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CASE REPORT

NON UNION 1/3 MIDDLE FEMUR FRACTURE SINISTRA AND OSTEOMYELITIS


Disusun untuk Memenuhi Sebagian Tugas Kepaniteraan Klinik
Bagian Ilmu Bedah di RSUD dr. H. Soewondo Kendal

Disusun oleh:
Ulfa Elsanata
01.211.6546
Pembimbing:
dr. Wisnu Murti, Sp.OT
ILMU BEDAH RSUD DR. H. SOEWONDO KENDAL
FAKULTAS KEDOKTERAN
UNIVERSITAS ISLAM SULTAN AGUNG
SEMARANG
2016
HALAMAN PENGESAHAN

Nama

Ulfa Elsanata

NIM

01.211.6546

Fakultas

Kedokteran

Universitas :

Universitas Islam Sultan Agung ( UNISSULA )

Tingkat

Program Pendidikan Profesi Dokter

Bagian

Ilmu Bedah

Judul

Non Union 1/3 Middle Femur Fracture Sinistra And Osteomyelitis

Semarang, April 2016


Mengetahui dan Menyetujui
Pembimbing Kepaniteraan Klinik
Bagian Ilmu Bedah RSUD Kendal

Pembimbing,

dr. Wisnu Murti Sp.OT


CHAPTER I
INTRODUCTION
A fracture is a discontinuity of bone, catilage, ephiphyseal cartilage both total and
partial. The femur is the largest and strongest bone and has a good blood supply. Because
of this and its protective surrounding muscle, the shaft requires a large amount of force to
fracture. Once a fracture does occur, this same protective musculature usually is the cause

of displacement, which commonly occurs with femoral shaft fractures. Traumatic femur
fractures in the young individual are generally caused by high-energy forces and are often
associated with multisystem trauma. In the elderly population, femur fractures are typically
caused by a low energy mechanism such as a fall from standing height.
Assessment of fracture healing (union) based on the union of clinical and radiology
union. Clinical assessment made by examining the fracture area by bending in the fracture
area, rotation and compression to determine the presence or feeling pain in patient. Union
radiology assessed by X-ray examination in the fracture line or callus and may be found of
the trabeculation that already connect the two fragments. At the advancednlevel include the
medulla or room in the fracture area. In the process of bone healing can occur undesirable
result, in which the bones have fused in line with expectation, either way the union nor the
time of unification. The healing process in question is malun ion, nonunion and delayed
union.

As with many orthopedic injuries, neurovascular complications and pain


management are the most significant issues in patients who come to the hospital. The rich
blood supply, when disrupted, can result in significant bleeding. Open fractures have added
potential for infection
Osteomyelitis is inflammation of the bone caused by an infecting organism.
Although bone is normally resistant to bacterial colonization, events such as trauma,
surgery, the presence of foreign bodies, or the placement of prostheses may disrupt bony
integrity and lead to the onset of bone infection. Osteomyelitis can also result from
hematogenous spread after bacteremia.

CHAPTER II
CONTENS REVIEW

I.

ANATOMY OF FEMUR

The
femur is
the

only

bone
located
within the human thigh. It is both the longest and the strongest bone in
the human body, extending from the hip to the knee. It is classed as a
long bone, and is in fact the longest bone in the body. The main function
of the femur is to transmit forces from the tibia to the hip joint.It acts as
the place of origin and attachment of many muscles and ligaments so
we shall split it into three areas; proximal, shaft and distal.

Picture 1. Femur; anterior and posterior view


Proximal
The proximal area of the femur forms the hip joint with the
pelvis. It consists of a head and neck, and two bony processes called
trochanters. There are also two bony ridges connecting the two
trochanters
Head Has a smooth surface with a depression on the medial
surface this is for the attachment of the ligament of the head. At the
hip joint, it articulates with the acetabulum of the pelvis.
Neck Connects the head of the femur with the shaft. It is
cylindrical, projecting in a superior and medial direction this angle of
projection allows for an increased range of movement at the hip joint.
Greater trochanter this is a projection of bone that originates from the anterior
shaft, just lateral to where the neck joins. It is angled superiorly and posteriorly, and can be
found on both the anterior and posterior sides of the femur. It is the site of attachment of
the abductor and lateral rotator muscles of the leg.
Lesser trochanter much smaller than the greater trochanter. It projects from the
posteromedial side of the side, just inferior to the neck-shaft junction. The psoas major
and iliacus muscles attach here.

Intertrochanteric line a ridge of bone that runs in a inferomedial direction on


the anterior surface of the femur, connecting the two trochanters together. The iliofemoral
ligament attaches here a very strong ligament of the hip joint. After it passes the lesser
trochanter on the posterior surface, it is known as the pectineal line.
Intertrochanteric crest similar to the intertrochanteric line, this is a ridge of
bone that connects the two trochanters together. It is located on the posterior surface of
the femur.
There is a rounded tubercle on its superior half, this is called the quadrate tubercle,
which is where the quadratus femoris attaches.

Picture 2. (A) Proximal femur in anterior view and (B) posterior view
The Shaft

The shaft descends in a slight medial direction. This brings the knees closer to the
bodys center of gravity, increasing stability. On the posterior surface of the femoral shaft, there
are roughened ridges of bone, these are called the linea aspera (Latin for rough line)
Proximally, the medial border of the linea aspera becomes the pectineal line. The lateral
border becomes the gluteal tuberosity, where the gluteus maximus attaches. Distally, the linea
aspera widens and forms the floor of the popliteal fossa, the medial and lateral borders form the
the medial and lateral supracondylar lines. The medial supracondyle line stops at the adductor
tubercle, where the adductor magnus attaches.
Distal
The distal end is characterised by the presence of the medial and lateral condyles, which
articulate with the tibia and patella, forming the knee joint.
Medial and lateral condyles rounded areas at the end of the femur. The posterior and
inferior surfaces articulate with the tibia and menisci of the knee, while the anterior surface
articulates with the patella.
Medial and lateral epicondyles bony elevations on the non articular areas of the
condyles. They are the area of attachment of some muscles and the collateral ligaments of the knee
joint.
Intercondylar fossa A depression found on the posterior surface of the femur, it lies in
between the two condyles. It contains two facets for attachment of internal knee ligaments.
Facet for attachment of the posterior cruciate ligament found on the medial wall of
the intercondylar fossa, it is a large rounded flat face, where the posterior crucitate ligament of the
knee attaches.

