It is sometimes called a seat belt injury or “chance
fracture”. Usually, the patient is restrained, back seat passenger that is
involved in a car accident and the person is wearing only a lap seat belt. The
chance fracture is a variant of the flexion/distraction injury. The terminology
is sometimes confusing, but a chance fracture could indicate a bony injury. It
may present itself with a minimal compression fracture of the vertebral body,
however, in this case all three columns of the spine are injured from
distraction and tension. When you deal with a traumatic compression fracture in
a young patient that is involved in a car accident, rule out a seat belt injury
or “chance fracture”. This condition could be misdiagnosed or not diagnosed.
Bowel trauma occurs in these cases due to crushing of the bowel between the lap
seat belt and the spinal column, which results in devascularization and acute
bowel rupture. In flexion/distraction injury, there will be an anterior wedge
fracture of the vertebral body plus horizontal fracture of the posterior
elements or distraction of the facet and the spinous processes. If it goes
unrecognized, it may lead to progressive kyphosis with pain and deformity. This
injury usually occurs in the thoracolumbar junction or in the midlumbar are.
The posterior column fails first because of the axis of rotation is anterior to
the vertebral body. The flexion/distraction injury is unstable in flexion and
usually needs surgery to restore the disrupted tension band and prevent
progressive deficit and pain, as well as enhance the functional recovery of the
patient. In patients with flexion/distraction injury of the lumbar spine, up to
50% of these patients have associated potential life threatening injures such
as visceral and gastrointestinal injury. Look for transabdominal ecchymosis;
you will probably need to consult a general surgeon, and this condition occurs
more in children. The hallmark of this injury is the axial split of the pedicle
which is seen on the sagittal CT scan. There will be little comminution and
since the center of rotation is the anterior longitudinal ligament, the
posterior ligaments will be disrupted or the posterior neural arch is fractured
transversely. Flexion/distraction injury or seat belt injury can be purely bony,
purely ligamentous, or mixed. The treatment of flexion/distraction injury,
especially if the injury is ligamentous, is usually a posterior reconstruction
of the tension part of the spine with short segment fusion with
instrumentation. Ligamentous injuries of the spine do not heal (needs to be
fused). The bony chance fracture can be stable in extension and the fracture
can heal. The fracture could heal, but the fracture will probably need long
term follow-up. The fracture could be treated in a TLSO (Thoracic Lumbar Sacral
Orthosis) brace and watch the fracture for the development of kyphosis.
Brown-Sequard Syndrome results from an injury to one half of
the spinal cord as seen in penetrating injuries. The spinothalamic tract fibers
cross the midline below the level of the lesion resulting in contralateral loss
of pain and temperature sensation. The posterior column and the corticospinal
tracts carry vibration, position, light touch sensation, and motor function
that are lost from the ipsilateral side of the body. The prognosis is usually
good. 90% of the patients recover. If the patient has a wound on the right
side, the patient will feel it on the left side. It is a hemisection lesion.
There is loss of vibratory, light touch and motor on the same side while pain
and temperature is lost on the other side.
25% of tibial shaft fractures can be open. Open fractures
can lead to complications including wound problems, osteomyelitis, nonunions,
and infected nonunions. The treatment of open fractures of the tibia can be
challenging. A lot of the concepts are not black and white; they may be in the
grey zone. We don’t know the best time for debridement. We don’t know what the
optimal irrigation solution is and what the optimal pressure for the fluid is.
We don’t know for sure the ideal duration of giving antibiotic prophylaxis, but
we know that it is important to give the appropriate antibiotics early and do
meticulous debridement. We know that the IM rod is better than the plate
fixation or external fixator, and the result of the reamed IM rod or unreamed
IM rod is the same. We need to close or cover the wound before 1 week and the
vac can be used provisionally when we cannot close the wound, primarily at the
optimal time. A grade I fracture is less than 1 cm. a grade II fracture is
1-10cm. A grade III fracture is more than 10 cm, and there is contamination.
Grade III fractures are divided into three types. Grade IIIa fractures require
adequate tissue for closure (or skin graft). Grade IIIb fractures require
extensive periosteal stripping and the patient will need a flap (rotational or
free flap). Grade IIIc fractures have a vascular injury that requires repair or
amputation. The relative indication for amputation is warm ischemia for more
than 6 hours, absent plantar sensation and severe ipsilateral foot trauma.
