Approach to Inflammatory Arthritis – Preop Planning

Pre-op planning
Approach to Inflammatory Arthritis – Preoperative Planning

– includes rheumatoids, SLE, ank spond, psoriatic arthritis

Pre-Operative Considerations

– beware the increased risk of infection: psoriatic arthritis patients have a higher risk of deep infection – probably from skin lesions colonized with bacteria. Rheumatoids also have higher risk of infection
– beware skin ulceration: rheumatoids may have skin vasculitis that makes them prone to ulceration
– beware atlanto-axial and atlanto-occipital instability in rheumatoids – may be asymptomatic in over 50% May also see instability in ank sponds. Does not require fusion – requires careful intubation (awake, fluoroscopic)
– beware limited chest wall expansion in ank sponds or other seronegative arthritides – need preop pulmonary function studies and careful positioning so as to not impede their diaphragmatic breathing
– beware pulmonary disease in rheumatoids – restrictive +/- nodules – need preop pulmonary function
– beware ileitis and colitis when associated with arthritis – increased risk of infection
– beware anemia of chronic disease – almost universal
– beware immune suppression, with and without steroid use
– beware variations in bone quality – rheumatoids have increased bone turnover in periarticular bone – may attribute to high loosening rates; be wary of using cementless fixation in this population
– beware soft tissue contractures and joint DEFORMITY in inflammatory arthritis – be prepared for difficult ligament balancing and soft tissue releases around the knee and hip
– beware the medications that they may be on – NSAIDs, steroids, methotrexate – all should be noted, and arguably stopped in lieu of their surgery

Flexion Contracture

Flexion contracture
Total Knee Replacement with Flexion Contracture

– this is common particularly in the inflammatory arthritides – rheumatoid, psoriatic, hemophilic – because they hold their knee flexed as that is the least painful for them.
– they may also have concomitant varus or valgus deformities

– do the approach and do the medial/lateral soft tissue balancing first.

– then decide how to deal with the flexion contracture. The basic approach is to start with soft tissue releases, then move on to bony changes if absolutely necessary.

– start with releasing the PCL – even though this opens up the flexion space more than the extension space, these severe deformities are a lot easier to deal with by starting with the obliteration of the PCL (how would you balance the PCL in a 25o valgus knee with a 30o flexion deformity anyways?)

– make sure all the medial and lateral osteophytes are resected so that the medial/lateral soft tissues aren’t draped over them.

– start dealing with the flexion contracture by flexing the knee up fully, and removing the osteophytes off the posterior condyles – then check the extension space again.

– if still tight, flex up the knee again, and use an elevator to elevate the capsule off the posterior condyles and femur; keep checking as you release, but you may have to go all the way and release the entire capsule and proximal heads of the medial and lateral gastrocs.

– if still tight in extension after this (rare) you have to think about doing bony work. The way to increase the extension gap is to cut more of the distal femur back – unfortunately, you will raise the joint line if you do this, so don’t be too aggressive. Raising the joint line 8 mm apparently really fucks up the extensor mechanism.

– the vast majority are manageable by getting rid of the posterior osteophytes first, then stripping the posterior capsule off next, then stripping the gastrocs off the distal femur. (ie – soft tissue procedures usually work!) Only after then should you consider resecting more off the distal femoral cut.

Lower Back Pain – Fusion 1

LBP-fusion1
Title: Lumbar Arthrodesis for the Treatment of Back Pain – Current Concepts Review

Reference: JBJS Volume 81-A, Number 5, May 1999
– Hanley, E.N., David, S.M., Dept of Orthopaedic Surgeyr, Carolinas Medical Centre, Charlotte, North Carolina

Main Message

– Much has been published on arthrodesis of the lumbar spine; most has used nonstandardized criteria for inclusion, and have used nonvalidated outcomes. This review attempted to determine which treatments are REASONABLE, which are UNREASONABLE, and those that are experimental. Ie. the literature kinda sucks, but some things can be gleaned from it. Some improvement occurs as a result of operative treatment in about 75% of patients (a generous number), but major or complete relief of pain and recovery of function are seen in less than 50% or less.

