Rangkuman Week 1 (PBL) - Fracture

Rangkuman Week 1 – Fracture 1. Bone Growth and Formation a. Intramembranous Ossification  Membentuk tulang-tulang pipih  Pembentukan tulang tidak didahului pembentukan tulang rawan.  Terdapat trabekel tulang. Proses: o Pembentukan ossification center o Calcification o Pembentukan trabekel o Perkembangan periosteum

b. Endochondral Ossification  Tulang terbentuk dari tulang rawan hyaline  Ada primary ossification center pada fetus dan infants  Ada secondary ossification center pada anak-anak, remaja dan early adulthood.  Membentuk hampir seluruh tulang pada skeleton manusia (selain yang dibentuk pada osifikasi desmal). Proses: o Perkembangan model tulang rawan o Pertumbuhan model tulang rawan o Perkembangan primary ossification center o Perkembangan medullary (marrow) cavity o Perkembangan secondary ossification center o Pembentukan articular cartilang dan eoiohyseal (growth)

c. Normal epiphyseal (growth) plate  Growth in the length of the metaphysis and diaphysis of a long bone.  Terjadi interstitial growth sel tulang rawan, membuat epiphysis terletak lebih jauh dari metaphysis  Terjadi calcification, death and replacement dari tulang rawan pada metaphysical surface melalui osifikasi endokondral.  Ada 4 zona pada epiphyseal plate: o Zona rehat:  Zona terdekat dengan epiphysis.  Terdiri dari kondrosit yang kecil. o Zona proliferasi  Terdapat yang kondrosit yang sedikit lebih besar.  Kondrositnya mengalami pertumbuhan interstitial. o Zona hipertrofi/maturasi  Kondrositnya sudah matang dan besar serta tersusun dalam kolomkolom. o Zona kalsifikasi  Kondrositnya kebanyaka telah mati.

2. Bone types ( cortical,trabecular, woven) and histologic features of each. cortical bone /compact bone system havers(osteon) :untuk menyalurkan sirkulasi ke tulang, terdiri dari lamel konsentrik yang mengikuti saluran havers. lamel interstisiales:lamel sisa osteon yang mengalami remodeling. volkmann’s canal:saluran havers yang menembus lamel-lamel,berguna untuk menyalurkan aliran darah,nerves. - canaliculi : menghubungkan antar lacuna dan central canal untuk menyampaikan nutrisi. osteosit :mature cell yang terletak didalam lacuna

woven bone / immature bone - pada skeleton embrio,yang matriksnya terusun dari proteogyclan dengan sedikit cement tetapi belum memiliki lamel. - Umumnya woven bone akan hilang dan digantikan dengan cortical bone pada usia >1tahun,tapi dalam keadaan patologis woven bone tetap ada pada orang dewasa .

trabecular bone/cancellous bone - less complex in lamellae arrangement making it thin in its trabeculae and nourished by vessels in the marrow spaces a. Basic structures of diaphysis, metaphysis bone and their blood supply Metaphysis Daerah perbatasan antara growth plate dan diaphysis,tersusun dari trabecular bone.Dan terdapat epiphyseal plate yang merupakan lapisan kartilago hyaline yang berfungsi dalam pertumbuhan memanjang dari diaphysis.Pada usia 18-21 tahun epiphyseal plate pada metaphysis akan digantikan oleh tulang,sehingga menjadi epiphyseal line. Aliran arah pada metaphyseal berasal dari arteri yang mensupply sendi,anastomose dengan diaphyseal kapiler dan berakhir di cortical bone,trabecular bone. Diaphysis Diaphysis adalah bagian dari tulang panjang yang terletak diantara metaphysis yang terdiri dari compact cortical bone.Pada bagian tengah diaphysis terdapat medullary canal yang berisi marro dan sedikit trabecular bone. Aliran darah pada diaphysis disupply oleh diaphyseal nutrient artery yang merupakan artery paling penting pada long bone,diaphyseal nutrient arteries melalui cortical bone secara oblique,artery ini dibedakan menjadi ascendant dan descendant dan mensupply 2/3 dari cortex dan medullary cavity. b. Structure of periosteum

