podiatry exam 2 2005 boards part 2

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  1. Diagnostic test for herpes simplex of the foot
    Herpes simplex is diagnosed with a Tzanck smear in which fluid from an intact vesicle is smeared on a glass slide, dried, and stained with Giemsa’s stain.
  2. pagets disease
    • Paget's Disease
    • A focal disorder of bone metabolism in which all the elements of bone remodeling are increased resulting in bony enlargement and deformities.The condition is often asymptomatic although pain and stiffness may develop. Symptoms include an enlarged skull, bowing of the long bones, and pathologic fractures.

    • What are the stages of Paget?
    • 1. Destructive – osteolytic
    • 2. Mixed – osteolytic and osteoblastic
    • 3. Sclerotic – osteoblastic

    OSTEOSARCOMA(osteogenic sarcoma)-malignant bone forming tumor-most common malignant bone tumor with exception of Multiple Myloma-age 10-25yrs, and >40yrs-male to female distribution is equal-most commonly found in the metaphyseal region around the knee(distal femur or proximal tibia)-usually occurs in teenagers during rapid growth spurts or in patients over 40 who have a preexisting condition most notably Paget's dz-Symptoms: Pain, swelling, and fever(R/0 OM), the osteoid producing nature of the tumor often yield an elevated alkaline phosphatase level-radiographic appearance: appearance is variable depending on osteolytic or sclerotic nature of lesion. Penetration of cortical bone usually occurs with a Codman's triangle or "Sunburst" appearance-prognosis is poor
  3. ankylosing spondylitis
    • SERONEGATIVE SPONDYLOARTHROPATHIES ANKYLOSING SPONDYLITIS(Marie-Strumpell's dz)
    • DESCRIPTION
    • A chronic inflammatory arthritis that affects the sacroiliac joint and to a lesser extent the rest of the spine. Pain and stiffness are early signs,but in advanced cases a poker spine(very stiff, inflexible backbone) is common.
    • SIGNS AND SYMPTOMS-onset is 15-35 yrs-male to female ratio(10:1)-lower back pain(sacroiliac jts)-kyphosis-Recurrent acute iritis in 1/3 of pts
    • DIAGNOSIS-increased sed rate-(+)HLA-B27-(+)Schoeber's Test- (A 10cm length is measured along the erect lower lumbar spine, the pt bends forward. This measurement should increase by at least 4cms.This test is positve in Ankylosing Spindylitis.)
    • X-ray-abnormalities at the sacroiliac jt-bamboo spine
    • TREATMENT
    • -PT-NSAIDS

    • Ankylosing Spondylitis
    • The criteria for the diagnosis of ankylosing spondylitis include:1. Limited motion of lumbar spine in anterior and lateral flexion and extension 2. History of pain or presence of pain in dorsolumbar junction or in lumbar spine 3. Limitation of chest expansion to one inch or less
    • Definite ankylosing spondylitis is confirmed by the presence of bilateral sacroiliitis associated with at least one clinical criteria. Probable ankylosing spondylitis exists in the presence of bilateral sacroiliitis associated with none of the clinical criteria. Common symptoms include low back pain, prolonged back stiffness, ascending back pain, heel pain,peripheral joint pain, fatigue, and diminished vision and/or eye pain. Roentgen signs vary with duration of the disease. Early signs include sacroiliac joint blurring, joint space narrowing and widening, subchondral sclerosis, diffuse osteoporosis of spine, apophyseal joint sclerosis, and straightening of spine. Advanced ankylosing spondylitis reveals apophyseal joint erosion, squaring of vertebrae, narrowed disc space, vertebral collapse,pelvic whiskering, and pubic symphysis involvement. Terminal roentgen signs include intervertebral disc calcification, paravertebral ligament calcification, vertical syndesmophytes,sacro-iliac joint fusion, and bamboo spine.
  4. RHEUMATOID ARTHRITIS
    • RHEUMATOID ARTHRITIS
    • Inflammatory, Symmetrical, Pain worse in morning or after rest, Osteopenia, Increased soft tissue density, (+)RA factor, Swan neck, ulnar deviation, Boutonniere, pannus
    • OSTEOARTHRITIS(DJD)Noniflammatory,Asymmetrical , Pain worse at the end of the day, Sclerosis,Soft tissue is normal,(-)RA factor

    • -do cervical spine x-ray pre-op(predisposed to atlas/axis dislocation)
    • -more prone to infection due to immunosuppressive medications

    • DESCRIPTION
    • Begins as a chronic symmetric peripheral polysynovitis with insidious aching and morning stiffness. Caused by an autoimmune response that progresses to destruction of articular and periarticular structures.
    • SIGNS AND SYMPTOMS-symmetrical inflammatory polyarthritis-pain and swelling worse in the morning and after rest(gets better with motion)-Gel phenomenon-after rest the pts jt stiffens and becomes painful to move-female to male ratio(3:1)-onset is 20-50 yrs of age-affects small jts in hands and feet(MPJs, wrists, MCJs, and PIPJ)-Possible low grade fever, fatigue, weight loss, and malaise-Rheumatoid nodules-benign subcutaneous painless masses found at sites usually subject to trauma-Boutonniere deformity-flexion of the PIPJ of the finger with hyperextension of the DIPJ-Swan neck deformity-hyperextension of the PIPJ of the finger with flexion of the DIPJ
    • -Baker's Cyst(popliteal cyst)-a synovial fluid filled cyst which develops in the popliteal fossa. When ruptured symptoms mimic a DVT-Felty's Syndrome-rheumatoid arthritis with associated splenomegalia.Patient presents with pigmented spots on the lower extremity-Pannus transformation-the synovium develops into a vasculature granulation tissue that produces inflammatory agents and immunoglobin-producing lymphoreticular-like elements that destroy the articular cartilage
    • DIAGNOSIS
    • Blood-increased Sed rate-(+)RA factor-normocytic MCV
    • X-ray-fibular/ulnar deviation of phalanges-marginal erosions, ulnar styloid process shows early erosions-increased soft tissue density-early increase in joint space(from pannus formation), later decreased joint space which can lead to ankylosis-juxta-articular osteopenia(metatarsal heads are washed out whilethe shafts may be relatively normal)
    • TREATMENT-rest(splints) during flare-ups, ROM exercise during remission-anti-inflammatory drugs-especially ASA-corticosteroids(prednisone)-Antimalarial drugs(Hydroxychloroquine)-Gold salts, Methotrexate

    • Rheumatoid Arthritis (RA) is a constitutional disease with inflammatory changes throughout the connective tissues. It is generally a wasting disease with muscle and bone atrophy.Chronic proliferative inflammation of the synovium exists and causes irreversible damage to joint capsule and cartilage, which are replaced by granulation tissue. Radiographically there is joint space narrowing, periarticular demineralization, bone erosion, "punched out" periarticular lesions, subluxation, deformity (arthritis mutilans), and osteoporosis. RA primarily affects the small joints of the hands and feet, most commonly the PIPJs and MTPJs. lt can also present in the hindfoot and ankle, with progressive metatarsal joint and subtalar joint subluxation and ankle pes valgus. Frequently the posterosuperior process ofthe calcaneus is involved. Clinical manifestations include post-static dyskinesia (pain that is worse after periods of immobility) and non-weight bearing, as well as stiffness. Post-static dyskinesia is a hallmark of any type of arthritis. Pain and stiffness often subside somewhat after motion has proceeded and the joint "warms up." Prolonged activity thereafter can lead to worsening of pain. Constitutional symptoms of weight loss, fever, coldness, numbness,ting ling, fatigue and malaise are common. The cardinal objective findings are bilateral,symmetrical small joint swelling (fusiform, sausage fingers and toes), tenderness to palpation (or even barometric pressure), and pain with motion. Swelling due to synovial hypertrophy is palpably spongy or rubbery, and often crepitant. Synovitis may lead to effusion. Limited motion over a long period is associated with muscle wasting, contracture,fibrosis, and ankylosis. Subcutaneous rheumatoid nodules (palisading granulomas) mayform in areas of bony prominence, weight bearing or contact.Diagnosis of RA is based on disease characteristics over time. Classic RA displays 7 of the following symptoms, the first 5 presenting for at least 6 weeks: morning stiffness, painful range of motion in at least one joint, swelling in at least one joint, swelling of at least one other joint, symmetrical joint swelling with simultaneous involvement ofthe same joint onboth sides of the body (except PIPJs), subcutaneous nodules, X-ray changes typical of RA(peri-articular osteopenia, joint narrowing, bone whittling), positive agglutination test(rheumatoid factor), poor mucin clot precipitate, characteristic histologic changes in synovial membrane, characteristic histologic granulomatous nodules. Five of these findings in combination represent definitive RA,3 represents probable RA. Possible RA is represented by any 2 of the following for 3 weeks: tenderness or pain with motion, morning stiffness, history of joint swelling, subcutaneous nodules, elevated ESR or CRP, or iritis.
    • Exclusions to RA include:1. Malar rash typical of systemic lupus erythematosus (SLE) 2. Rash typical of drug reaction 3. High concentration of lupus erythematosus (LE) cells 4. Histologic evidence of polyarteritis nodosa 5. Trunk or neck or pharyngeal weakness or swelling or dermatomyositis 6. Definite scleroderma 7. Rheumatic fever 8. Tophi or gout 9. Septic arthritis 10. Reiter's syndrome 11. Tubercle bacilli in joint 12. Shoulder-hand syndrome 13. Hypertrophic pulmonary osteodystrophy 14. Clinical picture characteristic of neuropathy 15. Homogentisic acid in urine 16. Histological evidence of sarcoidosis 17. Positive Kveim (sarcoid antigen) test 18. Multiple myeloma 19. Characteristic skin lesions of erythema nodosum 20. Leukemia or lymphoma 21. AgammaglobulinemiaLab Testing for RA includes CBC with slight to moderate normocytic hypochromic anemia,white count decreased or, in acute cases, elevated (PMNs may be increased with left shift),chronic normal to slight decrease ESR, moderate to marked increase rheumatoid factor(RF) with this agglutination test positive 75% after several months to a year, normal uricacid, altered plasma proteins (fibrinogen and globulin increased, albumin and total proteinand NG ratio decreased), normal Ca++ and P04, and the synovial fluid is cloudy withincreased WBCs and decreased viscosity. The differential diagnosis includes anypolyarthritic inflammatory disease with constitutional signs and symptoms.

    JUVENILE RHEUMATOID ARTHRITIS-RA factor is usually negative, however ANA is usually positive-not a life long disorder(fades with age)-onset is usually before age 16yrs-females to males(4:1)-usually involves the knees, elbows, ankles or neck-in addition to arthritis JRA is often associated with fever and skin rashand fusions of the cervical spine(especially C2-C4)-JRA is divided into three types1) polyarticular(40%)2) pauciarticular(40%)-associated with iridocyolitis3) Still's disease(20%)-associated with systemic manifestations(splenomegaly, generalizedadenopathy)-treatment is largely the same as with RA, including ASA and otherantiinflammatory modalites
  5. osteomalacia
    A condition marked by softening of the bones with pain, tenderness,muscular weakness, and loss of weight resulting from a deficiency of vitamin D and calcium.
  6. STJ coalition
    • TARSAL COALITIONS
    • DESCRIPTION
    • -a bridge between two or more tarsal bones that restrict motion-most common cause of peroneal spastic flatfoot(the spasm occurs as a response of the body to immobilize the STJ)-male > female-pain is usually insidious in onset or may follow athletics or minor trauma-occasionally anterior and posterior muscles are in spasm causing a varus deformity-incidence is ~1 % - 50 % B/L-TC and CN coalitions are roughly equal in distribution and account for over 90% of tarsal coalitions-common peroneal blocks may be used to relax the spastic peroneals and fully evaluate ROM
    • SYMPTOMS-deep, aching pain aggravated by activity, relieved by rest-decreased ROM-muscle spasm(peroneals are often fatigued from over use)-halo sign-talonavicular beaking-anteater nose sign
    • CAUSE-Congenital(failure of segmentation of primitive mesenchyme)-Aquired(infection, arthritis, trauma, iatrogenic)Fusion tissue type Syndesmosis-fibrous Synchondrosis-cartilaginous Synostosis-osseous
    • ORDERING A CT FOR STJ-coronal(frontal) plane scan-contiguous sections-between 2-5mm slices-from the posterior talo-calcaneal facet to the navicular

    • HARRIS-BEATH(SKI-JUMP)-good for posterior and middle STJcoalitions-angle unit 45°-patient stands on film with kneesand ankles flexed 15-20°-first take a scout lateral filmand determine the declinationangle of posterior facet of STJ.Then take 3 views; one at the angle determined by the lateral film,one 10° above and one 10° below-some advocate 3 arbitrary views at 35°, 40°, and 45°
  7. pulmonary embolism
    • Pulmonarv Embolism (PE)
    • PE is very common and a leading cause of death in the US. Lower extremity DVT accounts for 60-80% of PEs. Thrombi embolize from the lower extremities, traverse the pelvis and inferior vena cava, then enter the right side of the heart, and subsequently obstruct the pulmonary vessels. Pulmonary infarction ensues thereafter.
    • Clinical signs and symptoms vary with the degree of pulmonary occlusion and infarction, and include crushing chest pain, dyspnea,tachypnea, tachycardia, low grade temperature elevation (38 C [101 F]), neck vein distension, ipsilateral diaphragm elevation on standard chest X-ray, a positive ventilation perfusion lung scan (131/ or 51Cr), S-T segment depression (cardiac hypoxia) and other EKG changes, arterial blood gas abnormalities such as decreased P02 and PC02 and Ph, increased serum LDH and bilirubin in the presence of normal SGOT. The differential includes acute MI and pneumonia.
    • Treatment includes immediate anticoagulation with IV administration of 5,000-10,000 units of heparin, followed by continuous infusion of 800-1500 units/hr while monitoring the PH
    • Supportive measures include administration of 02, bed rest, and analgesia; while proceeding with definitive diagnostic measures. Thrombolytic therapy, or surgical phlebectomy, may be indicated. Septic pulmonary emboli may be observed as acomplication of infected pelvic thrombosis, in dwelling catheter, transvenous pacemaker,arteriovenous or ventriculovenous shunts, or in cases of IV drug abuse.
  8. DEEP VENOUS THROMBOSIS (DVT)
    • DEEP VENOUS THROMBOSIS(DVT) DESCRIPTION
    • Partial or complete occlusion of a vein by thrombus with secondary inflammatory reaction in the wall of the vein. Arises approximately 80% of the time in the deep veins of the calf. Contributing factors include those of Virchow's Triad such as: CHF, Ml, stroke,malignancy, Sx, trauma, immobilization, previous thromboembolic dz, obesity, pregnancy, oral contraceptives, and advanced age. The typical patient is a woman over 30 yrs old, on BCP's who smokes. There is a danger of pulmonary embolism in these patients. DVT usually results in destruction of the venous valves resulting in veins that are incompetent resulting in postphlebitic syndrome(venous insufficiency).
    • SIGNS/SYMPTOMS-Symptoms arise over a period of hours to 1-2 days.-Self limiting and lasts 1-2 weeks-Distention of superficial venous collaterals, and slight fever and tachycardia may develop.-Physical exam is normal in 50% of pts-Painful swollen leg with dilated superficial veins and a palpable cord-(-t-) Homan's sign-dorsiflexion of foot causes deep pain in calf-Pulses are usually present
    • DIAGNOSIS-Difficult to diagnose by Hx and PE-Venography remains the gold standard
    • TREATMENT-Leg should be elevated -15-20°, trunk should be kept horizontal-Bedrest until local tenderness and swelling disappears-Heparin(bolus of 5,000-10,000 units IV followed by a continuous IV infusion of 500 units/kg every 24hrs).-PTT should be checked 4-6hrs after initial therapy and then at least every 24hrs. PTT levels should be maintained at 2-3 times the control value-Monitor ABGs-Pt should later be started on long term anticoags(Coumadin) loading dose of 10mg is given each day until PT increases.Then a smaller dose (5-7.5mg) is given to maintain PT ~1.3-1.5 above the control value. Pts should be Tx for 3 months for the 1st episode.