The
most predictive factor for amputation is the severity of the soft tissue injury
in the ipsilateral extremity. When comparing limb salvage versus amputation,
the patient’s outcome is generally the same at 1-5 years. Lack of plantar
sensation does not predict poor outcome after limb salvage. Segmental fractures
are Grade III fractures, even if the open fracture is 1 cm. The ideal
irrigation solution and the pressure used to controversial. Timing of the
initial debridement is controversial. Irrigation and debridement within 6 hours
was the gold standard in the past. Debridement is performed as a priority
procedure no later than the morning after admission. There is no difference in
infection rate for a patient who has the initial surgery before or after 6
hours, including patients with Type III open fractures. More than 40% of the
patients usually wait longer than 6 hours for their initial surgery after
arrival at the hospital. Delayed surgery for less severe fractures is
acceptable as long as the debridement is done as a priority the following day.
Unless there is a gross contamination, evidence is not clear as to when is the
best time for the debridement. It seems like giving the patient antibiotics
promptly is more important than the time of debridement. The preferred solution
is normal saline and low pressure irrigation. Low pressure lavage may reduce
reoperation rates due to infection, nonunions, and wound healing problems.
Normally the tradition is to use 3, 6, and 9 liters of solution for Type I,
Type II, and Type III open fractures (just recommendations). There is increased
risk of wound healing with antibiotic solution. Meticulous irrigation and
debridement of open fractures is important in decreasing the infection risk.
Prophylaxis should be started as soon as possible. All patients with open
fractures should receive first generation Cephalosporin’s that will cover
gram-positive bacteria. You can give penicillin for farm injuries and
clostridia prone wounds. You will give clindamycin if there is a penicillin
allergy. In Type III open fractures, add aminoglycoside, such as gentamicin. It
was found that local antibiotics delivery at the site of injury decreased the
infection risk, such as cement beaded loaded with antibiotics. Antibiotic
should be given within 3 hours of the time of injury (preferably given as soon
as possible). There is reduction of 59% of acute infection in patients with
open fractures treated with antibiotics. The infection rate is 1.6 times
greater if antibiotics are given after 3 hours. Type I and Type II open
fractures require antibiotic coverage for 24 hours after wound closure. For
Type III open fractures, antibiotic administration should be given for a period
of 72 hours after the injury and no more than 24 hours after wound closure. After
the initial debridement, the patient will need staged debridement within 24-48
hours. There is a reduction infection rate, acute and chronic, for Type III
open fractures with the use of systemic antibiotics and aminoglycoside cement
beads compared with antibiotics alone. This combination of antibiotics lowers
the infection rate for any open tibial fracture that is treated with an IM rod.
Its affect is more noticed in Type III injuries. Plating of open fractures may
cause chronic infection and infected nonunion. The healing time is doubled with
plated open fractures. The IM rod resulted in a better alignment and lower
reoperation rate than using external fixator. Also, no difference in the
infection rate between the IM rod and the external fixator. You can use a
reamed nail or an unreamed nail. They both have a comparable result and no
difference in the outcome.
