Kompartemen sindrom

PENDAHULUAN Sindroma kompartemen adalah suatu kondisi dimana terjadi peningkatan tekanan intertisial di dalam ruangan yang terbatas, yaitu di dalam kompartemen osteofasial yang tertutup. Ruangan tersebut berisi otot, saraf dan pembuluh darah. Ketika tekanan intrakompartemen meningkat, perfusi darah ke jaringan akan berkurang dan otot di dalam kompartemen akan menjadi iskemik. Tanda klinis yang umum adalah nyeri, parestesia, paresis, disertai denyut nadi yang hilang. (1,2,3) Sindroma kompartemen dapat diklasifikasikan menjadi akut dan kronik, tergantung dari penyebab peningkatan tekanan kompartemen dan lamanya gejala. Penyebab umum terjadinya sindroma kompartemen akut adalah fraktur, trauma jaringan lunak, kerusakan arteri, dan luka bakar. Sedangkan sindroma kompartemen kronik dapat disebabkan oleh aktivitas yang berulang misalnya lari. (1) INSIDEN Di Amerika, ekstremitas bawah distal anterior adalah yang paling banyak dipelajari untuk sindroma kompartemen. Dianggap sebagai yang kedua paling sering untuk trauma sekitar 212%. Dari penelitian McQueen (2000), sindroma kompartemen lebih sering didiagnosa pada pria daripada wanita, tapi hal ini memiliki bias, dimana pria lebih sering mengalami luka trauma. McQueen memeriksa 164 pasien yang didiagnosis sindroma kompartemen, 69% berhubungan dengan fraktur dan sebagian adalah fraktur tibia. Menurut Qvarfordt, sekelompok pasien dengan nyeri kaki, 14% pasien dengan sindroma kompartemen anterior. Sindroma kompartemen ditemukan 1-9% fraktur pada kaki. (4,5) ANATOMI Fascia memisahkan serabut otot dalam satu kelompok. Kompartemen adalah merupakan daerah tertutup yang dibatasi oleh tulang, interosseus membran dan fascia yang melibatkan jaringan otot, saraf dan pembuluh darah. (6) Pada regio brachium, kompartemen dibagi menjadi 2 bagian yaitu : (9,10) 1. Kompartemen volar : otot flexor pergelangan tangan dan jari tangan, nervus ulnar dan nervus median. 2. Kompartemen dorsal : otot ekstensor pergelangan tangan dan jari tangan, nervus interosseous posterior. Pada regio antebrachium, kompartemen dibagi menjadi 3 bagian yaitu : (9,10) 1. Kompartemen volar : otot flexor pergelangan tangan dan jari tangan, nervus ulnar dan nervus median. 2. Kompartemen dorsal : otot ekstensor pergelangan tangan dan jari tangan, nervus interosseous posterior. 3. Mobile wad : otot ekstensor carpi radialis longus, otot ekstensor carpi radialis brevis, otot brachioradialis. Pada regio wrist joint, kompartemen dibagi menjadi 6 bagian yaitu : (9,10) 1. Kompartemen I : otot abduktor pollicis longus dan otot ekstensor pollicis brevis. 2. Kompartemen II : otot ekstensor carpi radialis brevis, otot ekstensor carpi radialis longus. 3. Kompartemen III : otot ekstensor pollicis longus. 4. Kompartemen IV : otot ekstensor digitorum communis, otot ekstensor indicis. 5. Kompartemen V : otot ekstensor digiti minimi. 6. Kompartemen VI : otot ekstensor carpi ulnaris. Pada regio cruris, kompartemen dibagi menjadi 4 bagian yaitu : (9,10) 1. Kompartemen anterior : otot tibialis anterior dan ekstensor ibu jari kaki, nervus peroneal profunda. 2. Kompartemen lateral : otot peroneus longus dan brevis, nervus peroneal superfisial. 3. Kompartemen posterior superfisial : otot gastrocnemius dan soleus, nervus sural.

