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Pathological Gait and Antalgic Gait - Complete Orthopaedic PG Guide

THE NORMAL GAIT CYCLE (Brief Review)

• Stance phase: Heel strike → Loading response → Mid-stance → Terminal stance → Pre-swing (toe-off)
• Swing phase: Initial swing → Mid-swing → Terminal swing

• Heel strike: Tibialis anterior (eccentric control)
• Mid-stance: Gluteus medius (prevents pelvis drop)
• Push-off: Gastrocnemius-soleus (plantar flexors)

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PATHOLOGICAL GAIT - CLASSIFICATION

MASTER TABLE OF GAIT ABNORMALITIES

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INDIVIDUAL GAITS IN DETAIL

1. ANTALGIC GAIT (Most important for Orthopaedics)

• Pain on weight-bearing → patient instinctively reduces time the painful limb supports the body
• Shortened stance phase on the affected side is the hallmark
• The swing phase on the opposite side is also shortened (patient hurries through)
• Body leans toward the painful side (reduces joint reaction force)
• Overall cadence may slow down

• Hip: OA, AVN, fracture, septic arthritis, Perthes disease, SUFE
• Knee: OA, meniscal tear, ligament injury
• Ankle/foot: Plantar fasciitis, ankle OA, metatarsalgia
• Spine: L4-L5/L5-S1 disc prolapse causing radicular pain
• Any painful bone/joint/soft tissue pathology

• Short contact time on the painful leg
• Patient appears to "hop" onto the good leg quickly
• May walk with a cane in the contralateral hand (to offload the painful limb)
• Trunk lean toward the affected side (reduces joint reaction force at hip)

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2. TRENDELENBURG GAIT (Waddling / Gluteal Gait)

• Bilateral involvement → classic waddling gait (side-to-side trunk sway like a duck)
• Unilateral → lurch to one side

• Muscular dystrophy (bilateral, hence waddling)
• Polio, superior gluteal nerve damage
• Congenital hip dislocation (bilateral waddling)
• Hip abductor weakness post hip replacement (damage to gluteus medius)
• Spinal muscular atrophy, inflammatory myopathies

• Trendelenburg = structural weakness (muscle/nerve problem)
• Antalgic = pain avoidance (intact muscle, but hurts to load)
• Both may coexist with hip pathology (painful hip with secondary muscle wasting)

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3. STEPPAGE GAIT (High-stepping / Foot-drop Gait)

• Common peroneal nerve palsy (fibular neck fracture, crossing legs)
• L4-L5 disc prolapse
• Charcot-Marie-Tooth disease
• Peripheral neuropathy

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4. HEMIPLEGIC GAIT (Spastic - Circumduction Gait)

• Affected leg is stiff and extended (spastic)
• Leg cannot flex freely at hip, knee, ankle
• To clear the foot, the leg swings outward in a semicircle = circumduction
• The foot scrapes the floor (toe of shoe wears out medially)
• Arm on the same side is flexed and carried stiffly

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5. SCISSOR GAIT (Spastic Paraparesis)

• Both legs are stiff, slightly flexed at knees
• Thighs adduct strongly → legs nearly cross with each step (scissoring)
• Looks like the patient is "wading waist-deep in water"
• Short, slow, effortful steps

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6. PARKINSONIAN (FESTINATING) GAIT

• Small steps (shortened stride length)
• Feet shuffle (barely lifted off ground, dragging sound)
• Forward stoop (flexed neck, trunk, elbows)
• Festination = involuntary acceleration of steps as if chasing center of gravity
• Freezing of gait at doorways, turning
• Reduced arm swing
• Difficulty initiating the first step
• Turns are done en bloc (as a whole block - cannot rotate trunk independently)
• Retropulsion (if pushed, falls backward in catching steps)

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7. SENSORY ATAXIC GAIT (Tabetic / Stamping Gait)

• Slightly wide base
• Stamps the feet forcefully (excessive force to get sensory feedback from the ground)
• Watches the feet and ground constantly (visual compensation)
• Romberg sign positive (falls with eyes closed)
• Worsens significantly in the dark or with eyes closed

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8. CEREBELLAR ATAXIC GAIT

• Wide base stance and walking
• Irregular, lurching, reeling steps (unpredictable deviations)
• Trunk sways even with eyes open
• Romberg sign negative (swaying both with eyes open AND closed - just slightly more with eyes closed)
• Cannot tandem walk (heel-to-toe)
• Veers toward the side of the cerebellar lesion

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9. CALCANEUS GAIT

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10. FRONTAL LOBE / MAGNETIC GAIT

• Feet appear "glued/magnetic" to the floor
• Extremely short steps ("marche à petit pas")
• Difficulty initiating (may shuffle in place before moving)
• Wide base
• Trunk held upright (unlike Parkinson disease)

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ANTALGIC GAIT - DETAILED ORTHOPAEDIC BREAKDOWN

Why is antalgic gait important in Orthopaedics?

