MCQs – Hand 2

MCQs-Hand 2
adducting the thumb metacarpal and keeping it there produces a webspace contracture!

Digital amputations: try replanting all thumbs; single digits that have been amputated DISTAL to the FDS insertion, and multiple digit injuries. Avoid trying to replant an avulsed, degloving-type amputation.

An intrinsic plus contracture or deformity usually shows up as MCP flexion, and IP joint extension. Intrinsic minus contracture (clawing) shows up as MCP extension, IP joint flexion.

The oblique pulley is the most important structure supporting thumb flexion (akin to the A2 pulley of the finger)

Hook of hamate fractures are best seen on CT or carpal tunnel views.

When excising hook of hamate fractures, beware of the deep branch of the ulnar nerve.

The best tendon transfer for opponensplasty is probably FDS of 4, brought through a little pulley made in FCU. (in the relevance of a low median nerve palsy, where opposition is severely limited by abductor pollicis brevis paralysis). “The motor has adequate power, more than sufficient excursion, and requires only slight change of direction by a pulley.” In high median nerve palsy, where FDS is also involved, probably have to do an extensor indices transfer through the 3rd metacarpal interspace.

Swan neck deformity can occur as the result of a long-standing mallet deformity. The distal extensor mechanism is lengthened, and allows dorsal migration of the lateral bands at the PIP joint.

If you cut your finger 1 mm proximal to the distal flexion crease and are unable to demonstrate DIP motion, you’ve cut the FDP. However, if you are also unable to demonstrate flexion of PIP with the other fingers held in extension, then you probably have a congenital absence of FDS, because 1 mm proximal to the distal flexion crease is probably still quite a bit distal to the broad insertion of FDS. Even if you got some of the FDS insertion, it is pretty broad, encompassing much of the volar surface of the middle phalanx – you are unlikely to have cut the whole tendon at this level, so close to the distal flexion crease.

Wartenberg’s Syndrome is a painful neuroma of the superficial radial nerve. If bothersome enough, dissect out the ends, and bury them in muscle.

The collateral ligaments are directly attached to the volar plate at the PIP joint.

A contracture of the oblique retinacular ligament will cause an extension contracture of the DIP, thereby limiting DIP flexion (part of the pathophysiology of Boutonniere deformities.) The oblique retinacular ligament appears to lie volar to the axis of rotation of the PIP, but then curls dorsally to lie on dorsal to the axis of rotation of the DIP. When contracted (as in the Boutonniere deformity), it maintains the extension of the DIP. Because it lies volar to the axis of the PIP, it contributes to the flexion deformity of the PIP.

The tight structures in a chronic Boutonniere deformity are the oblique retinacular ligament and the transverse retinacular ligament. The oblique retinacular ligament maintains the DIP extension, while the transverse retinacular ligament keeps the lateral bands subluxed volarly and maintains the PIP flexion. The oblique retinacular ligament, being volar to the axis of the PIP, also contributes to maintaining the PIP in flexion. The triangular ligament is attenuated because the lateral bands are pulled volarly.

If the intrinsics are paralyzed, the long extensors are best able to extend the IP joints with the MCPs in flexion. If they are not held in flexion, the long extensors tend to hyperextend the MCPs and lose there extension force on the proximal phalanges.

During the open volar approach to a complex MCP dislocation, the neurovascular bundle is most at risk.

Complex MCP dislocations are associated with skin dimpling, parallelism between the metacarpal and proximal phalanx, and a sesamoid within a widened joint space.

