MSK & Rheumatology review

Rheumatoid Arthritis Key Points

• The mc chronic inflammatory arthritis

• Symmetrical synovitis of small joints and wrists is the classical initial pattern

- spares the DIP joints

• Extraarticular manifestations should be seropositive

• Early and aggressive therapy

Scope of Rheumatoid Arthritis

• Affects 1% adults or 1.5 million American adults (with female to male 2-3:1)

• Tremendous negative impact on quality of life

• More than just joint pain - systemic disease that can cause wide ranging pathology - heart, lung, kidney, eye, skin disease

• Increased risk of cardiovascular events and increased risk of lymphoma

RA labs

• Erythrocyte sedimentation rate (ESR) elevated

- > 20 mm/hr = clinically significant

- can increase with age

• C-reactive Protein: Protein synthesized by the liver

- Often rises earlier and recovers earlier than ESR in the setting of acute insult

- marker for disease activity and other systemic inflammation

• Anti-CCP IgG

- Citrullinated peptide present in 50-70% of RA pts

- More specific, rarely present in other rheumatic diseases, autoimmune or infections

- Indicative of more progressive, joint destruction.

Rheumatoid factor

• Antibody directed against the Fc portion of IgG

• Present in approximately 60-75% of RA patients

• May be involved in disease pathogenesis

• Higher levels tend to be associated with poorer prognosis

• Found in other rheumatologic and non-rheumatologic conditions

• Not diagnostic because:

- positive 5% general population

- may/may not be positive in RA

- may be negative early, positive later

- positive in other diseases

RA presentations

• Swan neck, Bouchard deformities, rheumatoid nodule

• MCP subluxation, ulnar deviation

• MTP subluxation, callus

• Radiographic features:

- Periarticular soft-tissue swelling

- Juxtaarticular osteopenia

- Marginal erosions, Joint-space narrowing

- Symmetric involvement, Deformities in advanced disease

• Extraarticular:

- Interstitial Lung Disease (ILD), Rheumatoid nodules

- Interstitial nephritis and IgA nephropathy

- Sicca symptoms in eyes & mouth

- Increased risk for CV events and lymphoma

RA diagnosis

• Important to dx early as:

- RA is progressive, not benign

- structural damage/disability occurs within first 2-3 years

- slower progression linked to early tx

• Early RA: RA with duration of sx's of < 6 months, where "duration" denotes the length of time the patient has had symptoms/disease, not the length of time since RA diagnosis

• Established RA:

RA with duration of sx's of > 6 months

• ≥ 6 = definite RA

- dx can also be made if pt fulfills criteria over time

RA therapy

• Steroids (low/high dose, short term)

• Mono/Double/Triple therapy: Hydroxychloroquine (Plaquenil) +

Sulfasalazine or MTX + Leflunomide

• Tofacitinib (Xeljanz)

Upadacitinib (Rinvoq)

• TNF biologics: adalimumab, certolizumab, etanercept, golimumab, infliximab

• Non-TNF biologics:

- tocolizumab (Actemra) Sarilumab (Kevzara): monoclonal IL-6R inhibitor

- Rituximab (Rituxan): monoclonal against CD 20 on B cells

- Abatacept (Orencia): monoclonal blocks CD28, stops T and B cell communication

RA treatment goals & future steps

• Early Diagnosis

• Begin treatment early-within 3-6 months of onset of synovitis

• T2T ( Treat to Target) of low disease activity or remission

• RA treatments have changed dramatically: from paucity of treatments to dilemma of choice

• How do we decide which drug to use and when?

• Need to develop ways to predict:

- Which patient will respond to which drug

- Risk for AEs from treatment

- How and when to withdraw biologics for patients in remission

Juvenile Idiopathic Arthritis

• Chronic arthritides of childhood

• Term replaces JRA (juvenile rheumatoid arthritis)

• Heterogenous group of diseases

• Based on clinical and laboratory features, serology

• Few definitive tests

• Arthritis < 16 y/o, lasts > 6 weeks

• Can be diagnosed as JIA after 6 weeks but may take 6 months to classify into specific JIA subgroup

• Unknown cause: doesn't include reactive arthritis, acute rheumatic fever, lyme disease, SLE, metabolic disease

JIA subgroups

• Systemic JIA (10-15%)

• Oligoarthritis (30-60%)

• Polyarticular: RF negative (10-30%)

• Polyarthritis: RF positive (5-10%)

• Psoriatic arthritis (2-15%)

• Enthesitis related arthritis/Juvenile SpA (20%)

• Undifferentiated arthritis

JIA systemic

• Most serious short/long term morbidity

• Males = females

• Extra-articular symptoms can predate joints

• Typically joints involved in 3-12 months

- Wrists, knees, ankles, cervical spine, hands

• Daily fever ("quotidian"): once or twice (double quotidian)/day in repeated pattern

