Camptodactyly is a fixed flexion deformity at the PIP joint
of the little finger. The condition is an autosomal dominant trait involving
permanent flexion of the little finger. Camptodactyly may also be bilateral
affecting multiple digits. Unilateral 1/3 of the time and bilateral 2/3 of the
time. Camptodactyly occurs in less than 1% of the population, and it may be
associated with several congenital syndromes. Camptodactyly may be caused by
abnormal lumbricals and flexor digitorum superficialis insertion. Severe
camptodactyly may cause difficulty in grasping objects. Clinodactyly is
congenital curvature of the digit in the radioulnar plane. Treatment should be
done early with splinting, passive stretching, and physical therapy. Surgery
may be needed if the deformity is flexible, the patient may need tenotomy or
tendon transfer. If the deformity is severe and fixed, the patient may need
osteotomy or arthrodesis.
Female athlete triad is a condition that affects female
athletes such as gymnasts, dancers, or athletes with weight classifications
such as body builders. It is a syndrome in which amenorrhoea, osteoporosis, and
insufficient caloric intake affects certain groups of athletes. Each component
of the female athlete triad can occur from mild to severe. Not all components
need to be present, but if one component is found, the doctor should check for
the others. If you find a healthy, young female with stress fractures, ask
about her eating habits. The physician should examine the relationship between
the different components of the triad. The athlete will try to restrict their
diet in order to maintain lower body fat, and that may cause an imbalance of
energy (low caloric intake). This restriction of the athlete’s caloric intake
will lead to negative energy balance. Amenorrhoea results from energy
imbalance. Insufficient caloric intake is the most common cause of amenorrhoea
in female athletes, and it may or may not be associated with eating disorders.
Eating disorders can affect the brain’s regulation of the ovaries. This may
cause an absence of the menstrual cycle (amenorrhoea). It occurs in about 65%
of athletes such as runners and ballet dancers. There are two types of
amenorrhoea: primary and secondary. Primary amenorrhoea occurs when menstrual
cycles never start. Secondary amenorrhoea occurs when there is no menses for 6
months or absence of 3 or more consecutive menstrual cycles. Osteoporosis will
lead to bone fragility and often manifest as stress fractures. 90% of bone
mineral content occurs by the end of adolescence. The first step in treatment
is recognition of the disorder. Treatment includes prevention, correction of
the energy deficit, increase dietary calcium and vitamin D, maintaining bone
mass, resume normal menstrual function, and reduce training intensity. The
patient will need a multidisciplinary team including an athletic trainer, a
nutritionist, a psychologist, and a physician. Female patient with a history of
stress fracture should undergo a workup. This includes obtaining a menstrual
cycle history, nutritional consult, bone density, and psychological consult for
eating disorder.
Transient osteoporosis of the femoral head is not an
osteonecrosis of the femoral head. In transient osteoporosis, the symptoms are
usually more than the x-ray findings. It usually affects pregnant women, and it
also affects men during the 5th decade of life. On x-ray, you
probably will not find much. You may find osteopenia. The signal changes will
involve the femoral head and extend into the neck, and may include the
trochanteric area. In transient osteoporosis, there is no double density which
is seen in the MRI patients with osteonecrosis. Transient osteoporosis is not a
tumor, it is not an osteonecrosis, and it does not need surgery. Osteonecrosis
may be bilateral in about 80% of patients. Check the other hip even if the
patient is asymptomatic. Early diagnosis and treatment may improve the chances
for success of a head preserving surgical procedure, such as core decompression
or bone grafting. In late stages of osteonecrosis, the femoral head collapses and
cannot be saved. For the patient to have a good outcome, the femoral head will
need to be replaced at this late stage. MRI is usually the study of choice,
especially when the patient has persistent hip pain and the radiographs are
negative and the diagnosis of osteonecrosis of the femoral head is suspected,
especially if the patient has risk factors. On the T1 MRI, there will be a well-defined
band of low signal intensity usually within the superior anterior portion of
the femoral head. Decreased signal from the ischemic marrow, and there is a
single band-like area of low signal intensity (crescent sign). The crescent
sign represents the reactive interface between the necrotic and reparative
zone. The single line density demarcates the normal from the ischemic bone.
Double line sign is seen in T2 images. The subcortical lesion on T2 shows two
lines: low signal intensity line and high signal intensity line. The lesion
will show a high signal intensity inner border with a low signal intensity
peripheral rim (double line). The high signal intensity represents hyper
vascular granulation tissue. The size of the lesion is the most important
factor in determining the development of symptoms and the progression of the
disease. The best prognosis occurs in a small lesion with sclerotic margins.
The presence of bone marrow edema on the MRI is predictive of worsening of the
pain and future progression of the disease. Multifocal osteonecrosis is a
disease involving three or more sites such as the hip, the knee, the shoulder
and the ankle, occurs in about 3% of patients. A patient that presents with
osteonecrosis at a site other than the hip should undergo MRI of the hip to
rule out the asymptomatic lesion in the femoral head.
Osteoarthritis of the knee is the most common cause of
arthritis of the knee. The patient will complain of pain, swelling, stiffness,
and decreased range of motion of the knee. In arthritis, the cartilage of the
knee gets worn off. The meniscus which absorbs the shock, becomes degenerated
and tears. Which time, there will be more and more degeneration with wear and
tear on the knee joint. The joint space becomes narrower and narrower. When the
cushion of the cartilage is completely lost, the bone will rub against bone, causing
severe symptoms to the patient with severe pain, inability to walk, a lot of
swelling with the knee, and “giving way” (knee will be unstable). The x-ray
will show arthritis. When you ask the patient to stand or walk, the alignment
of the lower extremity is lost, and the patient may have varus or valgus
malalignment. With varus deformity, the bowing end of the leg occurs more with
medial osteoarthritis (common), and the patient will compensate for the
arthritis and pain in the knee by limping. The patient is trying to reduce the
weight being placed on the knee. The stance phase on the affected knee will be
shortened. The patient cannot take the pain any longer, so they are quick to
get the foot off the ground due to the painful knee. Arthritis can be mild,
moderate, or severe. To understand the arthritis, you need to know the anatomy
of the knee. Synovial fluid lubricates the knee joint. As you can see here at
the end of the femur and the tibia, there is hyaline articular cartilage which
is smooth and allows for smooth movement of the joint. There are no holes, no
fissures or cracks in the normal hyaline cartilage. For mild osteoarthritis of
the knee, the patient will have some discomfort, and the x-rays can appear
normal. The fabric of the articular cartilage breaks down. The process of wear
and tear, being overweight, and enzymes will affect the cartilage, and the
cartilage will break down (it is mild or minimal) which can be controlled by
nonsteroidal anti-inflammatory medication, weight loss and therapy. For
moderate osteoarthritis, there will be narrowing of the joint space on x-ray
due to degeneration of the cartilage. There will be cysts in the subchondral
space located underneath the cartilage, and there may be some osteophytes or
bony spurs. The joint will no longer be smooth (joint surface is roughened with
cracks and fissures). The patient’s pain will be worse with more swelling. This
is the time when the physician has a lot of options, but none of them are
optimal. You may try nonsteroidal anti-inflammatory medication or try weight
loss and exercises, steroid injection (viscosupplementation or hyaluronic acid
injections). Recently, long acting steroid injections is used. Other doctors
may try platelets and stem cells. None of the options are proven to be
successful. The only protocol that is proven to be successful is weight loss,
exercises, and nonsteroidal anti-inflammatory medication. For severe
osteoarthritis, the condition of the knee is bad. The joint space is severly
narrowed with total destruction of the cartilage. The knee is swollen and
painful with more osteophytes, and the bone is rubbing against the bone, and no
cartilage is left. There is no cushion and nothing to absorb the shock of the
weight, so the condition becomes very painful. The patient’s knee is like a car
that is running on its rim. Because the patient is walking on their own bone,
there will be decreased activity, and the patient will have an inferior quality
of life. Surgery is the best option for the patient and surgery is usually done
by a total knee replacement. Total knee replacement is like a house that has a
roof that leaked, you want to change the roof of the house. Total knee
replacement is the same thing. You need to fix the damaged roof of the house
and fix the destruction to the knee.
Infection of the finger is common, and it can vary in
severity. Serious infection of the fingers will require urgent surgical care.
Felon is a deep infection of the soft pad, or pulp, of the
fingertips. It is usually the result of a puncture wound. Swelling or pus is trapped
in the small compartments of the pulp or the tip of the finger. Symptoms
include unusual redness or swelling, firm swelling, throbbing pain at the tip
of the finger, or visible yellowish area of puss. If the infection goes
untreated, it may lead to severe symptoms such as skin necrosis, flexor
tenosynovitis, osteomyelitis, and arthritis of the distal interphalangeal
joint. Surgery is the usual treatment in the form of incision and drainage of
the felon. If there is no foreign body in the finger, you will do the midaxial
incision or the “J shaped” incision, and you will leave the wound open. If
there is a foreign body present, such as a splinter or a thorn, you will do the
volar longitudinal incision. Try to avoid doing the “fish mouth” incision; it will
lead to unstable finger pulp.
Symptoms of paronychia include swelling, redness, puss
formation, and pain in the soft tissue around the nail plate. Treatment is
antibiotics if the infection is caught early. Surgery is the usual treatment.
Incision and drainage with or without partial nail removal for subungual
abscess.
