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Injuries to the lumbosacral plexus

In the same way that the brachial plexus connects the spinal cord to the upper limb, the lumbo-sacral plexus provides all
the nerves to the lower limb. A complete or partial injury to the lumbo-sacral plexus therefore leaves the patient with a
deficit in the sensation and/or movement in the lower limb and pain which has got the typical characteristics of
burning/cramping or sometimes tingling. Movements of hip, knee, ankle, foot and toes can be affected to a different
degrees up to a complete injury where the whole limb is flail and there is no control of the hip with complete paralysis of
the gluteal muscles. If the gluteal muscles are still working the possibility of a lesion of the sciatic nerve proper is more
likely.
The treatment and the likelihood of full recovery depends on the cause and the delay between damaging event and
treatment itself. In some cases the lesion is at the level of the origin of the lumbo-sacral plexus and that means inside the
spinal canal where the nerves originate. In these cases the only surgical option is reconnection of the nerves at this level.
Sometimes the reconnection is performed with nerve grafts (nerves taken from other parts of the body, usually the sural
nerve) directly to the femoral and sciatic nerve).
Lumbar Plexus Neuralgia
What is lumbar plexus neuralgia?
The nerve roots that arise in the spinal column make up a network of nerves in the back. This is known as a plexus. Each
nerve that goes to the leg and the foot originates in this network. Lesions of the lumbar plexus are injuries to this network
of nerves in the back and may be the cause of pain.
Cause
The most common cause of this condition is a serious accident, but damage to this network of nerves can also be caused
by: sports injuries, stab wounds, and operations in this area.
Signs and symptoms
As well as varying degrees of paralysis and loss of feeling, neuropathic pain in the legs is the biggest problem. This pain
is continually present and is of a burning or stabbing character. At a later stage there are attacks of stabbing and shooting
pain. This pain normally occurs at the ends of the limbs: the lower arm, the hand and/or the fingers.
How is lumbar plexus neuralgia diagnosed?
The neurological examination particularly focuses on paralysis and loss of feeling in the legs.
Do I need additional examinations?

Diagnostic examination for other non-physical factors important for your pain, have already been done by yourself
trough filling out your pain questionnaires.

Additional examinations, in the event of a serious accident include standard radiographs, CT scan and MRI scan.

CT scan with contrast around the spinal cord.

EMG and SSEP.

What are my treatment possibilities?


Multidisciplinary treatment
Depending on the cause of your pain, your pain specialist will decide whether or not to start physical treatment. Based on
the results of the completed pain questionnaire, additional examinations can be carried out and, apart from physical
treatment, other methods of treatment will be suggested.
Non-physical treatment
If the results of your pain questionnaire are abnormal, your pain specialist will offer you one of the non-physical treatments
listed below:

Psychological Treatment

Depression Treatment

Cognitive-Behavioural Treatment

Rehabilitation Treatment

Physical Treatment
Medication

Neuropathic pain medication

Anti-inflammatories (short period)

Other Treatment

Physiotherapy

Interventional pain treatment

Spinal cord test stimulation

Spinal cord stimulation

Invasive pain treatment

If possible, restoring of the plexus by a neurosurgeon.

Overview
Neurologic signs of lumbosacral plexus injuries consist of motor deficit with flaccid paralysis associated with sensory
deficits to all types of stimulation in the territory of the damaged nerve roots: a lower motor neuron paralysis. Nonstructural
causes include radiation therapy, diabetes, vasculitis, and perivasculitis. Traumatic causes are mainly due to fractures of
the pelvic ring or acetabulum and hip joint replacements. In this article, the authors provide a systemic review of
lumbosacral plexus injuries from the published literature. They have included background information about the historical
notes, clinical manifestations, etiology, epidemiology, pathogenesis and pathophysiology, prevention, differential
diagnosis, diagnostic work-up, prognosis and complications, and management. In the recent update, the authors added
discussion of the preventive measures that can be considered during spine surgery to lower the risk of lumbar plexus
injury.
Key points

Symptoms of lumbosacral plexus injury include varying degrees of lower extremity weakness, sensation changes,
pain, and diminished reflexes.

Most lumbosacral plexopathies due to trauma are from very violent injuries, such as automobile-pedestrian
accidents, high-speed car accidents, or falls from heights, and are often associated with damage to internal organs,
blood vessels, and bony structures, especially the pelvic ring.

