Genu Valgum

Genu Valgum
Approach to Genu Valgum

First thing: consider the differential diagnosis
– physiologic knock knees – should max out at around 12+/-8o at 3-4 years of age
– bony dysplasia – MED, SED, Morquio’s,.
– hypophosphatemic rickets – usually varus, but can be valgus
– proximal tibial fracture – often develop valgus deformity once healed
– pseudoachondroplasia

As always, do a full history.
– What’s the time course of the problem? How old is the patient? – valgus should be turning around at 3-4 yrs
– Family history? Hypophosphatemic rickets is an x-linked dominant trait
– Overall health, weight gain, motor milestones, growth and development – short stature (rickets or one of the bony dysplasias)
The key is to be looking for hints that this is something other than simple physiologic knock knees
– on the exam, you fuckin’ better be thinking that this is not simple physiologic knock knees!

Do a physical
– measure the deformity and do a knee exam looking for laxity, etc.
– note the height of the patient (rickets patients are short!)
– do a general physical to rule out any dysmorphic features and examine the hips

Get standing AP x-rays, and have low threshold for getting entire femur to see hips and entire tib/fib to see ankles.
If you’re not sure if this is part of a generalize skeletal dysplasia, get a skeletal survey!


– in general, gnu valgum is associated with more patellofemoral problems than genu varum
– if they are 30-36 months old and otherwise completely normal – observe; even if they are >20 degrees, they may resolve.
– non surgical management is not practical for these patients.

For physiologic knock knees
– wait until they’re 10 years of age, have > 10 cm intermalleolar distance, or >15-20 degrees of valgus – then consider a hemi-epiphyseodesis if you are confident you know how much length they are going to gain on that other side; or medial physeal stapling if unsure (you can take out the staple – but you are not guaranteed that it will continue to grow once you take out the staple)

– ie. use a hemi-epiphyseodesis when you’re fairly certain that overcorrection will not occur, but use staples when you aren’t sure or when the growth parameters are abit weird.

Note: in general, if you are operating on a genu varus – you want to correct them bigtime (basically OVERcorrect them.) But in genu valgum, you want to just get them about neutral, maybe slight valgus. Do not overcorrect the valgus knee.

DDx Hip Pain

DDx Hip Pain
Differential Diagnosis of Unilateral Hip Pain

– congenital coxa vara (probably not painful until later)
– proximal femoral focal deficiency

– Slip capital femoral epiphysis
– Femoral neck, intertrochanteric fracture or stress fracture
– LT or GT avulsions, ASIS avulsion
– Ischial, pubic, ilium fractures

– dislocation/dysplasia (probably not painful quite as yet, but may be)
– developmental coxa vara
– idiopathic chondrolysis

– Perthes disease
– post-traumatic
– sickle cell, Gaucher�s, or idiopathic osteonecrosis

– toxic synovitis, bursitis, osteitis
– juvenile rheumatoid arthritis
– other seronegative spondyloarthropathies – Reiters, psoriatic, ank spond

– benign – UBC, ABC, EG, chondroblastoma, osteoid osteoma, osteoblastoma, fibrous dysplasia, GCT (abit young for this)
– malignant – ostosarcoma, Ewings, leukemia/lymphoma

– septic arthritis
– proximal femoral osteomyelitis
– psoas abscess

Metabolic – rickets??

RA Finger Deformities


– varying spectrum of deformities, caused by intrinsic tightness, lateral band displacement, rupture of the central slip, or abnormalities of the flexor or extensor tendons, including rupture or tenosynovitis

Intrinsic Plus Deformity (Intrinsic Tightness)

– with the intrinsics tending to flex the MCP�s and extend the IP�s, when the intrinsics are tight, they PIP joint cannot flex when the MCP is extended (The MCP extension tightens up the intrinsics even further so that the PIP cannot be flexed fully). When the MCP�s are flexed, the intrinsics are slackened, and the PIP can flex. This is the basis of the Bunnell test.
– be careful when doing the Bunnell test in rheumatoids – it must be done with the proximal phalanx in line with the metacarpal. If it is ulnarly deviated (which is common), the test will not be accurate.

Littler – release of intrinsic muscle contractures (Fig 75-10, page 3669)

– basically, incises the oblique fibers of the extensor aponeurosis into the extensor tendon. The transverse fibers are preserved to avoid hyperextension of teh MCP joints
– after the oblique fibers have been cut, the PIP joints should have full passive flexion with the MCP�s in extension.

