Febrian Brahmana ( BRO ) Notes

In this chapter
- DCO
- Management politrauma review
- Crush syndrome
- Pulmonary emboli
- ARDS
- Infection
- Bone cement implantation syndrome
- Prinsip dalam internal fiksasi dan eksternal fiksasi
- Disturbed bone healing ( AO course )
- Bone faal, Bone healing and remodelling
- Delayed union, non union, Malunion
- Bone garft

Damaged control Orthopaedi

- Definisi DCO : suatu pendekatan yang meliputi stabilisasi cedera orthopaedi sehingga fisiologi pasien membaik. Bertujuan
untuk menghindari kondisi pasien yang bertambah buruk oleh karena second hit dari procedure pembedahan orthopedic, dan
menunda terapi definitive sampai waktu dimana kondisi umum pasien optimal.
- teknik minimal invasive seperti Eksternal fiksasi, digunakan tahap awal. Focus pada bleeding control hemorrhage,
management sot tissue injury dan pencapaian stabilisasi fraktur.
- kelemahan :
bila terlalu lama length of stay di RS resiko : ARDS, Pneumonia dan Fat Emboli Syndrome

( DCO, JBJS, 2005 )

sesaat setelah trauma = respon SIRS terjadi dan diikuti CARS
-> The key players in the host response appear to be the cytokines, the leukocytes, the endothelium, and subsequent
leukocyte-endothelial cell interactions.
-> fenomena first hit = stimulasi mediator inflamasi immediate/sesegera setelah trauma.
Diikuti dengan meningkatnya konsentrasi plasma IL-6 dan IL-8 pada pasien dengan ISS >= 25.
-> setelah trauma,
 produksi interferon dan immunoglobulin menurun
 defek kemotaksis neurtrofil
 defek phagositosis
 defek konten enzim lisosomal
 hasil dari semua diatas adalah : status imunosupresi = menyebabkan infeksi dan sepsis setelah trauma

-> One hit = menyebabkan respon inflamasi berlebih = mengaktifkan system immune innate ( makrofage, leukosit, NK sel,
inflammatory cell migration enhanced by interleukin-8 (IL-8) production and complement components (C5a and C3a)
-> second hit ( sepsis/pembedahan) dapat mereaktifkan respon inflamasi
- Hyperstimulation of the inflammatory system, by either single or multiple hits, is consid- ered by many to be the key
element in the pathogenesis of adult respiratory distress syndrome and multiple organ dysfunction syndrome.

( DCO, JBJS, 2005 )

ISS ( injury severity score )

Politrauma = ISS > 17 dengan sequensial raksi sistemik trauma yang dapat berujung disfungsi / failure remote organ dan vital
system dimana organ / system organ tersebut bukan organ yang secara langsung terkena trauma ( AO Course )

Ingat = Fracture adalah „ luka / wound „ jaringan lunak = artinya adalah mustahil bila suatu fracture TIDAK disertai dengan
cedera soft tissue disekitarnya
Maka !!! bila terdapat fracture, ingat selalu bahwa PASTI ada soft tissue injury !!!!!
Panah biru = artinya memicu, merangsang, promote
Panah merah = artinya menghambat, memutus, inhibit

Edukasi keluarga + pasien

Analgesic IV
MORTALITAS
Tanggungjawab
ke Gusti Allah di
Akhirat

C Clamp, eksternal
fixation, pelvic bandange/
Sling
Cairan IV
Unstable pelvis
SIRS!! MODS
SEPSIS!! MOF

-> O2 terapi
Lihat X RAY
toraks !!! cari
hemotorakss,
peneumotoraks MORBIDITAS
X RAY servikal Maju Jumat
Weekly
Casting, splinting, traction Surgical Debridement +
‘Hold’ the fracture +
antibiotic coverage
Cedera soft tissue sekitar fracture = focus inflammasi

Open fracture, open wound ->

necrotic, devitalized, dead tissue

Mind Map = „ Orthoped Way To Think „ for optimized your Result

Pada pasien poli trauma

Tujuan Utama = Resuscitation untuk memastikan perfusi dan oksigenasi organ vital
Bisa dengan cara konservatif = intubasi, ventilasi dan penggantian volume
Bila usaha tersebut diatas tidak berhasil -> maka -> life saving surgery seperti :
- dekompresi = pneumotoraks, cardiac tamponade, EDH
 - bleeding control = unstable pelvis, crushed injury, whole limb amputation, hemotoraks, abdominal bleding

Within the locomotor system the

following conditions should be treated with high priority:
• Limb-threatening and disabling injuries (including open fractures) require at least “damage control”:
débridement, fasciotomies, reduction, fixation, and revascularization [7].
• Long bone fractures (especially femoral shaft fractures), unstable pelvic injuries, highly unstable
large joints, and spinal injuries require at least provisional reduction and fixation.
Definitive fixation may need to wait and the better option might be temporary stabilization by means of an external
fixator followed by a scheduled, definitive osteosynthesis (intramedullary nailing) during a window of opportunity
between days 5 and 10

There is a convincing body of evidence, from clinical experience as well as in the literature, that early fracture
fixation in polytrauma is beneficial in terms of mortality and morbidity

-> Maksudnya adalah seperti contoh pada unstable pelvis / fracture femur pada pasien poli trauma dapat
dilakukan fiksasi sementara ( EksFix )dalam usaha untuk :
 mengurangi insidensi ARDS, Fat Emboli, Pneumonia, MODS, Sepsis dan komplikasi thromboemboli
lain3
 memfasilitasi perawat ruangan baik di ICU maupun ruangan less intensif untuk early mobiilisasi, up right
chest position
 meminimalisir penggunaan analgetik yang dapat dipicu oleh unfixated fracture

End point resusitasi

 hemodinamik stabil
 tidak hypoxemia tidak byprcapnea
 lactat < 2 mmol/L
 koagulasi normal
 normotthermia
 UO > 1 ml/kgBB/jam
 Tiidak membutuhkan stimulasi vasoactive atau obat2an inotropic

Eleng2 sampe tuwek = Definitive osteosynthesis as “day-1-surgery”is advisable only when all the endpoints of
resuscitation have been accomplished

day 5-10 = window of opportunity secara imunologi

artinya fase hiperinflamasi diikuti dengan periode imunosupressi, saat dimana perekrutan sel inflamasi dan sintesis dari acute
phase protein terjadi

 Saat window of opportunity ini bisa dilakukan definitive surgery dari long bone / inta articular secara AMAN

Periode window of opportunity berlangsung selama 2 minggu = artinya bila dibutuhkan procedure rekonstruksi, bisa
direncanakan pada minggu ke 3 post trauma

Crushed Syndrome and crush injury

- Crushed injury : cedera yang diakibatkan oleh tekanan langsung oleh benda yang cukup berat mengakibatkan crushed
otot
- Crushed syndrome : cedera pada otot skeletal yang berakibat rusaknya suatu integritas sel, mengakibatkan lepasnya isi sel
ke sirkulasi, rhabdomiolisis berakibat suatu perubahan metabolic.
- compression syndrome : cedera otot yang indirect, akibat dari kompresi perlahan sejumlah kelompok otot, berakibat
iskemia, menyebabkan pelepasan isi sel kedalam sirkulasi.

Sejarah
- perang dunia I : dr. Myer Betz : muscle pain, weakness and brown urine
- perang dunia II : dr. Eric Bywaters : after London Blitz = crush injury

Patofisiologi
Crushed/ruptured muscle -> otot swollen, hard, cold, necrotic -> release myoglobin+Tamm-horsfell protein -> konversi ->
methilmyoglobin -> acid hematin, K, Mg, Phosphat, CKMM, LDH -> sirkulasi -> aktivasi NO -> vasodilatasi -> capillary
leak -> volume loss ( to the 3rd space ) -> hipotensi.
Myoglobin disraring ke glomerulus pada tubulus convoluted distal menyebabkan obstruksi
Serum CPK = penting sebagai index derajat muscle damage
Kalium (K) ke sirkulasi = mempengaruhi ritme jantung
acid hematin, K, Mg, Phosphat, CKMM, LDH (Toxic bila release ke sirkulasi pada jumlah yang besar)

crush > 1 jam : rentan crush syndrome

crush 4-6 jam : anatomical, functional changes
> 6 jam : muscle necrosis

klinis
- 1. shock
- petechial, blister, muscle bruising and superficial injuries
- muscle paralysis
- fever
- 2. Elektrolit problem ( cardiac aritmia ) = recipe for aritmia = asidosis + hyperkalemia + hypocalcemia
- urine berwarna tea/cola (tea or cola colored urine)
- oligouria
- 3. renal failure jenisnya acute tubular necrosis ( ATN )
- bisa terjadi kompartemen sindrom
- 4. kompartemen syndrome
- 5. Pulmonary :

laboratories

- creatinin kinase serum > 1000 IU/L -> biasanya 2-12 jam naik setelah cedera crush, puncaknya pada 1-3 hari. Dan
menurun setelah 3-5 hari
- hipokalsemia = karena influx Ca ke otot
- hyperkalemia = keluar dari sel ke sirkulasi
- hiperphospotemia
- hasil degradasi myoglobin :
o serum lactic acid
o serum urea
o serum creatinin
o serum potassium ( K ) = sebagai prediktor untuk hemodialysis
- pada urine = myoglobinuria, RBC, hematuria mikroskopik