CT for evaluation of bony injuries, MRI, and EMG/NCS are important diagnostic tools.

Because most traumatic plexopathies improve spontaneously, at least to some extent, they usually are treated
conservatively, but when surgical repair is attempted, it tends to yield better results.

Historical note and terminology


Involvement of the lumbosacral plexus appears in history in its congenital form, most often described as
myelomeningocele. Hippocrates and Arabic physicians described this condition with its devastating clinical problems.
Aristotle proposed infanticide to resolve this social problem. Even with modern technological advances, lumbosacral
plexus injury is not easy to describe. Books on the subject of trauma make only a brief mention of this entity (Huittinen
1972).
The lumbosacral plexus comprises 2 distinct portions: the lumbar plexus and the sacral plexus, each innervating a
different part of the lower limb. The lumbar plexus connects with the sacral plexus via the lumbosacral cord. The lumbar
plexus is formed by the ventral primary rami of L1-3 with contributions from the ventral rami of L4 and T12, which
separates into anterior and posterior divisions. The lumbosacral plexus sends muscular branches to the quadratus
lumburom (T12, L1-4), psoas minor (L1), psoas major (L2-3[4]), and iliacus (L2-3). The anterior rami (L2-4) form the
obturator nerve that innervates the adductor muscles of the thigh and the skin of the medial thigh. The posterior rami (L24) form the femoral nerve, which innervates the quadriceps femoris muscle, the anterior thigh, and the medial side of the
leg via medial and intermediate cutaneous nerves of the thigh and saphenous nerves, respectively. The predominantly
sensory iliohypogastric (L1), ilioinguinal (L1), genitofemoral (L1-2), and lateral cutaneous nerve of the thigh (L2-3) also
arise from lumbar plexus. The caudally located sacral plexus is formed by the lumbosacral cord (L4-5) and the ventral
rami of S1-3 and part of S4. The main branch is the sciatic nerve (L4-5, S1-3), and its 3 main branches (the peroneal,
tibial, and sural nerves) supply the hamstring muscles, all the muscles below the knee, and all the skin below the knee
except the area supplied by the saphenous nerve. The superior gluteal nerve (L4-5, S1; innervates the gluteus medius
and minimus), inferior gluteal nerve (L5, S1-2; innervates gluteus maximus), and the nerve to piriformis (S1-2) directly
arise from the sacral plexus. The posterior femoral cutaneous (S1-3) and pudendal (S2-4) nerves also arise from sacral
plexus.

Lumbosacral plexus neuropathies are rare syndromes, which are caused by damage to the nerve bundles in the
lumbosacral plexuses. After establishing the existence of a plexus lesion nerve by demonstrating that symptoms
cannot be explained by a lesion of a single nerve root or peripheral nerve the underlying pathology needs to be
unravelled. Most frequently, the lumbosacral plexus is damaged: in diabetics, by direct or indirect pelvic trauma,
by compression, or obstetric complications. Tumours, aneurysms and idiopathic or hereditary neuropathies are
more infrequent causes of a lumbosacral plexopathy. Treatment, course and prognosis largely depend on the
underlying disorder.
Clinical features
Lumbosacral plexus neuropathies are relatively rare, and fairly unknown clinical syndromes, which are caused by damage
to the nerve bundles in the lumbosacral plexuses.
One of the main causes for a lumbosacral plexus neuropathy is the so-called 'diabetic amyotrophy'. Another cause is the
idiopathic form of lumbosacral plexus neuropathy, the lower-extremity counterpart of the more well-known ParsonageTurner syndrome or neuralgic amyotrophy, which usually affects the brachial plexus(-es). Locally invasive tumour-growth
in the pelvic region can be another cause of a lumbosacral plexopathy.
The clinical features of a lumbosacral plexopathy depend on two things: the exact parts of the plexus and nerves that are
involved, and the underlying etiology. As localisation of a lesion is the first objective of any neurological evaluation, and
from then on a possible etiology can be inferred, the anatomical features will first be discussed.
The lumbosacral plexus (see picture) consists of the interwoven nerves bundles coming from the 3 rd, 4th and 5th lumbar
nerve roots, and the 1st, 2nd and 3rd sacral nerve roots, with small additions from the 2nd lumbar and the 4rd sacral nerve root
as well. Actually, the plexus consists of two separate parts, the lumbar and the sacral plexuses, that are connected by the
so-called lumbosacral trunk. The lumbar part of the plexus mainly lies embedded between and in the paraspinal quadratus
lumborum and psoas muscles, making it vulnerable to local trauma or compression (e.g. by a hematoma). On the other
hand, the sacral plexus lies in the pelvis, with the lumbosacral trunk crossing the pelvic brim, making it vulnerable to
intrapelvic pathology.