4. Kompartemen posterior profunda : otot tibialis posterior dan flexor ibu jari kaki, nervus tibia. ETIOLOGI Penyebab terjadinya sindroma kompartemen adalah tekanan di dalam kompartemen yang terlalu tinggi, lebih dari 30 mmHg. Adapun penyebab terjadinya peningkatan tekanan intrakompartemen adalah peningkatan volume cairan dalam kompartemen atau penurunan volume kompartemen. (9) Peningkatan volume cairan dalam kompartemen dapat disebabkan oleh : (9) Peningkatan permeabilitas kapiler, akibat syok, luka bakar, trauma langsung. Peningkatan tekanan kapiler, akibat latihan atau adanya obstruksi vena. Hipertrofi otot. Pendarahan. Infus yang infiltrasi. Penurunan volume kompartemen dapat disebabkan oleh : (9) Balutan yang terlalu ketat. PATOGENESIS Perkembangan sindroma kompartemen tergantung tidak hanya pada tekanan intrakompartemen tapi juga tekanan sistemik darah. Patofisiologi sindroma kompartemen melibatkan hemostasis jaringan lokal normal yang menyebabkan peningkatan tekanan jaringan, penurunan aliran darah kapiler dan nekrosis jaringan lokal akibat hipoksia. (1) Ketika tekanan dalam kompartemen melebihi tekanan darah dalam kapiler dan menyebabkan kapiler kolaps, nutrisi tidak dapat mengalir keluar ke sel-sel dan hasil metabolisme tidak dapat dikeluarkan. Hanya dalam beberapa jam, sel-sel yang tidak memperoleh makanan akan mengalami kerusakan. Pertama-tama sel akan mengalami pembengkakan, kemudian sel akan berhenti melepaskan zat-zat kimia sehingga menyebabkan terjadi pembengkakan lebih lanjut. Pembengkakan yang terus bertambah menyebabkan tekanan meningkat. (12,13) Aliran darah yang melewati kapiler akan berhenti. Dalam keadaan ini penghantaran oksigen juga akan terhenti. Terjadinya hipoksia menyebabkan sel-sel akan melepaskan substansi vasoaktif (misal : histamin, serotonin) yang meningkatkan permeabilitas endotel. Dalam kapiler-kapiler terjadi kehilangan cairan sehingga terjadi peningkatan tekanan jaringan dan memperberat kerusakan disekitar jaringan dan jaringan otot mengalami nekrosis. (5) DIAGNOSIS Sindroma kompartemen dapat didiagnosis berdasarkan pengetahuan tentang faktor resiko, keluhan subjektif dan adanya suatu tanda-tanda fisik dan gejala klinis. Adapun faktor resiko pada sindroma kompartemen meliputi fraktur yang berat dan trauma pada jaringan lunak, penggunaan bebat. (15,16) Gejala klinis yang umum ditemukan pada sindroma kompartemen meliputi 5 P, yaitu : (17) 1. Pain (nyeri) : nyeri pada jari tangan atau jari kaki pada saat peregangan pasif pada otot-otot yang terkena, ketika ada trauma langsung. 2. Pallor (pucat) : kulit terasa dingin jika di palpasi, warna kulit biasanya pucat, abu-abu atau keputihan. 3. Parestesia : biasanya memberikan gejala rasa panas dan gatal pada daerah lesi. 4. Paralisis : biasanya diawali dengan ketidakmampuan untuk menggerakkan sendi, merupakan tanda yang lambat diketahui. 5. Pulselesness (berkurang atau hilangnya denyut nadi) : akibat adanya gangguan perfusi arterial. Pengukuran tekanan kompartemen adalah salah satu tambahan dalam membantu menegakkan diagnosis. Biasanya pengukuran tekanan kompartemen dilakukan pada pasien dengan penurunan kesadaran yang dari pemeriksaan fisik tidak memberi hasil yang memuaskan. Pengukuran tekanan kompartemen dapat dilakukan dengan menggunakan

teknik injeksi atau wick kateter. (15,16) Prosedur pengukuran tekanan kompartemen, antara lain : (19) a. Teknik injeksi. Jarum ukuran 18 dihubungkan dengan spoit 20 cc melalui saluran salin dan udara. Saluran ini kemudian dihubungkan dengan manometer air raksa standar. Setelah jarum disuntikkan ke dalam kompartemen, tekanan udara dalam spoit akan meningkat sehingga meniskus salinudara tampak bergerak. Kemudian tekanan dalam kompartemen dapat dibaca pada manometer air raksa. b. Teknik Wick kateter. Wick kateter dan sarung plastiknya dihubungkan ke transducer dan recorder. Kateter dan tabungnya diisi oleh three-way yang dihubungkan dengan transducer. Sangat perlu untuk memastikan bahwa tidak ada gelembung udara dalam sistem tersebut karena memberi hasil yang rendah atau mengaburkan pengukuran. Ujung kateter harus dapat menghentikan suatu meniskus air sehingga dapat dipastikan dan diketahui bahwa dalam jaringan tersebut dilewati suatu trocar besar, kemudian jarumnya ditarik dan kateter dibalut ke kulit. TERAPI Penanganan sindroma kompartemen meliputi : 1. Terapi medikal / non bedah. (11) Menempatkan kaki setinggi jantung, untuk mempertahankan ketinggian kompartemen yang minimal, elevasi dihindari karena dapat menurunkan aliran darah dan akan lebih memperberat iskemia. Pada kasus penurunan volume kompartemen, gips harus dibuka dan pembalut kontriksi dilepas. Mengoreksi hipoperfusi dengan cara kristaloid dan produk darah. Pemberian mannitol, vasodilator atau obat golongan penghambat simpatetik. 2. Terapi pembedahan / operatif. Fasciotomi adalah pengobatan operatif pada sindroma kompartemen dengan stabilisasi fraktur dan perbaikan pembuluh darah. Keberhasilan dekompresi untuk perbaikan perfusi adalah 6 jam. (11) Terapi untuk sindroma kompartemen akut maupun kronik biasanya adalah operasi. Insisi panjang dibuat pada fascia untuk menghilangkan tekanan yang meningkat di dalamnya. Luka tersebut dibiarkan terbuka (ditutup dengan pembalut steril) dan ditutup pada operasi kedua, biasanya 5 hari kemudian. kalau terdapat nekrosis otot, dapat dilakukan debridemen, kalau jaringan sehat, luka dapat di jahit (tanpa regangan ), atau skin graft mungkin diperlukan untuk menutup luka ini.(8,20) Adapun indikasi untuk melakukan fasciotomi adalah : (21) 1. Ada tanda-tanda klinis dari sindroma kompartemen. 2. Tekanan intrakompartemen melebihi 30 mmHg. FASCIOTOMI PADA REGIO CRURIS Ada 3 pendekatan fasciotomi untuk kompartemen regio cruris : fibulektomy, fasciotomi insisi tunggal perifibular, dan fasciotomi insisi ganda. Fibulektomi adalah prosedur radikan dan jarang dilakukan, dan jika ada, termasuk indikasi pada sindrom kompartemen akut. Insisi tunggal dapat digunakan untuk jaringan lunak pada ektremitas. Teknik insisi ganda lebih aman dan efektif. (1,19) Fasciotomi insisi tunggal (davey, Rorabeck, dan Fowler) : Dibuat insisi lateral, longitudinal pada garis fibula, sepanjang mulai dari distal caput fibula sampai 3-4 cm proksimal malleolus lateralis. Kulit dibuka pada bagian anterior dan jangan sampai melukai nervus peroneal superficial. Dibuat fasciotomy longitudinal pada kompartemen anterior dan lateral. Berikutnya kulit dibuka ke bagian posterior dan dilakukan fasciotomi kompartemen posterior superficial. Batas antara kompartemen superficial dan