Swan-Neck Deformity

– described as a hyperextension deformity of the PIP and flexion deformity of the DIP, with flexion at Phillip E. 2
times of the MCP
– there seems to be a number of different ways for this deformity to form

– Start at the DIP: may begin with the disruption of the extensor tendon at the DIP, causing a mallet deformity; then, with secondary overpull of the central tendon, the PIP is hyperextended
– Start at the PIP: may begin with synovitis at the PIP causing tightening of the lateral bands and central tendon, and adherence of the lateral bands in a fixed dorsal position – thus, the PIP is hyperextended. With the lateral bands stuck in this dorsal position, they are unable to extend the DIP, and a mallet deformity may develop without actual rupture of the extensor tendon at the DIP. This requires synovectomy of the PIP, mobilization of the lateral bands, and release of the skin distal to the PIP.

Lateral band release is shown and described on page 3620

Nalebuff, Feldon, Millender – categorized swan-neck deformities into four types

Type I: flexible deformities
– require dermodesis, flexor tenodesis of the PIP, fusion of the DIP, reconstruction of the retinacular ligament

Type II: intrinsic muscle tightness
– require intrinsic release, plus one or more of the above procedures

Type III: stiff deformities but without joint destruction
– require joint manipulation, lateral band mobilization, and dorsal skin release

Type IV: stiff deformities with joint destruction
– require arthrodesis of the PIP or, in the ring and small fingers, Swanson arthroplasties

– consider flexor sublimis tenodesis at the PIP joint in addition to the release of the lateral bands. Beckenbaugh thinks that sublimis laxity due to tenosynovitis is a contributor to the development of these deformities, and he treats them with this sublimis tenodesis, brining the PIP down into about 30 degrees of flexion.

Arthroplasty of the PIP joint can only be undertaken when there is near normal function at the MCP joint proximally

Boutonniere Deformity

– common but not unique to rheumatoid arthritis
– caused by synovitis at the PIP causing the central slip to stretch out and the lateral bands to sublux volarly to a position where they maintain the flexion deformity at the PIP and cause the secondary hyperextension at the DIP. A compensatory hyperextension of the MCP may develop, but this is usually not fixed.

– if flexible, with normal x-rays, the lateral bands may be repositioned after PIP synovectomy and extensor tenotomy over the middle phalanx (Dolphin Fowler procedure)
– for moderate deformities with satisfactory xrays, the central slip can be reconstructed using the lateral bands or a tendon graft
– for severe deformities, the long,

Keinbock’s Disease

Keinbock’s Disease

What are the association/possible etiologies of Keinbock�s?
– trauma – repetitive or single; although, severe trauma (perilunate dislocations) often do not get this
– ulnar variance – the ulnar negative wrist
– vascular anomalies in supply – having only one feeding vessel rather than two
– shape
– it is bilateral in 15%

X-rays: remember that to assess ulnar variance (the ulnar variance view) the forearm must be in neutral rotation. The easiest way to do this x-ray is with the patient seated, shoulder abducted to 90, elbow flexed to 90, and the forearm in neutral rotation, and the x-ray aimed right at the wrist joint, not at the forearm or hand. Supination will make it look more ulnar minus (supination makes the ulnar look short), while pronation will make it look more ulnar positive (pronation prolongs the ulna).
What is ulnar minus? 3 millimeters is considered pathologic.

4 stages:
1 – pre-radiographic
2 – sclerosis
3A – fragmentation and early collapse without scaphoid rotation
3B – fragemetation and early collapse with scaphoid rotation
4 – collapse and arthritis – assess collapse with carpal height ratio – carpal height / 3rd metacarpal height

There are a number of scenarios. The first differentiation is the EARLY vesus ADVANCED Keinbock�s – based on the scaphoid rotation. – ie. Stages 1 to 3A versus 3B and 4

In stages 1 to 3A (pre-scaphoid rotation) and the ulna is short (ulnar minus), then start with a radial shortening, which seems to be simpler than the ulnar lengthening. Favero favors a volar approach to the distal radius through FCR sheath. Cuts the radius near the metaphyseal/diaphyseal junction so that he can get a plate with a few good screws in the distal fragment. Often you only need a few millimeters of shortening. Apply the plate and compress across the osteotomy.