Points of Interest

Etiology of Low Back Pain

Facets
– the facets have a controversial role. Facet blocks have had disappointing success as a therapeutic modality. �It is believed that so called facet syndrome is much less common cause of low back pain than are problems related to the intervertebral disk�.
– the predictive value of facet blocks for the success of lumbar arthrodesis is also questionable.
Discs
– MRI abnormalities exist in a significant (one/third) proportion of the normal population (Boden, 1990)
– the outer annulus is highly innervated, as is the endplate, and PLL. The outer layer of the annulus has most often been implicated as the tissue causing axial low back pain. Some authors have stimulated this layer (and the PLL) and have produced typical symptoms of back pain.
– the hypothesis that the disc is the source of pain is also supported by the observation that in the cervical spine, resolution of symptoms are sometimes seen with excision of the disc without arthrodesis.

Degenerative Instability

– this, like �facet pain�, is also thought to be uncommon. Poor outcome in spinal fusion has not been found to be associated with pseudarthrosis, so �abnormal motion� is not necessarily the problem.
– AAOS Definition of segmental instability: �an abnormal response to applied loads, characterized by motion in the motion segment beyond normal constraints�.
– Kirkaldy-Willis on the pathology of degeneration: 3 phases – Phase 1 is dysfunction (tearing of the annulus fibrosus, degeneration of the nucleus, arthropathy of the facets), phase 2 is instability (laxity of facets and discs), phase 3 is restabilization (formation of osteophytes and facet hypertrophy).

– the concept of segmental instability may be related to, but differs from, the diagnosis of so-called discogenic back pain (pain related to disc degeneration).
– it is difficult to quantify instability on x-ray, and there is no agreement on what is abnormal motion on flexion/extension films.

Diagnostic Studies

Provocative Discography – controversial. Varied results on the predictive value of discography in spinal arthrodesis.
1995 NASS position paper on discography indicates that it is supported for determining which disc level or levels reproduce the pain in those with non-radicular symptoms, or localizing discogenic sources of persistent pain after a previous unsuccessful procedure on the lumbar spine. They advocate using CT and MRI to support the discogram findings, and recommend against using discogram alone.

Non-Operative Treatment
– Strong evidence supports the use of NSAIDs and muscle relaxants in acute LBP. Evidence supports the use of excercise, back school, and manipulation in chronic LBP. Bed rest for no more than 2 days is advisable for severe acute pain.

MCQs – Spine 4

MCQs-spine 4
the lateral aspect of the superior facet, not inferior facet.

– epidural steroids are more therapeutic than just local block alone and can be done as an outpatient.

– pathophysiology of spondylolytic spondylolisthesis is related to stress fracture.

– clinical presentation of severe L5/S1 spondy – flat buttocks, lumbosacral kyphosis, lumbar lordosis, hip flexion contracture, hamstring spasm, signs of L5 radiculopathy

– Potts disease typically gets T12-L1

– nerve root impingement in the lumbar spine is most likely due to posterolateral disc, hypertrophic facet – most unlikely to be a intradural tumour!

– the young adult who presents with some discomfort and is found to have Scheurmans – observe with physio. They are unlikely to progress once hitting skeletal maturity.

– Scheurermann’s disease treatment begins with physio. Bracing can be used for curves in the 50-70 range, with the goal of achieving a curve near 50 at maturity. For surgery, curves greater than 75 degrees and anterior wedging in excess of 10 tend to lose correction with posterior fixation alone and require anterior surgery.

Posterior Shoulder Instability

Posterior Shoulder Instability

Relatively rare incidence, reported to be 2-4%

Pathoanatomy

Static stabilizers:
Studied in capsular cutting experiments
Schwartz et al., 1988 – posterior inferior capsule is the primary posterior restraint, with anterior superior capsule and superior glenohumeral ligaments providing secondary restraint.
Warren et al. 1984 – posterior dislocation occurred only after the anterior superior capsule was incised
Harryman et al., 1992 – posterior subluxation is resisted by an intact rotator interval capsule.
Intra-articular negative pressure

Dynamic stabilizers:
It is assumed that the rotator cuff will act to stabilize the humeral head in flexion, adduction, and internal rotation
Blasier et al, 1997 – all cuff muscles contributed to posterior stability, but the subscapularis was most significant.

