Ortho questions

Question 1

Define: “joint dislocation”; “joint subluxation”; and “joint reduction”

Answer 1

Joint Dislocation (also known as luxation) occurs when the joint surfaces become 
completely disengaged. A dislocation always results in damaged ligaments. 
Joint Subluxation is an incomplete or partial dislocation in a joint
Joint Reduction is the medical procedure in which manipulation brings a structure
back into its normal anatomic position. (This term also applies to the bones in the 
case of fracture.)

Question 2

Why is a traumatic hip dislocation typically worse than a shoulder
dislocation? (Contrast the mechanisms which prevents the normal
shoulder from dislocating with that of the hip joint, and consider what must
be damaged.)

Answer 2

In brief, the shoulder is a loose joint, held in place by soft tissue, not bone. This
allows for great ROM yet poor inherent stability The hip is held in place, by
contrast, via bony congruity: ball in socket (vs ball on golf tee).
This has two main implications:
1. A hip dislocation requires more force to get the joint out of place. And as a
higher energy injury, it is more likely to inflict other damage (local (pelvic)
fracture, visceral injury, etc)
2. Because the shoulder has so much natural freedom, the soft tissues are
not tethered as much and typically have fairly wide excursion. Thus, when
the shoulder is dislocated, it is correspondingly less likely that the blood
vessels and nerves are apt to be damaged.

Question 3

What is osteonecrosis (a/k/a avascular necrosis)? How does hip
dislocation disrupt this?

Answer 3

Avascular necrosis is the death of bone, secondary to loss of blood supply and
resultant ischemia.
Recall that bone is alive. Hence:
 If bone gets ischemic, it dies.
 If bone dies, it does not remodel (see below).
 If bone does not remodel, micro-damage does not get repaired.
 If enough micro-damage accumulates, the sub-chondral bone collapses.
 If the sub-chondral bone collapses the joint surface is no longer smooth.
 If the joint surface is no longer smooth it will eventually damage the other
surface.
Note: although you can observe/detect dead muscle right away (8 hours post
infarct for sure), acutely dead bone (at hour 8) under the scope looks normal.
Think of it this was: If you cut off the “water supply” to a person’s shower, they
don’t start stinking immediately.
Hip dislocation can cause disruption of the blood supply to the head and thus
lead to AVN
Note: the blood supply in the adult is NOT via vessels from the center
acetabulum (as it is in the neonate) and is NOT ripped when dislocation occurs.
Rather, the blood supply ascends from the profunda femoris to the circumflex
femoral arteries, which then ascend to the head; and the damage is via
stretching of these vessels. The key implication is that rapid reduction might
decrease the chance of AVN as mere reduction might restore flow (which is not
the case if the vessels were torn).

Question 4

Describe the process of bone remodeling. Why does this process exist?

Answer 4

Bone remodeling, in brief, is the process by which osteoclasts eat old bone and
stimulate osteoblasts to make new bone. 3
The activity of ostoeblasts is easy to comprehend: make bone where needed.
Osteoclasts are bit trickier: why resorb bone?
That process exists for two reasons, really: first, to liberate calcium and other
ions; and second, to clear out worn out pieces of the skeleton and promote the
deposition of newer, better material.
Osteoclastic resorption occurs by secretion of acid and proteolytic enzymes
which digest the bone matrix; Ca2+ and PO43- are then taken up by the
osteoclasts and released into the circulation.
Bone formation occurs by osteoblasts secreting an organic matrix (osteoid) and
then mineralizing the matrix.
 When the remodeling process is skewed over time such that there is more
eating than replenishing, you get osteoporosis.
 When the remodeling process is aborted, say in avascular necrosis, bad
bone accumulates leading to mechanical failure–and such mechanical
failure in subchondral (“under the cartilage”) bone can lead to arthritis*.
 When the remodeling process just can’t keep up with (new) mechanical
demands, like over-exercising, you get a stress fracture.
 When you get a long bone fracture, bone remodeling kicks in to literally
remodel the callus and lay down new bone (not scar).
 And to be sure, when the bone needs to liberate calcium and other ions, it
employs osteoclasts and invokes the process of bone remodeling; as such
bone remodeling is a key feature of metabolic bone disease
Bone resorption occurs from osteoclastic breakdown of trabecular bone via the
secretion of hydrolytic enzymes. This process occurs throughout life and is tightly
regulated by several factors: serum vitamin D, serum calcium, growth hormone,
PTH (increase resorption), and calcitonin (increase bone formation) levels, to
name a few.
Two things to recall:
1. you cannot “de-mineralize” the bone. You have to “de-bone” the bone, as
Dr Fred Kaplan termed it—that is, you must break down the matrix to get
the mineral out. Thus, even if the body need calcium ‘only for a minute’ it 4
takes a while get the skeleton restored (think of it as having to get a
mortgage if you wanted to borrow even a small amount; it’s a much bigger
hassle than a credit card overdraft!) Implication: lots of mineral flux =
immature bone, at best; maybe a deficit.
2. Metabolic needs trump skeletal needs. (makes sense: calcium is needed
for cardiac contractility and nerve transmission). Thus, in metabolic
diseases, the skeletal system can be harmed.

Question 5

Besides osteonecrosis, what other mechanisms may enable a dislocation
to cause arthritis?

Answer 5

Two things come to mind: initial cartilage damage itself and ongoing cartilage
damage inflicted by loose ligaments (just like a loose lug nut may cause your tire
to wear out)
Recall this picture: dislocation can be associated with an impaction injury to the
joint surface, and torn or stretched ligaments

Question 6

A patient falls on his outstretched hand and has normal appear xrays but
tenderness in the “anatomic snuff box” (between extensor pollicis longus
and abductor pollicis longus/extensor pollicis brevis). Why –thinking about
osteonecrosis—might such a patient be placed in a cast despite the normal
x-ray?

Answer 6

A fall on an outstretched hand can injure/ fracture the scaphoid carpal bone
(located at the base of the thumb). Blood supply to the scaphoid bone flows from
a distal to proximal direction through the palmar arches, and is tenuous.
Therefore, in the event of a scaphoid injury, it is imperative to prevent
displacement of the fracture and disruption of the blood supply and in turn
avascular necrosis of the scaphoid. Note that xrays may not be sensitive enough
to detect non-displaced fractures in the scaphoid during the early phase of the
injury; thus, preventative casting (to prevent fracture propagation and
displacement and follow up radiograph imaging is the standard of care following
a scaphoid injury.

Question 7

There are three tasks of bone: skeletal homeostasis, mineral homeostasis, and hematopoesis. How can problems related to these latter two non-structural tasks lead to fracture?