During the complex dislocation, the metacarpal head ruptures between the lumbrical radially and the flexor tendons ulnarly. These two

Forearm Fractures – General Principles

Forearm Fractures – General Principles

Anatomy
– distal radial physis closes about age 17 in girls, 18 in boys
– proximal radial physis closes about age 17-18
– because the radius and ulna are not completely cylindrical, you can tell malrotation by the width of the proximal and distal fragments at the fracture site.
– the annular ligament is most responsible for maintaining the proximal radioulnar joint – most stable in supination
– the TFC complex and ligaments is responsible for maintaining the DRUJ

Rotational Considerations
– supination tends to shorten the ulna on the radius (ulnar minus) while pronation tends to lengthen the ulna relative to the radius (hence, if looking for ulnar variance, must do it in neutral)
– interosseous membrane and space is narrowest in pronation, widest in neutral to 30 of supination
– 10 degrees of angulation in the midshaft limites rotation 20-27 degrees
– bayonet apposition does not limit rotation as long as the interosseous space is maintained

Deforming Forces
– biceps and supinator flex and supinate the proximal radius fragment
– pronator teres pronates the mid-radius fragment
– pronator quadratus pronates distally
– it is hard to predict how to immobilize the arm based on these deforming forces and the level of the fracture. Just be aware of them!

Remodeling Potential
– the amount of spontaneous correction is dependent on age, amount of residual angulation, the fracture to epiphyseal plate proximity, and relationship of deformity with plane of motion
– don’t depend on remodeling after age 11; best remodeling is seen in kids less than 8
– average rate of remodeling at the distal radius is .9 degrees per month, or 10 degrees per year
– volar and ulnar angulation result in a higher rate of correction than do dorsal angulation
– increased correction takes place when there is greater deformity
– bayonet apposition is acceptable and will remodel in a child less than 8-10 if rotation is correct, if interosseous space is preserved, and there is no angulation!

In general:
Accept no more than 10 degrees of angulation (maybe 20 in a child less than 8)
Accept no malrotation
Accept bayonet apposition only in a child less than 10.

MCQs – Hip Recon 3

MCQs-Hip recon 3
Volume of wear = K x load x distance Where K = constant for materials
– the highest K is with metal on metal; lowest K is with ceramic on poly; in between is metal on poly.
– notice that DISTANCE is an important factor – hence, the bigger heads have more volumetric wear because with each movement, there is more distance covered.

– the best treatment for staph epi is vancomycin

– the hardest bug to eradicate in THA is pseudomonas; it may in fact be staph epi, but in general, the gram negatives are hardest to get rid of.

– the most common bug in an indolent infection 6 months postop THA is going to be staph epi; in a fulminant infection, it is most likely staph aureus.

– in doing a THA after a patient has a Salter osteotomy – beware the lack of posterior wall. Their acetabulum has now been retroverted, so you don’t want to put your component in the same alignment as the native acetabulum. Note that when you put your cup in with adequate anteversion, because the acetabulum is so retroverted, there may be quite abit of anterior lip overhanging – you must cut this out or you’ll impinge.

– there are many factors to consider in doing THA in dysplastics
– Femur: short neck, small canal, straight canal, trochanter way around the back, significant anteversion, need for shortening osteotomy
– Acetabulum: antero/superior bone defect, high riding, need to find native floor

– the anticoagulated patient who develops a wound hematoma and complete femoral nerve palsy – reverse the anticoagulation and consider what to do next. Many questions suggest that you can just observe. Some authors suggest that you should decompress this. Hard to know what to do. I think I’m gonna go in and decompress this, or get radiology to put in a drain.

– to decrease the stress on a prosthetic stem, you can increase the cross sectional area of the stem. ???

– Stress = My/I where M=bending moment, y= linear distance from neutral axis, and I = moment of inertia. The moment of inertia is significantly increased (r to the 4th power) by increasing the radius, and hence the stress would decrease.

– from Campbell’s: “increasing the modulus of elasticity, the stem length, and the cross-sectional area of the stem increases the stress in the stem, but decreases the stress n the cement and proximal third of the femur” I think he means that you increase the stiffness of the stem and thus potentiate stress shielding.

