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

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