Clinically, the patient's symptoms can be attributed to a plexopathy if they are


localised to the peripheral nervous system, but neither fit the distribution of one
nerve root or one single peripheral nerve. For this conclusion, a careful and
detailed neurological examination is required. If the symptoms are attributable to
a plexus lesion, they must be further devided in mainly lumbar, mainly sacral or
diffuse or patchy lesions of the whole plexus. This localisation will then aid the
question of 'how' did the nerves get damaged (see: differential diagnosis).
For the patient, the symptoms of a lumbosacral plexopathy can be that of any
other peripheral nerve lesion: neuropathic (severe, shooting, burning or stabbing)
pains, tingling, numbness of certain skin areas or, conversely, areas that are very
hypersensitive to the touch, and weakness and wasting of certain muscles in the
thigh, buttock and leg region. Usually, when a lesion is acute, pain will be a
marked symptom, followed by weakness and wasting. More slowly progressive
lesions usually start with sensory symptoms such as numbness and tingling and
increasing pain, or sometimes just slowly increasing muscle weakness.
Natural course and prognosis
Not surprisingly, the course and prognosis will largely depend on the underlying disorder causing the lumbosacral
plexopathy, and especially on whether a treatable cause can be demonstrated (see Therapy section). Once a fixed plexus
deficit has been established, recovery of sensory and motor function can take months to years, depending on the degree
of axonal damage and the length new nerve fibers have to grow to reinnervate the affected muscles or skin parts.
Unfortunately, complete functional recovery is not always the rule, and many patients remain with functional impairments,
hindering daily activities such as walking or cycling.
Epidemiology
There are no data on the incidence or prevalence of lumbosacral plexopathies in the general population. For diabetics, the
prevalence of a proximal diabetic neuropathy is estimated at 8 per 1000 (type I and II diabetics combined); the prevalence
of type II diabetes alone in the general population is about 3% ( 500.000 people in the Netherlands). In trauma's, the
incidence of a lumbosacral plexus lesion with a sacral fracture is about 2%, in other types of pelvic fractures it's about
0.8%. After major gynaecologic pelvic surgery, the incidence of lumbosacral plexus lesions was 0.16% in a series of 1200
patients. The incidence of obstetric lumbosacral trunk lesions is estimated at 1 per 2000 - 6000 deliveries. In
coagulopathies, either during anticoagulant therapy or in hemophiliacs, the occurrence of an iliopsoas hematoma
compressing the lumbar plexus is rare, but does occur, especially after invasive procedures. Idiopathic lumbosacral
plexus neuropathy is a rare disorder, with a few hundred cases known in literature.
Differential diagnosis
The most important aspect in the differential diagnosis is establishing the existence of a plexus lesion, by demonstrating
symptoms that cannot be explained by a lesion of a single nerve root or peripheral nerve. However, there are some
disorders that can mimic this clinical picture. For example, a lumbar spinal stenosis can cause compressive lesions of
multiple nerve roots, which causes pain, sensory symptoms and sometimes paresis in a 'plexus' distribution. Usually, the
additional symptoms of lower back pain and provocation of symptoms by certain activities (e.g. walking) give a clue to this
diagnosis, and when in doubt, imaging of the lower spine should be performed. Also, an EMG examination will reveal
intact sensory conduction in the presence of sensory symptoms, localising the lesion proximal to the spinal sensory
ganglion. Another mimic of a lumbosacral plexopathy can be lower-limb motor neuron disease, for example idiopathic
(such as ALS) or infectious in endemic areas (e.g. poliomyelitis). A previously undiscovered tethered spinal cord can also
present with patchy paresis and sensory symptoms in the legs. Finally, if the patient suffers from a patchy peripheral nerve
disorder such as a mononeuritis multiplex, the symptoms can resemble a plexus lesion.
Once the clinical diagnosis of a lumbosacral plexopathy is established, one should consider the following etiological
categories (see table):
TABLE: Causes of lumbosacral plexopathy
Vascular:
proximal diabetic neuropathy / diabetic amyotrophy
vasculitis in connective tissue disease (PAN, RA, SLE)
Trauma:

pelvic ring disruption


obstetric complications
pelvic surgery
Compressive:
tumor retroperitoneal or pelvic
abdominal aortic or iliac aneurysm
retroperitoneal hematoma or abscess
invasion of nerves by metastatic tumour growth
Idiopathic:
lumbosacral plexus neuropathy
neuralgic amyotrophy
Hereditary:
hereditary neuralgic amyotrophy (HNA)
hereditary neuropathy with liability to pressure palsies (HNPP)
Infectious:
Herpes simplex (type II) or Herpes zoster
Borrelia
Most frequently, the lumbosacral plexus is damaged: in diabetics, by direct or indirect pelvic trauma, by compression, or
obstetric complications. Tumours, aneurysms and idiopathic or hereditary neuropathies are more infrequent causes of a
lumbosacral plexopathy. This also means that usually the cause of the plexopathy is relatively obvious or easily diagnosed
once the clinical diagnosis has been made. Two less obvious causes of a lumbosacral plexopathy will be discussed below.
Diabetic amyotrophy or proximal diabetic neuropathy is a syndrome which classically occurs in older type II diabetics, who
already have some signs of a diabetic symmetric distal polyneuropathy, but not yet an overt vasculopathy. It starts with a
subacute, burning neuropathic pain in the leg, thigh, buttock, or lower back, with weakness in the proximal leg muscles,
usually mainly in the distribution of the femoral or obturator nerve, and dysesthesias. Some patients suffer from
considerable weight loss. The neuropathic pain can last for as long as months, and gradually decreases, while strength
returns in months to years. The cause is probably ischemia, induced by a metabolically induced focal microvasculitis
[Dyck ea, 2002].
Idiopathic lumbosacral plexus neuropathy is characterized by extreme neuropathic pain at onset, rapidly followed by a
patchy paresis and striking atrophy of muscles in the thigh and leg. In about 30%-50% of the patients there are also
sensory symptoms such as paresthesias and subsequent hypesthesia in skin regions innervated by the lumbosacral
plexus.[van Alfen ea, 1997] Although the name of the disorder implies that all parts of the lumbosacral plexus can be
involved (and they sometimes are), the symptoms are usually localized to the lumbar plexus region. The severe pain
usually lasts for days to weeks, and recovery of strength can take months to years.
Ancillary investigations
Depending on whether there's an obvious or plausible cause for the lumbosacral plexopathy, there will be a need for
limited or more extensive ancillary investigations.
Imaging studies are warranted whenever any structural cause of the plexopathy is suspected.
If there is a direct or indirect trauma to the plexus, imaging of the region by CT or MRI scanning, sometimes by abdominal
or pelvic ultrasound, will help to clarify the extent of the lesion and identify treatable causes (such as a hematoma).
An electrophysiological examination, including needle examination (EMG) and nerve conduction studies (ENG) can help
to confirm the clinical diagnosis of a plexopathy, and identify the nerve structures involved. ENG will show reductions in
the sensory nerve action potential amplitudes in different lumbosacral plexus branches, excluding a purely radicular
problem. Motor nerve conduction studies are usually not very informative unless the paresis is severe, in which case the
compound motor action potentials will be reduced in affected nerves. ENG can also help in the differential diagnosis by
evaluating the presence or absence of pressure palsies, making HNPP as an underlying cause more or less likely. Needle
examination will identify neurogenic abnormalities in affected muscles, assess the severity of the lesions, and show if
there are signs of recovery. This also makes it an important tool in predicting the functional outcome.
Laboratory investigations or blood test can be helpful if for example a hematoma during anticoagulation therapy is likely,