In stages 1 to 3A (pre-scaphoid rotation) and the ulna is NOT short (ulnar neutral), then you cannot do a radial shortening. In this case, probably best to start with an intercarpal fusion – ie. STT fusion, or try to change the joint biomechanics by doing an osteotomy to increase the radial inclination (ulnar closing wedge or radial opening wedge). Other possibility would be a revascularization procedure, but these sound pretty experimental.

In stages 3B (post-scaphoid rotation), basically, you have some collapse of the carpus. The scaphoid rotates (flexes) as the capitate collapses. You�re kinda screwed here. At this stage, you can excise the lunate and do a limited carpal fusion (either an STT or scapho-capitate), or do a proximal row carpectomy if the proximal pole of the capitate is not severely degenerative.
NOTE: the prerequisites for doing a PRC are 1. an intact lunate fossa, and 2. an intact proximal pole of the capitate (although some say that mild degenerative changes on the capitate are not a contraindications to PRC).

In stage 4, there are fairly advanced degenerative changes. The choices here are pretty limited, and basically come down to the patient�s functional demands.
– If active and want some wrist motion – lunate excision and scapho-capitate fusion
– If just want pain relief and don�t mind the idea of a stiff wrist – wrist arthrodesis

Tendon Transfers

Tendon Transfers

– Planning – must know strength, amplitude of excursion, and consider the expendability
– muscles typically lose one grade when transferred
– tendon transfers should be surrounded in fat
– passive range of motion should be maintained
– the straighter the new course of tendon, the better


Restoration of Pinch – Restoration of Thumb Opposition
– Restoration of Thumb Adduction

Restoration of Index Finger Adduction

Restoration of Intrinsic Function

Restoration of Pinch – Restoring Thumb Opposition

– Thumb opposition is the ability of the thumb to move across the palm and oppose the other finger tips. This is a complex motion which is the result of coordinated function of all the long and short muscles of the thumb. There includes the actions of thumb abduction, MCP flexion, thumb pronation, proximal phalangeal radial deviation, and motion of the thumb towards the fingers.

– Conceptually, the act of “pinch” requires that the thumb be positioned, then a force be applied. Think of “opposition” as functioning predominantly to get the thumb into position, and “adduction” as functioning to exert power.

– Opposition is lost in low median nerve injuries and in polio – usually the loss is partial.

– The most important muscle in thumb apposition is the abductor pollicis brevis (median nerve); restoration of opposition is focused on restoring APB function.

APB – internally rotates and abducts the thumb away from the index metacarpal, abducts and internally rotates the thumb proximal phalanx on its metacarpal, and assists EPL in extending the IP joint

Before doing anything to restore the APB, you must consider any deformities and correct these first or concurrently. The EPL begins to act as an adductor in order to assist in pinch – this may draw the tendon into the web space, closing it, and leaving an external rotation deformity to the thumb. Correct the web-space contracture with Z-plasty, and get the thumb into position with a CMC arthroplasty or arthrodesis. Thumb MP or IP arthrodesis may also have to be performed.

Techniques to restore opposition

Many techniques – all have in common the selection of one extrinsic expendable tendon brough from an ulnar direction and transferred to a point on the thumb at a suitable angle to pull the thumb into opposition.

Riordan – FDS of ring finger brought through a loop in FCU, then to the base of thumb

Brand – FDS of ring finger brought through a subcutaneous tunnel just supeficial to the hook of the hamate

Burkhalter – extensor indices proprius brought volarly along the ulnar aspect of the wrist just superficial to pisoform, then across the palm to the base of the thumb

Restoration of Pinch – Restoring Thumb Adduction

Opposition is the refined, unique movement that places the thumb within the flexion arc of the fingers so that the tips of the thumb and fingers can oppose; adduction is the force that stabilizes the thumb in the desired position.

When the adductor pollicis is paralyzed (ulnar nerve palsy), firm pinch between the pulps of the thumb and the flexed index and middle fingers is impossible, and the thumb cannot be brought across the palm to contact the 4th and 5th.