lateral dan interval ini diperluas ke atas dengan memotong soleus dari fibula. Otot dan pembuluh darah peroneal ditarik ke belakang. Kemudian diidentifikasi fascia otot tibialis posterior ke fibula dan dilakukan inisisi secara longitudinal. (1,19) Fasciotomi insisi ganda (Mubarak dan Hargens) : Insisi sepanjang 20-25 cm dibuat pada kompartemen anterior, setengah antara fibula dan caput tibia. Diseksi subkutaneus digunakan untuk mengekspos fascia kompartemen. Insisi tranversal dibuat pada septum intermuskular lateral dan identifikasi nervus peroneal superficial pada bagian posterior septum. Buka kompartemen anterior kearah proksimal dan distal pada garis tibialis anterior. Kemudian dilakukan fasciotomi pada kompartemen lateral ke arah proksimal dan distal pada garis tubulus fibula. Insisi kedua dibuat secara longiotudinal 1 cm dibelakang garis posterior tibia. Digunakan diseksi subkutaneus yang luas untuk mengidentifikasi fascia. Vena dan nervus saphenus ditarik ke anterior. Dibuat insisi tranversal untuk mengidentifikasi septum antara kompartemen posterior profunda dan superficial. Kemudian dibuka fascia gastrocsoleus sepanjang kompartemen. Dibuat insisi lain pada otot fleksor digitorum longus dan dibebaskan seluruh kompartemen posterior profunda. Setelah kompartemen posterior dibuka, identifikasi kompartemen otot tibialis posterior. Jika terjadi peningkatan tekanan pada kompartemen ini, segera dibuka.(1,19) FASCIOTOMI PADA REGIO ANTEBRACHIUM Pendekatan volar (Henry) Dekompresi kompartemen fleksor volar profunda dan superficial dapat dilakukan dengan insisi tunggal. Insisi kulit dimulai dari proksimal ke fossa antecubiti sampai ke palmar pada daerah tunnel carpal. Tekanan kompartemen dapat diukur selama operasi untuk mengkonfirmasi dekompresi. Tidak ada penggunaan torniket. Insisi kulit mulai dari medial ke tendon bicep, bersebelahan dengan siku kemudian ke sisi radial tangan dan diperpanjang kea rah distal sepenjang brachioradialis, dilanjutkan ke palmar. Kemudian kompartemen fleksor superficial diinsisi, mulai pada titik 1 atau 2 cm di atas siku kearah bawah sampai di pergelangan.(1,19) Kemudian nervus radialis diidentifikasi dibawah brachioradialis, keduanya kemudian ditarik ke arah radial, kemudian fleksor carpi radialis dan arteri radialis ditarik ke sisi ulnar yang akan mengekspos fleksor digitorum profundus fleksor pollicis longus, pronatus quadratus, dan pronatus teres. Karena sindrom kompartemen biasanya melibatkan kompartemen fleksor profunda, harus dilakukan dekompresi fascia disekitar otot tersebut untuk memastikan bahwa dekompresi yang adekuat telah dilakukan.(1,19) Pendekatan Volar Ulnar Pendekatan volar ulnar dilakukan dengan cara yang sama dengan pendekatan Henry. Lengan disupinasikan dan insisi mulai dari medial bagian atas tendon bisep, melewati lipat siku, terus ke bawah melewati garis ulnar lengan bawah, dan sampai ke carpal tunnel sepanjang lipat thenar. Fascia superficial pada fleksor carpi ulnaris diinsisi ke atas sampai ke aponeurosis siku dan ke carpal tunnel ke arah distal. Kemudian dicari batas antara fleksor carpi ulnaris dan fleksor digitorum sublimis. Pada dasar fleksor digitorum sublimis terdapat arteri dan nervus ulnaris, yang harus dicari dan dilindungi. Fascia pada kompartemen fleksor profunda kemudian diinsisi.(1,19) Pendekatan Dorsal Setelah kompartemen superficial dan fleksor profunda lengan bawah didekompresi, harus diputuskan apakah perlu dilakukan fasciotomi dorsal (ekstensor). Hal ini lebih baik ditentukan dengan pengukuran tekanan kompartemen intraoperatif setelah dilakukan fasciotomi kompartemen fleksor. Jika terjadi peningktan tekanan pada kompartemen dorsal yang terus meningkat, fasciotomi harus dilakukan dengan posisi lengan bawah pronasi.