Answer 7

Mineral homeostasis involves maintaining the correct serum levels of calcium,
phosphate and magnesium and other ions. PTH increases serum calcium levels
by increasing GI calcium absorption, renal phosphate and calcium reabsorption
and releasing calcium from the skeleton by de-boning the bone (see above).
Hyperparathyroidism, to name one disease of aberrant nineral homeostasis, will
increase osteoclast activity and therefore weaken the bone Vitamin D deficiency
in adults, to name another process, can cause defective bone mineralization, and
will might lead to pathologic fractures.
In general, if the body needs minerals it will take them from the bones. You need
the right level of Calcium to have a heart beat. You need a skeleton (in
evolutionary terms) to get to food and mate(s). The former is more important, at
least on a minute to minute basis
Problems with hematopoesis problems can also lead to fracture–indirectly.
Basically, it’s the fact that the blood-making apparatus is in the bone –and thus
the bones are essentially part of the vascular system—that leads to problems.
Bad blood cells can get stuck there (sickled rbc  infarct/avn), and cancer cells
and infection can easily spread there (not to mention blood cell cancers that
original there).

Question 8

Define and contrast osteoporosis and osteomalacia (include histology,
radiology and clinical features)

Answer 8

Both osteoporosis and osteomalacia can cause weak bones. In osteoporosis, there is decreased bone mass with normal ration of mineral to matrix. In osteomalacia, the ratio of mineral to matrix is decreased.
Osteoporosis causes decreased bone mass with a normal ratio of bone mineral to matrix in addition to altered bone microarchitecture. The catch-phrase of osteoporosis to recall is “normal enough bone but not enough of it!”
Clinical features of osteoporosis include fractures from minimal trauma, particularly in the thoracic and lumbar spine, wrist and hip. Thoracic vertebral compression fractures can cause dorsal kyphosis (Dowager’s hump). Plain x-rays show decreased bone density - but only once at least 30% of bone is lost. Dual x-ray absorptometry (DEXA) is the diagnostic test for osteoporosis; it measures bone density of usually the lumbar spine or femoral neck in terms of T scores (deviations from the mean of normals). A DEXA > 2.5 is diagnostic of osteoporosis. Lab values of serum calcium, phosphorus and alkaline phosphatase are not diagnostic.
Osteomalacia (a process known in childhood as “rickets”) is characterized by decreased ration of bone mineral to matrix. Histologically, the un-mineralized osteoid appears as thickened layer of matrix. The disease causes characteristic symptoms of diffuse bone pain, tenderness and muscle weakness.
X-rays commonly show decreased bone density with thinning of the cortex.
Advanced disease can cause concavity of vertebral bodies (codfish vertebrae)
and bowed legs. In addition, bilateral and symmetrical fissures (Looser’s zones
or pseudo-fractures) are often seen perpendicular to the cortical bone at the
femoral neck and medial femoral shaft. Lab findings may show low serum and
urinary calcium and high serum alkaline phosphate.

Question 9

How is osteoporosis diagnosed, prevented and treated?

Answer 9

Diagnosis: index of suspicion in susceptible patients must be maintained; Dual-energy x-ray absroptimoetry (DEXA) is the diagnostic test for osteoporosis. The first low energy fracture (usually the wrist) should stimulate a work up.
Prevention: Primary prevention includes diet supplementation with calcium and
vitamin D. Pharmacology is typically not used in prevention, but
bisphosphonates and raloxifene are approved for preventative use, typically in
patients with a DEXA between 2.0 and 2.5. Weight bearing exercise also can
prevent osteoporosis. Exercise, avoiding excess alcohol use and smoking
cessation can also improve bone density.
Treatment: A first line treatment is calcium (1500mg daily) and vitamin D
supplementation (800 IU daily). First-line pharmacologic treatment includes
bisphophonates such as alendronate, which inhibit osteoclasts, reducing bone
resorption and turnover. Estrogen-progestin therapy is now rarely used in
postmenopausal women due to cardiovascular side effects.

Question 10

Describe the relationship between menopause and hip fracture risk.
Describe the relationship between body mass and hip fracture risk.

Answer 10

Menopause, with its decreased estrogen production, leads to increased
osteoclast activity and thus at menopause, women begin to experience a 2% loss
in bone mass per year as bone resorption outpaces bone formation.
A low BMI is a risk factor for hip fracture. A BMI of 20 is estimated to have a 2.0
relative risk of hip fracture compared to an individual with a BMI of 25.
There are two schools of thought why low BMI leads to fracture, both centered on
the role of fat. 1) Fat is a substrate for the synthesis of estrogen and thus is an 7
indirect source of osteoclast inhibition. 2) Fat provides soft tissue padding.
Maybe both. (The interested student is pointed to Bernstein, J., Grisso, J.A.
and Kaplan, F.S. Body Mass and Fracture Risk. Clinical Orthopedics and
Related Research. 364:227-230 1999)
(And a really low BMI is best thought of as cachexia –and that’s a sign of general
decline, bones included)
What is the practical distinction between the two mechanisms? Basically, it’s the
question of whether low energy fractures are an intrinsic bone problem or an
extrinsic, medical problem. (See question below on Heaney quote)

Question 11

What are the three fractures typically associated with osteoporosis?
Which is worst? Why is it so deadly?

Answer 11

The three fractures typically associated with osteoporosis are hip, wrist, and
vertebral compression fractures. Hip fractures are the worst: there is a 30%
mortality within the first year of fracture. That may be because of its affect on
mobility, or maybe because getting a fracture in the first place is a sign of the
dwindles…
And don’t forget: a low energy wrist fracture is a sign suggestive of underlying
osteoporosis—a wrist fracture from a fall should be the initiator of an
osteoporosis work up, or empiric treatment.

Question 12

Heaney wrote “Although bone mass is certainly the most extensively studied of
the fragility factors, low bone mass is not the whole of the osteoporosis story and
may not even be its most important component (despite frequent assertions to
the contrary). If one could magically normalize bone mass in everyone, would
one eliminate osteoporotic fractures? The best answer that can be given today is
“no.” There would be fewer such fractures, but there would still be many,
especially hip fractures.” (Heaney RP Bone Mass, Bone Loss, and Osteoporosis
Prophylaxis. Annals Internal Medicine 15 February 1998 128: 313-314)
What else (besides abnormal bone) might lead to low energy hip fractures?

Answer 12

(This is to ask, as I think Heaney implied, What else besides intrinsic bone
problems could cause hip fracture?)
Old people get the dwindles. They fall more and when they fall, the risk of
fracture is higher because they can’t catch themselves. A risk of falls (like bad
vision, say, or a neuro disease) is an independent risk factor for a hip fracture. Ie,
if you have normal bones but a higher propensity for falling, you are at higher risk
of hip fracture.8
The key point to know and recall is that the amount of energy needed to break a
hip is only a fraction of the energy available from a typical fall. That most falls do
not cause fracture is a testament to the normally present energy-absorbing
processes (catching yourself, basically).
So if you fall frequently and if you can’t catch yourself as you fall, you are going
to break bones.
A related point: that’s why patients falling off the OR table is such a potential
disaster: sleeping patients can’t catch themselves! (and anecdotally, some of the
worst fractures I have seen are in the inebriated.)