- Pt toxic with chills and malaise during fevers

• Salmon colored rash once or twice/day with fever

• 75% with lymphadenopathy/hepatosplenomegaly

• Serositis: pericarditis and pleuritis

• MAS (macrophage activation syndrome)

JIA: Oligoarticular

• Oligoarticular: < 5 joints total

• MC category

- Persistent: less than 4 joints at 6 months

- Extended: more than 4 joints at 6 months

• Most present before 5 years old (peak 1-3 years)

• Females more than males (2:1 persistent; 5:1 extended)

• Usually present with limp and less with pain

• A "hot" joint (red, warm, swollen) may be sepsis instead

• Knees (47%) then ankles, hands and elbows

• No constitutional sx's

• Labs: negative SED, CRP, CBC, RF

• Labs: positive ANA (40-85%).

• ANA associated chronic anterior uveitis

- May be asx so needs regular eye exams (can lead to blindness)

JIA: polyarthritis

• 25% of JIA patients

• ≥ 5 joints in first 6 months

• Divided into RF + and RF - groups

JIA: Polyarticular RF-

• Presentation throughout childhood

• Low grade fevers

• Mild hepatosplenomegaly

• Symmetric joint involvement

• Knees, wrists, ankles, hands, cervical

• Hands: MCP/PIP/tenosynovitis

JIA: Polyarticular RF+

• May be same as adult seropositive RA. 12-16 years old

• Mostly female, systemic rare

• Symmetrical small joint involvement

• Rheumatoid nodules, erosions, flexer tenosynovitis

• RF/CCP positive

• Growth retardation (micrognathia)

JIA: Psoriatic Arthritis

• RF negative, Psoriasis, Nail pitting

• Dactylitis (sausage digits) from tendon inflammation

• Asymmetric joint involvement, DIP joints involved, Inflammatory back disease

JIA: Enthesitis-related Arthritis

• Females>males 4:1

• Median age 11 (usually after 9 years old)

• HLA -B27 positive

• Lower extremity arthritis, Enthesitis

• Some develop into sacroillitis in future

• Some develop AS/spondyloarthropathy, Iritis (15 -25%)

JIA: Undifferentiated Arthritis

• Hard to classify in any category

• Aspects of multiple categories

• Up to 20% of all JIA patients

JIA therapy

• Systemic steroid

• NSAID

• DMARD

• Biologics

What is an autoimmune disease?

• The job of the immune system is to fight against bacteria, viruses and to survey for cancer cells

• An autoimmune disease entails one's immune system erroneously attacking their own tissues

• Disease manifestations will depend on which organs are involved

What causes lupus?

• Genetically susceptible individual--> environmental factors--> autoantibody production--> Inflammation--> damage-->

What is SLE?

• An autoimmune disease that affects multisystem

• 1.5 million cases in the US per Lupus Foundation, and many millions worldwide have some forms

• Women > Men - 9:1 ratio

• African Americans, Asian, and Latino > Whites

• Onset usually between ages of 15 and 45 years

SLE presentation

• A myriad of symptoms

• A heterogeneous disease with a continuum of disease activity

• Some can have organ threatening diseases like lupus nephritis or Diffuse alveolar hemorrhage.

• Some may have predominant skin and joint symptoms.

• Common sx's (> 60%): malaise, fatigue, arthralgia, myalgia, photosensitivity/rashes

• Other sx's: fever, arthritis, serositis with pleuritis and pericarditis, hair loss/alopecia areata, Raynaud's, HTN, oral ulcerations

SLE: polymorphic disease

• Lupus can affect any organ

• Each patient's lupus will look different depending on the constellation of sx's

• This makes SLE a difficult disease to grasp

SLE diagnosis

• Old ACR criteria: Butterfly rash, Discoid skin lesion, Photosensitivity, Oral ulcers, Arthritis, Serositis, Neurologic, Hematologic, Renal, Immunologic (anti-DNA, anti-Sm, false pos STS), Anti-nuclear antibody (ANA)

• NEW criteria: Requires ≥ 4 criteria (at least 1 clinical & 1 laboratory) OR bx proven lupus nephritis with (+) ANA or anti-DNA

- clinical: acute/chronic cutaneous lupus, oral/nasal ulcers, non-scarring alopecia, arthritis, serositis, renal, neuro, hemolytic anemia, leukopenia, thrombocytopenia

- immunologic: ANA, anti-DNA, anti-Sm, antiphospholipid ab, low complement, Direct Coombs test

SLE: serositis-pulmonary

• Pleuritis with or without effusion

• Interstitial inflammation

• Diffuse alveolar hemorrhage

SLE cardiac manifestations

• Pericarditis

• Myocarditis

• Fibrinous endocarditis (Libman-Sacks)