Phase analysis of antalgic gait:

Distinguishing antalgic from other limping gaits:

• Antalgic = pain is the primary driver, short stance phase
• Trendelenburg = weak abductors, full stance but trunk lurch, positive Trendelenburg test

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HIGH-YIELD EXAM POINTS (Quick Recall)

1. Antalgic gait = SHORT stance on AFFECTED side (pain avoidance)
2. Trendelenburg gait = TRUNK LURCH to affected side (weak gluteus medius)
3. Waddling gait = BILATERAL Trendelenburg (bilateral hip abductor weakness - muscular dystrophy, bilateral CDH)
4. Steppage gait = HIGH STEP + FOOT SLAP (foot drop, peroneal nerve palsy, L4-L5)
5. Scissor gait = CROSSING LEGS while walking (spastic paraparesis, cerebral palsy)
6. Festinating gait = QUICKENING SHORT STEPS forward (Parkinson's disease)
7. Stamping gait = PROPRIOCEPTION LOSS, stamps loudly, Romberg positive (posterior column disease)
8. Cerebellar gait = WIDE BASE + REELING + Romberg negative (Romberg is a discriminating sign)
9. Calcaneus gait = WALKS ON HEEL (weak gastrocnemius-soleus, S1)
10. Magnetic/frontal gait = FEET STUCK TO FLOOR, NPH triad (wet, wobbly, wacky)

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ORTHOPAEDIC MNEMONIC FOR ANTALGIC GAIT

• Pain is primary cause
• Affected limb has short stance
• Intact neurology (no weakness)
• Not Trendelenburg (abductors normal unless wasted)
• Lean toward affected side (offload joint)
• Investigate the joint for OA, infection, fracture, AVN
• Minimized weight bearing time
• Pelvis level (no pelvic drop unlike Trendelenburg)

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GAIT CYCLE IMAGE

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• Adams and Victor's Principles of Neurology, 12th Ed - Types of Abnormal Gait, Table 6-1
• Goldman-Cecil Medicine - Table 366-2, Characteristic Gait Disorders
• Miller's Review of Orthopaedics, 9th Ed - Gait Evaluation section
• Bailey and Love's Short Practice of Surgery, 28th Ed - Gait (Foot & Ankle examination)
• Gray's Anatomy for Students - Trendelenburg's sign
• Firestein & Kelley's Textbook of Rheumatology - Antalgic gait in hip and foot pathology

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SHOCK: Complete Orthopaedic PG Exam Guide

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DEFINITION OF SHOCK

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CLASSIFICATION OF SHOCK

1. HYPOVOLEMIC SHOCK

• Hemorrhagic - blood loss (trauma, fracture, GI bleed)
• Non-hemorrhagic - plasma loss (burns, pancreatitis, severe vomiting/diarrhea)

2. CARDIOGENIC SHOCK

• Myocardial infarction (most common - anterior wall MI)
• Myocardial contusion (trauma)
• Arrhythmias
• Severe valve disease

3. DISTRIBUTIVE SHOCK

• Septic shock (most common distributive shock)
• Neurogenic shock (spinal cord injury)
• Anaphylactic shock (histamine-mediated vasodilation)
• Adrenal insufficiency

4. OBSTRUCTIVE SHOCK

• Tension pneumothorax
• Cardiac tamponade (Beck's triad: hypotension + distended neck veins + muffled heart sounds)
• Massive pulmonary embolism
• IVC obstruction

HEMODYNAMIC FINGERPRINT TABLE (High-yield for exams)

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TRAUMATIC SHOCK (important for Orthopaedics)

• Blood and plasma loss
• Soft tissue injury and bony injury releasing DAMPs (damage-associated molecular patterns)
• Inflammatory/immune activation (same receptors as bacterial products)
• MODS (multiple organ dysfunction syndrome) develops much more easily than with simple hemorrhage

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HEMORRHAGIC SHOCK

ATLS CLASSIFICATION (Most important table for Orthopaedic exams)

• Class I = 15% loss = "minor", only tachycardia as first sign
• Class II = 30% loss = anxiety + narrowed pulse pressure
• Class III = 30-40% = THE TURNING POINT - confusion, needs blood
• Class IV = >40% = immediately life-threatening, near death

