Vertical Talus

Vertical Talus
Approach to Congenital Vertical Talus

This is the at the extreme spectrum of flatfeet; ie. the ultimate flatfoot.

Look for associated conditions: spinal dysraphism, sacral agenesis, arthrogryposis, neurofibromatosis, DDH, CP, polio, SMA, and iatrogenic (overcorrection of a clubfoot)

Basically, the TN joint is dislocated, with the navicular riding dorsolaterally on the talar head. The calcaeneocuboid joint may also be subluxed dorsally – the whole midfoot and forefoot are swung way out into abduction

The diagnosis is made by the rigidity of the hindfoot, and the “Persian slipper” appearance.


There is no role for conservative management. Cast them only as a temporizing measure to stretch things out as best as possible prior to operating on them.

Can do a one or two stage open reduction of the TN and CC joints.

Drennan: single stage
– posterolateral release (calcaneofibular ligament), release tendoachilles, expose NV bundle, open reduction of TN joint, cut interosseous talocalcaneal ligaments, then K-wires the joint.

MCQs – Peds Foot 3

MCQs-peds foot 3
vertical talus – hindfoot equinovalgus, forefoot dorsiflexion and abduction/valgus.

– a 16 year old with symptomatic talonavicular coalition with degenerative changes should probably undergo triple arthrodesis.

– the prognosis for tarsal coalition excision is better if the bar is fibrous or cartilaginous rather than bone. The most common types are calcaneonavicular and talocalcaneal.

– initial treatment of a coalition is symptomatic control – bracing, NSAIDs, etc.; failing this, excise if no degenerative changes exist.

Complex Regional Pain Syndromes (CRPS) – Presentation


In general, there is a history of a noxious event (may be trivial, or non-existent), usually accompanied by a period of immobilization. It should be remembered that this is a multi-symptom phenomenon that usually involves severe pain, swelling, stiffness, and discoloration of the extremity. The entire symptom complex is rarely observed in one patient.

Signs and Symptoms

Huge constellation of signs and symptoms, often changing as the disease progresses.

Pain (Hyperpathia) – usually burning sensation, but also described as �cutting�, �searing�, �pressure�. However described, the magnitude is out of proportion to the severity of injury. It is usually constant, but is aggravated by attempts to move the limb. Associated with this is allodynia (pain produced by non-noxious stimuli), where light touch is very painful.

Swelling – usually the first and most constant physical sign. Like the pain, it is out of proportion to what would be expected for the injury, and tends to worsen rather than improve, spreading through the extremity. In early RSD, the swelling is soft, but in time becomes hard and brawny. Periarticular swelling is a late finding, and produces tremendous thickening and stiffness of the joints.

Stiffness – again, much worse than would be expected for the injury. Initially, the stiffness is probably due to edema and pain; later, motion becomes limited by the brawny, thick edema, and eventually by intense fibrosis.

Skin Discoloration – this is related to vasomotor instability. Initially, vasodilation takes place and the extremity is erythematous; in later stages, vasoconstriction persists and the hand may appear pale, grayish, or cyanotic. Vasomotor instability is similarly responsible for temperature changes, with the extremity feeling warm during vasodilation, cool during vasoconstriction.

Hyperhidrosis (Excessive Sweating) – in the early stages of disease, this represents excessive adrenergic stimulation of apocrine glands. In advanced stages, diminished sweating or a dry hand is more commonly seen. Sudomotor activity is either increased or decreased, depending on the stage.

Osteoporosis – usually greater in degree than that caused solely by disuse. Demineralization usually starts in the ends of the long bones, but then spreads throughout. Early in the course, demineralization in a speckled, punched-out pattern has been referred to as Sudeck�s atrophy.

Trophic Changes – smooth, shiny skin with disappearance of skin wrinkles, initially due to edema, but later due to atrophy of the skin and subcutaneous tissues; atrophy of fat pads produce �pencil-pointing� fingers.

Palmar Fasciitis – observed in a number of patients, with the formation of acute nodules and thickening of the bands of palmar fascia.