Herpetic Whitlow is a painful infection caused by the herpes
simplex virus that usually affects the fingers or the thumb. It is seen in
dentists, respiratory therapists, anesthesiologists, and toddlers (children who
suck their thumb). Symptoms include swelling, tenderness, redness, fever,
swollen lymph nodes, burning pain, and vesicle formation on the finger. It can
be grouped together with inflammation and redness at the base of the finger.
The fluid in the vesicle is usually clear (not purulent). The infection is
self-limiting. Conservative treatments include antiviral treatments applied to
the skin (acyclovir). Antibiotics are not used unless secondary infection is
present. Do not do surgery, surgery can make the situation worse.
Flexor tenosynovitis is a relatively common infection of the
hand usually caused by Staphylococcus aureus. It usually occurs due to prior
penetrating trauma and infection. The index, middle, and ring fingers are most
commonly affected. Symptoms include painful swelling of the finger that hurts
worse with motion. Flexor tenosynovitis has Kanavel’s four cardinal signs:
uniform swelling of the entire finger (fusiform swelling, finger looks like a
sausage), the finger is flexed, intense pain when attempting to straighten the
finger (occurs early), tenderness along the course of the tendon sheath (most
important sign). If the infection is caught early, treat with IV antibiotics.
If the infection is severe, do early open drainage of the infection to avoid
skin loss, tendon necrosis, and osteomyelitis. Surgical incisions used to drain
the flexor sheath infection. Use a midaxial or Bruner incision. Use two small
incisions, one proximally at A1 pulley and one distally at A5 pulley. Use an
angiocath for irrigation. Give culture specific IV antibiotics. Infection may
spread from the tendon into the deep palmar space or into the Parona’s space in
the forearm. The little finger communicates with the ulnar bursa. The thumb
communicates with the radial bursa. The radial and ulnar bursa communicate
proximal to the carpal tunnel. Infection may travel from the little finger into
the ulnar bursa to the Parona’s space. Infection can also travel from the thumb
into the radial bursa to the Parona’s space. Infection may cause “horse shoe”
tenosynovitis. Infection travels from the thumb through the radial bursa to the
ulnar bursa infecting the little finger. May need combination of incisions for
drainage.
The most common joint affected by gout is the first
metatarsophalangeal joint. The most common joint affected by pseudogout is the
knee joint. Gout and pseudogout both show a sudden onset of pain, redness, and
swelling typically affecting a single joint in 80% of the cases. Gout and
pseudogout are similar problems with different causes. Gout is caused by the
buildup of uric acid and the deposit of uric acid crystals inside a joint. The
best test to diagnose gout is with a joint fluid analysis. Gout crystals are
needle shaped and negatively bifringent. When placed under polarized light,
they will be yellow. 90% of patients suffering from gout are men between the
ages of 40-60 years old. Uric acid buildup in the body occurs by two main
mechanisms: excessive urate production and diminished urate clearance. Uric
acid is produced from the breakdown of proteins inside the body and from the
proteins of food that is eaten. Gout symptoms and signs include joint pain,
swelling and arthritis. Patients with gout have periarticular erosions along
with the formation of uric acid soft tissue masses in and around the joint
which can be seen on x-ray. Soft tissue tophus deposition with periarticular
erosions “punch-out” lesions. The tophi occurs due to deposition of uric acid
crystals. The tophus aspirate may look like tooth paste. The sudden attack of
gout can be brought on by anything that increases the level of uric acid in the
blood such as: dehydration, increased consumption of alcohol, eating large
amounts of meat or seafood, or trauma/surgery. Other risk factors for gout are
obesity, hypertension, and diuretics. Red meats, seafood, liquor, beer, all
increase the risk of gout. Vegetables, wine, dairy products, and total proteins
do not increase the risk of gout. Aspiration and analysis of the joint fluid is
the best method for diagnosis. Elevate uric acid is not diagnostic. 80% of
people with elevated uric acid will not get a gouty attack. There are blood
tests such as white blood cell count, C-reactive protein, sedimentation rate,
and uric acid level that are helpful in supporting the diagnosis if elevated,
but if these levels are normal, it cannot definitively rule out gout or
pseudogout. Every time you aspirate a joint and you get synovial fluid, you
need to analyze it for cell count differential, find out if you have crystals
or not and send the fluid for culture and sensitivity if you suspect infection.
It might be difficult to differentiate an acute gouty attach from acute septic
arthritis. Patients with an acute gouty arthritis may not have an elevated
serum uric acid level. A patient with acute gouty arthritis may present with
symptoms and a clinical picture that is similar to septic arthritis. Aspirate
the joint fluid, and the joint fluid will look like pus, but it could be gout.
You will take the fluid and examine it under the microscope (you will find
needle shaped, intracellular crystals, and you will think that it is gout). The
cell count of the aspirate may be high (may be 50,000-60,000) and the
neutrophils may also be high (may be 80%). The incidence of gout and associated
septic arthritis of a joint is low (about 1.5%). The incidence of septic
arthritis will increase to 11% or more if the cell count is more than 50,000.
We aspirate the joint (aspirate will look cloudy, like pus). We look for
crystals and if there is crystals, then it is gout, but the presence of uric
acid crystals does not exclude septic arthritis. We look at the cell count
(will be high, 50,000 or more). The neutrophil count may be 80% or more (we
think there is an infection in addition to gout or maybe gout alone). We need
to culture the fluid. After we aspirate the fluid and send the fluid for culture,
then we give the patient empiric intravenous antibiotics pending the culture
result. Remember that gout and septic arthritis can occur together, but the
incidence is low. The incidence will increase significantly if the cell count
is more than 50,000. Pseudogout or chondrocalcinosis is the deposition of
calcium pyrophosphate dihydrate crystals in the hyaline cartilage or
fibrocartilage (CPPD). Pseudogout is a metabolic disease where calcium
pyrophosphate dehydrate crystals (CPPD) are formed within the joint space.
Pseudogout most often affects the knee, occurs more in older patients, and is a
calcification of fibrocartilage (chondrocalcinosis). Pseudogout crystals are
rhomboid shaped and positively birefringent. Crystals will be blue when placed
under polarized light. Associated conditions include hyperparathyroidism,
rheumatoid arthritis, and gout. Aspirate to see if it is pseudogout or
infection, because you do not want to inject the knee with steroids when there
is an infection. You need to look for the rhomboid crystals of pseudogout.
X-rays in pseudogout will show thin calcification in the articular cartilage or
menisci. Calcifications of the synovium, tendon, and ligaments can also occur.
Acute gout can be treated with indomethacin or colchicine if the patient cannot
tolerate NSAIDs. Colchicine inhibits the inflammatory mediators and is
indicated if the patient cannot tolerate indomethacin. Chronic gout can be
treated with allopurinol to prevent buildup of uric acid. Allopurinol is a
xanthine oxidase inhibitor. Pseudogout is treated with NSAIDs and
intraarticular injections.
The knee bursa is a small, fluid filled sac located between
the front of the patella (knee cap) and the overlying skin. The bursa allows
the knee cap to slide freely underneath the skin as we bend and straighten the
knee. This is an inflamed bursa over the top of the knee cap. When the bursa
becomes inflamed, it is called bursitis, which causes pain, swelling,
tenderness and a lump in the area on the top of the knee cap. It may be
difficult to kneel down and put the knee the floor due to the tenderness and
swelling. Types of knee bursitis include suprapatellar, prepatellar (most
common), and infrapatellar. Knee bursitis can be caused by trauma such as a
direct injury or a fall into the knee which damages the bursa with the
development of sudden large swelling. Knee bursitis can also be caused by
occupational kneeling. Bursitis is chronic and develops slowly as seen in
carpet layers, tilers, and wrestlers. Infection can cause knee bursitis as well.
Inspect the bursa for any breaks in the skin leading to infection. Red, hot,
painful, and swollen bursa is a sign of possible infection. Wrestlers may have
abrasions of the knee, and this can lead to knee bursitis that may be infected.
Inflammation of the bursa can also cause knee bursitis. Treatment of knee
bursitis includes anti-inflammatory medications, ice therapy, aspiration, or
surgery. Do aspiration if infection is suspected or confirmed. Aspirate first
before you give antibiotics and send the fluid for culture and crystals.
Surgery is debridement and excision of the bursa may be needed. Protective
covering should be placed around the knee while avoiding activities that
aggravate the condition.
The patellar tendon attaches the patella (knee cap) to the
top of the tibia. The quadriceps muscle is attached superiorly to the patella.
A small part of the quadriceps tendon then continues over the front of the
patella to become the patellar tendon. The patellar tendon works with the
quadriceps tendon to straighten the leg. Several bursae are seen around the
patella: suprapatellar, prepatellar, and infrapatellar. These bursae allow the
knee cap to slide freely underneath the skin while bending and straightening
the knee. Patellar tendonitis may develop due to repeated stress being placed
on the patellar tendon. Patellar tendonitis is often referred to as “jumper’s
knee”. It is an overuse condition that often occurs in athletes who perform
repetitive jumping activities. Patellar tendonitis is a knee pain that is
associated with focal patellar tendon tenderness, and it is usually activity
related. Younger adults will get patellar tendonitis. Older adults will get
quadriceps tendonitis. Jumper’s knee can occur above the patella, below the
patella, or at the tendon insertion into the tibia. The most common area for
patellar tendonitis (jumper’s knee) to occur is just below the knee cap.