Merupakan jaringan double layer yang melapisi seluruh permukaan tulang yang tidak dilapisi oleh articular cartilage.  Pada lapisan luar periosteum berhubungan langsung dengan pembuluh darah dan terdiri dari jaringan fibrosa,pada lapisan dalam terdiri dari lapisan osteogenic dimana terdapat sel osteoprogenitor. Periosteum berhubungan dengan tulang melalui serat kolagen yang kuat, Sharpey’s fibres. Fungsi periosteum: -Sebagai tempat menempelnya tendon dan ligament -berperan penting dalam proses bone healing. -memberi nutrisi pada sel-sel tulang melalui pembuluh darah yang terdapat di periosteum c. Major bone cells and their function Osteoblast - Merupakan diferensiasi dari sel mesenkim,berfungsi dalam proses osteogenisis atau osifikasi. - Osteoblast mensintesis kolagen dan komponen organic lainnya yang digunakan untuk membuat matrix extracellular agar dapat terjadi proses kalsifikasi,jika sudah tertutupi oleh matrix extracellular maka osteoblast berubah menjadi osteosit - Sel osteoblast yang belum mengalami kalsifikasi disebut osteoid (prebone) pada tahap ini tulang masih lunak. - Tidak mengalami mitosis dan tidak dikelilingi matrix. Osteosit - Mature bone cells dikelilingi matrix yang berasal dari osteoblast. - Berfungsi untuk mengatur metabolism tulang dalam pertukaran nutrisi dan waste dengan aliran darah - Tidak mengalami mitosis. Osteoclast - Berfungsi sebagai bone resoption karna memiliki enxim lisosom dan acid yang berguna untuk melisis komponen protein dan mineral dalam matrix extracellular tulang. - Peran penting dalam proses pertumbuhan,perkembangan dan bone repair. - Mengatur kadar kaslium dalam darah - Secara mikrokopik berada diluar trabekel tulang dengan ukuran sel yang besar dan memiliki banyak inti. Osteoprogenitor -bone stem cell yang berasal dari mesenkim dan mengalami perkembangan menjadi osteoblast. -terletak pada periosteum tulang.

d. Component of bone matrix Bone matrix consist of: - organic component - anorganic component -Organic component(35%)= - osteoprogenitor cell - osteosit - osteoblast - osteoclast - osteoid(sel osteoblast yang belum mengalami kalsifikasi) -Inorganic component(65%)= - Hydroxyapatite (mineral salts) - calcium phosphate [Ca3(PO4) 2.(OH) 2] (menjadikan tulang kuat) -calcium carbonate, fluoride, magnesium. e. Common type of collagen Collagen ada 2 jenis:collagen 1 dan collagen 2. collagen type I - major collagen pada kulit,tulang,fibrokartilago,meniskus - berfungsi untuk menguatkan tulang - ada 2 jenis: COL1A1 COL1A2 -collagen type 1 terdiri dari 2rantai procollagen 1α1menjadi COL1A1 1rantai procollagen 1α2menjadi COL1A2 jika terjadi mutasi pada kolagen type 1 maka dapat menyebabkan osteogenesis imperfect. collagen type 2 - banyak terdapat di kartilago,articular cartilage,vitreous(eyeball) - dalam jumlah kecil ditemukan pada jaringan skeleton pada awal masa pertumbuhan. - Berfungsi untuk menguatkan connective tissue pada otot,sendi. Jika terjadi mutasi makan dapat menyebabkan chondrodisplasia(dwarfism) f. Describe the mineralization of bone The mineralization of soft callus begins about 1 week later, after the formation of new soft callus. The increased oxygen tension leads to the production of osteoid(visible on radiographs) The presences of osteoid provides rigidity within the callus  id dependent on the relative stability of the fracture site, the larger callus is prevent this motion.  been gained across the fracture site,the patient may resume limited activity.  callus may take anything from 4 to 16 weeks and is a quicker process in children and spongy bones.

