Presentan Kelompok 18
Rizky Rizal A
Fatimah Putri NW 12
Identitas Pasien
Nama : Tn. YY
Usia : 49 th
Jenis Kelamin : Laki-laki
Alamat : Ujung Berung
Tanggal masuk RS : 12 juli 2022
Tanggal Pemeriksaan : 13 juli 2022
Keluhan Utama
Pasien datang ke RS Al-Islam oleh keluarganya dengan keadaan lutut kiri sudah
diperban dan ditahan 3 papan, pasien dengan keluhan nyeri pada lutut kiri sisi depan sejak
1 hari yang lalu akibat kecelakaan bermotor. Pasien menggunakan motor pada malam hari jam
02.00 menggunakan helm dengan keadaan jalan gelap mencoba untuk belok kanan, kemudian
ditabrak oleh motor dari arah kiri dengan kecepatan sekitar 40 km/jam.
Pasien mengatakan keluhan disertai adanya luka terbuka sekitar 2 cm dan terdapat
perdarahan aktif. terdapat bengkak pada pergelangan tangan kanan, lecet pada tungkai
bawah kiri sisi kiri.
Pasien menyangkal kepalanya terbentur saat kejadian, hilang kesadaran, mual, muntah, perdarahan
dari hidung, maupun dari telinga. ketika dicoba digerakan secara aktif kaki pasien masih dapat
menggerakan seluruh jari kaki kiri dan mengangkat paha kiri, atau memutar ke arah luar maupun
kedalam meski terbatas karena lutut yang sakit.
Pasien sebelumnya ke ahli tulang di Cijambe tetapi tidak dilakukan apa apa, langsung
disarankan untuk ke RS. kemudian pasien ke RS Hermina dilakukan foto x-ray, pembersihan luka,
penjahitan, penutupan luka dan pemasangan papan. kemudian dirujuk ke RS Al-Islam untuk
dilakukan operasi. pasien tidak memiliki riwayat darah tinggi, atau penyakit gula.
Status Generalis
● Keadaan Umum : Tampak sakit sedang
● Nilai GCS : 15 (E4M6V5)
● Kesadaran : Compos Mentis
Tanda Vital :
● TD : 120/80 mmHg
● N : 80x/menit
● RR : 20x/menit
● SpO2 : 98%
● Suhu : 36 4 C
Pemeriksaan Fisik
Non Farmakologi
● wound debridement
● bandage kompresi tanpa hecting
● traksi dan Imobilisasi dengan 3 splint
Farmakologi
● ketolorac
● pemberian ATS dan TT
Pro rujuk
ke spesialis Sp.B OT untuk mempertahankan fungsi patela dan knee joint
dengan cara ORIF dan (TBW) tension band wiring
Konseling
Edukasi mengenai penyakit pasien
Edukasi mengenai tatalaksana pasien
Edukasi mengenai prognosis penyakit pasien
Prognosis
Quo ad Vitam : Ad bonam
Quo ad Functionam : Ad bonam
Quo ad Sanationam : Ad bonam
Open Fracture
Fracture
• Fraktur adalah terputusnya kontinuitas tulang
dan ditentukan sesuai jenis dan luasnya.
Fraktur dapat terjadi jika tulang dikenai stress
yang lebih besar dari yang dapat diabsorbsi.
Klasifikasi fraktur "
eksternal.
Komplikasi
• Komplikasi awal
• Kerusakan Arteri
+
Compartement Syndrom
•
Fat Embolism Syndrom
•
• lnfeksi
• Avaskuler Nekrosis
• Shock lama
• Delayed Union
Komplikasi dalam waktu
• Non Union
• Mal Union
Pengkajian:
• Aktivitas/istirahat
• Sirkulasi
•
Neurosensori
•
• Nyeri/kenyamanan
• Keamanan
Penyuluhan/Pembelajaran
TENSION BAND WIRING
Teknik tension band wiring (TBW)
Teknik tension band wiring (TBW) adalah perawatan umum untuk
fiksasi fraktur olekranon hingga tiga fragmen. Literatur dan ahli
bedah menggambarkan TBW sebagai operasi yang tidak rumit,
selalu tersedia dan nyaman yang menghasilkan hasil yang sangat
baik.
Pendahuluan
Fraktur olecranon mencapai hingga 40% dari semua fraktur di
sekitar sendi siku. Fraktur olecranon yang tidak rumit dianggap
sebagai cedera umum.
Tujuan utama dari tension band wiring (TBW) adalah reposisi yang
tepat dari permukaan artikular dan pembentukan kembali stabilitas
pada sendi humero-ulnaris.
● Mesenchymal stem cells (MSCs), growth factors, and inflammatory mediators play a temporospatial role.
● Articular cartilage repair remains a difficult problem, but newer techniques are promising.
● Bone is a unique tissue among all musculoskeletal tissues because it heals via formation of normal bone,
as opposed to scar tissue.