Patellar tendonitis affects about 20% of jumping athletes. Patellar tendonitis
will cause anterior knee pain at the inferior border of the patella with
tenderness to palpation at the distal pole of the patella in extension and not
in flexion. Patellar tendonitis is a sport specific problem. Examples of sport
activities that are typically associated with patellar tendonitis include
basketball, volleyball, soccer, and it also may occur in runners. It occurs in
younger age athletes, taller body stature, higher body weight, and occurs more
in male volleyball players. Predisposing factors include quadriceps
inflexibility and atrophy, hamstring tightness, playing on a hard surface,
increased training frequency, or patellar hypermobility. Patellar tendonitis
occurs due to irritation of the tendon, and it progresses to tearing and
degeneration of the tendon. It is degeneration and not inflammation. The
condition causes micro tears of the tendon due to repetitive, eccentric
forcible contraction of the extensor mechanism with poor flexibility of the
hamstrings and quadriceps. Hamstring inflexibility places excessive stress on
the extensor mechanism which causes increased forces on the patellar tendon
during contraction. We should focus on screening and treating poor quadriceps
and hamstring muscle flexibility to prevent patellar tendonitis in athletes.
X-rays will appear normal. MRI and ultrasound will show degenerative changes in
the tendon and tendon hypertrophy. Ultrasound with colored doppler may show
increased vascularity. Examine the patient for flexibility of the lumbar spine
as well as the hamstrings and quadriceps muscles. Stiffness may cause patellar
tendonitis. Treatment is rest, anti-inflammatory medications, stretching and
strengthening (stretch the hamstrings and the quadriceps and use eccentric
exercise program). A patellar tendonitis strap can help relieve knee pain
caused by patellar tendonitis. Early stages of patellar tendonitis will respond
well to nonoperative treatment. Treatment can also be injections. Do not inject
steroids into the tendon, it may rupture the tendon. If you think injection is
necessary, inject around the tendon. Surgery is done in severe cases. It is
debridement and repair of the tendon. If conservative treatment fails for 6-12
months, then surgical treatment is indicated. When the patient continues to
have pain during activity and rest, then conservative treatment won’t work.
Surgery consists of excision of the degenerated parts of the tendon at the
inferior pole of the patella. At 12 months, 90% of the athletes return to
pre-injury level of activity.
Fat embolism can occur when fat globules are released from
the bone, usually during long bone fractures. These fat globules can travel to
the lungs and obstruct the pulmonary vessels. Release of these fat globules can
also occur during reaming of the intramedullary canal. These fat globules also
cause the release of inflammatory mediators which cause endothelial lung damage
and hypoxemia. Fat embolism usually occurs in trauma patients with multiple
fractures, especially the fractures which involve the pelvis and long bones.
Fat embolism occurs more with closed fractures. The fat globules may also
travel to the brain; this is called cerebral embolism. The fat globules may
also travel to the skin capillaries. The classic triad for fat embolism includes
respiratory changes, neurologic signs, and petectial rash. The fat globules
affect the pulmonary vessels, and the patient will have difficulty in breathing
(dyspnea, hypoxia). You see this from the history, the physical examination of
the patient, the patient’s vital signs and blood gases. The fat globules may
travel to the brain. The patient may have confusion or alteration of the mental
status. In severe cases, the patient may have seizures. The fat globules can
affect the dermal capillaries. Patient history is important in diagnosis. The
mortality rate involving fat embolism is about 10%. Fat embolism usually occurs
earlier than deep venous thrombosis (DVT). Patients with femur fractures,
nonoperative treatment, overreaming of the fracture, or pathologic fractures
are at risk for fat embolism. Patients with pathological fractures are especially
at risk in bilateral femur fractures; try not to fix bilateral pathological
femur fractures in the same sitting. Multiple trauma patients are always at
risk of fat embolism. There are diagnostic signs. Major respiratory signs
include shortness of breath- hypoxemia (oxygen saturation less than 60mmHg) or
pulmonary edema. Major neurological signs confusion, agitation, altered mental
status, or drowsiness. Major petectial rash signs include axillae, conjunctiva,
or palate. Rash occurs in about 20-50% of cases and usually appears within 36
hours. Rash is usually self-limiting and usually disappears in about 7 days.
Minor signs include tachycardia, pyrexia, anemia, thrombocytopenia, or fat in
the urine. Early stabilization of long bone fractures will reduce risk of fat
embolism. High index of suspicion is needed for diagnosis. Treatment of fat
embolism is supportive treatment such as oxygen or In severe cases, mechanical
ventilation with high levels of PEEP. The outcome of the patient post fat
embolism depends on the pre-injury condition of the heart and the lungs.
Fractures of the radial head and neck in children are not
common. The fracture can be non-displaced, displaced, tilted, or translocated. These
types of fractures are rare. They usually occur around 9 years of age, usually
due to valgus force. The fracture may involve the physis (growth plate). It is
a Salter-Harris Type II fracture, or the fracture may involve the radial neck
at the metaphysis. There is a mnemonic statement that can be used to remember
the names and order of the elbow ossification centers: CRITOE. 1, 3, 5, 7, 9,
11 are the approximate ages when the ossification centers appear around the
elbow. Capitellum 1 year, Radial head 3 years, Internal epicondyle (medial) 5
years, Trochlea 7 years, Olecranon 9 years, External epicondyle (lateral) 11
years. An AP and lateral view of the elbow including the forearm should be
taken. The radial head should align with the capitellum in all views.
Radiocapitellar view may be helpful to view the radial head. The
radiocapitellar view is an oblique lateral view; the elbow will be flexed to
90-degrees with the thumb pointing upwards, and the beam is directed 45 degrees
proximally. Nondisplaced fractures of the radial head may not be seen on x-ray
and then you are going to look for the fat pad sign. If you find the posterior
fat pad, this is not normal and means that there is a fracture. In radial neck
fractures, part of it is extra-articular, so if there is a fracture there, the
fat pad sign may not be present even if there is a fracture. Treatment for a
non-displaced fracture is immobilization. Immobilization is used if angulation
is less than 30 degrees; up to 30 degrees of angulation is acceptable. Closed
reduction is used if angulation is greater than 30 degrees. Reduction of the
radial neck fracture is done with elastic bandage around the forearm and elbow
or with extension of the elbow, traction, supination, and direct varus pressure
over the radial head. Push the radial head medially and push the radial shaft
laterally. If the reduction is acceptable, treat with immobilization. After
reduction, the radial head usually stays in its position by the periosteum.
K-wire joystick may be used for reduction in some cases. You will attempt
closed reduction first before you use K-wire percutaneous reduction. Use the
k-wire percutaneous reduction if the closed reduction failed. Open reduction
can be done if more than 45 degrees or residual angulation after failure of
reduction, either closed or by percutaneous methods. Complications include
synostosis, loss of motion, osteonecrosis, and nonunion. Synostosis is fusion
of the radius to the ulna; reflected periosteum is a possible cause of the
synostosis. Osteonecrosis occurs due to interruption of the blood supply.
Nonunion is rare. Interposition of the periosteum is a possible cause of nonunion.
Risks and complications increase with open reduction. Open reduction should be
the last resort in radial head and neck fractures in children. The worst
outcomes are seen in children older than 10 years. With fracture of the radial
head in children, repeat neurovascular examination should be done. Compartment
syndrome of the forearm should be suspected in case of increased pain or
increased analgesia requirements.
Osteochondritis Dissecans (OCD) is a condition that affects
the articular cartilage and the subchondral bone of the knee. The lesion
usually occurs in the knee on the lateral and posterior aspect of the medial
femoral condyle (70% of lesions are in the postero-lateral aspect of the knee).
OCD lesions are distributed around the knee, 85% medial femoral condyle, 13%
lateral femoral condyle, 1% patella, 1% trochlea. The chances of the lesion
occurring at the lateral femoral condyle and patellar aspect of the knee is
rare. Lateral condyle and patellar lesions will have a bad prognosis. The
mechanisms and causes of injury for OCD lesions may be multifactorial. It is
usually caused by repetitive overloading causing fragmentation and separation
of bony fragments. It can occur in juveniles with an open epiphysis usually
during the ages 10-15 years old. Prognosis is usually very good when the
patient has an open epiphysis. It can also occur in adults with a less
favorable prognosis. Osteochondritis Dissecans of the knee is classified in
four stages. Stage I is depressed OCD with intact cartilage and a small area of
compressed subchondral bone. Stage II is a partially detached fragment. Stage
III is the most common type and has a completely detached but non-displaced fragment.
Stage IV is completely detached and displaced. The displaced fragment can be a
loose body. Symptoms include activity related pain, poorly localized
tenderness, effusion, and swelling and stiffness with or without mechanical
symptoms. Mechanical symptoms indicate an advanced problem. The Wilson’s Test
is a test used to detect the presence of Osteochondritis Dissecans of the knee.
To perform the Wilson’s test, ask the patient to sit on a table with his legs
dangling over the edge. The patient’s knee should be flexed at a 90-degree
angle. Grasp the patient’s leg and internally rotate the tibia. Instruct the
patient to extend the leg until pain is felt. The test is positive when the
patient reports pain in the knee about 30-degrees from full extension. When
rotating the leg back to its normal position, the pain disappears. Internal
rotation causes impingement of the tibial eminence on the OCD lesion of the
medial femoral condyle which causes the pain. external rotation moves the
eminence away from the lesion, which relieves the pain. For x-ray images, do
weight-bearing AP and lateral view radiographs and use the Tunnel View
(intercondylar notch view). On MRI, check the size of the lesion, signal
intensity surrounding the lesion, and the presence of any loose bodies.
Prognosis correlates with age; the younger the age, the better the prognosis.