• Myocardial infarction

SLE neuropsychiatric presentations

• 19 presentations

• Seizures, Cranial/peripheral neuropathy (10-15%)

• Memory and reasoning difficulty

• HA: if excruciating, often indicate acute flare

• Psychosis: must distinguish from steroid-induced psychosis

SLE renal presentation

• Check a urinalysis to look for proteinuria

• Diagnosis is made with a kidney bx, which shows various levels of glomerular involvement and immune complex/antibody deposition

SLE Heme manifestations

• Anemia- Anemia of chronic disease or hemolytic anemia

• Leukopenia

• Thrombocytopenia

SLE labs

• Anti-Nuclear Antibody (ANA) used as a screening test

- Exceedingly sensitive, False positive

- If a patient has a positive ANA, no other sx's and no other antibodies, they DO NOT have lupus

- At the lower titer of 1:80 up to 5-10% of the population can have a positive ANA

- For every year after age 50, percentage of ANA positivity increases 1%/year (ex. Age 50 = 1%, Age 55 = 5%, Age 60 = 10%)

Abnormal Antibodies

• Anti-SSA/SSB= aka anti Ro and anti La --> Sjogren’s disease

• Anti-SSA = Risk of cutaneous lupus

• Anti SM= Most specific antibody for SLE

• Anti –RNP= Mixed connective tissue disease

• dsDNA= Goes up with disease activity

- Increased risk of kidney disease

• C3/C4= Go down with disease activity

• Anti-Ribosomal P= Increased risk of CNS involvement

Drug-Induced Lupus (DIL)

• Approximately 80 offending agents can cause DIL

- Procainamide, Hydralazine, Enbrel/Remacade/Humira, Minocycline, Diltiazem, Penicillamine, INH, Quinidine

• Usually a rash, arthritis and positive ANA

• 99% disappear within 3 months of stopping the medicine

• Labs: anti-Histone antibody

Neonatal lupus

• Risk in women who have SSA/AAB antibodies

• Not true lupus

• Trans-placental transfer of anti SSA or SSB abs

• 5-7% babies will have a transient rash, resolves by 6-8 months

• 2% of babies will have cardiac complications with congenital heart block

SLE treatment

• Patient Education

1. Avoidance of sun

2. Use of SPF > 35 sunblocks UVA and UVB

3. Sun-protective clothing

4. Promote exercise

5. Healthy diet (low chol, low sugar, low salt)

6. Smoking cessation

7. Avoidance of stress (animal models)

8. Good sleep hygiene

• Meds:

- Oral and IV steroids have the quickest onset of action

- Hydroxychlorquine (Plaquenil ), mycophenolate (Cellcept), azathioprine (Imuran), MTX, cyclophosphamide (Cytoxan), Belimumab (Benlysta), anifrolumab (Saphnelo)

SLE prognosis

• Dramatically improved over time

• Normal life expectancy for pts with drug induced lupus, cutaneous lupus, lupus without organ involvement

• Increased risk of infection and CV disease

• Poor Prognostic Factors:

- Renal disease with lupus nephritis (esp DPGN), HTN, Male sex

- Young age, Older age at presentation, Poor socioeconomic status (SES)

- Black race, which may primarily reflect low SES

SLE causes of death

• Infection

• Active SLE

• Cardiovascular disease-accelerated atherosclerosis

• malignancy

SLE summary

• A prototypal autoimmune disease

• Skin and MSK are the mc clinical entities

• It can be life endangering on the initial encounter

• The goal of therapy is to prevent organ damage, and accrual organ damage

• Great progress has been made with 10-yr survival of 85-90%.

Henrich Sjögren's work

• A monograph on arthritis and dry eyes in 1933

• Rose Bengal staining to identify cornea lesions

• Keratoconjunctivitis sicca (KCS)

What is Sjögren's Syndrome?

• The mc autoimmune disease

• MC symptoms - KCS, xerostomia, and parotid gland swelling

• Antibodies against Ro/SS-A and La/SS-B are the serologic hallmark of Primary SS

• A minor salivary gland (MSG) lip biopsy with a chronic lymphocytic infiltrate is the gold standard for diagnosis.

Who gets Sjögren?