    • Venous Thrombosis and Pulmonary Embolism-the deep veins of the lower extremity include the plantar arch, posterior tibial, peroneal, anterior tibial, sural, popliteal, superficial femoral, and deep femoral. Venous thrombosis, particularly of the deep system at or above the popliteal fossa, is associated with pulmonary embolism (PE), and for this reason can be fatal or extremely morbid. Predisposing factors for venous thrombosis include congestive heart failure, malignancy, trauma, surgery, pregnancy, and thrombocytosis. Other risk factors include cigarette smoking, oral contraceptive use, obesity, advanced age, bed restor confinement, and paraplegia. Deep venous thrombosis prophylaxis should be instituted in patients at risk (Tables 3-6 and 3-7).Lower extremity deep vein thrombophlebitis (DVT, also known as venous thromboembolism,or VTE) presents with deep, aching pain and tightness in the calf or thigh. Pain upon active dorsiflexion ofthe ankle, or resistance to ankle dorsiflexion is known as Homan's sign, and is a nonspecific and unreliable clinical diagnostic maneuver. Tenderness upon calf or thigh muscle compression is a more specific test for DVT, when associated with edema and local increase in skin temperature. Superficial thrombophlebitis, which conveys a lower likelihood of PE, more commonly displays local heat, edema, erythema, and a palpable cord consistent with the thrombosed vein. Application of a tourniquet above the suspected thrombosis may cause pain at the level of thrombosis within 30-45 seconds, and is strongly suggestive of DVT. Comparison of calf circumference will often show enlargement of the affected side. Constitutional findings may include temperature elevation (39.5°-40.5° C), chills,and malaise. Arterial embolism is usually more painful early on, with less swell ing,exaggerated distal temperature decrease, and early sensory deficit. Severe venous thrombosis effecting retrograde arterial flow decrease may result in phlegmasia ceruleadolens, which can result in pedal ischemia and gangrene. Coagulation studies are usually normal unless full blown disseminated intravascular coagulation (DIC). familial antithrombin III deficiency, or lupus erythematosus clotting inhibitors exist. The laboratory diagnosis of DVT hinges on venous non-invasive duplex Doppler examination, andmagnetic resonance venography or contrast venography may be employed if ultrasound is equivocal. Radioactive 1251-fibrinogen scanning, in conjunction with occlusion impedence plethysmography is also a sensitive combination for DVT of the calf. Use ofthe D-dimert est may also be useful, however combined clinical and venographic tests are more reliable. An accurate diagnosis of DVT is made upon identification of predisposing factors and clinical observation, combined with duplex Doppler ultrasound and, perhaps, magnetic resonance venogram or contrast venography.Prevention of DVT is recommended, and can be achieved in several different ways (Tables 3-6 and 3-7). Prophylactic therapy in the low-risk patient involves mini-dose subcutaneous administration of 5000 units of heparin every 8 or 12 hours beginning about 60 minutes preoperatively. Adjunct physical measures include support hose, intermittent sequential pneumatic compression of the lower extremity, leg elevation with the knee flexed, and out-of-bed activity at an early stage after surgery. In high-risk patients, DVT prophylaxis is administered preoperatively with mini-dose heparinization, however in the postoperative phase, the heparin dose is adjusted upward to keep the PH within 4 seconds of high normal. Despite statistically more postoperative hemorrhage, this form of DVT prophylaxis appears to be worthwhile in the high-risk patient. A baseline platelet count is recommended prior to mini-dose heparinization, and should be monitored periodically if it is observed to be low. High-risk patients may also be prophylaxed with a combination of mini-dose heparin and dihydroergotamine, which causes venular constriction and rapid venous return.Other prophylactic combinations include heparin and antithrombin III administration, and the use of low molecular weight heparin administered once daily has been shown to be effective and popular (see risk stratification and guidelines for prophylaxis, below).Coumadin, which inhibits the vitamin K-dependent clotting factors II, VII, IX, X, and proteins G and S, can also be administered preoperatively and during the postoperative phase to effect DVT prophylaxis.
    • TABLE 3-6. DVT RISK STRATIFICATION (ASSIGN POINTS BASED ON PROCEDURE,DISEASE, AND OTHER PATIENT-RELATED FACTORS).
    • Risk factorsOperating room time> 105 minTourniquet time >90 minRearfoot or ankle surgeryAge 40-60 yearsPregnancy or postpartum <1 monthVaricose veinsObesity (>20 Ibs over ideal body weight)Diabetes mellitusHypertensionHyperlipidemiaSmokerPolycystic ovary syndromeImmobilized in BK or AK cast for> 1 weekPatient confined to bed for >72 hoursCentral venous accessAge >60 yearsOral contraceptive useHormone repla cement therapyInflammatory bowel diseaseCongestive heart failureAnkle, pilon or tibial fractureSevere sepsis/infectionMultiple traumaAcute spinal cord injury• Cancer treatmentCurrently treated or history of DVT or PERisk factor points assigned235Ch.3 Selected Diseases and Pathological Conditions 57TABLE 3-7. DVT RISK STRATIFICATION AND GUIDELINES FOR PROPHYLAXIS.Risk Risk Clinical Prophylaxispoints stratum features0 Low " <40 years old • Patient education"Minor surgery • Early ambulation<30 minutes1-2 Moderate "40-60 years old • Patient education, early ambulation, elastic+ minor surgery stockings• General anesthesia '1 ntermittent pneumatic compression (if>30 minutes NWB)" Minor surgery • Low dose unfractionated heparin+ 1 or more other risks (5000 units sq), or low molecular weightheparin (enoxaparin 30 mg sq q 12 hours or40 mg sq qd)• Mechanical therapy starting 1-2 hoursbefore surgery, or 12-24 hours postop ifneeded to achieve adequate hemostasis• Continue therapy while inpatient or duringinitial recovery, then decide whethertoextend 7-14 days3-4 High ">60 years old + • Patient education, early ambulation, elasticminor surgery + stockingsno other risks • Intermittent pneumatic compression" >40 years old + (if NWB)minor surgery + • Low dose unfractionated heparinany other risk (5000 units sq), or low molecular weightheparin (enoxaparin 30 mg sq q 12 hours or40 mg sq qd)• Mechanical therapy starting 1-2 hoursbefore surgery, or 12-24 hours postop ifneeded to achieve adequate hemostasis• Continue therapy throughout hospitalizationand up to 7-14 days, then decide durationbased on degree of immobilization, ROMand WB status~ 5 Very high "> Past PE, cancer • Patient education, early ambulation,or major trauma elastic stockings"> 40 years old + '1 ntermittent pneumatic compressionmajor surgery + (if NWB)any other risk factor • Low molecular weight heparin (enoxaparin30 mg sq q 12 hours or 40 mg sq qd), orfondaparinux, or adjusted dose heparin• Warfarin (therapeutic when INR 2-3)• Start therapy 1-2 hours preop, or 12-24hours postop if needed to achieveadequate hemostasis• Continue therapy 10-14 days or entire timeof immobilization• Encourage early ROM and/or WBif indicated58 Selected Diseases and Pathological Conditions Ch.3Treatment of DVT involves assessment of the PT and PTI, followed immediately by IVinfusion of heparin 5000-10,000 units. Thereafter, heparin is infused continuously at a rate of800-1500 units per hour, maintaining the PTI at 2-2.5 times the baseline value, and the INRat 2.0-3.0. The patient is maintained at bed rest with the lower extremities elevated at 15degrees to 20 degrees above the level of the heart. It takes approximately one week forthrombi to become firmly adherent to endothelium and thereby diminish the risk of PE.Coumadin is started as soon as longterm anticoagulation is planned, and takes 3-5 days tobecome therapeutic monitoring the PT. The patient is maintained in an anticoagulated statefor 4-6 weeks for the treatment of isolated calf DVT, and for 3-6 months for more proximalvein thrombosis. Clinical and/or venographic evidence of clot propagation indicates theneed for vascular surgical consultation regarding the potential benefits of Greenfield filter(umbrella) placement in the inferior vena cava. Moreover, thrombolytic therapy, orphlebectomy in rare instances, may be indicated. Postphlebitic syndrome may ensue, andinvolves venous insufficiency, chronic venous stasis dermatitis, permanent calfenlargement and predisposition to recurrent superficial and deep thrombophlebitis,postphlebitic neuritis, and the need for indefinite use of support hose and perhaps otherphysical measures.
  9. Which agent is associated with drug-induced systemic lupus erythematosus?
    Patients who take procainamide for prolonged periods often develop anticardiolipin antibodies as well as anti-DNA and anti-histone antibodies. Drug induced systemic lupus erythematosus is rare and usually subsides once the medication is discontinued.
  10. SYSTEMIC LUPUS ERYTHEMATOSUS(SLE)
    • SYSTEMIC LUPUS ERYTHEMATOSUS(SLE)
    • DEFINITION
    • A chronic, remitting, relapsing, inflammatory, and often febrile, multisystemic disorder of connective tissue, acute or insidious in onset.Drug induced lupus may be caused by: Procainamide, Hydralazine,Chlorpromazine, Isoniazid, Penicillamine, Griseofulvin
    • SIGNS/SYMPTOMS-age of onset 15-35 yrs-joint pain in 90% of patients(an early manifestation)-primarily small joints of the hands and feet-mainly in young women(10:1)-more common in blacks-fever(90% of patients)-abdominal pains-butterfly rash-skin lesions in sun exposed areas(photosensitivity)-fatigue, weight loss, and anorexia-Raynaud's phenomenon-alopecia-vision problems-proximal nail fold telangiectasis-renal, cardiac, splenic, and pulmonary problems
    • DIAGNOSIS-increased sed rate-(+)ANA(antinuclear antibody test)-antibodies to double-stranded DNA-decreased hemoglobin, WBC, and platelets
    • TREATMENT-symptomatic steroids antimalarials (chloroquine) immunosuppressants avoid sunlight
  11. MELANOCYTES
    MELANOCYTES-intermingled amongst the basal cells-melanocytes produce melanin which absorbs ultraviolet light and protects the tissue-ultraviolet radiation activates melanocytes(tanning)

    • Melanoma
    • DESCRIPTION-malignant tumor of the melanocytes-arising from pre-existing nevi orde novo-found primarily on sun exposedareas of fair skinned individuals-predilection for the backs of menand the legs of women-when it occurs in blacks it is oftenfound on the palms, soles, or nailbeds-majority present between 30-60years of age-any pigmented skin lesion withrecent change in appearanceshould be suspectTYPESa) Superficial Spreading Melanoma-Most common(70%)-Occurs in younger patients-Spreads radially before invading deep-Pigmented macular/papular lesion with irregular bordersb) Nodular Melanoma-15% of cases-Worst prognosis(becomes invasive early)-Uniformly pigmented bizarrely colored nodule-Commonly ulceratesc) Lentigo Maligna Melanomafmalignant freckle)-5% of Melanomas-Slowest growing, least likely to metastasize-Macular patch of mottled pigmentation-Enlarged radially before spreading deep-Occurs on sun exposed areas-More common in older pts >60yrsd) Acral lentiginous Melanoma-10% of Melanomas-Aggressive, invades early-Occurs chiefly on the palms and soles, often on the digits or subungual(melanotic whitlow)-Usually found on nonwhite individuals
  12. shin splints
    Shin splints are a common injury in runners and are most symptomatic when a person is running on hills. Overpronation is often the etiology.
  13. rheumatoid arthritis
    • Which of the following is a chronic inflammatory disease characterized by proliferative synovitis with subsequent bony erosion and destruction of the articular cartilage?
    • Rheumatoid arthritis is characterized by synovial inflammation. Joint destruction in rheumatoid arthritis targets articular cartilage, ligaments, tendons,and bone.

    • RHEUMATOID ARTHRITIS
    • DESCRIPTION
    • Begins as a chronic symmetric peripheral polysynovitis with insidious aching and morning stiffness. Caused by an autoimmune response that progresses to destruction of articular and periarticular structures.
    • SIGNS AND SYMPTOMS-symmetrical inflammatory polyarthritis-pain and swelling worse in the morning and after rest(gets better with motion)-Gel phenomenon-after rest the pts jt stiffens and becomes painful to move-female to male ratio(3:1)-onset is 20-50 yrs of age-affects small jts in hands and feet(MPJs, wrists, MCJs, and PIPJ)-Possible low grade fever, fatigue, weight loss, and malaise-Rheumatoid nodules-benign subcutaneous painless masses found at sites usually subject to trauma-Boutonniere deformity-flexion of the PIPJ of the finger with hyperextension of the DIPJ-Swan neck deformity-hyperextension of the PIPJ of the finger with flexion of the DIPJ
    • -Baker's Cyst(popliteal cyst)-a synovial fluid filled cyst which develops in the popliteal fossa. When ruptured symptoms mimic a DVT-Felty's Syndrome-rheumatoid arthritis with associated splenomegalia.Patient presents with pigmented spots on the lower extremity-Pannus transformation-the synovium develops into a vasculature granulation tissue that produces inflammatory agents and immunoglobin-producing lymphoreticular-like elements that destroy the articular cartilage
    • DIAGNOSIS
    • Blood-increased Sed rate-(+)RA factor-normocytic MCV X-rav-fibular/ulnar deviation of phalanges-marginal erosions, ulnar styloid process shows early erosions-increased soft tissue density-early increase in joint space(from pannus formation), later decreased joint space which can lead to ankylosis-juxta-articular osteopenia(metatarsal heads are washed out whilethe shafts may be relatively normal)
    • TREATMENT-rest(splints) during flare-ups, ROM exercise during remission-anti-inflammatory drugs-especially ASA-corticosteroids(prednisone)-Antimalarial drugs(Hydroxychloroquine)-Gold salts, Methotrexate

    JUVENILE RHEUMATOID ARTHRITIS-RA factor is usually negative, however ANA is usually positive-not a life long disorder(fades with age)-onset is usually before age 16 yrs-females to males(4:1)-usually involves the knees, elbows, ankles or neck-in addition to arthritis JRA is often associated with fever and skin rash and fusions of the cervical spine(especially C2-C4)-JRA is divided into three types1) polyarticular(40%)2) pauciarticular(40%)-associated with iridocyolitis 3) Still's disease(20%)-associated with systemic manifestations(splenomegaly, generalized adenopathy)-treatment is largely the same as with RA, including ASA and other antiinflammatory modalites

    • Rheumatoid Arthritis (RA) is a constitutional disease with inflammatory changes throughout the connective tissues. It is generally a wasting disease with muscle and bone atrophy.Chronic proliferative inflammation of the synovium exists and causes irreversible damage to joint capsule and cartilage, which are replaced by granulation tissue.
    • Radiographically there is joint space narrowing, periarticular demineralization, bone erosion, "punched out" periarticular lesions, subluxation, deformity (arthritis mutilans), and osteoporosis. RA primarily affects the small joints of the hands and feet, most commonly the PIPJs and MTPJs.lt can also present in the hindfoot and ankle, with progressive metatarsal joint and subtalar joint subluxation and ankle pes valgus. Frequently the posterosuperior process of the calcaneus is involved.Clinical manifestations include post-static dyskinesia (pain that is worse after periods of immobility) and non-weight bearing, as well as stiffness. Post-static dyskinesia is a hallmark of any type of arthritis. Pain and stiffness often subside somewhat after motion has proceeded and the joint "warms up." Prolonged activity thereafter can lead to worsening of pain. Constitutional symptoms of weight loss, fever, coldness, numbness,ting ling, fatigue and malaise are common. The cardinal objective findings are bilateral,symmetrical small joint swelling (fusiform, sausage fingers and toes), tenderness to palpation (or even barometric pressure), and pain with motion. Swelling due to synovial hypertrophy is palpably spongy or rubbery, and often crepitant. Synovitis may lead to effusion. Limited motion over a long period is associated with muscle wasting, contracture, fibrosis, and ankylosis. Subcutaneous rheumatoid nodules (palisading granulomas) may form in areas of bony prominence, weight bearing or contact.
    • Diagnosis of RA is based on disease characteristics over time. Classic RA displays 7 of the following symptoms, the first 5 presenting for at least 6 weeks: morning stiffness, painful range of motion in at least one joint, swelling in at least one joint, swelling of at least one other joint, symmetrical joint swelling with simultaneous involvement of the same joint on both sides of the body (except PIPJs), subcutaneous nodules, X-ray changes typical of RA(peri-articular osteopenia, joint narrowing, bone whittling), positive agglutination test(rheumatoid factor), poor mucin clot precipitate, characteristic histologic changes in synovial membrane, characteristic histologic granulomatous nodules. Five of these findings in combination represent definitive RA,3 represents probable RA. Possible RA is represented by any 2 of the following for 3 weeks: tenderness or pain with motion, morning stiffness, history of joint swelling, subcutaneous nodules, elevated ESR or CRp, or iritis.Exclusions to RA include:1. Malar rash typical of systemic lupus erythematosus (SLE)2. Rash typical of drug reaction3. High concentration of lupus erythematosus (LE) cells4. Histologic evidence of polyarteritis nodosa5. Trunk or neck or pharyngeal weakness or swelling or dermatomyositis6. Definite scleroderma7. Rheumatic fever8. Tophi or gout9. Septic arthritis10. Reiter's syndrome11. Tubercle bacilli in joint12. Shoulder-hand syndrome13. Hypertrophic pulmonary osteodystrophy14. Clinical picture characteristic of neuropathy15. Homogentisic acid in urine16. Histological evidence of sarcoidosis17. Positive Kveim (sarcoid antigen) testCh.3 Selected Diseases and Pathological Conditions 6318. Multiple myeloma19. Characteristic skin lesions of erythema nodosum20. Leukemia or lymphoma21. AgammaglobulinemiaLab Testing for RA includes CBC with slight to moderate normocytic hypochromic anemia,white count decreased or, in acute cases, elevated (PMNs may be increased with left shift),chronic normal to slight decrease ESR, moderate to marked increase rheumatoid factor(RF) with this agglutination test positive 75% after several months to a year, normal uric acid, altered plasma proteins (fibrinogen and globulin increased, albumin and total protein and NG ratio decreased), normal Ca++ and P04, and the synovial fluid is cloudy withincreased WBCs and decreased viscosity. The differential diagnosis includes any polyarthritic inflammatory disease with constitutional signs and symptoms.

    • What are the Criteria for the Classification of Rheumatoid Arthritis according to the American Rheumatology Association?
    • 1.Morning stiffness (for at least 6 weeks).2.Arthritis of 3 or more joint areas (for at least 6 weeks).3.Arthritis of hand joints (for at least 6 weeks).4.Symmetric arthritis (at least 6 weeks).5.Rheumatoid nodules.6.Serum rheumatoid factor.7.Radiographic changes.For classification purposes, a patient has RA if they satisfy at least 4 of these 7 criteria.

    • What is the course of joint destruction seen in rheumatoid arthritis?
    • Erosion of juxta-articular bone around the margins of the pannus and invasion of subchondral tissue by the pannus.

  14. OSTEOARTHRITIS
    • OSTEOARTHRITIS( D e g e n e r a t i v e Joint Dz) DJD
    • DESCRIPTION
    • Osteoarthritis is the most common arthritis and occurs as a result of wear and tear on joints. The cartilage that cushions the impact on the joint gradually deteriorates. As the cartilage wears down, subchondral bone is exposed which becomes sclerotic, the surface becomes worn and polished in a process called eburnation. Over time, the ends of the bones also are affected, with bone growing along the sides producing lumps. There is usually a predisposing factor such as trauma or prior inflammatory arthritis.
    • SIGNS AND SYMPTOMS-asymmetrical noninflammatory arthritis-pain worse at end of day(after use)-pain in joint before a change in weather-loss of flexibility-Heberden's nodes(bony protuberances at the margins and dorsal surface of the DIPJs)-Bouchard's nodes(bony protuberances at the margins and dorsal surface of the PIPJs)-joints most commonly affected(neck, back, knees, hips, shoulder,1st MPJ and the 1st radiocarpal jt)
    • DIAGNOSIS
    • X-ray-subchondral sclerosis-loose bodies(jt mice)-asymmetrical jt space loss-soft tissue is normal
    • TREATMENT
    • -ROM exercises for stiffness-Joint replacements-Synovial fluid viscosupplements-lnjected into joints to cushions and lubricate joint space SYNVISC(Hylan G-F 20)-an elastoviscous fluid containing hylan polymers-indicated in OA-supplied in 2.25mL syringe containing 2mL-intra-articular injections once a week for a total of 3 injections HYALAGAN(Sodium Hyaluronate)-a viscous solution consisting of high molecular weight fraction of purified sodium hyaluronate-indicated in OA-2mL vials or 2mL pre-filled syringes-intra-articular injections once a week for a total of 5 injections
    • 

    Osteoarthritis (OA) can be idiopathic and defined as primary OA; or the result of repetitive mechanical strain, and defined as secondary ~A. Secondary OA is also termed degenerative joint disease or "wear and tear" arthritis, and is generally not inflammatory beyond the confines of the joint. Chronic subtalar joint and metatarsophalangeal joint hyperpronation is a common cause of degenerative joint disease in the foot. with resultant pes valgus, forefoot supinatus and hallux limitus/rigidus, plantarfascitis, flexor stabilization induced hammertoes, and medial Lisfranc breakdown. Any joint can be subject to degenerative joint disease, particularly when subjected to weight bearing or in the post-traumatic phase. There are three cardinal roentgen signs of OA, including joint space narrowing, subchondral sclerosis, and osteophytosis. The classic dorsal "flag" of hallux rigidus (dorsal bunion). first metatarsal-cuneiform exostosis, and the anterior tibial exostosis are examples of advanced osteophytosis. Clinical manifestations include PSD,joint pain without acute inflammation, stiffness, fine and/or coarse crepitus, and symptoms that worsen with weight-bearing activity. Although range of motion may be diminished,there is rarely ankylosis. OA usually affects middle-aged or older individuals, with history of insidious onset (unless post-traumatic), with gradual progression. The differential diagnosis includes rheumatoid arthritis, gout. and Charcot neuroarthropathy.

