Anatomi Pergelangan Tangan

Anatomi Pergelangan Tangan Struktur anatomis telapak tangan terdiri dari dua bagian utama yaitu : a. Bagian tulang : Carpal, metacarpal, dan phalangs b. Bagian lunak : Otot, saraf, vascular, jaringan lemak, dan jaringan ikat sendi (Snell, 2006)

1) Tulang Telapak Tangan a. Carpal Tulang carpal terdiri dari 8 tulang pendek yang berartikulasi dengan ujung distal ulna dan radius, dan dengan ujung proksimal dari tulang metacarpal. Antara tulang-tulang carpal tersebut terdapat sendi geser. Ke delapan tulang tersebut adalah scaphoid, lunatum, triqutrum, piriformis, trapezium, trapezoid, capitatum, dan hamatum. (Moore, 2002). b. Metacarpal Metacarpal terdiri dari 5 tulang yang terdapat pada pergelangan tangan dan bagian proksimalnya berartikulasi dengan distal tulang-tulang carpal. Khususnya di tulang metacarpal jari 1 (ibu jari) dan 2 (jari telunjuk) terdapat tulang sesamoid (Moore, 2002) c. Phalangs Tulang-tulang phalangs adalah tulang-tulang jari, terdapat dua phalangs di setiap ibu jari (phalangs proksimal dan distal) dan 3 di masing-masing jari lainnya (phalangs proksimal, medial, dan distal). Sendi engsel yang terbentuk antara tulang phalangs membuat gerakan tangan menjadi lebih fleksibel terutama untuk menggenggam sesuatu. (Moore, 2002)

2) Bagian Lunak Telapak Tangan a. Otot Otot-otot tangan intrinsik digolongkan menjadi 4 kelompok, yaitu : a) Otot-otot Thenar dalam kompartemen thenar b) Musculus adductor pollicis dalam kompartemen adductor c) Otot-otot hypothenar dalam kompartemen hyphothenar d) Otot-otot tangan pendek (Musculi lumbricales dalam komparteman tengah dan musculi interossei antara ossa metacarpi) (Snell, 2006). Otot-otot thenar (musculus abductor pollicis brevis, musculus flexorpollicis brevis, dan musculus opponens pollicis terutama berfungsi untukmengadakan oposisi pollex (digitus primus). Gerak majemuk ini dimulai dengan ekstensi, lalu dilanjutkan dengan abduksi, fleksi, endorotasi, dan biasanya aduksi.(Moore, 2002).

b. Saraf Saraf- saraf telapak tangan adalah nervus medianus dan nervus ulnaris. Nervus ulnaris akan mempersarafi musculus flexor carpi ulnaris, musculus flexor digitorum profundus/ FDP (untuk fleksi DIP joint/ distal inter phalang joint jari 4 dan 5), dan sebagian besar otot intrinsik tangan termasuk mm. lumbricales (untuk fleksi MCP/Metacarpo phalangeal 4 dan 5). Cedera pada nervus ulnaris akan menyebabkan kecenderungan tertarik ke depan oleh FDP tanpa adanya tarikan lumbricales, kondisi yang demikian disebut Claw Hand (main en griffe). (Moore, 2002). Nervus medianus mempersarafi semua otot antebrachium kompartemen anterior flexor - kecuali m. flexor carpi ulnaris dan m. FDP / flexor digitorum profundus jari ke-4 dan ke-5 (bagian radial). N. Medianus juga mempersarafi otot regio thenar (m. flexor policis brevis, m. abductor policis brevis dan m. opponens policis (Snell, 2006). Cedera nervus medianus bagian proksimal akan

memberikan

gambaran

obstetricus

hand/

Benedict,

accoucheur’s hand, Pitcher’s Hand. Cedera nervus medianus akan menyebabkan gambaran ape hand (Moore, 2002). c. Arteri a. Arteri Ulnaris Arteri ulnaris mempercabangkan ramus profundus dan kemudian berlanjut ke telapak tangan sebagai arcus palmaris superficialis. Arcus palmaris superficialis adalah lanjutan langsung arteri ulnaris. Di lateral, arcus ini dilengkapi oleh cabang arteria radialis. Empat arteriae digitales

dipercabangkan dari bagian cembung arcus dan berjalan ke jari (Snell, 2006). b. Arteri Radialis Arteri radialis membelok ke medial di antara caput obliqum dan caput tranversum musculi adductor pollicis dan berlanjut sebagai arcus palmaris profundus. Arcus palmaris profundus merupakan lanjutan langsung arteri radialis. Arcus arterial palmaris superficialis dan profundus diikuti oleh arcus venosus palmaris superficialis dan profundus yang menerima darah dari cabang yang sesuai. (Snell, 2006).