Potassium ( kalium ) Hyperkalemia, cardiotoksik, diprovokasi oleh hipovolemia dan hipocalcemia

Phosphate Hyperphospatemia memperburuk hypocalcemia dan kalsifikasi metastatic
Organic acids Metabolic asidosis dan aciduria
myoglobin Myoglobinuria dan nephrotoksik
CK kreatinin kinase
thromboplastin DIC

treatment ( rescue, resusistasi, recognition, rehabilitation )

rescue
- potassium binder
-
resusistasi
- fluid teraphy ( saline, NACL jangan RL krn mengandung K ), pada 6 jam pertama
 - cegah metabolic acidosis = kasih bicarbonate 50 mmol/liter saline
- insulin teraphy drip untuk hyperkalemia
- ( diuresis ) jaga UO minimal 300 ml/24 jam

dialisis
- anuria
- BUN dan serum kreatinin level
- Kalium > 7 meq/l
- 2/3 kali sehari
- profilaksis bila beresiko tinggi hiperkalemia

pentyebab kematian pasien dengan crushed syndrome

- shock ( hari ke 0 sampai ke 4 )
- hyperkalemia (hari ke 0 sampai ke 4 )
- renal failure ( hari ke 3 sampai ke 7 )
- infection ( late )

prediksi poor outcome dari pasien crushed syndrome :

- level CK serum > 100.000
- Oligouria
- Serum creatinin tinggi
- PLT rendah
- Hypotensi
- Hyperkalemia
- Fever
- Albumin rendah
- fever

Pulmonary emboli

Pulmonary embolism atau Emboli paru adalah peristiwa infark jaringan paru akibat tersumbatnya
pembuluh darah arteri pulmonalis oleh peristiwa emboli

Gambaran klinis meliputi spectrum luas, mulai dari suatu gambaran klinis yang asimptomatik sampai
keadaan yang mengancam nyawa berupa hipotensi, shock kardiogenik dan keadaan henti jantung yang
tiba2

-> Penyebab utama = thromboemboli Vena, namun bisa berupa emboli udara, lemak, cairan amnion,
fragment tumor dan sepsis.

Patofisiologi menurut Rudolf Virchow 1856 ( Trias )

- trauma lokal pada dinding pembuluh darah

- Hiperkoagulobilitas darah
- Stasis Vena

Diagnosis

- klinis : Dispnoe merupakan gejala yang paling sering muncul, dan tachypnoe adalah tanda
emboli paru yang paling khas. Pada umumnya, dispnoe berat, sinkop atau sianosis merupakan
tanda utama emboli paru yang mengancam nyawa. Nyeri pleuritik menunjukkan bahwa emboli
paru kecil dan terletak di arteri pulmonalis distal letak dekat dengan pleura
-
- Penunjang = D Dimer test, CT angiografi

Emboli paru pada pasien dengan hipotensi highly suspected bila : terdapat Bukti thrombosis Vena atau
faktor predisposisi emboli paru

Faktor risiko terjadinya thromboemboli Vena yang bisa berujung pada PE

Probabilitas dihitung dengan skor modified wells :

Clinical Characteristic Score

Previous pulmonary embolism or deep vein thrombosis + 1.5

Heart rate >100 beats per minute + 1.5

Recent surgery or immobilization (within the last 30 d) + 1.5

Clinical signs of deep vein thrombosis +3

Alternative diagnosis less likely than pulmonary embolism +3

Hemoptysis +1

Cancer (treated within the last 6 mo) +1

Clinical Probability of Pulmonary Embolism Score

Low 0-1

Intermediate 2-6

High ≥6

Atau revised Geneva Scorring System

Risk factors
- Usia lebih dari 65 tahun 1
- Riwayat DVT sebelumnya / emboli pulmonalis sebelumnya 3
- Riwayat bedah dengan GA fraktur ekstremitas bawah 1 bulan terakhir 2
- Kondisi keganasan aktif ( solid/hemorhagic , currently active / considered Cured < 1 tahun
2
Symptoms
- Unilateral lower limb pain 3
- Hemoptysis 2
Clinical Signs
- Heart rate 75-94 beats/min 3
- Heart rate ≥95 beats/min 5
- Pain on lower limb deep venous palpation and unilateral edema 4
Clinical Probability Score
0-3
- Low
total
4-10
- Intermediate
total
- High

-
-
ARDS

Updated definition of ARDS

ARDS is a syndrome with multiple risk factors that trigger the acute onset of respiratory insufficiency.

-> The pathogenic mechanisms vary depending on the inciting insult, but as demonstrated on autopsy findings, there are a
number of common pathological pulmonary features, such as:

- increased permeability as reflected by alveolar edema due to epithelial and endothelial cell damage, and

- neutrophil infiltration in the early phase of ARDS.

Until recently, the most accepted definition of ARDS for use at the bedside or to conduct clinical trials (1,8) was the
American-European Consensus Conference (AECC) definition, published in 1994 (9).

ARDS was defined as:

-> the acute onset of respiratory failure,

-> bilateral infiltrates on chest radiograph,

-> hypoxemia as defined by a PaO2/FiO2 ratio ≤200 mmHg, and

-> no evidence of left atrial hypertension or a pulmonary capillary pressure <18 mmHg (if measured) to rule out cardiogenic
edema.

In addition, Acute Lung Injury (ALI), the less severe form of acute respiratory failure, was different from ARDS only for the
degree of hypoxemia, in fact it was defined by a 200 < PaO2/FiO2 ≤300 mmHg.

Berlin definition 2013

- Oksigenasi

In the Berlin definition, ARDS was classified as mild, moderate and severe according to the value of PaO 2/FiO2 ratio
Importantly, the PaO2/FiO2 ratio value is considered only with a CPAP or PEEP value of at least 5 cmH 2O.

- Timing of acute inset

The timing of acute onset of respiratory failure to make diagnosis of ARDS is clearly defined in Berlin definition.
It defines the exposure to a known risk factor or worsening of the respiratory symptoms within one week.
It is important to identify risk factors that explain the context of acute respiratory failure arised from

- Chest x ray

The chest radiograph is characterized by bilateral opacities involving at least 3 quadrants that are not fully explained by
pleural effusions, atelectasis and nodules.
In the absence of known risk factors, a cardiogenic origin of edema is to be excluded by objective evaluation of cardiac
function with echocardiography. Consequently, the wedge pressure measurement was abandoned because ARDS may coexist
with hydrostatic edema caused by fluid overload or cardiac failure

BCIS ( bone cement implantation syndrome) = cement emboli disease

Bone cement implantation syndrome (BCIS) is characterised by :

- hypotension,
- hypoxaemia,
- cardiac arrhythmias,
- cardiac arrest or any combination of these,
-
leading to death in 0.6–1% of patients.
 One of the mechanisms suggested to explain these complications is diffuse microembolisation of the
lungs as a consequence of extrusion of the bone marrow content by the pressurised bone cement.
 the release of methyl methacrylate (MMA) cement monomer into the circulation following cementation.
 histamine release, complement activation and endogenous cannabinoid-mediated vasodilatation have also been
proposed

Hipotensi pada BCIS ec = penurunan resistansi vaskuar secara sistemik dan/atau reduced cardiac output

By reducing intramedullary pressure and changing the operative technique, BCIS can be diminished, but
deaths still occur.
An anaphylactoid mechanism as a major factor in BCIS is receiving renewed attention since increased plasma
histamine levels were recently demonstrated after the implantation of bone cement and a prosthesis.

Factor resiko antara lain :

- usia tua
- reduced cardiopulmonary function
- poor health
- osteoporosis / bony metastasis / previous hip fracture = meningkatkan abnormal vascular channels dimana bisa
dilewati marrow ke system sistemik

cara reduksi factor resiko :

 - VS monitored closely pre-op
- Menggunakan low pulsatile lavage, menghilangkan fat dan marrow dari canal
- Removal debris from femur ( blood, cancellous debris )

Strain
Grade 1 : the muscle or tendon is overstretched. Small tears to muscle fibers may or may not occur. You may have mild pain
with or without swelling. Grade I strain is also called mild muscle strain.
Grade 2 : Also called moderate muscle strain, grade II strain occurs when the muscle or its tendon is overstretched with more
of the fibers torn but not complete. Symptoms may include marked pain with swelling. The area of injury is tender. Bruising
may occur if small blood vessels at the site of injury are damaged as well. Movement may be difficult because of pain.
Grade 3 : Grade III strain, or severe muscle strain, is the most serious among the three grades of muscle strains. Most of the
muscle fibers are torn. In some cases, the muscle is completely torn or ruptured. Pain, swelling, tenderness, and bruising are
usually present. Movement is usually difficult.