Insisi lurus dari epikondilus lateral sampai garis tengah pergelangan. Batas antara ekstensor carpi radialis brevis dan ekstensor digitorum komunis diidentifikasi kemudian dilakukan fasciotomi.(1,19) DIAGNOSIS BANDING Diferensial diagnosis dari sindroma kompartemen meliputi tendinitis, fatigue fraktur dan shin splints. Keadaan ini dihubungkan berdasarkan nyeri pada tungkai bawah akibat latihan. Namun memberikan gejala yang sama dengan sindroma kompartemen. (22,23) Gejala pada tendinitis biasanya muncul setelah latihan, nyeri sering diakibatkan oleh regangan pada tendo. Pada fatigue fraktur, daerah tulang yang diserang meluas dari satu sisi tulang ke tulang yang lain. Pada shin splints, nyeri biasanya hanya pada puncak belakang tibia medial, sering pada pertemuan setengah dan sepertiga distal tibia. (22,23) KOMPLIKASI (21,24) Kegagalan dalam mengurangi tekanan intrakompartemen dapat menyebabkan nekrosis jaringan, selama perfusi kapiler masih kurang dan menyebabkan hipoksia pada jaringan tersebut. Kontraktur volkmann adalah deformitas pada tungkai dan lengan yang merupakan kelanjutan dari sindroma kompartemen akut yang tidak mendapat terapi selama lebih dari beberapa minggu atau bulan. Infeksi. Hipestesia dan nyeri. Komplikasi sistemik yang dapat timbul dari sindroma kompartemen meliputi gagal ginjal akut, sepsis, dan Acute Respiratory Distress Syndrome (ARDS) yang fatal jika terjadi sepsis kegagalan organ secara multisistem. PROGNOSIS Sindroma kompartemen akut cenderung memiliki hasil akhir yang jelek. Toleransi otot untuk terjadinya iskemia adalah 4 jam. Kerusakan irreversibel terjadi bila lebih dari 8 jam. Jika diagnosa terlambat, dapat menyebabkan trauma saraf dan hilangnya fungsi otot. Walaupun fasciotomi dilakukan dengan cepat dan awal, hampir 20% pasien mengalami defisit motorik dan sensorik yang persisten. (11) DAFTAR PUSTAKA 1. Azar Frederick. Compartment syndrome in Campbell`s operative orthopaedics. Ed 10th. Vol 3. Mosby. USA. 2003. p : 2449-57 2. DeLee C Jesse, Drez David. Compartment syndrome in DeLee & Drez`s orthopaedic sports medicine. Ed 2nd. Vol 1. Saunders. USA. 2003. p : 13-4 3. Argenta C Louis. Compartment syndromes in Basic sciense for surgeons. Saunders. Philadelphia. 2004. p : 143-4 4. Paula Richard. Compartment syndrome, extremity. Available at http://www.emedicine.com. Accessed on May 28th 2007. 5. Rasul Abraham. Compartment syndrome. Available at http://www.emedicine.com. Accessed on May 29th 2007. 6. Cameron Peter, Jelinek George. Compartment syndrome in Textbook of adult emergency medicine. Ed 2nd. Churchill Livingstone. New York. 2004. p : 84-5

7. Anonym. Compartment syndrome. Available at http://www.AAOS.com. Accessed on May 28th 2007. 8. Andrew L, Chen. Compartment syndrome. Available at http://www.medlineplus.com. Accessed on May 28th 2007. 9. Marc F Swiontkowski. Compartmental syndromes in Manual of orthopaedics. Ed 5th. Lippincott Williams & Wilkins. USA. 2001. p : 20-8 10. Preston R Miller, John M Kane. Compartment syndrome and rhabdomyolysis in The trauma manual. Ed 2nd. Lippincott Williams & Wilkins. USA. 2002. p : 335-7 11. Wallace Stephen. Compartment syndrome, lower extremity. Available at http://www.emedicine.com. Accessed on June 4th 2007. 12. Anglen J, Banovetz. Pathophysiology of compartment syndrome in The well leg resulting from fracture table positioning. Clinical Orthopaedics & Related Research. 1994. p : 239-42 13. Kearns, Daly, Sheehan, Murray. Oral vitamin C reduces the injury to skeletal muscle caused by compartment syndrome. Journal of Bone and Joint Surgery. Aug 2004. 14. Solomon Louis, Warwick David. Compartment syndrome in Appley`s system of orthopaedics and fractures. Ed 8th. Oxford University Press. New York. 2001. p : 563-4 15. Townsend M Courtney, Beau Champ. Acute compartment syndrome in Textbook of surgery. Ed 17th. Elsevier Saunders. USA. 2004. p : 554-7 16. Pink P Mitchell, Abraham Edward. Compartment syndrome in Textbook of critical care. Ed 5th. Elsevier Saunders. USA. 2005. p : 2099 17. McRae Ronald, Esser Max. Compartment syndromes in Practical fracture treatment. Churchill Livingstone. New York. 2002. p : 99 18. Flandry Fred. Compartment syndrome : swelling out of control. Available at http://www.hughston.com. Accessed on May 28th 2007. 19. Amendola, Bruce Twaddle. Compartment syndromes in Skeletal trauma basic science, management, and reconstruction. Vol 1. Ed 3rd. Saunders. 2003. p : 268-92 20. Brian J Awbrey, Shingo Tanabe. Chronic exercise-induced compartment syndrome of the leg. Harvard Orthopaedic Journal. 21. Kalb L Robert. Compartment syndrome evaluation in Procedures for primary care. Mosby. USA. 2003. p : 1419-29 22. Frederick A. Compartmental syndromes. Available at http://www.wikipedia.org. Accessed on June 4th 2007. 23. Braver Richard. Surgical pearls : How to test and treat exertional compartment syndrome. American College of Foot and Ankle Surgeons. May 2002. p : 22-4 24. Anonym. Compartment syndrome. Available at http://www.wikipedia.org. Accessed on May 29th 2007.

Chronic Exercise-Induced Compartment Syndrome of the Leg

Brian J. Awbrey, MD Shingo Tanabe, MD, PhD Massachusetts General Hospital

Vigorous exercise results in increased muscle volume due to increased perfusion. This expansion of muscles can cause increased pressure within an unyieldingosteofascial compartment, particularly in the leg. In most people these elevated muscular pressures return to normal within seconds following rest.1 Some people experience prolonged elevation of intracompartmental pressures. When these abnormally high pressures are associated with pain or neurological symptoms, the condition has been described as an exercise-induced compartment syndrome.1-3 Exercise-induced compartment syndrome is one of many causes of exercise related pain in the leg.4 Definitive diagnosis and distinction from other causes of exercise-induced leg pain can be difficult. It is the general consensus of most practitioners that the diagnosis must rest on measurement of abnormal resting and post-exercise intracompartmental pressures, but the threshold pressure values to define the condition and a rapid and reliable method to measure pressures have not been consistent. In addition, there are various techniques for performing intracompartmental pressure measurement tests before, during, and after exercise, and technique can have a substantial affect on recorded pressure. The difficulties associated with reliable diagnosis of the condition make it difficult to interpret data regarding treatment since patients from different series may not be comparable. We have been interested in chronic exercise-induced compartment syndromes for many years. This paper will discuss our work in the context of an overall review of the topic. Anatomy The leg is commonly divided into four compartments on the basis of separate fascial envelopes: the anterior, lateral, superficial posterior, and deep posterior compartments. In the management of exercise-induced compartment syndrome, some have suggested that the tibialis posterior functions as if it were its own compartment (the so-called fifth compartment of the leg) and may be selectively vulnerable to exercise-induced compartment syndrome.5