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PATHOPHYSIOLOGY OF HEMORRHAGIC SHOCK

STEP 1: Blood Loss → Reduced Venous Return

STEP 2: Baroreceptor Activation (within seconds)

• Norepinephrine + epinephrine release from adrenal medulla
• Vasoconstriction of skin, muscle, gut, kidney (NOT brain or heart - they have autoregulation)
• Tachycardia + increased myocardial contractility
• Venules and capacitance vessels constrict → auto-transfusion of 300-500 mL back to central circulation

STEP 3: Hormonal Response (hours)

• Renin-Angiotensin-Aldosterone System (RAAS): Renal hypoperfusion → renin → angiotensin II → aldosterone → Na and water retention
• ADH (Vasopressin): Released from posterior pituitary → water retention + vasoconstriction
• Cortisol: ACTH-mediated → gluconeogenesis, maintains BP

STEP 4: Interstitial Fluid Shift (the "transcapillary refill")

STEP 5: Cellular Hypoxia - The Critical Point

• Aerobic → Anaerobic metabolism → lactic acid accumulation → metabolic acidosis
• ATP depletion → failure of Na-K ATPase pump → cells swell with Na and water
• Intracellular Ca2+ overload → mitochondrial damage
• Cell membranes lose integrity → cells die (necrosis)

STEP 6: Microcirculatory Failure (Prolonged Shock)

• Arteriolar sphincters become refractory and relax (lose ability to vasoconstrict)
• Postcapillary sphincters remain constricted
• Capillary hydrostatic pressure rises → fluid leaks out to interstitium
• Plasma volume depletes further → worsening shock (vicious cycle)

STEP 7: Coagulopathy of Trauma ("Lethal Triad")

1. Hypothermia (poor coagulation, impaired enzyme function)
2. Acidosis (from anaerobic metabolism - impairs coagulation factors)
3. Coagulopathy (dilution from IV fluids, consumption of clotting factors, platelet dysfunction)

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REPERFUSION INJURY

What is it?

Mechanisms of Reperfusion Injury (4 key mechanisms):

• During ischemia: damaged mitochondria generate partially reduced oxygen intermediates
• On reperfusion: sudden oxygen delivery + activated neutrophils generate superoxide (O2-), hydroxyl radical (OH-), hydrogen peroxide (H2O2)
• Antioxidant defense mechanisms (SOD, catalase, glutathione) are DEPLETED during ischemia → cells cannot neutralize this oxidative burst
• Result: lipid peroxidation of cell membranes, protein oxidation, DNA damage

• Ischemia starts Ca2+ influx due to membrane damage
• Reperfusion: more Ca2+ floods in through damaged membranes and damaged sarcoplasmic reticulum
• Ca2+ overload → opens the mitochondrial permeability transition pore (mPTP)
• mPTP opening = ATP depletion → cell death
• Ca2+ activates destructive enzymes (phospholipases, proteases, endonucleases)

• Ischemia releases "danger signals" (DAMPs) and cytokines from dead/injured cells
• Reperfusion brings in circulating neutrophils that were activated by these signals
• Neutrophils extravasate and release proteases + more ROS = "oxidative burst"
• Endothelial cells upregulate adhesion molecules (ICAM-1, selectins) → more leukocyte sticking
• Result: massive tissue injury, endothelial disruption, microvascular leak, interstitial edema

• Some IgM antibodies deposit in ischemic tissues (unknown mechanism)
• On reperfusion: complement proteins bind to these deposited IgM antibodies and activate
• Complement activation → membrane attack complex (MAC) → cell lysis + more inflammation

Clinical Consequences of Reperfusion Injury:

• ARDS (Acute Respiratory Distress Syndrome): pulmonary microvascular injury → alveolar flooding
• ACS (Abdominal Compartment Syndrome): visceral edema
• MODS (Multi-Organ Dysfunction Syndrome): kidneys, liver, gut, brain
• No-reflow phenomenon: despite opening the vessel, no blood reaches the tissue

Why does reperfusion injury matter in Orthopaedics?