When reaming, you can use a bigger rod that provides
better stability. Reamed nailing is superior in closed tibial fractures, but it
is not superior in open tibial fractures. Reaming can cause increased pressure
and disruption of the endosteal blood supply, can cause thermal necrosis and
fat embolism with increased intramedullary risk of infection. The unreamed rod
uses smaller nails and results in less stability but preserves the endosteal
blood supply. Unreamed IM tibial rod appears to have a shorter time to union
and fewer incidence of knee contractures when compared with circular wire
external fixator. Nowadays, more and more orthopedic surgeons are using reamed
nails for open fractures of the tibia. If you have a spiral fracture of the
distal 1/3 of the tibia, you will need to get a CT scan of the ankle to
identify a posterior malleolar fracture, which should be fixed before insertion
of the IM rod. There is a lack of evidence to support the value of external
fixator over the IM rod in open factures of the tibia. Due to patient
discomfort, the high incidence of pin tract infection and loss of alignment,
external fixator should not be used as a definitive fixation. Use external
fixator temporarily (less than 4 weeks) and replace it with a rod in about 14
days. External fixator may be utilized for severely contaminated open
fractures. Tibial fractures treated with a shorter duration of external fixator
has reduction of the infection risk by 80%. When there is a shorter interval
between removal of the external fixator and insertion of the IM rod of the
tibia, there is a reduction of the risk of infection by 85%. In less severe
soft tissue injuries, you do primary closure without tension. In cases of
delayed closure, soft tissue coverage should be done within 7 days. Soft tissue
coverage beyond 7 days will increase the infection. There is no difference in
the incidence of infection in patients who had primary closure and delayed
closure of the wound. It is recommended to do primary closure for Type I, Type
II, and Type IIIa fractures with tension free closure and after timely
antibiotic prophylaxis and adequate debridement. Intraoperative culture after debridement
has no value. It does not predict future infection. In the upper 1/3 of the
tibia, you can treat it by a medial gastrocnemius flap. In the middle 1/3 of
the tibia, you can treat it by a soleus rotational flap. The use of a free flap
for soft tissue coverage was less likely to have wound complications than the
use of a rotational flap. The zone of injury may be larger than expected, and
it may include the rotated muscle flap. The negative pressure wound therapy
(the vac) is used frequently. The vac provides provisional coverage for wounds
where the physician cannot do primary closure. There is decreased infection
rate when using the vac. The vac is used for coverage after the initial
debridement of the open fracture until the definitive coverage is done. It is a
good temporizing dressing and can also be used in fasciotomy wounds. The vac
promotes local wound healing. Bone morphogenetic protein (BMP2) decreases the
need for secondary surgery and is used in acute open tibial fractures treated
with IM rod.
The syndesmosis gives stability to the ankle. It resists
external rotation and axial and lateral displacement of the talus. Syndesmotic
injuries of the ankle can be challenging in the diagnosis and in the treatment.
It may not be easy to obtain and maintain reduction of the syndesmosis.
Approximately 50% of the patients with operatively treated supination/external
rotation type fracture of the ankle have syndesmotic injury on stress
radiographs intraoperatively. Anatomic reduction of the syndesmosis is crucial
for a good clinical outcome. Restoration of the normal fibular length and
alignment, as well as obtaining and maintaining the alignment of the
syndesmosis significantly impacts the functional outcome of the patient. Malreductions
of the tibiofibular syndesmosis is not uncommon, and it can occur in up to 30%
of the patients. Fluoroscopy, direct visualization and reduction of the
syndesmosis could improve the anatomic reduction. Syndesmotic injuries are
common. They are found in sports injuries (high ankle sprain) or in ankle
fractures such as supination/ external rotation Type IV, pronation/ external
rotation and pronation/ abduction injuries. It does not occur with
supination/adduction injury. In this injury, you will see vertical fracture of
the medial malleolus and the talus will go medially. Syndesmotic fixation
probably is needed more with an ankle fracture that has a high fibular fracture
and deltoid ligament injury, than an ankle fracture that has fracture of the
fibula with medial malleolus fracture. The higher the fracture in the fibula,
the more incidence of syndesmotic disruption and the need for syndesmotic
fixation. In fact, the high fibular fracture plus deltoid injury equals
syndesmotic screw fixation (means syndesmotic screw fixation is needed more). To
diagnose a syndesmotic injury, you will find an unstable mortise; it can be
evident or occult.
You also need to suspect syndesmotic injury in proximal
fibular fracture, which is called Maisonneuve fracture. Look at the disruption
of the interosseous membrane and the syndesmosis. You do this by looking at the
ankle and get an x-ray. You also suspect syndesmotic injury with sports
injuries where there is a positive squeeze test (high ankle sprain). 20% of
syndesmotic injuries of the ankle can be undetected on clinical examination.