Facet for attachment of anterior cruciate ligament found on the lateral wall of the
intercondylar fossa, it is smaller than the facet on the medial wall, and is where the anterior
cruciate ligament of the knee attaches.

Picture 3. C. Posterior Surface of the Shaft , (D) Anterior and (E) Posterior Surface of the
Distal Portion of the Femur

Arteries of Femur
The main artery of the femur is femoral artery. It is a continuation of the external iliac
artery (terminal branch of the abdominal aorta). The external iliac becomes the femoral artery
when it crosses under the inguinal ligament and enters the femoral triangle.
In the femoral triangle, the profunda femoris artery arises from the posterolateral aspect of
the femoral artery. It travels posteriorly and distally, giving off three main branches:

Perforating branches Consists of three or four arteries that perforate the adductor

magnus, contributing to the supply of the muscles in the medial and posterior thigh.

Lateral femoral circumflex artery Wraps round the anterior, lateral side of the
femur, supplying some of the muscles in the lateral side of the thigh.

Medial femoral circumflex artery Wraps round the posterior side of the femur,

supplying the neck and head of the femur. In a fracture of the femoral neck, this artery can easily be
damaged, and avascular necrosis of the femur head can occur.

Picture 4. Arteries of femur

II.

FEMUR FRACTURE

Femoral head fractures


Femoral head fractures are relatively uncommon injuries; however, appropriate
treatment of these fractures is of prime importance to help prevent the development of posttraumatic osteoarthritis. Approximately six to 16 % of posterior hip dislocations have been
noted to be associated with a femoral head fracture. Since the first description of a femoral head
fracture, several case series have been published; however, no firm conclusions have been
reached regarding optimal treatment. Historically, these fracture patterns have been associated
with poor functional outcomes.
The vast majority of patients that present with a fracture-dislocation of the hip have
been involved in high-energy trauma. A thorough history and physical examination is thus
crucial not only to diagnose the hip injury but also to identify any associated injuries. It is
imperative that concomitant injuries, such as head, intra-abdominal, and chest injuries are
identified and treated appropriately.
The classic mechanism of injury for femoral head fracture is traumatic posterior
dislocation of the hip. Shear forces against the femoral head as it exits the contained acetabulum
are thought to cause the femoral head fracture during hip dislocation. Due to the inherent
stability of the hip joint, dislocation of the hip with associated femoral head fracture requires
high amounts of energy, most often due to motor vehicle collisions, fall from a height, motor
vehicle-pedestrian accidents, and sports injuries. A common position of the upper extremity
during dislocation of the hip is akin to the position during a dashboard injury to the knee, in
which the hip is positioned in flexion, adduction, and internal rotation.
The Pipkin classification is the most widely used classification system, which is based
on the location of the femoral head fracture in relation to the femoral head fovea and the present
of any associated fractures. Type I femoral head fractures occur when the fracture is inferior to

the fovea centralis, whereas type II femoral head fractures extend superior to the fovea centralis.
Type III is any femoral head fracture that is associated with a concomitant femoral neck
fracture, and a type IV is associated with an acetabular fracture. Brumback et al. designed a
more comprehensive classification system with the attempt to eliminate the ambiguity of the
Pipkin classification and to provide treatment guidelines for each fracture type. Fractures are
divided into one of five categories and then are further delineated into subsets A and B. Many
orthopaedists, however, continue to use the traditional Pipkin classification system when
describing and reporting these fracture patterns.
Fracture-dislocation of the hip is a true orthopaedic emergency. Provided that no
contraindications exist (e.g., associated femoral neck fracture), emergent closed reduction
should be attempted as soon as feasible, preferably within 6 hours, given the direct relationship
between delayed reduction and the increased risk of femoral head osteonecrosis. An irreducible
fracture-dislocation of the hip or a femoral head fracture with associated femoral neck fracture
are indications for emergent open reduction.
In these settings, a preoperative CT scan should be obtained if feasible in a timely
manner.
The goals of definitive treatment of femoral head fractures are to achieve an anatomic
reduction, achieve and maintain joint stability, and remove any interposed bone fragments. This
may be obtained either nonsurgically or surgically. The size, location, and displacement of the
fracture are factors in this decision-making process.

Picture 5. a A fracture-dislocation of the hip is evident on the routine trauma


anteroposterior (AP) pelvis radiograph. The dislocated femoral head is incongruent with the
acetabulum and is displaced superiorly overlapping the acetabular sourcil with an apparent
break in Shentons line. There is also an associated femoral neck fracture. b. A posterior
approach with a trochanteric-flip osteotomy provides excellent exposure for reduction and
internal fixation. c, d. Post-operative radiographs demonstrate anatomic reduction and fixation
of the femoral head and neck fractures, in addition to a congruent hip joint
Neck of femur fractures (NOF)
Neck of femur fracture is common injury sustained by older patients who are both more
likely to have unsteadiness of gait and reduced bone mineral density, predisposing to fracture.
These fractures are often associated with multiple injuries and high rates of avascular
necrosis and nonunion.
Elderly osteoporotic women are at greatest risk. In elderly patients, the mechanism of
injury various from falls directly onto the hip to a twisting mechanism in which the patients
foot is planted and the body rotates. There is generally deficient elastic resistance in the
fractured bone. The mechanism in young patients is predominantly axial loading during high

force trauma , with an abducted hip during injury causing a neck of femur fracture and an
adducted hip causing a hip fracture-dislocation.
Garden described the classification of femoral neck fractures. In this classification,
femoral neck fractures are divided into the following 4 grades based on the degree of
displacement of the fracture fragment:
Grade I is an incomplete or valgus impacted fracture.
Grade II is a complete fracture without bone displacement.
Grade III is a complete fracture with partial displacement of the fracture fragments.
Grade IV is a complete fracture with total displacement of the fracture fragments.
Frandersen et al concluded that clinically differentiating the 4 grades of fractures is
difficult. Multiple observers were able to completely agree on the Garden classification in only
22% of the cases. Hence, classifying femoral neck fractures as nondisplaced (Garden grades I or
II) or displaced (Garden grades III or IV) is more accurate. See the illustration depicted below.