    Myxoid cysts or synovial cysts of the distal dorsal fingers are associated with which type of arthritis? Osteoarthritis.
  15. gouty arthritis
    • CRYSTALINE-INDUCED ARTHRITIS
    • GOUT
    • DESCRIPTION
    • A recurrent acute arthritis that affects peripheral joints, most notably the 1st MPJ. The arthritis stems from a build up of monosodium urate crystals in and around joints and tendons. Supersaturated hyperuricemic body fluids crystalize causing a severe red hot swollen joint. The arthritis may become chronic and deforming. Not all hyperuricemic persons develop gout. A build up of uric acid crystals in the joint may be from excessive breakdown or over production of purines. Gout classically begins in the evening or early morning and tends to occur in previously damaged joints.
    • SIGNS AND SYMPTOMS-asymmetrical monoarticular arthritis-sudden onset, red hot swollen joint-low grade fever is sometimes present-more common in men(20:1)-joint sparing(chronic gout may be joint destructive)-most commonly first attacks the 1st MPJ(called Podagra), followed by Lisfranc's and then the heel-crunchy tophi felt in ears, olecranon bursa, and Achilles tendon. NOTE: Formalin dissolves gouty tophi
    • DIAGNOSIS
    • X-ray-rat bites-cloud sign-punched out lesions-Martel's sign-overhanging margins
    • Aspiration-negatively birefringent yellow needle shaped crystals, when parallel to axis of the lens and blue when perpendicular.
    • Blood work-Hyperuricemia(>7.5mg/dl ) not conclusively diagnostic for gout
    • TREATMENT
    • For effective Tx determination must be made as to whether the pt. is an over producer of uric acid (metabolic gout) or an under excreter (renal gout).

    -Avoid foods and medications that exacerbate gout-organ meat(liver sweetbread, kidney, heart, brains)-lard-anchovies and sardines-ETOH especially red wine-diuretics(increases osmolarity)

    • Gouty Arthritis
    • Chronic hyperuricemia can result in monosodium urate crystal deposition in joints and soft tissues. The four main etiological forms of gout include:
    • 1. primary metabolic gout - chronic over-production of uric acid, often dietary in origin
    • 2. secondary metabolic gout - myeloproliferative disease with high rate of cellular turnover causing over-production of uric acid
    • 3. primary renal gout - under-excretion of uric acid due to primary kidney disease
    • 4. secondary renal gout - under-excretion of uric acid due to renal disease other than primary kidney lesion (certain diuretic medications).
    • Serum uric acid levels of 7 mg/dl for males and 6 mg/dl for females indicate a supersaturated state wherein crystals may precipitate in joints and the kidneys
    • Clinical forms of gouty arthritis include acute gouty arthritis, intercritical or quiescent, and chronic gouty arthritis. Acute gouty arthritis presents as monoarticular, sudden onset and intensely painful inflammation (red, hot. swollen, excruciating pain). stiffness and antalgic guarding, and overlying cutaneous desquamation. Chronic gouty arthritis presents insidiously with gradual, progressive tophus formation; intermittent acute gouty attacks; and is associated with indurated tophus formation (advanced monosodium urate deposition) in subcutaneous and/or tendon, auricular helix, and the small joints of the hand and foot; and advanced deformity (bunion, hammertoes, nodular lesions) effecting cutaneous compromise. A draining tophus reveals a white, chalky exudate of monosodium urate crystals. The diagnosis of gout is confirmed by the presence of strongly birefringent monosodium urate crystals identified on joint aspiration. The presence of a phagocytosed monosodium urate crystal within a granulocyte is pathognomonic, and termed the "martini sign." Serum uric acid, which is chronically elevated in chronic gout, is normally 8 mg%;however the serum value can actually be within the normal range during an acute gouty attack. Roentgen signs of acute gouty arthritis consist primarily of increased soft tissue density and volume; while chronic gouty arthritis reveals punched out or "rat bite" defects of bone at the capsular attachment. Overtime, chronic erosion and ankylosis may develop.The most common locations of gouty arthritis are the first MTPJ, posterior heel at the Achilles insertion, the plantar inferior calcaneus, other pedal articulations (lesser MTPJ,MTJ), the ankle; the hand, wrist and elbow, and knee. The differential diagnosis includes pseudogout; suppurative arthritis, acute bursitis, and rheumatoid arthritis.
    • Oral therapy consists of indomethacin 50 mg Q 6 hours x 24 hours, followed by 50 mg Q 8hours x 24 hours, followed by 25 mg Q 8 hours x 24 hours. Alternatively, one may usecolchicine (inhibits PMN migration) 0.5 mg Q 1 hour or 1 mg Q 2 hours until the symptomssubside, or GI distress develops, or a total of 6 mg has been administered without relief.Colchicine can also be administered intravenously as an initial2 mg bolus followed by 1 mgIV Q 6 hours for two additional doses. In surgical or traumatized patients with a history ofacute gouty arthritis, prophylactic therapy using colchicine can be administered as 0.5 mgPO Q 8 hour for one week, beginning two days preoperatively. Patients with hyperuricemiarequire medical evaluation, including 24 hour urine uric acid analysis, and may benefitfromlongterm anti-hyperuricemic therapy. In such patients, if the uric acid excretion is lessthan 700 mg/24 hour period, then probenecid sulfinpyrazone is used; and if the uric acidexcretion is over700 mg/24 hours, then Allopurinol is used regularly for an indefinite periodoftime.

    PSEUDOGOUT(Chondrocalcinosis, Calcium pyrophosphate dihydrate, CPPD)DESCRIPTION-associated with acute or chronic inflammatory arthritis-caused by deposition of calcium pyrophosphate dihydrate(CPPD)crystals in the joint-symptoms are similar to those of gout but it tends to run a longercourse(reaches maximum severity at 1-3 days, and resolves in 1week or longer)-the knee is most often involved(50%) followed by the ankle, wrist,and shoulder-risk increases with age, trauma, patients hospitalized for othermedical conditions and those with metabolic dz(hypothyroidism,hyperthyroidism, gout, amyloidosis)-associated with high grade fever198 POCKET PODIATRICS 3RD EDITIONARTHROPATHIESDIAGNOSIS-microscopic examination of joint aspiration reveals rhomboid crystals-radiographically-calcifications of the articular cartilage or meniscusTREATMENT-immobilization, NSAID, analgesics

    • -most commonly first attacks the 1st MPJ(called Podagra), followedby Lisfranc's and then the heel
    • The most common locations of gouty arthritis are the first MTPJ, posterior heel at theAchilles insertion, the plantar inferior calcaneus, other pedal articulations (lesser MTPJ,MTJ), the ankle; the hand, wrist and elbow, and knee.

    Martel's sign-overhanging margins
  16. psoriatic arthritis
    • PSORIATIC ARTHRITIS
    • DESCRIPTION
    • An inflammatory arthritis seen in approximately 7% of patients with dermatological psoriasis. Usually peripheral joints are involved, but there may be associated back pain. The skin disease typically precedes the joint disease, however arthritis can occasionally precede the psoriasis by months to years.
    • SIGNS AND SYMPTOMS-asymmetrical arthritis of large and small (especially the DIPJs) joints,including the sacroiliac and the spine-male=female-peak age ~40yrs-associated psoriatic skin and nail lesions(pitting)
    • DIAGNOSIS-(+)HLA-B27-radiographic- "Pencil in cup" deformity"whittling" of the distal tufts of the phalanges
    • TREATMENT-NSAIDS

    Psoriatic arthritis-pitting and onycholysis, discoloration, subungual hyperkeratosis,splinter hemorrhages; usually treated with systemic control of arthritis, localprotection and palliative care.

    Psoriatic Arthritis is an often severe polyarthropathy that is more common in females (3:2 M:F ratio), and can affect patients of any age. Patterns of psoriatic arthritis include polyarthritis with DIPJ involvement and nail disease, symmetrical seronegative polyarthritis simulating rheumatoid arthritis, monoarthritis or asymmetrical oligoarthritis,sacroiliitis and spondylitis, and arthritis mutilans. Diagnostic features include papulosquamous skin lesions and nail dystrophy (pitting, onycholysis, flaking, hypertrophy, nonsuppurative paronychia); DIPJ arthritis, fusiform digital swelling (sausage toes), unilateral sacroiliitis, simultaneous exacerbation of cutaneous psoriasis and arthritis, absence of subcutaneous nodules, and serum negative for rheumatoid factor. Roentgen signs include bone resorption with "pencil-in-cup" IPJ osteolysis and mineral resorption (DIPJ involvement with erosion and expansion of base of distal phalanx with proximal osteolysis)'oligoarthritis, sacroiliitis, and spinal column invo lvement.
  17. Sever's Disease
    • Sever's Disease-osteochondrosis of the calcaneus(apophysis)-caused by excessive traction of the Achilles tendon-occurs between ages 6-12yrs-more common in patients with equinus-radiographic diagnosis is difficuIt-the normal epiphysis can have 2 or more centers(appearing fragmented), irregular borders, and is often sclerotic
    • Treatment
    • -RICE-NSAIDS-elimination of sports-heel lifts-Achilles stretching exercises

    Sever's disease-osteochondritis of the calcaneal apophysis, observed in children 8-14years of age and most common in boys.

    Sever's disease could best be described as: A traction apophysitis.

    What are the common mechanical abnormalities associated with Sever's disease? Excessive pronation; Equinus.
  18. Kaposi's Sarcoma
    Malignant melanoma would produce the type of pigmented skin changes that could mimic Kaposi’s sarcoma.

    • Kaposi's Sarcoma-a multicentric systemic vascular tumor characterized by violaceous nodules and by edema secondary to lymphatic obstruction-prior to HIV was uncommon and seen in greatest frequency in Eastern Europe and Jewish and Italian immigrants over 60 years of age-now occurs mainly in homosexual males with HIV
    • PRESENTATION-bluish-red, purple to violaceous or dark brown macules, nodules,and patches that spread and may coalesce to form large plaques or nodules-often associated with edema-most lesions are asymptomatic
    • LOCATION OF LESIONS-most frequently found on the feet or legs
    • TREATMENT-in HIV patients treatment is not often indicated since infection usually dominates the clinical cause

    Kaposis sarcoma- is a vascular malignancy comprised of a proliferation of capillaries and connective tissue, seen traditionally in males over the age of 50 years, and of Mediterranean descent. There is also a high incidence in patients suffering with AIDS. The lesions are bluish, or purple nodules or plaques. Treatment is observation (pending general medicalstatus) or excision.

    Name four types of Kaposi's sarcomaClassic, African, immuno-suppressed patient, and AIDS-related.
  19. OSTEOID OSTEOMA
    Which of the following tumors is associated withnight pain that is relieved by salicylates?

    • Which of the following bone lesions ischaracterized by dense bone surrounding a lyticcentral nidus?
    • Osteoid osteoma is a small benign osteoblastic tumor.It initially appears as a sclerotic bone island with a central lucent defect.

    Below the knee, osteoid osteomas are most commonly found in the:: Half of all osteoid osteomas are seen in the tibia and femur, making the tibia the most likely location below the knee.

    To prevent recurrence on removing an osteoid osteoma surgically, the surgeon must do what? Excise central lucent nidus.

    Why is osteoid osteoma pain worse at night? Diurnal production of prostaglandins.

    Osteoid osteomas are most frequently encountered in which foot bone? The talus.

    OSTEOID OSTEOMA-benign bone forming tumor-occurs in the 1st and 2nd decade of life-M>F-occurs in the diaphysis of long bones(esp. tibia and femur) and may be located in the cortex, medullary canal, or parosteally. Occurs in the foot5-8% of the time and the talus and calcaneus are most commonly involved-symptoms are pain, worse at night, relieved by aspirin-radiographic appearance: oval or round radiolucent area, measuring<1cm in diameter surrounded by a zone of uniform bone sclerosis

    Osteoid osteoma- usually observed in children and young adults, marked by nocturnal pain. eleviated with aspirin. displaying a round osteolytic defect surrounding a central radiodense (sometimes lucent) nidus that is usually no larger than 1 cm in diameter. This lesion is common in the foot.
  20. giant cell tumor
    GIANT CELL TUMOR-benign fibrohistocytic tumors composed of connective tissue, stromal cells and giant cells-occurs during the 3rd and 4th decade of life-male to female distribution is equal-usually originates in the metaphysis but quickly extends into the epiphysis and subchondral bone-seen in long tubular bones especially around the knee(distal femur or proximal tibia)-symptoms include pain, with possible swelling and limitation of motion-may be associated with Paget's dz-radiographic appearance: eccentric osteolytic lesion extending to the subchondral bone. Large extensive periostitis is generally not present-Have a tendency to reoccur

    Giant cell tumor- usually observed in the 3rd to 4th decade well after growth plates have closed (skeletally mature), localized to the diaphysis as well as metaphysis and epiphysis Displays thin, delicate trabeculae that have a "soap bubble" appearance, expanding into adjacent cortex, and known to undergo malignant transformation.
  21. aneurysmal bone cyst
    Cystic lesions ofthe calcaneal body are not uncommonly encountered. The three most frequently encountered biopsy proven lesions are:Simple bone cyst, intraosseous lipoma, and aneurysmal bone eyst.

    Name three benign bone tumors that can have a "soap bubble" matrix?Aneurysmal bone cyst, giant cell tumor, chondromyxoid fibroma.

    ANEURYSMAL BONE CYST-benign blood filled cyst-occurs during the 1st, 2nd, 3rd decade of life-F>M-unusual in that it is a rapidly growing painful lesion yet it is benign-lesions are usually located in the metaphysis of long tubular bones and the spine-symptoms include pain and swelling, possible pathologic fx-radiographic evaluation: an eccentric, osteolytic(possibly trabeculated)expansive lesion which may extend out into the soft tissue-trauma is a possible etiology

    Aneurysmal bone cyst -a benign, blood-filled lesion that is usually observed in the 1stto 3rd decade. It is expansile, with horizontal, parallel trabeculae that are readily observed onMRI. The lesion is difficult to distinguish from malignancy.
  22. osteosarcoma
    Osteosarcoma is chiefly a disease of individuals of less than 20 years of age. What pre-existing condition can result in a secondary peak in incidence for older adults?Paget's disease.

    What is the most common site for metastases of osteosarcoma? Lung.

    OSTEOSARCOMA(osteogenic sarcoma)-malignant bone forming tumor-most common malignant bone tumor with exception of Multiple Myloma-age 10-25yrs, and >40yrs-male to female distribution is equal-most commonly found in the metaphyseal region around the knee(distal femur or proximal tibia)-usually occurs in teenagers during rapid growth spurts or in patients over 40 who have a preexisting condition most notably Paget's dz-Symptoms: Pain, swelling, and fever(R/0 OM), the osteoid producing nature of the tumor often yield an elevated alkaline phosphatase level-radiographic appearance: appearance is variable depending on osteolytic or sclerotic nature of lesion. Penetration of cortical bone usually occurs with a Codman's triangle or "Sunburst" appearance-prognosis is poor
  23. pagets
    • Which of the following is normally associatedwith Paget's disease?(B) Increased osteoblast and osteoclast activity
    • Osteoblast and osteoclast activity both increase inPaget’s disease.

    Paget's Disease A focal disorder of bone metabolism in which all the elements of bone remodeling are increased resulting in bony enlargement and deformities.The condition is often asymptomatic although pain and stiffness may develop. Symptoms include an enlarged skull, bowing of the longbones, and pathologic fractures.

    • Which of the following is associated with an increased incidence of osteosarcoma?(A) Paget's disease
    • The most serious complication of Paget’s disease is sarcomatous degeneration. Osteosarcomas are most common but fibrosarcomas and chondrosarcomas can also be seen.

    Phase I Paget's disease manifests radiographically with? Advancing osteolysis with a well-defined zone of transition.

    Barring injuries, the differential diagnosis for inferior calcaneal heel pain should include?Plantar fasciitislheel spur syndrome, inferior calcaneal bursitis, heel pad atrophy, nerve entrapment (posterior tibial, medial calcaneal, 151 branch of lateral plantar nerve), seronegative spondyloarthropathies, rheumatoid arthritis, gout, pseudogout, sarcoidosis, thyroid abnormalities, Paget's disease, and infections.
  24. bacterial endocarditis
    • In a patient with bacterial endocarditis who has no known allergies, the most appropriateprophylactic drug is
    • amoxicillin
    • Prophylaxis against Staphylococcus aureus and Staphylococcus epidermidis consists of amoxicillin3 gm orally 1 hour before the procedure and 1.5 gmorally 6 hours later.

    • What is the predominant causative organism for subacute bacterial endocarditis in IV drug abusers?
    • Staphylococcus

    AMOXICILLIN-used for prophylaxis against bacterial endocarditis-dosage 3g PO before and 1.5g PO 6 hours after the procedure or2g IV 30 minutes before and 1g IV 6 hours after the procedure

    ERYTHROMYCIN-used for prophylaxis against bacterial endocarditis in Pen allergic patients-dose depends on the preparationCLINDAMYCIN-used for prophylaxis against bacterial endocarditis in Pen allergic patients-dosage 300mg PO before and 150mg PO 6 hrs after theprocedure or 300mg IV 30 minutes before and 150mg IV 6 hrs afterthe procedure
  25. describe the posterior tibial muscle (function, attachments,etc)
    Which of the following is a muscle that directly prevents the longitudinal arch from collapsing?

    The posterior tibial muscle, an inverter of the foot, is the only muscle listed that is powerful enough to support the arch and counteract the effect of fibularis(peroneus) brevis, an everter of the foot. One of the main characteristics of posterior tibial dysfunction is loss of the arch.