• Female disease:♀/♂ : 9/1

• Common (1-4%)

• 30-50 years old. It has rarely been reported in children

• Slowly progressive

Types of Sjögren Syndrome

• Primary Sjögren Syndrome: Can occur as an autoimmune disease by itself

• Secondary Sjögren Syndrome: can occur in the settings of SLE, RA or any other autoimmune disease

Sjögren Syndrome symptoms

• Subjective:

- Exocrine organ-Dry eyes, mouth, and vaginal dryness

- Jaw swelling (Parotid Gland Swelling)

- Dry skin, Rashes, arthritis

• Objective:

- Reduced Saliva pool under the tongue

- Dry eyes, Poor dentition

Extraglandular Presentations of Primary SS

• Fatigue, Arthralgia/arthritis, Raynaud's

• Esophageal dysfunction, Autoimmune thyroiditis

• Lymphadenopathy, Vasculitis, Annular skin lesions

• Lung, Kidney, Liver involvement, Peripheral neuropathy, CNS disease, Myositis, Hematology-Lymphoma (B cell), cryoglobulinemia, pancytopenia

Sjögren Syndrome diagnosis

• Abnormal Labs: elevated inflammatory markers (ESR and CRP), Anti SSA/SSB, anti-nuclear antibody (ANA)

• Schirmer's test: tape in eye ≤ 5mm/5min

• Rose Bengal Staining

• Send the patient for a bx of lip minor salivary gland or parotid gland

- Lip bx shows focal lymphocytic infiltrate

• Check C3, C4, IgA, IgM, IgG and SPEP

Sjögren Syndrome treatment

• Dry eyes: preservative-free artificial tears, Restasis for severe case

• Dry mouth: Lozenges, Biotene mouthwash, Pilocarpine, Cevimeline

• Hydroxychloroquine, Methotrexate, Imuran, Leflunomide, rituximab

Sjögren Syndrome Summary

• Chronic Course with variable progression

• Glandular dysfunction can progress/plateau

• Extraglandular conditions occur over time

• Lymphoma 44 fold increase - an uncommon complication

• Overall mortality not increased

• Rare for primary SS to progress to another autoimmune syndrome

Myositis

• An autoimmune disease

• Muscle involvement-Proximal weakness in both upper and lower extremities

• Dermal manifestation

• Antibodies: myositis specific antibodies (MSA), and associated antibodies (MAA)

• PM and DM: Autoimmune diseases attacking the skin and muscles

PM & DM symptoms

• Main presenting sx: symmetrical proximal muscle weakness

- usually starts with lower extremity

• May also complain of non-specific sx's including fever, weight loss, arthralgia, and etc.

• Potential life threatening symptoms

- If diaphragm involvement--> lead to respiratory failure

- In adults, dermatomyositis can be a sign of underlying malignancy

- High risk for interstitial lung disease

• Skin findings: Gottron's papules, periungal telangiectasia, Raynaud's, Heliotrope rash, Shawl sign

PM & DM diagnosis

• History & Physical, Laboratory

• Labs:

- Creatinine Kinase (CK) elevation in almost any pts at some time during the course of active disease at several thousand to tens of thousand

- Aldolase level

- liver enzyme (AST/ALT)

- ESR and CRP frequently elevated

- Myositis Specific Antibodies may be present

- ANA (+) in 40%

• Electromyogram (EMG)/Nerve Conduction Study (NCS)

- EMG has a good sensitivity (85%), but low specificity (33%), it should be done on One Side

- A guide for the location of tissue bx on the contralateral side given its symmetrical distribution, and false (+) from damage from the needles insertion

• Muscle bx (important): Should be performed in most cases to confirm and differentiate types of myositis or myopathy (PM, DM, Inclusion Body Myositis, Necrotizing autoimmune myopathy or metabolic myopathy)

• MRI

Myositis specific antibodies

• Jo-1 ab (aka anti-tRNA synthetase ab): interstitial lung disease, mechanics hands

• Anti-Mi-2: older women, Shawl sign, good prognosis

• Anti SRP (signal recognition protein): polymyositis/scleroderma overlap

• Anti P140/P155: strong association with malignancy

Childhood dermatomyositis

• 3x more common in girls than in boys, affect 6-9 years old

• Presentation is similar to adult dermatomyositis except the cutaneous manifestation are more common

not associated with malignancy

• More commonly associated with abnormal soft tissue calcification

- dystrophic calcification

PM & DM screening for malignancy

• Screening investigation when malignancy is suspected should include chest/abdo/pelvis CT + Age appropriate colonoscopy & mammogram

• Malignant disease particularly ovarian, lung, pancreatic, stomach and colorectal

PD & DM differentials

• Statin- induced myopathy

- Most patients improve when the medication is stopped

- Some pts develop auto-antibodies to HMG-CoA reductase and can have persistent sx's

PM & DM treatment & prognosis

• Oral/IV steroids depending on presentaion

• IVIG if acute life threatening

• Azathioprine, methotrexate, cyclosporine, cyclophosphamide, tacrolimus, rituximab

• Early and regular PT

• Prognosis: Similar 5-yr survival rates between 77-85%

- clinical factors (old age, ILD, dysphagia, cardiac, neoplastic disease

- serologic factors (Anti-Mi2, Anti-SRP with 5 yr survival 30%, Anti 155/140 with cancer)

Patients with arthritis commonly feel pain in the ____________.