– remember: modulus of elasticity is a material property, not a structural property. Modulus does not change with thickness, length, cross-sectional area, etc. The overall stiffness of an implant may change though, but this is not the same as the modulus. Note that viscoelastic materials do change with time, and so their modulus would change a little over time (eg. Polyethylene)

– lucency in zones 1 and 7 represent loosening in a PCA component where the beads are all up at the top (in zones 1 and 7)

– if you see a patient who dislocates her THA during the transfer but you get it reduced in the PAR – treat the patient with bed rest and an abduction pillow if you are happy with the components otherwise.

– if you get huge bleeding after putting a retractor around the anterior column – you’ve hit the femoral artery.

– AVN in adults is mostly likely to be associated with injury to the lateral epiphyseal artery

– AVN typically involves the anterosuperior aspect of the head.

– Alcaptonuria is not a cause of AVN of the femoral head. Alcaptonuria is the excretion of black urine and is seen in patients with Ochranosis, a deficiency of the enzyme to break down homongentisic acid. AVN is seen with Gaucher’s, sickle cel, Caisson’s disease, and dislocation

– the appearance of AVN on MRI – would see a double line sign on T2; on T1 the dead area is DARK, on T2 the dead area is BRIGHT.

“The earliest finding in AVN is a single-density line (low signal) on T1 that presumably represents the separation of normal and ischemic bone. On T2 images, a second, high signal

MCQs – Knee Recon 1

MCQs-Knee recon 1
MCQs-Knee recon
– HTO – young active patients with less than 15 of varus, less than 10 degree flexion contracture, and primarily unicompartmental changes. The lack of an ACL is NOT a contraindication to HTO.

– watch out for posterior sag in patients with PCL retaining knees – their PCL may not be so good and they may develop significant AP instability

– porous ingrowth is dependent on a few things: avoidance of micromotion; approximation of the surfaces; and size of pores (150-400 microns). The optimal pore volume or volume fraction porosity is 30-40%. Obtaining intimate bone contact and avoiding micromotion are the most important factors for bone ingrowth. Titanium has not been shown to be more conducive to bone ingrowth than cobalt chrome.

– cement failure in femoral components is caused by microfracture and fragmentation of cement

– ultimate postop knee ROM is most predicted by PRE-OP knee ROM

– for medial unicompartmental knee replacement, to maximize longevity of the prosthesis it should neither rock nor tilt as the knee is put through a range of motion. The principles of uni’s are different from total knee. It is NOT recommended to put the knee in valgus, as this can lead to deterioration of the lateral side. Slight mechanical varus is acceptable, especially with implants that rest on cortical bone. Tibial loosening is the biggest problem with uni’s, so it is important that the component be well-positioned – it should not “yawn” anteriorly with knee flexion.

– comparing simultaneous bilateral vs staged total knee replacements: the only significant difference has been duration and cost of hospitalization. There is no significant difference in P.E., ROM, infection, or component loosening.

– PCL retention supposedly improves femoral rollback in flexion.

– in rheumatoids, do their hips before knees – it is easier to rehab after the total hip.

– in patients less than 55 yrs, the 10 year survivorship is actually pretty good – comparable to older patients. They are better than those in really young though.

– reducing cement porosity improves the compressive modulus of cement (increases its strength)

– The presence of a varus alignment with a high adductor moment actually predicts a poor response to HTO.

– in aspirating TKA – there is a 25% false negative result rate – need to go by clinical history and suspicion!

– the more constrained the TKA, the higher the rate of component loosening – particularly the tibia. Thus, a hinged component would be worse than a TCIII, which would be worse than a regular TKA.

– there are four independent factors that are associated with a significantly LOWER risk of failure: PRIMARY total knee arthroplasty, rheumatoid arthritis, age over 60, and the use of metal backing for the tibial component

– for osteochondral allografting of the femoral condyle lesions – tissue matched fresh osteochondral grafts produce excellent incorporation; cryogenically preserved grafts unfortunately lose most of the chondrocytes. Non-matched fresh grafts are immunogenic and are broken down.