Question 13

Describe the 2 main types of bone healing.

Answer 13

The two mechanisms of bone healing are primary bone healing and secondary
bone healing. JUST LIKE SKIN: you can sew it up or it can scab.
Primary bone healing involves a direct attempt by the cortex to re-establish
itself after interruption without the formation of a fracture callus. This only works
when the edges are touching exactly and is the less commonly seen type of
healing (in fact, this method is employed only after rigid surgical fixation, or with a
partial crack in the bone –a “unicortical” fracture (where the remaining bone holds
everything rigid). The basic science, in brief, Primary bone healing is lead by the
formation of a so-called cutting cone (consisting of osteoclasts at the front of the
cone to remove bone and trailing osteoblasts to lay down new bone) across the
gaps to form a secondary osteon.
Secondary bone healing involves the classical stages of injury, hemorrhage
inflammation, primary soft callus formation, callus mineralization, and callus
remodeling.
1. Right after injury, a hematoma (blood clot) forms.
2. From this hematoma, a primary soft callus, composed of granulation
tissue (made from fibroblasts and new blood vessels) is formed.
3. The cells in this soft callus make cartilage.
4. The cartilage is then mineralized producing “woven” or “lamellar” ie
disorganized, bone.
5. Last, the woven bone remodels into normal bone (ie, structurally oriented
in direction of load). (There is a picture on the answer key that is said is important)

Question 14

One of the two methods above looks a lot like bone formation. What are the
implications of that similarity?

Answer 14

Indirect bone healing closely resembles endochondral ossification (which
involves a cartilage template being replaced by bone). This suggests that indirect
bone healing results in re-formation of bone with essentially the same
mechanical properties as the original bone, if not better.
Key point: healing in a sense recapitulate growth. So fracture healing can lead to
completely new bone, not scar. (At the other extreme: cartilage: it heals poorly—
it not only forms just scar, the scar is poor mechanical quality. Scientists among
you: fix this!)

Question 15

What are the necessary conditions for appropriate bone healing (leading to
minimal functional residuals) and how may physicians thus optimize the
chances for healing?

Answer 15

Successful bone healing requires a variety of factors, including adequate blood
supply, relative mechanical stability, sterility and intact surrounding soft tissue.
Physicians may optimize chances of healing by
 Reducing (aligning) the fracture;
 making sure the blood supply and soft tissue envelope are in good shape;
 keeping infection out;10
 minimizing edema (more for pain control and compartment syndrome
prevention, perhaps, but also to promote perfusion)
 and allowing just enough force to stimulate bone growth but not so much
to ruin the reduction or prevent hardening of the fracture callus. (gross
motion at the fracture will lead to a so-called fibrous union: some tissue
there, but not hard tissue)
Summarized as: promote the proper mechanical and biological environment

Question 16

Plating a fracture clearly disrupts the soft tissue envelope around a
fracture. Why, then, is surgical plating ever used?

Answer 16

One famous orthopaedic surgeon said “fractures heal despite internal fixation, not because of it.”
Surgical implantation of bone plates are bad for healing, ie increase risk of nonunion, but we need them to restore alignment, especially near the joint line, where even slight deformities are poorly tolerated. Yes, the bone can heal without the plate, – healing is probably more likely without it – but that healing will be misshapen, a so called MALUNION.

Question 17

Suggest how a femoral shaft fracture can be a lethal condition.

Answer 17

A femoral shaft fracture can be lethal by complications such as deep vein
thrombosis and pulmonary embolism. Recall that bone is vascular and fractures
let marrow contents (fat especially) out into the circulation. The marrow contents
is thrombogenic and when it lands in the lung or the brain unhappiness results.11
Other serious co-morbidites of femoral shaft fractures include shock from
significant blood loss and visceral injuries from the initial hit (MVA?) that broke
the bone.

Question 18

What is compartment syndrome and how is it prevented, diagnosed, and
treated? What are the consequences of not treating a compartment
syndrome and over-treating a (falsely) suspected compartment syndrome?

Answer 18

KNOW THIS

Compartment syndrome is the process of increased pressure within an enclosed fascial space, which leads to muscle and nerve death from ischemia.
This could occur from tibia fractures (bleeding), compressive devices (casts, ace wraps), IV infiltration or burns. (Reperfusion after vascular repair is a non-musculoskeletal cause too.)
The hallmark symptom of compartment syndrome is severe pain that is out of
proportion to what is expected from the given injury/situation. One clue is pain
that increases over time (by contrast, a splinted fracture should start hurting less
once inmobilized).
In more advanced cases, symptoms may also include decreased sensation, pale
skin, and weakness of the affected area. Physical exam will reveal: severe pain
when moving the affected area, tensely swollen and shiny skin, and pain when
the compartment is squeezed.
Confirming the diagnosis of compartment syndrome involves directly measuring
the pressure in the compartment, which is done by inserting a needle attached to
a pressure meter into the compartment—or treating empirically if needed.
Treatment (prevention, actually) is a surgical procedure, fasciotomy, where long
surgical cuts are made in the fascia to relieve the pressure. The incisions are
generally left open to be closed during a second surgery about 48-72 hours later.
If compartment syndrome is not prevented treated, permanent nerve injury and
loss of muscle function can result and in severe cases amputation may be
required. Performing a fasciotomy can potentially increase the risk of infection
but overall the risk of NOT operating is way higher
Basically: the issue is that if you have increased extrinsic pressure, you
can’t perfuse the tissue, and if so, the tissue dies. Sometimes, the only sign
is PAIN OUT OF PROPORTION TO THE INJURY

Question 19

What is a stress fracture? How is a stress fracture treated in a normal
person? What are the consequences of a stress fracture which is not treated?
Why might a young woman with an eating disorder be at particular risk for stress
fracture?