Groin

Special tests for the hip

• Obers Test- IT band tightness

• Nobles Test (overlap with the knee): ITBFS

• Stinchfield maneuvers: Hip OA and internal derangement

• Logroll exam: Hip fracture

• FABERs (Patricks Test)- Piriformis/SI and FADIRs- FAI/labrum

• Thomas Test: Iliopsoas/flexor strains/tightness

• Trendelenburg Test/sign: Glute med/abductor weakness

• Ortolani/Bartlow: Infantile/congenital hip dysplasia

Common/Important injuries to the hip

• Fractures, very common among elderly, particularly women as well as trauma (falls, MVA).

• Dislocations, commonly associated with fractures or hip replacements.

• Chronic:

- OA/Labral tearing/FAI

- Overuse (ITBFS, piriformis, abductor weakness).

- Low back pain (SI joints, lumbar radiculopathy)

• Acute: Muscle strains (hip flexor, hamstring, lumbar), Labral tears

FAI (femoracetabular impingement)

• Cam type: femoral head-based deformity.

• Pincer type: Acetabular based deformity.

-Can be combined.

• Pathophysiology: Femoral head abuts acetabulum

- Can cause labral tearing (degenerative), cartilage damage, and early OA.

• Presentation: Groin pain increased with flexion activities, pain with prolonged sitting, mechanical sx's.

- Can be generalized lateral pain too.

FAI diagnosis & treatment

• Who gets this: mc in runners and anatomic congenital malformations (hip dysplasia).

• Tests: FABER/FADIR, Stinchfield

• Exam: Pain elicited in groin with flexion, externally rotated stance.

• Imaging: Xray may or may not show deformity; MRI gold standard. Only needed for unknown Dx or surgical planning.

• Treatment:

- Conservative ideal: NSAIDs, PT, ergonomics, strengthen abductors!

- If failed: Osteotomy, Labral repair/debridement/THA.

Hamstring Injuries

• Etiology: Forceful knee extension with hip flexion.

• Largely athletes/"weekend warriors."

- Rapid acceleration sports: jumping, sprinting.

• Most occur in myotendinous junction, small risk of avulsion fracture (ischial tuberosity, mostly in adolescents).

• Four muscles?

• Strain vs. Tear, Grade 1 through 3.

• Presentation: Intense pain, limping, hx of athletic/applicable event, virtually never atraumatic.

• Exam: Posterior palpable pain, abnormal gait, bruising common, limited motion.

• Dx: CLINICAL! MRI can confirm if severe/atypical diagnosis or for rare surgical planning.

• Tx: Virtually all resolve with PT, even grade 3.

- Surgical repair not recommended in almost all cases.

Greater trochanteric bursitis

• One of the MC injuries encountered.

• Largely occurs from falling on affected hip, over-applying pressure (sedentary lifestyle, prolonged sitting/driving, side-sleepers).

• Body habitus plays a large role; more common In women due to stress of wider pelvis.

• Pain can be excruciating, localized to direct point tenderness over lateral hip

• Can be confused/coinciding with sciatica/LBP.

• Imaging: Unnecessary but will come back on an MRI.

• Tx: Exclusively conservative.

- Aggravation avoidance, PT, NSAIDs, great option for cortisone injections.

- Severe/recurrent cases: TENJET/bursectomy.

IT band (Friction) Syndrome/ITBFS

• Can be from tightness, biomechanics, weakness.

• More sx's at the knee (d/t mechanical irritation).

• Almost always an overuse syndrome (running, cycling).

• Large overlap or concurrence with GTB and PFPS.

• Presents with: Tightness, pain with increased activity such as running/cycling, much better with rest.

• Pain at lateral knee w/wo "snapping."

• Exam:

- Tight IT band (Ober's Test).

- Mechanical crepitation felt at Gerdy's Tubercle with flex/ext (Noble's test).

- Often patellar maltracking and weak abductors (Trendelenburg).

• Dx: Clinical

• Imaging: Not needed

• Tx: PT, NSAIDs, activity modifications/mechanical technique corrections.

Hip osteoarthritis

• Very common, can be younger than you think

- mc after age 40-50

• Caused from many things: Previous Trauma/surgeries, Weight, Overuse/profession, Undiagnosed FAI/hip dysplasia, Alcohol/substance abuse

• Classic signs: deep pain in GROIN when weightbearing, stiffness/crepitation

• Limp is classic, especially in end-stages.