Growth
Apositional growth = sirkumferential growth, yang bertanggung jawab adalah periosteum, tumbuh menebal
Longitudinal growth = yang bertanggung jawab adalah physis, melewati fase cartilaginous, tumbuh memanjang

Macam2 Arthroplasty (Dr tjuk)

- Interposition (fascia latta, lacertus fibrosus for elbow arthroplasty, kienbock using palmaris longus, sacrifice FDS One belly
One muscle)
- Resection
- excision

Internal fiksasi

Nailing

Mechanics of IM Nailing The original concept of Küntscher was based on the principle of elastic deformation or “elastic
locking” of the nail within the medullary canal.
-> To increase the elasticity , the hollow cloverleaf nail was slotted and reaming of the canal enlarged the area of contact and
friction between the nail and the bone (working length).
Nails with larger diameters had an increased bending and torsional stiffness.
The weak point of the first nails remained the poor resistance to axial (telescoping) forces and rotation especially in
comminuted fractures.

The introduction of interlocking screws and bolts at the proximal and distal end of the nail addressed these issues rather well,
there remains however the problem of the strength and purchase of the lock-ing screws in the bone.
 This problem is not yet completely solved as twisted blades and an increase in screw diameter and number (larger
and more holes) may weaken the nail ends.
Based on the positive experience and data of Lottes who presented very low infection rates in open tibia fractures with the
use of solid nails that were introduced without reaming, thin-ner, solid tibia nails with holes for interlocking were developed.
At the beginning those thin nails were to be inserted without reaming with mandatory interlocking as a temporary splint in
open tibia fractures.

The clinical experience as to the infection rate in open fractures was most encouraging however the time to union took
longer, especially as in the majority of cases the original concept of secondary exchange nailing to a thicker nail was not
followed. The enthusiasm for the new nails without reaming rapidly extended their indications and use also to closed and
highly complex tibia and femur fractures.
-> This resulted in a higher incidence of delayed and malunions due to a poorer mechanical stiffness of the construct
especially in long bone fractures of the lower extremity .

Pathophysiology of IM Nailing Depending on the

- surgical technique,
- nail design, and
- anatomical region the use of intramedullary nails has both local and systemic effects,
some of which may be beneficial, others how-ever detrimental to the patient and fracture healing.

Local Effects

The insertion of a nail into the medullary canal is inevitably associated with damage of the endosteal blood supply , which
was shown to be reversible within 8 to 12 weeks.
-> Experi-mental data have also shown that the cortical blood perfusion is significantly reduced after reaming of the
medullary canal, if compared to a series without reaming.
-> Accordingly the return of cortical blood flow takes considerably longer after reaming than in the unreamed cases, which
may have an influence on the resistance to infection especially in open fractures.
Furthermore tight-fitting nails appear to compromise the cor-tical blood flow to a higher degree than loose fitting ones.32

-> Reaming of a narrow medullary canal may be associated with a risk of heat necrosis of the bone and surrounding tissues
especially if blunt reamers and/or a tourniquet are used.

On the other hand the bone debris produced during the reaming has been shown to act like an autogenous bone graft
enhancing fracture healing.
Meta-analysis of current clinical studies found “gentle” reaming superior to the undreamed technique for reliable healing of
long bone fractures in closed and low-degree open fractures.

Systemic Response

Reaming of the medullary canal has been associated with :

- pul-monary embolization,
- coagulation disorders,
- humoral, neural, immunologic, and
- inflammatory reactions.

The development of post-traumatic pulmonary failure after early femoral nail-ing in the polytrauma patient with chest injury
appears to be more frequent following reaming of the medullary canal than without it.
-> In clinical and experimental studies the pas-sage of large thrombi into the pulmonary circulation has been demonstrated
with intraoperative echocardiography especially during the reaming process and to lesser extent, already when introducing
the reaming guide.
Measurements of the intramedullary pressure have shown values between 420 and 1,510 mm Hg during reaming procedures
compared with 40 to 70 mm Hg when thin solid nails were inserted without reaming.
Nevertheless there is an ongoing controversy between the advocators of reamed nailing also in the multiply injured patient
and those who are recommending the use of thinner solid or cannulated nails without reaming. Especially the young adult
with a simple transverse femoral shaft frac-ture and a high ISS (>25) appears to have an increased risk for pulmonary
complications, which is why there is the recommendation for a staged nailing procedure according to the concept of damage
control surgery (DCS) under such circum-stances.

-> DCS starts as soon as possible with the stabilization of the femoral shaft fracture with an external fixator followed by a
conversion to an intramedullary nail after 5 to 10 days (window of opportunity).

The described systemic responses of IM nailing of femoral shaft fractures seem to be much more critical than in tibial shaft
fractures, where such effects have hardly ever been observed.

Implants for Nailing There is a great variety of intramedullary nails and entire nail-ing systems available for the femur, tibia,
and humerus. Fore-arm nails are also on the market, but until now they have not proven to be superior or as versatile as the
fixation with plates. Originally intramedullary nails were offered in a tubular, usu-ally slotted form, while today solid and
especially cannulated nails are most popular. In children the elastic nails according to Ligier et al. 46 have become the
implant of choice for long bone fractures. The implant material is either stainless steel or a titanium alloy . The holes or
openings for interlocking devices are usually situated at either end of the implant and oriented in different directions, some
nails have also locking possibilities throughout the entire nail length. Accordingly the indications have increased from
originally midshaft fractures to fractures involving the proximal and distal femur and tibia as well as the proximal humerus.
The nail design and the dimensions have to be adapted to the shape of the medullary cavity and the bone. The correct
diameter and length of the nail should to be selected before-hand, unfortunately the accuracy of templates is rather poor. The
best tool is probably a radiolucent ruler placed on the intact contralateral leg under C-arm control or the measure-ment with
the intramedullary guidewire. A very important issue is the correct entry point and starting trajectory of the nail, which varies
from one type of nail to the other (Fig. 7-41).
Eksternal fiksasi

- monoplane
- Circular plane
Hold reduksi fragment fracture
Memberikan stabilitas relatif, sambil menunggu definitif terapi
Sifatnya hanya relatif stability tidak akan pernah bisa mencapai absolut stability

Monolateral as well as circular frames can also be used to bring areas of metaphyseal or metadiaphyseal bone into close
contact through the use of compression techniques.
This may be useful in arthrodesis, osteotomy, or nonunion repair
Similarly, distraction forces can also be applied across pin groups to effect deformity correction, intercalary bone transport,
or limb lengthening

Components No matter what the biomechanical function of the frame type, the most important factor regarding the longevity
and performance of the frame is the strength and competency of the pin–bone interface.
Pin loosening with subsequent pin sepsis continues to be problematic.

There are many biomechanical factors, which have been evaluated for the prevention of pin tract problems.

1. Pin geometry and thread design

- Diameter pin lebih besar lebih kuat
- Placing a screw hole greater than 20% or 30% of the bone's diameter will substantially increase the risk for pinhole fracture

2. Pin biomaterials and biocompatibility

- the use of titanium alloy external fixator pins in distal radial fractures may reduce pin-related complications and
significantly reduce pain levels compared with the stainless steel pin fixators
- Among the many different techniques to enhance the pin– bone interface fixation, coating the pins with hydroxyapatite
(HA) has been shown to be one of the most effective
- The HA coating provides a significant increase in direct bone apposition with a decrease in the fibrous tissue interposition
at the pin–bone interface. There is significantly less pin loos-ening in studies comparing HA-coated pins with other pin
material groups.

3. Pin insertion techniques and pin–bone interface mechanics

Monolateral Frame Types

Monolateral frames are subdivided into those fixators that come with individual separate components, that is, separate bars,
attachable pin bar clamps, bar-to-bar clamps, and separate Schanz pins.
These “simple monolateral” frames allow for a wide range of flexibility with “build-up” or “build-down” capabilities.

These components are available with various diameter connection bars as well as multiple clamp sizes and pin clamp
configurations. These are often available in “mini” configurations as well for the stabilization of smaller areas of involvement
such as for the fingers, wrist, and hand, as well as foot and ankle involvement

As noted above, pin diameters should be undersized especially when stabilizing lesser diameter bones
This allows the surgeon to apply a frame specific to the clinical and biomechanical needs of the pathology addressed (Fig. 8-
22).