A. Definisi Tenosynovitis adalah suatu peradangan yang melibatkan tendon dan selubungnya yang mengakibatkan pembengkakan dan nyeri. Beberapa penyebab dari

pembengkakan ini adalah trauma, penggunaan yang berlebihan dari repetitive minor trauma, strain atauinfeksi. Beberapa contoh dari tenosynovitis adalah Dequervain’s, Volar Flexor Tenosynovitis (trigger finger) dan flexor tenosynovitis. A. Epidemiologi Tenosynovitis supuratif mempunyai insiden yang lebih tinggi (75%) di kalangan wanita berbanding lelaki. Kebanyakan kasus terjadi pada individu antara 52 dan 62 tahun. Penyakit ini sering terjadi pada kedua tangan B. Tanda Gejala Menurut Chaidir (1998) pada kasus Tenosynovitis Supuratif, pasien dengan luka penetrasi dating dengan sakit kemerahan pada tangan dan demam. Pemeriksaan fisik menunjukkan adanya 4 tanda dari kanavel, yaitu: 1. Jari dalam posisisedikit fleksi 2. Bengkak dalam bentuk fusiform 3. Nyeri tekan sepanjang flexor tendon sheath 4. Nyeri pada saat dilakukan pasif fleksi jari Gejala kanaval ada beberapa yang tidak terlihat, seperti pada keadaan: 1. Pemberian antibiotika segera 2. Kondisi yang sangat dini 3. Status immunocompromised 4. Infeksi kronik Tenosynovitis is inflammation of a tendon and its sheath (see the image below). Most acute cases of flexor tenosynovitis (FT)—which involves disruption of normal flexor tendon function in the hand—result from infection. However, FT also can develop secondary to acute or chronic inflammation from a noninfectious cause, such as diabetes, overuse, or arthritis. Cases of infectious FT that present early and have no comorbidities have a good prognosis, but patients with fulminant infection, chronic infection, or an impaired immune status have increased risk of long-term complications and impairment.

Signs and symptoms Infectious tenosynovitis Patients with infectious FT can present at any time following a penetrating injury, with complaints of pain, redness, and fever. Physical examination reveals Kanavel signs of flexor tendon sheath infection, which are as follows:  Finger held in slight flexion  Fusiform swelling  Tenderness along the flexor tendon sheath  Pain with passive extension of the digit Clinical features of gonococcal tenosynovitis include the following:  Erythema, tenderness to palpation, and painful range of motion (ROM) of the involved tendon(s)  Fever - A common sign  Dermatitis - Also a common sign; it occurs in approximately two thirds of disseminated gonococcal infections; it is characterized by hemorrhagic macules or papules on the distal extremities or trunk Inflammatory flexor tenosynovitis  Usually the result of an underlying disease process  Presentation is indolent but progressive if therapy is not initiated  Similar findings to those found in infectious FT eventually present  Swelling is the most common initial finding  Hallmark is a difference in active, versus passive, flexion  As the tissue expands and impingement occurs, pain and restricted motion ensue Delayed presentations can have the appearance of fulminant FT with all Kanavel signs or may involve tendon rupture if the patient delays seeking treatment long enough. Diagnosis If infection is suggested, culture of the suppurative synovial fluid is mandatory prior to beginning definitive antimicrobial treatment. These cultures should include the following samples:  Aerobic  Anaerobic  Fungal  Acid-fast bacilli (AFB)  Atypical AFB Diagnostic arthrocentesis is indicated if joint effusion is present with tenosynovitis, because most patients with disseminated gonococcal infection have coexistent septic arthritis. Hematologic studies  Complete blood count (CBC)  Erythrocyte sedimentation rate (ESR)  Rheumatoid factor - If rheumatoid arthritis is a consideration Biopsy

Synovial biopsy for histopathologic examination is helpful in diagnosing granulomatous changes observed in Mycobacterium infections and in cases of chronic processes. Imaging Obtain standard anteroposterior and lateral radiographs to rule out bony involvement or a foreign body. [1] See Workup for more detail. Management Infectious flexor tenosynovitis Prompt medical management of acute nonsuppurative flexor tenosynovitis (FT) may preclude the need for surgical intervention. Nonoperative treatment for infectious FT includes the following:  IV antibiotics - May be included in initial treatment if the patient presents very early with suspected infectious FT  Elevation - Initially, until infection is under control  Splinting - In "safe position"  Rehabilitation - ROM exercises and edema control, initiated once FT is under control Inflammatory flexor tenosynovitis Nonoperative management is the primary treatment for inflammatory FT. The mainstay of therapy for FT caused by overuse syndromes is cessation of the insult by modification of activity. Therapy also includes the following:  Icing and elevation of the affected area  Administration of a nonsteroidal anti-inflammatory drug (NSAID) if tolerated by the patient  Consideration of a short course of oral steroids  Administration of flexor tendon sheath or carpal tunnel corticosteroid injections to decrease pain and the inflammatory response  Splinting - If used, splinting should be limited in area to a pain-free ROM  Rehabilitation - Slow rehabilitation prevents reinitiation of the inflammatory phase Treatment for rheumatoid inflammatory FT includes ice, NSAIDs, rest, splinting, hydroxychloroquine, gold, penicillamine, and methotrexate. Drainage The indication for surgical drainage includes history and physical examination consistent with acute or chronic FT. In certain circumstances when acute FT presents within the first 24 hours of infection development, medical management may initially be used. Prompt improvement of symptoms and physical findings must follow within the ensuing 12 hours; otherwise, surgical intervention is necessary.