– unlike anterior dislocators, capsular detachment is uncommon – 10% (Bigliani, 1995)

Hottya et al., AJR, Sept 1998
MR evaluation of 4 acute posterior dislocations
found posterior capsular disruption, partial tears of teres minor, labral tears and fraying

Classification Noble, Morin in Shoulder Injuries in the Athlete, Hawkins ed. 1996

Acute posterior dislocation
With impression defect in humeral head
Without impression defect in humeral head (rare)

Chronic posterior dislocation
Locked (missed) with impression defect

Recurrent posterior subluxation
Voluntary
Habitual (willful)
Muscular control (not willful)

Involuntary
Positional (demonstrable)
Nonpositional (not demonstrable).

Acute Traumatic Posterior Dislocation

extremely rare to not have an impression defect in the humeral head
indirect violent trauma, including seizures, electrical shock, MVA, or a posteriorly directed blow on the forward, outstretched extremity with the arm in flexion, adduction, and internal rotation.
both acute posterior subluxations and dislocations reduce spontaneously, making it difficult to distinguish the two.
the arm is held in fixed adduction and internal rotation, with no external rotation ability.
the humeral head may be palpable posteriorly, with an empty glenoid fossa.
treatment is by closed reduction – performed by flexion and adduction with longitudinal and lateral traction
no real consensus on how long it should be immobilized for, if at all
recurrence rate is felt to be uncommon

Chronic Posterior Dislocation (Locked/Missed)

a posterior dislocation in the presence of an impression defect with the humeral head remaining subluxed posteriorly
if presenting late (missed), pain will be diminished, but functional deficit will be the chief complaint, particularly the inability to externally rotate the arm. (may lead to the diagnosis of “frozen shoulder”)
the key to diagnosis is the internal rotation deformity
treatment depends on a variety of factors: duration of dislocation, size of impression defect, presence of changes in the glenoid,

Size of Defect Duration of Dislocation Treatment

20% 50% 50% > 6 months Hemiarthroplasty (0o retroversion)

Subscapularis transfer – McLaughlin procedure, Neer & Foster modification

Fowler – Modified Brostrom

Fowler-Modified Brostrom
-chronic lateral ankle instability
-antero-lateral incision

Chordoma

Chordoma

– arises from remnants of primitive notochord found in midline at either end of the spine (sacrum > shnooccipital region) in middle-aged men

Signs & Symptoms:
– gradual onset of pain & usu long duration prior to diagnosis
– large presacral rectal mass
– bowel or bladder dysfunction

Xrays:
– destructive bony lesion associated with an expansile soft tissue mass

Histology:
– polyhedral cells with eosinophilic cytoplasm & many vacuoles which displace the nucleus = physaliphorous cells
– cells disposed in cords, trabeculae or sheets which are separated by abundant mucoid & myxoid matrix

Treatment:
– wide excision (may have to sacrifice sacral roots)
– radiation if not resectable
– frequent metastases to lungs, liver & other tissues

MCQs – Pathology 2

MCQs-pathology 2
production and osteoblastic activity.

– widened osteoid seams are seen in osteomalacia (Looser’s lines); they are areas of uncalcified osteoid that surround mineralized bone. Seen in osteomalacia and rickets.

– most common area of mets from a rhabdomyosarcoma – lymph nodes

– UBC’s often recur after curettage and bone grafting; they also often do not heal after fracture. Most common site is the proximal humerus

– gout can be seen after leukemia, multiple myeloma, polycythemia and lesch Nyan syndrome. It is not seen with hemophilia.

– osteogenesis imperfecta – the collagen crosslinking is abnormal. “In patients with OI, several recent reports have shown a considerable increase in concentrations of types III and V collagen and a marked variation in cross-linking”.
(Lovell and Winter)

– look for intra-osseous ganglia in carpal bones (scaphoid in particular)

– osteoblastoma – most common location is posterior elements of the spine.