Approach to Spondylolisthesis

Wiltse Classification (“Did Tim Pass”)

I – Dysplastic
– IA – axially oriented facets; IB – sagitally oriented facets
– dysplastic facets permit forward translation – higher chance for neural compression as the intact posterior elements move forwards

II – Isthmic
– IIA – lytic defect in pars; IIB – elongated (partially healed lytic lesion)

III – Degenerative

IV – Traumatic

V – Post-Surgical

– children get isthmic spondylolysis and spondylolisthesis at L5/1; adults get degenerative spondy at L4/5
– an acquired disorder; possibly a stress fracture of the pars after repetitive microtrauma
– increase in slippage is seen during adolescent growth spurt; progression is unlikely after adolescence; therefore, like in adolescent scoliosis, get an idea of how skeletally mature they are when deciding about risk of progression.
– initial slippage of 50% is predictive of further slippage
– slip angle measures lumbosacral kyphosis and is associated with a higher risk of progression
– look for a rounded off sacrum or trapezoidal L5 body – higher chance of progression

Grade I and II slips that are asymptomatic (found spuriously)
– observation semiannually until age 15, then annually until the end of growth
– may give them advise about avoiding hyperextension activities and contact sports
– a 20% slip that progresses to 35% is not necessarily an indication for fusion – assess the above factors and watch – look at skeletal maturity, high slip angle, rounded sacrum or trapezoidal shape of L5 as useful markers of progression.
closesly. A 20% slip that progresses to 50% is probably an indication that you better get on an fuse it.

Grade I and II slips with pain
– activity restriction, NSAIDs, local measures, stretching exercises
– if continues to have pain – thoracolumbar orthosis
– if pain persists with orthosis, can do a L5-S1 posterolateral in-situ fusion with bone graft followed by single or double leg hip spica cast

Grade III or IV slips with or without symptoms
– gets a L4-S1 posterolateral in situ fusion with bone graft as a preventative measure for further progression if they are asymptomatic. Must extend fusion up to L4 because of the biomechanical disadvantage of the fusion mass.

– instrumented fusions are becoming popular but do not have the long-term track record of the standard posterolateral uninstrumented in-situ fusion. Instrumented reduction is hazardous to the nerve roots
– if they have documented MOTOR weakness, you should probably decompress them, which also means that you are going to go midline and destablize them – they need to be instrumented.
* when you position them prone in the OR, position them with their hips and legs EXTENDED – if you allow them to flex like they normally do, their lumbosacral kyphosis worsens, and they are apt to get a cauda equina syndrome. Cauda equina can occur with reductions and with in-situ fusions as well – requires sacroplasty

Osteonecrosis Of The Hip

Osteonecrosis of the Hip

– often in young patients (30-50)
– natural history (we think) is that of progressive collapse (in 80%)
– higher failure rate in these young patients with this diagnosis, even when accounting for age and activity level;
? necrotic bone with altered remodeling?
– pathophysiology is not well understood. Four hypothesis exist – none are particularly solid:
1. Direct cellular mechanisms – death of osteocytes
2. Extraosseous arterial mechanisms – reduction in blood flow to the head
3. Extraosseous venous mechanisms – venous stasis
4. Intraosseous extravascular mechanisms – inflammatory marrow edema
– in truth, the disease is probably multifactorial, and there is a concept of “multiple hits” of multiple insults, superimposed on what might be a genetic susceptibility.

Classification – Ficat Classification – University of Pennsylvania
0 – asymptomatic, normal x-rays – abnormal MRI 0 – asymptomatic, normal x-rays, abnormal MRI
I – normal x-rays I – normal x-rays
II – sclerosis or cystic lesions II – sclerosis or cystic lesions
III – crescent sign with subchondral collapse III – cresent sign only
IV – osteoarthrosis IV – subchondral collapse
V – early arthritis
VI – late arthritis * A, B, C depending on size of lesion
(For any given stage)

Head Preserving Treatment:

Core Decompression
– good results in Ficat I and II; moderate in Ficat III (47% survival)
– probably best for Ficat I and II, small, central lesions in young, non-obese patient not on steroids
– success rate is closer to 20% in post-collapse

– to move the diseased part of the head into a less weightbearing area
– critical size is 30% or 200o combined necrotic arc angle on AP and lateral – beyond this, don’t try osteotomy!
– probably effective only for Ficat I and II, and very early stage III hips.

Nonvascularized Grafting
– structural grafting through the core decompression track
– cancellous and cortical grafting through femoral neck and head
– osteochondral grafting

Vascularized Grafting
– decompresses the femoral head, provides structural support, removes dead bone, increases vascularization, and provides additional cancellous bone
– in general, best for young patients with early disease (like all the rest)
– patients over 55 are not candidates, as are patients on continued corticosteroids
– still has somewhat limited results in hips with more than 30% head involvement

* in general – when the lesion is >200o combined necrotic angle or greater than 30% head involvement, the head preserving techniques have not been very successful (including vascularized grafting)

High Tibial Osteotomy

High Tibial Osteotomy

The IDEAL Candidate:
– young (age 65)
– severe tricompartmental disease
– severe ligamentous laxity on the concavity of the deformity (medial side)
– medial/lateral subluxation of 1 cm – this is BAD – HTO will not resolve this instability
– excessive deformity (>15o varus)
– inflammatory arthritis
– obesity

In general:
– patients can expect to maintain a high level of activity
– patients should be warned to expect less than full pain relief
– patients should expect that disease progression will probably allow the pain relief to last 5-7 years. (ie. A temporizing procedure)

The single most important factor in outcome is the post-operative alignment of the knee. Exactly how much correction required is unclear, but it appears that you need an OVERcorrection to an anatomic valgus of 8-10o. Patients with 7-13 degrees of valgus do far better than those with less than 7!