• Uncommon to be unilateral

Hip OA diagnosis & treatment

• Crepitation/limited motion, Positive Stinchfield maneuvers, gait deformities, Pain reproduced deep in groin with movements and motion.

• Very straightforward dx

• Radiographs always to start (AP pelvis best to assess contralateral comparison).

- ALWAYS WEIGHT BEARING!!

• Advanced Imaging: Often unnecessary unless severe symptoms with limited radiographic OA

- helpful for surgical planning

• Tx: no treatment prior and based on symptoms: trial of oral steroids/PT OK.

- Age should NEVER be a requirement.

-Arthritis does not equal arthroplasty

-Injective therapies are great intermediate options.

-Total hip arthroplasty is eventual need for almost all.

Septic THA/TKA

- Medical urgency needed.

- Immediate OR, wash-out, explantation.

- Followed by IV antibiotic regimen (PICC) line and a short antibiotic "Holiday."

- Eventually revision reimplantation.

- High Morbidity rate.

Types of injections

• Intraarticular

• Bursa

• Tendon Sheath

• Types: Corticosteroids, Visco supplementation (IA only), Biologics

Contraindications for cortisone

• Diabetes (A1c at least under 8.0)

• Active infection

• Active immunosuppression/cancer

• Allergy

• Severe bone loss/necrosis to area.

• Not a contraindication

- "I can't take NSAIDs"

- Anticoagulation

- If needle phobic: consider procedural sedation

Athletic Pubalgia (Sports Hernia)

• Inguinal hernia: MC hernia in groin such as intestines pushes through abd wall defect

• Sports Hernia: Strain/tear of soft tissue (usually adductors).

- Often no true hernia

• More common in males, Athletes in "planting" sports

• Dx is clinical

• Tx: Conservative, RICE, NSAIDs, PT.

Slow to recover and heal (persistent).

High rate of re-injury so return to activity at appropriate time is key

Acetabular fractures

• Common in traumatic dislocations from femoral head abutting the acetabulum.

• Easily diagnosed with Xray in most.

- CT if questionable.

• Little displacement: Protected WB 6-8 weeks.

• Displaced: Operative.

Usually, ORIF.

Femur fractures

• By far the mc orthopedic hip fractures (proximal).

• Can be anywhere on the Femur but proximal mc

- Femoral Head/neck/intertrochanteric.

Intertrochanteric fractures

• 50% of all hip fractures.

• More elderly, but can happen to anyone

• Usually, easy dx on Xray

- CT for better identification

- MRI if occult is suspected.

• Surgical unless pt's morbidity risk is high.

• Surgery: Screw vs. Intramedullary nailing.

- If failed: Can convert to hemi/total THA.

Types of trochanteric fractures

• Greater/Lesser: Non-Op v. Screw

• Subtrochanteric: IM Nailing/ORIF

• Intertrochanteric: Screw vs. Nail.

• Femoral Neck/humeral head:

Hemiarthroplasty if good bone.

• Total arthroplasty

Cemented v. Non-cemented.

Pelvic fractures

• Stable pelvic fracture patterns include:

- Iliac wing fracture

- Sacrum fracture

- Superior pubic ramus fracture

- Inferior pubic ramus fracture

• Unstable pelvic fracture patterns include:

- AP compression fracture

- Lateral compression fracture

- Vertical shear fracture

Meralgia Paresthetica

• Damaged lateral femoral cutaneous nerve-usually compressed

• Classically from tight pants/belts, common in men.

• Burning/hypersensitivity to lateral thigh region.

- easily confused with sciatica/lumbar radiculopathy.

• Management:

- ergonomics/adjustments in - wardrobe/function

- Proper fitting clothing, Wt loss measures.

Knee special tests: Meniscus

• McMurray's: flexion with valgus/varus stress. (very low specificity/sensitivity)

• Thesaly's: single leg squat with rotation (best)

• Apley's compression: Prone, 90 degrees, axial compression with rotation applied.

• Circumduction maneuvers: Flexion with rotation.

Knee special tests: ACL & PCL

ACL

• Lachman Test: Best test

• Anterior Drawer Test (beware of false negatives due to hamstrings).

• Pivot shift test

PCL

• Posterior drawer test

• Sag sign

Patellofemoral region tests

• Apprehension test: patellar instability, MPFL tears/incompetency, patellar subluxations/dislocations.

• Patellar grind test (Clarke's test): Patellofemoral OA/chondromalacia.

• Patellar glide test: Patellar mobility/chondromalacia.

• Ballotable patella, wave/fluctuation testing, bulge sign: Effusion

Effusion vs. Swelling

Effusion

• Intra-articular, Feels like a “water balloon.”

• Indicates significant debris, fluid, and intraarticular damage present

• Easiest to identify suprapatellar region.

• Can be blood, debris, synovial fluid, infection.