3. Bone Remodelling. a. Cortical (Compact) bone - Characterized by the concentric arrangement dari lamella dan complex formation dari sistem havers atau osteon. b. Cancellous (trabecular) bone - The arrangement dari lamelanya lebih sederhana dibandingkan dengan cortical bone karena trabekelnya thin dan dapat dinutrisi oleh pembuluh darah disekitarnya dan marrow spaces. c. Wolff’s Law  Bone Reaction o Ada 4 basic ways of bone reaction to abnormalities:  Local death: keadaan sebuah area pada tulang telah completely deprived of its blood supply.  An alteration of bone deposition:  Increased deposition: peningkatan pembentukan matrix dengan kalsifikasi normal  Decreased deposition: pengurangan pembentukan matrix atau hypo-calcification  An alteration of bone resorption: increased resoprtion dan decreased resorption  Mechanical failure or fracture o Reaksi-reaksi tulang lainnya terhadap disorders and injuries:  Osteoporosis (Marble Bones)  Acromegaly  Osteoporosis (Osteopenia)  Rickets in children, Osteomalacia in adults.  Degenerative Osteoarthritis  Fractures  Infection  Osteosclerotic Neoplasms  Rheumatoid Arthritis  Osteolytic Neoplasms  Bone Healing o Formation of fracture hematoma: Blood vessels crossing the fracture line are broken. As blood leaks from the torn ends of the vessels, a mass of blood (usually clotted) forms around the site of the fracture. This mass of blood, called a fracture hematoma, usually forms 6 to 8 hours after the injury. Swelling and inflammation occur in response to dead bone cells, producing additional cellular debris. Phagocytes (neutrophils and macrophages) and osteoclasts begin to remove the dead or damaged tissue in and around the fracture hematoma. o Fibrocartilaginous callus formation: Fibroblasts from the periosteum invade the fracture site and produce collagen fibers. In addition, cells from the periosteum develop into chondroblasts and begin to produce fibrocartilage. These events lead to the development of a fibrocartilaginous (soft) callus, a mass of repair tissue consisting of collagen fibers and cartilage that bridges the broken ends of the bone. Formation of the fibrocartilaginous callus takes about 3 weeks. o Bony callus formation: osteogenic cells develop into osteoblasts, which begin to produce spongy bone trabeculae. The fibrocartilage is converted to spongy bone, and the callus is then referred to as a bony (hard) callus. The bony callus lasts about 3 to 4 months. o Bone remodeling: The final phase of fracture repair is bone remodeling of the callus. Dead portions of the original fragments of broken bone are gradually resorbed by osteoclasts. Compact bone replaces spongy bone around the periphery of the fracture.

 Diaphyseal Healing o Stage of Healing from Soft Tissue Osteogenic cells yang berproliferasi dari lapisan dalam periosteum untuk membentuk external callus dan to a lesser extent from endosteum untuk membentuk internal callus. o Stage of Clinical Union Temporary external and internal callus mengelilingi fracture site dan membentuk “biological glue” yang memperkeras saat cartilaginous components dari callus digantikan dengan tulang melalui osifikasi endokondral. o Stage of Radiographic Union Seiring waktu berjalan, the temporary callus digantikan oleh mature lamellar bone. Pada saat tulang yang belum matang telah digantikan oleh mature lamellar bone dan tulang sudah kembali ke diameter yang hampir normal, fraktur itu sudah bisa dikatakan radiographic union.  Metaphyseal Healing Diawali dengan pembentukan internal atau endosteal callus, walaupun external atau periosteal callus yang mengelilingi thin shell of cortex juga memegang peran penting. Karena banyaknya suplai darah pada thin trabeculae dari cancellous bone sehingga terjadi sedikit necrosis tulang. The Osteogenic repair cells berproliferasi membentuk primary woven bonedi internal fracture hematoma. Saat telah terjadi Union, fraktur sudah clinically united. Lalu, woven bone digantikan oleh lamellar bone saat fraktur telah radiographic united.  Growth Plate Reaction o Ada 3 basic ways:  Increased Growth:  Generalized:  Arachnodactyly (Hyperchondroplasia) (Marfan’s Syndrome)  Pituitary Gigantism  Localized:  Chronic Inflammation  Displaced fracture of the shaft long bone  Congenital Arteriovenous Malformations  Decreased Growth  Generalized:  Achndroplasia  Pituitary Dwarfism (Lorain type)  Rickets  Localized:  Disuse retardation  Thermal Injury  Ischemia  Infection  Torsional Growth  Localized: when a growing long bone and its epiphyseal plate are subjected to either continual or intermittent twisting forces. Ex: Knock Knees  Bone Deformity o Loss of Alignment: Terjadi pada long bone. Bisa karena twisted in its long axis (torsional deformity) atau karena crooked (angulatory deformity). o Abnormal Length