Each of the four major compartments contains a nerve with a sensory component. Increased pressure in the anterior compartment may cause diminished sensation in the dorsum of the first web space of the foot (deep peroneal nerve). Elevated pressure in the lateral compartment might cause sensory loss of the dorsum of the foot (superficial peroneal nerve). The sural nerve lies within the superficial posterior compartment and increased pressures may cause numbness over the lateral aspect of the leg and foot. The deep posterior compartment contains the tibial nerve and the sole of the foot may therefore become numb with increased pressures. Abnormalities of motor function, such as a transient foot drop, may also occur with exercise-induced compartment syndrome. We have found that this transient foot drop is present in nearly all patients with exercise compartment syndrome and have coined the term Slap Sign to describe the onset of weakness during the course of running exercise. Transient pressure elevation within a compartment during exercise is not abnormal and reflects both transient increases in tissue perfusion and the pressure of muscle contraction, which may cause pressures upwards of 80 mm Hg in a normal muscle.6 The amount of stretch placed upon a muscle (i.e. the position of adjacent joints) also affects compartment pressures. These factors must be taken into account when interpreting pressure measurements. Muscle herniation through fascial defects has been identified in upwards of 40% of patients with chronic compartment syndromes, compared to only 5% of controls.2 The importance of this finding is not known. Presentation The typical history associated with exercised-induced compartment syndrome was outlined by Detmer and colleagues.7 Most patients are avid runners who are completely asymptomatic in the off-season but gradually develop an aching pain in the lower leg as training progresses. The pain is initially present near the end of a run and disappears shortly thereafter. As symptoms progress, the pain may persist after the activity, even into the next day. Paresthesias may develop on the sole of the foot with a deep posterior compartment syndrome and on the dorsum of the foot in an anterior compartment syndrome. These two locations account for over 80% of all exercise-induced compartment syndromes in the leg.2, 5 The physical examination is usually normal. Athletes report a progression of the onset of symptoms with time and severe pain with their sport, combined with weakness and a positive Slap Sign. NEXT PAGE | TOP OF PAGE | HOJ HOME Chiefs Reports | Osgood Day | Cartilage Regeneration and Repair, Where Are We? A Harvard Orthopaedic Presence in China | Scientific Articles | Alumni

Diagnosis Differential Diagnosis Active young patients complaining of exercise-induced leg pain may suffer from medial tibial stress syndrome, stress fracture, nerve entrapment, or exerciseinduced compartment syndrome.4 Bone scans and radiographs can usually identify the first two conditions. In medial tibial stress syndrome, the bone scan shows diffuse activity along the posteromedial cortex. Stress fractures cause a focal area of uptake. Radiologic investigations are normal with nerve entrapment conditions and, generally, negative in exercise-induced compartment syndrome, which may show areas of nucleotide uptake along the tibia by bone scan. Office Standing Exercise Test Results: A Comparison of Compartment Syndrome vs. Medial Tibial Stress 1. Exercise Test Time to Characteristic Pain (4-minute Excercise Test): Exercise Compartment Syndrome Medial Tibial Stress Syndrome Normal Subjects In <2 minutes all tested subjects develop severe pain No pain No pain

2. Increase In Calf Size After 4-Minute Exercise Test (mean) Exercise Compartment Syndrome Medial Tibial Stress Syndrome Normal Subjects +0.6 cm +1.4 cm +1.75 cm

Intracompartmental Pressure Monitoring To test for an exercised-induced compartment syndrome, most authors have the patient perform running or isokinetic exercises until either pain or fatigue limit further activity. Measurements are taken pre and post-exercise. The position of the knee and ankle must be standardized since joint position can effect compartment pressure. The wick and slit catheter techniques have been popular instruments for obtaining pressure measurements. This abbreviated measurement method has several drawbacks, but does provide the practitioner with a crude measure of muscular pressures associated with exercise. Diagnostic criteria for exercise induced compartment syndrome vary. Rorabeck and co-workers required both a resting pre-exercise pressure of 10 mm Hg and a 15 minute post-exercise pressure greater than 15 mm Hg for diagnosis.3 Pedowitz and colleagues accepted any one of the following as diagnostic: 1) preexercise pressure greater than 15 mm Hg; 2) a one-minute post-exercise pressure greater than 30 mm Hg; or 3) a five-minute post-exercise pressure greater than 20 mm Hg.2 Our initial studies focused on the development of a miniaturized fluid pressure monitor for office use, which was found to be practical, accurate and rapid.1 Our current technique involves pressure measurements of symptomatic compartments in the office setting using a hand-held digital monitor (Stryker Corporation, Kalamazoo, MI). In an effort to provide complete and sophisticated pressure data, each compartment is monitored continuously starting at rest, during the course of four minutes of in-office exercise, and after exercise for five minutes. Most recently, this test has been adapted from a four-minute outdoor running test (which proved to be inconsistent) to our present use of a four-minute provocative supine exercise test. During the test the patient performs a vigorous isometric muscle contraction against the force of the examiner during pressure measurement. This brief office-based testing program consistently reproduces the patients symptoms and provokes pressure elevation. Our parameters for the diagnosis of chronic exercise-induced compartment syndrome include: 1. Elevated resting muscular compartment pressures (>12 mmHg); 2. Elevated relaxed muscle pressures during exercise (>60 mmHg), 3. Post-exercise pressure elevated above rest pressure at 5 minutes, and 4. The onset of characteristic pain during the four minute study. All four criteria were required for diagnosis. Those patients with compartment syndrome were found to consistently have resting pressures in the low twenties, exercise pressures of 90-110 and elevated post-exercise pressures.