Trochanteric fracture
Trochanteric fracture is a fracture involving the greater and/or lesser trochanters of
the femur.
Classification
Fractures in these region can be classified as:

Intertrochanteric

Subtrochanteric

greater trochanteric avulsion fracture

lesser trochanteric avulsion fracture


Intertrochanteric fracture
Evan classified intertrochanteric fracture based on fragment fracture:

Type I: Fracture line extends upwards and outwards from the lesser trochanter (stable).
Type I fractures can be further subdivided as :

Type Ia: Undisplaced two-fragment fracture


Type Ib: Displaced two-fragment fracture
Type Ic: Three-fragment fracture without posterolateral support,

owing to displacement of greater trochanter fragment

Type Id: Three-fragment fracture without medial support, owing to


displaced lesser trochanter or femoral arch fragment

Type Ie: Four-fragment fracture without postero-lateral and medial


support (combination of Type III and Type IV)
Type II: Fracture line extends downwards and outwards from the lesser trochanter
(reversed obliquity/unstable). These fractures are unstable and have a tendency to drift medially.

The Boyd and Griffin classification is based on the involvement o subtrochanteric


region:

type I linear intertrochanteric


type II with comminution of trochanteric region
type III with comminution associated with subtrochanteric

component

type IV oblique fracture of shaft with extension into subtrochanteric

region

Subtrochonteric fracture
The Fielding classification of subtrochanteric fractures is based on the level of the
subtrochanteric region through which the fracture extends:

type I: at the level of the lesser trochanter (most common)


type II: within the region 2.5 cm below the lesser trochanter
type III: within the region 2.5 cm to 5 cm below the lesser

trochanter (least common)


The Zickel classification (modified from Fielding) of subtrochanteric fractures takes
into consideration the level and obliquity of the fracture line as well as the presence or
absence of comminution.

type I short oblique


o
linear
o
comminuted

type II long oblique


o
linear
o
comminuted

type III transverse


o
high level
o
low level
Treatment and prognosis
Subtrochanteric fractures generally have a good prognosis due to the good supply of
blood and adequate collateral circulation to this region of the femur with low incidence of

avascular necrosis and non-union. Postoperative infection, however, is a potentially serious


compilation.
Femur Shaft Fracture
Femoral shaft fractures in young people are frequently due to some type of highenergy collision. The most common cause of femoral shaft fracture is a motor vehicle or
motorcycle crash. Being hit by a car as a pedestrian is another common cause, as are falls
from heights and gunshot wounds.
A upper-force incident, such as a fall from standing, may cause a femoral shaft fracture
in an older person who has weaker bones.
A femoral shaft fracture usually causes immediate, severe pain. You will not be able
to put weight on the injured leg, and it may look deformed shorter than the other leg and
no longer straight.
Femur fractures are classified depending on:

Picture 8. Femoral Shaft Fracture according OTA classification

Picture 9. Femoral Shaft Fracture according Winquist and Hansen classification


Management
Surgical Treatment
Timing of surgery.
If the skin around fracture has not been broken, the surgery should wait until the
condition of the patients are stable. Open fractures, however, expose the fracture site to the
environment. They urgently need to be cleansed and require immediate surgery to prevent
infection.
For the time between initial emergency care and surgery, the leg should be placed either
in a long-leg splint or in skeletal traction. This is to keep the broken bones as aligned as
possible and to maintain the length of your leg.
Skeletal traction is a pulley system of weights and counterweights that holds the
broken pieces of bone together. It keeps the leg straight and often helps to relieve pain.
External fixation. In this type of operation, metal pins or screws are placed into the
bone above and below the fracture site. The pins and screws are attached to a bar outside the
skin. This device is a stabilizing frame that holds the bones in the proper position so they can
heal.
External fixation is usually a temporary treatment for femur fractures. Because they
are easily applied, external fixators are often put on when a patient has multiple injuries and
is not yet ready for a longer surgery to fix the fracture. An external fixator provides good,
temporary stability until the patient is healthy enough for the final surgery. In some cases, an
external fixator is left on until the femur is fully healed, but this is not common.

External fixation is often used to hold the bones together temporarily when the skin
and muscles have been injured. Intramedullary nailing. Currently, the method most surgeons
use for treating femoral shaft fractures is intramedullary nailing. During this procedure, a
specially designed metal rod is inserted into the marrow canal of the femur. The rod passes
across the fracture to keep it in position.
An intramedullary nail can be inserted into the canal either at the hip or the knee
through a small incision. It is screwed to the bone at both ends. This keeps the nail and the
bone in proper position during healing.
Intramedullary nails are usually made of titanium. They come in various lengths and
diameters to fit most femur bones.

Intramedullary nailing provides strong, stable, full-length fixation. Plates and


screws. During this operation, the bone fragments are first repositioned (reduced) into their
normal alignment. They are held together with special screws and metal plates attached to
the outer surface of the bone.
Plates and screws are often used when intramedullary nailing may not be possible, such
as for fractures that extend into either the hip or knee joints.

Picture 8. (Left) This x-ray shows a healed femur fracture treated with intramedullary
nailing. (Right) In this x-ray, the femur fracture has been treated with plates and screws.
Recovery
Most femoral shaft fractures take 4 to 6 months to completely heal. Some take even
longer, especially if the fracture was open or broken into several pieces.
Weightbearing
Many doctors encourage leg motion early in the recovery period. It is very important
to follow the doctor's instructions for putting weight on injured leg to avoid problems.
In some cases, doctors will allow patients to put as much weight as possible on the leg
right after surgery. However, the patient may not be able to put full weight on leg until the
fracture has started to heal. It is very important to follow the doctor's instructions carefully.
When the patient begin walking, they will most likely need to use crutches or a walker for
support.
Physical Therapy
With trauma-related femur fractures, physical therapy following stable fixation of the
fracture to improve hip and knee range of motion, strengthening and gait training is
recommended. Weight-bearing status is dependent upon fracture pattern and surgical
intervention. Ambulatory aids, such as crutches, are used in the initial stages. The goal of the