– when looking for osteonecrosis of the femoral condyle, look on T1 MRI for loss of the high intensity signal from the marrow fat

– patients with inflammatory arthritis should not be left with their native patella in TKA. They should be resurfaced because they will have significantly less peripatellar pain than in those who do not undergo resurfacing.

– beware trying to do any reconstruction in a patient with previous sepsis, especially pseudomonas! Do arthrodesis instead.

– external rotation of the femur is a good thing for patellar tracking

– the most common cause of failure in revision TKA are patellar malalignment, component loosening, and sepsis. The most common is extensor mechanism or patellar problems.

– 10-15 year survival of TKA is about 90%

– when doing an HTO, make sure you don’t cut the medial cortex – you’ll destabilize the thing!

– successful knee arthrodesis is most dependent on the degree of bone loss.

Knee – Medial Anatomy

knee-medial anatomy
THE MEDIAL COMPARTMENT

The Medial Collateral Ligament

The medial collateral ligament originates from the adductor tubercle and proceeds distally 10-12 cm, fanning out and inserting over a broad area of the tibia under the pes anserinus, blending with the periosteum. It has a superficial and a deep component. The superficial ligament has no attachments to the underlying structures. The deep portion inserts into the superior aspect of the medial meniscus. The ligament can also be thought to have anterior and posterior fibers. The anterior fibers are thick and tighten during knee flexion, while the posterior fibers are relaxed.

The Medial Capsuloligamentous Complex

The medial capsuloligamentous complex is a complicated structure. Anatomically, it has three layers, which are numbered with Roman numerals I, II, and III from superficial to deep.

Deep Layer (III)

This is the capsule of the knee. It can also be conceptualized as anterior, midportion, and posterior components. It is thin anteriorly. The midportion is the deep layer of the medial collateral ligament, which has attachments to the medial meniscus. The posterior component fuses with the middle layer (II) to become the posterior oblique ligament. Further posteriorly, the layer thins, and is reinforced by the semimembranosus tendon, which is an important stabilizer of this posteromedial corner of the knee.

There are five reflections of the semimembranosus tendon: 1. oblique popliteal ligament. 2. posterior oblique ligament and medial meniscus rim. 3. posteromedial tibial metaphysis. 4. anteromedial tibial metaphysis, running deep to the superficial MCL. 5. investing fascia around the popliteus muscle

Intermediate Layer (II)

This layer contains the superficial medial collateral ligament. Posteriorly, this layer and the deep layer form the posterior oblique ligament which has an attachment to the posterior portion of the medial meniscus. This area is an important insertion for the semimembranosus tendon, as a secondary stabilizer in the ACL deficient knee. Some controversy exists about whether the posterior oblique ligament is truly a separate ligament or simply the posterior portion of the superficial MCL

Superficial Layer (I)

This layer consists of the deep fascia of the thigh and leg, and sartorius muscle. Anterior to the superficial MCL, the fibers of the intermediate and superficial layers are inseparable.

The “Posteromedial Capsule”

The “posteromedial capsule” refers to the confluence of the capsuloligamentous layers II and III posterior to the medial collateral ligament but anterior to the posterior cruciate ligament. The posteromedial capsule plays a crucial role in the medial and rotatory stability of the knee; the integrity of the capsular complex directly affects the prognosis of injuries to the MCL because it adds a component of rotation to the tears.

Fowler – Exertional Compartment Syndrome

Fowler-Exertional Compartment syndrome
-2 incision fasciotomies (ant-lat)
-find nerve distally
-subcutaneous tunnel
-long 9 inch scissors

MCQs – Metabolic 2

MCQs-Metabolic 2
with decreased rates of mineral apposition on tetracycline labeling.
– vitamin D resistant rickets is also known as familial hypophosphatemic rickets and is inherited as a sex-linked dominant trait; it is caused by a renal inability to handle phosphate (there are a number of types of vitamin D resistant rickets, of which this is type I.