Adults have a worse prognosis. Lesions in the lateral femoral condyle and
patella have a worse prognosis. Synovial fluid appearing behind the lesion on
MRI correlates with a worse prognosis. Fluid signal on MRI behind the lesion
indicates that the fragment is unstable and is less likely to heal.
Nonoperative treatment is observation, limitation of activity, crutches, trial
of non-weight bearing for six weeks, and close follow-up. Stable lesions in
children with open physis are an indication of nonoperative treatment. The
majority will heal as long as the physis is open (good prognosis). Operative
treatment is indicated if the fragment is detached, unstable or loose in patients
where the physis has already closed, is near closing, or if there is failure of
the non-operative treatment. Surgical treatment usually includes arthroscopy
and removal of the loose fragment, fixation of the unstable lesion, or
microfracture (drilling of the lesion). Arthroscopic drilling of the subchondral
bone is done in children who approach skeletal maturity. Drilling of the lesion
has a high success rate especially if the lesion is stable.
If the transverse atlantal ligament ruptures, you can see
that the spine becomes translationally unstable in the sagittal plane, and the
odontoid will be displaced posteriorly. The ADI will increase more than 3mm,
and the spinal cord area will be narrowed, and you may get spinal cord
compromise as the odontoid process moves posteriorly towards the spinal cord.
This rupture of the transverse ligament is usually apparent on the x-rays or CT
scan as the odontoid moves posteriorly, and the ADI increases, compromising the
spinal cord. If the condition is not diagnosed properly, it can result in
spinal cord compression, respiratory arrest and a catastrophic outcome. This
condition usually requires surgery because ligaments do not heal (they need to
be fused), so it will probably require posterior atlanto-axial arthrodesis.
Facet dislocations of the cervical spine include unilateral
facet dislocation and bilateral facet dislocation. In unilateral facet
dislocation, displacement of the vertebrae is less than 50% of the cervical
body width and may need surgery. Bilateral facet dislocation is more serious;
the displacement is greater than 50% of the vertebral body width. Obtain a
preoperative MRI to rule out disc herniation associated with facet
dislocations.
Spinal cord compression is more common with cervical spine
injuries and thoracic spine injuries. Bone within the canal increases the risk
of spinal cord compression and injury. Neurogenic shock resulting from spinal
cord injury may complicate resuscitation of the patient and should be
differentiated from hypovolemic shock. Look for hypotension and bradycardia in
neurogenic shock. Emergency management involves resuscitation and hemodynamic
stabilization of the patient with a concurrent, adequate and frequent
neurologic examination. Definitive treatment is usually stabilization of the
unstable spinal injuries.
Cauda equina syndrome results from injury to the lumbosacral
nerve roots within the spinal canal. It presents with involvement of the
bladder, bowel, and lower limbs and usually results from fractures or central
disc herniation. Central disc herniation or bony fragments result in
compression of the nerve roots. Early diagnosis of the condition is important
for eventual improvement on the outcome. Treatment is urgent decompression by
the removal of the central disc herniation or decompression and stabilization
of the fracture.
McMurray’s test is a commonly used test in orthopaedic
examination to test for tears of the meniscus. The McMurray’s test is a
rotational maneuver of the knee that is frequently used in the examination of
the patient to help in the diagnosis of meniscal tears. Meniscus injuries are
very common. When the patient sustains an injury of the knee and has a meniscal
tear, usually the patient complains of knee pain localized to the medial or
lateral side of the knee. The patient may also have locking and clicking.
Sometimes the patient will have an effusion and sometimes this effusion is
small (swelling of the knee). Joint line tenderness is the most sensitive
finding. Joint line tenderness can be on the medial side (medial meniscal tear)
or on the lateral side (lateral meniscal tear). There will be minimal swelling
of the knee and possible extension lag (locked knee) due to a displaced bucket
handle tear of the meniscus. Pain at a higher level than the joint is usually
associated with medial collateral ligament tear. If an MCL tear is present, it
is usually avulsed from the medial femoral condyle. The MCL is rarely avulsed
from the tibia. Pain at a lower level is usually associated with the pes
anserine bursitis. McMurray’s test is a knee examination test that shows pain
or a painful click as the knee is brought from flexion to extension with either
internal or external rotation of the knee. The McMurray’s test uses the tibia
to trap the meniscus between the femoral condyles of the femur and the tibia.
When performing the McMurray’s test, the patient should be lying supine with
the knee hyperflexed. The examiner then grasps the patient’s heel with one hand
and places the other hand over the knee joint. To test the medial meniscus, the
knee is fully flexed, and the examiner then passively externally rotates the
tibia and places a valgus force. The knee is then extended in order to test the
medial meniscus. To test the lateral meniscus, the examiner passively
internally rotates the tibia and places a varus force. The knee is then
extended in order to test the lateral meniscus. A positive test is indicated by
pain, clicking or popping within the knee joint and may signal a tear of either
the medial or lateral meniscus when the knee is brought from flexion to
extension. There are mixed reviews for the validity of this test. There are
other clinical tests that are as good as the McMurray’s test, however MRI is
making the diagnosis of a meniscal tear easier. MRI is very sensitive, and it
also excludes other associated injuries. I find that the McMurray’s test is
valuable in getting insurance approval for performing an MRI. If you state that
the McMurray’s test is positive, then the insurance will approve the MRI.
Nowadays though, the McMurray’s test does not give us a lot of valuable
clinical information, because we get the information from other tests.
The trapezius is a large superficial muscle that extends
from the back of the skull, back of the neck, and back of the thorax. The upper
fibers of the trapezius muscle arise from the external occipital protuberance
and the medial third of the superior nuchal line. The middle fibers arise from
the ligamentum nuchae and the spinous process of C7. The lower fibers arise
from the spinous processes and supraspinous ligaments of all twelve thoracic
vertebrae. The trapezius is inserted into the lateral third of the clavicle,
and from the acromion process and the spine of the scapula. The trapezius
muscle allows for rotation and lift of the scapula. Dysfunction of the
trapezius muscle may cause lateral winging of the scapula. Winging can occur
after radical neck surgery, but it usually occurs after biopsy or tumor
dissection. The spinal accessory nerve will be injured, and the patient will
have difficulty with overhead activity. If injury to the spinal accessory nerve
occurs early, explore the nerve. If injury is late, do a muscle transfer. The
spinal accessory nerve provides motor innervation to the sternocleidomastoid
and the trapezius muscle. The spinal accessory nerve courses obliquely across
the posterior triangle on the surface of the levator scapula muscle and reaches
the trapezius. Within the posterior triangle of the neck, the nerve is
vulnerable since it is superficial and only covered by skin and subcutaneous
fascia. Extreme caution should be taken for any surgical procedure done in the
posterior triangle of the neck.
To study the involvement of any nerve root we look for
sensory change, motor changes, reflex changes. A herniated disc at T12-L1
affects the L1 nerve root. The sensory of the L1 nerve root is half the
distance between the inguinal ligament and mid-thigh. Motor involvement is hip
flexion. There are no reflexes of L1. A herniated disc at L1-L2 affects the L2
nerve root. The sensory of the L2 nerve root is mid-anterior thigh. Motor
involvement is hip flexion, hip adduction, and knee extension. There are no
reflexes of L2. A herniated disc at L2-L3 affects L3 nerve root. The sensory of
the L3 nerve root is distal part of the thigh including the knee area. Motor
involvement is hip flexion and knee extension. A herniated disc at L3-L4
affects the L4 nerve root. The sensory of the L4 nerve root is medial side of
the leg down to the medial side of the foot. Motor involvement is L4 ankle
dorsiflexion (tibialis anterior) and knee extension. L4 reflex changes will be
a positive femoral stretch test. The test is positive if pain is felt in the
ipsilateral anterior thigh. If the test is positive, it means that there is
probably a disc herniation between L3-L4, affecting the L4 nerve root. The
patellar reflex is mainly L4. A herniated disc at L4-L5 affects the L5 nerve
root. The sensory of the L5 nerve root is dorsum of the foot and leg. Motor
involvement is hip abduction (gluteus medius) and extension of the big toe. L5
nerve root is very popular in the exam. If you see a big toe extension, this
involves the L5 nerve root (L4, L5 disc herniation). The patient may have
Trendelenburg gait due to injury to the L5 nerve root (disc herniation between
L4, L5 affecting the L5 nerve root). Both the gluteus medius and minimus
muscles are innervated by the L5 nerve root. Straight leg raise can be positive
with L5 nerve root irritation. This test is used to determine if the patient
with low back pain has an underlying herniated disc irritating the nerves. A
herniated disc at L5-S1 affects the S1 nerve root. The sensory of S1 nerve root
is lateral and plantar aspects of the foot. Motor involvement is S1 hip
extension (gluteus maximus), S1 ankle plantar flexion (gastro-soleus), and S1
foot eversion (peroneus longus and peroneus brevis). Positive straight leg
raise examination to determine whether patient with low back pain has an
underlying component of a herniated disc or not (stretch test). Reflexes are S1
ankle reflex.
Fractures of the capitellum are rare and usually occur in
the coronal plane and can be difficult to diagnose. Fracture of the capitellum
is similar to Hoffa fracture of the distal femur. Both fractures are coronal,
difficult to diagnose, and the x-ray may miss the fracture. failure to diagnose
this fracture and treat it appropriately can lead to a poor patient outcome.
