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Fracture Healing ( System of Orthopaedics and Trauma, Apley and Solomon)

HEALING BY DIRECT UNION


(PRIMARY BONE HEALING)
If the fracture site is absolutely stable – for example, an impacted fracture in cancellous bone, or a
fracture
held by a metal plate with absolute stability – there is no stimulus for callus. Instead, osteoblastic new
bone
formation occurs directly between the fragments. Where the exposed fracture surfaces are in intimate
contact and held from the outset with absolute stability, internal bridging may occasionally occur without
any intermediate stages (contact healing). Gaps between the fracture surfaces are invaded by new
capillaries and osteoprogenitor cells growing in from the edges, and new bone is laid down on the
exposed surface (gap healing). Where the crevices are very narrow (less than 200 μm), osteogenesis
produces lamellar bone; wider gaps are filled first by woven bone, which is then remodelled to lamellar
bone. By 3–4 weeks the fracture is solid enough to allow penetration and bridging of the area by bone
remodelling units, i.e. osteoclastic ‘cutting cones’ followed by
osteoblasts (Figure 23.4). With rigid metal fixation, however, the absence of callus means that there is a
long period during which the bone depends entirely upon the metal implant for its integrity, increasing the
risk of implant failure. Moreover, the implant diverts stress away from the bone, which may become
osteoporotic
and may not recover fully until the metal is removed.
HEALING BY CALLUS (SECONDARY BONE HEALING)
Healing by callus, though less direct (indirect healing) has distinct advantages: it ensures mechanical
strength while the bone ends heal, and with increasing stress the callus grows stronger and stronger
(according to Wolff’s law) (see Figure 23.6). At least for the secondary bone healing, surgical
stabilization is not always necessary but it can prevent malunion. Secondary bone healing is the most
common form of healing in tubular bones; in the absence of rigid fixation, it proceeds in five stages
(Figure 23.5):
1 Haematoma formation – At the time of injury, bleeding occurs from the bone and soft tissues.
2 Inflammation – The inflammatory process starts rapidly when the fracture haematoma forms and
cytokines are released, and lasts until fibrous tissue, cartilage, or bone formation begins (1–7 days
postfracture). Osteoclasts are formed to remove the necrotic ends of bony fragments.
3 Soft callus formation – After 2–3 weeks, the first soft callus is formed. This is about the time when the
fragments can no longer move freely. The strain applied to the cells in the fracture gap modifies their
growth factor expression and progenitor cells are stimulated to become osteoblasts. The cells form a cuff
of woven bone periosteally. The fracture can now still angulate but is stable in length.
4 Hard callus formation – When the fracture ends are linked together, the hard callus starts and lasts until
the fragments are firmly united (3–4 months). Bone callus forms at the periphery of the fracture
and progressively moves centrally.
Gait (Orthopedics Physical Assesment, Magee D et al)
Antalgic (Painful) Gait
The antalgic or painful gait is self-protective and is the result of injury to the pelvis, hip, knee, ankle, or
foot.
The stance phase on the affect~d leg is shorter than that on the nonaffected leg, because the patient
attempts
to remove weight from the affected leg as quickly as possible; therefore, the amount of time on each leg
should be noted. The swing phase of the uninvolved leg is decreased. The result is a shorter step length on
the uninvolved side, decreased walking velocity, and decreased cadence.28 In addition, the painful region
is often supported by one hand, if it is
within reach, and the other arm, acting as a counterbalance, is outstretched. If a painful hip is causing the
the painful hip. This shift decreases the pull of the abductor muscles, which decreases the pressure on the
femoral head, from more than two times the body weight to approximately body weight, owing to vertical
instead of angular placement of the load over the hip.
Arthrogenic (Stiff Hip or Knee) Gait

The arthrogenic gait results from stiffness, laxity, or deformity, and it may be painful or pain free. If the
knee or hip is fused or the knee has recently been removed from a cylinder cast, the pelvis must be
elevated
by exaggerated plantar flexion of the opposite ankle and circumduction of the stiff leg (circumducted
gait) to provide toe clearance. The patient with this gait lifts the entire leg higher than normal to clear the
ground because of a stiff hip or knee.

Ataxic Gait
If the patients has poor sensation or lacks muscle coordination, there ini tendency toward poor balance
and a broad base. The gait of a person with cerebellar ataxia includes a lurch or stragger, and all
movement are exaggerated. The resulting gait is irregular, jerky, and weaving

Contracture Gaits
Joints of the lower limb may exhibit contracture if immobilization has been prolonged or pathology to the
joint has not been properly cared of. contracture often results in increased lumbar lordosis and extension
of the trunk combined with knee flexion to get the foot on the ground. With a knee flexion contracture,
the patient demonstrates excessive ankle
dorsiflexion from late swing phase to early stance phase on the uninvolved leg and early heel rise on the
involved
side in terminal stance. Plantar flexion contracture at the ankle results in knee hyperextension (midstance
of affected leg) and forward bending of the trunk with hip flexion (midstance to terminal stance of
affected leg). Heel rise on the affected leg also occurs earlier.28
Heel rise on the affected leg also occurs earlier.