Bisa abnormally pendek atau memanjang. Kalau hanya terjadi pada salah stu kaki atau salah satu tangan disebut limb length discrepancy. o Bony Outgrowth: A lesion, seperti Osteochondroma.  Bone Neoplasm o Neoplasm-like Lesions of Bone  Osteogenic  Osteoma (ivory exostosis)  Single Ostechondroma (osteocartilaginous exostosis)  Multiple Osteochondroma (multiple hereditary Osteoma)  Osteoid Osteoma  Benign Osteoblastoma  Chondrogenic  Echondroma  Multiple Echondromata (Ollier’s Dyschondroplasia)  Fibrogenic  Subperiosteal cortical defect (metaphyseal fibrous defect)  Nonosteogenic fibroma (nonossifying fibroma)  Monostotic fibrous dysplasia  Polyostotic fibrous dysplasia  Osteofibrous dysplasia (Campanacci syndrome)  “Brown tumor” (hyperparathyroidism)  Angiogenic  Angioma of bone (hemangioma and lymphangioma)  Aneurysmal bone cyst (ABC)  Uncertain origin  Simple bone cyst (Unicameral bone cyst (UBC)) o True Primary Neoplasm of Bone  Osteogenic  Osteosarcoma (Osteogenic Sarcoma)  Surface osteosarcoma (periosteal sarcoma)  Chondrogenic  Benign chondroblastoma  Chondromyxoid fibroma  Chondrosarcoma  Fibrogenic  Fibrosarcoma of Bone  Malignant fibrous histiocytoma of bone  Angiogenic  Angiosarcoma of bone  Myelogenic  Myeloma of bone (Multiple myeloma)  Ewing’s sarcoma (Ewing’s tumor)  Hodgkin’s lymphoma of bone  Non-Hodgkin’s lymphoma (reticulum cell sarcoma)  Skeletal reticuloses (Langerhan’s cell histiocytoses)  Leukemia  Uncertain origin  Giant cell tumor of bone (Osteoclastoma)

4. Muscle Physiology a. Describe the innervations of muscle and neuromuscular junction.

b. Explain the physiology of muscle contraction

c. Explain the mechanism of muscle growth (hypertrophy, atrophy, growth in length) and contracture. i. Muscle Hypertrophy - Aerobic, short-duration, high intensity resistance training (weight lifting) results in muscle enlargement by increase in its diameter (hypertrophy) of fast, glycolytic fibers during powerful contractions. - Muscle enlargement by thickening of myosin and actin filament, allowing cross-bridge interaction and increase the muscle’s contractile strength. - During contraction, muscle fiber triggers signaling proteins that turn on genes to direct synthesis of more of these contractile proteins. Thus, exercises with endurance compared to brief periods are more effective. ii. Muscle Atrophy - When muscle is not in use, actin and myosin content decreases as its fibers becomes smaller and eventually atrophies and weaker.  Disuse Atrophy Occurs when muscle is not in use for a long time. Ex. when casting or brace is worn for prolonged period.  Denervation atrophy Occurs after nerve supply to a muscle is lost which can be treated by stimulation electricity, but this doesn’t fully treat denervation. Thus, muscle contraction is important as it activates ACh for nerves to work.