• Present with most/all ACL tears, severe OA, complex meniscus tears

• Does not indicate acuity, can be chronic, localized/encapsulated.

Swelling

• Can be anywhere in the body; SC tissue and extraarticular structures

• Body’s inflammatory response to trauma, can be diffuse

• Common in sprains, muscular/tendinous injuries, cellulitis/infection, blunt force trauma.

• R/O concern for compartment syndrome if rigid swelling

ACL injuries: overview

• Extremely common, not just in athletes

• Women show predisposition, controversial on why

• Usually the injury results in a tear, rarely can be "sprained."

• Timely MRI for good outcome, time to surgery matters.

• Start PT immediately, preferably same/next day to prevent quad atrophy, range of motion, and stability.

• Can be isolated/multiple structures involved

• Mechanisms: rotational (mc), hyperextension, direct trauma to posterior tibia

ACL exam

• Hx: often very traumatic, feels unstable, heard an obvious "pop", "Twisted/rotated my knee."

- Adolescents have a very high rate.

- Can be chronic, usually atraumatic with pain, weakness, or instability.

• Exam: very limited motion (not always), inability to extend/raise the leg straight (extensor lag), limp, WB trouble common, large effusion common, joint line pain.

- Lachman is key (bilateral comparison).

- Anterior drawer and pivot shift helpful.

- R/O and identify additional ligaments and structures that may be involved.

- Quad atrophy/lack of contraction of VMO if late presenting

ACL diagnosis & treatment

• Xray to r/o tibial plateau fracture, only if in-house available.

• STAT MRI within the week preferred.

- Immediate pre and postop PT

• Generally requires 9-12 months of PT for full recovery.

• Almost always treated arthroscopically unless chronic and OA.

- Chronically unstable knee and early OA if left torn.

- Autograft (preferred) if bone quality/tissue health allows.

- Bone-patella-bone and hamstring mc

- Allograft for older patients

MCL injury

• Very commonly injured.

• Pain at inside of knee with twisting force or force or blow to outside of leg.

• Great blood supply to ligament so rarely needs surgery and has great healing potential

- Less instability, more pain.

- Large majority: bracing, activity accommodations, PT.

- Typical full recovery in 4-6 weeks for most.

- MRI not usually needed unless not improving.

LCL injury

• Less common than MCL d/t mechanism (blow or force to inside of leg).

• Much stronger more fibrous ligament, but smaller.

• Usually treated nonsurgical in most cases but lower threshold than MCL for surgery given worse blood supply.

• Can start with PT and activity modifications w/o imaging, imaging if not improving.

PCL imaging (forgotten ligament)

• Provides stability to the knee, much less than ACL.

• Mechanism is almost always fall directly onto knee or blow to anterior tibia in posterior direction (skateboarding, football, MVA).

• Pain can be very nonspecific, often posterolateral. Can be felt deep and internal as well.

• Often pain when past 90 degrees (can present similar or also involve meniscus as well).

PCL exam/treatment

• Often limited in flexion; sometimes instability, not always.

• Effusion common early.

• Assess for additional ligamentous/IA pathology.

• Posterior sag/drawer testing.

• Xray always to rule out Fx.

• MRI is never the wrong idea if large effusion and instability

• Tx: conservative unless additional ligaments/structures involved.

- PT, activity modifications, RICE

- Slow to improve so often expectation management and assurance

Multiligament injuries

• Often d/t significant trauma (football/contact sports, severe fall injuries, high impact trauma such as MVA).

• Often includes multiple ligaments and Meniscus involvement.

• Common in true knee dislocations.

-"Terrible triad."

• Medical emergencies, Air casting/stabilization

• Vascular assessment is most immediate need

• Immediate surgical intervention once stable after STAT MRI.

- May require multiple surgeries

• Poor prognostic outcomes

Knee osteoarthritis: overview

• Medial compartment (mc)= varus deformity.

• Lateral (less common)= valgus deformity.

• Can be patellofemoral, often Tricompartamental

• Common causes: idiopathic, weight, trauma/surgeries, autoimmune conditions, substance abuse.

• By far the mc orthopedic

• Hx: Long/chronic history of progressive WB pain, external malalignment/osteophytic deformity, limps common, all weight-bearing activities make sx's worse, stiffness

Knee OA exam & treatment

• Almost always flexion deficit

• Early OA: rather benign exam

• Joint line pain/effusion very common, weakness/atrophy in late-stage disease.