Pinch against the index finger is facilitated by FPL in this case (produces Froment’s sign)

Techniques to restore adduction

Brand – FDS of ring finger through the natural openings of the fascia between the ring and long fingers at the distal third of the palm, then subcutaneously into the radial aspect of the thumb

Boyes – brachioradialis or ECRL to a free tendon graft (plantaris or palmaris longus) dorsally, through the 3-4 webspace, then across the palm to the base of the thumb.

Royle-Thompson (modified) – FDS of ring finger split into two limbs, then tunneled subcutaneously to the base of the thumb, with one slip going to EPL, the other going dorsally to the tendon of adductor pollicis.

Restoring Index Finger Abduction

Abduction of the index finger is important for

Flatfoot In Adults 2

Flatfoot in Adults-2

Posterior Tibial Tendon Dysfunction
– Tib post inserts into the plantar aspect of the navicular and into the medial and middle cuneiforms
– main function of the tendon is to invert the subtalar joint (stabilizes the hindfoot with gastrocs) and adduct the forefoot; inverting the heel stabilizes the subtalar joint.
– the peroneus brevis is the main antagonist, everting the subtalar joint and abducting the forefoot
– if the tib post is weak, the peroneus brevis is a significant deforming force (conversely, if peroneus brevis is disrupted, the hindfoot is pulled into varus and the forefoot into adduction by tib post)]
– tib post dysfunction is largely a degenerative problem, preceded by synovitis.
– the history is that of a slow progressive discomfort
– physical demonstrates significant sagging of the medial malleolus and talar head, with the forefoot abducted. Standing on toes is difficult, and the calcaneus will not invert.
– ankle joint motion is usually good, but subtalar motion is variable, as is transverse tarsal motion; these are important to note in planning treatment
– muscle strength can be tested by resisted inversion in plantarflexion (to decrease the influence of tib ant) and in maximal eversion.
– look for the relationship between the forefoot and the hindfoot; as the hindfoot falls into valgus, the forefoot may swing into varus and this deformity may become fixed. This may need to be corrected.

– careful physical exam to note synovial thickening, subtalar motion, ankle motion, transverse tarsal motion, and the degree of hindfoot versus forefoot rotation.
– if synovitis is the major problem, try an NSAID and cast immobilization
– if chronic and rigid, try foot orthosis
– if flexible, try an orthosis or UCBL insert
– Surgery: reconstruction or fusion
– for reconstruction, the foot must be supple in both the hindfoot and forefoot; if the mobility is not present, or the forefoot varus is too advanced, a tendon transfer will fail.
– tendon transfer is probably superior in young patients with supple feet
– Mann describes a technique of reconstructing tib post with flexor digitorum longus strung up into the navicular.
-Arthrodesis – the basic premise is that the more flexible the foot, the less disability the patient has
– what to fuse depends on what the anatomy is. Options include
– isolated subtalar fusion if there is a supple, easily correctable transverse tarsal joint and no fixed forefoot deformity
– talonavicular arthrodesis – if subtalar joint and forefoot are flexible.
– double arthrodesis – talonavicular and calcaneocuboid – if subtalar joint is supple
– triple arthrodesis – must get the hindfoot back to neutral or 5o of valgus

Rheumatoid Arthritis
– has a predilection for the forefoot, with ankle involvement.
– rarely involves the tarsometatarsal joints
– treatment involves immobilization, perhaps AFO; surgery should be aggressive before huge deformity exists.

Arterial Injury

Arterial Injury

– ischemia time of 6 hours is the cutoff: most limbs can be salvaged if revascularization occurs before this; after 8 hours, the amputation rate is between 72% and 90%
– intimal tear with subsequent development of thrombosis can lead to a picture of palpable pulses initially that disappear (delayed loss of pulse)
– children are particularly prone to ischemia and gangrene due to arterial spasm, a rare problem in adults.

Any diminution of pulse, even if the pulse is detectable by Doppler testing, pressure, or palpation,
should be considered abnormal.

– all major arterial injuries should be repaired; venous injuries are controversial
– autogenos vein grafting is preferred
– surgical shortening of the bone may facilitate vascular repair, and leg length can be dealt with later
– ideally, fracture stabilization should precede vascular repair – may require temporary shunting; this needs to be decided upon by the surgeons
– prophylactic fasciotomy is a good thing!