    • A 47-year-old patient has pain in the right ankle ofseveral weeks’ duration. The patient remembers noinciting event but says the pain worsens withincreased activity. The right foot appears morepronated than the left foot on weightbearing; onattempts to rise to the toes, the patient hasconsiderable pain and the rearfoot does not invert.Pain is found on palpation just proximal to the navicular tuberosity.
    • The tibialis posterior muscle acts as a supinator of thesubtalar joint, counterbalancing the effects of thefibularis (peroneus) brevis muscle, which acts as apronator. Posterior tibial tendinitis will result inweakness of the muscle, causing a more pronatedappearing foot, as well as discomfort at the tendon’sinsertion on the navicular tuberosity.

    What is the most common cause of tendon rupture of the posterior tibialis tendon? Chronic or acute stress on an already degenerated tendon.

    Describe the usual mechanism of injury for a navicular tuberosity fracture. Usually an avulsion type fracture. When foot is forcibly everted, the posterior tibialis tendon exerts its force and causes the avulsion.

    • TIBIALIS POSTERIOR MUSCLE
    • Origin: posterior two thirds of the interosseous membrane and the adjacent tibia and fibula
    • Insertion: plantarly on the navicular (major insertion site), medial and intermediate cuneiform, and base of the second, third, and fourth metatarsal
    • Action: invert the foot, adduct foot, plantarflex ankle Innervation: tibial nerve(L4, L5)
    • Arterial Supply: sural, peroneal, and posterior tibial arteries
  26. Following lesser digital arthroplasty, the digit should be splinted in which of the following positions?
    • Metatarsophalangeal Proximal Interphalangeal Distal Interphalangeal
    • (C) Slightly Plantarflexed Straight Straight

    slightly overcorrect for the preoperative hammer toe deformity and are the positions most likely to prevent recurrence.

    What is extensor substitution?Extensor substitution occurs when the long extensor muscles overpower the lumbricales. The lumbricales act to stabilize the digits during swing phase and counteract the extensor digitorum longus pull. When the lumbricales are weakened a high-arched foot develops with hammer toes.

    • Extensor Substitution
    • Extensor muscles normally contract to dorsiflex the ankle to allow the foot to clear the ground during swing phase. With extensor substitution the extensors gain a mechanical advantage over the lumbricles and the extensors will contract the MPJs. There is normally no adductovarus deformity. Causes include anything that will give the extensors a mechanical advantage over the lumbricles.
  27. Windlass mechanism
    -As the hallux is dorsiflexed the plantar fascia is pulled under the head of the metatarsal. This brings the calcaneus toward the head of the 1st metatarsal, thereby creating an elevated medial longitudinal arch.
  28. Flexor Stabilization
    Occurs in flat feet with excessive pronation. STJ pronation allows hypermobility and unlocking of the midtarsal joint leading to hypermobility of the forefoot. The flexors fire earlier and longer than normal in an attempt to stabilize the forefoot. The flexors overpower the interosseous muscles and cause digital hammering or clawing. There is also an possible associated adductovarus of the fourth and fifth toes because the quadratus plantae loses its mechanical advantage.
  29. Flexor Substitution
    Occurs with weak triceps surae, the deep posterior leg and lateral leg muscles try to compensate for lack of plantarflexion. In doing so, they create a high arched supinated foot and contract the digits. There is usually no adductovarus deformity of the digits.
  30. Extensor Substitution
    Extensor muscles normally contract to dorsiflex the ankle to allow the foot to clear the ground during swing phase. With extensor substitution the extensors gain a mechanical advantage over the lumbricles and the extensors will contract the MPJs. There is normally no adductovarus deformity. Causes include anything that will give the extensors a mechanical advantage over the lumbricles.

    Extensor Substitutio~this is associated with pes cavus, foot drop, and anterior compartment weakness, wherein the EDL overpowers the lumbricales during swing phase,and causes dorsiflexion of the MTPJs; results in a high degree of MTPJ subluxation and retrograde plantar buckling of the metatarsus.

    "too many toes"

    Describe the extensor substitution phenomenon as an etiology for hammertoes? Extensor substitution occurs during propulsion, swing phase, and heel contact when the extensor digitorum longus and brevis muscles are active. It may occur as a result of an equinus and an anterior cavus foot type and may manifest as a result of peripheral neuropathy, as the intrinsic muscles are often affected first.
  31. CONGENITAL VERTICAL TALUS
    Vertical talus presents with which of the following x-ray changes?(B) Dislocated navicular

    Congenital vertical talus presents as the talus fixed in a vertical position with hypoplasia of the talar neck and head. The navicular is dislocated and articulates with the dorsal aspect of the talar neck. The tibionavicular and dorsal talonavicular ligaments are contracted preventing reduction of the navicular.

    Congenital vertical talus is a complex deformity involving bone, tendon, capsule, and soft tissue abnormality. It has a similar appearance at birth to talipes calcaneovalgus, but there is lack of motion at the subtalar joint and ankle joint within 6 months after birth, a negative calcaneal inclination angle, and complete dislocation of the talonavicular joint. It cannot be reduced with serial casting.

    What iatrogenic problem can occur with derotational casting for clubfoot by aggressive dorsiflexion for the equinus component?Vertical Talus.

    How is congenital calcaneovalgus deformity easily distinguished from congenital convex pes plano valgus deformity on clinical examination?Congenital calcaneovalgus is flexible and allows for passive correction.

    • CONGENITAL VERTICAL TALUS A.K.A.Congenital Convex Pes Plano Valgus.Reverse Clubfoot. Persian Slipper.Rockerbottom Flatfoot)
    • DESCRIPTION-Primary dislocation of the navicular dorsally on the neck of the talus locking the talus in a vertical position-Forefoot is abducted and dorsiflexed at the midtarsal joint-Calcaneus is in valgus and equinus-RIGIDITY is the hallmark of the deformity -Contracted gastrocsoleus, and elongated spring ligament-Majority B/L-R>L-Often occurs with other congenital deformities most notably Arthrogryphosis-Foot may actually touch the front of the tibia at birth-Walking is not delayed because the condition is not painful in childhood, however gait is awkward, clumsy and almost peg-like and shoes may be difficult to wear-Talar head is prominent on medial plantar aspect of foot and may have a callus over it from bearing most of the body weight-STJ facets are abnormal Anterior-absent Middle-hypoplastic Posterior-malformed(misshapen)
    • RADIOGRAPHIC EVALUATION-Definitive diagnosis is determined by taking a lateral x-ray and comparing it to a second lateral x-ray with the foot maximally plantarflexed demonstrating that the talonavicualar relationship does not change. Navicular is not evident radiographically until age 3 so it is difficult to establish its subluxation.-Line bisecting talus(on lateral x-ray) is parallel to tibia-Talocalcaneal angle on A/P is increased, usually > 40°-Talar neck is hypoplastic and so may have an hourglass shape and may have a flat surface-Navicular articulates with the dorsal neck of the talus-(-)Hubscher maneuver
    • TREATMENT CLOSED REDUCTION-rarely successful-Manipulation and casting is recommended as a means of stretching the soft tissues for future definitive surgical treatment in an attempt to avoid skin sloughing
    • OPEN REDUCTION 3 MONTHS-3YEARS-If closed reduction fails, open reduction should be performed at 3 months of age-Many procedures have been described, they all involve a posterior release and reduction of the talonavicular joint 3-6YEARS-In addition to open reduction an extra-articular arthrodesis(Green-Gricetype) or arthroereisis may be attempted to maintain reduction and stabilizethe STJ 6 YEARS AND UP-At this point it's best to postpone surgery until skeletal maturity(10-14years of age) at which time a triple arthrodesis is performed which may require removal of the head and neck of the talus to obtain reduction

    Congenital Vertical Talus (Congenital Convex Pes Valgus, Rocker Bottom Foot)-this idiopathic anomaly, a form of clubfoot, is characterized by a foot that may actually contact the pretibial surface at birth. The plantar surface is convex (rocker bottom), and the talar head can be identified on the medial plantar aspect of the longitudinal arch, with the hindfoot in equinovalgus. Deforming muscle groups displaying contracture include- gastrosoleus complex (ankle equinus); ankle dorsiflexors (TA, EDL, EHL.) and the peroneal tendons; and the peroneal and tibialis posterior are relatively more anteriorly migrated than normal. Ligamentous shortening involves the dorsal talonavicular, tibionavicular,calcaneofibular, calcaneal-cuboid, interosseous talocalcaneal ligaments; and the posterior AJ and STJ capsules are tightened. The spring ligament, conversely, is elongated.Radiographic evaluation employs use of the Ap, lateral and forced plantarflexion views(Figure 9-11 ).In the lateral view, the long axis of the talus appears vertical and parallel to that of the tibia while the calcaneus is in equinus and the forefoot dorsiflexed. In the AP view,the TCA is increased to >400 The navicular cannot be radiographically evaluated until 3-4years of age, when it ossifies. When it has ossified, the navicular is identified in a dorsallydislocated position. The stress plantarflexion latera l view allows comparison of the firstmetatarsal on standard lateral and the stress view, so that rigidity of the deformity can bedetermined. Normally, the talar and first metatarsal axes are parallel; however in thepresence of a rigid plantarflexed talus, the talar axis passes through sole of foot and the firstmetatarsal ax is passes dorsal to head of talus. In the forced plantarflexion view, thisrelationship will not be reduced. Convex pes valgus is categorized as either Type I or TypeII. Type I involves dislocation ofthe TNJ, subluxation ofthe TCJ, and a normal CCJ. Type IIis more rigid and involves dislocation ofthe TNJ, subluxation of the TCJ and CCJ, and ankleequinus. The differential diagnosis for calcaneovalgus includes talipes calcaneovalgus,severe pes valgoplanus with gastrosoleus equinus, paralytic pes valgoplanus,myelomeningocele, polio, and rigid pes valgus due to tarsal coalition. Associateddeformities include cleft palate, arthrogryposis, and spastic equinus due to CP and others.Treatment of congenital vertical talus focuses on restoring the normal TN, TC, andCCJ relationship as soon as possible. This condition is notoriously res istantto nonsurgicaltreatment As with ta lipes equinovarus, manipulation and serial corrective casting(Ponsetti method) are useful. At birth, gentle manipulation is used to stretch the contractedsoft tissues. Manipulation entails stretch oftriceps surae and calcaneofibular ligament viadistal and medial traction, plantarflexion and adduction of the FFto stretch dorsiflexors andeverters, and distal traction of the FF and TNJ to effect adductus and varus stretch of thetibionavicular and talonavicular ligam ents. The stretch is held for 15 seconds and thenreleased, and the exercise is continued for 15 minutes after which the cast is applied. Thecast is changed twice per week for six weeks. As correction ensues, focus more on TNreduction by means of distal FF traction until the head of the talus dorsiflexes and thecalcaneus is pulled under the ta lus. It may become necessary to maintain the closedreduction with percutaneous pin stabilization. If, after 4-6 months of closed reduction,Figure 9.11Ch.9 Congenital Deformities and Juvenile Surgery 241impasse is reached, then open reduction should be performed. The longer the TNdislocation persists, the more the soft tissue contracture deforms bone and surroundingjoints. Surgical repair of congenital vertical talus employs a medial, curvilinear skinincision extending from the medial aspect ofthe Achilles tendon at a point 4-6 cm proximalto the ankle, around the tip of the medial malleolus, and onward to the junction of the firstmetatarsal and medial cuneiform. The neurovascular bundle is retracted, after which theAchilles, TA, EHL, and peroneal tendons are Z-plasty lengthened. The tibionavicular, TN,bifurcate, and dorsal calcaneocuboid, calcaneofibular and TC interosseous ligaments arethen sectioned. The talar head is manipulated dorsally and the navicular moved in aplantar direction with inversion. A smooth 0.062" K-wire is then driven from the posterioraspect ofthe talus across the reduced TNJ, and continued anteriorly across the NCJ. Thespring ligament is then reefed tightly, and an AK cast used to maintain the correction for12-16weeks. The K-wire can be removed around 6 weeks postop. Avascular necrosis ofthetalus is a possible complication. Excision of the navicular has been effective in the treatmentof rigid arthrogryposis in patients 3-6 years of age. In children >6 years old, rigid bone andjoint adaptation may indicate the need fortriple arthrodesis.
  32. Windswept deformity
    (Met adductus on one foot and calcaneal valgus on the other)
  33. CALCANEOVALGUS
    • In patients under 1 year of age, what is one of the most common forerunners of pes valgus deformity?
    • Congenital calcaneovalgus deformity.

    • How is congenital calcaneovalgus deformity easily distinguished from congenital convex pes plano valgus deformity on clinical examination?
    • Congenital calcaneovalgus is flexible and allows for passive correction.

    -characterized by excessive dorsiflexion of the ankle and eversion of the foot-caused by abnormal intrauterine position-dorsal surface of the foot is in contact with the anterior surface of the leg-usually resolves spontaneously with growth but may require serial casting

    • Congenital Calcaneovalgus-this congenital anomaly presents the foot in an acutely extended position with the dorsal surface in contact with the anterolateral surface of the leg. The entire foot, including the heel, is in complete valgus to the point that when the neonatal foot is pulled into plantarflexion, the following are noted: flexion is limited to the neutral position, or perhaps slightly beyond; skin and subcutaneous tissues are stretched tightly due to contracture that reveals a prominent, tight band that blanches in comparison to surrounding normal skin; the underlying tendons usually not contracted; the calcaneus(heel) is in valgus with the rest of the foot, and there is no frontal plane deviation of the forefoot in relation to the hindfoot; and the foot is fairly flexible so that the heel and midfoot can be brought into a corrected varus position (a nonrigid deformity). Normal neonatal ankle dorsiflexion is approximately 45°, unlike the calcaneovalgus foot that can dorsiflex to become flush with the pretibial surface of the leg. Normal neonatal ankle plantarflexion is about 50°, whereas the calcaneovalgus foot only gets to neutral or a few degrees of plantarflexion. Increased plantarflexion of talus will be visible on the lateral radiograph,and Kite's angle will be >35° in the AP view.

    As with many pedal misalignments, the parents usually do not seek an opinion or care until the child is 6-8 months of age, when the child first stands. In weight bearing, a complete absence of the arch and severe valgus are noted. Conservative treatment employs corrective casting using two layers of cast padding after applying skin adherent (tincture of benzoin). An assistant holds the foot by the toe tips and maintains as much of an equinus position as possible, while maintaining a neutral relationship of the FF to the hindfoot, and adduction of the FF to correct the TN alignment. The cast is then applied from the toe tips to below-the-knee, molding into the arch and about the heel. A lateral X-ray is obtained to confirm reduction, and correction is maintained for 2-3 weeks, changing the cast every 3-4 days in the neonate.
  34. METATARSUS ADDUCTUS
    • What is the relationship between metatarsus adductus and cavus foot?
    • Metatarsus adductus is a structural defonnity in which the metatarsals are excessively adducted in relation to the lesser tarsus at Lisfranc's joint. This deformity usually leads to an adducted gait with pronation being the compensation, thus unlocking the MTJ and allowing abduction at Chopart's joint, which masks the adduction at Lisfranc's joint. A skewfoot, or "Z" shaped foot results. When anterior cavus is superimposed on the met adductus foot, the ground reactive forces are increased adding to the severity of the deformity.

    • What deformity cannot be present if the Evans procedure is planned? Metatarsus Adductus.
    • o What is the consequence if the Evans is performed in a foot with the above deformity? Unmasking and exaggeration of the metatarsus adductus and an in-toe gait.
    • What musculoskeletal deformity usually accompanies juvenile HAV in the absence of extrinsic and systemic etiologies? Metatarsus adductus.

    • METATARSUS ADDUCTUS
    • DESCRIPTION-Adduction of the FF at tarso-metatarsal joints-Rearfoot is normal-1 in 1000 live births-55% B/L-males=females-prominent styloid process-intoed gait with frequent tripping-the severity of the adduction progressively decreases from medial to lateral-Usually idiopathic, rarely associated with neuromuscular disease-10% are associated with dislocated hip-86% resolve satisfactorily without treatment, spontaneous improvement should be almost complete at about 3 months if it is to occur
    • CAUSE-intrauterine position-tight abductor hallucis muscle-absent or hypoplastic medial cuneiform-abnormal insertion of anterior tibial tendon
    • CLASSIFICATIONS
    • Dynamic-baby is born with straight feet for 1st 7-8 months, then baby develops a"C" shaped foot due to tightening or contracture of the abductor hallucis tendon. Hallux is pulled into adduction with WB. Treatment involves cutting or lengthening the abductor muscle
    • Flexible-strainghtens out or over corrects when force is applied to the medial aspect of the foot. Treatment is with straight last shoe
    • Rigid-little change in FF to RF position with medial pressure. Biggest problem is shoe fit (prominent styloid process). Treatment is serial casting or surgical.
    • Crawford and Gabriel Classification
    • Stroking the lateral border of the foot will cause peroneal muscle contractions which will demonstrate the degree of active forefoot mobility Type II Partial flexibility(does not correct to neutral actively but does passively)Type I Flexible(forefoot will correctpast neutral intoslightly overcorrected) Type III Rigid(does not correct toneutral actively orpassively)
    • Bleck Classification Bisect the heel and extend the line distally to see where it falls onthe toesNormal(between 2nd-3rd toe)Mild(through 3rd toe)
    • MEASURING THE METATARSUS ADDUCTUS ANGLE
    • CLASSIC METHODReference pointsMedial-proximal aspect of 1st metatarsal baseMedial-distal aspect of the talo-naviculararticulationLateral-proximal aspect of the 4th metatarsal baseLateral-distal aspect of the calcaneo-cuboid jointMetatarsus adductus angle above 20° isconsidered adductedMTA angle at birth is 25-30°, at 1 year(beginwalking) it's -20° and by 4 years it's at the adultnormal of -15°Moderate Severe(beween 3rd-4th toe) (between 4th-5th toe)
    • LEPOW TECHNIQUE
    • Take the perpendicular of a line passingthrough the lateral base of the 5th andmedial base of the 1st metatarsals andcompare with the 2nd metatarsal-values are comparable to values obtainedby the traditional methodMTA angle at birth is 25-30°,at 1 year(begin walking) it's -20°and by 4 years it's at the adultnormal o f - 1 5°ENGLE'S ANGLEBisect the intermediate cuneiform andcompare with the 2nd metatarsal. Anormal value using this method is 24°.The angle increases with an adductedfoot.TREATMENTCONSERVATIVE(children < 3 years old)-manipulation and serial casting are the standard treatment-shoes, orthotics-splints(Ganley), bracesPOCKET PODIATRICS 3RD EDITIONPEDIATRICS499CHAPTER 29SURGICALCHILDREN 2-6 or 8 YEARS-SOFT TISSUE PROCEDURESHeyman, Herndon, and Strong-release all soft tissue structures at Lisfranc's jt except lateral andplantar lateral ligaments-initially described using one transverse skin incision, revised to 2 or 3longitudinal incisionsThompson procedure-resection of the abductor hallucis muscle-release medial head of FHB if necessaryLange-capsulotomy of the 1st metatarsal-1st cuneiform joint-division of the abductor hallucisLichtblau-sectioning of the hyperactive abductor hallucisCHILDREN 8 YEARS AND OLDER-OSSEOUS PROCEDURESBerman and Gartland-laterally based crescenticosteotomies of metatarsal baseLepird-closing wedge osteotomy of 1 and 5 metatarsal bases-oblique rotational osteotomies of the three central metatarsals500CHAPTER 29POCKET PODIATRICS 3RD EDITIONPEDIATRICSJohnson osteochondrotomy-closing abductory base wedge osteotomy ofthe 1 st metatarsal-resection of osteocartilaginous 2.5mmwedge from the lesser metatarsalsFowler-opening wedge osteotomy of the medialcuneiform with insertion of bone graftPeabody-Muro-excision of the base of the central threemetatarsals-osteotomy of 5th metatarasal-mobilization of the 1st-metatarsal-cuneiformjointSteytler and Van Der Walt-oblique osteotomy of all metatarsalsMcCormick and Blount-arthrodesis of 1st-metatarsal-cuneiform jt-osteotomy of metatarsals 2, 3, and 4-possible wedge resection of cuboid