Answer 19

Mental image to keep: Bending a paperclip right to the breaking point gives
it a stress fracture.
A stress fracture occurs when a bone breaks after being subjected to repeated
tensile or compressive stresses, none of which would be large enough
individually to cause the bone to fail, in a person who is not known to have an
underlying disease that would be expected to cause abnormal bone fragility.
A stress fracture is believed to develop with abrupt increase in the duration,
intensity, or frequency of physical activity without adequate periods of rest.
Important risk factors for developing stress fractures include a history of prior
stress fracture, low level of physical fitness, increasing volume and intensity of
physical activity, female gender and menstrual irregularity, diet poor in calcium,
poor bone health, and poor biomechanics.
THE TREATMENT OF AN OVERUSE INJURY IS UNDER-USE. (stop beating
up the bone and just let it heal)
Not listening to the instructions to stop is a sign of not being normal…If they don’t
listen, a stress fracture can lead to “real” (separated) fracture.
Women with eating disorders are at particularly high risk for stress fractures
because they typically lack adipose (a chemical precusor for many hormones
and do not have proper estrogen levels). As such, because osteoclasts are
estrogen sensitive, these women have bad bone remodelling weak bones.
Eating disorders are one third of the so-called female athlete triad (eating
disorders, amenorrhea, and osteoporosis).

Question 20

What is the definitional distinction between grade I, II and III sprains?
How would these various grades of injury present distinctly on examination?

Answer 20

A grade I sprain results from mild stretching of a ligament with microscopic tears.
Patients have mild swelling and tenderness. There is no joint instability on
examination, and the patient is able to bear weight and ambulate with minimal 13
pain. Due to their SEEMINGLY benign nature, these injuries are not frequently
seen in the office.
A grade II sprain is a more severe injury involving an incomplete
tear/macroscopic stretchin of a ligament. Patients have moderate pain, swelling,
tenderness, and ecchymosis. There is mild to moderate joint instability on exam
with some restriction of the range of motion and loss of function. Weight bearing
and ambulation are painful.
A grade III sprain involves a complete tear of a ligament. There is significant
mechanical instability on exam and significant loss of function and motion.
Patients are unable to bear weight or ambulate. Paradoxically, perhaps, this may
hurt less than a grade 2, as once the ligament is torn, it no longer is provoked
with every step.
Note: there are proprioceptive nerves are within the ligament, informing the brain
just how bent the joint is you might say, and even a grade I sprain can cause
proprioceptive disruption.

Question 21

What is the function of the Anterior Cruciate Ligament (ACL) in the knee?

Answer 21

The main function of the ACL is restraint of anteroposterior translation of the tibia
relative to the femur. It also acts as a secondary restraint to tibial rotation and
valgus or varus stress.

Question 22

How is the ACL torn?

Answer 22

The mechanisms of injury is commonly noncontact, such as sudden deceleration
or rotational maneuvers. (Direct contact injuries often result in hyperextension or
valgus stress on the knee, resulting in cruciate ligament injury along with a
collateral ligament injury as well). It is important to note that ACL is one of the
most common injuries to the knee accounting for 40-50% of all ligamentous knee
injury. The common theme is that a force sends the tibia one way and femur
another (typically because the foot is planted and the body spins), and the
secondary restraints (the hamstrings mostly) are overwhelmed or not helping and
the ligament is exposed to forces it cannot bear.

Question 23

Along those lines, why might it be the case (as we suspect) that skiing-related ACL tears occur disproportionately after 2 pm?

Answer 23

This is all hypothetical/theoretical, but the idea is that at 10am your still-powerful
hamstrings protect the ACL; at 2pm, when the tibia starts to subluxate, the14
hamstrings just say ‘screw it, I am done’ and let the bone go on its path of
subluxation– and bam, the ligament fails.

Question 24

How is an ACL tear detected on exam?

Answer 24

An ACL tear is suspected first by history. A “pop: heard by the patient, immediate
pain and swelling after a twist are typical features.
To test for an ACL tear on physical exam one can use the anterior drawer and
Lachman tests. The Lachman test is the gold standard because it is thought to
focus just on the ACL and not all of the other possibly stabilizing structures.
The Lachman test is performed by placing the knee in 30 degrees of flexion and
then stabilizing the distal femur with one hand while pulling the proximal tibia
anteriorly with the other hand, thereby attempting to produce anterior translation
of the tibia. An intact ACL limits anterior translation and provides a distinct
endpoint. Increased translation compared to the uninjured knee and a vague
endpoint suggest ACL injury.
The anterior drawer is performed with the patient lying supine and the knee
flexed at 90 degrees. The proximal tibia is gripped with both hands and pulled
anteriorly, checking for anterior translation. Often the clinician sits on the foot
while performing the test to provide stability. The test is positive if there is
anterior translation.
In brief, if there is a good story on history; effusion; what you think is maybe a
positive lachman or drawer then get MRI
(Wanna be a smart PCP? Learn how to tap a knee. (We teach that in
ortho-300). If there is blood in the knee it’s bad and needs an orthopaedic
surgeon soon. Even in the face of normal xrays, blood in the knee has a
cause in need of surgical Rx more than 90% of the time)

Question 25

Why is it that a tear (grade III sprain) of the ACL typically requires surgical replacement whereas a grade III sprain/tear of the medial collateral ligament of the knee can heal with immobilization and rehab?

Answer 25

The MCL heals and the ACL does not. A glib answer to the question Why? is that the MCL has the right biological and mechanical environment and the ACL does not. In fact, that glib answer applies: The ACL is in the joint (the MCL is not) and joint fluid dissolves clots and impeded healing (says Martha Murray, Penn Med ’92ish, now a Harvard Professor). Also, it’s hard to immobilize the knee in such a way that the ACL is protected yet the joint can move (whereas a hinged brace does that for the MCL)

Question 26

What is the function of the meniscus in the knee? What is the 15 consequence of tearing a meniscus? Why are most symptomatic meniscal tears removed and not repaired?

Answer 26

A torn meniscus is a disruption of the fibro-cartilage pads located between the femoral condyles and the tibial plateaus. The medial and lateral meniscus provide shock absorption, help with anterior/posterior stability of the knee, and provide a broad base of contact surface. A lost meniscus leads to  Pain with loading, such as jumping (because of lost shock absorption)  Less anterior/posterior stability of the knee (because of loss of chock block effect on airplane wheel  DJD (because lost broad base of contact surface leads to focal load bearing and overstimulation of bone formation and in turn stiff, injury prone subchondral bone). We remove menisci, in light of the above, only when we have to. And we usually have to remove symptomatic tears because they don’t heal. (A glib answer to the question Why? is that the meniscus does not have the right biological and mechanical environment for healing—biological in particular: there is no blood supply except at the edges.)

Question 27

What is rotator cuff tendinitis? What are the consequences of labeling it (perhaps incorrectly) as an “—itis"? What are the consequences of labeling rotator cuff tendinitis as “impingement syndrome”?