Gluteus Maximus Gait


If the gluteus maximus muscle, which is a primary hip extensor, is weak, the patient thrusts the thorax
posteriorly
A initial contact (heel strike) to maintain hip extension of the stance leg. The resulting gait involves a
characteristic backward lurch of the trunk.

Gluteus Medius Gait


If the hip abductor muscles are weak, the stance phase is lost, and the patients exhibits an excessive
lateral list in which the thorax is thrust laterally to keep the center of gravity over the stance leg.

Equinus Gait

This childhood gait is seen with talipes equinovarus (club foot). Weight bearing is primarily
on the dorsolateral or lateral edge of the foot, depending on the degree of deformity. The weight-bearing
phase on the affected limb is decreased, and a limp is present. The pelvis and femur are laterally rotated to
partially compensate for tibial and foot medial rotation.

Hemiplegic gait

Gait swings the paraplegic leg outward and ahead in a cirle.

Parkinsonian Gait

Gait characteristic are by shuffling or short rapid step at times.


During the gait, patient may lean forward and walk progressively faster as throught unable to stop.

Plantar Flexor Gait

If the plantar flexor muscles are unable to perform their function, ankle and knee stability are greatly
affected.
Loss of the plantar flexors results in decrease or absence of push-off. The stance phase is less, and there
is a shorter step length on the unaffected side.

Psoatic Limp
The psoatic limp is seen in patients with conditions affecting the hip, such as Legg-Calve-Perthes disease.
The patient demonstrates a difficulty in swing-through, and the limp may be accompanied by exaggerated
trunk and pelvic movement.28 The limp may be caused by weakness or reflex inhibition of the psoas
major
muscle. Classic manifestations of this limp are lateral rotation, flexion, and adduction of the hip.
The patient exaggerates movement of the pelvis and trunk to help move the thigh into flexion.

Quadcriceps Gait
If the quadriceps muscles have been injured (e.g., femoral nerve neuropathy, reflex inhibition, trauma),
the
patient compensates in the trunk and lower leg. For plantar flexion causes the knee to extend
(hyperextend).
If the trunk, hip flexors, and ankle muscles cannot perform this movement, the patient may use a hand to
extend the knee. 28
Scissors Gait
This gait is the result of spastic paralysis of the hip adductor muscles, which causes the knees to be drawn
together so that the legs can be swung forward only with great effort (Fig. 14-21). This is seen in spastic
paraplegics and may be referred to as a neurogenic or spastic gait.

Short leg Gait


If one leg is shorter than the other or there is a deformity in one of the bones of the leg, the p'!tient
demonstrates a lateral shift to the affected side, and the pelvis tilts down on the affected side, creating a
limp. The patient may also supinate the foot on the affected side to try to "lengthen" the limb.
The joints of the unaffected limb may demonstrate exaggerated flexion, or hip hiking may occur during
the swing phase to allow the foot to clear the ground.28 The weight-bearing period may be the same
for the two legs. With proper footwear, the gait may appear normal. This gait may also be termed painless
osteogenic gait.

Stepapge or drop Foot Gait


Patient has weak or paralyzed dorsiflexor muscles, resulting in a drop foot.