The other major category of monolateral frames is a more constrained type fixator which is supplied preassembled with a
multi pin clamp at each end of a long rigid tubular body. The telescoping tube will allow for axial compression or distraction
of this so-called “mono tube”-type fixator.

“Simple monolateral fixators” have the distinct advantage of allowing individual pins to be placed at different angles and
varying obliquities while still connecting to the bar. This is helpful when altering the pin posi-tion relative to the areas of soft
tissue compromise. The advantage of the monotube-type fixator is its simplicity. Pin placement is predetermined by the
multipin clamps. Loosening the universal articulations between the body and the clamps allows these frames to be easily
manipulated to reduce a fracture. Similarly, compression (dynamization) or distraction can be accomplished by a simple
adjustment of the monotube body

“Simple” Monolateral Fixators

The stability of all monolateral fixators is based on the concept of a simple “four-pin frame.”
- Pin number,
- pin separation, and
 - pin proximity to the fracture site, as well as bone–bar distance and the diameter of the pins and connecting bars,
all influence the final mechanical stability of the external fixator frame

Most simple monolateral frames allow for individual placement of pins prior to the application of the connecting bars.
This permits the surgeon to place pins out of the zone of compromised skin or away from the fracture hematoma. The
versatility of contemporary pin/bar clamps have multiple degrees of freedom built into the clamp which allows a single bar to
attach to all four clamps while still retaining the ability to reduce the fracture.
The pins do not have to be placed in precise alignment as was required by earlier monolateral frame designs
If aligned pin placement is contraindicated because of soft tissue or other concerns, the fractures can still be reduced by
simply adding additional connecting bars and using the proximal and distal pin groupings as reduction handles.

Once reduction is achieved, the bar-to-bar connecting clamp is tightened and reduction maintained
-> Simple four-pin system rigidity can be increased by maximizing pin separation distance on each side of the fracture site as
well as the number of pins used.
In the case of a four-pin system, two pins on each limb segment with maximal pin spread, and minimizing the bone-
connecting bar distance also increases stability
However, single and double stacked bar anterior four-pin frames have the best combination of clinical and mechanical
features

When the connecting bar to bone distance increases, implant stability decreases.
This is clinically significant when dealing with patients who present with wide areas of soft tis-sue compromise, which may
preclude the ability to place the connecting bar close to the subcutaneous border of the bone. To counteract this, a standard
four-pin fixator should be augmented by increasing the number of pins applied in each fracture segment.
The materials that the connecting bars are constructed of have a significant effect on overall frame stability.
The weakest part of the system is the junction between the fixator body and the clamp or between the fixator clamp and the
Schanz pins.
Insufficient holding strength on a pin by a clamp may result in a decrease in the overall fixation rigidity, as well as increased
motion and cortical bone reaction at the pin–bone interface.
-> Cyclic loading of external fixators has been shown to loosen the tightened screws in the pin clamps.
Thus, one needs to be aware of the mechanical yield charac-teristics of the clamps, bars, and pins throughout the course of
treatment.
Because of the gradual fatigue of components and loosening of pin-to-bar and bar-to-bar connections, the clinical practice of
regular tightening of the device during the course of treatment should be routine.
-
-
Joint Basic Miller
Cartilage
-> Lapisan cartilage ;
- zona tangential memiliki konsentrasi serabut kolagen yang tinggi, paralel terhadap articular surface
- zona calcified cartilage membentuk zona transisional, intermediate stiffness, terletak antara articular cartilage
dan subchondral bone

-> metabolism cartilage

- sintesis collagen
- katabolisme collagen
- sintesis proteoglycan
- katabolisme proteoglycan

-> lubrications and wear mechanism articular cartilage

- elastohydrodinamik lubrication = mekanisme primer lubrikasi saat fungsi dinamis. Koefisien friksi bergantung
pada bahan lubricants
- boundary lubrication = non deformable bearing surface, lubricant secara parsial memisahkan permukaan
- boosted lubrication
- hydrodynamic lubrication = cairan memisahkan kedua permukaan
- weeping lubrication = cairan bergeser ke area beban

Faktor yang menurunkan friksi Faktor yang meningkatkan friksi

- fluid film formation - fibrilasi
- synovial formation
- elastic deformation dari articular cartilage
- efflux fluid from cartilage

-> artkular cartilage healing

- deep laceration extending below the tidemark + penetrasi ke subchondral bone = healing dengan fibrocartilage
- superfisial articular cartilage, tidak melewati tidemark = proliferasi dari kondrosit namun tidak healing
- CPM promote cartilage healing
 - imoblization lead joint atropi or cartilage degeneration
- 4 minggu imobilisasi pada knee = menurunkan rasio proteoglikan terhadap collagen dimana kemabli normal
dengan mobilisasi joint selama 8 minggu
- joint instability = penurunan hyaluronan, sedangkan kalau disuse tidak mengakibatkan penurunan hialuronan

-> sinovium = sebagai mediator exchange nutrient antara blood dan joint (synovial fluid)
terdapat 2 sel pada sinovium yaitu :
- sel A = untuk fagositosis
- sel B = produksi synovial fluid
- sel C = tipe intermediate
cairan synovial terdiri dari hyaluronic acid, lubricin. Proteinase, collagenase dan prostaglandin
cairan synovial : sebagi lubricant articular cartilage dan nourishment melalui proses difusi
- no RBC
- no clotting factors
- no HB

-> meniscus

anatomi meniscus knee : struktur triangular semilunar, batas tepi melekat pada kapsul sendi
- medial meniscus berbentuk semilunar
- lateral meniscus sirkuler
-
inervasi dan bloodsupply meniscus
- 2/3 perifer nerve ending tipe I, II
- divaskularisasi oleh a geniculate ( cabang nya memvasularisasi 25% tepi RED ZONE dan sisanya mendapat
vaskularisasi dari difusi WHITE ZONE )
- defek pada red zone healing melalui fibrovascular scar, sedangkan white zone ga bisa healing
- sel fibrocondrocyte bertanggungjawab pada proses healing meniscus, lebar defek < 4 mm sembuh dengan baik
Infeksi dari tulang dan sendi dibedakan menjadi 4 :

- pyogenic infection = AHO,CHO, ASA, necrotizing fascitis

- granulomatous infection = TB infection, TB osteomyelitis, TB arhtritis
- viral infection
- non spesifik infection = rheumatoid arthritis, ankylosing spondylitis, psoriasis, Reiters
syndrome, rheumathoid fever

TBC infection
Patologi : mycobacterium tuberculosis –> masuk paru (droplet infection) / GUT / skin -> menyebabkan infeksi pyogenic
infection -> granulomatous reaction = tissue necrosis + casseation

Military tubercle = dibentuk oleh histiocytes, yang menjadi macrophages fagositic yang memakan bacilli. Tubercle bacilli
bisa berkembang didalam intracellular. Sekelompok macrophages yang bergabung membentuk GIANT CELLS.

Tubercle bersifat avaskular, ditengah-tengahnya menajdi massa casseosa karena koagulasi nekrosis.

Imun normal dapat menghasilkan respon imun untuk sembuh berujung dengan fibrosis->kalsifikasi->dorman state = bisa
sewaktu-waktu reaktifasi (khususnya pada pasien poor nutrition, imunocompromised, chronic fatigue.

3 bentuk :

- primary kompleks = lesi inisal pada paru, usus = menyebar via limfatik ke kelenjar limfe regional terdekat,
terjadi pembesaran kelenjar ( masih belum maifestasi klinis ) namun terjadi 2 kemungkinan
o didialam nodes, sembuh/kalsifikasi
o tubuh telah terangsang oleh toksin yang dihasilkan
- secondary lesion
penyebaran via hematogen -> military TB/meningitis TB/multiple lesi TB => bacilli meyebar ke jaringan
ekstrapulmonary
- tertiary
tulang dan sendi terlibat sekitar 5% (corpus vertebrae dan synovial joint yang besar)
sulit menentukan apakah infeksi berasal dari sendi ke sekitarnya atau sebaliknya karena synovial membrane dan
subchondral bone memilki vascularisasi bagus tentunya dapat terinfeksi secara simultan

karakteristik lesi mikroskopik granuloma TB/tuberkel.

kumpulan epiheloid dan multinucleated giant cell disekeliling area nekrosis dengan round sel yang kebanyakan
adalah limfosit mengelilingi perifer.