• Compartment syndrome → fasciotomy (reperfusion injury)
• Crush injuries
• Replantation surgery (limb revascularization)
• Tourniquet release during surgery

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PRINCIPLES OF TREATMENT OF HEMORRHAGIC SHOCK

IMMEDIATE PRIORITIES (ATLS - "C-ABCDE" in trauma):

1. STOP THE BLEEDING

• Direct pressure, wound packing, tourniquet
• Surgical or interventional radiology (embolization) for internal bleeding
• Damage Control Surgery (DCS): temporary control of hemorrhage, pack and close, return for definitive repair after resuscitation

2. SECURE AIRWAY

• High-flow O2 to maximize oxygen delivery
• Intubate if obtunded or airway compromised

3. VOLUME RESUSCITATION

• Class I and II: Crystalloid (Normal saline or Lactated Ringer's - LR preferred as it avoids hyperchloremic acidosis)
• Class III and IV: Blood products (Packed Red Blood Cells + Fresh Frozen Plasma + Platelets in 1:1:1 ratio = "Damage Control Resuscitation")

• Minimize crystalloid (crystalloid dilutes clotting factors, causes coagulopathy)
• Target 1:1:1 ratio of pRBC : FFP : Platelets
• Goal is to prevent/treat the lethal triad (hypothermia + acidosis + coagulopathy)

• In penetrating trauma with active uncontrolled hemorrhage - accept a lower BP (systolic ~80-90 mmHg) until surgical hemorrhage control
• Rationale: higher BP dislodges clots, pushes more blood out
• NOT used in TBI (traumatic brain injury needs higher MAP to maintain cerebral perfusion)

4. VASOPRESSORS (if BP not responding to fluids)

• Norepinephrine first-line
• Added after adequate fluid resuscitation

5. PREVENT/TREAT THE LETHAL TRIAD:

• Hypothermia prevention: warm IV fluids, warm blankets, warm environment, warming blankets
• Acidosis correction: adequate perfusion (definitive), bicarbonate only if pH <7.1
• Coagulopathy: FFP, cryoprecipitate, platelets, TXA (tranexamic acid)

6. TRANEXAMIC ACID (TXA)

• Anti-fibrinolytic - prevents clot breakdown
• CRASH-2 trial: if given within 3 hours of injury, significantly reduces mortality
• Dose: 1g IV over 10 min, then 1g over 8 hours
• Must give within 3 hours - after 3 hours, actually harmful (increases clotting complications)

7. MONITORING END-POINTS OF RESUSCITATION:

• Urine output >0.5 mL/kg/hr (best simple bedside marker)
• Normalization of base deficit and lactate (best metabolic markers)
• Heart rate normalization
• BP normalization
• CVP / PCWP (if monitored)

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NEUROGENIC SHOCK

DEFINITION

MECHANISM (PATHOPHYSIOLOGY)

1. Sympathetic outflow from T1-L2 is interrupted
2. Loss of vasoconstrictor tone → massive vasodilation of arteries AND veins below the level of injury
3. Venous dilation = loss of venous return → preload drops → CO drops
4. Arterial dilation = peripheral resistance falls → BP drops
5. Cardiac sympathetic fibers (T1-T4) may also be disrupted → BRADYCARDIA instead of compensatory tachycardia
6. Combined vasodilation + bradycardia = warm shock (dilated vessels feel warm) + hypotension

CLASSIC CLINICAL FEATURES

LEVEL OF INJURY MATTERS:

• T6 and above (cervical/upper thoracic): Most severe - both cardiac and peripheral sympathetics lost → bradycardia + hypotension
• Below T6: Loss of peripheral sympathetics but cardiac sympathetics partly preserved - less bradycardia

SECONDARY SPINAL CORD INJURY:

IMPORTANT NOTE:

MANAGEMENT OF NEUROGENIC SHOCK

• CT, FAST, clinical exam - exclude other sources of bleeding

• Crystalloid first to restore relative hypovolemia
• Caution: don't over-fluid - loss of pulmonary vasomotor tone → pulmonary edema risk
• Monitoring of cardiac preload is important

• Dopamine or Norepinephrine: to restore peripheral vasomotor tone
• Miller's Ortho: Treat with dobutamine and dopamine
• Norepinephrine: primarily alpha-agonist → vasoconstriction (preferred if pure vasodilation)
• Dobutamine: beta-1 agonist → inotrope (useful if myocardial depression)

• For bradycardia (if heart rate < 50 and causing hypotension)

• Maintain MAP >85-90 mmHg for first 7 days (to protect the cord)
• Maintain SpO2 >95% (oxygen delivery)
• Avoid hyperthermia

• Definitive surgical decompression and stabilization

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SEPTIC SHOCK

DEFINITION (Sepsis-3, 2016)

• Sepsis = life-threatening organ dysfunction caused by dysregulated host response to infection
• Septic shock = Sepsis + hypotension despite adequate fluid resuscitation + need for vasopressors to maintain MAP ≥65 mmHg + serum lactate >2 mmol/L