Drug Affected Non Union ( Factors contributing to non-union of fractures : Venkatachalapathy Perumal,
Craig S. Roberts)
Nonsteroidal anti-inflammatory drugs
NSAIDs inhibit osteogenic activity and fracture healing. Glassman et al., in a retrospective review of 228
patients who underwent instrumented spinal fusion, reported an odds ratio with a five-fold increased
chance of non-union with NSAIDs. The pathogenesis of NSAID-inhibiting osteogenesis is not clearly
understood. Animal studies show reversibility of NSAID effects when prostaglandin E2 levels are
gradually restored after short-term treatment. Late exposure to NSAIDs, 61–90 days after a humeral shaft
fracture, was associated with non-union. There is a correlation between the use of NSAIDs and non-
union, especially when NSAIDs are used for more than 4 weeks. In this series, 70% of patients with non-
union had taken NSAIDs. Although all NSAIDs inhibit fracture healing, cyclooxygenase-2 (Cox-2
inhibitors) have been shown to inhibit fracture healing more than the less specific NSAIDs. Current
evidence suggests that avoidance of NSAIDs in the post-operative and post-injury period may prevent
nonunions.
Neglected Fracture ( Himpunan makalah Prof Soelarto, www. Eprints.undip.ac.id)
Neglected fracture dengan atau tanpa dislokasi adalah suatu fraktur dengan atau tanpa dislokasi yang
tidak ditangani atau ditangani dengan tidak semestinya sehingga menghasilkan keadaan keterlambatan
dalam penanganan, atau kondisi yang lebih buruk dan bahkan kecacatan.
Menurut Prof dr. Subroto Sapardan, dalam penelitiannya di RSCM dan RS Fatmawati Jakarta, Februari –
April 1975, Neglected fracture adalah penanganan patah tulang pada extremitas (anggota gerak) yang
salah oleh bone setter (dukun patah), yang masih sering dijumpai di masyarakat Indonesia. Pada
umumnya neglected fracture terjadi pada yang berpendidikan dan berstatus sosio-ekonomi yang rendah.
Berdasarkan pada beratnya kasus akibat dari penanganan patah tulang sebelumnya, neglected fracture
dapat diklasifikasikan menjadi 4 derajat :
1. Neglected derajat satu: Bila pasien datang saat awal kejadian maupun sekarang, penanganannya tidak
memerlukan tindakan operasi dan hasilnya sama baik.
2. Neglected derajat dua: Keadaan dimana apabila pasien datang saat awal kejadian, penanganannya tidak
memerlukan tindakan operasi, sedangkan saat ini kasusnya menjadi lebih sulit dan memerlukan tindakan
operasi. Setelah pengobatan, hasilnya tetap baik.
3. Neglected derajat tiga: Keterlambatan menyebabkan kecacatan yang menetap bahkan setelah dilakukan
operasi. Jadi pasien datang saat awal maupun sekarang tetap memerlukan tindakan operasi dan hasilnya
kurang baik.
4. Neglected derajat empat: Keterlambatan di sini sudah mengancam nyawa atau bahkan menyebabkan
kematian pasien. Pada kasus ini penanganannya memerlukan tindakan amputasi.

Non Op Modalities for non Union (Campbell : Operative Orthopaedics, Canale S T, Beaty J H)

 LOW-INTENSITY ULTRASOUND
Xavier and Duarte in Brazil first reported the successful use of low-intensity ultrasound (30 mW/cm 2) to
heal nonunions in humans in 1983. Before their report, several studies suggested that the stimulation of
bone ends by ultrasound in animals would accelerate or enhance bone healing. Some studies showed
increases in cellular activity at osteotomy sites and increases in mineralization of the bone and metabolic
activity. It has been theorized that ultrasound stimulation promotes bone healing because it stimulates the
genes involved in inflammation and bone regeneration. Another theory suggests that ultrasound increases
blood flow through dilation of capillaries and enhancement of angiogenesis, increasing the flow of
nutrients to the fracture site. Some studies have suggested that chondrocyte stimulation is enhanced by
ultrasound, which leads to an increase in enchondral bone formation.
The overall success rate in the United States has been reported to be between 70% to 93% for nonunions
and delayed unions. The current protocol is to use the ultrasound equipment for 20 minutes once a day.
Rubin et al. noted in their 2001 review article that double-blind prospective clinical trials showed that
healing times of fresh fractures can be reduced 40% with the use of ultrasound. They estimated a cost
savings of $15,000 per case with the early use of ultrasound on fresh fractures, considering the number of
fractures that progress to nonunion. A systematic review and a meta-analysis of relevant randomized
controlled studies of low-intensity pulsed ultrasound on the rate of fracture healing by Busse et al. also
found a benefit to the use of ultrasound in fracture management. Ultrasound seems to be a reasonable,
noninvasive treatment for fractures in which healing is delayed or at risk for nonunion.

 ELECTRICAL AND ELECTROMAGNETIC STIMULATION


Improvements in electrical and electromagnetic bone growth stimulators continue to progress. Bone
growth stimulators usually are used in conjunction with cast immobilization and weight bearing. External
electrical stimulation is especially advantageous in infected nonunion management or when surgical
intervention is contraindicated. At least three electrical and electromagnetic methods are available for the
treatment of nonunions. These methods are either invasive, requiring the implantation of electrodes, or
semi-invasive, requiring the percutaneous application of multiple electrodes. Devices that use inductive
coupling differ in their configuration; some try to re-create the Helmholtz configuration, and others use a
U-shaped coil. U-shaped coils with inductive coupling used for 3 or more hours per day has been
successful in healing nonunions of long and short bones, open or closed fractures, long-standing
nonunions, infected nonunions, and those with fracture gaps up to 1 cm. Several electrical and
electromagnetic waveforms, including direct current application, square-wave generators, and other
unusual waveforms, also have proved to be of benefit. In delayed union or nonunion of the tibia, square
wave signals have been shown to be beneficial; however, the prolonged immobilization required poses
problems with rehabilitation. DeHaas et al. recommended that nonunions with a gap between tibial
fragments (pseudarthroses) be treated with bone grafting and internal fixation before electrical
stimulation. They also recommended that infected fractures be débrided before electrical stimula tion.
Extracorporeal shock-wave therapy remains popular in Europe and is gaining more usage in the United
States despite the lack of conclusive level I evidence.

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