We have also developed a noninvasive four-minute standing exercise test. In a review of 33 patients, we found that this test accurately distinguished patients with exercise-induced compartment syndrome from those with medial tibial stress syndrome.(unpublished data) Patients with exercise-induced compartment syndrome consistently reproduced their characteristic disabling pain and all had a significantly diminished increase in calf circumference with exercise compared to normal subjects. Primary Symptoms of Exercise-Induced Compartment Syndrome Severe pain with exercise Sharp pain Numbness Tingling SLAP SIGN* 100% 100% 91% 82% 70%

* Slap Sign: Exercise-Induced peroneal palsy leading to transient foot drop Treatment Patients with exercise-induced compartment syndrome do not require surgery if they are willing to curtail inciting sports activities. In our experience, 95% of patients desire to remain active in exercise and sport. Nonoperative treatment has not been effective. Patients that want to remain active in their sport usually require operative treatment. Operative treatment requires fascial release of the involved compartments. Many surgeons attempt to do this through a limited incision.8 Our experience with the operative treatment of exercise-induced compartment syndrome suggests that limited skin incisions with extensive subcutaneous release of involved compartments are preferable. Among patients requiring operative release of an exercise-induced compartment syndrome under our care 55% involved the anterolateral compartments, 24% the posterior compartments, and in 21% both areas. Both legs were involved in 82% of patients. We performed two-incision fasciotomy, with the subcutanous fascial incisions extended from ankle to knee. As a gauge of complete fasciotomy, compartment pressures were measured before and after release. Preoperative pressure measurements recorded in the operating room matched those measured at rest in the office setting. In 32% of patients, post-fasciotomy pressure measurements were found to be greater than 15 mm Hg. Exploration of the release identified numerous fibrous bands overlying the fascia in each case. When these additional bands were released, the final resting pressure was below 9 mm Hg in each case. Overall, the resting pressure had decreased from an average of 23 mm Hg pre-op to an average of 7 mm Hg post-op. Nearly all of the patients had satisfactory relief of pain with return to full sports activities.

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Conclusions We have attempted to simplify the office diagnosis of exercise-induced compartment syndrome of the leg and have developed methods for measurement. Measurement of muscle pressures during the described exercise test differentiates exercise compartment syndrome from other disorders causing exercise pain. Although conservative treatment methods have failed, the results of operative fascial release have been highly successful. We recommend extensive subcutaneous fascial release of each involved compartment and intraoperative pressure monitoring. With careful diagnosis and treatment, the results of operative treatment can be rewarding. Brian J. Awbrey, MD is an Attending Surgeon at Massachusetts General Hospital and Clinical Instructor of Orthopaedic Surgery at Harvard Medical School Shingo Tanabe, MD, PhD was a visitor from the Departments of Physiology and Sports Medicine at the The University of Tokushima School of Medicine and The Kanzaki Central Hospital, Tokushima, Japan Address Correspondence to: Brian J. Awbrey, M.D.; Department of Orthopaedic Surgery; Massachusetts General Hospital; 151 Merrimac Street, Suite 202; Boston, MA 02114

References 1. Awbrey B, Sienkiewicz P, Mankin H. Chronic exercise-induced compartment pressure elevation measured with a miniaturized fluid pressure monitor. Am J Sports Med 1988;16:610-615. 2. Pedowitz R, Hargens A, Mubarak S, Gershuni D. Modified criteria for the objective criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990;18:35-40. 3. Rorabeck C, Bourne R, Fowler P, Finlay J, Nott L. The role of tissue pressure measurement in diagnosing chronic anterior compartment syndrome. Am J Sports Med 1988;16:143-146. 4. Andrish J. The leg. In: DeLee J, Drez D, eds. Orthopaedic sports medicine: Principals and practice. Philadelphia: W.B. Saunders, Co., 1994:1603-1631. vol 2. 5. Davey J, Rorabeck C, Fowler P. The tibialis posterior muscle compartment. Am J Sports Med 1984;12:391-397. 6. Logan J, Rorabeck C, Castle G. The measurement of dynamic compartment pressure during exercise. Am J Sports Med 1983;11:220-223. 7. Detmer D, Sharpe K, Sufit R, Girdley F. Chronic compartment syndrome: Diagnosis, management, and outcomes. Am J Sports Med 1985;13:162-170. 8. Fronek J, Mubarak S, Hargens A, et al. Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop 1987;220:217-227. 9. Mubarak S, Owen C. Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg 1977;59A:184.