Answer 27

Rotator cuff tendinitis is not inflammatory. It is a degenerative wearing out of the tendon, owing to repetitive use, poor blood supply and aging. It should be “treated” with an anti-inflammatory only to the extent that the medicine is also a pain reliever. There is no proof that anything is impinging on the cuff (C Neer, Penn Med ’42 came up with this theory sans evidence and it stuck, no fooling) and hence no evidence that we should surgically remove anything (though we do) . The interested student is pointed to the best (and only; hence worst too) discussion of orthopaedic surgery semiotics (the pernicious effect of mis-naming things) : Bernstein, J. In the Beginning was the Word.. Journal of Bone and Joint Surgery. 88: 442-445 2006

Question 28

Back pain is a common, self-limited condition in many people. Discitis, cancer and cauda equine syndrome are causes of back pain which are not 16 innocent and self-limiting. First, by way of background, define "cauda equina syndrome", discitis and the common cancers are found in the spine. Next, name some questions a physician might ask to help detect the diagnoses?

Answer 28

Cauda Equina Syndrome is a serious neurologic condition in which there is acute loss of function of the lumbar plexus. The “cauda equina” are the nerve roots that branch off of the lower end of the spinal canal beneath the termination of the spinal cord (conus). The cauda equina contain the nerve roots from L1-L5 and S1-S5. Cauda Equina syndrome occurs when the nerves of the cauda equina are compressed or disturbed such as by a tumor/lesion, trauma, spinal stenosis, or inflammatory conditions. It is associated with weakness of the muscles innervated by the compressed roots, sphincter weaknesses causing urinary retention, and post-void residual incontinence. There may also be decreased anal tone; sexual dysfunction; saddle anesthesia; bilateral leg pain and weakness; and bilateral absence of ankle reflexes. Pain may, however, be entirely absent. The diagnosis is usually confirmed by an MRI scan or CT scan. Treatment typically involves URGENT surgical decompression. Discitis is an infection in the intervertebral disc space. Pathogens can reach the bones of the spine by hematogenous spread from a distant site or focus of infection, direct inoculation from trauma or spinal surgery, or contiguous spread from adjacent soft tissue infection. Staphylococcus Aureus accounts for more than half of cases in developed countries. Symptoms include severe back or neck pain, which often lead to immobility. Fevers have been noted in some patients. The diagnosis is usually confirmed by an MRI scan. Treatment usually includes antibiotics and using a back brace or a plaster cast to reduce the mobility of the region. Spinal metastasis is the third most common site for cancer metastases (behind lung and liver). The patient may not know s/he has a primary tumor! The most common cancers that metasticize to the spine are lung and breast. The key questions are Is there pain at rest?; Are there constitutional symptoms?; and Do you have neurological complaints? A positive response to any should prompt investigation.

Question 29

A so-called herniated disc may compress a nerve root and cause radicular complaints/findings. What are the classic motor and sensory findings of involvement of L4? What are the classic sensory and motor findings of involvement of L5? What are the classic findings of involvement of S1?

Answer 29

L4 disc hernation often presents with quadriceps and tibialis anterior weakness, medial knee and shin sensory loss and pain distributed down the anterior thigh. L5 disc herniation classically presents with weakness in extension of the big toe, sensory loss in the big tow, and pain distributed down the back of the thigh and lateral gastrocnemius. S1 disc herniation classically presents with weakness of the gastocnemius causing impaired ankle plantar flexion, sensory loss of the lateral foot and heal and pain distributed down the back of the thigh and gastrocnemius.

Question 30

Why, given that an MRI can localize the disc herniation, if present, should/must a student know the motor and sensory findings of each nerve root level?

Answer 30

We need to be able to match the likely “positive” findings on MRI with the findings on exam! Dr Major will say “clinical correlation suggested”. How else can one do this, if not by knowing what each lesion might cause!

Question 31

Suggest a rationale for not obtaining an MRI in a patient with low back pain and no neurological features. (To be sure, there are public health consequences to this MRI-happy approach. I am thinking about the personal costs to the [fully insured] patient.)

Answer 31

MRIs of healthy patients can lead to false positives and incorrect diagnoses that cause unnecessary stress, psychosocial difficulties and even psychiatric morbidity AND MOST ESPECIALLY OVERTREATMENT. I believe that MRI is a “gateway test” to many (perhaps unnecessary) procedures.

Question 32

What is neurogenic claudication (and contrast with vascular claudication)?

Answer 32

“Claudication” (Latin: limp) refers to painful cramping and/or weakness. It is important to differentiate neurogenic from vascular claudication. “Neurogenic” refers to the fact that the problem originates from a problem at a nerve, but the common theme is ischemia. Neurogenic claudication is often found in patients with spinal stenosis. Neurogenic claudication can cause bilateral or unilateral lateral calf, buttock, or thigh discomfort, pain, and/or weakness. In some patients, it is precipitated by walking or prolonged standing. The pain is typically relieved by a change in position or flexion of the waist. The cause is believed to be ischemia of the lumbosacral nerve roots secondary to compression from structures such as 18 hypertrophied facets, ligamentum flavum, bone spurs, scar tissue, and bulging or herniated discs. Vascular claudication is due to a circulatory problem. Bad circulation leads to ischemia of the calf muscles. Neurogenic claudication can be differentiated from vascular claudication, by the following features: Neurogenic claudication: more proximal, not always present but can be present at rest, not dose dependent and may be relieved by postural changes (leaning forward to make more space in the spine). Basically: vascular claudication causes ‘dose dependent calf pain’—walk more, hurt more; stop, feel better. All the time, every time.

Question 33

What is idiopathic scoliosis and what is its relationship to back pain?

Answer 33

Scoliosis is a lateral curvature of the spine that is usually accompanied by rotation. Idiopathic scoliosis does not have a clear causal agent and it is generally believed to be multifactorial. It is a diagnosis of exclusion. Adolescents with idiopathic scoliosis (“adolescent type”) may present in several ways. In some patients, scoliosis is incidentally found on physical examination. Others have complaints related to the deformity that is caused, such as asymmetry of the shoulders, flank creases, hips, scapulae, or breasts. Still others present because an abnormality was noted during a scoliosis screening at school. Most patients with adolescent idiopathic scoliosis have little, if any, functional limitation or pain. In practice, the presence of scoliosis not be consider an adequate explanation for acute or severe back pain—at least in the sense that if somebody presents with idiopathic scoliosis and pain, the clinician must not simply attribute the pain to the idiopathic scoliosis.

Question 34

Provide a brief description of Carpal Tunnel Syndrome.