therapy program should be eventual full weight-bearing and restoration of normal function.
Pulmonary therapy is often needed in patients sustaining major trauma requiring prolonged
bed rest.
For femoral stress fractures, discontinue crutches once pain-free walking is possible.
Increase low-impact upper extremity aerobic training (e.g., swimming, biking, elliptical
trainer) as symptoms permit. Attempt to identify causative factors of the femoral stress
fractures (e.g., improper training techniques, footwear, diet).
One treatment algorithm that has been suggested consists of a graduated four-phase
program, each of which last three weeks in duration. Transfer to the next phase is based on
the result of fulcrum and hop tests carried out at the end of each phase. If the tests were
positive (i.e., a failed test), the patient was returned to the beginning of that phase. In the
first phase athletes walked with the help of crutches and were instructed to be non-weightbearing on the affected leg. In the second phase normal walking was permitted, and
swimming and exercising on the unaffected extremities was allowed. In the third phase the
patients performed exercises with both upper and upper extremities using light weights.
Patients were also permitted to run in a straight line every other day and ride a stationary
bicycle. The distance that the subjects were allowed to run was gradually increased. In the
fourth phase the patient resumed normal training. In this study all seven patients returned to
normal activitywithin 12-18 weeks with no recurrences noted at 48-96 month follow up.
Distal Femoral fracture
Distal femur fractures vary. The bone can break straight across (transverse fracture)
or into many pieces (comminuted fracture). Sometimes these fractures extend into the knee
joint and separate the surface of the bone into a few (or many) parts. These types of fractures

are called intra-articular. Because they damage the cartilage surface of the bone, intraarticular fractures can be more difficult to treat.

(Left) A

transverse

fracture

across

the

distal

femur

(Center)

An

intra-articular fracture that extends into the knee joint (Right) A comminuted fracture that
extends into the knee joint and upwards into the femoral shaft.
According to the common principles of the AO classification, type A fractures are
extra-articular and type B fractures are partial articular, which means that parts of the
articular surface remains in contact with the diaphysis. Type C fractures are complete
articular fractures with detachment of both condyles from the diaphysis. The fracture types
are further subdivided describing the degree of fragmentation and other, more detailed
characteristics. Further subdivision of type B fractures includes Bl (sagittal, lateral condyle),
B2 (sagittal, medial condyle) and B3 (frontal, Hoffa type). Fracture type C is divided in C1
(articular simple, metaphyseal simple), C2 (articular simple, metaphyseal multifragmentary)
and C3 (multifragmentary).

Distal femur fractures can be closed meaning the skin is intact or can be open. An
open fracture is when a bone breaks in such a way that bone fragments stick out through the
skin or a wound penetrates down to the broken bone. Open fractures often involve much
more damage to the surrounding muscles, tendons, and ligaments. They have a higher risk
for complications and take a longer time to heal.
When the distal femur breaks, both the hamstrings and quadriceps muscles tend to
contract and shorten. When this happens the bone fragments change position and become
difficult to line up with a cast.

Pisture 10. In this x-ray of the knee taken from the side, the muscles at the front and
back of the thigh have shortened and pulled the broken pieces of bone out of alignment.
III.

Fracture Healing Process


The healing process of a fracture starting fractures occur as the body's attempt to
repair the damage - the damage suffered. Healing of fractures is influenced by
several factors, local and systemic factors, while local factors:
a. location of the fracture
b. Types of bone fracture.
c. Reposition anatomical and immobilasi stable.

d. Contact between fragments.


e. The presence or absence of infection.
f. Levels of fracture.
The systemic factors are:
a. The general state of the patient
b. Age
c. malnutrition
d. Systemic disease.
Fracture healing process consists of several phases, as follows:
1. Phase Reactive
a. Phase hematoma and inflammation
b. Granulation tissue formation

2. Phase Reparatif
a. Phase formation of callus
b. Lamellar bone formation
3. Phase Remodelling
a. Bone remodeling to its original shape
In terms of classical histology, fracture healing fracture healing has been divided into
primary and secondary fracture.
Fracture Healing Process Primary
Healing occurs in this way internal remodeling that includes a direct attempt by the cortex to

rebuild itself when continuity interrupted. In order to be united fractures, bone on one side of
the cortex must be fused with the bone on the other side (direct contact) to establish a
mechanical continuity.
No association with callus formation. Remodeling of the internal occur haversian system
and unification edge fracture fragments of the broken bone
There 3 remodeling at the fracture site is:
1. Implementation of appropriate reduction
2. Fixation stable
3. The existence of an adequate blood supply
The use of dynamic compression plate in the osteotomy models have been shown to cause
primary bone healing. Remodeling active haversian seen at around week four fixation.
Secondary Fracture Healing Process.
Healing response in the secondary cover periostium and external soft tissues. The process of
fracture healing is broadly be divided into five phases, namely phase hematoma (swelling),
the proliferative phase, the phase of callus, ossification and remodeling.

1. Phase Inflammation:
Inflammatory phase lasts a few days and disappear with the reduced swelling and pain.
Bleeding in the injured tissue and hematoma formation at the site of fracture. The tip of the
bone fragments of devitalized because the breakdown of the blood supply hypoxia and
inflammation induced gene expression and promotes cell division and migration to the
fracture site to begin healing. Production or release of specific growth factors, cytokines, can

create conditions suitable for the micro:


(1) Stimulating the formation of osteoblasts and periosteal ossification intra membrane at the
site of the fracture,
(2) Stimulates cell division and migration to the fracture site, and
(3) Stimulates chondrocytes to differentiate in soft callus with accompanying endochondral
ossification.
Blood gathering phase initially suspected hematoma due to laceration local blood vessels
that are focused on a particular place. But on further development of hematoma is not only
caused by tearing of blood vessels but also instrumental factors that cause inflammation
localized swelling condition. The timing of this process begins when fractures occur until 23 weeks.
2. Phase proliferation
Approximately 5 days hematoma will experience the organization, formed threads of fibrin
in the blood clot, forming a network for revascularization, and the invasion of fibroblasts
and osteoblasts. Fibroblasts and osteoblasts (the developing of osteocytes, endothelial cells,
and cell periosteum) will produce collagen and proteoglycan matrix of collagen in bone
fracture. Formed fibrous connective tissue and cartilage (osteoid). From periosteum, growth
looks circular. The callus cartilage is stimulated by micro minimal movement on the site of
fracture. But the excessive movement will damage the structure of the callus. Bones that are
actively growing shows electronegative potential. In this phase started in week 2-3 after
fracture and ended in week 4-8.
Phase 3. Establishment of Callus