Chapter 13 Compartment Syndromes Bruce C. Twaddle, M.D., F.R.A.C.S., Annunziato Amendola, M.D., F.R.C.S.(C.) HISTORY Compartment syndrome is a condition characterized by raised pressure within a closed space with a potential to cause irreversible damage to its contents. Clinical awareness of the condition is attributed to the work of Richard von Volkmann. In 1881, he published an article in which he attempted to relate the state of irreversible contractures of flexor muscles of the hand to ischemic processes occurring in the forearm. Volkmann believed that the pathophysiology of the contracture is related to massive venous stasis associated with simultaneous occurrence of arterial insufficiency. He thought that the condition may be caused by tight bandages, an observation that proved to be accurate.[121] Other investigators confirmed Volkmann's conclusion [0140] [1050] and Petersen,[91] in 1888, described surgical treatment of a Volkmann contracture, demonstrating some return of function after release of contracted scarred tissue, further supporting the observation that the causative factor is related to an ischemic event. Others at that time theorized that neurologic damage secondary to ischemia was causally related to the Volkmann contracture. [0850] [1200] [1210] It was Hildebrand[47] in 1906 who first used the term Volkmann's ischemic contracture to describe the end-point of an untreated compartment syndrome and suggested that elevated tissue pressure may be causally related to ischemic contracture. He speculated that the underlying problem was a result of venous obstruction causing increased pressure in muscle and compromising arterial circulation to the muscle itself. Thomas,[120] in 1909, attempted to review the data concerning the cause of Volkmann's ischemic contracture published up to that time. In his published review of 112 cases, fractures were found to be a causative factor in most end-stage Volkmann ischemic contractures. Other predisposing causes of the condition were noted, however, including arterial injury, embolus, and tight bandaging. Of the 112 cases reported up to that time, 107 had occurred in the upper extremity. Whereas the early investigators into the cause of compartment syndrome concentrated mainly on the development of the contracture, Rowlands,[105] in 1910, was the first to suggest that reperfusion after a prolonged period of ischemia could result in postischemic congestion and edema of muscle and nerve and could lead to the development of acute compartment syndrome. In 1914, Murphy[85] was the first to suggest that fasciotomy, if done before the development of the contracture, may prevent the contracture from occurring. He was also the first to suggest the relation among tissue pressure, fasciotomy, and the development of a subsequent contracture. Brooks and colleagues[14] further investigated the cause of acute compartment syndrome. After a series of extensive investigations, they suggested that the late picture of Volkmann's ischemic paralysis could be explained only on the basis of acute venous obstruction causing diminished perfusion of the extremity. After release of the obstruction (bandage or splint), a period of swelling, heat, and rapidly developing contracture is likely to occur. During and after World War II, many cases of Volkmann's contracture were seen as a complication of high-velocity gunshot wounds causing fractures of the upper or lower extremities.[16]

Although the existence of arterial trauma complicating a fracture was well known, the concomitant need for fasciotomy at the time of arterial repair was not generally appreciated. Many surgeons of the day thought that treatment of an impending Volkmann ischemia should be directed toward relief of the arterial spasm. Often, direct arterial injury could not be demonstrated at the time of surgery. In spite of that, however, surgical exploration of the damaged artery frequently led to reestablishment of flow distally and, in some cases, to reversal of the acute impending compartment syndrome.[88] It is highly likely that, while exposing the artery, the vascular surgeons were actually performing a limited fasciotomy, and this may have been the reason for the improvement in the patient's symptoms. In 1970 Patman and Thompson,[88] after an extensive review of 164 patients with peripheral vascular disease in whom fasciotomy had been performed after arterial reconstruction, concluded that fasciotomy has much to offer for limb salvage and implied that it should be performed more often after restoration of arterial inflow to an extremity. Similar observations were made in 1967 during the Vietnam War by Chandler and Knapp,[19] who also suggested that, had more fasciotomies been performed after arterial repair to the extremities, the long-term results might have been better. Many early cases of compartment syndrome seemed to be confined to the upper extremity. Increased attention focused on the lower extremity, however, after the report by Ellis[26] in 1958 of a 2 percent incidence of ischemic contractures occurring as a complication of tibial fractures. Most early descriptions of compartment syndrome involving the lower extremity were related to the development of the condition in the anterior compartment, but after the reports of Seddon[99] in 1966 and of Kelly and Whitesides[50] in 1967, the existence of four compartments in the leg and hence the need to decompress more than the anterior compartment were pointed out. Compartment syndrome of the foot has been indirectly alluded to since the description of gangrene as a complication of Lisfranc fracture-dislocations, and increasing reports of this condition have appeared in the literature. [0550] [0860] Similarly, the involvement of thigh and gluteal compartments is now well recognized, particularly as a complication in the multiply traumatized patient. [0160] [1070] [1080] The anatomy of these various compartments has been documented in the past and has been revisited by several authors in an attempt to define the ideal surgical approaches. [0490] [0860] The pathophysiology has been elucidated by a number of researchers, who correlated end-stage muscle contracture with such underlying pathophysiologic factors as raised interstitial pressure and muscle and nerve ischemia. [0810] [0870] [1020] [1030] [1100] [1230] These investigators also noted that a compartment syndrome can occur in any of the compartments of the leg or arm if the prerequisites for its development are present.[56] PATHOPHYSIOLOGY The prerequisites for the development of a compartment syndrome include a cause of raised pressure within a confined tissue space. Distortions in the relation between volume and pressure interfere with circulation to the compartment leading to the d evelopment of an acute
compartment syndrome.[56] Any condition that increases the content or reduces the volume of a compartment could be related to the development of an acute compartment syndrome. Excess tissue pressure secondary to increased volume of a compartment has been shown to occur in