You should get stress-rays. You also suspect it in supination/external rotation
Type II injury that has a fibular fracture. Provocative tests or the stress
views are used in fibular fractures supination/external rotation Type II to see
if it is really a Type II injury or if the injury is a Type IV and there is a
hidden occult deltoid and syndesmotic injury. To do the provocative tests to
diagnose an occult injury or syndesmotic injury of the ankle, do the gravity
test or do the abduction/external rotation stress views or do weight bearing
film. In weight bearing films, the dorsiflexion of the ankle can eliminate any
errors on the medial side. Sometimes when the ankle is plantar flexed, the
medial side looks widened, but it is not a true widening. Look for the
tibiofibular clear space, look for the tibiofibular overlap, and look for the
widened medial clear space (more than 5mm). The tibiofibular clear space will
be greater than 5mm with syndesmotic injury. The tibiofibular clear space is
probably the best radiologic measure because it is not affected by the position
of the leg. If the syndesmosis is unstable, you need to fix it. It is the last
part of ankle fracture fixation. You must have anatomic reduction of the
syndesmosis. Before you fix the syndesmosis, you will need to evaluate the
reduction of the syndesmosis. This can be done by direct inspection and
reduction or by x-rays. You may need x-rays of the other side to assess
accuracy of reduction of the syndesmosis intraoperatively. In surgery, you can test
the stability of the syndesmosis. You can use the cotton test, use a bone hook,
or pull on the fibula by levering it out by hemostat, by a freer or an
elevator, or you can see the movement of the fibula. You can also do the
abduction/external rotation test. You will do x-ray intraoperatively and check
if the syndesmosis is stable or not and if it is reduced or not. So you want to
restore the fibular length and see if the medial clear space and tibiofibular
overlap are OK or not. Make sure that you do not have mortise instability,
which is displacement of the talus out of the mortise. You want to restore the
fibular length because this is key. The fibula must sit properly in the
incisura. The morphology of the incisura is variable and that encourages
malreduction. If the incisura is shallow, the fibula can be pushed anteriorly.
If the incisura is deep, then the fibula can be pushed posteriorly, and this
can cause malreductions and malrotation. Syndesmotic malreduction can occur
from positioning of the reduction clamps. Anterior clamps can cause
malreduction. Avoid translation of the fibula anteriorly when using anteriorly
based clamps. Clamp placement in a neutral anatomical axis reduces syndesmotic
malreduction. While oblique placed clamps results in syndesmotic malreduction,
variation in the angulation of the reduction clamp and screw placement can
cause iatrogenic syndesmotic malreduction and displaces the fibula in external
rotation. Fixation of the fibula in as much as 30 degrees of external rotation
may go undetected using intraoperative fluoroscopy. The malreduction may not be
clinically significant if it is minimal; however, it can be very significant if
the malreduction is significant. Screw fixation is supposed to be the gold
standard for syndesmotic fixation; however, this is no longer the gold standard
fixation method. You can fix the syndesmosis by screws, by suture buttons, and
by a variety of different techniques. Patients with suture buttons return to
work early and less frequently need their implant removed. The controversy is
that there is no gold standard for the number of screws used, the number of
cortices, the level of placement of the screws, the type of screws (3.5 or
4.5). I personally use 3.5 screws and rarely use 4.5 screws. I may also use
cross screws in severe situations. I also use a plate in Maisonneuve fractures,
not just screws over the fibula, the screws have to go through a plate to help
the stability of the screws. You must have anatomic reduction of the fibula, as
well as alignment. Achieving the fibular length can be a problem, especially if
the fibula is comminuted. In this situation, you need to fix the medial
malleolus first, then restore the fibular length.
The Dime Sign, the Shenton’s
line, and the uninterrupted subcortical line. Syndesmotic screws are rigid, and
they can break or loosen. The tight rope fixation avoids the problem of the
rigid fixation, so it maintains the reduction while allowing physiological
movement of the fibula (tight rope fixation has its own problems). I used to
remove all syndesmotic screws, but now I don’t remove them unless it is
necessary for pain or stiffness. I make the patient walk on it around 10-12
weeks. 17% of the screws will break, 13% become loosened, and ¼% of the screws
are removed due to symptoms. The screws look bad on x-rays when they are broken
or loosened, but these screws don’t cause a lot of trouble. If you keep the
screws, it is just an x-ray problem and not a functional problem. If you leave the
screws or if you remove the screws, there is no difference in functional
outcome between screw removal and nonremoval. They found that when the
syndesmosis is malreduced and then you remove the screws, then the patient
feels better and the movement gets better. Retained, broken screws had a better
functional outcome than the retained, intact screws. Fixation of the posterior
malleolus adequately stabilizes the syndesmosis. If the fragment is minimally
displaced, then the screws can be directed anteriorly to posteriorly. If the
fragment is large, you can fix it with a buttress plate posteriorly. The
posterior malleolar fixation restores the stiffness to 70% and the syndesmotic
screw fixation restores the stiffness to 40% compared to intact specimens. There
is a strong association between obesity and loss of syndesmotic reduction.