Alignment Issues

The Normal Mechanical Axis
– from center of hip to center of ankle
– normally lies in 1.2o of varus (ie, it is not quite vertical) – but everything is a lot easier to think about if you call it 0o.
– normally goes through the central third of the knee
– generally speaking, it parallels the anatomic axis of the tibia

The Anatomic TibioFemoral Angle = 5-7o of valgus
– the distal femur is in about 8-9o of valgus
– the proximal tibia is in about 3o of varus (hence the approximate 5-7 of valgus for the anatomic tibiofemoral anlge)

The Anatomic Femoral Axis = 6o of valgus to the mechanical axis

So even though the anatomic tibio-femoral angle is 5-7, you want them overcorrected to 8-10!

A high pre-operative lateral thrust/adductor moment is bad – these patients have a higher loss of correction.

Spinal Stenosis

Spinal Stenosis

Reference: JBJS 81-A, No. 4, April 1999, Instructional Course Lecture
– Garfin, Herkowitz, Mirkovic, San Diego, Michigan, Chicago

Main Message

Spinal stenosis is a syndrome that associates cauda equina compression with inflammation and pain (compression alone is not enough, as many asymptomatic people demonstrate compression). For those with severely disabling symptoms, operative care gives good results. The indications for operative care are a bit soft.

Points of Interest

Something we don’t understand about spinal stenosis is that the severity of symptoms is not necessarily associated with the magnitude of compression. ? Is it that we don’t understand the pathophysiology? Is our imaging insufficient?


– the disc degeneration takes place over time; begins with degeneration and decreased production of proteoglycan in the nucleus, so that the water content of the nucleus diminishes and the ability to distribute stress is diminished and fissures/tears are formed in the annulus. The disc height decreases, as annular bulging, disc herniation, and early osteophyte formation is seen. Facet joints are then placed at increasing stress (although facet arthritis can precede disc degeneration) and degeneration leads to hypertrophy of the facet joint, thickening of the overlying capsule, and more osteophytes.
– if disc degeneration exceeds alteration to the facets, retrolisthesis may occur; as the facets erode, the subluxation reverses to more anterior listhesis.

– Degenerative changes are noted in most people over 60; but most who have evidence of mechanical nerve root compression do not have pain.


Nerve Compression
– alone, compression does not independently cause pain; there must be inflammation and irritation of the root. Compression of a normal nerve leads to paresthesia, sensory and motor loss, and reflex abnormalities, but pain usually does not occur. If an inflammed nerve, on the other hand, is compressed, then pain develops in addition to the objective signs.
– compression may be static or dynamic – flavum buckling, disc protusion, osteophyte impingment, nerve/vascular tethering
– the force of compression, duration of compression, and rate of compression are all important factors. Blood flow/ischemia is probably the final pathway, effecting changes in nerve root nutrition.


– usually insidious onset
– classically, poain, numbness, and tingling in the posterior or posterolateral aspect of the limb. Exacerbated in extension, relieved in flexion. (Look at Table III for distinctions from vascular claudication).

Physical Examination

– specific motor deficits are uncommon, although weakness is a common complaint.
– watch for long tract signs – there may be a cause more cephalad in the cord!
– SLR is usually negative


– severe debilitating neurological deterioration in patients managed nonoperatively is RARE
– operative treatment can usually be deferred, and a significant number may improve
– the decision to operate is based on symptoms and quality of life; the symptoms most amenable to treatment are the leg symptoms, not back pain.

Decompressive laminectomy and nerve root decompression – the standard procedure

– the controversy centers around when to add a fusion: Pre and Intraoperative considerations

Preoperative Structural Alterations
– degenerative spondylolisthesis – an indication for additional fusion; there is good evidence to support this concept, that after decompressing these, fusion is definitely recommended.
– scoliosis or kyphosis – factors to encourage arthrodesis are: 1. A very flexible curve. 2. documented progression. 3. Radiculopathy on the concavity. 4. Lateral slip. 5. Loss of normal lumbar lordosis (want to correct the sagittal alignment). 6. Failed surgery requiring further decompression (and destabilization). 7. Removal of 50% of the facet (renders the motion segment unstable).