– rhabdomyosarcoma – mets to lymph nodes (along with leiomyosarcoma, synovial sarcoma, epitheliod sarcoma)

– multiple myeloma, sarcoidosis, thyrotoxicosis, and metastatic breast Ca all cause hypercalcemia; medullary carcinoma of the thyroid does not (it produces calcitonin, which decreases calcium)

– amyloidosis is often seen with multiple myeloma (10%)

– dystrophic calcification is calcification of DEGENERATIVE TISSUE
– ivory vertebrae – lymphoma!

– GCT’s are one of the few benign lesions to have a predeliction for the ANTERIOR spinous elements.

– fracture through the distal radius with a big GCT – probably best to do a wide excision and primary arthrodesis

– anterolateral bowing of the tibia that shows up at birth – congenital pseudarthrosis of the tibia

– for patients with soft tissue sarcomas with postop XRT – watch for radiation induced osteonecrosis of adjacent bones. They do not get bony metastasis!

– synovial cell sarcoma: classically a biphasic pattern with 2 distinct cell populations – spindle cells and epitheloid cells. The spindle cells are predominant, and are plump and form an interlacing pattern. The epithelioid cells form glandlike structures.

ORIF Acetabulum 1

ORIF Acetabulum, 1

ORIF Acetabulum, Triradiate approach

50 year old gentleman with multiple right lower extremity injuries from a motorcycle vs truck MVA. We fixed his tibia first supine, then flipped him into the lateral position and fixed his distal femur, then approached his acetabulum. He had a complex 2 column injury that looked initially like a T type fracture because it looked as if part of his ilium was still connected to the acetabulum. Intra-operatively it appeared as if this was not the case.

Surgeon: O’Brien

Positioning: Lateral on Jackson table to allow C-arm access

Description:

The triradiate approach is centered on the GT – the Kocher Langenbach approach is posterior, and O’Brien makes his anterior incision almost horizontal at the level of the GT, and then curves it up to the ASIS, rather than cutting straight at the ASIS from the GT. The posterior approach is as for the Kocher Langenbach. The fascia overlying the G. Max is incised, and the G.max is split – not too high, as this dennervates it. The abductors are revealed. The fascia lata is split longitudinally and the dissection is carried bluntly via fingers posteriorly to get into the fat around the sciatic nerve. The nerve is then identified. The piriformis is then identified superior to the nerve. It is followed to its insertion and the tendon is tagged then cut. Then the superior and inferior gemelli muscles are identified. They are identified by looking for the rectangular quadratus femoris, and going proximal to it. The obturator internus tendon lies beneath the gemelli, and is identified by directing your finger down from above the superior gemelli, and up from below the inferior gemelli – you can feel the tendon deep beneath the muscles. This tendon is similarly tagged then cut. The obturator internus is the key to the deep dissection of the posterior column.

The anterior incision is carried through the subcutaneous tissue to the fascia overlying tensor fascia lata. The reason O’Brien carries his incision quite horizontally from the GT is that the incision through the TFL is then more distal and therefore less of the muscle is denervated. The fascia overlying TFL is incised with a knife, and the TFL muscle is then incised with cautery. Make sure you make the fascial incision clean with a knife because it is these edges that are repaired in the end – the muscle does not hold suture.

The fascia deep to TFL is then examined. Look for the ascending branch of the lateral femoral circumflex vessel in this area, between rectus and gluteus medius. The anterior border of gluteus medius must be identified and dissected out so that the abductors may be taken up off the capsule once the trochanter is osteotomized. Watch for bleeding in this area.

The trochanter is osteotomized by making stabs into the soft tissue with the cautery, and directing a 3.2 mm drill through to the medial side to exit just at the level of the lesser trochanter. The holes are drilled parallel to one another and tapped for 6.5 mm cancellous screws. The final step in preparing to take off the trochanter is to go posteriorly and dissect the g.minimus off the capsule. This can be done with mets. Once this layer has been dissected off, a lauer is delivered from posterior to anterior and a Gigli saw is passed. The trochanter is then osteotomized.