● The events of fracture healing mimic embryonic development, and the phases of fracture healing include
inflammation (duration up to 37 days after injury), a reparative phase including soft callus (2 weeks) to
hard callus (6+ weeks), and a remodeling phase (months to years after injury).
● Fracture healing can also be temporally divided into the following four stages; however, there can be
significant overlap:
● Initially after a fracture, there is an increase in blood flow, hematoma formation, and inflammation.
● Tumor necrosis factorα (TNFα), interleukin (IL)1, IL6, IL11, and IL18 are all involved to recruit inflammatory cells and promote angiogenesis.
● Macrophages express TNFα, which peaks at 24 hours, may recruit other cells, and induces osteoblastic differentiation of MSCs.
● The central command orchestrating the initiation of hematoma formation, local inflammation, and tissue regeneration is largely unknown.
● It is possible that the interplay between the periphery (eg, neural, endocrine) and the central nervous system (CNS) is important to the process.
● For example, the weight of the pituitary gland begins to increase 30 minutes after fracture and peaks at 2 to 4 hours and 24 hours after fracture.
● The precise mechanism by which the CNS and/or peripheral nervous system (PNS) initiate the inflammatory process and orchestrate the
temporospatial release of growth factors, cell recruitment, and so on has yet to be elucidated.
Cartilage Formation and Calcification
● During and after inflammation, MSCs are recruited from the periosteum’s cambium layer, the
endosteum, surrounding musculature, and systemically.
● Recruited MSCs differentiate into chondrocytes or osteoblasts depending on the local mechanical
environment.
● Fracture healing can be divided into primary and secondary healing depending on the local mechanical
and physiologic factors.
● In primary healing, the cortex attempts to reestablish itself without the formation of callus (osteonal
or haversian healing) via direct woven bone formation.
● This primary healing occurs when the fracture is anatomically reduced, the blood supply is preserved,
and the fracture is rigidly stabilized by internal fixation.
● Local factors such as highoxygen tension and high pH also predispose to osteoblast stimulation.
Secondary fracture healing results in the formation of callus (cartilage intermediate) and involves the
participation of the periosteum and external soft tissues.
● Lowoxygen tension and low pH favor the MSC differentiation into chondrocytes. This fracture
healing response is enhanced by motion and is inhibited by rigid fixation.
● During secondary bone healing, fractures heal from the periosteum in a centrifugal pattern (ie, radially
outward).
● This increase in the diameter of the fracture callus increases the moment area of inertia, thus
improving stability of the healing tissue. Many fractures entail a combination of both primary and
secondary fracture healing patterns due to variation in local microscopic mechanical strain.
The amount of fracture motion has been demonstrated to affect the differentiation pathway of periosteal
progenitor cells in mice.
● Growth factors and cytokines derived from platelets and other cells are essential for angiogenesis, cellular chemotaxis, proliferation, and
differentiation.
● These growth factors induce MSC differentiation as well as production of type I collagen, type II collagen, and a proteoglycan extracellular matrix
(ECM).
● The transforming growth factorβ (TGFβ) superfamily is critical to the process of matrix production.
● Bone morphogenetic protein2 (BMP2) is important to cell differentiation and/or recruitment during this process.
● During matrix production, the bony fracture ends are resorbed with a decrease in porosity and stiffness; this change in the fracture ends is frequently
● This “leeching” of local bone serves several purposes. First, it provides a local source of calcium.
● It also lowers the elastic modulus of the adjacent bone to minimize stress shielding and allows for physiologic mechanotransduction of adjacent
healing tissue.
● Once this matrix has formed with a subsequent increase in mechanical stability, it is now a soft callus and clinically manifested by a decrease in the
patient’s pain.
Cartilage Resorption and Bone Formation
● During this phase, cartilage cells undergo apoptosis, and ECM is removed to allow for vascular
invasion.
● Vascular endothelial growth factor (VEGF) is expressed by osteoblasts and hypertrophic chondrocytes
to allow for vascular ingrowth and to transform the ECM into osseous tissue.
● There are several mediators of this process including macrophage colonystimulating factor (MCSF),
receptor activator of nuclear factor kappa B ligand (RANKL), osteoprotegerin (OPG), and TNFα.
● The Wnt family of molecules has also been demonstrated to play a role in MSC osteoblastic
differentiation during this process. It has recently been shown that chondroblasts can transdifferentiate
into osteoblasts. In other words, these cells are “plastic” in that they do not need to dedifferentiate and
redifferentiate into an osteoblast—they can “jump” cell lineages to perform required functions.
Bone Remodeling
● After the initial hard callus is formed, the bone continues to remodel as it adapts to local
mechanical factors.
● The hard callus woven bone is typically irregular and provides initial mechanical stability
suitable for loading.
● However, during remodeling, the intramedullary canal is restored, and the woven bone is
replaced by lamellar bone arranged in osteonal systems.
● This remodeling process attempts to restore the Haversian canal system and strengthens the
quality of the bone.
● During this phase, IL1 and TNFα have been shown to be highly expressed.
● The remodeling process begins during hard callus formation but can continue for years as the
bone continues to remodel based on local mechanical factors.