disekitar area infeksi tampak casseous necrosis, bisa menjadi larger yellowish mass / centre bisa breakdown
(rusak) membentuk abses mengandung pus dan fragment tulang nekrotik
lesi tulang menyebar dengan cepat, cartilage epifisis is no barrier to invasion dan selanjutnya infeksi mencapai
joint. Hanya corpus vertebra dan trochanter mayor (jarang)/metatarsal/metacarpal. Infeksi menetap dan menjadi
kronik osteomyelitis
bila synovium terinfeksi, menjadi tebal, edematous, mengakibatkan efusi
pannus dari jaringan granulasi dapat meluas ke dari synovial reflection -> across the joint
 artikular cartilage hancur secara perlahan, destruksi secara cepat komplit oleh organisme pyogenic does not
occur in the absence of secondary infection.
Pada tepi sendi, dekat dengan refleksi synovial, dapat terjadi erosi tulang yang aktif, lebih-lebih dapat terjadi
peningkatan vaskularitas mengakibatkan osteoporosis
-> Bila tidak mendapatkan terapi, infeksi dan massa kaseosa menyebar ke soft tissue sekitar membentuk COLD
ABCESS (cold hanya sebagai perbandingan dengan infeksi pyogenic). Disebut cold abses karena abses terjadi
tanpa disertai tanda2 inflamasi seperti kemerahan, panas, dll dan prosesnya lama kronik
-> abses ini bisa merusak kulit diatasnya lalu membentuk sinus/ulkus tuberkulosa, atau bila terdapat jalan lain
bisa ke tempat jauh
-> infeksi sekunder oleh bakteri piogenik ditemukan sering
-> bila infeksi diterapi pada stadium awal, maka hasil resolusi bisa didapatkan
-> bila terlambat maka infeksi akan merusak cartilage dan sembuh berakhir dengan fibrosis/ankilosing dengan
deformitas yang progresif
didalam masa fibrocasseosa, mycobakteri terperangkap didalamnya, sewaktu waktu dapat flare up

klinis

- riwayat kontak dengan penderita TB, riwayat minum OAT, riwayat batuk kronis berdahak
- demam, keringat malam hari
- nafsu makan turun -> berat badan turun
- sendi = nyeri, tenderness, stiff, swelling, night cries : sendi terasa sakit sekali secara mendadak karena saat jam
bangun, sendi tersplinting dengan otot yang spasme, namun saat tidur, otot relaks dan mengakibatkan efek
splinting tadi hilang yang berakibat nyeri
- atropi otot
- synovial thickening
- ROM terbatas pada semua arah gerakan
- Pembesaran kelenjar limfe regional
- Pada spine : abses, kifosis, gibbus, weakness lower limb, back pain

X Ray

Pada sendi selain spine

- soft tissue swelling, proses inflamasi berawal dari synovium
- periarticular osteoporosis
- RAT BITE phenomenom
- Erosi subartikular bone : on both sides of the joint
- Penyempitan celah sendi
- Lesi cystic pada bone end namun tanpa reaksi periosteal
-
Pada spine :

- intervertebral disc space berkurang

- colaps corpus vertebrae
- paravertebral absess sebagai soft tissue shadow along the spine

laboratoris : WBC , ESR , mantoux test (+),

aspirasi cairan sendi : didapatkan cairan berwarna putih berawan (CLOUDLY), konsentrasi protein  , WBC 
kultur cairan sendi : acid fast bacilli (+)
biopsy synovial : acid fast bacilli (+)

TB sendi harus dibedakan dengan 5 penyakit sendi yang memiliki manifestasi serupa:

- transient synovitis,
- monoartikular RA,
- sub-acute arthritis,
- hemorrhagic arthritis,
- pyogenic arthritis

Tuberculosis osteomyelitis - Adalah infeksi sekunder yang terjadi dibagian tubuh yang lain yang selalu menyertai infeksi
TB

- Infeksi ini menyebar melalui peredarah darah

- Infeksi ini tidak seperti infeksi pyogenic yang menyerang daerah metafisis, namun sering
menyerang spine (vertebra)
treatment

- rest : prolonged, uninterrupted, rigid (traksi, splintage) untuk mencegah spasme otot dan joint colaps. Selama 6 bulan
sampai 1 tahun. Namun dengan adanya obat2an kemoterapi saat ini, traksi dan splintage tidak mandatory

- kemoterapi : obat anti TB meliputi wajib isoniazid dan rifampicin. (obat anti TB mnimal harus 1 tahun)

Fase inisial : selama 6 bulan tujuan untuk illed bakteria attack

- isoniazid 300-400 mg (I)

- rifampicin 450-600 mg (R)
- floroquinolon

dilanjutkan fase : intensif

- isoniazid 300-400 mg (I) + pyrazinamide 1500 mg/hari (4,5 bulan)

- isoniazid 300-400 mg (I) + rifampicin ( 4,5 bulan selanjutnya )

dilanjutkan fase profilaktik

- isoniazid 300-400 mg (I) + ethambutol 1200 mg / hari selama 3-4 bulan selanjutnya

- operasi

- drainage + pembersihan focus TB

- cold abses harus segera di aspirasi / drainase

umbrella drugs for TB ??

Tentiran dr tjuk malang nov 16

- Bila hip trauma = posisi hip internal rotasi adduksi

- Bila hip infeksi = posisi hip eksternal rotasi, abduksi

Pada infeksi = cek Ada tidaknya multiple sinus / multiple cicatrix scar

Kebanyakan pada infeksi piogenic hip = head hilang

Kebanyakan pada infeksi granulomatous = head masih ada meskipun tidak utuh

Pada kasus trauma, thomas test tidak diperlukan, kecuali ada suatu kecurigaan infeksi yang terjadi prior trauma

Thomas test wajib pada kasus infeksih hip

Heterotrophic kalsifikasi pada hip (jarang, seringnya pada elbow) krn hematoma comes out from the joint

PTO = post traumatic myositis ossificans

Subchondral cyste = post trauma

Untuk konfirmasi arah dislokasi selain diprediksi dari foto pelvis AP yaitu hip axial

Bila terdapat bilateral dislokasi, yang dioperasi pertama kali adalah sisi yang paling sakit

Gambaran x ray yang buruk belum tentu memberikan gejala pain yang berat oleh karena ligament, kapsular, dan soft tissue
sekitar already destroyed dan komponen propioseptik juga ikut rusak

Crescent like app pada x ray = stage III

Bone Healing

Terdapat 2 jenis :

- direct : tanpa melalui pembentukan callus

callus (-), weaker dibandingkan indirect,
melalui mekanisme cutting cone, direct osteonal remodelling
hasil dari stability ABSOLUTE stability only

Contoh dari stabilitas absolut : Lag screw, compression plates

Macam direct healing :

o Kontak healing = bila the gap between bone ends is less than 0.01 mm and
interfragmentary strain is less than 2% = terbentuklah cutting cones pada osteon
deket ujung fracture side
- The tips of the cutting cones consist of osteoclasts which cross the fracture line,
generating longitudinal cavities at a rate of 50–100 μm/day
- These cavities are later filled by bone produced by osteoblasts residing at the rear
of the cutting cone.
- This results in the simultaneous generation of a bony union and the restoration of
Haversian systems formed in an axial direction
- re-established Haversian systems allow for penetration of blood vessels carrying
osteoblastic precursors.
-
The bridging osteons later mature by direct remodelling into lamellar bone resulting
in fracture healing without the formation of periosteal callus.

o GAP Healing
- It occurs if stable conditions and an anatomical reduction are achieved, although
the gap must be less than 800 μm to 1 mm
- this process the fracture site is primarily filled by lamellar bone oriented
perpendicular to the long axis, requiring a secondary osteonal reconstruction unlike
the process of contact healing
- The primary bone structure is then gradually replaced by longitudinal
revascularized osteons carrying osteoprogenitor cells which differentiate into
osteoblasts and produce lamellar bone on each surface of the gap
- This lamellar bone, however, is laid down perpendicular to the long axis and is
mechanically weak.
- This initial process takes approximately 3 and 8 weeks, after which a secondary
remodelling resembling the contact healing cascade with cutting cones takes place.

Bila suatu fracture terfiksasi dengan stabil anatomis namun masih ada GAP < 1 mm
maka akan terjadi direct healing dengan proses cutting cones yang dimulai 3-8 minggu
lebih lambat dibanding bila GAP < 0.01 mm
 - indirect : melalui fase callus
callus (+), stronger than direct healing
melalui mekanisme callus
hasil dari stability RELATIVE = still some small intrafragmentary motion under normal load

missal : ORIF intramedullary nailing / bridging plate, eksternal fixation, plate pada fracture comminutive

o paling sering,
o terdiri dari endochondral dan intramembranous bone healing
o enhanced by micromotion and weight bearing ( hati2 dengan much motion -> resiko non/delayed
union )

Stage of indirect bone Healing

Hemorrhage / perdarahan Tujuan = agar mencapai proses hemostasis

Inflamasi ( 1-7 days post fracture )

Hematoma ( sel dari perifer/intramedullary + bone marrow )

sebagai „callus template‟

Respon inflammasi akut : puncak pada 24 jam pertama dan

berakhir 7 hari setelah fracture
Agen proinflamasi : The fracture results in:
- makrofag -> TNF alfa • Soft-tissue damage
- IL – 1 • Disruption of blood vessels in bone
- IL – 6 Promote
• Separation of small bony fragments
- IL – 11 ANgiogenesis
- IL - 18

Hematoma forms and the periosteum ruptures partly.