• Radiographs

• MRI for those with normal radiographs but symptoms with WB

• Stepwise approach:

- Very early/no treatment: oral NSAIDs daily, activity mods, diet/exercise measures

- Mild to severe OA: injections, or biologics (PRP, stem-cell)

- End stage/failed all above: TKA (total knee arthroplasty)

Knee injections

• Cortisone: lots of myths, bad rep, can be highly effective, very minimal risks with potentially life-changing benefits for most

• Pros: cheap, readily available/largely covered, easy to train/perform, very low risk

-Can wear off very quickly for some (medically resistant)

• Cons: limited with T2DM (A1c >8.0), limited with immunosuppression/infection, cannot give within 3 months of a knee replacement, can receive one every 3 months.

Visco injections

• Binds to CD44 and stimulate synoviocytes to increase secretion of hyaluronic acid

- Hyaluronic acid: thick viscous lubricant (think aloe vera)

• Made from gelatinous chicken embryo of Roosters, now synthesized from bacterial fermentation

• More painful both before and initially after injection

• Much longer to kick in: weeks, can continue to increase in effect for 6 weeks

• Receive one every 6 months

• FDA approved as viscoelastic agent to improve lubrication and mechanics of the knee joint

• Much more expensive than cortisone, limited insurance coverage

Biologics

• Still controversial, limited literature but growing rapidly (better for early OA/cartilage delamination)

• faster growth in other countries

• May have spiritual/ethical barriers to treatment

• Extraordinarily expensive (5-10K per injection)

• Many formulations (WBCs, RBCs, plasma, bone marrow, stem-cells).

-Requires high level of facilities/training, not widely available

TKA considerations

• Most injections are simply buying patient time for a TKA

• 90% effective as of 2025

• Nobody "needs" a knee replacement (quality of life matters).

• Nobody is too young for a knee replacement

• 20-25 years of life on modern prosthetics, advancing quickly

• Careful consideration of pts with T2DM, obesity (BMI 45-50), and smoking

Meniscus tears

• Second MC injury to encounter in clinic for the knee (most common among all age groups)

• Can be acute/chronic

• Include ligament injuries (younger) and arthritis component (older)

• Acute: presents similar to ACL/ligament injuries

• Chronic: presents similar to OA

• Hx is the most important piece of exam

Meniscus tears: H&P, exam, imaging

• Acute: rotational, hyperextension, twisting, running

• Chronic: atraumatic gradual WB pain, swelling, weakness

- hx of surgeries, trauma, or previous tears

• S/S: sx's worse with WB activities, kneeling, squatting, pivoting, stairs, crepitation/catching; locking is not common

• Can be unstable.

• Exam: flexion limitations, pain with deep flexion, crepitation on joint line/through flexion, effusion

- McMurrays, Thesalys, Apleys, circumduction (all very limited)

• Imaging: Baseline Xray (assess OA/effusion)

- MRI if locking/massive effusion/ligament damage (ACL) suspected

Meniscus tears: treatment

• Conservative: RICE/NSAIDs and/or cortisone injection, PT

- try to preserve cartilage vs. early arthroscopic meniscectomies

• If complex, high-level athlete, very young, no cartilage wear/locking: Surgery can be more aggressive

• If extensive underlying OA (common): Meniscectomies are not ideal, conservative until needing/qualifying for a TKA

• Younger pts: meniscus repairs

• Older/OA/chondromalacia: Meniscectomies

Patellar dislocations/subluxations

• Common, but often missed and underdiagnosed.

- mc in women

• Can be highly traumatic and involve IA structures: large effusion, gross limitations, WB difficulty

• Atraumatic and chronic: minimal sx's, often maltracking

• Exam

- Apprehension Test, patellar glide (hypermobility)

- Pain in MPFL region and around patella, may dislocate

• Dx: Xray (situation, r/o fx), MRI for other structures involved

• Tx: conservative for acute (J-Brace)

• Recurrent: requires MPFL repair

Patellofemoral pain syndrome

• One of most common idiopathic knee pain conditions in teens/adults

• Pain suprapatellar and in distal quad region worse with sitting/repetitive activities

• D/t weakness in VMO/Quad.

• Common with patellar instability, obesity

Patellar tendon tear

• Urgent injury.

• Almost always traumatic.

• Severe pain + inability to extend knee with "divot" deformity

• Commonly from jumping and landing forcefully, severe hyperextension, or trauma (MVA).

• Patella alta

• Xray (r/o avulsion fracture)

• MRI STAT

• OR few days to no more than a week

• Tx: Always surgical unless CI

- Very long recovery.

- Relatively good outcome

Quad rupture

• Ruptures at distal attachment

• Medical urgency (d/t massive bleeding/scarring)

• Patella Baja

• S/S: Divot sign, severe pain/inability to flex and often extend knee, inability to bear weight, massive ecchymosis/swelling

• MRI STAT is key

• Tx: surgical unless CI

- Very long, arduous recovery with rehab process.

- Poorer prognosis than patellar tendon ruptures