PATHOPHYSIOLOGY

1. LPS/bacterial products bind to Toll-Like Receptors (TLRs) on macrophages
2. Macrophages release inflammatory mediators:
   • TNF-α (first responder - causes vasodilation, endothelial injury)
   • IL-1, IL-6, IL-8
   • Nitric Oxide (NO) - most important! - causes profound vasodilation
3. Endothelium activates → increased vascular permeability → fluid leaks into tissues
4. Widespread vasodilation → SVR falls → BP drops
5. Microvascular thrombosis (coagulation activation) → organ ischemia

TWO PHASES: WARM SHOCK vs COLD SHOCK

• Peripheral vasodilation → warm, flushed extremities
• Compensatory elevated CO (heart tries to compensate)
• High CO + low SVR = "warm shock"
• Bounding pulse, fever, confusion

• Myocardial depressant factors released (cardiac depressants from bacteria + inflammation)
• CO falls
• Peripheral vasoconstriction (compensatory)
• Cold extremities, mottling, oliguria
• Progressive acidosis, MODS

MICROVASCULAR DERANGEMENTS:

• Endothelial dysfunction → capillary leak → massive tissue edema
• Fluid requirements in septic shock EXCEED those in other shocks
• Abdominal compartment syndrome from massive fluid resuscitation
• Inappropriate oxygen utilization even when oxygen delivery is adequate (mitochondrial dysfunction by bacterial toxins like LPS)

WHY IS LACTATE ELEVATED DESPITE HIGH OXYGEN DELIVERY?

• Bacterial toxins (LPS) directly impair mitochondrial function
• Cells cannot use oxygen even when it's delivered
• Called "distributive" pattern - oxygen is delivered but not utilized

MANAGEMENT OF SEPTIC SHOCK

• Find and eliminate the infection source
• Drain abscess, debride infected tissue, remove infected implant
• Delay of even a few hours in antimicrobial therapy significantly increases mortality

• Broad-spectrum empiric antibiotics first
• Then de-escalate based on cultures
• Every hour of delay in antibiotics = increased mortality

• Initial bolus: 30 mL/kg crystalloid (within 3 hours) - Surviving Sepsis Campaign
• LR preferred over Normal Saline (avoids hyperchloremic acidosis)
• Reassess after each bolus with clinical signs, lactate

• Start if MAP <65 mmHg despite fluid resuscitation
• Norepinephrine = first-line vasopressor (alpha-1 and beta-1 agonist)
• Vasopressin: add if norepinephrine doses escalating
• Dopamine: now second-line (more arrhythmias)
• Avoid phenylephrine in high-output states

• Measure lactate
• Blood cultures before antibiotics
• Broad-spectrum antibiotics
• 30 mL/kg crystalloid for hypotension/lactate >4
• Vasopressors if MAP <65 despite fluids

• Oxygen and ventilation (lung-protective ventilation in ARDS)
• Glycemic control (target 140-180 mg/dL)
• DVT prophylaxis
• Stress ulcer prophylaxis
• Corticosteroids: Hydrocortisone 200-300 mg/day if refractory to vasopressors (relative adrenal insufficiency)

SEPTIC SHOCK IN ORTHOPAEDICS:

• Post-operative wound infection → sepsis
• Open fractures with contamination
• Prosthetic joint infection (PJI) - organism in biofilm very difficult to treat
• Haematogenous osteomyelitis with systemic spread
• Necrotizing fasciitis (surgical emergency - débridement within hours)
• Crush syndrome → secondary infection

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COMPARISON TABLE: All Three Shock Types for Orthopaedics

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HIGH-YIELD EXAM SUMMARY

1. Shock Class III/IV = needs blood products (Class I and II = crystalloid alone)
2. Lethal triad = Hypothermia + Acidosis + Coagulopathy (hemorrhagic/traumatic shock)
3. TXA (Tranexamic acid) must be given within 3 hours of injury
4. Neurogenic shock = bradycardia + hypotension + warm skin (unique - all others have tachycardia)
5. Neurogenic shock is diagnosis of exclusion - always rule out hemorrhage first
6. Reperfusion injury causes: ROS, Ca2+ overload, Neutrophil activation, Complement
7. Septic shock = WARM early (high CO, low SVR), COLD late (low CO, high SVR)
8. Norepinephrine = first-line vasopressor for both neurogenic and septic shock
9. Urine output >0.5 mL/kg/hr = simplest resuscitation endpoint
10. Damage Control Resuscitation = 1:1:1 (pRBC:FFP:Platelets) - minimize crystalloid
11. "Permissive hypotension" (SBP ~80-90 mmHg) in uncontrolled penetrating hemorrhage - NOT in TBI
12. MAP >85 mmHg for 7 days in neurogenic shock - protects the ischemic spinal cord
13. Hour-1 Sepsis bundle: lactate + blood cultures + antibiotics + 30mL/kg fluid + vasopressors