The Bryan and Morrey Classification has four types. Type I is a large fragment
of bone and articular cartilage sometimes with trochlear involvement. Type II
is a shear fracture of the articular cartilage. The articular cartilage is
separated with a small shell of bone. Type III is a comminuted fracture of the
capitellum. Type IV is the Mckee Modification; it is a coronal shear fracture
that extends medially to include the capitellum and trochlea. You can see double
bubble or a double arc on the lateral x-ray of the elbow. One arc represents
the capitellum, and the other arc is the lateral ridge of the trochlea. The
double arc sign is a pathognomic finding of the capitellar fracture and is
usually seen in the lateral elbow x-rays. In more than 50% of the time,
capitellum fracture may be associated other injuries such as radial head
fracture or lateral ulnar collateral ligament injury. Fracture of the
capitellum can cause mechanical block to movement of the elbow. The fracture
can be seen on the lateral x-ray of the elbow, however CT scan is helpful in
showing the fracture adequately. Nonoperative treatment for nondisplaced fracture
is to give the patient a splint for less than 3 weeks followed by range of
motion. Open reduction internal fixation is done for displaced fractures. We
rarely excise the capitellum, but you may get into this situation if the
fragment is displaced and causing symptoms and if most of the fragment is
cartilage attached to a thin piece of bone and the fragment could not be fixed.
You will try to fix it first before you excise it. Excision is done for Type
III fractures, for comminuted and displaced fractures, especially if there is a
block to movement of the elbow. Small displaced, insignificant fractures can be
excised if it is causing pain or mechanical block to elbow motion. Excision of
a large fragment of the capitellum can create a problem of developing arthritis
or instability, especially if the medial collateral ligament is injured. Do total
elbow arthroplasty when there is a comminuted fracture of the capitellum that
extends to the medial column and the fracture is unreconstructable and the
patient is old. For open reduction internal fixation, the ideal visualization
of the fracture is usually provided by a lateral approach (Kaplan or Kocher
approach). The patient is usually in the supine position. Elevate the common
extensor tendons and the capsul anteriorly off the lateral column and use
headless compression screws from anteriorly to posteriorly. The fracture is
partial articular and vertical shear. Going anteriorly to posteriorly will
allow excellent compression and stability of the fracture. Countersink the
screws. Bury the screw heads beneath the articular cartilage anteriorly. Try to
avoid destabilizing the lateral ulnar collateral ligament and try to make the
dissection more anterior to the equator of the radial head. Try to avoid
disruption of the capitellum blood supply that comes from the posterolateral
area. Stay anteriorly to avoid these two problems. A complication of capitellar
fractures is elbow stiffness. Surgery to fix the capitellar fracture will help
in gaining the functional range of motion, but the patient will have residual
stiffness. Surgery is probably better than no surgery, but the reoperation rate
is high due to the residual stiffness of the elbow.
Salter-Harris fracture is a common injury in children that
involves the growth plates. 15% of all fractures in children involves the
growth plate, and it occurs more in boys than in girls. The growth plate
injuries occur more distal than proximal, such as distal radius, distal tibia,
and distal phalanges. Growth plate injuries in children are common in the bones
of the lower (tibia and fibula). It is important to diagnose these fractures as
they may affect the growth of the bone if not diagnosed and treated properly.
There are generally five types of Salter-Harris fractures. The higher of the
type number, the more complications associated with the fracture and worse
prognosis. Growth plates produce the longitudinal growth bones. The reserve
zone of the growth plate is the inactive zone. The proliferating zone of the
growth plate has cellular proliferation and longitudinal growth, and this zone
makes a person tall or short. The hypertrophic zone of the growth plate has
maturation, degeneration, and provisional calcification. The majority of growth
plate injuries occur in the hypertrophic zone. The hypertrophic zone is weak.
In fact, the hypertrophic zone is weaker than the ligaments, and it provides a
cleavage zone for the fracture to occur. Type I Salter-Harris fracture is
difficult to diagnose; 5% of fractures are Type I. The fracture occurs through
the growth plate, and there may not be an obvious displacement. Sometimes the
diagnosis is a clinical one. Fracture occurs through the weak zone of
provisional calcification. Type I is known by fast healing and rare
complication rate. Type II is a fracture through the growth plate and the
metaphysis, sparring the epiphysis. 75% of fractures are Type II. The corner of
the metaphysis separates (Thurston-Holland Sign). With Type II, the fragment
usually stays with the epiphysis while the rest of the metaphysis will
displace. Healing is fast and growth is usually okay. Injury to the distal
femur will cause a high rate of growth abnormality. Type III is a fracture
through the growth plate and epiphysis, sparring the metaphysis. The fracture
splits the epiphysis. 10% of the fractures are Type III. Fracture extends into
the articular surface of the bone (intraarticular fracture). It requires
anatomic reduction of the joint and internal fixation. An example of Type III
is the Tillaux fracture of the distal tibia. CT scan may be needed to diagnose
this fracture. Type IV fracture passes through the epiphysis, the growth plate,
and the metaphysis; 10% of fractures are Type IV. It can cause complications
such as growth disturbances and angular deformity. Type V is uncommon; about 5%
are Type V. It is a compression or crush injury of the growth plate. There is
no associated fractures of the epiphysis or metaphysis. Initial diagnosis may
be difficult. Type V has the highest incidence of growth arrest and
disturbance. Type I and Type II usually do not require surgery and will have a
better prognosis than Type III, Type IV, and Type V. In Type I and Type II, the
reduction of the fracture may not be anatomic. Despite this, the prognosis is
usually good. In Type III and Type IV, the fracture is usually intraarticular
and anatomic reduction is necessary. Type III and Type IV do not require
surgery and the prognosis is usually fair. Type V is rare and has a poor
prognosis. In general, the distal femur contributes to approximately 9-10mm of
growth per year. The proximal tibia contributes to approximately 6mm of growth
per year. Girls complete growth at the age of 14 years. Boys complete growth at
the age of 16 years. In situations of child abuse, you may find growth plate
injury or physeal separation as you can see in transepiphyseal separation of
the distal humerus in children.
Hoffa fracture is a coronal split of the posterior condyle
of the femur. Hoffa fracture is a rare intra-articular fracture of the
posterior femoral condyle occurring from violent trauma, and generally occurs
in young adults. Three types of Hoffa fractures are described. This
classification is based on the location of the fracture within the condyle.
Hoffa fracture can be an isolated fracture; however, it is often associated
with other distal femur fractures. 38% of intra-articular distal femur
fractures may have a Hoffa fracture (coronal plane fracture). The Hoffa
fracture is a lot more common in open fractures than in closed fractures.
Fracture may occur in either condyle, but the lateral condyle is the most
common one to be affected by Hoffa fracture. It affects a single condyle in
about 75% of the time, and the lateral condyle in about 85% of the time. Hoffa
fracture occurs due to axial compression in a flexed knee. The mechanism of
injury is controversial. The fracture is coronal, and it can be missed on routine
lateral x-rays. The undisplaced fracture of the condyle may become displaced if
the fracture is missed. The Hoffa fracture is almost like the capitellar
fracture of the elbow. This fracture has the same story as the capitellar
fracture, it is hidden, and you can miss it on the x-ray (you must look for
it). CT scan is very helpful in the diagnosis of Hoffa fracture and will give
you great details about the articular surface of the distal femur, especially
if the fracture is comminuted. X-rays are not very good in diagnosing the Hoffa
fracture. 20% of Hoffa fractures are diagnosed with x-rays only, so the CT scan
is the best study for diagnosing the Hoffa fracture. Use a high degree of
suspicion in the diagnosis of this fracture because the fracture may be subtle,
and you may not be able to see it on routine x-rays. Treatment is reduction and
stabilization of the fracture. stabilization of the fragment is usually done by
headless compression screws and can be buried underneath the surface. Fixation
can be done from either the anteroposterior (AP) direction or the
posteroanterior (PA) direction. It can be temporarily fixed with k-wires.
Permanent fixation is done with headless compression screws.