Cells migrate into the fracture hematoma.

Bone necrosis is seen at the ends of the fracture
fragments. Injury to the soft tissues and
degranulation of platelets results in the release of
powerful cytokines that produce a typical
inflammatory response,

Coagulation starts. Fibrin fibers are formed and

stabilize the hematoma
(hematoma callus).
 The inflammation stage. Formation of hematoma
resolving into granulation tissue with the typical
inflammatory cascade.
Osteoclasts in this environment remove necrotic
bone at the fragment ends.
Soft callus formation ( 2-3 weeks postfracture )

Terdapat beberapa fase :

Pain and swelling decrease

Phase 1:
New blood vessels invade the organizing
hematoma
Decrease of pain and swelling
Phase 2:
Fibroblasts, derived from periosteum, invade and
colonize the hematoma.
Once injury occurs, the natural process of bone healing
Phase 3:
begins with the creation of soft callus—a cascade of
Fibroblasts produce collagen fibers (granulation cellular differentiation occurs.
tissue).
Phase 4:
Collagen fibers are loosely linked to the bone
fragments.
Phase 5:
The cells of the granulation tissue gradually
differentiate to form fibrous tissue and subsequently
Fibrocartilage (replacing hematoma).

Endochondral = terjadi pada masing masing fracture

ends dan eksternal terhadap periosteal
Intramembraneous, appositional bone growth starts
on these surfaces away from the fracture gap,
forming a cuff of woven bone subperiosteally, and
filling the intramedullary canal.

Kedua proses diatas dibawah pengaruh TGF Beta

-> Ingrowth of capillaries into the callus and

increased vascularity follows.( dipicu oleh VEGF )
-> Closer to the fracture gap, mesenchymal
progenitor cells proliferate and migrate through the
callus, differentiating into fibroblasts or
chondrocytes, each producing their characteristic
extracellular matrix and slowly replacing the
hematoma dengan collagen I dan II
Intramembraneous ossification forming bone cuffs
away from the fracture gap. Replacement of the
granulation tissue elsewhere in the callus by fibrous
tissue and cartilage, and ingrowth of vessels into the
calcified callus. This starts at the periphery and
moves towards the center.
 At the end of soft callus formation, stability
is adequate to prevent shortening,
although angulation at the fracture site
may still occur.
Had Callus ( 3-12 weeks posttrauma )

As intramembraneous bone formation continues, the

soft tissue within the gap undergoes endochondral
ossification and the callus is converted into rigid
calcified tissue (woven bone).

Bone callus growth begins at the periphery of the

fracture site, where the strain is lowest.

The production of this bone reduces the strain more

centrally, which in turn forms bony callus. Thus, hard
callus formation starts peripherally and progressively
moves towards the center of the fracture and the
fracture gap.
Endochondral ossification converts the soft callus to
The initial bony bridge is formed externally or within woven bone starting at the periphery and moving
the medullary canal, away from the original cortex. towards the center, further stiffening the healing tissue.
Then, by endochondral ossification, the soft tissue in This continues until there is no more interfragmentary
the gap is replaced by woven bone that eventually movement.
joins the original cortex.

Bila hard callus (+) = boleh mulai weight bearing

Remodeling Proses ( Taking months to years )

he remodeling stage begins once the fracture has

solidly united with woven bone

The remodeling stage:

- conversion of woven bone into lamellar bone through
surface erosion and osteonal remodeling once
interfragmentary movement ceases.
Fracture healing becomes complete with remodeling of
the medullary canal and removal of parts of the
external callus.

Perbedaan healing antara cortical bone vs cancellous bone

Cortical bone Cancellous bone

Seperti dijelaskan diatas healing in cancellous bone occurs without the

 formation of significant external callus.

After the inflammatory stage, bone formation is

dominated by intramembraneous ossification.

This has been attributed to the tremendous

angiogenic potential of trabecular bone as well as
the fixation used for metaphyseal fractures, which is
often more stable.

In unusual cases with substantial interfragmentary

motion, intermediary soft tissue may form in the gap,
but this is usually fibrous tissue, which is soon
replaced by bone.

Apa itu Osteon ? ( AO Slide )

Adalah basic contruction unit, haverssian system

Each osteon has a central canal, containing blood vessels and a small amount of connective tissue
with interconnecting channels surrounded by cocentric layers of bone, the laminae. There are no
osteons in cancellous bone.
• Osteoclasts are present where new bone is being resorbed.
• Osteoblasts participate in the ossification process, present when new bone is formed.
Osteocytes are trapped within the bone lacunae, is active in the constant remodeling of bone.
Lacunae communicate with each other and the canal of the osteons through canaliculae.
Due to the activity of cutter cones, tunnels are cut through the compact bone, resulting in the creation of new
haversian osteons in their wake.

Bone Formation ( Miller )

1. Endochondral bone formation / mineralization

Stem cell -> kondrosit -> osteoprogenitor dating -> osteoclast resorb cartilage dan osteoblast menjadi tulang
Note = bone replaces the cartilage , bukan cartilage konversi menjadi bone
Contoh = longitudinal growth physis, fracture callus

 Physis =
Growth plate pada tulang mature long bone tedapat 2 :
- Physis, horizontal growth plate
- Epiphysis , spherical growth plate

Physeal cartilage dibagi berdasarkan growth dan fungsi

Bagian cartilage dari growth plate dimulai dari puncak reserve zone, dan berakhir pada intak transverse septa pada
dasar sel kolumn zona hiperthropik

a. Reserve zone / resting zone

Oksigen tension rendah
Bukan bersifat germinal layer, namun lebih ke arah storage
More lipid bodies dan vakuola dibandingkan zona lainnya namun matrixnya mengandung lipid yang minimal
contains the lowest amount of alkaline and acid phosphatase,
Lipid, glycogen (+) pada sitoplasma, proteoglycan aggregates for later growth, abundant reticulum endoplasmic
= indikasi kuat bahwa daerah ini bertugas untuk sintesis protein
They appear to store lipid and other materials and perhaps are held in reserve for later nutritional
requirements
Sel lebih sediit bila diandingkan dengan zona yang lain namun antar sel dengan sel terpisah oleh
matrix extrasellular yang lebih banyak dari zona lain
that the blood vessels that pass through this zone in cartilage canals to arborize at the top of the
proliferative zone do not actually supply the reserve zone itself.

b. Proliferate zone
Oksigen tension tinggi = berfungsi untuk produksi matrix dan proliferasi celluler
Metabolisme aerob terjadi
They are aligned in longitudinal columns with the long axis of the cells perpendicular to the long axis
of the bone
Inhibit calcification
Aktivitas lisosom paling tinggi
Fungsi zona proliferative : produksi matriks dan proliferasi seluler -> Longitudinal growth occur,
Namun cartilage tidak bertambah
This, of course, is due to the vascular invasion that occurs from the metaphysis with the resultant
removal of chondrocytes at the bottom of the hypertrophic zone, events that, in the normal growth
plate, exquisitely balance the rate of cartilage production.

c. Hipertrohic zone
Kondrosit melebar membesar
Sel membesar sebanayk 5x meningkatkan kandungan kalsium dan mitokordia dan lalu mati
Matinya sel ini melapaskan kalsium dari vesikel matriks
Osteoblast lalu terbenam dalam sinusioin darah, lalu menjadikan cartilage sebagai scaffold selama bone
formation
Low oksigen tension dan proteoglycan rendah = menandakan zona ini avascular
Metabolism anaerob terjadi
hypertrophic zone has the lowest diffusion coefficient in the entire growth plate.
Zona ini mengandung high mineral konten, dan menandakan adanya kejadian seqensial meliputi :
1. Calcification occurs.
2. Diffusion of nutrients and oxygen to the hypertrophic chondrocyte is decreased.
3. Anaerobic glycolysis with glycogen consumption occurs until all the glycogen is depleted.
4. Mitochondria release calcium.
5. Nucleation occurs in the matrix vesicles.
6. Calcification of the matrix occurs.