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• Miller's Review of Orthopaedics, 9th Ed - ATLS Table, hemorrhagic shock classification
• Schwartz's Principles of Surgery, 11th Ed - Hemorrhagic shock, neurogenic shock pathophysiology
• Mulholland & Greenfield's Surgery, 7th Ed - All types of shock, ischemia-reperfusion injury, complications
• Robbins & Kumar Basic Pathology / Robbins Pathologic Basis of Disease - Ischemia-reperfusion injury mechanisms
• Goldman-Cecil Medicine - ATLS Classification table, gait overview
• Washington Manual of Medical Therapeutics - Septic shock management bundles

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INTRODUCTION

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ANATOMY RELEVANT TO TKA

• Medial and lateral tibiofemoral compartments
• Patellofemoral compartment
• Stabilized by MCL, LCL, PCL, ACL (ACL is removed in TKA)
• Blood supply: geniculate artery branches (anastomotic network)
• Innervation: femoral, obturator, sciatic nerve branches

• Normal mechanical axis: line from center of femoral head → center of knee → center of ankle (Mikulicz line - should pass through center of knee)
• Normal anatomic-mechanical angle of femur: 5-7° valgus
• Normal tibial plateau slope (posterior slope): 3-7° posteriorly

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INDICATIONS FOR TKA

1. Debilitating pain affecting activities of daily living - this is the PRIMARY indication
2. Pain NOT well controlled by conservative measures (failed conservative treatment for minimum 3-6 months)
3. Medical fitness for surgery (patient can tolerate anaesthesia and procedure)
4. No active infection anywhere (dental, urinary, skin - all must be treated first)

• Primary osteoarthritis (most common indication - ~95%)
• Rheumatoid arthritis
• Post-traumatic arthritis
• Avascular necrosis (AVN) of femoral condyles
• Psoriatic arthritis, ankylosing spondylitis
• Charcot arthropathy (requires higher constraint)

Conservative Treatment to Try First:

• Weight loss
• Activity modification
• Physiotherapy and strengthening
• NSAIDs, analgesics
• Viscosupplementation (hyaluronic acid injections)
• Corticosteroid injections (avoid within 2 weeks before TKA - risk of infection)
• Bracing (unloader brace for unicompartmental disease)

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CONTRAINDICATIONS

• Active infection (local or systemic - must be cleared first)
• Neuropathic (Charcot) arthropathy - relative (may need constrained design)
• Extensor mechanism deficiency (patella alta with non-functional quad - relative)
• Significant peripheral vascular disease (healing concern)
• Medically unfit for surgery

• Obesity (BMI >40) - higher complication rate, less improvement in outcomes
• Young age (<55) - concern about implant longevity
• High-demand activity requirements
• Severe osteoporosis
• Prior infection at same site

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PREOPERATIVE PLANNING

Radiographic Assessment:

• Standing full-length AP X-ray (hip to ankle) - to measure mechanical axis, identify deformity
• Standing AP knee - joint space narrowing, osteophytes
• Lateral knee - posterior slope, patellar height (Insall-Salvati ratio), bone stock
• Merchant/Skyline view - patellofemoral joint assessment
• Single-leg stance X-ray - if varus thrust gait is evident (reveals severity of ligament stretch-out and instability)

What to Identify on Radiograph:

• Bone defects (require augmentation or bone graft)
• Joint subluxation
• Ligament stretch-out
• Deformity magnitude and location
• Anticipated ligament releases
• Extent of constraint needed (simple PS vs. constrained vs. hinged)

Templating:

• Implant sizing (femur size, tibia size, poly thickness)
• Entry point for IM rod (identify any femoral deformity, hip implant in situ)
• Identify bone defects needing augments

Preoperative Medical Optimization:

Antirheumatic Medications (ACR/AAHKS Guidelines):

• Methotrexate - continue (anytime)
• Hydroxychloroquine - continue
• Sulfasalazine - continue
• Leflunomide - continue

• Biologics (TNF inhibitors like Adalimumab, Etanercept) - withhold for 1 dosing cycle + 1 week before surgery
• JAK inhibitors (Tofacitinib, Baricitinib) - withhold 3 days prior
• Mycophenolate, Azathioprine - withhold 1 week prior