An ankle fracture needs anatomic reduction & absolute
stability. Anatomic reduction and stable fixation of the posterior malleolus is
very important. In a trimalleolar ankle fracture with syndesmotic instability,
anatomic reduction and fixation of the posterior malleolus provides greater
syndesmotic stability, and it lessens the need for syndesmotic screw fixation. It
restores the stability better than placing syndesmotic screws. Failure of
fixation or conservative treatment that gives us undesirable result of ankle
fracture treatment. You see the patient with hardware failure, syndesmotic
problems, and malalignment of the ankle. Some of these patients are treated
surgically and did not do well. Some of these patients are treated
conservatively and did not do well. Some of these patients may have
redisplacedment of the syndesmosis after syndesmotic fixation. Some of these
patients may have malreduction of the syndesmosis that may or may not be
obvious. Some of the patients may have shortening of the fibula. Some of the
patients may have conservative treatment and the ankle is not well aligned, so
you will need to do revision surgery. Ankle fracture malalignment due to
failure of fixation. The presentation is that of an older fracture that healed
improperly, or it was fixed, and the fixation failed, so you need to revise the
treatment. The first thing that you want to do is to look at the ankle and see
if you have arthritis. If you have some arthritis and the patient is young,
then you can revise the ankle treatment. You want to make sure that you do not
have a lot of arthritis before you do this big surgery. The question is, are we
going to revise the syndesmosis alone, because one way or the other, the
syndesmosis is malaligned. If the Shenton’s line is interrupted or if the dime
sign is interrupted, then the fibula is short. If the patient has peripheral
neuropathy or Charcot arthropathy, there will be more complications. If you are
going to handle a diabetic patient, you will need to do surgery and you will
need to put more hardware and prolong the area of non-weight bearing (instead
of 6 weeks, it will be 3 months). We do external rotation stress view x-rays
before surgery to look at the medial clear space, and you will check the
integrity of the deltoid ligament. If you do stress view x-rays before surgery,
it is done to see if the deltoid ligament is injured or not in an ankle
fracture when you are not sure if the deltoid ligament is injured. If deltoid
ligament turns out to be injured, then the patient will need surgery, and if it
is not injured, then the patient will not need surgery. When you do the stress
view, and if the medial clear space does not widen, then the fracture is
external rotation Type II that is treated conservatively. When you do the
stress view, and the medial clear space is widen, then the deltoid ligament is
ruptured and surgery is needed (external rotation Type IV). Before surgery, you
will check the medial clear space to check the integrity of the deltoid
ligament. During surgery, when you check the integrity of the syndesmosis, you
check the tibiofibular clear space. The tibiofibular clear space will be
greater than 5mm with syndesmotic injury. To perform the cotton test, pull on
the fibula with a bone hook and assess the integrity of the syndesmosis. During
surgery, when you check the integrity of the syndesmosis, you can also check
the medial clear space in addition to the tibiofibular clear space. If it is a
pilon fracture and the patient starts weight-bearing now, then the patient can
start driving 6 weeks from now. For the ankle fracture, return to driving is 9
weeks from the day of surgery. The type of fixations, type of screws, and how
many screws used, and if you remove the screws or not all are controversial
points. What is not controversial is that the syndesmotic reduction of the must
be anatomic. You must restore adequate length, rotation, and alignment of the
fibula. That will help anatomic alignment of the syndesmosis. Watch for
reduction of the syndesmosis, because there is a lot of malalignment. If you
are not sure, direct inspection and reduction of the syndesmosis can be
helpful. Failure of the syndesmotic fixation can occur in over-weight patients,
and it can also occur from surgical errors that may not be recognized during
surgery. Supination-adduction mechanism of injury is characterized by vertical
medial malleolus fracture associated with injury to talus and tibial plafond,
movement of the talus medially, and impaction on anteromedial aspect of the
ankle. Supination-adduction injuries are treated by screws parallel to the
ankle joint or anti-gliding plate. In pronation injuries, the fibula is comminuted,
usually at or above the syndesmosis. In supination-external rotation injury,
the fracture goes anterior to posterior direction. This is the direction of the
fracture in supination-external rotation. You see the fibular fracture in the
lateral view, and you are not going to see the fracture well in the AP view. If
you use lateral plate, it will decrease the peroneal tendon irritation, but the
patient may feel the plate, and the screws may violate the joint. If you use
posterior plate on the fibula, it is more stable and biomechanically better. It
will cause more irritation of the peroneal tendons, especially if the plate is
placed low and the screw heads are prominent.
The coronoid process provides anterior buttress against
posterior subluxation or displacement. The radial head prevents valgus
instability, and the coronoid process prevents varus instability. The coronoid
process also provides attachment for the anterior bundle of the MCL and
attachment to the anterior capsule. The anterior capsule attaches 6mm distal to
the tip of the coronoid process. The anterior bundle of the medial collateral
ligament attaches to the sublime tubercle 18mm distal to the tip of the
coronoid process. You need to know the difference between the insertion of the
MCL and the insertion of the brachialis as seen here. If the fracture of the
coronoid process tip is small, the brachialis should insert distal to the tip
of the coronoid process. There are two types for the mechanism of injury: posterolateral
rotatory displacement and varus and posteromedial rotatory displacement.
Posterolateral rotatory displacement is a fracture of the radial head, fracture
of the coronoid process tip, and dislocation of the elbow. Varus and
posteromedial rotatory displacement are associated with fracture of the
anteromedial coronoid process. The LCL tears from the humerus, and the MCL may
not be ruptured. In posterior elbow dislocation and posterolateral instability,
the lateral side fails first with the medial side failing last. This valgus and
supination can result in the terrible triad. Patient with instability after
elbow fracture dislocation always has a coronoid fracture, and it can
redislocate in a cast or after surgery. Elbow dislocation with Type II coronoid
process fracture and non-reconstructable comminuted radial head fracture. Treated
by repair of the lateral collateral ligament, do radial head arthroplasty, and
do ORIF of the coronoid process. This is an example of the terrible triad
(dislocation of the elbow, coronoid fracture, and radial head fracture) and you
need to fix all these injuries. Address each injury to restore elbow stability.
If you have an elbow dislocation with fracture of the olecranon tip fracture
and a radial head fracture, the likely pattern of instability is valgus
posterolateral rotatory instability. There will be rupture of the LCL from the
humerus and varus force will cause medial facet fracture, and this is the
malignant fracture pattern. To recognize the posteromedial facet injury, look
at the AP view x-ray in addition to the lateral view x-ray (in the lateral view
you may miss it). In large medial coronoid fracture and elbow dislocation,
there probably will be varus posteromedial rotatory instability, and it will
affect the anteromedial facet of the coronoid. In fracture of the coronoid
process, the x-ray is difficult to interpret. The fracture may be mistaken for
a radial head fracture. The structures overlap, and we may miss the fracture.
In the lateral view radiograph, you find a chip a bone. AP view radiograph will
find a nondislocated elbow with an anteromedial coronoid process fracture. if
you miss the anteromedial coronoid process fracture, you will get progressive
narrowing of the joint space from lateral to medial between the medial trochlea
and the coronoid process. This entity (anteromedial facet fracture) that gives
posteromedial instability, occurs in conjunction with lateral collateral
ligament injury. When you see this fracture, suspect anteromedial coronoid
fracture, especially when you cannot find a radial head fracture. You may also
find narrowing of the joint space between the medial trochlea and the coronoid
process. CT scan is usually very helpful. There are two known classification
systems: Regan & Morrey Classification and O’Driscoll Classification. Regan
& Morrey Classification is based on viewing the lateral x-ray. In Regan
& Morrey Classification, there are three fracture types based on viewing
the lateral x-ray. Type I is a shear fracture of the tip of the coronoid
process. Type II involves up to 50% of the coronoid process. Type III involves
more than 50% of the coronoid process. This is a very simple classification
system, but the problem is that it does not show the malignant fracture
pattern. The O’Driscoll classification is very helpful, and it will show the
anteromedial facet fracture that will create posteromedial instability. The
O’Driscoll classification can be the tip, anteromedial facet, or basal. The
O’Driscoll classification recognized the anteromedial facet fracture caused by
varus posteromedial rotatory force. This fracture could be missed on the x-ray
and can cause degenerative joint disease.
The scratch collapse test is a provocative test for nerve
entrapment or compression. This is becoming a popular test, and it is one of
many examination techniques used in the diagnosis of nerve compression,
entrapment, or injuries. The scratch test is a simple examination test that is
similar in sensitivity to other examination tests in the diagnosis of cubital
tunnel syndrome and other entrapment areas of the different nerves, such as
radial tunnel syndrome, pronator teres syndrome, and other nerve entrapment
areas. This test supplements, but does not replace, other information that we
collect during obtaining the history and physical examination of the patient. It
is really an added, helpful test that will precisely localize the site of nerve
compression. Do this test if you need to. Not only can this test add or provide
confirmation where entrapment of the nerve is located, but it can also
precisely localize the area of the entrapment of the nerve that `is known to
have different sites of entrapment, such as the ulnar nerve. If the patient has
a nerve entrapment at a specific site, after the scratch, the patient will
temporarily lose the ability to resist the internal rotation force to their
arm. The arm will collapse in the direction of internal rotation. The mechanism
is unknown, and it could be a reflex response. Because after you scratch or
stroke the skin above the nerve, the arm seems to have no power, and it
collapses as we test the resistance and internally rotate the arm. There might
be bias from the examiner due to the subjective evaluation of the brief,
temporary loss of resistance or loss of power after the scratch. To perform the
test, have the patient standing or sitting with the arms at the sides and the
elbows flexed to 90 degrees. Have the fingers and the wrist extended, then the
examiner applies force against the patient’s forearm to internally rotate the arm
and ask the patient to resist this force. The examiner and the patient will
both assess the baseline resistance of the patient. The skin over the potential
nerve entrapment area is scratched by the examiner, and then the examiner
immediately repeats the test. The change in resistance is assessed. Positive
scratch collapse test occurs when the patient has no resistance to the
examiners force and the arm collapses in internal rotation. There should be no
delays in retesting the patient because it may produce a false negative result.
Adding ethyl chloride (the cold spray) will temporarily numb or anesthetize the
skin superficial to the nerve of interest. It will freeze out a response to
scratching. It also may show secondary areas of compression of the same nerve
or different nerves. It also may show secondary areas of compression of the
same nerve or different nerves. After you apply the cold freezing spray to the
area of interest, the test is repeated. The cold spray should freeze out the
response to scratching. If you suspect multiple sites of entrapment, use the
freezing spray to numb the area then scratch it, and usually the patient will
have strength return after scratching the area. The freezing spray can make the
examiner eliminate sites or add sites of entrapment to the differential
diagnosis. It could be helpful in identifying multiple areas of compression for
the same nerve.