An advanced phase of the phase hematoma and proliferation of bone tissue begins to form
the chondrocyte bone tissue starts to grow or commonly referred to as the cartilage tissue.
Actually, the cartilage is still subdivided into lamellar bone and wovenbone. Continued
network growth and cartilage growth cycle reaches the other side until the gap is plugged.
Fragments of bone fracture combined with fibrous tissue, cartilage, and bone mature fibers.
Callus shape and volume dibutuhkanuntuk linking effect is directly related to the amount of
damage and bone shifts. It can take three to four weeks to allow the bone fragments
belonging to the cartilage or fibrous tissue. Clinically bone fragments can no longer be
moved. Regulation of callus formation during fracture repair mediated by the expression of
growth factors. One of the most dominant factor of the many growth factors are
Transforming Growth Factor-Beta
1 (TGF-B1) which indicates involvement in regulating the differentiation of osteoblasts and
extra cellular matrix production. Other factors are: Vascular Endothelial Growth Factor
(VEGF), which plays an important role in the process of angiogenesis during fracture
healing.
The center of the soft callus is kartilogenous then along osteoblasts will differentiate to form
a chain network of osteocytes, are signs of bone cells and the ability to anticipate the
mechanical stress.
The rapid process of soft callus formation which then continues until the remodeling phase
is a critical period for the success of fracture healing.
Types of Callus
Known to some kind of callus which corresponds to the callus callus was formed primarily

as a result of the fracture occurs within 2 weeks Bridging (soft) callus occurs when the edges
of the bone fracture is not contiguous. Medullary (hard) will complete the bridging callus
Callus slowly. External callus is outermost regions under the periosteum fracture periosteal
callus formed between the periosteum and bone fractures. Interfragmentary callus was
formed callus and fracture fills the gap between the fractured bone. Medullary callus formed
in medullary bone around the fracture area.
4. Stadium Consolidation
With the activity of osteoclasts and osteoblasts continually, immature bone (woven bone)
converted into mature (lamellar bone). The bones become stronger so osteoklast can
penetrate tissue and debris in the area of the fracture followed by osteoblasts that will fill the
gap between the bone fragments with a new one.
This process goes slowly for a few months before the bone is strong enough to accept the
normal load.
5. Remodelling Stadium.
Fractures have been associated with strong bones sheath with a different shape with normal
bone. Within months or even years of a process of formation and bone resorption continuous
lamella thick will be formed on the side with high pressure. Medullary cavity diameter are
formed back and spine back to its original size. Finally, the bones will be returned close to
its original form, especially in children.
In these circumstances the bone has healed clinically and radiology.

IV.

FRACTURE COMPLICATION
Early complications
Local:

Vascular injury causing haemorrhage, internal or external


Visceral injury causing damage to structures such as brain, lung or bladder
Damage to surrounding tissue, nerves or skin
Haemarthrosis
Compartment syndrome (or Volkmann's
ischaemia) Wound infection, more
common for open fractures
Systemic:

Fat embolism
Shock
Thromboembolism (pulmonary or venous)
Exacerbation of underlying diseases such as diabetes
or CAD Pneumonia

Compartment syndromes

Fractures of the limbs can cause severe ischaemia by damage to a major artery or by
increasing the osteofascial compartment pressure by swelling due to bleeding or

oedema.
capillary flow muscle ischaemia. more oedema more pressure

capillary flow. Thus rapid pressure build-up, leading to muscle and nerve necrosis.
Compartment syndromes can also result from crush injuries (falling debris or simple
compression if patient unconscious for length of time) or an over-tight cast.
Any compartment, but tibia shaft # & forearm # greatest risk. Esp if age<35years
Presentation
Signs of ischaemia (5 P's: Pain, Paraesthesia, Pallor, Paralysis, Pulselessness)
diagnosis should be made before all these features are present. The presence of a

pulse

does not exclude the diagnosis.

Signs of raised intracompartmental pressure:


o
Swollen arm or leg
o
Tender muscle - calf or forearm pain on passive extension of digits
Pain out of proportion to injury
o
Redness, mottling and blisters
o
Watch for signs of renal failure (low-output uraemia with
acidosis)
When uncertain, measure intracompartmental pressure
directly.
Management

Remove/relieve external pressures


Prompt decompression of threatened compartments by open fasciotomy
Debride any muscle necrosis
Treat hypovolaemic shock and oliguria urgently
Renal dialysis may be necessary
Complications

Acute renal failure secondary to rhabdomyolysis


DIC
Volkmann's contracture (where infarcted muscle is replaced by inelastic fibrous

tissue

Fat embolism
This is a relatively uncommon disorder that occurs in the first few days following
trauma with a mortality rate of 10-20%. Various theories: Fat drops from bone marrow
following #, coalesce and form emboli in pulmonary capillary beds and brain, with a 2
inflammatory cascade and platelet aggregation. Alternative theory suggests that FFAs are
released as chylomicrons following hormonal changes due to trauma or sepsis. Also seen
following severe burns, CPR, bone marrow transplant and liposuction.
Risk factors

Closed fractures
Multiple fractures
Pulmonary contusion
Long bone/pelvis/rib fractures
Presentation

Sudden onset dyspnoea


Hypoxia
Fever
Confusion, coma, convulsions
Transient red-brown petechial rash affecting upper body, especially axilla

Management

Supportive treatment
Corticosteroid drugs (used in treatment, more controversial in
prevention) Surgical stabilisation of fracture

Late Complications

o
o
o
o

Local:
o Delayed Union
o Non-union Malunion
Joint stiffness
Contractures
Avascular necrosis
Osteomielitis

Systemic:
o Gangrene, tetanus, septicaemia

o Fear of
mobilising
o Osteoarthritis

Problems with bone healing (non-union, delayed union and malunion)


Non-union = no signs of healing after >3-6 months (depending upon # site). Nonunion is one endpoint of delayed union. 1% of all #, but 19% in upper leg #. Malunion
occurs when the bone fragments join in an unsatisfactory position, usually due to
insufficient reduction.