by measuring the bleeding time or INR, or when an auto-immune or infectious cause is suspected. In these cases, a
lumbar puncture should also be considered, for identification of an auto-immune or infectious response in the
cerebrospinal fluid which could affect the nerve roots. Ofcourse a blood glucose will help to evaluate the diabetic patient;
but the chance that a proximal diabetic neuropathy is the first sign of diabetes mellitus is very small.
If an underlying genetic disorder (HNA or HNPP) is suspected because of a family history with similar signs and
symptoms, a DNA sample can be tested for a PMP22 deletion or point mutation which will identify patients with HNPP.
For HNA, DNA testing in individuals is not yet available.
Therapy
For space-occupying lesions, relieving the compression of the plexus by tumour debulking or irradiation, hematoma
evacuation or abscess drainage, should be the first goal of therapy. For diabetic and idiopathic lumbosacral plexopathy, an
early treatment with high-dose corticosteroids could be helpful, by mitigating the inflammatory response in the nerves.
Ofcourse, when an infectious process is suspected, treatment should be aimed at eradicating that infection, e.g. by
antibiotics for Borrelia, or aciclovir in case of a Herpes infection.
If neuropathic pain is present, an attempt should be made to alleviate this, first by a trial of a long-acting NSAID, such as
diclofenac slow-release 100 mg twice a day, combined with a strong opiate such as morphine in a slow-release formula
twice or three times a day. If this does not provide adequate relief, the best option is probably the use of a co-analgesic
from the group of anti-epileptic drugs, such as gabapentin or carbamazepine. As these are not 'ordinary' painkillers, one
needs to carefully instruct patients on their (prolonged) use and side-effects. We start with an increasing dose of
gabapentin, until a maintenance dosage of 2400 mg per day (in 2 or 3 gifts) is reached, and evaluate its effect after 4-6
weeks. If the side-effects are acceptable, but the pain not sufficiently suppressed, the dosage is increased to a maximum
of 3600 mg per day.
The musculoskeletal pain that can ensue from altered mechanical stability of the hip, knee or ankle joint, is best treated by
a combination of physiotherapy for maintaining a normal posture and mobility, and NSAID's if necessary. Some patients
find the use of a TENS apparatus helpful. During physiotherapy, there is little sense in pure strength training, as this is a
near-impossible task for denervated muscle groups. However, the patient should be encouraged to use the limb as fully
as possible. There is no indication that inadvertent overexertion worsens the nerve damage.
For many patients, the advice of a rehabilitation doctor can be very useful in helping them overcome practical difficulties in
everyday life, and finding their way back to their work or occupation. Because the recovery is usually slow and gradual, it
can take up to 2 or 3 years before the final residual symptoms and impairments can be assessed. This should be taken
into account for example, when advising patients on how to deal with occupational disability. In the Netherlands, the first
assesment of any permanent occupational disability is made after six months, and after one year it is decided if, and for
which part or percentage, the patient is unable to work ('WAO', or 'wettelijk arbeidsongeschikt'). For patients with a fixed
lumbosacral plexopathy, the timing of this decision can just be too early.

New Ways to Heal Broken Bones


Jacqueline Wallace, of Phoenix, sat enjoying the December 1993 holidays at her son's home in Gaithersburg, Md. But
when she stood up and took a step, her holiday took a turn for the worse. Wallace fell and fractured her hip.
"My foot dragged a little, not exactly a stumble," Wallace says. "I don't know whether the bone broke because I fell, or I fell
because the bone broke."
Despite her 84 years and weak heart, Wallace had a lot going for her after her fall: modern medical practice and
determination to walk again. Surgery to implant an artificial hip joint took under 45 minutes. (The x-ray at left shows the
artificial left hip in sharp contrast with the bones of the normal right hip.) Spinal anesthesia and sedation were
administered instead of general anesthesia because they are thought to pose less risk. And her physical therapy began
the day after the operation.
"I fussed," she says. "I was afraid it was going to hurt or I'd fall. But they said if you want to go home, you have to do this.
And I did. It was more scary than painful."
Wallace's fracture was one of 1.5 million--including 336,000 hip fractures--reported in 1993, the latest year for which the
National Center for Health Statistics has figures.
Besides surgical repair, treatments for broken bones include bone manipulation to reduce the fracture, use of a cast, and
bone stimulation. Central to fracture healing is bone biology. Many treatments, some on the horizon, are designed to
improve the natural course of healing.
Bones at Work
For skeletal growth and maintenance, the body's 206 dynamic, living bones renew themselves lifelong through a continual
breakdown, build-up process known as remodeling. This process is also involved in the remodeling of fractures, says
Martin Yahiro, M.D., a Baltimore orthopedist in private practice and a consultant on fracture treatment devices to the Food
and Drug Administration's Center for Devices and Radiological Health.
In remodeling, complex chemical signals prompt cells called osteoclasts to break down and remove (resorb) old bone,
and others called osteoblasts to deposit new bone. Many elements influence remodeling. Among them: weight-bearing,
vitamin D, growth factors, prostaglandins, and various hormones, including estrogen, thyroid, parathyroid, and calcitonin.
As 80 percent of the mature skeleton, compact cortical bone supports the body, providing extra thickness mid-shaft in long
bones to prevent their bending. Cancellous bone, whose porous structure with small cavities resembles a sponge,
predominates in the pelvis and the 33 vertebrae from the neck to the tailbone. A fibrous membrane called the periosteum
covers bone.
For healing and health, living bone must have a steady supply of nutrients. Blood vessels permeate bone to provide this
lifeline. Blood-forming elements fill the long bone inner canals.
When a Bone Breaks
Fracture breaks continuity of bone and of important attached soft tissue--including blood vessels, which spill their contents
into surrounding tissue.
Even before treatment, the body automatically seeks to repair the injury. Inflammatory cells rush to destroy, dilute or
isolate invaders and injured tissue. Tiny new blood vessels called capillaries begin growing into the site. Cells proliferate.
The injured person usually must endure pain, swelling, and increased heat at the breakage site for one to three days.
New tissue bonds the fractured bone ends with a soft callus, a mass of connective tissue and exudate (matter escaped
through blood vessel walls). Remodeling begins. Within a few months, a hard callus replaces the soft one. Remodeling
restores the inner canal. >
Once restoration is complete, which may take years, the healed area is brand new, without a scar. Usually thicker, the
new bone may even be stronger than the old, Yahiro says, adding that if the bone should break again, it's unlikely to be at
the same place.
And children's bones have a healing boost: They're growing.