When the subtalar dislocation happens, the talonavicular
joint also becomes dislocated. There are two types of subtalar dislocations:
medial subtalar dislocation and lateral subtalar dislocation. Medial
dislocations are 4 times as common as lateral dislocations. Some of these
dislocations can be open and urgent reduction is important to decrease skin
necrosis and interruption of the circulation of the foot. After either closed
or open reduction, the subtalar joint is usually stable. Lateral subtalar
dislocation means that the foot goes lateral. As the foot goes lateral, the
structure in the medial side becomes trapped. The posterior tibial tendon
blocks successful closed reduction of the lateral subtalar dislocation. Lateral
subtalar dislocation is a bad type. It is worse than the medial subtalar
dislocation and is not as common. The foot goes lateral and as the foot goes
lateral, the medial structures get pulled from also trying to go lateral. As
you try to reduce the foot to its normal position, then there can be some
entrapment, usually the posterior tibial tendon. This tendon will be interposed,
and you will be unable to do closed reduction. This lateral subtalar
dislocation will have a high incidence of fractures of the surrounding tarsal
bones, and the subtalar joint could be unstable after reducing the dislocation.
Lateral subtalar dislocations are more open than the medial subtalar
dislocations. Open subtalar dislocations have a high incidence of infection. If
the patient sustained an open injury to the foot with complete extrusion of the
talus, the treatment should be to give the patient antibiotics and debride the
wound, clean the talus using betadine solution or normal saline with
antibiotics, and after the wound is debrided, implant the talus back into its
bed. You may want tot use external fixator after that. The medial subtalar
dislocation is different. Rarely the dislocation is irreducible (it usually
reduces easily). Irreducible dislocation can be due to: impaction fracture of
the head of the talus, interposition of the extensor digitorum brevis tendon
(popular in exams), or interposition of the peroneal tendons. In medial
subtalar dislocation, the foot appears supinated. In lateral dislocation, the
foot appears pronated. The majority of both dislocations can be managed by
closed reduction and immobilization, which the closed reduction should be done
as soon as possible to decrease the risk of skin complications. Closed
reduction is probably difficult in about 5-10% of medial dislocations and
15-20% of lateral dislocations. The dislocation can be reduced easily, and you
will get an x-ray to evaluate and see if the dislocation is reduced or not, but
you will probably also see it clinically. If you do not have a fracture or any
fragments in the post-reduction x-rays, then the success rate with a splint or
immobilization cast is very good. The medial dislocation has a better prognosis
than the lateral dislocation. In the medial subtalar dislocation, the late
instability is rare, and the duration of immobilization should be short (about
3-4 weeks). If you have a lateral subtalar dislocation, you may want to
evaluate the foot by CT scan after closed reduction and splinting the patient.
The reason that you get a CT scan, is to see if you have any bony fragments
that need to be removed or fixed, and that can also be done for the medial
subtalar dislocation if you think it is necessary. These bony fragments can
cause the subtalar joint to be unstable. The lateral subtalar dislocations are
a high energy injury. They are frequently associated with small osteochondral
fractures. Larger fragments should be fixed, and a small fragment that is
entrapped in the joint should be excised. If you think the joint is unstable
after reduction, check for the presence of a large intra-articular fracture and
try to reduce it and fix it. You want to start early range of motion, so
immobilize the patient for a short period to avoid stiffness but try to avoid
the recurrence of the dislocation or the instability. The subtalar dislocations
can cause stiffness of the subtalar joint and degenerative arthritis. If you
can’t do closed reduction then you need to do open reduction, and you need to
know that the extensor digitorum brevis is usually the entrapped in medial
subtalar dislocation, and the tibialis posterior is the one that is usually
entrapped in the lateral subtalar dislocation.
Lisfranc injury is a tarsometatarsal fracture dislocation
that involves the medial cuneiform and the base of the second metatarsal. The
severity of the injury can range from a mild sprain to severe dislocation or
fracture dislocation. The Lisfranc dislocation can be a purely ligamentous
injury, boney injury, or a combination of both. The metatarsals are usually
dislocated dorsally and laterally. The condition could be missed and may result
in progressive foot deformity, disfunction, chronic pain, and arthritis. The
oblique interosseous ligament (Lisfranc ligament) is the strongest ligament.
The region is stable because the bony architecture is connected to strong
ligaments, especially the Lisfranc ligament. Osseous stability is provided by
the roman arch arrangement of the metatarsals, and the Lisfranc ligament
stabilizes the 2nd metatarsal to maintain the midfoot arch. The
Lisfranc ligament is between the medial cuneiform and the base of the 2nd
metatarsal. The keystone configuration is formed by the base of the 2nd
metatarsal that fits into the mortise, which is made by the medial cuneiform
and the recessed middle cuneiform. The mechanism of injury results from axial
loading on a plantar flexed foot. Diagnosis is done by a combination of
clinical exam and x-rays. Clinical presentation could show midfoot pain,
plantar ecchymosis, and tenderness on the dorsal aspect of the midfoot. When you
see that clinical situation, you need to suspect Lisfranc injury even if the
x-ray is negative. The fleck sign is a small avulsion fracture at the medial
base of the second metatarsal. It represents an avulsion of the Lisfranc
ligament. The diastasis between the 1st and 2nd
metatarsal of more than 2 mm is considered to be a Lisfranc injury. The injury
may be subtle and can be missed. You will need to get standing weight bearing
x-rays if the injury is suspected (compare the x-ray to the other side). If you
purely ligamentous injury, the treatment will be early fusion of the 1st
and 2nd tarsometatarsal joints. Ligamentous injuries to the
tarsometatarsal and intermetatarsal joints resulted in a worse outcome
following open reduction and internal fixation than Lisfranc injuries that
involve fractures. Ligamentous Lisfranc injuries will give a better result if
they are treated by primary arthrodesis. If the Lisfranc injury is treated by
open reduction internal fixation, it will result in a higher rate of secondary
surgery and a lower function outcome. Anatomic reduction is important if the
surgeon selects open reduction and internal fixation. If you do open reduction
and internal fixation for a ligamentous injury, the patient may have persistent
pain and arthritis. Closed reduction and percutaneous pinning do not give a
good result. Post-traumatic arthritis and altered gait is common.
Injuries of the distal phalanx can be a fingertip injury,
which will be a different topic by itself. Fracture of the distal phalanx is
the most common phalangeal fracture, and it can occur from a crushing injury
that produces major soft tissue injury. It can involve the tuft, the shaft, or
the base of the phalanx. If it involves the tuft, then it is usually a crush
injury and may be associated with a nail bed injury. Usually it is associated
with subungual hematoma. If the hematoma involves more than 25% of the nail,
especially if there is a fracture, then you need to remove the nail, as well as
explore and suture the nail bed. Most of the time the fracture is comminuted
and probably will need a splint. In some cases, the fracture may need k-wire
fixation. The fracture may fail to unite. Fracture of the distal phalanx shaft
is usually stable and can be treated conservatively by a splint or buddy
taping, and surgery is rarely needed. Distal phalanx nonunion, if symptomatic
and painful, do reduction and internal fixation with bone graft. With fracture
of the distal phalanx base, there are two types jersey finger and mallet
finger. The patient that is unable to flex the DIP joint is the patient that
has a Jersey finger, or volar base fracture. The patient with a mallet finger,
or dorsal base fracture, is unable to extend the DIP joint. If the fracture is
large, there may be a volar subluxation of the distal phalanx. Be aware of
avulsion fracture at the base of the distal phalanx, because it must be
evaluated thoroughly. It could be an avulsion of the insertion of the flexor or
the extensor tendon, and the fracture appearing small and benign. If the
fragment is large or if there is volar subluxation of the joint, then this can
be treated by different techniques. K-wire utilization is a very common
technique. The goal is to keep the DIP extended until the bone or the tendon
heals. Some orthopaedic surgeons will continue to treat this injury by closed
means (splint), even if there is a volar subluxation of the joint. The rationale
is that a stiff finger that is treated by closed means is better than a stiff
finger that is treated by surgery. When the tendon is avulsed with a bony
fragment, the tendon with a piece of bone could be retracted at different
levels, and it can be seen in the x-ray. In general, if the tendon is retracted
to the palm, then the blood supply could be affected and surgery should be done
within 10 days. If the fragment is large, then usually the retraction is
limited to the DIP. The finger lies in extension relative to the other fingers,
and the patient will not be able to do active DIP flexion. Seymour fracture is
an epiphyseal fracture of the distal phalanx. It is a flexion injury that leads
to physeal separation between the extensor tendon dorsally and the flexor
digitorum profundus volarly. This flexion injury causes an avulsion of the nail
from the nail fold with disruption of the nail matrix. The patient’s finger
will appear flexed, which looks like a mallet finger, and the nail appears to
be larger compared to the nail on the other side. This injury is really an open
fracture and needs to be treated by antibiotics, removal of the nail,
irrigation and debridement of the fracture, reduction and pinning of the
fracture and nail bed repair.