Causes of delayed
o union include: Severe
o soft tissue damage
o Inadequate blood
o supply Infection
o Insufficient splintage
o Excessive traction
For non-union: as above plus bone separation & interposition of
periosteum, muscle or cartilage
Presentation

Pain at fracture site


Non-use of extremity
Tenderness and swelling
Joint stiffness (prolonged >3 months)
Movement around the fracture site (pseudarthrosis)
X-Ray

Absence of callous (remodelled bone) or lack of progressive change in the callous


Closed medullary cavities suggest non-union.
May look avascular (known as atrophic non-union) or have excessive bone
formation on either side of the gap (known as hypertrophic non-union).

Management

Early weight bearing and casting may be helpful. Surgical treatments include:
Debridement to establish a healthy infection-free vascularity at fracture site

Internal fixation to reducing and stabilize fracture.


Bone grafting to stimulate new callous formation

I.

OSTEOMYELITIS
The bony skeleton is divided into two parts: the axial skeleton and the

appendicular skeleton. The axial skeleton is the central core unit, consisting of the
skull, vertebrae, ribs, and sternum; the appendicular skeleton comprises the bones
of the extremities. The human skeleton consists of 213 bones, of which 126 are
part of the appendicular skeleton, 74 are part of the axial skeleton, and six are part
of the auditory ossicles.
Hematogenous osteomyelitis most commonly involves the vertebrae, but
infection may also occur in the metaphysis of the long bones, pelvis, and clavicle.
Vertebral osteomyelitis involves two adjacent vertebrae with the corresponding
intervertebral disk. (See the image below.) The lumbar spine is most commonly
affected, followed by the thoracic and cervical regions.
i.

OSTEOMYELITIS PATHOPHYSIOLOGY
Bone is normally resistant to infection. However, when microorganisms

are introduced into bone hematogenously from surrounding structures or from


direct inoculation related to surgery or trauma, osteomyelitis can occur. Bone
infection may result from the treatment of trauma, which allows pathogens to
enter bone and proliferate in the traumatized tissue. When bone infection persists
for months, the resulting infection is referred to as chronic osteomyelitis and may
be polymicrobial. Although all bones are subject to infection, the upper extremity
is most commonly involved.
Some important factors in the pathogenesis of osteomyelitis include the
virulence of the infecting organism, underlying disease, immune status of the
host, and the type, location, and vascularity of the bone. Bacteria may possess

35

various factors that may contribute to the development of osteomyelitis. For


example, factors promoted by S aureus may promote bacterial adherence,
resistance to host defense mechanism, and proteolytic activity.
Hematogenous osteomyelitis
In adults, the vertebrae are the most common site of hematogenous
osteomyelitis, but infection may also occur in the long bones, pelvis, and clavicle.
Primary hematogenous osteomyelitis is more common in infants and
children, usually occurring in the long bone metaphysis. However, it may spread
to the medullary canal or into the joint. When infection extends into soft tissue,
sinus tracts may eventually form. Secondary hematogenous osteomyelitis is more
common and occurs when a childhood infection is reactivated. In adults, the
location is also usually metaphyseal.
S aureus is the most common pathogenic organism recovered from bone,
followed by Pseudomonas and Enterobacteriaceae. Less common organisms
involved include anaerobe gram-negative bacilli. Intravenous drug users may
acquire pseudomonal infections. Gastrointestinal or genitourinary infections may
lead to osteomyelitis involving gram-negative organisms. Dental extraction has
been associated with viridans streptococcal infections. In adults, infections often
recur and usually present with minimal constitutional symptoms and pain.
Acutely, patients may present with fever, chills, swelling, and erythema over the
affected area.
Contiguous-focus and posttraumatic osteomyelitis
The initiating factor in contiguous-focus osteomyelitis often consists of
direct inoculation of bacteria via trauma, surgical reduction and internal fixation
of fractures, prosthetic devices, spread from soft-tissue infection, spread from

36

adjacent septic arthritis, or nosocomial contamination. Infection usually results


approximately one month after inoculation.
Posttraumatic osteomyelitis more commonly affects adults and typically
occurs in the tibia. The most commonly isolated organism is S aureus. At the
same time, local soft-tissue vascularity may be compromised, leading to
interference with healing. Compared with hematogenous infection, posttraumatic
infection begins outside the bony cortex and works its way in toward the
medullary canal. Low-grade fever, drainage, and pain may be present. Loss of
bone stability, necrosis, and soft tissue damage may lead to a greater risk of
recurrence.
Septic arthritis may lead to osteomyelitis. Abnormalities at the joint
margins or centrally, which may arise from overgrowth and hypertrophy of the
synovial pannus and granulation tissue, may eventually extend into the
underlying bone, leading to erosions and osteomyelitis. One study demonstrated
that septic arthritis in elderly persons most commonly involves the knee and that,
despite most of the patients having a history of surgery, 38% developed
osteomyelitis. Septic arthritis is more common in neonates than in older children
and is often associated with metaphyseal osteomyelitis. Although rare,
gonococcal osteomyelitis may arise in a bone adjacent to a chronically infected
joint.
Patients with vascular compromise, as in diabetes mellitus, are
predisposed to osteomyelitis owing to an inadequate local tissue response.
Infection is most often caused by minor trauma to the feet with multiple
organisms isolated from bone, including Streptococcus species, Enterococcus
species, coagulase-positive and -negative staphylococci, gram-negative bacilli,

37

and anaerobic organisms. Foot ulcers allow bacteria to reach the bone. Patients
may not experience any resulting pain, because of peripheral neuropathy, and
may present with a perforating foot ulcer, cellulitis, or an ingrown toenail.
Physical examination may reveal decreased sensation, poor capillary
refill, and decreased dorsalis pedis and posterior tibial pulses. Treatment is aimed
at suppressing infection and improving vascularity. However, most patients
develop recurrent or new bone infections. Resection or amputation of the affected
tissue is sometimes necessary. Debridement, incision and drainage, and tendon
lengthening are attempted first.
ii.