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IMPLANT DESIGN

3 Basic TKA Designs Based on PCL Management:

1. Cruciate Retaining (CR-TKA)

• PCL is preserved
• Tibial polyethylene insert is flat or slightly congruent
• PCL provides posterior stability (prevents tibial translation during flexion)
• Advantage: preserves normal knee kinematics, PCL proprioception, bone stock
• Disadvantage: requires intact and functional PCL; PCL must be balanced - technically demanding
• No tibial post on the poly insert

2. Posterior Stabilized (PS-TKA) - Cruciate Sacrificing

• PCL is excised
• Tibial polyethylene insert has a central tibial post that engages the femoral component box ("cam-post mechanism")
• The post-cam mechanism recreates femoral rollback during flexion
• Advantage: easier soft tissue balancing (PCL removed, only MCL and LCL to balance)
• Disadvantage: femoral "box" cut weakens distal femur (closed box = no retrograde nail); risk of post fracture; less femoral rollback than CR
• Most commonly used design worldwide

3. Ultra-Congruent (UC) / Bicruciate Retaining (BCR)

• Attempts to retain both ACL and PCL (rarely used)
• High-congruency polyethylene replaces PCL function in UC design

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TYPES OF TIBIAL COMPONENT

Modular Metal-Backed Tibial Component

• Most common
• Metal base plate with a polyethylene (PE) insert that clips/locks in
• Advantage: PE insert can be exchanged without removing metal base
• Disadvantage: risk of PE delamination at locking mechanism, backside wear

All-Polyethylene Tibial Component (APT)

• No metal backing - solid PE block cemented directly to tibia
• Advantage: lower cost, no backside wear, no locking mechanism failure, better cement penetration
• Disadvantage: cannot exchange PE independently; need to remove entire component for revision
• No difference in outcomes vs. modular component (AAOS 4-star evidence)
• Failure mechanism: PE bends at periphery (no metal support) → cement fractures → loosening

Tibial Rotating Platform (Mobile-Bearing TKA)

• PE insert can rotate on the metal tray
• Theoretical advantage: reduces PE wear by allowing rotation (decouples rotation from fixed position)
• Clinical advantage over fixed bearing: NOT proven in randomized trials

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CONSTRAINT LEVELS

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SURGICAL TECHNIQUE

Patient Positioning:

• Supine on standard operating table
• Foot of table lowered to allow 90° knee flexion
• Tourniquet applied to proximal thigh (inflated to 250-350 mmHg)
• Contralateral limb protected

Approach - Standard: Medial Parapatellar Approach

• Subvastus approach (lateral subluxation of patella, no quad tendon incision) - better patellar blood supply
• Mid-vastus approach - split vastus medialis oblique (VMO) fibers
• Lateral parapatellar approach - for severe valgus deformity with lateral contracture

Steps of TKA (in sequence):

• Intramedullary (IM) guide rod inserted through entry hole in distal femur (2-3 cm anterior to PCL attachment, medial to notch)
• Cutting jig set to valgus cut angle (typically 5-7°) - this corrects for the angle between anatomic and mechanical femoral axes
• Cut perpendicular to the Mechanical Axis of Femur (MAF)
• Typical resection: 9-10 mm (to match implant thickness)

• Size the femur (A-P sizing)
• Rotational alignment of femoral component (critical step):
  • Transepicondylar Axis (TEA) - gold standard for rotation reference
  • Posterior condylar axis (PCA) - 3° internal rotation from TEA (as posterior lateral condyle is smaller)
  • Whiteside's line (AP axis) - perpendicular to this = femoral rotation
  • Flexion gap - balance medially and laterally
  • Malrotation → patellar maltracking, flexion instability

• Tibial cut made perpendicular to mechanical axis of tibia (MAT)
• Most cases: AAT (anatomic axis) = MAT → cut angle = 0°
• Extramedullary guide: centered over medial 1/3 of tibial tubercle distally, 2nd metatarsal proximally
• IM guide: through tibial tubercle entry point
• Typical resection: 8-10 mm from the less damaged side
• Posterior slope of cut: 3-5° (matches normal tibial slope)

• CR design: preserve PCL
• PS design: excise PCL

1. Remove osteophytes (often corrects 5-10°)
2. Deep MCL (capsule and coronary ligament)
3. Superficial MCL (posterior oblique for extension tightness, anterior for flexion tightness)
4. Pes anserine tendons (semimembranosus)
5. Posteromedial capsule