The L5 nerve root is part of the lumbosacral plexus. It is
an important component of the sciatic nerve. The L5 nerve root causes ankle
dorsiflexion, which also comes from the L4 nerve root. The tibialis anterior is
the primary dorsiflexor of the ankle, and the innervation comes from the deep
peroneal nerve. Injury of the L5 nerve root can cause weakness of the tibialis
anterior muscle, and this can lead to a foot drop. The L5 nerve root also
causes dorsiflexion of the toes through innervating the extensor hallucis
longus and extensor digitorum longus, and this innervation comes from the deep
peroneal nerve. Of particular interest, is the extensor hallucis longus. Weakness
of the big toes extension is usually present when disc herniation affects the
L5 nerve root. So, when the L5 nerve root is affected, the extensor hallucis
longus could become weak. The tibialis posterior is an important muscle that
runs behind the medial malleolus, and its innervation comes from the posterior
tibial nerve (L4-L5). The function of the tibialis posterior is to invert the
foot, to assist in plantar flexion of the ankle, and to maintain the medial
longitudinal arch. The L5 nerve root also innervates the muscles that cause hip
extension, and the muscles are the hamstrings, which is innervated by the
tibial nerve, and the gluteus maximus which is innervated by the inferior
gluteal nerve. The hamstring muscles are also a major flexor of the knee. The L5
also innervates the hip abductors (gluteus medius and gluteus minimus), and the
innervation comes from the superior gluteal nerve, injury of L5 nerve root can
cause weakness of the hip abductors, and this can lead to Trendelenburg Gait. The
L5 nerve root is really an important nerve root that supplies a lot of muscles.
The L5 nerve root gives sensory innervation to the top of the foot. If you do
not remember anything about the L5 nerve root, try to remember that injury to
this nerve can cause weakness of the big toe extension, weakness of ankle
dorsiflexion (foot drop), and weakness of the hip abductor muscles which will
give you Trendelnburg Gait.
The sternoclavicular joint is composed of the proximal
end of the clavicle and the manubrium of the sternum. Sternoclavicular joint
injuries are uncommon shoulder injuries. In young patients, the injury is usually
a physeal injury. Medial clavicle physeal fracture occurs in a patient less
than 25 years old. Th epiphysis ossifies at the age of 18 and closes between
20-25 years of age. Anterior dislocation is more common than posterior
dislocation. The AP x-ray is difficult to interpret, and we get what is called
the Serendipity view X-ray, which is 40° cephalic tilt view with the beam
focused on the manubrium, then you compare both clavicles. The serendipity view
allows for identification of the anterior or posterior translation. In practice
clinically, the anterior dislocation will be obvious. The posterior dislocation
will not be obvious. The patient will have pain, order a CT scan. A CT scan is
the best study to evaluate acute, traumatic injuries of the sternoclavicular
joint. It will help determine what type of injury or dislocation (anterior or
posterior). A Ct scan will show if the injury is a physeal injury or if it is a
true dislocation. It shows the status of the mediastinal structures. Anterior
dislocation is common. The patient will have pain, a bump, or swelling that is
increased by abduction of the arm. Anterior dislocation is unstable if you
reduce it, but it is benign. If it is acute, try to reduce it, otherwise accept
the deformity. Observe the patient and treat the patient symptomatically. The
anterior sternoclavicular dislocation is rarely symptomatic when left
unreduced. Most of the time the patient will do very well, and it will not
affect function or range of motion (resuming of unrestricted activity in 3
months). If the injury is chronic and symptomatic, then you will do surgery.
The type of surgery that is done is a resection of the medial part of the
clavicle. Resect less than 15 mm of the medical clavicle. Do soft tissue
stabilization of the residual medial clavicle with costoclavicular ligament
reconstruction. Reconstruction of the sternoclavicular joint utilizing tendon
graft (allograft or autograft can be used). The hamstring tendon technique is popular,
and the figure eight technique is commonly used because it provides great
stability. The posterior sternoclavicular dislocation is less common and is a
true orthopaedic emergency. 1/3 of the posterior dislocations may have
compressive effect by exhibiting pressure on the great vessels, esophagus of
the trachea. It may cause dyspnea, tachypnea, dysphagia, or paresthesia and it
needs reduction. It has minimal, visible clinical findings. Sometimes the
affected shoulder is shortened with forward thrust. The posterior
sternoclavicular dislocation will be stable after reduction. You will have
general anesthesia with thoracic surgeon backup. With a posterior
sternoclavicular dislocation start with closed reduction with the hand or with
a towel clip and lift the clavicle up. When you do closed reduction, the
initial position for the extremity is the same for anterior and posterior
dislocation. You will have general anesthesia and you will do abduction and
extension of the shoulder. For the posterior dislocation, you will do abduction
and extension. There will be a bump underneath the medial scapula. You will
manipulate the medial clavicle with a towel clamp or with the fingers, lifting
the clavicle up and reducing the joint. The posterior dislocation is usually
stable, so give the patient a sling for 3-4 weeks. For the anterior
dislocation, you will do direct pressure. If the reduction is stable, you will
use a figure 8 strap or sling, and do therapy at 3-4 weeks. If posterior
dislocation is unstable or irreducible, you will do reduction or excision of
the medial clavicle plus stabilization of the soft tissue. If it is chronic,
recurrent, or symptomatic, you will do excision of the medial clavicle plus
soft tissue stabilization. Do not try to do closed reduction in late or chronic
cases, because there are mediastinal adhesions that may cause problems inside
the chest.
Interpretation of elbow radiographs can be complicated.
There are a lot of ossification centers in the elbow that can be confusing.
Elbow trauma and injuries are common and ossification centers can look like
bony fragments, and bony fragments can look like ossification centers. Knowing
the time of development of the normal ossification centers can be important.
Although this timing may be variable, you can guess the approximate time of the
appearance of the ossification centers by using the mnemonic CRITOE. CRITOE, 1
3 5 7 9 11, are the ages when the ossification centers appear around the elbow.
The time of appearance of these ossification centers is reliable, although they
can be variable, especially in girls where they can occur earlier than in boys,
sometimes by two years earlier. A rough timing estimate that is easy or simple
will be helpful. This is more helpful in looking for the medial epicondyle for
example, after an elbow dislocation that is avulsed and may be trapped in the
joint, and you could not find it in its normal location because you could not
remember if the ossifications center was even developed. If you find the
trochlea ossification center and you do not find the medial epicondyle
ossification center in its normal location, then look inside the joint,
especially if you know the age of the patient and you know that the internal or
the medial epicondyle should be developed by then. The internal epicondyle
(medial) should be seen because it develops before the trochlear ossification
center. One of the most important things is to know the age of the patient.
Look for the normal position of the ossification center. Finding what appears
to be a fracture or an ossification center in the area of the olecranon or the
lateral epicondyle in a young child (5 years) should not be interpreted as an
ossification center which should be developed later.
Iliac bone fractures have unique characteristics. You can
have stable fractures such as avulsion of the iliac spine, anterior superior
spine, due to pull of the Sartorius muscle. There may also be avulsion of the
anterior inferior iliac spine (AIIS) due to the pull of the direct head of the
rectus femoris muscle. The iliac bone can be part of acetabular fractures, and
when it breaks as part of the acetabular fracture, it can be an associated both
column fracture, and the iliac fracture will be seen in the CT scan in a
coronal view. You can also see the “spur sign” which is part of the posterior
ilium in its undisplaced position, and this can be seen in the obturator view.
The fractured ilium can also be a part of pelvic fractures. This can be
partially stable, such as posterior iliac bone fracture in the crescent type.
The fractured pelvis can also be unstable, and you will have unilateral iliac
fracture and complete disruption of the posterior arch complex. If it is not
treated adequately, it can lead to malunion, deformity of the iliac wing and
leg length discrepancy. Isolated iliac fracture occurs due to a direct blow to
the pelvis. It is usually rotationally and vertically stable and is usually
treated conservatively. It is not a benign injury; it can be a serious injury,
especially if the fracture ilium is comminuted. Comminuted iliac fractures are
uncommon and difficult to treat. There can be significant associated injuries
such as soft tissue injury. Iliac and flank soft tissue injuries such as iliac
and flank degloving injuries that is called Morel-Lavallee lesion. In the
internal degloving injury, the fat is sheared off of the fascia. An open
fracture and entrapment of the bowel within the fracture site. There may be a
variety of abdominal, vascular and neurological injuries. If the fracture extends
into the greater sciatic notch, then the patient may have an arterial injury or
a lumbosacral plexus injury. In general, treatment is nonoperative if the
fractured ilium is isolated and nondisplaced. Surgery is done by open reduction
and internal fixation for displaced fractures. In case of open fracture, the
patient may need a colostomy.
Crescent fractures of the pelvis is a sacroiliac joint
fracture dislocation. The fracture of the iliac wing enters the sacroiliac
joint. The fracture of the iliac wing enters the sacroiliac joint. There is a
varying degree of injury to the sacroiliac joint ligament (combination of iliac
fracture and sacroiliac joint disruption). The posterior ilium remains attached
to the sacrum by the posterior sacroiliac ligaments. The anterior ilium has an
internal rotational deformity. The posterior superior iliac spine remains
attached to the sacrum. This injury is known to be rotationally unstable;
however, some people believe it is more than that. Crescent fracture occurs by
a laterally directed force applied to the anterior part of the involved iliac
wing. There are three types of fractures based on the Young-Burgess
Classification. Type I is a small impacted fracture of the anterior sacrum.
Type II is a crescent fracture of the pelvis which is partially stable. Type
III is an unstable fracture type with ipsilateral lateral compression and
contralateral anteroposterior compression (windswept pelvis). CT scan defines
the posterior pelvic fracture adequately, and it also can define the crescent
fracture type. You can fix it by two screws from posterior to anterior, and you
can add a reconstruction plate on top of it. The whole idea is to achieve
anatomic reduction of the iliac wing, and the sacroiliac joint dislocation and
stable fixation. The fixation can be done by extra-articular internal fixation
using intertable lag screws and outer table neutralization plates. It can be
done through a posterior approach, and this will be fixing the iliac component.
The fixation can also be done percutaneously, and it also can be done with
screws through the sacroiliac joint.