ETIOLOGY
Posttraumatic osteomyelitis accounts for as many as 47% of cases of

osteomyelitis. Other major causes of osteomyelitis include vascular insufficiency


(mostly occurring in persons with diabetes; 34%) and hematogenous seeding
(19%).
Motor vehicle accidents, sports injuries, and the use of orthopedic
hardware to manage trauma also contribute to the apparent increase in prevalence
of posttraumatic osteomyelitis. Osteomyelitis may complicate puncture wounds
of the foot, occurring in 1.8%-6.4% of patients following injury.
iii.

PROGNOSIS
Inadequate therapy may lead to relapsing infection and progression to

chronic infection. Because of the avascularity of bone, chronic osteomyelitis is


curable only with radical resection or amputation. These chronic infections may
recur as acute exacerbations, which can be suppressed by debridement followed
by parenteral and oral antimicrobial therapy. Rare complications of bone infection

38

include pathologic fractures, secondary amyloidosis, and squamous cell


carcinoma at the sinus tract cutaneous orifice.

II.

39

CHAPTER II
I.
a.
b.
c.
d.
e.
f.
g.
h.
II.

IDENTITY
Name
Age
Sex
Religion
Address
Room
Register number
Date of in patient

: Mr. F
: 37 years old
: male
: Islam
: Kendal
: Kenanga
: 487.401
: 18 March 2016

ANAMNESA
Autoanamnesa with the patient and held on March 22, 2016 in Kenanga

room and also supported by medical records.


Main complaints: Pain in the left medial thigh
Present status:
Patients come to orthopedic department hospitals in Kendal with
complaints of pain in the left thigh post ORIF 2 month ago, since 2 days ago.
Patients complain of pain in the left medial thigh because previous patient fall on
the bathroom. Patient fall it self and not treat to the doctor but to quack massage.
After several days, the patient felt no improvement, but getting worse. The patient
feels pain when he walk, patient difficulty in moving his left thigh. Patient no
fever, no problems with urination and defecation, and patient just pain and cant
move his left thigh.
Medical condition history:
-History femur trauma(fracture) : yes about 2 month ago
- History of asthma and allergies: denied
- History of heart disease
: denied
- History of hypertension
: denied
- History of diabetes
: denied
Family history:
- History of asthma and allergies: denied
- History of heart disease
: denied
- History of hypertension
: denied
- History of diabetes
: denied
Socioeconomic status :
Patients working as an employee.
Impression: enough in socioeconomic.
III.

Physical Examination
40

Held on March 22, 2016 at 7 a.m in Kenanga room of Kendal Hospital


General Condition : Looks weak
Awareness: Composmentis, GCS 15
Vital Signs
1. Blood pressure
: 120/80 mmHg
2. Heart rate
: 78 x / minute, regular
3. Temperature
: 36,5oC
4. Breathing
: 20 x / min
Status generalis
Skin
Head
Eyes
Ear
Nose
Mouth
Neck
Thorax :

: turgor (+)
: mesocephal, wound (-)
: anemis (-/-), icteric (-/-)
: discharge
(-/-)
: deviation septum (-), discharge (-/-)
: sianosis (-)
: simetris, trachea deviation (-)

Cor :
Inspection : ictus cordis (-)
Palpation: ictus cordis palpable at SIC V 2cm medial to line
midclavicularis, pulsus sternal (-), pulsus epigastrium(-)
Percussion : heart border
Bottom left : SIC 2 cm medial line midclavicularis
Top left : SIC II linea sternalis sinistra
Top right : SIC III linea sternalis dextra
Bottom right : SIC III linea parasternalis sinistra
Auscultation : Heart sound I-II reguler, gallop (-), murmur (-)
Pulmo :
Inspection : normochest, simetris, retraction (-)
Palpation : simetris, nothing widening between the ribs, retraction (-)
Percussion : sonor (+/+)
Auscultation : vesiculer (+/+)
41

Abdomen
Inspection
Auskultation
Perkussion
Palpation

: flat, meteorismus (-), mass(-)


: bowel (+), normal
: tymphani (+)
: supel , pain (-), hepar lien are not papble

EXTREMITY
Cold extremity
Oedem
Capillary refill
Lesion
Hematom

IV.

SUPERIOR
-/-/<2
-/+/-

INFERIOR
-/-/<2
-/+
-/-

Backbone : inspection : kifosis and lordosis (-)


Palpation
: pain (-)
Localized status of left Thigh

Thigh
Look : deformity (+), hematom (-), wound (-), blood (-), oedem
(+),sikatric (+), striae (-)
Feel : painfulness when it given a palpation on left thigh, skin
temperature warm.
Move : motorik (+), muscle strenght (5/3), limited movement of
the left medial thigh.
Measurement

lower extremity
LLD

Dextra

Sinistra

True lenght

76

75

Appearance

81

80

lenght
Anatomical

44

43

lenght

42

Extension
Flexion

Active

Passive

(+)

(+) minimum

minimum
(+)

(+) minimum

endorotation

minimum
Hard to

exorotation

evaluate
(+)

(-)
(+) minimum

minimum

V.
1.

Laboratory Results
Blood laboratory

Examines
Hb
Leucosite
Trombosite

Results
14,6 gr%
7.500 cell/mm3
360.000

Ht
PT
APTT
GDS
Ureum
Creatinin

cell/mm3
47,1 %
11,4 seconds
30,4 seconds
99
20
1,19

Normal Results
13 18 gr%
4.000 10.000 cell/mm3
150.000 500.000
cell/mm3
39 54 %
11,3-14,7 seconds
27,4 39,3 seconds
75-115 mg/dl
10-50 mg/dl
0,5-1,1 mg/dl

43

2. Radiology

X- ray Femur Sinistra (AP- Lateral) Position


Open Reduction Internal Fixation 19-01-2016

44

Before surgery post ORIF 18-03-2016

After Open Reduction Internal Fixation 23-03-2016

VI.

DIAGNOSE
Non union femur 1/3 middle sinistra and osteomyelitis

45

VI. PLANNING THERAPY

Medical
Infus RL 20 tpm
Inj. Cefazoline 2x1 gr
Inj. Ketorolac 3x 30mg
Inj. Ranitidin 2x1 amp

a.
b.
c.