Pathophysiology Infectious flexor tenosynovitis

Infection can be introduced directly into the tendon sheaths through a skin wound (most often) or via hematogenous spread, as occurs with gonococcal tenosynovitis. Infectious FT is a closed-space infection. Sheaths of the index, middle, and ring fingers run from the metacarpal neck at the level of the first annular (A1) pulley proximally to the insertion of the flexor digitorum profundus distally. The small finger and thumb sheaths are continuous with the ulnar and radial bursae in the palm, respectively (see the image below). Because the radial and ulnar bursae are contiguous, infections in either the small finger or the thumb are at risk of communicating and potentially progressing to the carpal tunnel. Infection in any of the fingers may spread proximally into the wrist and forearm (Parona space). The initial infection also may move into the fascial spaces within the hand, adjacent osseous structures, or synovial joint spaces, or it may erode through the layers of the skin and exit superficially. The tendon sheath is made up of an inner visceral layer and an outer parietal layer. Between the two layers is the synovial space, which is filled with synovial fluid. The visceral layer is in close approximation to the flexor tendon. The parietal layer is reinforced by a series of five annular pulleys (A1-5) and three cruciform pulleys (C1-3). The A2 and A4 pulleys are critical for flexor tendon function and should be avoided during surgical manipulation of the infected sheath. With the accumulation of pus in flexor tendon sheath infections, pressure can increase within the closed-space compounds of the flexor tendon sheath, thus inhibiting the inflammatory response. In one study, eight of 14 patients with flexor tendon sheath infections had hand tendon sheath pressure in excess of 30 mg Hg. The increased pressure also inhibits blood flow and adds to the destructive process. Tendon ischemia increases the likelihood of tendon necrosis and rupture. Flexor tendons of the fingers receive their nutrient supply from a combination of direct vascular sources and diffusion from synovial fluid. An avascular segment of the flexor digitorum superficialis has been found at the proximal phalangeal level. The flexor digitorum superficialis has two distinct vascular supplies, and three have been identified for the flexor digitorum profundus. As a result, the profundus has two avascular segments, which are located over the proximal and middle phalangeal regions. Inflammatory flexor tenosynovitis Inflammatory FT occurs through a process different from the one that produces infectious FT, though it can lead to similar complications. In inflammatory FT, proliferation of fibrous tissue occurs until there is impingement or constriction of the tendon and surrounding structures. The flexor tendons and the flexor retinaculum can create a tourniquet effect, producing distal swelling and pain. Nodularity of the tendons can lead to crepitus and sometimes frank triggering as the tendon becomes impinged adjacent to a thickened segment of the tendon sheath. [2, 3] Overuse Overuse syndromes go through predictive stages that can lead to FT. Overuse is defined as repetitive microtrauma that is sufficient to overwhelm the ability of the tissue to adapt. Pathologic stages of overuse include inflammation, proliferation, and, finally, maturation. They proceed as follows:

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Inflammatory stage - Starts immediately following injury, with release of chemotactic and vasoactive substances; the resulting inflammatory cells create pain, swelling, erythema, and warmth; this stage can last from 48 hours to 2 weeks unless further injury occurs Proliferative stage - Lasts up to 2 weeks and is characterized by the production of collagen and ground substances; the tendon is extremely vulnerable to injury during this period Maturation stage - Lasts up to 12 weeks, during which time the healing phases are completed; unrestricted activity should be avoided until this stage is complete; if the inflammatory response is reinitiated at this time, fibrosis can result from repeated or continued release of inflammatory substances

Tendon rupture Several causes of tendon rupture in rheumatoid arthritis (RA) exist. An attrition rupture may occur after the tendon has passed over roughened bony surfaces or has been eroded by chronic synovitis. The tendon also may be weakened by direct invasion of the rheumatoid tenosynovium or by ischemic necrosis secondary to surrounding pressures and diminished vascular supply.