Obese patients are 12 times more likely to lose syndesmotic reduction than
nonobese patients. In regards to the syndesmotic injury, you will need to
recognize it and fix it when the syndesmosis is unstable. Evaluate the
reduction of the syndesmosis. Avoid malreduction. Remove syndesmotic screws
only if needed.
There are only a few cases of compartment in the neonate.
This can be a difficult diagnosis. Compartment syndrome in the neonate does not
present itself with the classic “P’s” as seen in adult patients. Compartment
syndrome in the neonate does not present itself with the classic “P’s” as seen
in adult patients. There are 5 P’s: pain/swelling, paresthesia, pulselessness,
pallor, and paralysis. Diagnosis in neonate is usually made retrospectively
after the patient has complications. The condition of compartment syndrome
usually occurs within the first 24 hours of birth. It usually occurs in the
forearm, is usually unilateral and occurs more in the dorsal aspect of the
forearm. Risk factors are the mother may be diabetic, some hypercoagulable
state (like polycythemia), and prematurity. The actual cause is not known,
however it can be a combination of extrinsic compression and hypercoagulable
state. Make sure to avoid missing the diagnosis of compartment syndrome. The
infant will have a swollen, tense forearm associated with skin lesions on the
forearm. The skin may have erythema, bullae, and edema. The skin lesions will
be present at birth and usually at the forearm. The patient may also have
pseudoparalysis, may lack spontaneous limb movement, and there might be some
nerve injury involved also. The clinical diagnosis of compartment syndrome will
be made after exclusion of other conditions such as infection, vascular injury,
and amniotic band syndrome. The clinical diagnosis of compartment syndrome will
be made after exclusion of other conditions such as infection, vascular injury,
and amniotic band syndrome. Infection could be cellulitis or can be necrotizing
fasciitis. Both should be excluded! Treatment of neonatal compartment syndrome
of the forearm should be early diagnosis and immediate fasciotomy. Ischemic
muscle contracture will develop from missing the diagnosis and delaying the
treatment.
The column principle divides the acetabulum into an anterior
and posterior column which becomes important when considering acetabular
fractures and their management. The anterior column is composed of the anterior
ilium, the anterior wall and dome of the acetabulum and the superior pubic
ramus. The posterior column extends from the obturator foramen through the
posterior aspect of the weight bearing dome of the acetabulum and then
obliquely through the greater sciatic notch. The ischiopubic ramus is a complex
structure that consists of the inferior pubic ramus and the inferior ramus of
the ischium. It forms the inferior border of the obturator foramen. The pelvis
is oriented to form an inverted “Y” shape. The obturator artery is a branch of
the anterior division of the internal iliac artery. It arises in the pelvis and
it enters the obturator canal. The obturator artery the divides into two
branches: the anterior and posterior branches of the obturator artery form a
vascular circle around the outer surface of the obturator membrane. An
acetabular branch reaches the hip joint and joins the ligamentum teres to
supply the head of the femur. It usually supplies a small portion of the head
of the femur. Corona mortis is a connection between the internal iliac branch
(obturator) and the external iliac or its branch, the inferior epigastric.
Corona mortis is predominantly a venus connection and the arterial connection
is much less. Its location on the superior pubic ramus is variable. It is about
3-7 cm from the symphysis pubis. It is located behind and on top of the
superior pubic ramus and one must be careful with lateral dissection of the
superior pubic ramus. The Corona Mortis is susceptible to injury in pelvic
trauma and in pelvic surgery especially during the ilioinguinal approach.Be aware that the sciatic nerve
can be split, and this can be a normal variant. Keep the knee flexed and the
hip extended during posterior approach to the acetabulum. This will protect the
sciatic nerve. The sciatic nerve is posterior to the obturator internus muscle
and anterior to the piriformis muscle. When using the sciatic nerve retractor
in the lesser sciatic notch, the muscle and tendon of the obturator internus
protects the sciatic nerve. It acts as a buffer layer between the retractor and
the nerve, because the nerve is posterior to the muscle. Sliding trochanteric
osteotomy allows exposure of the dome and the superior aspect of the
acetabulum. This type of osteotomy keeps the muscles intact and this will
balance its pulling forces. There will be less of a chance of displacement of
the greater trochanter this way. The superior gluteal nerve is close to the
superior gluteal artery at the greater sciatic notch. The superior gluteal
nerve can be injured from approaches that involve more than 5 cm above the
acetabulum. Excessive traction or attempt to control the bleeding from the
superior gluteal artery at the greater sciatic notch, may injure the nerve by a
suture or by a vascular clip that may entangle the nerve. Injury to this nerve
may affect the gluteus minimus. Injury to this nerve affects the abductors of
the hip joint and the patient may end up with Trendelenburg Gait. The inferior
gluteal nerve may also be injured. It innervates the gluteus maximus muscle.