Doing angiography: the question of whether to do angiography or not depends on the perfusion status of the limb.
– If the limb is perfused adequately, and there is no rush to stabilize the bone, then do the angiogram
– If the limb is white and non-perfused, then you may as well assume the injury to the artery is at the level of the fracture and just get on with exposing it.
– If the limb is broken at a number of levels and you are unsure where the injury is, get the angio.

Proximal Femur Fractures

Proximal Femur Fractures

There now appears to be a limited role for closed treatment and hip spica casting in any of these injuries

Delbert Classification (1907)
I – transepiphyseal fracture – AVN almost 100%
II – transcervical fracture – AVN 50-60%
III – basicervical fracture – AVN 30-40% – much higher than in adults
IV – intertrochanteric fracture

– current recommendations are to do capsulotomy and fixation

– watch for AVN and for early physeal arrest leading to coxa breva and GT overgrowth; LLD secondary to physeal arrest is usually not a huge problem.
– coxa vara is common if the reduction is fucked up.
– nonunion is rare, but can be treated with valgus subtrochanteric osteotomy.

Hip Dislocation

– closed reduction under general anesthetic
– CT to show concentricity of reduction and intra-articular loose body
– open reduction, if necessary is done through Kocher Langenbeck – head may be buttonholed through the capsule


Title: Osteotomies about the Hip for the Prevention and Treatment of Osteoarthrosis

Reference: Millis, Murphy, Poss, Instructional Course Lectures, 1996

Main Message
– the finite lifespan of arthroplasty makes osteotomy a consideration, particularly in the young patient.

Points of Interest

Many joints degenerate for MECHANICAL reasons – elevated joint contact pressure seems to be related directly to the onset of degeneration of articular cartilage. Osteoarthritis begins when the magnitude of UNIT LOAD experience by the joint exceeds the tolerance level of the articular cartilage and subchondral bone.

Most OA Of the hip is secondary to some pre-existing anatomic deformity – primary OA caused by biological failure of articular cartilage in the absence of any mechanical derangement is RARE.

Aronson – 474 patients with end-stage OA – 76% had some disorder (dysplasia, Perthes, slip)

Average unit load of articular cartilage: 25kg/cm2 (remarkably consistent among species)

The sourcil in normal hips has a symmetric density, reflecting a nice distribution of forces. In dysplastic hips, the sourcil becomes eccentric, with increased density laterally and anteriorly.

Varus osteotomy: seeks to restore congruency (and therefore decrease unit load); seeks to decrease muscle forces about the hip by elevating and lateralizing the GT and by medializing the abductors and the psoas.

Valgus osteotomy: seeks to increase congruency and to transfer the center or rotation of the hip from the superior aspect of the acetabulum towards the medial aspect.
Ideal patient for reconstructive osteotomy: young, good range of motion, minimal symptoms, good function, congruent surfaces with minor degenerative changes if any.

Patients who have an osteotomy usually neither gain nor lose overall motion of the hip. Contractures do not necessarily represent a contraindication to a realignment osteotomy as long as the patient has a pain-free flexion/extension arc of at least 80o.

The false profile view is taken with the patient standing, the pelvis pointing 25o towards the beam, with the ipsilateral foot and knee lying perpendicular to the beam. Provides a true lateral radiograph of the acetabulum. This is good for showing subtle acetabular dysplasia with anterior coverage defect.

Examination of the hip under fluoro may be helpful in determining the incongruity of the joint.

Selecting the site of osteotomy
– if CE angle

High Tibial Osteotomy – Complications 2

Persistent pain
– the most important determinant of sustained pain relief is accuracy of correction
– patients with > 15 of varus will likely do poorly, because you will not get them over farenough.
– also, patients with a high adductor moment may not do as well

Patient Selection
– what side is the angular deformity on.
– varus closing wedge osteotomies do poorly for valgus knees – the joint line is made oblique, the nerve is stretched, and if the MCL is stretched out, the closing of the medial side will simply make this more loose – DO THE VALGUS KNEE FROM THE FEMORAL SIDE.
– if there is significant MCL laxity in the varus knee, consider medial OPENING wedge osteotomy
– avoid inflammatory arthritides

Preoperative planning

– beware the calculation of correction based on angles alone. In a short person, a 15o wedge will not create a greater change than in a tall person!
– Try to consider where the osteotomy will put the mechanical axis – it should be shifted into the medial one third of the lateral compartment, approximating a 183 to 185 degree valgus weightbearing axis.