Dibagi lagi menjadi 3 bagian yaitu :

- Maturasi
- Degenerai
- Kalsifikasi provisional = terjadi fracture
 Metafisis
The metaphysis begins just distal to the last intact transverse septum at the base of each cell column of
the cartilage portion of the growth plate.
It ends at the point at which narrowing or funnelization of the bone end ceases, that is, where the wider
metaphysis meets the narrower diaphysis.
-> In the first part of the metaphysis just distal to the cartilage portion of the plate, the oxygen tension is
low -> The low oxygen tension, as well as the rouleaux formation of the red cells frequently seen just
distal to the last intact transverse septa, indicates that this is a region of vascular stasis.
-> an enzyme active in anaerobic metabolism, are found in this region and are compatible with vascular
stasis
Osteoblasts, which are plump, oval-shaped cells with eccentric nuclei, line up along the calcified bars.
Between the osteoblasts lining the calcified bars and the capillary sprouts are seen osteoprogenitor
cells, cells with little cytoplasm but with a prominent ovoid to spindle-shaped nucleus.
-> This region of vascularized calcified cartilage with little or no bone formation occurring on the
calcified bars is termed the primary spongiosum.
A short distance (within a cell or two) further down the calcified longitudinal septa, the osteoblasts
begin laying down bone (termed endochondral ossification, i.e., bone formation within or upon
cartilage). The further down or into the metaphysis one progresses, the more bone is formed on the
calcified cartilage bars. At the same time, the bars gradually diminish in thickness until they disappear
altogether. This region, where bone is laid down on calcified cartilage bars, is termed the secondary
spongiosum
 Still further down in the metaphysis, the fiber bone that was formed originally is replaced with lamellar
bone. This gradual replacement of the calcified longitudinal septa with newly formed fiber bone, as well as the
gradual replacement of fiber bone with lamellar bone, is termed internal or histologic remodeling.

osteoblasts are also seen subperiosteally around the outside of the metaphysis where it diminishes in
diameter to meet the diaphysis. This narrowing or funnelization of the metaphysis is termed external or anatomic
remodeling.

The functions of the metaphysis therefore, are vascular invasion of the transverse septa at the bottom of the
cartilaginous portion of the growth plate, bone formation, and remodeling, both internal and histologic (removal
of calcified cartilage bars and replacement of fiber bone with lamellar bone) and external or anatomic
(funnelization of the metaphysis).

 Perifer dari physis, kommponen fibrous dan fiibrokartilaginous , terbagi menjadi 2 elemen yaitu :
encircling the typical long-bone growth plate at its periphery are a wedge-shaped groove of cells,
termed the ossification groove, and a ring or band of fibrous tissue and bone, termed the perichondrial
ring of La croix
- Groove of ranvier = suplai kondrosit ke perifer untuk berperan dalam pertumbuhan melebar
contains round to oval cells, the function of the groove of Ranvier is to contribute chondrocytes to
the growth plate for the growth in diameter, or latitudinal growth, of the plate

- Pericondral ring of La Croix = jaringan ikat padat yang melekat sebagai jangkar untuk support physis
perichondrial ring is a dense fibrous band that encircles the growth plate at the bone-cartilage
junction and in which collagen fibers run vertically, obliquely, and circumferentially.
continuous at one end with the group of fibroblasts and collagen fibers in the ossification groove
and at the other end with the periosteum and subperiosteal bone of the metaphysis.

Hence the function of the ossification groove is to provide chondrocytes for the growth in width of the growth
plate, and the function of the perichondrial ring is to act as a limiting membrane that provides mechanical
support to the growth plate.

mineralisasi : seeding dar collagen hole zone dengan calcium hidroksiapatite crystal trough branching and accretion ( Crystal
growth )

efek of hormone and growth factor n the growth plate

2. Intramembranous bone formation / ossifikasi

 Tanpa melalui proses kartilago

3. Appositional ossifikasi

Bone Formation Pada Diafisis ( khusus hanya pada diafisis )

Indikasi terjadinya / adanya cartilage model pada long bone adalah = thin collar (ring or sleeve) of osseous tissue around the
middle

The formation of the osseous collar is induced when the cartilage cells in the area mature and hypertrophy, and
the matrix they have produced becomes mineralizable. The collar of bone, which represents the first stage in
the development of the cortex of the evolving bone, is formed through intramembranous ossification from
osteoblasts in the inner or osteogenic layer of the perichondrium.

This fibrous tissue layer, because of its location, should be called periosteum. The cortical shell consists of a
loosely woven matrix with more cells per unit area than that which occurs in mature bone.

Periosteal Vascular buds Primitive vessels masuk ke Endochondral

osseous collar dari periosteum cartilage yang degenerasi, ossification +
element mesenkimal menjadi formation
osteoblast, osteoclast dan hematopoietic
Degeneration / death chondroclast marrow
cartilage cell

As the diaphysis elongates, the cortical shell of bone continues to develop adjacent to the growth plate and
remains at, or slightly beyond, the level of the zone of hypertrophied cartilage cells, providing structural support
for the cartilaginous epiphysis. This extension of the cortical shell forms a three-dimensional cup and is called
Ranvier's ossification groove (encoche deRanvier)

During the rapid advance of enchondral ossification toward the epiphyseal ends of the elongating young bone,
growth is also occurring subperiosteally in the diaphysis. The periosteum becomes quite thick, and spicules of
new bone are deposited more or less perpendicularly between the cambium layer of the periosteum and the
original cortical shell.

Remodelling Cortical Bone

This remodeling is accomplished by osteoclasts, the number and activity of which are influenced by circulatory,
metabolic, and mechanical factors.

The initial event in remodeling is the removal by osteoclasts of matrix that was previously deposited by
osteoblasts. This occurs through the action of a "cutting cone" of osteoclasts, which progresses more or less
longitudinally along the developing shaft of the bone. The cutting cone advances along the course of the vessel,
producing a resorption cavity

Following along behind the cutting cone, osteoblasts become aligned on the walls of the resorption cavity and
secrete a layer of mucopolysaccharides on the surface of the cavity, which is referred to as a cement or reversal
line.

Successive generations of osteoblasts then produce layers of bone that fill in the resorption cavity in centripetal
fashion, leaving a small central canal that contains vessels and nerves. This process results in the production of
an osteon or haversian system, which consists of the central canals with their blood vessels, canaliculi, and the
concentric lamellae of bone
 Setiap kompleks yang terdiri dari central canal dan
matrix ring
Lamella : lingkaran konsentrik dimana lacunae are
arranged
Canaliculi : Tiny canals that radiate outward from
the central canals to all lacunae. They form a
transportation system that connects all the bone
cells to the nutrient supply through the hard bone
matrix.

Terdapat 2 macam canal pada bone yaitu ( prof siki

sering Tanya tentang ini )

Kanal havers : kanal berorientasi vertical, sesuai axis

longitudinal long bone, dimana lamella dan lacuna are
arranged

Kanal Volkmann : transversal, perpendicular terhadap

axis long bone

The canaliculi contain osteocytic processes during life and radiate from the central canal, thereby
interconnecting the osteocytic lacunae. Thus, each haversian system or osteon is a single metabolic unit
nourished by the vessel in the central canal, with nourishment proceeding outward through the canaliculi

As cutting cones remodel bone, they do so with a "skew" determined by mechanical stresses.

Therefore, the cutting cone may cross osteonal lines, removing portions of several osteons. When these
resorption cavities are refilled, portions of the original osteons are left behind. After several waves of such
activity, numerous interstitial fragments remain. Since a cement or reversal line is deposited following the
formation of the cavity, the interstitial fragments are not directly connected to any haversian blood supply.
With the passage of years and many waves of remodeling activity, the number of interstitial fragments
becomes greater and greater.

Volkmann's canals course transversely through the cortex, connecting adjacent haversian systems and providing
intercommunication between the medullary and the periosteal blood supply. These canals are not surrounded
by concentric layers of bone, as are the osteons.

Fracture healing AO course

Tergantung pada factor factor berikut ini :

- Kompleksitas fraktur
- Derajat besarnya soft tissue injury
- Open atau closed injury
- Apakah ada periosteal stripping
- General status of the patient, komorbid ??

Requirement for Bone Healing

- BHO bone healing organ is a hipotetical temporary structure, migrating pluripotent mesenchymal cell :
o Fracture hematoma
o Local/systemic regulatory factors
o Extracellular matrix as the scaffold
- Bone blood flow is the major determinant
- Vascularization of the bone fragment and especially the periosteum
- Soft tissue condition
- Need appropriate mechanical stability

Yield tolerace AO Course

- Bone = 2 %
- Cartilage = 10 %
- Granulation tissue = 100 %

Secara natural untuk menaham strain : large soft callus -> strain decrease -> bony bridge (+)

Bila Gap terlalu kecil : semua intrafragmentary strain minimal = no bony bridge (-)

Low strain on the large gap = bony bridge (+)

 Pada fase awal healing, masih banyak soft tissue = fracture masih mentoleransi deformasi / strain jaringan yang
besar
 Pada fase healing yang lanjut, dimana kalus sudah banyak mengandung jarngan kalsifikasi, = fracture mampu
menahan strain yang lebih rendah

Bony bridging between the distal and proximal callus can only occur when local strain (ie, deformation) is
less than the forming woven bone can tolerate.
Thus, hard callus will not bridge a fracture gap when the movement between the fracture ends is too great

Nature deals with this problem by expanding the volume of soft callus. This results in a decrease in the local
tissue strain to a level that allows bony bridging. This adaptive mechanism is not effective when the fracture
gap has been considerably narrowed so that most of the interfragmentary movement occurs at the gap,
producing a high-strain environment. Thus, overloading of the fracture with too much interfragmentary
movement later in the healing process is not well tolerated

Multifragmentary fractures tolerate more motion between the two main fragments because the overall
movement is shared by several fracture planes, which reduces the tissue strain or deformation at the
fracture gap.