With the trochanter off, the abductors are then reflected superiorly. Subperiosteal dissection is carried out to lift the abductors off the outer table of the pelvis. This can be done all the way anteriorly to the ASIS. Similarly, the posterior dissection can be brought right down onto the ischium.

Technical tricks to reduction:

A large hook can be used to pull on the femoral head and apply traction to the head/capsule. An incision can be made in the capsule to look inside the joint and visualize the intra-articular derangement.

If there is a fracture through the iliac wing, screws applied to each side can be inserted and a reduction clamp applied to the screws –

Amputations II – 2

AMPUTATIONS 2

BELOW-KNEE AMPUTATION

The most proximal level at which near-normal function is available.

INDICATIONS (Haimovici, 1996)
� Gangrene of several toes, extending to or beyond the adjacent metatarsal lesion and showing no tendency to demarcate.
� Spreading gangrene of the foot, with or without associated gangrene of the heel or ankle.
� Spreading gangrene of the toes, associated with uncontrollable infection of the foot.
� Failure of a transmetatarsal or Syme amputation.
� Trauma
� Neoplasia

CONTRAINDICATIONS
� Inadequate circulation for healing!
� Extensive gangrene and infection of the leg with absence of femoral pulses
� Gangrene of the foot associated with irreducible flexion contracture of the knee joint.
� Recent acute occlusion of the femoral or iliac artery with inadequate collateral supply at the below-knee level. (Need a 2-3 month interval for the development of collateral circulation.)
� The nonambulatory patient with a dysvascular limb and flexion contracture of the knee – will be better off with a knee dysarticulation. (McCollough et al., 1981)

TECHNICAL OPTIONS

Long Posterior Myocutaneous Flap
� Most common. Takes advantage of the vascularity of the posterior musculature.
� Moore et al. (1972, Am. J. Surg): superior healing rate (89% vs 72%) after changing from equal AP flaps.

Equal Anterior and Posterior Myocutaneous Flaps
� Still popular in some centres, though falling out of favor.

Equal Medial and Lateral (Sagittal) Myocutaneous Flaps
� Reduces the amount of poorly vascularized anterior skin, utilizes wide-based, short flaps, may provide better bony coverage and wound drainage, and is useful if necrotic skin is present posteriorly.
� Persson, (1974, J. Bone Joint Surg): superior healing rate (74% vs 41%) in 58 pt compared to 40 with equal AP flaps.
� Termansen, (1977, Acta Orthop. Scand): equal healing rate (58% vs 59%) in 41 pt compared to 47 with long posterior flap.

Suffice to say, that in certain situations (trauma in particular), the flap configuration may be dictated by the pattern of tissue loss, so it is important to be aware that there are more than one way to perform the operation.

TECHNICAL OPTIONS (cont�)

Osteomyoplasty
� Requires raising two one-inch osteoperiosteal flaps from the anteromedial and lateral tibia. The tibia and fibula are divided at the level of the osteoperiosteal flap hinge (the fibula 5mm shorter). The flaps are then swung over and attached to the fibula. An osseous bridge then develops between the tibia and fibula, which is believed to stabilize the fibula and improve the end-bearing characteristics of the stump.
� Questionable role in vascular disease – requires the sacrifice of 7.5 cm of stump length, and significantly increased operative time.
� May be indicated in young patients to provide a stronger stump, or in revisions of traumatic supramalleolar amputation. (McCollogough, 1981)

POSTOPERATIVE STUMP MANAGEMENT

Drain vs No Drain?

� A hematoma is a major complication, predisposing to infection which may delay wound healing or sabotage it completely. Revision surgery or more proximal amputation have been known to be caused hematoma formation.
� Kacy et al. (1982, Surg. Gynecol. Obstet.) 113 BKA’s in 100 patients. Wound complications in 55% of drained patients, 16% in those not drained (Penrose drains)
� Tripses and Pollak (1981, Am. J. Surg.) 64 BKA patients. 46% infection rate in drained patients, 20% in undrained.

Conclusion: Meticulous hemostasis is critical. Open drainage is hazardous. Closed drainage may be useful if the patient is oozing a great deal at the conclusion of the case.