    METATARSUSADDUCTUS ANGLE-normal 15°-less than 15° is a rectus foot-MTA angle at birth is -30°, at1 year(begin walking) it's -20°,by 4 years it's at the adultnormal of -15°

    Metatarsus Adductus-this transverse plane deformity displays medial deviation of the metatarsals with the apex of the deformity at Lisfranc's articulation. Metatarsus adductus(MAdd) occurs in lout of every 1,000 live births, is familial, and the presence of the deformity conveys a 1 in 20 chance that a sibling will also have the anomaly, and it occursbilaterally in 55% of cases. Clinical findings include a C-shaped foot with convex lateral and concave medial borders in the transverse plane, adducted metatarsals with the more medial metatarsals being more adducted (1)2>3>4>5). a high arch if there is no STJ compensatory pronation, a skewfoot (toes abducted, metatarsals adducted, tarsus abducted) with heel valgus if compensatory ST J pronation is available, separation between the first and second digits, inability to abduct the metatarsals past midline of the foot. hypertonicity and spasm of tibialis anterior in gait or upon striking in open chain, and possible hyperactivity of abductor hallucis. lf the hindfoot is in rigid equinus and varus, ruleout clubfoot. Total MAdd involves all five metatarsals, whereas atavistic MAdd localizes tothe first ray, and is termed congenital metatarsus primus adductus or varus. MPV displays a first intermetatarsal angle of 10 or greater. Radiographic assessment of MAdd isnecessary to quantify the degree of deformity. The AP view is used, and the long axis ofthelesser tarsus or that of the second cuneiform can be compared to the long axis of thesecond metatarsal (Fig 9-6). Using the long axis of the lesser tarsus, the normal met-addangle is 15-21 0, and 250 when using the middle cuneiform reference. The Podiatry Instituteradiographic classification system employs the long axis of the lesser tarsus, and definesmet-add as follows: normal (rectus foot) 0-150, mild 16-250, moderate 26-350, and severe>350. In the AP view, long-term compensation will show moderate-severe hallux abductus,cuboid abduction, and digital abductus as toes align with rearfoot. and increased Kite'stalocalcaneal angle as the talus adducts medial to the navicular. In the lateral view ofthe compensated deformity, an anterior break in the cyma line indicates hyperpronationand is usually associated with a decreased CIA. The uncompensated foot will displaycharacteristics of pes cavus.Points plotted for deremination oflogitudinal bisection of lesser tarsus.Figure 9.6LTAxLesser tarsal axis (LTAx) representsperpendicular to bisector of lessertarsus. Line "EF" is bisector oflesser tarsus. Line "G" is bisectionof second cuneiform.Ch.9 Congenital Deformities and Juvenile Surgery 235Conservative treatment can be effective if instituted in a timely fashion. For patients <3months of age, manipulation, taping or casting, can be effective. For patients <3 years of age,altering sleeping habits to avoid adduction, use ofthe Ganley splint or corrective casting areuseful. Casttherapy involves three point bending ofthe foot in the transverse plane (Figure9-n and should be maintained an additional period of time equal to half ofthe time that wasrequired to eliminate the deformity. If cuboid abduction increases, then over correction isoccurring and casting should be discontinued. The BK cast should entail limited padding,and effect abductoryforce atthe first metatarsal head and medial aspect ofthe heel, withan adductory force applied to the cuboid-fifth metatarsal junction. The hindfoot and ankleare maintained in neutral position. Medial tibial torsion, if present, can simultaneously beaddressed with an AK derotating cast. The cast is changed every 1-2 weeks. Followingcorrection, a reverse last shoe may be useful for up to 6-12 months.Surgical treatment is indicated in patients >2 years of age who have reached animpasse with nonsurgical methods, and offer treatment options for patients up to 8 yearsof age. The Heyman, Herndon and Strong (HHS) procedure is performed through either atransverse or three longitudinal incisions, and entails sectioning of the medial2!3 of thecapsule and ligaments of the tarsometatarsal joints, followed by K-wire stabilization andcasting. The Thompson procedure can be used in the infant or youngster to correct halluxvarus associated with metatarsus primus adductus or varus. Johnson's chondrotomytechnique entails laterally based (medial apex) wedge resection (2.5 mm) of thecartilaginous metatarsal base of the lesser metatarsals and a closing abductory basewedge, distal to the physis, on the first ray; in addition to lengthening abductor hallucis. TheLange procedure involves first metatarsal -c uneiform capsulotomy with recession ofabductor hallucis, followed by serial casting. The Lichtblau procedure entails sectioning ofa hyperactive abductor halluc is, much like Thompson's procedure, and is indicated in theequinovarus foot with metatarsus adductus Brown described transfer of tibialis posteriorinto the navicular from anomalous insertion, combined with medial cuneiform-navicularcapsulotomy. Ghali described an anterior-medial release ofthe first metatarsocuneiformand naviculocuneiform joints with division oftibialis anterior atthe medial aspect of medialcuneiform. Osseous procedures are indicated in patients 8 years of age or older. McCormickand Blount described arthrodesis ofthe first metatarsocuneiform joint with lateral closing. wedge osteotomy ofthe second, third, and fourth metatarsals and the cuboid. Peabody andMuro described mobilization of the first metatarsocuneiform joint combined with excisionof the second, third, and fourth metatarsal bases and lateral closing wedge osteotomy ofthe fifth metatarsal. Steytler & VanDerWalt described pan metatarsal oblique laterally basedclosing wedge osteotomies. The Berman-Gartland procedure is a popular technique thatemploys lateral closing base wedge osteotomies of all five metatarsals distal to the growthplates (Figure 9-8). The Lepird procedure (Figure 9-9) is a refinement on the BermanGartlandtechnique that varies with the use of through-and-through rotational osteotomiesof the intermediate metatarsals, combined with lateral closing base wedge osteotomies ofthe first and fifth metatarsals. The through-and-through osteotomies are made parallel to thesubstrate and are initially made with preservation of the dorsal-distal-medial cortex, whichis completed only after interfragmental screw placement has been positioned and priortoachieving final screw purchase after swiveling the metatarsals into corrected alignment.Fowler described an opening wedge osteotomy of the medial cuneiform, and Ganleyrefined the technique to address a deformed LASA (Lisfranc articular set angle) that displaysa severely oblique first met-cuneiform articular interface directed from proximal-medial todistal-lateral. Ganley performed a medial cuneiform opening wedge osteotomy with236 Congenital Deformities and Juvenile SurgeryABMetatarsus adductus angle. Correction is gained by compressingthe rearfoot. Metatarsals are thenabducted on stable resrfoot.Figure 9.7Figure 9.8Figure 9.9Ch. 8Ch.9 Congenital Deformities and Juvenile Surgery 237autogenous bone graft in conjunction with a laterally based closing wedge osteotomy ofthecuboid. The resected corti co cancellous cuboid bone is harvested for transplant into themedial cuneiform. The osseous work is combined with appropriate soft tissue releases andsubsequent casting. Bankhart described excision of the cuboid, and Tachdjian-Gricedescribed a combination of hindfoot extra-articular arthrodesis with forefoot soft tissuerelease for correction of skewfoot.

    What is the relationship between the 1M angle and the metatarsus adductus angle?As the metatarsus adductus angle increases above 15 degrees, the 1M angle becomes more significant at a lower angle. A simple formula which helps demonstrate this concept is: Effective 1M angle Metatarsus Adductus angle 15 degrees + the measured I M angle. In other words, every degree of MA angle over 15 degrees is added to the 1M angle.

    When evaluating an A-P view of a 6-year-old child with metatarsus adductus where would you observe the position of the navicular? Lateral to talar head.

    According to Rushford what percentage of infants with metatarsus adductus spontaneously corrects? 86%.
  35. PLANTAR LAYERS OF THE FOOT
    • First Layer (superficial)
    • 1. Abductor Hallucis Muscle 2. Flexor Digitorum Brevis Muscle 3. Abductor Digiti Minimi(quinti)
    • Second Layer
    • 1. Quadratus Plantae Muscle 2. Lumbricales 3. Flexor Hallucis Longus Tendon 4. Flexor Digitorum Longus Tendon
    • Third Layer
    • 1. Adductor Hallucis Brevis Muscle2. Flexor Hallucis Brevis Muscle3. Flexor Digiti Minimi Brevis Muscle
    • Fourth Layer(deep)
    • 1. Plantar Interossei 2. Dorsal Interossei 3. Tibialis Posterior Tendon 4. Peroneus Longus Tendon

    Netter 532-537

    • MYOLOGYThe intrinsic pedal muscles comprise 4 layers in the plantar vault. innervated by the deepperoneal (EOB; 2nd, 3rd and 4th dorsal 10), medial plantar (FOB, FH B, abductor hallucis,1st lumbrical), and lateral plantar (GP, abductor digiti minimi, flexor digiti minimi, all 10,ailiumbricals exceptthe 1st, and adductor hallucis) nerves.
    • Plantar Laver I
    • Abductor Hallucisorigin-medial calcaneal wall.insertion-tibial sesamoid and medial base of proximal phalanx of hallux (Fig. 1.5).
    • Flexor Digitorum Brevisorigin-calcaneal tuberosity, divides at base of proximal phalanx.insertion-plantar surface of middle phalanx (Fig. 1.6).
    • Abductor Digiti Quintiorigin-lateral calcaneal wall.insertion-lateral aspect base of proximal phalanx (Fig. 1.7).Figure 1.5MedialplantarnerveMedialplantararteryMedialplantarnerveIlIIln:IUL-MedialFigure 1.6plantararteryFigure 1.7LateralplantarnerveLateralplantararteryII-Ch. l Pertinent Anatomy & Normal Physiology
    • Plantar layer II
    • Quadratus Plantae origin-2 calcaneal heads.insertion-lateral aspect of FDl tendon before it divides (Fig. 1.8).
    • Lumbricales7origin-1st. from medial aspect of FDL to 2nd toe; 2nd, from contiguous aspects of 1st and2nd FDL tendons; 3rd, from contiguous aspects of 2nd and 3rd FDl tendons; 4th, fromcontiguous aspects of 3rd and 4th FDL tendons.insertion-medial aspect of mid-portion of proximal phalanges and fibrous expansion ofthe dorsal hood ofthe 2nd-5th toes (Fig. 1.9).DeepTendon of m.metatarsalflexor digitorumarterieslongus Deep branchof lateral MedialLateral plantar nerve plantarplantar nervenerveLateralplantararteryFigure 1.8 Figure 1.98Plantar Layer IIIFlexor Hallucis BrevisPertinent Anatomy & Normal Physiology Ch. 1origin-medial arm from tendons oftibialis posterior inserting into the metatarsal bases, andlateral arm from the cuboid, 3rd cuneiform, peroneus longus tendon, and long and shortplantar ligaments.insertion-base of proximal phalanx on medial and lateral aspects, after investing 1st MTPJsesamoids and plantar plate (Fig. 1.10).Adductor Hallucisorigin-oblique head arises from 2nd, 3rd, 4th metatarsal bases.insertion-into fibular sesamoid, plantar plate, and lateral aspect base of proximal phalanxorigin-transverse head arises from plantar plates of 3rd, 4th, 5th MTPJs.insertion-into fibular sesamoid, plantar plate, and lateral aspect base of proximal phalanx(Fig. 1.11).Flexor Digiti Minimi Brevisorigil}-plantar aspect of cuboid and 5th metatarsal base.insertion-plantar aspect base of proximal phalanx of 5th toe (Fig. 1.12).If';i,'+-F:ir~t plantarmetatarsalFirst plantarmetatarsalartery~~,*-Deep branchFigure 1.10Superficialbranch of lateralplantar nerveLateral --fll~plantararteryFigure 1.12Figure 1.11of lateralplantar nerveCh.1Plantar Laver IVDorsal Interossei (10)Pertinent Anatomy & Normal Physiology 9orjgj~1 st, adja cent surfaces of 1 st and 2nd metatarsals; 2nd, adja cent surfaces of 2ndand 3rd metatarsals; 3rd, adjacent surfaces of 3rd and 4th metatarsals; 4th, adjacentsurfaces of 4th and 5th.jnsertjo~ 1 st, base of proximal phalanx of 2nd toe medially; 2nd-4th, lateral aspect of basesof proximal phalanges of toes 2, 3, and 4 (Fig. 1.13).Plantar Interossei (10)orjgj~medial aspect of 3rd, 4th, 5th metatarsal shafts and bases.jnsertjo~media l aspect of bases of proximal phalanges of toes 3, 4, and 5 (Fig .. 1.14).
  36. Steindler Stripping
    -Plantar fascia, and the long plantar ligament is released-Abductor hallucis, FDB, and abductor digiti quinti are stripped from theperiostium of the calcaneus

    What is the difference between a subcutaneous plantar fasciotomy and a Steindler Stripping?A subcutaneous fasciotomy releases only the plantar aponeurosis. The Steindler stripping releases both the plantar aponeurosis and the plantar musculature.
  37. OSHA
    • OSHA regulations require that an employer do which of the following?.(B) Post OSHA regulations in a highly visiblearea for all employees.
    • OSHA regulations state that it is “mandatory to post”regulations in a location all employees routinely visit.

    • In addition to gloves, OSHA-designated personalprotective equipment includes(A) gowns and eye protection
    • In addition to gloves, OSHA-designated personalprotection includes gowns and eye protection, whichprovide protection especially from blood splatter.
  38. lumbricales
    • LUMBRICALES
    • Origin: Tendon of the flexor digitorum longus after its separation into 4 slips
    • Insertion: Medial aspect of the extensor expansion, slightly more dorsally than plantarly
    • Action: Flex the 2nd-5th MPJ and extend the IPJs of these same toesInnervation: The 1st(medial) lumbricalis innervated by the medial plantar nerve L5, S1. The lateral 3 lumbricales are innervated by the deep branch of the lateral plantar nerve S1, S2
    • Arterial Supply: Plantar metatarsal arteries

    Extensor Substitutio~this is associated with pes cavus, foot drop, and anteriorcompartmentweakness, wherein the EDL overpowers the lumbricales during swing phase,and causes dorsiflexion of the MTPJs; results in a high degree of MTPJ subluxation andretrograde plantar buckling of the metatarsus.

    • Which of the following tendons is exposed during neuroma surgery performed on the third interspace through a dorsal approach?(C) Lumbrical to the fourth toe
    • Of the options listed, the only tendon encountered in the third interspace is the lumbrical to the fourth toe.

    • A patient presents with a second toe that is dislocated in the sagittal plane. One year ago,the proximal phalangeal base of the toe was removed. The most likely cause of the dislocation is loss of attachment of the(A) first lumbrical and the first and second dorsalinterossei(B) first lumbrical and the first and secondplantar interossei(C) first and second lumbricals and the firstdorsal interosseous(D) first and second lumbricals and the firstplantar interosseous
    • 32 AThe first lumbrical and the first and second dorsalinterossei all insert in the base of the proximalphalanx of the second digit.

    • Which of the following tendons is found plantar to the deep transverse metatarsal ligament?(A) Lumbrical tendon(B) Abductor tendon(C) Plantar interosseous tendon(D) Dorsal interosseous tendon
    • The lumbrical tendon is located plantar to the deep transverse metatarsal ligament.

    What is the "hood apparatus"?The "hood apparatus" or "extensor expansion" is the medial and lateral fibrous extensions of the extensor tendon. It is composed of tendinous contributions from the long and short extensor tendons as well as from the lumbricales and interossei. The "hood apparatus" functions such that the pull of the long and short extensor tendons creates dorsiflexion of the proximal phalanx at the metatarsophalangeal joint via the "sling" portion of the apparatus.

    What is the relationship between the deep transverse intermetatarsal ligament (DTlL) and the interossei and lumbricales?The plantar and dorsal interossei lie dorsally and the lumbricales plantar.
  39. abductors (hallucis, digiti minimi etc
    Infracalcaneal nerve (nerve to the abductor digiti minimi) -a.k.a.Baxter's nerve

    • ABDUCTOR HALLUCIS
    • Origin: Medial process of the calcaneal tuberosity Insertion: The tendons of abductor hallucis and the medial head of the flexor hallucis brevis insert together on the medial side of the plantar aspect of the base of the proximal phalanx. Somefibers also attach to the medial sesamoid.
    • Action: Abduct the hallux.
    • Innervation: Medial plantar nerve(L5, S1,S2)
    • Arterial Supply: Medial plantar artery.

    • ABDUCTOR DIGITI MINIMI QUINTI
    • Origin: Lateral process of the calcaneal tuberosity.
    • Insertion: Lateral side of the plantar aspect of the base of the 5th proximal phalanx.
    • Action: Abduct the 5th toe and assist with flexion.
    • Innervation: Lateral plantar nerve S1, S2
    • Arterial Supply: Lateral plantar nerve.

