High Tibial Osteotomy – Complications

High Tibial Osteotomy – Complications

Undercorrection – the most common complication
– basically, anything less than 7 degrees of valgus is undercorrected. Must get them to 8-10 degrees of valgus (representing an overcorrection of 3-5 degrees from normal valgus)

Overcorrection – second most common complication
– going too far is bad also; > 15 degrees of valgus is poorly tolerated and can cause patellofemoral tracking problems

Deep Peroneal Nerve Injury – third most common, but most dreaded complication
– caused by tight post-op bandages, tight casts, transient anterior compartment syndrome, and direct injury
– in general, it is not recommended to go expose it – just keep the knee flexed during the procedure; exposing it and even gentle handling of it can cause a neuropraxia.
– 0-40 mm from tip is where the motor branch to tibialis anterior arises
– 68-153 mm from tip is where motor branch to EHL arises – EHL weakness postop is frequently seen because of failure to recognize this. The safe zone is 160 mm from tip of fibula.

Vascular Injury & Compartment Syndrome
– do prophylactic fasciotomy and use drain if necessary

Delayed Union/Nonunion
– preserve the medial osseoperiosteal hinge! It is critical to stability of the osteotomy.
– osteotomy proximal to the tibial tubercle has a lower rate of nonunion than distal

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.

C-Spine Outcome 2

c-spine outcome2

– there was no mention of the complications that the surgical patients endured.

– they concluded that half of patients continued to have neurologic symptoms, and that the statistically significant improvement was only seen in the surgical group (though the medical group did improve). The fact that many did not improve suggested to the authors that they were not dealt with soon enough, and that surgery should have been offered sooner – pretty far stretching conclusion.

In the end, it is really difficult to derive much from this study. How to treat the individual who shows up with a cervical radiculopathy? Surgery or medical treatment? Because the two groups were different to begin with and no randomization was performed, it is difficult to compare the results between the two groups! Sure, they showed an improvement in the surgical group, but the indications for surgery were not listed, and so it is difficult to know how to apply these observations.
They did, however, indicate that a significant number of surgical patients (over 25%) continue to have severe pain – they offer no explanation for this.

So, if the question is “how do I treat patients with cervical radiculopathy?” it is difficult to say that this paper offers much help in answering that….

Knee – Medial Anatomy

knee-medial anatomy

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.

MCQs – Sports Knee 2

MCQs-sports knee 2
lateral release and VMO advancement

– if you have lateral patellar tilt but otherwise normal tracking, start again with physio, then you can do an arthroscopic lateral release. “LPCS” or lateral patellar compression syndrome is associated with a tight lateral retinaculum and excessive lateral tilt.

– in terms of risk factors for arthrofibrosis after ACL reconstruction – a toss up between MCL repair and reconstruction within 2 weeks. Lots of papers describe increased stiffness when doing ACL plus meniscal repair and ACL plus MCL repair (the latter does worse – ie. doing the MCL leads to more stiffness than the meniscus); lots describe increased stiffness when doing them acutely. But nothing I’ve seen compares the addition of MCL repair versus timing of surgery as risk factors.

– graft placement within the knee is critical in ACL reconstruction – on the femur, placing it too anteriorly makes it too tight in flexion, placing it too posteriorly makes it too tight in extension. On the tibia, placing the hole too anteriorly makes it too tight in flexion and makes it impinge in extension

– the ACL and PCL are extra-synovial

– the tibial attachment of the ACL is stronger than the femoral origin – check this out!

– the saphenous nerve is most in danger when doing outside in mensical repair

– most LCL injuries can be managed non-operatively. This typically causes problems in the varus knee only.

– the best predictor of outcome after HTO is the postop alignment.

– for distal femoral varus osteotomy, you are aiming for a femoral-tibial angle of ZERO (or maybe a tiny bit of valgus at most)

– the Q angle is not increased by externally rotating the femur; it is increased by anteversion of the hip (internal rotation of the femur) and external rotation of the tibia (lateralizes the insertion of the patellar tendon)

– on the function of the meniscus – takes 50% of load in extension, 85% of load in flexion; as a shock absorber, it is decreases shock by 20%. As a stabilizer, it is not very important until the ACL is torn, at which point the medial meniscus becomes a very important stabilizer – it is stressed and often tears with chronic ACL insufficiency.

Fowler – Exertional Compartment Syndrome

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

Langerhans Cell Granulomatosis

Langerhans Cell Granulomatosis

– eosinophilic granuloma – solitary lesion in long bones, pelvis, ribs & vertebrae of young kids (5-10 yrs)
– nonneoplastic proliferation of Langerhans cells associated with eosinophils & chronic inflammatory cells
– Hand-Schuller-Christian disease – systemic process involving multiple bones (esp skull) as well as liver, lungs, spleen & skin
– Letterer-Siwe disease – skeletal lesions with aggressive clinical course due to widespread involvement of skin, viscera & lymphatics

Signs & Symptoms:
– localized pain & swelling

– in long bones: – metaphyseal or diaphyseal lesions with endosteal scalloping
– local periosteal reaction if cortical destruction
– spinal lesions – vertebra plana (2o compression of vertebral body)

– Langerhan’s cells – vesicular, indented nucleus with small, centrally placed nucleolus & abundant pale, granular eosinophilic cytoplasm
– arranged in sheets or clusters & surrounded by eosinophils, various chronic inflam’y cells & macrophages
– electron microscope – ‘Birbeck granules’ = racquet-shaped cytoplasmic structures

– depends on location of lesion
– intralesional steroid injection vs curettage & bone grafting

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

Midtarsal Injuries

Midtarsal Injuries

Reference: Heckmann, James, in Rockwood and Green, 1996, Chapter 32

Main Message

These are often overlooked injuries that require a keen index of suspicion.

Points of Interest

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

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.