Answer 34

Carpal Tunnel Syndrome (CTS) is an entrapment neuropathy due to compression of the median nerve as it passes through the carpal tunnel. The tunnel is at the base of the palm, right above the wrist. It has four sides: 3 of which are carpal bones and the 4th side/top of structure being the transverse carpal ligament. The key clinical point is based on the anatomy: the signs and symptoms must be in the median nerve only; and they need to be related to targets of the median nerve distal to the tunnel itself. That is, objective median nerve function in the forearm should not be affected! (pain is sometimes found there, though) Factoids about who gets CTS (and why): 1. occurs most commonly in patients between 30-60 years of age 2. more common in females. 3. Risk/causative factors: a. anatomical decreases in size of the carpal tunnel (bony abnormalities of carpal bones, fracture) b. POSITIONAL: extreme flexion/extension of wrist may produce symptoms when the hand is in this position (this may be why typing a lot causes symptoms). c. increases in contents of canal (forearm/wrist fractures, tumors (rare) arthritis with bone spurs or synovitis), d. neuropathic conditions (DM, alcoholism, etc), e. inflammatory conditions (RA, gout, nonspecific tenosynovitis, infection), f. alterations of fluid balance (pregnancy, menopause, eclampsia, thyroid disorders, obesity, SLE, amyloidosis, Raynaud disease, etc), and g. external forces (jackhammer?).

Question 35

What are the (chief) complaints in Carpal Tunnel Syndrome?

Answer 35

Numbness and paresthesias in the anatomic distribution of the median nerve: radial 3 ½ fingers (thumb, index, middle, and radial side of ring). Patients may experience pain radiation proximally into the forearm. A common early complaint is awakening in the night due to numbness or pain in these fingers (night-time worsening). Patients may also complain of swelling in the hands, dry skin, and cold hands (less common symptoms). Later, patients may report constant numbness, motor disturbances, and decreased strength (tendency to drop objects)

Question 36

What are the main competing differential diagnoses? What complaints would make you think that a patient has one of these, and not Carpal Tunnel Syndrome?

Answer 36

- C6 or C7 radiculopathy - with radiculopathy expect to see neck pain and pain proximal to the wrist - Osteoarthritis - this may exist concurrently with CTS, but would see tenderness and crepitus on exam (and EMG would be normal unless CTS co-exists) - Ulnar neuropathy - just like CTS but wrong nerve! The sensory sx are on the medical aspect of the hand, distal forearm and 4th and 5th fingers (instead of radial 3 1/2 fingers). No thumb weakness - De Quervian tenosynovitis - extensor tendinitis of the thumb. with this, tend to see pain with movement of thumb and/or wrist along with hardening and thickening of radial styloid. EMG is normal (unless CTS co-exists)

Question 37

What may you find on examination of a patient with moderate or advanced Carpal Tunnel Syndrome?

Answer 37

 Flattening of the thenar eminence;  Weakness of the thenar intrinsic muscles (clinically tested by abduction of thumb against resistance)  Diminished or absent sensation to pin prick in the median nerve distribution  Positive results for Phalen test or Tinel’s test  EMG would likely show focal slowing of conduction velocity in median nerve across carpal tunnel (A note to the interested student: the accuracy/sensitivity/specificity of various diagnostic maneuvers or tests is hard to define: What is the reference standard? If all are compared to, say, “positive EMG” we have a problem, as there people without any Carpal Tunnel symptoms who have a positive EMG; likewise there are some with normal EMGs who seem to have the syndrome… Recall, the word “syndrome” means that the condition is somewhat ill-defined. As treating doctors, we don’t necessarily want to know what the patient has, we want to know what to do with them therapeutically. So the reference question should be “What percentage of patients with a positive Phalen’s test, say, get relief from surgery?” But that is not only an assessment of the test, but also the patients in the study and the surgeon doing the work…)

Question 38

How is Carpal Tunnel Syndrome treated? Why?

Answer 38

There are many treatment options for individuals with CTS, and the treatment choice depends on the severity of the nerve dysfunction, patient preference, and 21 availability. Non-operative treatment options include: rest, wrist splinting, NSAISDs, and oral steroids or corticosteroid injections. In patients who do not respond to more conservative treatment modalities or in patients with signs of atrophy or muscle weakness, carpal tunnel release surgery –cutting the transverse carpal ligament --should be considered. This surgery is performed to decrease pressure on the median nerve. Obviously if there is a precipitating cause (like a wrist fracture) that cause should be addressed expeditiously

Question 39

Is Tinel’s sign a true sign?

Answer 39

Tinel’s sign: tap over median nerve as it passes through the carpal tunnel in the wrist. A positive response is a sensation of tingling in the median nerve distribution over the hand. This is not a sign because it reports a subjective sensation. Signs are objective. I think this is better termed a “wign”. I defined wign as a subjective reaction to a provocative examination maneuver deemed to have some valid relationship to the underlying pathology. This word is pronounced “whine” to remind us it is a spoken response, and its spelling echoes that of sign, reminding us likewise a wign is more definitive than a generalized complaint. The response to Tinel’s test can be considered a wign: pain or paresthesia is a subjective response, but the test is deemed positive only when the complaints match the distribution of the median nerve. (Radiating paresthesia to the fifth finger, ulnar nerve territory, would not be classified as positive.) Other examples include Lasègue’s wign, Kernig’s wign, and Lhermitte’s wign, to name a few. Because symptoms, unlike signs, pass through (and are affected by) the prism of patients’ perceptions, the diagnostic value of a wign may be appropriately less than a true sign.

Question 40

Contrast osteoarthritis with rheumatoid arthritis.

Answer 40

Osteoarthritis: - deterioration of cartilage and overgrowth of bone often due to "wear and tear" that occurs with age - more often affects the larger weight-bearing joints, such as the hips and knees - worse pain at the end of the day, when wear and tear builds up - not a systemic disease, as far as we know - lab tests normal - bone spurs, sclerosis common - 10x more common than RA Rheumatoid arthritis - autoimmune inflammation of the synovial membranes, which leads to the destruction of the articular cartilage - more often affects the smaller joints of the hands, wrists and feet - the stiffness is worse after rest, such as the first thing in the morning and often lasts at least 30 minutes or more - systemic disease: other organs can be affected as well - RA is 3x more common in females vs males - no bone spurs; rather osteopenia more common - 80% of patients are sero-positive (have + rhematoid factor blood test)

Question 41

Given the typical (degenerative) etiology of Osteoarthritis, how then might a 20 year old person have this condition?

Answer 41

Trauma, for sure. Damage to the articular surface directly or via chronic damage from loose ligaments (s/p dislocation). Deformity, such as DDH or SCFE (see below) Maybe genetic?23 The take home point is that DJD in a young person is possible, but not likely, and should be a diagnosis of exclusion.

Question 42

What is the role of body mass vis a vis osteoarthritis? Why might we think that this not be a pure mechanical phenomenon? (hint: Framingham)

Answer 42

Excess body mass increases the load placed on joints which increases stress and accelerates the breakdown of cartilage. However, OA may not be a pure mechanical phenomenon because being overweight has also been associated with higher rates of hand OA --this suggests that a circulating systemic factor may also play a role.