    • PLANTAR LAYERS OF THE FOOT
    • First Laver(superficiah1. Abductor Hallucis Muscle2. Flexor Digitorum Brevis Muscle3. Abductor Digiti Minimi(quinti)Second Layer1. Quadratus Plantae Muscle2. Lumbricales3. Flexor Hallucis Longus Tendon4. Flexor Digitorum Longus TendonThird Layer1. Adductor Hallucis Brevis Muscle2. Flexor Hallucis Brevis Muscle3. Flexor Digiti Minimi Brevis MuscleFourth Laver(deep)1. Plantar Interossei2. Dorsal Interossei3. Tibialis Posterior Tendon4. Peroneus Longus Tendon

    • SESAMOIDAL ATTACHMENTSLIGAMENTOUS ATTACHMENTSIntersesamoid Ligament -(tibial & fibular)Medial metatarsosesamoid Suspensory Ligament-(tibial)Lateral metatarsosesamoid Suspensory Ligament -(fibular)Medial Sagittal Hood Ligament (tibial)Lateral Sagittal Hood Ligament -(fibular)Medial Sesamophalangeal Ligament-ff/b/a/JLateral Sesamophalangeal Ligament -(fibular)
    • TENDON ATTACHMENTSAdductor Hallucis Conjoined Tendon-(fibular)Abductor Hallucis Ter\dor\-(tibial)Flexor Hallucis Brevis Tendon(Medial head)-(tibial)Flexor Hallucis Brevis Tendon(Lateral head)-(fibular)OTHER ATTACHMENTSPlantar Fasc\a-(tibial & fibular)Plantar Intermetatarsal Ligament -(fibular)Plantar P\ate-(tibial & fibular)
    • Name the muscles and tendons visible in dissection when performing the Young's procedure. Tibialis anterior tendon, tibialis posterior tendon, abductor halluc is muscle.

    What are the possible points of entrapment of the first branch of the lateral plantar nerve (to the abductor digiti quinti)?The first point occurs on its course to the abductor digiti quinli muscle. It is compressed by the deep fascia of the abductor hallucis muscle and the medial head of the quadratus plantae muscle. The next point is where the nerve crosses just distal to the medial calcaneal tuberosity in the vicinity of the heel spur. Here it may be compressed against the bone and ligaments.

    The Hiss procedure is?A transfer of the abductor hallucis to the dorsomedial proximal phalanx of the hallux.

    A common mechanical factor in the development of abductor hallucis muscle strain occurring in a runner may be ______.Hypermobility of the 1st ray requiring the abductor hallucis to overwork in attempt to try to stabilize the 1st ray on the ground/supporting surface.

    What tendon transfer could be useful in the correction of a hallux varus deformity? Abductor hallueis transferred from the medial to lateral side ofthe hallux (adjunctive procedure).
  40. plantar interosseous
    • How many interossei muscles are there and where do they insert?
    • Three plantar interossei which insert on the base of the proximal phalanx, medially and four dorsal interossei which insert on the base of the proximal phalanx laterally except the first dorsal interossei which inserts from medially. Together with the flexor digiti quinti brevis, there are eight intrinsic muscles that function as a pair for each lesser digit.

    o What are the forces and functions of the interossei muscles?The pull of the interossei muscles neutralizes the force of the flexor muscles at the metatarsophalangeal joints.

    • DORSAL INTEROSSEI
    • Origin: Originate from adjacent sides of adjacent metatarsal bones.
    • Insertion: The base of the proximal phalanx and the extensor expansion.
    • Action: Abduct the toes away from the midline of the foot(the second toe).
    • Innervation: 1st-Deep branch of the lateral plantar nerve and an extra branch, the medial branch of the deep peroneal nerve. 2nd-Deep branch of the lateral plantar nerve and an extrabranch, the lateral branch of the deepperoneal nerve. 3rd-Deep branch ofthe lateral plantar nerve. 4th-Superficialbranch of the lateal plantar nerve.
    • Arterial Supply: Dorsal metatarsal arteryNOTE: Mnemonic-DAB, Dorsal-Abduction

    • PLANTAR INTEROSSEIOrigin: Medial side of the bases of the3rd, 4th, and 5th metatarsal bones
    • Insertion: Medial side of the bases of theproximal phalanges, the metatarsophalangealjoint capsules, and the extensor expansion of the same digit on which they originate.
    • Action: Adduct the third, fourth, and fifth toes toward the midline of the foot.
    • Innervation: The 1st and 2nd are innervated by the deep branch of the lateral plantar nerve, The 3rd is innervated by the superficial branch of the lateral plantar nerve.
    • Arterial Supply: 2nd, 3rd, and 4th plantarmetatarsal arteries.NOTE: Mnemonic-PAD, Plantar-ADduction
  41. compartments of the foot
    • In the foot, there are 3 main longitudinal compartments: 1) medialcompartment-containing abductor hallucis and FHB; 2) superficial compartment- whichis plantar central and contains FOB; and 3) lateral-which contains abductor digiti minimiand flexor digiti minimi brevis. The forefoot also houses 5 smaller compartments:4 intermetatarsal (interosseous) spaces containing the interossei; and the adductorhallucis compartment plantarly. The hindfoot houses a single deep compartment, referredto as the calcanean compartment. which contains the quadratus plantae.
  42. metatarsus primus adductus
    • INTERMETATARSAL ANGLE
    • (Metatarsus Primus Adductus angle)-normal is 8-12° in a rectus footand 8°-10° in an adductus foot-an IM greater than 16° a base wedgeosteotomy is indicated

    • BUNION EVALUATION
    • Stage I -Subclinical subluxation of the first metatarsal joint
    • Stage II -Development of clinical hallux abduction deformity
    • Stage III -Development of metatarsus primus adductus deformity
    • Stage IV -Clinical subluxation/dislocation of the first MPJ
  43. Psuedogout
    What is the most common cause of acute monoarticular or oligoarticular arthritis in the elderly?Acute pseudogout.

    What joints are most commonly involved in pseudogout?Knee (58%), wrist (33%), ankle joint.

    What is the most common joint involved in the foot?Talonavicular joint. Pseudogout involves the foot in only 5% of cases.

    What are the differences in clinical presentation between gout and pseudogout?Patients with pseudogout tend to be older, and complain less of pain. Males and females are involved equally. Pseudogout does not respond as dramatically to colchicine as does gout.

    Does the finding of chondrocalcinosis in the knee, wrist symphysis pubis, or any other joint require treatment for pseudogout?Most people with chondrocalcinosis remain asymptomatic. 60% ofpeople over the age of 80 have chondrocalcinosis.

    • PSEUDOGOUT
    • (Chondrocalcinosis, Calcium pyrophosphate dihydrate, CPPD)
    • DESCRIPTION-associated with acute or chronic inflammatory arthritis-caused by deposition of calcium pyrophosphate dihydrate(CPPD)crystals in the joint-symptoms are similar to those of gout but it tends to run a longer course(reaches maximum severity at 1-3 days, and resolves in 1week or longer)-the knee is most often involved(50%) followed by the ankle, wrist,and shoulder-risk increases with age, trauma, patients hospitalized for othermedical conditions and those with metabolic dz(hypothyroidism,hyperthyroidism, gout, amyloidosis)-associated with high grade fever
    • DIAGNOSIS-microscopic examination of joint aspiration reveals rhomboid crystals-radiographically-calcifications of the articular cartilage or meniscus
    • TREATMENT-immobilization, NSAID, analgesics
  44. diabetes mellitus
    • A podiatric physician is examining a 57-year-oldpatient who has a 21-year history of poorlycontrolled diabetes mellitus. A neurosensoryexamination reveals a loss of proprioception.Further examination of the patient would mostlikely reveal a(B) loss of protective sensation with 10-grammonofilament
    • A patient with a loss of proprioception will also havea loss of protective sensation, which is best detectedwith a 10-gram monofilament.

    • A Charcot joint is caused by(B) sensory neuropathy
    • Charcot joint is caused by impairment of deep pain sensation or proprioception, which affects the joint’s normal protective reflexes. It commonly occurs in patients with diabetes in joints formed by the tarsal bones.

    • A patient presents with a hemoglobin A1c of 8.0and a fasting blood glucose level of 210 mg/dL.Clinical examination strongly indicates thatsensory polyneuropathy is present. A symptomof this would be
    • The 5.07 (10-gram) monofilament is used to screenfor protective sensation loss in patients with diabetes.

    • A 38-year-old patient with diabetes mellitus is in the preoperative holding area and surgery has been delayed for 2 hours. One-half of the patient’s prescribed AM NPH insulin dose was administered at 7:00 AM. It is now 9:30 AM and the patient suddenly becomes disoriented and begins to perspire profusely. Which of the following actions would be most appropriate?.(B) Perform a finger-stick blood glucose evaluation.
    • Blood glucose levels should be measured preoperatively and postoperatively. The need for additional measurements is determined by the duration and magnitude of surgery and the stability ofthe diabetes. Signs of hypoglycemia include tachycardia, hypertension, and diaphoresis.

    On the morning of surgery a patient with non-insulin dependent diabetes, hypothyroidism, and hypertension should be told to take all of their medication except?They should not take their oral hypoglycemic because they have been NPO and could become severely hypoglycemic and go into insulin shock.

    CUTANEOUS MANIFESTATIONS OF DIABETESNecrobiosis Lipoidica Diabeticorum

    • Xanthoma Diabeticorum
    • Bullous Diabeticorum
    • Diabetic Dermopathv

    • DIABETES-6% of Americans(12 million people) have diabetes-glucose levels >200mg/dl-when treating a diabetic with Insulin one should always error on theside of hyperglycemia; hypoglycemia results in permanent neurondestruction
  45. limb length discrepancy
    • LLD
    • (limb length discrepancy)-a true LLD requires a 5mm discrepancy or more to cause significant functional and structural problems-children typically walk with a shoulder drop-during stance the foot of the longer leg is usually pronated and the shorter leg is supinated-by age 13-14 years compensatory scoliosis may develop-with a difference of 1/i " or more, will have some change in their shoulders

    Unequal limb length - may be structural within the thigh, leg or both femoral and t ibial!fibular segments; or functional secondary to scoliosis induced pelvic tilt with lower side of pelvis effecting functionally longer limb, unilateral supination or pronation of the foot.Compensation for limb inequity involves pedal pronation on the longer side, along with ipsilateral inferior pelvic tilt (tilts downward) due to hyperpronating hindfoot, ipsilateral shoulder tilt downward, scoliosis, ipsilateral head tilt toward longer limb, increased stance phase on the longer side. On the short side, the hindfoot supinates, pelvis rises, shoulderrises, and there is less stance phase weight bearing.
  46. pronation
    • Open kinetic chain
    • Open kinetic chain pronation can be described as abduction, evertion, and dorsiflexion of the foot.
    • Closed kinetic chain.Closed kinetic chain pronation can be described as talar plantarflexion and adduction in the ankle joint, and calcaneal evertion.
    • Flexor Stabilization Occurs in flat feet with excessive pronation
    • tarsal tunnel-biomechanical(excessive pronation-results in stretching of the tibialnerve)
    • Kites Angle-long axis of talus and long axis of calcaneus-normal range is 20°-40°-increased in pronation, decreased in supination
    • osteoarthritis: Chronic subtalar joint and metatarsophalangeal jointhyperpronation is a common cause of degenerative joint disease in the foot. with resultantpes valgus, forefoot supinatus and hallux limitus/rigidus, plantarfascitis, flexor stabilizationinduced hammertoes, and medial Lisfranc breakdown.
  47. ANKYLOSING SPONDYLITIS
    • SERONEGATIVE SPONDYLOARTHROPATHIES
    • ANKYLOSING SPONDYLITIS(Marie-Strumpell's dz)DESCRIPTION
    • A chronic inflammatory arthritis that affects the sacroiliac joint and to a lesser extent the rest of the spine. Pain and stiffness are early signs,but in advanced cases a poker spine(very stiff, inflexible backbone) is common.
    • SIGNS AND SYMPTOMS-onset is 15-35 yrs-male to female ratio(10:1)-lower back pain(sacroiliac jts)-kyphosis-Recurrent acute iritis in 1/3 of pts
    • DIAGNOSIS-increased sed rate-(+)HLA-B27-(+)Schoeber's Test-X-ray-abnormalities at the sacroiliac jt-bamboo spine
    • TREATMENT-PT-NSAIDS

    • Ankylosing Spondylitis
    • The criteria for the diagnosis of ankylosing spondylitis include:1. Limited motion of lumbar spine in anterior and lateral flexion and extension 2. History of pain or presence of pain in dorsolumbar junction or in lumbar spine3. Limitation of chest expansion to one inch or less
    • Definite ankylosing spondylitis is confirmed by the presence of bilateral sacroiliitis associated with at least one clinical criteria. Probable ankylosing spondylitis exists in the presence of bilateral sacroiliitis associated with none of the clinical criteria. Common symptoms include low back pain, prolonged back stiffness, ascending back pain, heel pain,peripheral joint pain, fatigue, and diminished vision and/or eye pain. Roentgen signs vary with duration of the disease. Early signs include sacroiliac joint blurring, joint space narrowing and widening, subchondral sclerosis, diffuse osteoporosis of spine, apophyseal joint sclerosis, and straightening of spine. Advanced ankylosing spondylitis reveals apophyseal joint erosion, squaring of vertebrae, narrowed disc space, vertebral collapse,pelvic whiskering, and pubic symphysis involvement. Terminal roentgen signs include intervertebral disc calcification, paravertebral ligament calcification, vertical syndesmophytes,sacro-iliac joint fusion, and bamboo spine.
  48. SYSTEMIC LUPUS ERYTHEMATOSUS(SLE)
    • CONNECTIVE TISSUE DZ
    • SYSTEMIC LUPUS ERYTHEMATOSUS(SLE)
    • DEFINITION
    • A chronic, remitting, relapsing, inflammatory, and often febrile, multisystemic disorder of connective tissue, acute or insidious in onset.Drug induced lupus may be caused by: Procainamide, Hydralazine,Chlorpromazine, Isoniazid, Penicillamine, Griseofulvin
    • SIGNS/SYMPTOMS-age of onset 15-35 yrs-joint pain in 90% of patients(an early manifestation)-primarily small joints of the hands and feet-mainly in young women(10:1)-more common in blacks-fever(90% of patients)-abdominal pains-butterfly rash-skin lesions in sun exposed areas(photosensitivity)-fatigue, weight loss, and anorexia-Raynaud's phenomenon-alopecia-vision problems-proximal nail fold telangiectasis-renal, cardiac, splenic, and pulmonary problems
    • DIAGNOSIS-increased sed rate-(+)ANA(antinuclear antibody test)-antibodies to double-stranded DNA-decreased hemoglobin, WBC, and platelets
    • TREATMENT-symptomatic steroids antimalarials(chloroquine) immunosuppressant savoid sunlight

    • What are the Criteria for the Classification of Systemic Lupus Erythematosus according to the American Rheumatology Association?
    • 1.Malar rash.2.Discoid rash.3.Photosensitivity (by history or physician observed).4.Oral ulcers (or nasopharyngeal observed by a physician).5.Arthritis ( nonerosive involving 2 or more joints).6.Serositis (pleuritis or pericarditis).7.Renal disorder (proteinuria or cellular casts).8.Neurologic disorder (seizures or psychosis).9.Hematologic disorder (hemolytic anemia, or leukopenia, or lymphopenia, or thrombocytopenia).10.Immunologic disorder (pos. LE eell prep., or anti-DNA, or anti-Sm or false positive serologic test for syphilis confirmed by FTA).11.AntinueJear antibody.For eJassification purposes, a patient has Lupus if they satisfy at least 4 or more of these II criteria serially orsimultaneously.

    • o What are Lupus Anticoagulants?Paradoxically named blood coagulation inhibitors, which are associated with thrombosis, not with hemorrhage.They are found in Lupus as well as other conditions. Anticardiolipin antibodies and Lupus anticoagulants are bothantiphospholipid antibodies. The thrombotie manifestations, in addition to DVT and pulmonary emboli, may involve retinal vasculature, renal veins, coronary or mesenteric vessels and large peripheral arteries.
    • o Which drug is tbe most frequent cause of a drug induced Lupus syndrome?Procainamide. Other drugs which have been reported to cause Lupus like syndromes include hydralazine, hydantoin anticonvulsants, isoniazid, alpha methyldopa, propylthiouracil, methimazole, quinidine and the sulfonamide:s as well as penicillin.

    o What is the standard screening test for SLE'? The fluorescent antinuclear antibody (ANA) test.
  49. Kidner procedure
    • What is a Kidner procedure?Excision of an accessory navicular with advancement of the posterior tibial tendon plantarly.
    • o When excising an accessory navicular or hypertrophic navicular tuberosity, how much bone should be resected?The hypertrophic tuberosity should be resected flush with the medial cuneiform.
    • o What are the indications for a Kidner procedure?The Kidner procedure is not a corrective procedure for flatfoot deformity; it should be used for symptomatic prominence about an enlarged navicular tuberosity.
  50. McBride procedure
    List the following steps in a McBride bunionectomy in the order in which they are performed (from first to last).(A) Section of the deep transverse intermetatarsal ligament (B) Release of the conjoined adductor tendon (C) Medial capsulotomy (D) Removal of the fibular sesamoid (E) Exostectomy

    Sequence: Key60 The order is: C E A B DThe McBride procedure is an important historical procedure for hallux valgus correction in which the sequence of steps is medial capsulotomy,exostectomy, section of the deep transverse intermetatarsal ligament, release of the conjoined adductor tendon, and removal of the fibular sesamoid.
  51. Keller procedure
    removal of proximal phallanx
  52. The Hoffman-Clayton procedure
    • The Hoffman-Clayton procedure is most commonly indicated for which of the following conditions?(A) Pes cavus(B) Hallux valgus(C) Hammer toe(D) Rheumatoid arthritis
    • 19 DThe severe debilitating effects of rheumatoid arthritiscommonly require complete excision of the lesser metatarsophalangeal joints, a technique known as the Hoffman-Clayton procedure.
  53. Dwyer procedure
    What surgical procedure addresses the frontal plane component of posterior cavus or rearfoot varus?The Dwyer calcaneal osteotomy, an extra-articular procedure addresses this component of cavus foot.
  54. Jones Suspension
    • What is a Jones Suspension?An isolated transfer of the extensor hallucis longus to the neck of the first metatarsal. Additionally, the hallux IPJ is fused. This procedure compensates for an overpowering peroneus longus and flexor hallucis longus.
    • o What is a prerequisite for a Jones Suspension? An adequate dorsiflexory range of motion of the first ray.
    • o What are the consequences of over-correction following a Jones Suspension? Hallux limitus.