"The growing skeleton is just geared to make bone," Yahiro says. "A very young child's wrist bones grow a millimeter a
month, to rapidly correct misalignment or length defects. An adult may take six to eight weeks to heal a wrist fracture, a 5year-old only three."
>When the ends of a fractured bone, such as an arm bone, form an abnormal angle, the doctor must decide whether to
push the ends together (manipulation) to reduce the fracture, possibly under anesthesia. Simple x-rays aid evaluation.
"If it's a large angle, we'd want to reduce that fracture," Yahiro says. "But if it's a small angle, especially in a young child
whose growth will correct it, we'd probably just put the limb in a cast."
What are the treatment options for a bone fracture?
Bone healing is a natural process which in most cases will occur automatically. Fracture treatment is usually aimed at
making sure there is the best possible function of the injured part after healing. Treatment also focuses on providing the
injured bone with the best circumstances for optimum healing (immobilization).
For the natural healing process to begin, the ends of the broken bone need to be lined up - this is known as reducing the
fracture.
The patient is usually asleep under a general anesthetic when fracture reduction is done. Fracture reduction may be done
by manipulation, closed reduction (pulling the bone fragments), or surgery.
Immobilization - as soon as the bones are aligned they must stay aligned while they heal. This may include:

Plaster casts or plastic functional braces - these hold the bone in position until it has healed.

Metal plates and screws - current procedures use minimally invasive techniques.

Intra-medullary nails - Internal steel rods are placed down the center of long bones. Flexible wires may be used
in children.

External fixators - these may be made of metal or carbon fiber; they have steel pins that go into the bone directly
through the skin. They are a type of scaffolding outside the body.

Usually the fractured bone area is immobilized for between two to eight weeks. The duration depends on which bone is
affected and whether there are any complications, such as a blood supply problem or an infection.

While you are pain-free under general or local anesthesia, a surgical cut is made over the fractured bone. The bone is
placed in the proper position. Screws, pins, or plates are attached to or placed in the bone temporarily or permanently.
Long bones may be fixed with nails placed in the bone cavity.
Any disrupted blood vessels are tied off or burned (cauterized). If a lot of bone has been lost due to the fracture
(especially if there is a gap between the broken bone ends), the surgeon may decide to do a bone graft. Bone grafting
may be performed using the patient's own bone, usually taken from the hip. Or, bone taken from a donor can be used.
If bone grafting is not necessary, the fracture can be repaired by the following methods:

One or more screws may be inserted across the break to hold it.

A steel plate held by screws may be drilled into the bone.

A long, thick metal pin (sometimes called a rod or nail) with holes in it may be driven down the shaft of the bone
from one end. Screws are then passed through the bone and through a hole in the pin.

In some cases, blood vessels and nerves are repaired with microsurgery. The opening in the skin is then closed. If the
broken bone has pierced the skin, the bone ends need to be washed with sterile fluid in the operating room to prevent
infection. The washing process may need to be repeated if the wound is dirty or becomes infected.