Question 43

What are the cardinal signs of Osteoarthritis of the knee on plain radiographs? How (mechanistically) do they appear?

Answer 43

Cardinal signs of OA of the knee on plain radiographs are evidence of osteophytes, Asymmetric joint space narrowing, subchondral sclerosis, and subchondral cysts. Osteophytes typically develop. Why? Maybe as a (futile/foolish) reparative response. Maybe because of abnormal loads stimulating bone. Asymmetric joint space narrowing occurs as articular cartilage is lost is areas of abnormal load. Subchondral sclerosis is simply the deposition of bone in area under areas of stress—Wolff’s law. Cysts form when joint fluid seeps through the cracks in the cartilage and get into bone and cysts develop as increased blood flow and other changes develop in the subchondral layer with OA.

Question 44

Why is Osteoarthritis painful?

Answer 44

In osteoarthritis, the cartilage may wear away in some areas, greatly decreasing its ability to act as a shock absorber. As the cartilage deteriorates, the joint tips (collapses where cartilage is lost) and soft tissue may stretch (on the tensile side), perhaps causing pain. Fluid in the knee could be under pressure and also painful by simple distension. But the short answer is: we are not sure. Cartilage does not feel pain. It must be the bone or the synovium—but not all “ugly” joints hurt. You cannot look at an xrays and predict necessarily if somebody has pain

Question 45

If both rheumatoid arthritis and osteoarthritis can lead to end-stage destruction of the joint -and both can-why is it important to differentiate between the two?

Answer 45

- because RA is a systemic disorder that can affect many organs of the body; therefore, it is important to check for, manage and prevent other manifestation of the disease - RA has a different prognosis, in terms of overall health as well as joint specific - the diagnosis affects treatment: treatment for RA is not just symptomatic, and it also targets the root cause of the disease: immune abnormalities. This is accomplished with biologics and disease-modifying anti-rheumatic drugs (DMARDS) and Biologics. The goal is not just palliation but to stop disease progression.

Question 46

What is septic arthritis? What are its causes?

Answer 46

Septic arthritis is a bacterial (and less commonly fungal or mycobacterial) infection of a joint. It can be caused by hematogenous spread (most common), direct inoculation (ie: trauma, during surgery) or contiguous spread from infected periarticular tissue. It is possible to get an autoimmune arthritis after a systemic infection; but in that case the joint space itself is sterile. This condition is termed “reactive arthritis” and is grouped under rheumatological, not infectious, diseases.

Question 47

How is septic arthritis diagnosed definitively? What are the temporal limitations regarding our ability to diagnose definitively? How do we get around that?

Answer 47

Septic arthritis is definitively diagnosed by culturing bacteria from synovial fluid. Yet diagnosis by this method is delayed due to the amount of time it takes to grow out the bacterial culture. Waiting is bad as the damage begins once the white cells hit the joint. While waiting for culture results, we can use a clinical decision rule to make a good guess if infection is present: COUNT THE WHITE CELLS AND ASSUME THAT A HIGH COUNT MEANS INFECTION.25 (A positive gram stain may help, but it is specific, not sensitive; and even seeing “bugs” does not tell you which bug is present)

Question 48

How is septic arthritis treated? Why must septic arthritis be treated expeditiously?

Answer 48

Septic arthritis is treated removal of the joint fluid and IV antibiotics. The key consideration is that the body’s own response to the infection may inflict horrible damage on the sensitive articular cartilage. Joint fluid with high white counts is toxic! So even if we don’t think the patient is at risk for getting systemically sick from a joint infection, we must “wash it out” to save the joint itself. Whether you believe this should be done by serial needle aspirations or by surgery says more about your guild membership (surgeon vs non-surgeon) than about your scientific acumen.

Question 49

What is osteomyelitis? What are its causes?