    JONES TENOSUSPENSION-EHL tendon is transected and rerouted medial to lateral through the head of the 1st metatarsal and sewed back on itself. Kirk modification pass tendon from top to bottom(dorsal to plantar), this technique requires less tendon-the distal stump of the EHL is then attached to the EHB to maintain some extensor function of the hallux-arthrodesis the 1st IPJ to prevent overpowering of the EHL and hammering-performed for pressure problems under the 1st metatarsal head-Indications: flexible cavus foot, flexible plantarflexed 1st ray
  55. Heyman Procedure
    What is a Heyman Procedure?Transfer of all five long extensor tendons to their respective metatarsal heads. This procedure helps to reduce flexible anterior cavus. This procedure is rarely used today. It is technically difficult and has many complications.
  56. Hibbs Procedure
    • o What is the Hibbs Procedure?
    • Transfer of the extensor digitorum longus to the third cuneiform to reduce a flexible anterior cavus. The original description included a plantar fascia and plantar muscle release.

    HIBBS TENOSUSPENSION-the EDL tendon slips are detached from their insertion combined and reattached to the 3rd cuneiform or the base of the 3rd metatarsal-the EDB tendon are transected and reattached to the stump of the corresponding EDL tendon, the 4th and 5th longus slips are both attached to the 4th EDB slip-releases the buckling force at the MPJ's and elevates the forefoot-Indications: equinus with or without clawtoes

    • Hibbs Suspension (Figure 6-8)Goals- decrease MTPJ buckling and increase ankle dorsiflexion
    • Indications-anterior weakness (mild), flexible anterior cavus with extensor substitution, claw toes often with associated IPK
    • Contra indications-posterior weakness, weak interossei, gross EDL weakness,structural rigidity, osseous instabilityAftercare-BK weight bearing cast 4-6 weeks
  57. STATT Procedure
    o What is a STATT Procedure?The split tibialis anterior tendon transfer is an adjunctive procedure for treatment of flexible cavus foot. Thc lateral one half of the anterior tibial tendon is anastomosed to the peroneus tertius tendon near its insertion into the base of the fifth metatarsal. This is used when the EHL and EDL muscles are weak but the anterior tibial is a full strength.

    SPLIT TIBIALIS ANTERIOR TENDONTRANSFER(STATT)-tibialis anterior is split from it's insertion up just proximal to the superior extensor retinaculum-the lateral fibers are passed through the peroneus tertius sheath and sutured to the tendon or attached to the cuboid-the procedure increases dorsiflexion of the foot and balances the force laterally-Indications: flexible rearfoot varus, excessive supination, dorsiflexory weakness
  58. Cole Procedure
    • What is a Cole Procedure? A lesser tarsal osteotomy designed to reduce a fixed anterior cavus. It preserves subtalar and midtarsal motion. It does not correct varus of the calcaneus or compensate for muscle imbalance.
    • o How is the Cole procedure done?This is a dorsal wedge osteotomy, apex plantarly, base dorsally, which extends from the cuboid laterally to opposite sides of the navicular-cuneiform joint medially. After the wedge is excised the forefoot is dorsiflexed to close the osteotomy and is fixated with pins or screws. A fasciotomy is performed if necessary to release a tight fascia.
    • o What are the disadvantages of the Cole procedure?This osteotomy results in a shorter, thicker, wider foot because the deformity is corrected by shortening of the dorsal convex surface of the foot.
  59. Japas Procedure
    • What is a Japas Procedure? This is a midtarsal "V" shaped osteotomy in which the apex is proximal, usually within the navicular, and the lateral limb of the "V" extends through the cuboid while the medial limb extends through the first cuneiform. The medial limb can extend through the first metatarsal base when a plantarflexed first metatarsal is present. No bone is excised. The proximal part of the distal bone segment is then shifted dorsally on the proximal segment elevating the forefoot and correcting the cavus. Pins are used to fixate the osteotomy. A fasciotomy is performed first.
    • o What are the disadvantages of the Cole and Japas procedures?Both proeedures are diffleult to control accurately and both cause significant trauma to the lesser tarsal -midtarsal area. Healing is slow and the amount of correction possible is less than with a triple arthrodesis. They generally result in less than a cosmetically pleasing result.
  60. Calcaneal osteotomies
    Calcaneal osteotomies are classified (by Jacobs and associates) into three groups. Name the groups. extra-articular, anterior, and posterior osteotomies.o Name the procedures in each category above.Extra-articular Chambers, Baker-Hill, Selakovieh.Anterior = Evans.Posterior = Gleich, Dwyer, Silver, Koutsogiannis.
  61. Evans procedure
    • Where is the osteotomy made for the Evans procedure? Approximately 1.5 em proximal and parallel to the C-C joint.
    • o How is this osteotomy (Evans) directed and why? Directed anteriorly to avoid the middle facet ofthe STJ.

    • What deformity cannot be present if the Evans procedure is planned? Metatarsus Adductus.
    • o What is the consequence if the Evans is performed in a foot with the above deformity? Unmasking and exaggeration ofthe metatarsus adductus and an in-toe gait.
  62. Miller procedure
    What joint(s) is/are fused in the Miller procedure? Navicular-l st cuneiform joint and cuneiform-lst metatarsal joint.

    Which procedure(s) in the correction of flatfoot includes naviculocuneiform arthrodesis? Miller (navicular-l st cuneiform joint fusion), Hoke (navicular-) st,2nd cuneiform fusion).
  63. kessel & bonney procedure
    Describe the Kessel & Bonney procedure.This is a procedure to address a hallux limitus deformity, in which a dorsal wedge osteotomy is performed on the base of the proximal phalanx of the hallux, to bring it into a more dorsal position. This allows the limited joint motion to occur in a more dorsal manner.
  64. Regnauld procedure
    o What is a Regnauld procedure'!This is a procedure in which one third of the base of the proximal phalanx is resected, removed from the surgical site, fashioned into a hemi implant configuration, and then reinserted back into the proximal phalanx as an autogenic bone graft. Sometimes referred to as the enclavement procedure. This allows for preservation of the joint while also shortening the proximal phalanx, which reduces the internal cubic content ofthe joint and "loosens it up".
  65. Waterman procedure
    o Describe a Waterman procedure.This is a procedure to address a hallux limitus deformity, in which a dorsal wedge osteotomy is performed on the head of the 1st metatarsal. The plantar cartilage is thus directed more dorsally which brings the hallux more dorsally.

    WATERMANN-indicated in hallux limitus-plantar cortex is left intact
  66. Molluscum Contagiosum
    • -contagious viral infection of the skin-common in children, in adults it's often sexually transmitted
    • CAUSE-poxvirus
    • PRESENTATION-discrete, round, smooth,umbilicated, pearl-white or skincolored papules-usually measuring 1-3mm indiameter-lesions are asymptomatic unless secondarily infected-lesions may be a single isolated lesion or multiple scattered lesions-often disappear spontaneously within 1-2 years
    • TREATMENT-liquid nitrogen
  67. Verruca
    • Verruca(plantar wart)-plantar warts are common contagious benign tumors caused by a virus-more common in older children-caused by human papillomavirus-must be distinguished from a callus(see table below)-only painful when on WB surfaces
    • TREATMENT-surgical excision, liquid nitrogen,various topical acids, laser, oral ranitidine (See p. 74)-spontaneous remission occurs in-60% of cases with or without treatment, may reoccur at the sameor a different site
    • WART CALLUS-skin lines go around lesion-WB or NWB surfaces-pain on lateral pressure-center-pale/spongy punctate bleeding-affects children and young adults-skin lines go through lesion-WB surfaces-pain on direct pressure-center-hard-affects middle-aged and adults
  68. Contact Dermatitis
    • DERMATITIS/ECZEMA
    • Contact Dermatitis-dermatitis caused by contact with certain substances found in the environment causing inflammation of the epidermis and dermis-the most common and classic example of this is poison ivy-another common cause is nickel which is widely used in jewelry and inmetal clasps on women's underclothes. In podiatry contact dermatitis iscommonly due to the rubber found in the toe box of most shoes or thecement used to bind shoes together
    • CLASSIFICATIONa) Irritation contact dermatitis-non-immunologicmechanisms-a single exposure causesa reaction-i.e. detergents, fiberglassb) Allergic contact dermatitis-acquired immunologicresponse-first contact causes noreaction, but the exposuresensitizes the skin to futureexposures-i.e. poison ivy
    • PRESENTATION-irregular poorly demarcated patches of erythema and edema onwhich are superimposed closely spaced vesicles, punctate erosionsexuding serum and crust.-may be seen with a subchronic or chronic lesion lichenification
    • TREATMENT-avoid contact with the offending agent-increase aeration: avoid shoes with plastic uppers, wear cotton orwool socks instead of synthetic ones, apply drying powders-topical hydrocortisone cream for pruritis-in moderate to severe cases treat pruritis with oral meds(Benadryl,Atarax, Vistaril)-astringent soaks(Burrow's solution, Epsom salt) will decreaseinflammation and reduce weeping-moisturizing lotions may also be soothing and help withlichenification and fissuring-topical Abx for secondary bacterial infections

    • What is an id reaction and how is it managed?
    • Immune mediated, sympathetic response to acute tinea. Sterile eruptions distant from the acute site i.e.: fingers palms chest or back. Treat the primary tinea and the id reaction will resolve with it.
    • o Explain the pathogenesis of allergic contact dermatitis.Allergic contact dermatitis is a delayed cell mediated hypersensitivity reaction. First a hapten contacts skin and forms a protein complex. Langerhans skin cell present the complete antigen to the T-helper cell causing mediator release. Sensitization takes 5-21 days. Upon re-exposure there is proliferation ofactivated T cells, mediator release and migration of cytotoxic T cells resulting in cutaneous eczematous inflammation at the site of contact. This takes 4-72 hours after re-exposure. Small exposure can trigger eruptions in sensitized persons.
    • o Name the two types of contact dermatitis. Primary irritant and allergic contact dermatitis.
  69. Bullous Diabeticorum
    Bullous Diabeticorum-occur as spontaneous atraumatic lesions usually on the extremities, especially the feet-blisters are sterile and filled with clearfluid that range from a few millimeters to several centimeters in diameter-blisters start as tense lesions, but as itenlarges it becomes flaccid-the exactcause of the blisters is unknownalthough photosensitivity has beensuggested as initiating factor-blisters heal over a 6 week periodwithout scarring-lesions are asymptomatic and require no treatment, however theblisters may be incised and drained if they are in a precarious position
  70. chf
  71. Flexor tendon transfer
    Surgically changing the insertion of the flexor digitorum longus tendon from the base of the distal phalanx to the dorsal aspect of the proximal phalanx will correct the proximal interphalangeal joint contracture of the hammer toe by pulling the proximal phalanx into a more congruous positionwith the middle phalanx.

    • What are the advantages in the use of the flexor tendon transfer for digital surgery?Possible prevention of a joint fusion; Decreased incidence of mallet toe; Realignment of the metatarsophalangeal joint.
    • o What is a more common reported disadvantage of the flexor tendon transfer in digital surgery? Prolonged edema and stiffness.

    Flexor tendon transfer (Girdlestone, Foerster and Brown}--can also be useful for the correction of hammertoes and clawtoes, however care must be taken to transfer the sectioned flexor tendon slips from plantar to dorsal on the phalanx in a subperiosteal fashion (to avo id constriction of digital vessels), or through a drill hole in the phalanx, and itis possible to effect a PIPJ rocker-bottom deformity unless arthrodesis is performed(obviating the need for flexor tendon transfer). Sgarlato's modification of the Girdlestone procedure can be used for the correction of hammertoes and clavvtoes with MTPJ subluxation, and serves to redirect the long extensor tendon's pull to that of a stabilizing influence on the toe and MTPJ. Two incisions are used, 1 medial or lateral aspect at theproximal phalanx, and an adjunct dorsal incision more to the side opposite the medial orlateral incision. The long flexor tendon is split and transferred dorsally in a subfascial fashion and sutured to itself and the dorsal hood expansion as a sling dorsally at the levelofthe proximal phalangeal shaft. Care must be taken to transfer the sp littendon segmentsin a subfascial (deep fascia) fashion, in order to avoid circumferential constriction of thesubcutaneous neurovascular elements coursing to the toe tip. The transfer results indecreased PIPJ range of motion. Dockery and Kuwada modified the transfer by use of adorsal-to-plantar drill hole in the anatomic neck ofthe proximal phalanx. Moreover, a rockerbottom PIPJ or swan-neck deformity can be created iftoo much tension is placed within thetransferred long flexor. PIPJ arthrodesis is generally considered a more effective andlasting method to stabilize the digit and convert the long flexor to a stabiliz ing influence onthe MTPJ, particularly for the intermediate lesser digits. A flexor tendon transfer may beapplicable to the fifth toe, or in the presence of congenital absence of the middle phalanx.
  72. Rocker sole or rocker bar use?
    Rocker sole modification is used for any type of pathologic or pathomechanical condition that limits normal movement of the ankle, metatarsal, or metatarsophalangeal joint. A rocker sole is a dynamic lever that assists with the normal movement of the lower extremity during gait and prevents flexing of the sole of the shoe during all phases of gait.

    • -rocker bottom soles-may be added to either shoe type to provideadditional offloading of forefoot
    • Nonsurgical treatment of HL/HR involves use of a metatarsal bar or tapered rocker-sole, orthosis control of hypermobility, and range of motion physical therapy; and these measures are combined with anti-inflammatory intervention, intraarticular chondroprotective agent (chondroitin sulfate and glycosaminoglycanpreparations), and alteration of activities.

    List 3 methods of conservative treatment for hallux limitus/rigidus which can be used in athletes.Morton's extension.Stiffen the sole ofthe shoe or select a running shoe with a stiffer sole.Choose a shoe with more ofa "rocker bottom."
  73. first intention
    • Primary intention closure-involves direct wound margin reapproximation secured with skin sutures. It results in immediate closure that seals with epithelium after 24-48 hours,and usually results in a fine-line scar. Primary skin closure requires wound margin mobility that allows approximation of the edges.
    • Secondary intention closure-involves wound granulation, contraction and epithelialization,and slowly progresses over several days to weeks, depend ing upon local andsystemic factors. This is often the preferred method of closure following incision and drainage of an abscess or osteomyelitis, or when the wound presents chronic contamination and necrosis, such as ulceration in a debilitated patient.
    • Tertiary intention (delayed primary) closure-involves an initial period of secondary intention healing, followed by additional surgical wound debridement and primary intention suture closure. Primary, secondary or tertiary intention healing are the preferredmethods of wound closure, and should be attempted whenever clinically indicated.Indications include a clean wound with beefy red granulations and resolution ofsurrounding cellulitis and edema. Generally, other methods of closure, such as skin plasty,grafts, and flaps, entail a greater risk of dehiscence, dysvascularity, slough or othercomplication, and should be reserved for those cases where simpler methods aredeemed inadequate.
  74. talar dome
    During ankle joint dorsiflexion, the anterior andwidest portion of the talar dome is wedged in theankle mortise. With inversion, the lateral border ofthe talar dome is compressed against the lateralmalleolus.

    • OSTEOCHONDRITIS DISSECANS
    • (Talar dome fractures)
    • MECHANISM OF INJURY LOCATION OF LESION
    • Dorsiflexion-lnversion Anterior-Lateral
    • Plantarflexion-lnversion Medial-Posteriormnemonic-DIAL-A-PIMP
    • CLASSIFICATION(Berndt-Harty)
    • Type I Small area of subchondral bone compression with the overlying cartilage intact
    • Type II Partial detached osteochondral fragment
    • Type III Completely detached fragment remaining in crater
    • Type IV Displaced osteochondral fragment

    • Talar Dome Fractures-talar dome defects can develop secondary to ankle sprain orfracture, and are known to be debilitating in all age groups. The Berndt and Harty classification (Table 10-9) is the standard system for identification of talar dome lesions.Talar dome osteochondral defects develop as a result of shearing under compressive load between the distal tibial bearing surface and the dome. The injury causes AVN of the subchondral trabecular and cortical bone, which eventually heals with cortical irregularity, and resultant development of post-traumatic arthritis.
    • TABLE 10-9. THE BERNDT AND HARTY CLASSIFICATION OF TALAR DOME LESIONS.
    • Stage Description ofthe injury
    • I A small area of subchondral bone compression
    • II A partially detached osteochondral fragment
    • III A completely detached fragment, remaining in its crater
    • IV A displaced osteochondral fragment

    The incidence of posteromedial talar dome defect is 56%, while anterolateral defects occur in 44% of cases. Medial lesions are caused by ankle inversion and plantarflexion, while lateral lesions are caused by ankle inversion with dorsiflexion (Figs. 10-22 and 10-23).Treatment for all Stage I, II, and medial Stage III lesions is 6-12 weeks of BK non-weightbearing cast immobilization, with consideration to use of a patellar tendon bearing brace andpartial weight bearing; and surgical intervention for recalcitrant pain. Stage IV and lateralStage III lesions are treated surgically by means of fragment excision, saucerize the crater,drill hole fenestration of the subchondral bone to aid revascularization and enhance fibrocartilage production. Medial lesions may require medial malleolar osteotomy and subsequent replacement with lag screw fixation. Lateral lesions may be combined with secondary repair of chronic lateral ankle instability if this condition exists. Very large fragments may be amenable to reduction and fixation with either absorbable pin or screw fixation. The use of autogenous osteochondral plug grafts (OATS) harvested from non contact articular cartilage from the head of the talus, or the knee, as well as allogeneic grafts, and/or autogenous cultured cartilage cells, provide other reconstructive options. Early postoperative range of motion in a non-weight bearing fashion is indicated, with resumption of weight bearing at about 2-3 weeks postop. Salvage by means of ankle fusion,or total ankle replacement may also be considered (explained elsewhere in this manual).
  75. hemolytic anemia
    normochromic, normocytic

    Increased: Urobilinogen, bilirubin, LDH, SGOT

    Thalassemia: A hereditary group of hemolytic anemias marked by a decrease in production of hemoglobin.

    Remember the phrase "90, 30, 30," for normal MCV, MCH, and MCHC values.Normocytic anemia can be observed with acute hemorrhage, hemolytic anemia, andabnormal hemopoiesis. Macrocytic anemia occurs with pernicious anemia, sprue,pregnancy, antimetabolic therapy, and other megaloblastic conditions. Microcytic anemiaoccurs with iron deficiency or malabsorption, hemorrhage, and increased iron metabolism.
  76. iron deficiency anemia
    • hypochromia (abnormal decrease in the Hb content of RBC's), microcytic
    • What is the most common reason a male patient would have iron deficiency anemia? GI blood loss.

    o Hypochromia and microcytosis are morphological findings in which type of anemia? Iron Deficiency anemia.