Non-Medical :
Ip. Operative
Can be perfomed by ORIF ( Open Reduction of Internal Fixation )
Ip. Monitoring
General situation, vital sign, the result of supporting examination
Education
Educate patient about weight bearing after operative treatment
Tell the patient to do some simple exercise after the treatment received

VII. PROGNOSIS
Quo ad vitam
: dubia ad bonam
Quo ad sanam
: dubia ad bonam
Quo ad fungsionam
: dubia ad bonam

CHAPTER IV
DISCUSSION
Anamnese :
Patients come to orthopedic department hospitals in Kendal with
complaints of pain in the left thigh post ORIF 2 month ago, since 2 days ago.
Patients complain of pain in the left medial thigh because previous patient fall on
the bathroom. Patient fall it self and not treat to the doctor but to quack massage.
After several days, the patient felt no improvement, but getting worse. The patient
feels pain when he walk, patient difficulty in moving his left thigh. Patient no

46

fever, no problems with urination and defecation, and patient just pain and cant
move his left thigh.
Physical Examination
Left of Thigh
Look : deformity (+), hematom (-), wound (-), blood (-), oedem
(+),sikatric (+), striae (-)
Feel : painfulness when it given a palpation on left thigh, skin
temperature warm.
Move : motorik (+), muscle strenght (5/3), limited movement of
the left medial thigh.

Measurement

lower extremity
LLD

Dextra

Sinistra

True lenght

76

75

Appearance

81

80

lenght
Anatomical

44

43

lenght

Extension
Flexion

Active

Passive

(+)

(+) minimum

minimum
(+)

(+) minimum

minimum
47

endorotation
exorotation

Hard to
evaluate
(+)

(-)
(+) minimum

minimum
We need a supporting examination to find the right diagnosis. We did X-ray
examination of the femur sinistra with AP and Lateral position.
After we did the radiographic examination we can conclude that the true
diagnosis of this case is nonunion 1/3 middle os femur sinistra and osteomyelitis.
When we find the true diagnosis we can give the patient the right therapy. For this
patient we did surgical treatment, the treatment for this patient is ORIF.

PLANNING THERAPY
Theraphy ;
Infus RL 20 tpm
Inj. Cefazoline 2x1 gr
Inj. Ketorolac 3x 30mg
Inj. Ranitidin 2x1 amp

48

CHAPTER V
CONCLUSION
The spectrum of femur

fractures is wide and ranges from non-

displaced femoral stress fractures to fractures associated with severe comminution and
significant soft-tissue injury. Femur fractures are typically described by location
(proximal, shaft, distal). These fractures may then be categorized into three major
groups; high-energy traumatic fractures, low energy traumatic fractures through
pathologic bone (pathologic fractures) and stress fractures due to repetitive overload.
Fracture healing process Primer Healing occurs in this way internal remodeling that
includes a direct attempt by the cortex to rebuild itself when continuity interrupted. In
order to be united fractures, bone on one side of the cortex must be fused with the
bone on the other side (direct contact) to establish a mechanical continuity.
No association with callus formation. Remodeling of the internal occur haversian
system and unification edge fracture fragments of the broken bone
There 3 requirements for Haversian remodeling at the fracture site is
1. Implementation of appropriate reduction
2. Fixation stable
3. The existence of an adequate blood supply
The use of dynamic compression plate in the osteotomy models have been shown to
cause primary bone healing. Remodeling active haversian seen at around week four
fixation.
Secondary Fracture Healing Process is Healing response in the secondary cover
periostium and external soft tissues. The process of fracture healing is broadly be
divided into five phases, namely phase hematoma (swelling), the proliferative phase,
the phase of callus, ossification and remodeling

49

In a minority of cases delayed union gradually transformed into non union


-which is clear that the fracture will never unite without intervention. Movement can
cause reduced pain at the broken bone fragments. The distance to the fracture into a
type of pseudoarthrosis.
Osteomyelitis Is an infection of the tissue that covers the bone marrow and bone
cortex may be exogenous (infections have come from outside the body) or
hematogenous (infection from the body). Pathogens can enter through an open
fracture wounds, penetrating wounds, or during surgery. Gunshot wounds, long bone
fractures, open fractures are visible bones, amputation injuries due to trauma and
fractures - fractures with compartment syndrome or vascular injuries have a greater
risk of osteomyelitis.

50

REFERENCES
1.

Jong WD, Sjamsuhidajat R. Patah Tulang dan Dislokasi. Dalam : Buku

Ajar Ilmu Bedah. EGC. Jakarta, 1997 : 1138.


2.
Rasjad Chairudin. Pengantar Ilmu Bedah Orthopedi. Bintang
lamumpatue : Ujung Pandang, 1998 : 327.
3.
Schnackenburg kE, Macdonald HM, Ferber R, Wiley JP, Boyd SK.
Bone quality and muscle strength in female athletes with upper limb stress fractures.
Med Sci Sports Exerc. Nov 2011;43(11):2110-9.
4.
Brukner P. Sports medicine. The tired athlete. Aust Fam Physician.
Aug 1996;25(8):1283-8.
5.
Lakstein D, Hendel D, Haimovich Y, Feldbrin Z. Changes in the
pattern of fractures of the hip in pattiens 60 years of age and older between 2001 and
2010 : A radiological review. Bone Joint J. Sept 2013;95-B(9):1250-4.
6.
Maitra RS, Johnson DL. Stress fractures. Clinical history and physical
examination. Clin Sports Med. Apr 1997;16 (2):259-74.
7.
Bloomfeldt R, Tornkvist H, Ponzer S. Internal fixation versus
hermiathroplasty for displaced fractures of the femoral neck in elderly patients with
severe cognitive impairement. J Bone Joint Surg Br. Apr 2005;87(4):523-9.
8.
Heetveld MJ, Raaymakers EL, van Eck-Smit BL. Internal fixation for
displaced fractures of the femoral neck. J Bone Joint Surg Br. Mar 2005;87(3):367-73.
9.
Mostofi SB. Fracture Classifications in Clinical Practice. Pelvis and
Upper Limb. United Kingdom : University of London. 2006.35-7.
10.
Apley, AG., Salomon, L, (1993). Apleys System of Orthopaedics and
Fractures. 7th Edition. London : Butterworth Heinemann

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