Fracture: structural break in continuity. Types of Fracture: Direction

of

fracture

Transverse

lines

Oblique

Spiral

Comminuted

Comminuted (Segmental)

Comminuted (Butterfly)

Impacted

Anatomic location Alignment

(Degree

angulation

of

of

Proximal Middle Distal Good alignment

distal

fragment and proximal fragment) Angulation

Displacement

Associated

soft

Partial apposition Displaced Distracted

tissue

Closed (uncomplicated)

injury Stability

Open (complicated) Stable Unstable

SPECIAL FEATUED FRACTURE

Colles Fractures results from fall on an outstretched hand, often in osteoporotic women. The deformed and painful wrist looks like a “dinner fork”. The main lesion is a dorsally displaced, dorsally angulated fracture of distal radius. Treat with close reduction and long arm cast.

Smith Fracture Smith's fractures are either extra or intraarticular. These fractures are essentially inverted Colle's fracture since there is apex dorsal angulation. If the fracture is intraarticular, it is called a Barton's fracture.

Monteggia fracture result from direct blow to the ulna (such as on a raised protective arm hit by a nightstick). There is diaphyseal fracture of the proximal ulna, with anterior dislocation of the radial head.

Galeazzi fracture is the mirror image of the previous one: the distal third of the radius gets the direct blow and has the fracture, and there is dorsal dislocation of the distal radioulnar joint. In both of these, the broken bone often requires open reduction and internal fixation, whereasthe dislocated one is typically handled with closed reduction.

KLASIFIKASI OPEN FRACTURE

Bone Healing Process

WAKTU PENYEMBUHAN Perkins rules 

Fractures of cancellous (metaphyseal) bone (e.g. those around joints) will take 6 weeks to unite.



Fractures of cortical (diaphyseal) bone (e.g. shafts of long bones) will take 12 weeks to unite.



Fractures of the tibia (because of poor blood supply), will take 24 weeks to unite.



Time to union for children equals the age of the child in years plus one, e.g. tibial fracture in a 2-year-old child will unite in 3 weeks. Common sense needs to be applied when applying the rule to fractures of cancellous bone in older children.

DIAGNOSIS X-ray (rule of 2) -

2 views

-

2 joints

-

2 limbs

-

2 injuries

-

2 occasions

TREATMENTS 1. CLOSED FRACTURE a. Reduce i. Closed Reduction ii. Open reduction b. Hold Reduction i. Continuous traction 1. Skin traction 2. Skeletal traction 3. Fixed traction (Thomas Splint) 4. Balanced traction 5. Combined traction ii. Cast Splintage iii. Functional Bracing iv. Internal Fixation 1. Interfragmentary screw 2. Wires (transfixing, cerclage and tension band)

3. Plates dan screw v. External Fixation 2. OPEN FRACTURE a. Debridement b. Wound closure c. Stabilization of fracture d. Aftercare e. Sequels to open fracture

COMPLICATION OF FRACTURE 1. EARLY COMPLICATION a. Visceral injury b. Vascular injury c. Nerve injury d. Compartment syndrome e. Hemarthrosis f.

Infection

g. Gas gangrene h. Fracture blister i.

Plaster sores and pressure sores

2. LATE COMPLICATION a. Delayed Union: failure of union to occur in 1.5 times the normal time for fracture union. b. Non-Union: failure of union to occur within 2 times the normal time to fracture union. However, expect open fractures to normally take 2 times the normal Perkins rule. Non-union can be broadly divided into: i. hypertrophic: normally due to excess mobility, i.e. good healing potential; ii. atrophic: normally due to poor blood supply, i.e. poor healing potential. c. Mal-Union d. Avascular Necrosis e. Growth Disturbances  epiphyseal fracture in children f.

Bed Sores  elderly/paralyzed patients

g. Myositis ossificans  heterotopic ossification in the muscle h. Tendon lesion i.

Nerve compression

j.

Muscle contracture

k. Joint instability l.

Joint stiffness

m. Algodysthropy (Complex regional pain syndrome)

Osteoarthrytis