    Koilonychia(spoon nail)-Seen in long standing iron deficiency anemia or Plummer-Vinson syndrome(a combination of koilonychia, dysphagia,and glossitis primarily seen in middle-age women), aka Plummer's nails.
  77. folate deficiency anemia
    What are causes of macrocytic, megaloblastic anemia?Vitamin B12/folate deficiency

    • Impaired DNA synthesis - maturation of nucleus delayed relative to maturationof cytoplasm.
    • Findings: hypersegmented neutrophils, glossitis, -folate, l' homocysteine but normalmethylmalonic acid.
    • Etiologies: malnutrition (e.g., alcoholics), malabsorption, impaired metabolism(e.g., methotrexate, trimethoprim), i requirement (e.g., hemolytic anemia,pregnancy).
  78. lead poisoning anemia
    MICROCYTIC ANEMIA

    What are causes of microcytic, hypochromic anemia?Iron deficiency, thalassemias, lead poisoning

    HYPERURICEMIA

    What specific radiographic finding is seen in lead poisoning in pediatric bone? Dense white transverse bands in metaphysis.
  79. forefoot valgus
    • What is a flexible forefoot valgus deformity?
    • A flexible forefoot valgus is one in which the MTJ has sufficient ROM to compensate for the everted forefoot.
    • o What is a rigid forefoot valgus?A rigid forefoot valgus is one in which there is inadequate MTJ ROM to compensate, so the STJ must supinate to bring the forefoot to the ground. The pathomechanics are that the forefoot is everted at forefoot loading, the long axis of the MTJ supinates and the STJ supinates.
    • o What happens to the foot with a rigid forefoot valgus?The foot is high arched nonweightbearing and weight bearing. The heel is inverted when standing. There is restricted motion of the MTJ and contracted lesser digits. There are calluses under the 1st and 5th metatarsal head and the lateral heel.
    • o What is the rigid forefoot valgus foot type associated with?The rigid forefoot valgus deformity is associated with sesamoiditis, chronic inversion ankle sprains, tibial stress fractures and medial knee pain, and low back pain.

    • A patient with 3º forefoot valgus was casted forfunctional orthoses, but the negative castreflected 10º of forefoot valgus. This most likelyoccurred because the clinician(C) pronated the subtalar joint when locking themidtarsal joint
    • A pronated subtalar joint would result in pronation of the midtarsal joint, and forefoot valgus would increase.

    • HAGLAND'S DEFORMITYfPump Bump)A painful bony prominence and bursitis of the lateral posterior superioraspect of the calcaneus above the insertion of the Achiles tendon.Usually involving the retrocalcaneal bursa between the calcaneus andthe Achilles tendon, an adventitious bursa between the tendon and theskin may also develop. The most common cause is a compensated rearfoot varus, a compensated forefoot varus, a compensated forefoot valgus, or a plantarflexed 1st ray.
    • Tailor bunion
    • CAUSES-enlarged 5th metatarsal head or hypertrophied plantar chondyles-lateral bowing of the 5th metatarsal shaft-increased 4lh IM angle-biomechanicalcavus footuncompensated rearfoot varusun, compensated forefoot varussplay footmetatarsus adductus, forefoot valgus

    • What is the relationship between forefoot valgus and cavus foot?
    • Forefoot valgus can be thought of as medial column or the 1st, 2nd, 3rd metatarsals, the cuneiforms, and navicular being plantarflexed in respect to the rearfoot. This compensates with subtalar or midtarsal supination. In subtalar supination the foot functions as a high arched foot with no pronation and little shock absorbing capability. Lateral ankle instability may result due to the inverted position of the calcaneus. With midtarsal supination the joint becomes unlocked, making the forefoot unstable, which can lead to subtalar pronation.
  80. Talar Neck Fractures
    • Talar Neck Fractures- anatomically, 2/3 of the talus is covered with articular cartilage,therefore most fractures of the talus are intra-articular. No muscles or tendons originate from or insert into the talus. The extended neck with its tenuous blood supply is vulnerable to injury.
    • The blood supply to the talus entails:
    • Body-artery of tarsal canal from the posterior tibial and deltoid branch.
    • Head and neck-artery of tarsal sinus from perforating peroneal and DP
    • Posterior talus- calcaneal branches of PT.
    • Avascular necrosis (AVN) is likely to occur when 2/3 of the vascular channels are disrupted. Hawkins noted that it takes until 6-8 weeks after the injury to recognize the presence of AVN, and it may not appear until 1-4 months have passed.
    • Signs and symptoms of talar AVN include intractable pain, relative radiographic sclerosis, or opacity of the dead bone, best observed on the AP view of the ankle. Hawkins noted the presence of subchondral bone revascularization as radiolucency in the dome of the talus on the AP view, and this is referred to as Hawkins' sign and is indicative of healing.
    • The treatment of AVN is non-weight bearing in BK cast for 6-8 months until revascularization occurs, with electrical bone growth stimulation. The Hawkins classification (Table 10-8) of talar neck fractures can be useful in regard to anticipating the development of avascular necrosis(Fig. 10-21).
    • TABLE 10-8. THE HAWKINS CLASSIFICATION OFTALAR NECK FRACTURES.TypeIIIIIIIVFractureVertical non-displacedfracture oftalar neckVertical fracture throughneck with dislocationof ST J (not ankle)Vertical fracture of neckwith dislocation ofST J and ankleVertical fracture of neckwith dislocation ofSTJ, ankle, and TNJFigure 10.21Clinical characteristicsOccurrence is 20%, only the blood supplyto the neck disrupted, 0-15% incidence of AVNOccurrence is 42%, with 2 areas of disruptedblood supply, neck and body; 15-50%incidence of AVNOccurrence is 34%, and all 3 sources oftalar blood supply are disrupted; 90-100 %incidence of AVNOccurrence is 4%, disrupts all 3 areas oftalarblood supply; 90-100% incidence of AVN,.-------------------_.. .-Ii272 Management of Foot and Ankle Trauma Ch.l0
    • The treatment of talar neck fractures is based on the degree of injury and bloodsupply. Hawkins Type I fractures are managed in a BK non-weight bearing cast for 6-8weeks. Alternatively, an AK cast with the foot plantarflexed for 3-4 weeks followed by a BKcast neutral for an additional 4 weeks can be used. Weight bearing and motion are notinitiated until adequate signs of healing are observed radiographically. Hawkins Type II, III,and IV fracture/dislocations are initially closed reduced, however ORIF with lag screwfixation of the neck is most effective. Immobilization and WB status are the same asdescribed previously for non-surgical treatment. Complications of talar neck fracturesinclude AVN, degenerative arthritis of the ankle and STJ, nonunion or mal-union, and infection related to open fracture or surgery.
  81. hypothyroidism
    • Which of the following conditions may causedelayed relaxation of Achilles tendon reflexes?(D) Hypothyroidism
    • In hypothyroidism, the relaxation of Achilles tendon reflexes is delayed. This is sometimes referred to as hypothyroid neuropathy.

    alkaline phosphate decreased, increased cholesterol

    Hypothalamic thyrotropin-releasing hormone stimulates pituitary release of thyroidstimulating hormone, which activates thyroidal uptake of iodine and production ofthyroxine(T4) and triiodothyronine (T3), which exert negative feedback inhibition of pituitary thyroid stimulatinghormone release. Thyroid hormones regulate metabolism. Enlargement of the thyroid gland is referred to as a goiter, and may be associated with overactive or underactivefunction. Hypothyroidism can occur due to surgical or medical (radioactive iodine) ablation,or inflammation (Hashimoto's disease) of the thyroid gland; or secondary to hypothalamic or pituitary dysfunction (tumor, CVA, trauma, other). Hypothyroidism effects myxedema, which specifically presents as non-pitting edema, associated with facial changes that include swelling and a thickened nose, dry or hoarse voice, dry and waxy skin, and mucinous deposition in tissues. Hypothyroid patients display fatigue, general malaise, weight gain,bradycardia, and may become comatose (myxedema coma) in severe disease. Thyroid supplementation with T4 (Synthroid) and T3 (Cytome/), or natural preparations, as well as supportive therapy are used as indicated.

    Hyperthyroidism, or Grave's disease, effects exophthalmos (lid lag), tachycardia, profuse diaphoresis, nervousness, restlessness, finetremors, emaciation, and psychosis. Treatment involves supportive measures and drugs thatalter hormone metabolism or the end-organ effects of the hormone. Thyroid storm is amedical emergency wherein severe hyperthyroidism effects organ damage and death. Drugsthat inhibit hormone formation and release include thiourea derivatives that blockorganification of iodine, iodide which blocks thyroid hormone synthesis, and lithium whichblocks release of thyroid hormone. Propranolol controls the peripheral manifestations ofthyroid hormone. Radioactive iodine destroys thyroid tissue, thereby decreasing thyroidfunction and possibly effecting hypothyroidism (which can be treated with thyroidsupplementation).
  82. hyperparathyroidism
    The radiographic hallmark of hyperparathyroidism is: Subperiosteal resorption.

    Hyperparathyroidism, which can affect bone in manyways, appears on radiographs as osteopenia. Excess parathyroid hormone results in an increase in bone metabolism, which may appear as microfractures,bone cysts, brown tumors, and pathologic fractures.

    Which two radiographic features of secondary hyperparathyroidism (HPT) are infrequently encountered in the picture of primary HPT?Osteosclerosis and periostitis.

    Acrolysis of the mid-portions of multiple distal phalanges in a bilateral symmetric pattern should suggest one of 3 conditions:Hyperparathyroidism, acroJysis ofHajdu & Cheny, and PVC overexposure (tank cleaners).

    • INFRACALCANEAL HEEL SPURSHARP WELL DEFINED HEEL SPUR-RA-normal variant-DISH-Reiter's syndrome-Acromegaly
    • FLUFFY ILL DEFINED HEEL SPUR-psoriatic arthritis-hyperparathyroidism-RA-Reiter's syndrome-ankylosing spondylitis

    • increased: calcium, alkaline phosphate
    • decreased: phosphate
  83. Osteomalacia
    • Osteomalacia
    • A condition marked by softening of the bones with pain, tenderness,muscular weakness, and loss of weight resulting from a deficiency of vitamin D and calcium.

    Of scurvy, cougenital syphilis, rickets, osteomalacia, and congenital rubella, the disorder most frequently associated with pseudofractures?Osteomalacia.
  84. OSTEOSARCOMA
    • OSTEOSARCOMA(osteogenic sarcoma)-malignant bone forming tumor-most common malignant bone tumor with exception of Multiple Myloma-age 10-25yrs, and >40yrs-male to female distribution is equal-most commonly found in the metaphyseal region around the knee(distalfemur or proximal tibia)-usually occurs in teenagers during rapid growth spurts or in patientsover 40 who have a preexisting condition most notably Paget's dz-Symptoms: Pain, swelling, and fever(R/0 OM), the osteoid producing nature of the tumor often yield an elevated alkaline phosphatase level-radiographic appearance: appearance is variable depending on osteolytic or sclerotic nature of lesion. Penetration of cortical bone usually occurs with a Codman's triangle or "Sunburst" appearance-prognosis is poor
    • Osteosarcoma is chiefly a disease of individuals of less than 20 years of age. What pre-existing condition can result in a secondary peak in incidence for older adults?Paget's disease.

    What is the most common site for metastases of osteosarcoma? Lung.
  85. AIDS
    • AQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
    • AIDS is caused by infection with the cytopathic human immunodeficiency virus (HIV) retro virus(RNA virus), which causes cell death. The CD-4 surface glycoprotein is the essential molecule recognized by the retrovirus, on the surfaces of T-4 lymphocytes, monocytes, and macrophages. T-helper lymphocytes also become infected and destroyed, which greatly impairs the immune system. Natural killer lymphocytes are also destroyed, which impairs immune surveillance against neoplasms and virus infected cells. Approximately 40% to 50% of patients infected with HIV, and possessing less than 400 T-helper cells, develop AIDS within 2 years of HIV infection. Eighty-five percent of patients with T-helper cells less than200, will develop AIDS within 2 years of infection.
    • Four Stages of HIV Infection
    • Stage 1- manifesting acute HIV, wherein the patient displays general malaise and "mono-like" symptoms
    • Stage 11- chronically infected with HIV, often asymptomatic while developing antibodies to HIV
    • Stage III - persistent generalized lymphadenopathy
    • Stage IV - serious manifestations of immunodeficiency, frequent serious infectionsand debilitationSubgroups of Manifestations of HIV InfectionSubgroup A - Constitutional symptomsSubgroup B - Neurological syndromesSubgroup C - Associated with infectious diseasesC(l) - Defect in cell mediated immunity (Pneumocystis pneumonia)C(2) - Less profound infectionsSubgroup D - Secondary cancers (e.g. Kaposi's sarcoma)Subgroup E - Chronic lymphoid interstitial pneumonitisThe treatment of AIDS includes supportive measures, as well as suppressive anddisease modifying agents such as AZT. Therapeutic regimens have been shown to be mosteffective when disease modifying agents are used in synergy. Maternal transmission of thedisease to the fetus has been controlled with AZT. Treatment regimens are very expensive.Any patient suspected of being HIV positive should be counseled regarding the importanceof testing to confirm the presence of antibody, then appropriately referred for infectiousdisease consultation. Social services consultation is also important. as various agencies maybe able to assist with therapy. Regardless of whether or not you suspect a patient of being HIVpositive, universal precautions are the standard of care in ALL aspects of health care.
  86. Sarcoidosis
    Sarcoidosis-chronic, progressive, systemic granulomatous disease of unknown etiology, affecting any organ system, a common cause of pulmonary hilar adenopathy, histologically showing noncaseating epithelioid cell tubercles (tuberculin negative usually).
  87. Ivory Phalanx
    • PSORIATIC ARTHRITISSeen in 7-15% of pts w/ psoriasis (80% if pt has nail changes.)Typically affects 20-50 y/o, M:F equal. HLA-B27 frequentlypositive, particularly w/ SI involvement. Distribution isasymmetrical and is most common in the DIPJs. Oftenconfused w/ RA (for some reason.)Classic radiographic featuresJoint margin erosions working in to the center (similar to RA)– eventually leads to “pencil in cup” appearanceIncreased synovial fluid w/ increased intracapsular pressureApparent wide joint space (due to erosions)Acroosteolysis – resorbtion of the distal phalangeal tuftSausage digitsAbundant periosteal activity (resulting in “whiskering”)Ivory Phalanx – due to abundant endosteal activity
    • Osteopenia secondary to reduced activity
  88. -loose bodies(jt mice)
    OSTEOARTHRITIS( D e g e n e r a t i v e Joint Dz)DESCRIPTIONOsteoarthritis is the most common arthritis and occurs as a result ofwear and tear on joints. The cartilage that cushions the impact on thejoint gradually deteriorates. As the cartilage wears down, subchondralbone is exposed which becomes sclerotic, the surface becomes wornand polished in a process called eburnation. Over time, the ends of thebones also are affected, with bone growing along the sides producinglumps. There is usually a predisposing factor such as trauma or priorinflammatory arthritis.SIGNS AND SYMPTOMS-asymmetrical noninflammatory arthritis-pain worse at end of day(after use)-pain in joint before a change in weather-loss of flexibility-Heberden's nodes(bony protuberances at the margins and dorsalsurface of the DIPJs)-Bouchard's nodes(bony protuberances at the margins and dorsalsurface of the PIPJs)-joints most commonly affected(neck, back, knees, hips, shoulder,1st MPJ and the 1st radiocarpal jt)DIAGNOSISX-ray-subchondral sclerosis-loose bodies(jt mice)-asymmetrical jt space loss-soft tissue is normalTREATMENT-ROM exercises for stiffness-Joint replacements-Synovial fluid viscosupplements-lnjected into joints to cushions andlubricate joint spaceSYNVISC(Hylan G-F 20)-an elastoviscous fluid containing hylan polymers-indicated in OA-supplied in 2.25mL syringe containing 2mL-intra-articular injections once a week for a total of 3 injectionsHYALAGAN(Sodium Hyaluronate)-a viscous solution consisting of high molecular weight fraction ofpurified sodium hyaluronate-indicated in OA-2mL vials or 2mL pre-filled syringes-intra-articular injections once a week for a total of 5 injections190 POCKET PODIATRICS 3RD EDITIONARTHROPATHIESRHEUMATOID ARTHRITISInflammatorySymmetricalPain worse in morning or after restOsteopeniaIncreased soft tissue density(+)RA factorOSTEOARTHRITIS(DJD)NoniflammatoryAsymmetricalPain worse at the end of the daySclerosisSoft tissue is normal(-)RA factor
  89. -Martel's sign-overhanging margins
    GOUTDESCRIPTIONA recurrent acute arthritis that affects peripheral joints, most notably the1st MPJ. The arthritis stems from a build up of monosodium urate crystalsin and around joints and tendons. Supersaturated hyperuricemicbody fluids crystalize causing a severe red hot swollen joint. The arthritismay become chronic and deforming. Not all hyperuricemic personsdevelop gout. A build up of uric acid crystals in the joint may be fromexcessive breakdown or over production of purines. Gout classicallybegins in the evening or early morning and tends to occur in previouslydamaged joints.SIGNS AND SYMPTOMS-asymmetrical monoarticular arthritis-sudden onset, red hot swollen joint-low grade fever is sometimes present-more common in men(20:1)-joint sparing(chronic gout may be joint destructive)-most commonly first attacks the 1st MPJ(called Podagra), followedby Lisfranc's and then the heel-crunchy tophi felt in ears, olecranon bursa, and Achilles tendon.NOTE: Formalin dissolves gouty tophiDIAGNOSISX-ray-rat bites-cloud sign-punched out lesions-Martel's sign-overhanging marginsAspiration-negatively birefringent yellow needle shaped crystals, when parallelto axis of the lens and blue when perpendicular.Blood work-Hyperuricemia(>7.5mg/dl ) not conclusively diagnostic for goutTREATMENTFor effective Tx determination must be made as to whether the pt. is anover producer of uric acid(metabolic gout) or an under excreter(renalgout).
  90. Hardcastle
    • LISFRANC'S FX/DISLOCATION CLASSIFICATION
    • (Hardcastle)
    • Type A total or homolateral)-disruption of the entire Lisfranc jt complex in a sagittal or transverse plane (almost always lateral)-most common type
    • Type B(partial)
    • Type B1-medial incongruity with the 1st metatarsal forced medially-medially displacement involving the 1stmet alone or with met's 2, 3, 4, but not 5.Type B2-lateral incongruity with the lesser metatarsalsforced laterally I556CHAPTER 32POCKET PODIATRICS 3RD EDITIONTRAUMAType C(diverqent)Type C1-partial divergence with the 1st met mediallyand the 2nd met laterally displacedType C2-total divergence with the 1st met displacedmedially and the lesser met's displaced laterally

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