– secondary gout is associated with myeloproliferative and lymphoproliferative disorders such as multiple myeloma, leukemia, erythrocytosis, and hemolytic diseases such as sickle cell

– for newly diagnosed CPPD, you should get the following bloodwork: calcium, magnesium, phosphorus, glucose, alk phos, ferritin, iron and iron binding capacity, TSH, and uric acid. Patients with hemochromatosis often get a CPPD picture, and you should rule this out. Ochronosis is also associated with CPPD.

Ochronisis (Alkaptonuria) – rare, inherited deficiency of homogentisic acid oxidase; homogentisic acid is retained in the body and deposited as a pigmented polymer in the cartilage, skin, and sclerae (the darkening of these tissues is called ochronosis). Because the pigment is preferentially deposited in cartilage, a degenerative arthropathy is inevitable, beginning in the 4th decade. It begins in the spine with multiple vacuum discs, then the entire spine showing ossification of discs and or narrowing and collapse. Look for chondrocalcinosis in multiple joints. Look for a history of passing dark urine, or fresh urine turning black on standing.

Hemochromatosis – autosomal recessive disorder causing excessive body iron stores and deposition of hemosiderin causing tissue damage and organ dysfunction. Markedly elevated ferritin; increased serum iron concentration with at least 60% saturation of serum iron-binding transferrin. Diagnosis is confirmed by liver biopsy (the liver is radiodense too) showing hemosiderin in parenchymal cells; also may show fibrosis, cirrhosis, or even hepatoma. Chondrocalcinosis is characteristic of the arthropathy and a radiographic feature at some time in 50% of patients. The finding of chondrocalcinosis should always suggest the possibility of hemochromatosis. The arthropathy usually is of the hands, especially MCP (2 and 3) and PIP joints. May also get shoulders, knees, hips.

– the large, radiodense liver is the MCQ tip-off to think of hemochromatosis!

– PTH influences calcium hemostasis by influencing vitamin D production (amongst other things). Also gets osteoclasts working, and increases renal excretion of phosphate. Via vitamin D, it increases calcium absorption in the gut, increases calcium reabsorption in the kidney, and increases calcium breakdown from bone.

– vitamin D (1,25 (OH)2 Vit D) is the most important for gut absorption of calcium

– PTH does not work on the hydroxylation of vitamin D in the liver; it works at the kidney!

– osteocytes are directly stimulated by calcitonin and inhibited by PTH; ? decrease serum calcium with calcitonin is due to osteocytes working to lay down bone?

– carpo-pedal spasm is caused by hypocalcemia

– remember Mankin’s rules: nerve, brain, skeletal muscle – irritability is inversely proportional to calcium; while cardiac muscle irritability is directly proportional to calcium.

– hypercalcemia – polyuria (phosphate diuresis), poydipsia, constipation, lethargy, disorientation, hyporeflexia,

– renal osteodystrophy patients may have leg pain from extraskeletal calcification, fractures through Looser’s lines, periostitis, and osteitis fibrosa (subperiosteal erosions)

– steroids produce bone loss primarily by suppressing osteoblasts. It inhibits intestinal calcium absorption, leading to mild secondary hyperPTH and osteoclastic absorption. It also stimulates renal calcium excretion.

– myositis ossificans progressiva – has increased alk phos

– The x-ray findings of patients with rickets: widened physis. The epiphyseal line is irregular, cupped, or widened. The zone of provisional calcification, which is ordinarily a thin dense white line on x-rays, appears

Amputations I – 3

Amputations 3
Krukenberg’s Amputation This kineplastic operation transforms the
transradial residual limb into radial and ulnar pincers capable of strong
prehension and excellent manipulative ability due to the retention of
sensation. Due to psychologic considerations, it is generally restricted to
blind bilateral amputees who cannot use visual cues to operate their
prostheses (Fig. 2).