The Lateral Femoral Cutaneous Nerve can become injured during the ilioinguinal
approach for acetabular fixation. The Lateral Femoral Cutaneous Nerve usually
passes under the ilioinguinal medial to the anterior superior iliac spine
(ASIS).
Injury to the Corona mortis may lead to significant hemorrhage which may be
difficult to control. The superior gluteal artery passes through the greater
sciatic notch. Injury to the superior gluteal artery can be associated with
acetabular fractures, especially fractures that involve the posterior column of
the acetabulum. The superior gluteal artery cam ne damaged by aggressive
retraction of the abductor muscles during posterior approach to the hip. The
Medial Femoral Circumflex Artery (MFCA) can be damaged due to dislocation of
the femoral head or from taking down the quadratus femoris from the femur
instead of the ischium. You need to leave a tag of 1 cm for the piriformis and
the obturator internus from the greater trochanter to preserve the deep branch
of the medial circumflex artery. If you detach these two tendons too close to
the trochanter, this could injure the deep branch of the medial femoral
circumflex artery. The medial femoral circumflex is the main blood supply to
the femoral head. The sciatic nerve is close to the acetabulum and can be
injured. In fact, sciatic nerve injury is the most common traumatic and
iatrogenic nerve injury connected to the acetabulum. Sciatic nerve injury can
be approximately 10% with hip dislocation. The incidence may be higher with
posterior acetabular fractures. When you examine a patient with an acetabular
fracture, always check the sciatic nerve function. Check dorsiflexion of the
ankle and the toes. It is peroneal division of the sciatic nerve that will be
affected. Check for numbness on the top of the foot. Repeat the exam again just
before surgery. Partial sciatic nerve injury can get worse from acetabular
surgery. The sciatic nerve anatomy is variable but well described. There may be
variations in its anatomy. These diagrams show the incidence of the most common
patterns of the relationship between the sciatic nerve and the piriformis
muscle.
The adductor longus muscle is one of the adductor muscles of
the hip located within the thigh. There are six adductor muscles for the hip
and here is a diagram showing the arrangement of these adductor muscles. The
adductor longus muscle arises from the anterior surface of the superior pubic
ramus, just lateral to pubic symphysis. It is inserted into the middle third of
the medial lip of the linea aspera on the posterior surface of the shaft of the
femur. The adductor longus muscle is innervated by the obturator nerve which
arises from the L2, L3, and L4 ventral rami of the lumbar plexus. Outside the
obturator foramen in the proximal part of the thigh, the obturator nerve
divides into anterior and posterior divisions. It is the anterior division of
the obturator nerve which supplies the adductor longus muscle. The adductor
longus muscle adducts and flexes the thigh, and helps to laterally rotate the
hip joint. Adductor strains may occur in hockey players or soccer players. It
is sometimes called a “pulled groin.” Adductor strains usually involve the
adductor muscles, especially the adductor longus muscle. It occurs due to
eccentric contraction of the muscle. The injury occurs due to external rotation
of an abducted leg. The patient will have groining pain and pain at the site of
the injury, usually near the pubic ramus. The patient will also have weak
adduction. It may be difficult to differentiate an adductor strain from a sport
hernia. X-rays are usually normal. MRI will show avulsion of the adductor
muscles from the pubic ramus. Adductor strain treatment includes: ice, rest,
protected weight bearing, and patient will go through a rehabilitation program.
Surgery is rarely done and the role of surgery is not well defined.