various conditions, including hemorrhage, fractures, increased capillary permeability after burns, and a temporary period of ischemia resulting in post-ischemic swelling. * Regardless of the underlying cause, raised tissue pressure ultimately leads to some degree of venous obstruction within a closed space. Pressure continues to rise until the low intramuscular arteriolar pressure is exceeded. At that point, no further blood enters the capillary anastomosis, resulting in shunting within a compartment. If the pressure increase is allowed to continue untreated, muscle and nerve ischemia occurs, leading to irreversible damage to the contents of the compartment. [0440] [1010] [1020] Using a canine model, it was demonstrated that the extent of tissue injury depends on pressure and time. Rorabeck and colleagues [1010] [1020] found that interference with muscle and nerve function becomes progressively more severe according to the duration of applied pressure. They found that a pressure of 30 mm Hg must be maintained in the anterior compartment of a dog's leg for 8 hours before changes in conduction velocity can be demonstrated in the peroneal nerve. However, conduction velocity changes can be shown sooner if higher pressures are introduced and maintained. [0350] [0470] [0610] [0680] [0790] A compartment syndrome occurring as a complication of arterial injury is usually observed after restoration of arterial inflow to the compartment. Diminished arterial inflow caused by the injury results in a period of nerve and muscle ischemia within the compartment. The period of hypoxia experienced by the muscle and nerve allows transudation of fluid through capillary basement membranes and the capillaries of striated muscle.[98] It is also thought that the basement membranes may sustain some anoxic damage secondary to impaired arterial inflow. When arterial inflow to the extremity has been reestablished, fluid continues to leak through the basement membrane into the interstitial spaces. This leakage occurs soon after restoration of arterial inflow and, as a result, the pressure within the compartment continues to increase because of the unyielding fascial walls encasing the compartment. The pressure rise continues until the critical closing pressure of the small arterioles is reached. After that point, no further blood enters the striated muscle of the compartment and shunting occurs. The raised compartment pressure further increases the local venous pressure, thereby reducing the arteriolar-venous gradient. Regardless of the cause of acute compartment syndrome, however, pressure within the compartment never rises sufficiently to obstruct totally the systolic or diastolic pressure in the major vessel traversing the compartment.[98] Both laboratory and clinical studies have demonstrated that compartment syndrome is not directly comparable to an episode of pure ischemia. [0430] [0440] Heppenstall and associates demonstrated in an animal model the importance of episodes of hypotension in increasing the extent of irreversible muscle ischemia and confirmed the difference between mean arterial pressure and compartment pressures in determining flow and muscle survival. McQueen and Court-Brown[71] demonstrated this distinction clinically, suggesting that a difference between diastolic pressure and compartment pressure of less than 30 mm Hg has a high clinical correlation with development of a compartment syndrome. This difference between diastolic and compartment pressure was labeled p and is probably the most important clinical parameter to identify. Blood flow studies employing technetium 99m and xenon 133 have demonstrated that skeletal muscle blood flow is reduced during acute compartment syndrome in the experimental animal. [1020]

[1030]

Because of the patchy distribution of muscle necrosis found at the time of fasciotomy, however, variations in muscle blood flow probably occur among areas within the same muscle. Crush syndrome and crush injury have, at times, been grouped with compartment syndrome in pathophysiology and treatment. This grouping is probably conceptually incorrect. These patients present originally with a history of having been trapped or crushed with pressure on a limb or limbs for an extended period of time. They characteristically have a painless flaccid paralysis initially, followed by the rapid development of swelling and rigid compartments in the affected part of the limb. However, it is now clear that the elevation of compartment pressure in crush injury is secondary to intracellular muscle damage rather than being the causative factor and that treatment guidelines are different. [0720] [0940] In particular, fasciotomy is contraindicated in crush syndrome and is associated with higher morbidity and mortality. The anesthetized or sedated patient is at particular risk for development of a compartment syndrome, which may go unnoticed. Patients who are intubated very early in their initial care need accurate assessment of their injured extremities while in the intensive care unit. Because unrecognized injuries can lead to compartment syndrome in these patients, remembering to perform a secondary survey of all patients involved in high-velocity accidents resulting in ventilatory support is essential. Prolonged positioning of a limb, particularly with the use of a post or traction, or both, such as with hip fracture fixation or femoral nailing, can place the compartments involved at risk,[69] especially if there is ongoing bleeding related to injury. Compartment syndrome may, however, also occur in the uninjured leg if positioning restricts venous return. Hyperextension of the hip to improve imaging of a fractured femur or tibia in the lateral position may result in a risk of compartment syndrome in the well leg. A reperfusion phenomenon, as occurs with vascular repair, may also result in compartment syndrome in the well limb if the positioning of this limb affects arterial flow. Therefore, any patient who undergoes prolonged or unexpectedly protracted surgery, particularly to the lower limb, should have careful clinical assessment of the compartments of both the operated and un-operated limbs several times after surgery. Considering the underlying pathophysiology, the cause of a compartment syndrome may be related more specifically to conditions that decrease the size or increase the content of a compartment.[58] The most common cause of compartment syndrome associated with decrease in the size of the compartment is the application of a tight cast, constrictive dressings, or pneumatic antishock garments. [0200] [0300] [0520] [0700] [1190] Closure of fascial defects has been demonstrated to be associated with the development of acute compartment syndrome.[73] This condition most commonly occurs in the anterior compartment of the leg in patients who present with symptomatic muscle hernias and symptoms suggestive of chronic compartment syndrome. Failure to recognize the pitfalls in closing the muscle hernia in this situation can have disastrous consequences for the patient and the surgeon. [0730] [0890] [1100] Attempts to close the anterior compartment after surgery in this region, such as with a tibial plateau fracture, may also increase the risk of compartment problems. Care should be taken when assessing closure of this layer, taking into consideration the extent of swelling, any sign of ongoing bleeding, and the coagulation status of the patient.

A number of conditions have been shown to increase compartment contents and lead to compartment syndrome. These conditions involve hemorrhage within the compartment or accumulation of fluid (edema) within the compartment. The former is most commonly associated with fractures of the tibia, elbow, forearm, or femur, whereas the latter is most commonly associated with post-ischemic swelling after arterial injuries or restoration of arterial flow after thrombosis of a major artery. * The compartment syndrome described after arthroscopic treatment of tibial plateau fractures is likely to be related to extravasation of fluid into the compartment through the fracture itself.[9] This event is much more sinister than the fluid extravasation into the superficial soft tissues that can occur during regular arthroscopy because this fluid is generally outside the fascial layer. The use of arthroscopic fluid pumps to increase fluid flow increases the risk of this type of fluid accumulation. Compartment syndromes have also been reported to occur after other conditions or therapies, including soft tissue injury to an extremity, hereditary bleeding, dialysis, anticoagulant therapy, osteotomy, intraosseous fluid resuscitation in children, and excessive skeletal traction.[] As can be seen, the causes of acute compartment syndrome touch on several medical disciplines, including orthopaedic, general, and vascular surgery and traumatology.[]