JA, Joglar F, Onigman T, Rybin 59. Pruitt BA Jr. Protection from excessive resuscitation: ‘‘pushing the pen- D, Doros G, Eberhardt RT. Early fasciotomy in patients with extremity dulum back’’. J Trauma. 2000;49:567Y568.

1348 * 2014 Lippincott Williams & Wilkins