MCQs – Shoulder 2

MCQs-shoulder 2
If they are not having much PAIN and are just limited by weakness – not sure exactly how this changes things. Typically, in older patients we operate to help the pain. If a young patient were to sustain a sudden injury and have rotator cuff symptoms, that patient I’d fix right away.

– the best test for rotator cuff after MRI is arthrography.

– acromial morphology is best associated with incidence of full thickness rotator cuff tearing. (Type III)

– adhesive capsulitis is seen with diabetics in particular. Also with other “fibromatosis” – peyronies, dupuytrens, plantar fibromatosis, Garrods nodes, hypothyroidism, phenobarbitol use.

– for the acute proximal biceps tendon rupture – do nothing; physio to get them moving. No reason to go in and fix.

– Charcot arthropathy secondary to syrinx – NONoperative Rx only.

– onset of shoulder pain with deltoid atrophy and triceps atrophy – C5 and C7 – weird. Probably a plexus neuritis to affect them both.

– the most important risk factor for clavicular nonunion is displacement of fracture

– staple capsuloraphy has a high rate of complication when used in the shoulder; all arthroscopic stapling procedures are frought with complications.

– the pitcher subluxes his shoulder during late cocking (begins with the pitcher putting his foot down); The severe abduction and external rotation in late cocking causes posterosuperior impingement and levers the anterior head out the front – thus stretching out the anterior capsule. The rotator cuff hast to work harder to keep the shoulder in. When the cuff fatigues – more instability. Note: if this pt comes in with labral pathology, you need to address the instability primarily, not just the labral pathology.



– malignant plasma cell tumor originating from marrow that usu presents with multiple bony lesions
– males > females; presents in 6th decade with pain usu involving vertebrae, ribs or pelvis

– anemia, elevated serum Ca, plasmocytosis in bone marrow (>30%)
– serum electrophoresis – globulin spike
– immunoelectrophoresis – high levels of monoclonal immunoglobulins (M components) in serum
– monoclonal light chains in urine (Bence Jones proteinuria)

– multiple or single small, well-circumscribed ‘punched-out’ lytic lesions
– little or no reaction by surrounding bone but endosteal scalloping & medullary expansion
– with long bone involvement, may be cortical destruction with soft tissue mass

– tightly packed plasma cells with eccentrically located nucleus, abundant pink cytoplasm & pale-stained juxtanuclear halo
– nodular foci or broad areas of amyloid deposits with no background stroma
– intracytoplasmic inclusions (Russell bodies)

– chemotherapy & radiation (for solitary lesions)
– internal fixation for pathologic or impending pathologic #s

Calcaneal 2

Calcaneal 2
eccentrically on the calcaneus. Looking at it from the back, the talus lies medial to the center of the calcaneus, and thus it shears off the anteromedial piece. How far lateral that primary fracture line extends depends on the position of the foot and subtalar joint when the impact hits it.

Secondary Fracture Line(s) – runs through the posterolateral (tuberosity) fragment. Two distinct fracture patterns are seen depending on where this secondary fracture line exits – Tongue type or Joint depression. (Essex-Lopresti classification)

Tongue type – the secondary fracture line goes posteriorly from the crucial angle to the tuberosity, creating a large, posterior superior and lateral fragment, with a portion of the posterior facet on its anterior part.
Joint depression – the secondary fracture line goes posteriorly from the crucial angle but exits just back from the articular facet, creating a fragment separate from the tuberosity – the “thalamic portion” which contains a portion of the posterior facet.
– in either of these two types, the secondary fracture line creates a fragment that usually tips downwards, leaving a significant sagittal incongruity in the subtalar joint
– the magnitude of the injury is what causes the comminution of the tuberosity fragment; it is in this fragment that the secondary fracture line is created, and more energy creates more fracture lines and comminution, often blowing out the lateral wall, and extending anteriorly to the calcaneocuboid joint.

Compartment Syndromes

– severe claw-toe deformities can result from these
– need to review the articles from Myerson and Manoli to figure out what it is that they are decompressing.


– Nonoperative – no need to immobilize – these heal just fine. Early ROM
– Operative – the full Monty – extensile lateral approach with rigid fixation, bone graft
– L shaped incision behind the sural nerve; large skin/soft tissue flap elevated. Take down the calcaneofibular ligament, peroneal tendons, elevate them anteriorly

– the degree of subtalar incongruity is the most important prognostic facteor
– decrease in Bohler’s angle is important, but not as much as the subtalar incongruity; a decrease to -0o or less has been associated with poor results.