Today there is clinical experience and experimental proof that flexible fixation can stimulate callus formation,
thereby accelerating fracture healing. This can be observed in diaphyseal fractures splinted by
intramedullary nails, external fixators, or bridging plates.

- If the interfragmentary strain is excessive (instability), or the fracture gap is too wide, bony
bridging by hard callus is not obtained in spite of good callus formation, and a hypertrophic
nonunion develops

- Callus formation requires some mechanical stimulation and will not take place when the strain is
too low. A low-strain environment will be produced if the fixation device is too stiff, or if the fracture
gap is too wide. Delayed healing and nonunion will result.

The capacity to stimulate callus formation seems to be limited and may be insufficient when large fracture
gaps are to be bridged. In such cases dynamization (unlocking of the intramedullary nail or external fixator)
may permit bony bridging by allowing the fracture gap to consolidate and increase its stiffness.

 dynamization may be the solution to the problem. If a patient is too immobile to load the operated
leg, an externally applied load might be the way to stimulate callus formation

Factors promoting fracture healing

Movement of the limb
• Increases muscle activity
• Stimulates vascularity (venous and arterial flow)
• Stimulates callus maturation
• Prevents thromboembolic complications

Motion of the limb aids functional recovery, but if it causes strain at the healing fracture site, it increases the risk
of tears in the repaired tissue and compromise of callus formation, which is a potential cause of delayed or
nonunion.

- Metabolic regulasi
Bone Blood Flow - Humeral
fraktur - autonom Vasoactive agent :
- B adrenergic
- musicarinic
Disruption vacular anatomy at the fracture site - thromboxane
- prostaglandin

Decreased bone Blood flow ( initial response )

 Vasokonstriksi
Bone blood flow increase during hours to days after trauma
Resiko terjadi :
Peaks at the 2 weeks after trauma - osteonecrosis
- non union

Getting normal at the 3-5 monts after trauma

Bone Circulation ( sebagai sebuah organ, tulang menerima 10% cardiac output )

Tulang panjang menerima aliran darah dari 3 sumber yaitu :

1. Nutrient artery system

Nutrient arteri masuk ke tulang melalui foramen nutricia, cabang dari major vessel. Setelah masuk ke canalis
medularis, bercabang menjadi :
- Cabang desendent
- Cabang ascendant

yang semuanya bercabang lagi menjadi arterioles yang menembus korteks endosteal -> suplai inner 2/3 diafisis
matur, yang berjalan transversal melalui harversian system

ini adalah system high pressure

2. Metaphyseal epiphyseal system

Ini berasal dari plexus periartikular seperti a. genicularis disekitar lutut

3. Periosteal system
Sebagia besar berbentuk kapiler -> suplai outer 1/3 matur diafisis
Ini adalah low pressure system

Bone Blood Flow Direction

1. Setrifugal ( pada system nutrient arteri, endosteal system ) -> high pressure system
Dan low pressure system
2. Sentripetal bila terjadi fracture displaced -> endosteal system rusak -> tekanan berbalik -> yang mendominasi
adalah system periosteal
3. Sentripetal pada immature bone -> karena periosteum highly vascular = predominasi aliran darah
4. Sentripetal = aliran darah vena

Tissue surrounding the bone

1. Periosteum
Jaringa ikat yang menyelimuti tulang
Sangat berkembangpada tulang anak yang kaya deposisi cortical bone yang bertanggungjawab pada prtumbuhan
tulang secara melebar ( diamtere )
Memiiki 2 layer yaitu :
- Inner ( cambium ) = lebih vascular, loose dan mmiliki sel yang memiliki kemampuan menjadi osteoblast
Bila tulang dalam keadaan normal = berperan dalam pertumbuhan diamteter tulang
Bila tulang dalam keadaan fracture = berperan membentuk periosteal callus
- Outer ( fibrous ) = yang less cellular, berlanjut menjadi kapsul sendi saat mendekati sendi

2. Bone marrow
Kontrol pertumbuhan diameter tulang internal
Memiliki 2 jenis
- Red marrow = bersifat hematopoietic ( 40% air, 40% lemak, 20% protein )
Red marrow dapatbberubah menjadi yellow marrow dengan bertambahnya umur
- Yellow marrow = bersifat inactive ( 15% air, 80% lemak, 5% protein )
Disturbed Bone Healing ( AO Course )

Terdapat 3

- delayed union : gagal konsolidasi dalam waktu normal yang diharapkan berdasarkan tipe dan lokasi
- Non union : memperkirakan bahwa healing tidak akan terjadi, tanpa intervensi
- Pseudoarthrosis : peembentukan false joint dimana fibro-cartilaginous dengan synovial membrane.

Delayed Union ( Noted : That a bone is delayed in its union does not mean that it will become a nonunion )

by definition, is present when an adequate period of time has elapsed since the initial injury without achieving
bone union, taking into account the variables : umur, tulang yang cedera, sifat/bentuk fracture dan cedera soft
tissue yang menyertai

Classically the stated reasons for delayed union are problems such as :

- inadequate reduction,

- inadequate immobilization, sesuai dengan teori Perrent tentang relative motion at fracture site ( Strain Teory )

- distraction,

- loss of blood supply, and

- infection.

Non Union

Nonunion is defined as the cessation of all reparative processes of healing without bony union.

Since all of the factors discussed under delayed union usually occur to a more severe degree in nonunion, the
differentiation between delayed and nonunion is often based on radiographic criteria and time.

In humans, failure to show any progressive change in the radiographic appearance for at least 3 months after
the period of time during which normal fracture union would be thought to have occurred, is evidence of
nonunion

Tanda-tanda = klinis dan radiologis

Klinis = nyeri tekan pada fracture site, false movement still

Radiographic =

- a radiolucent line through the fracture site,

- sealing off of the medullary cavity with sclerosis at the edge of the fractured bone, and
- bony resorption or regional osteoporosis above and below the fracture site.
- The bone ends may be somewhat rounded, and a large hypertrophic callus may be present. This
"elephant foot" appearance of the callus has been thought of as one of the hallmarks of nonunion.
- Rarely, an atrophic nonunion is seen without any callus at the fractured bone ends = biasanya
disebabkan oleh soft tissue injury yang massive dan loss of vascularity

Malunion

defined as a healing of the bones in an abnormal position;

Malunions can be classified as functional or nonfunctional. Functional malunions are usually those that have
small deviations from normal axes that do not incapacitate the patient.

Malunions can occur with both axial deviations and rotational deformities.
 - Axial deformities such as the valgus or lateral deviation of the forepaw that occurs with a poorly set
fracture may cause secondary degenerative joint disease of the carpus because of continued weight
bearing in an abnormal position. Very often these axial deviation malunions will develop associated
joint problems.
- Rotational malunions also occur and are usually those of external rotation. These deformities allow
a surprising degree of function in most animal species. Conversely, internal rotational deformities
may cause more serious problems but are uncommon. Most external rotational deformities are not
even appreciated if they are less than 10 degree

Fractures associated with physeal injuries may also lead to deformities that are usually not classified as
malunions. These deformities are associated with premature closure of the growth plate. Very often the
deformity in these cases is the same as that of malunion, but it occurred after the time of union because of
further growth of one or more bones in relationship to other nongrowing bones.

Bone graft

- osteokonduktif matriks = Framework dimana bone growth terjadi

- osteokonduktif faktor = Growth faktur untuk memicu bone growth

- struktural integrity =

- osteogenic cells = osteosit, osteoblast, mesenkimal Cell

Macam2 jenis spesifik graft

- Cancellous bone graft sering dipakai untuk non union dan defek yang bersifat cavitary, Krn remodelling cepat dan
incorporated melalui creeping substitusi
- cortical bone graft remodelling dan incorporated lambat, sering dipakai untuk defek struktural namun haversian sistem
mengalami remodelling sehingga weakens the graft, lalu diikuti dengan deposisi of the new bone yang memperkuat tulang

Lamellar masih utuh namun resorpsi hanya pada batas

- sintetis bone graft ( terusin atas kalsium silicon alumunium )

Vascularized bone graft : bila defek jaringan cukup lebar luas, namun donor site morbidity cukup besar