Elbow Disarticulation/Transhumeral Amputation Functionally, both
levels require two acts to develop prehension, making these amputations
significantly less functional and making the prosthesis heavier than the
prosthesis for amputation at the transradial level. The length and shape of
elbow disarticulation provides improved suspension and lever arm capacity
compared to the transhumeral amputation. The drawback is cosmetic, because
the elbow will be too far distal and the forearm shank too short for the
limbs to be of equal length. Prosthetically, the best function with the
least weight at the lowest cost is provided by hybrid prosthetic systems
combining myoelectric, traditional body-powered, and body-driven switch
componentry for elbow disarticulation or transhumeral amputation.

Patients with a complete unreconstructable brachial plexus injury can
achieve function by amputation of the insensate dead-weight arm, leaving a
sensate residual limb which can be fitted with a prosthesis. If no
voluntary shoulder motion remains, shoulder fusion allows scapulothoracic
motion to drive the prosthesis.

Shoulder Disarticulation/Forequarter Amputation These levels of
amputation provide minimal function, because the patient must sequentially
control two joints and a terminal device. Limited function can be achieved
with a manual universal shoulder joint positioned by the opposite hand,
combined with a lightweight hybrid prosthetic components.

Lower Limb

Two major recent advances in lower limb prosthetics are socket design
and fabrication, and dynamic-response feet. New plastics allow sockets to
be lighter and more flexible, and therefore, more comfortable.
Computer-assisted design and fabrication allow more efficient fabrication
with the newer materials. The standard quadrilateral prosthetic socket for
transfemoral amputees is gradually being replaced by the newer ischial
containment socket designs, which more efficiently transfer load by total
contact. Silicone sleeves, used primarily in transtibial levels, improve
comfort and suspension. Dynamic response feet now provide spring and
push-off to the amputee’s gait, probably lessening the energy demands for
walking or running.

Toes The great toe, primarily, and the lesser toes act as
stabilizers during stance phase. Ischemic patients generally ambulate with
an apropulsive gait pattern, so they suffer little disability from toe
amputation. Traumatic amputees will lose some late stance-phase stability
with toe amputation. When amputation of the great toe is necessary, an
attempt should be made to salvage the proximal aspect of the proximal
phalanx with the insertion of the flexor hallucis brevis in order to
maintain some stabilizing function. Isolated second toe amputation should
be amputated just distal to the proximal phalanx metaphyseal flare to act
as a buttress that prevents late hallux valgus.

Ray Resection Single outer (first or fifth) ray resection functions
well in standard shoes. Resection of more than one ray leaves a narrow
forefoot that is difficult to fit in shoes. Central ray resections are
complicated by prolonged wound healing, and rarely outperform midfoot
amputation.

Midfoot Amputation There is little functional difference between
transmetatarsal and tarsal-metatarsal (Lisfranc) amputation. The long
plantar flap used in these amputations acts as a myocutaneous flap and is
preferred to fish-mouth dorsal-plantar flaps. Transmetatarsal amputation
should be performed in the distal shaft to retain lever arm length, or
through the proximal metaphyses to prevent late plantar pressure ulcers
under the residual bone ends. A percutaneous Achilles tendon lengthening
should be performed with the Lisfranc amputation to balance the foot to
prevent the late development of equinus or equinovarus. Late dynamic varus
occurring during stance phase of gait can be corrected with lateral
transfer of the tibialis anterior tendon. Midfoot amputees rarely require
the stability of high-topped shoes, generally being sufficiently stable
with standard tie shoes.

Forearm – Volar Approach (Henry’s)

Forearm – volar approach (Henry’s)

* position – supine with tourniquet

*

41 – Tibia/Fibula Proximal

41-Tibia/Fibula Proximal

A-Extra-articular
41-A-1 avulsion
41-A-2 metaphyseal-simple
41-A-3 metaph.-comminuted
B-Partial articular
41-B-1 pure split
41-B-2 pure depression
41-B-3 split-depression
C-Complete articular
41-C-1 simple articular + simple metaphysis
41-C-2 simple articular + comminuted metaphysis
41-C-3 comminuted articular