Answer 49

``` Osteomyelitis is and infection of the bone. Osteomyelitis too can be cause by hematogenous spread, contiguous spread from adjacent soft tissues or joints, or direct inoculation (ie: during trauma or surgery) ```

Question 50

Although bone is part of the vascular system (and therefore fractures can cause hemorrhage and metastatic cells can lodge in the skeleton) why might IV antibiotics have trouble reaching areas of infected bone?

Answer 50

Bone grows over the infection, producing a “sequestrum”—ie, infected bone gets walled off. This is a good thing, perhaps, if we had no antibiotics to deliver; but we do, so this wall-it-off strategy is a problem!

Question 51

What is Developmental Dysplasia of the Hip? & How is Developmental Dysplasia of the Hip diagnosed in the neonate and why is it critical to detect this, if present, as soon as possible?

Answer 51

It may be better to think of this condition in terms of its old name “congenital dislocation of the hip” (CDH): the baby is born with the hip out of the socket or unstable. Being out of socket is not good, of course, yet not so much for present function – the baby is not walking on it—but because for the hip joint to grow properly, the (mostly cartilage) head has to be in the socket. If the head is not in the socket, it will be grow to be mal-formed (“dysplastic”). Prompt detection and expeditious treatment allows the hip to remodel and form properly. DDH can be detected on exam – there are a variety of physical exam maneuvers that can be used for diagnosis, including the Ortolani reduction maneuver (abduction and elevation to feel for reduction) and the Barlow provocation test (adduction and posterior pressure to feel for dislocation)—but in high risk patients (Breech position, female gender, first born children, and a positive family history are risk factors) ultrasound is used.

Question 52

What is a Slipped Capital Femoral Epiphysis?

Answer 52

First, you have to know that the femoral head (capitus) has a physis (a growth plate). Then you have to know that the bone towards the end, across the physis, is called the epiphysis Then you have to know that the physis is cartilage-like, and therefore weak And then you can know/imagine that the epiphysis can slip off, a form of a growth plate fracture, really. So what else do you need to know?28 a. who gets this? 1 in 10,000 kids, 4x more common in blacks, usually during early puberty, when the physis active. Obesity and endocrinopathies are risk factors b. How do you diagnose? Xray—but not that the complaint may be KNEE pain! c. How do you treat? Pin it in situ d. Why do you treat? Prevent progression, symptom relief

Question 53

What is Perthes (rhymes with Her’-Sneeze) Disease?

Answer 53

Perthes is AVN of the femoral epiphysis (without a slip) in kids. The typical patient is a 10 year old boy with a limp. The cause is not known. The treatment is supportive—non weight bearing to prevent further collapse, maybe, and hope that the epiphysis revascularizes (which can happen). It is often unilateral. The older the patient, the worse the prognosis (consider: AVN with collapse in an adult has no cure; the closer one gets to being “adult” the more the disease behaves like the adult form of AVN.)

Question 54

Both gout and septic arthritis can cause acute pain and swelling of a joint. How can they be distinguished?

Answer 54

Symptoms of both gout and septic arthritis include redness and swelling present in just one joint and pain that is worse with movement. The key distinction is the results of a culture of the joint fluid obtained by aspiration: a positive culture defines an infection. One could consider the history (patients with known gout are of course more likely to have gout as the cause, as compared to patients without that history; patients with immune suppression are of course at higher risk for infection). One could also measure the concentration of white blood cells in the aspirate: the number of cells is higher in cases of infection. The problem is that there is no cut off that perfectly segregates the two. One can also examine the aspirate under the microscope: crystals suggest gout, and bacteria indicate infection. Yet crystals can be seen in cases of infection as well (where both conditions are present simultaneously). Because culture results are not known immediately, all of the information listed above should be considered, especially when urgent treatment is needed.

Question 55

Developmental Dysplasia of the Hip, a Slipped Capital Femoral Epiphysis and Perthes Disease might cause arthritis of the adult hip (ie, later in life). Why might successfully treated Developmental Dysplasia of the Hip have the best prognosis whereas untreated Developmental Dysplasia of the Hip might present the biggest treatment (surgical reconstruction) challenges?

Answer 55

DDH is truly treatable: relocate the hip before it malforms, and that is tantamount to a cure. SCFE pinning is basically halting progression. “treatment” of Perthes is lots of prayer At the other extreme, untreated DDH is the worst, because not only do you have bad arthritis –as you might with the other two, too—but you don’t even have normal anatomy with which to reconstruct the hip! There is no socket either—the pelvis, too, needs normal anatomy on the other side of the joint, ie femoral head, to form correctly. If either is missing, then the other side of the joint can be marred.

Question 56

What is “club foot”? Club foot is technically known as congenital talipes equinovarus (talipes is from Latin talus=ankle + pes=foot; equino-=of or resembling a horse and –varus=turned inward)

Answer 56

1. Club foot is a developmental deformity of the foot in which one or both feet are excessively plantar flexed, with the forefoot swung medially and the sole facing inward. 2. The main anatomic abnormality is in the TALUS but screwing up (overflexing) a bone in the middle of the action messes up evertying else: the talo-calcaneo-navicular joints; the soft tissues on the medial side of the foot; and the gastrocsoleus/Achilles;etc. 3. The forefoot is “normal” but because the hindfoot is bad, the forefoot does not strike the ground normally. Patients with (untreated) club foot often appear to walk on their ankles, or on the sides of their feet. 4. Most cases are idiopathic, but some are associated with chromosomal anomalies. 5. Dr Ponsetti, from Iowa via Spain, 1915-2009 (roughly), devised a method that WORKS for manipulating the foot back to normal with serial casts. One of the few areas where low tech beats high tech so decidedly that even in America we do it this way

Question 57

What is a Charcot joint?

Answer 57

1. if you don’t feel pain, you hand stays in the fire; likewise, if you don’t feel overuse in your joints you won’t let up and will destroy the joint 2. hence: decreased sensation in cases of peripheral neuropathy leads to JOINT DESTRUCTION (mental image: pimple on one butt cheek, sit on the other side or get a bed sore) 3. alternative or complimentary theory: micro-vascular disease of DM leads to altered bone metabolism 4. main cause today: diabetes. Historically: syphilis (NB: syphilis would tend to support theory of lost sensation as cause, I say, thinking out loud) 5. affects the foot mostly 6. may look like cellulitis/infection 7. vicious cycle: deformity leads to bony prominences leads to ulcers leads to infection leads to more bony deformity.

Question 58

Why might a 12 year old boy with a swollen ankle and pain on the distal fibula be treated with a cast despite normal xrays?

Answer 58

TAKE HOME MESSAGE: 12 year olds don’t get sprains. (OK, Maybe they do, but you have to assume that a sprain is a non-displaced growth plate fracture. If you want to save the patient the torture of wearing a cast that may not be needed, an MRI can be used. That’s what my son got…but hard to argue that this was cost effective. To consider the questions about ankle sprains and Achilles injuries, let’s first go over the anatomy, AP view to the left, lateral on the right: In this next view, I have added the calcaneo-fibular ligament –one of the major supporting structures that is stretched with an inversion sprain (twisting your ankle medial side up, like when you partially land on another player’s shoe). And now I have added the fibular growth plate31 Ok, so you are 12 year old and twist your ankle medial side up, by partially landing on another player’s shoe The force is shown in blue. This is TENSILE on the lateral side and compressive medially: Something’s got to give: If you have no growth plate, left panel, you sprain your CF ligament; but in a twelve year old, the growth plate is weaker, so it gets injured. Now, it there are “normal xrays” then by definition this a non-displaced fracture. This is an urgent medical situation, however, as we want to keep it non-displaced! It needs a cast, typically.

Question 59

Why do 40 year old men (in particular) rupture their Achilles tendons? What are the biological and mechanical steps leading to tissue failure?

Answer 59

40+ year old men, don’t ask me how I know, reside in that strange place of a) having accumulated plenty of tissue damage over the years (walking 1 mile a day for 45 years is almost 100,000,000 steps) yet b) have not quite caught on that they are old and decrepit So they try to do too much. The Achilles tendon not only gets beaten up, it is about as far from the heart as a tendon can get, and does not have a great blood supply. So why does the tendon fail? Well, what does it do? The Achilles powers plantar flexion (left) but also resists dorsiflexion (right) [the light blue signifies the STARTING position] and the blue arrow shows the motion of the foot The motion of the muscle on the right is called an eccentric contraction—the muscle actually lengthens as it works (“negative” work is how the weight lifters call it) It turns out that ripping the tendon almost always happens with resisting dorsiflexion, like when you land. Ditto patellar tendon and quad tendon. We can’t avoid eccentric contraction, because it happens with every step of gait. You land on the ball of your feet, and the gastroc/soleus decelerates your heel as it “lands” on the ground. The importance of this is that if you wanted to prevent Achilles injuries in middle aged men, you could do this with an extension block on the shoe or with a soft heel cup (do you understand why?—the extension block on the TOP of the shoe prevents excessive dorsi-flexion; the heel cup takes it easy on the gastroc. Extra credit: which would be better for PAIN control (not just tear prevention) Hint: which does Dr Scholl’s sell?

Question 60

The phrase “just a sprain” may grossly understate the impairment such an injury imparts. Why might a grade ONE ankle sprain cause long term impairment?

Answer 60

Let’s revisit that inversion sprain. There are two injuries here, really. Tension on the CF ligament and compression on the talus. Even if the CFL is not stretched or torn, you a) can get damage to the proprioceptive nerve fibers in it and get a sense of unsteadiness despite being intact b) post traumatic arthrosis (arthritis) of the tibio-talar joint