1. Remove osteophytes
2. Lateral capsule (anterolateral ligament)
3. Iliotibial band (key structure - tight in extension) → release off Gerdy's tubercle OR pie-crust technique
4. Popliteus tendon (key structure - tight in flexion) → release off anterior portion of lateral epicondyle
5. LCL (released last - affects both extension and flexion)

• Patella measured (minimum 12-13 mm bone must remain after resection)
• Cut flat or domed depending on implant
• Sizing of patellar button
• Patellar tracking assessed with "no thumb" test (observe tracking without holding patella - should track within the trochlear groove without lateral tilt or subluxation)
• Patella should track in the groove without sutures (lateral retinacular release only if still maltracking)

• Trial femur, tibia, and poly components inserted
• Assess: flexion-extension arc, varus-valgus stability, patellar tracking, posterior capsule tightness

• Bone surfaces prepared (pulsatile lavage + drying)
• Cement mixed (PMMA - polymethylmethacrylate)
• Cemented TKA is gold standard (better long-term data than uncemented)
• Femoral component cemented first, then tibial component, then patellar button
• Excess cement removed before hardening

• Medial parapatellar capsule closed in layers (interrupted sutures)
• Subcutaneous and skin closure
• Drain: AAOS evidence supports NOT using a drain (no difference in complications or outcomes)
• Tourniquet released before or after closure (controversy)

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ALIGNMENT TECHNIQUES (Modern Concepts)

1. Mechanical Alignment (Most Common, Traditional)

• Goal: Neutral mechanical limb line (Mikulicz line passes through knee center)
• Distal femur cut: perpendicular to MAF (mLDFA = 90°)
• Proximal tibia cut: perpendicular to MAT (mPTA = 90°)
• Requires soft tissue balancing in both coronal and sagittal planes
• Disadvantage: balancing in 2 planes is technically difficult; instability may result

2. Kinematic Alignment

• Goal: Maintain native limb alignment (don't change the patient's natural axis)
• Cuts made to restore natural femoral and tibial articular planes
• Ligament balancing usually NOT needed (native ligaments already adapted)
• Advantage: preserves native soft tissue tension; potentially more natural feel
• Disadvantage: recreating individualized alignment can lead to asymmetric implant loading → decreased implant survival

3. Computer-Assisted Surgery (CAS) / Navigation

• Uses intraoperative computer tracking to improve accuracy of cuts
• AAOS 4-star evidence: No difference in outcomes or complications with navigation → NOT recommended routinely

4. Robotic-Assisted TKA

• Haptic robotic arms constrain saw within planned boundaries
• Improves accuracy of implant positioning
• Growing evidence for improved short-term outcomes; long-term data pending

5. Patient-Specific Instrumentation (PSI)

• Custom cutting jigs made from CT/MRI data preoperatively
• AAOS 4-star evidence: No difference in pain or functional outcomes compared to conventional instrumentation → NOT routinely recommended

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PATELLAR TRACKING IN TKA

1. Femoral component rotation (most important) - malrotation = most common cause of maltracking
2. Tibial component rotation
3. Q-angle of the patient
4. Implant design (trochlear groove depth and shape)
5. Lateral retinacular tightness

• AAOS 4-star evidence: No difference in pain or function with or without patellar resurfacing
• Selective resurfacing is most common practice

• Patella positioned abnormally low
• Measured by Insall-Salvati ratio (<0.8)
• Risk factors: previous tibial tubercle osteotomy, previous tibial fracture, aggressive post-op therapy
• Prevents full knee flexion
• Prevention: avoid excessive proximal tibial resection, avoid tibial tubercle procedures

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PERIOPERATIVE MANAGEMENT

Anesthesia:

• Regional (spinal/epidural) preferred over general - lower DVT, blood loss
• Combined spinal-epidural (CSE) popular

Pain Management (AAOS 4-star evidence):

• Periarticular infiltration (PAI/PAB): Multiple small-volume injections around the joint (local anesthetic cocktail = ketorolac + epinephrine + bupivacaine + corticosteroid) - decreases pain and opioid use
• Adductor Canal Block (ACB): Block at medial-anterior midthigh; sensory block only (preserves quadriceps strength) → allows early ambulation; equivalent to femoral nerve block for pain but safer
• Femoral Nerve Block (FNB): Motor + sensory block → quad weakness → fall risk → needs knee immobilizer
• iPACK block: Posterior knee sensory block; eliminates "pseudo-DVT pain" (posterior knee pain from missed posterior nerves)
• Best combination: ACB + iPACK for optimal pain control with preserved quad function

Tourniquet Use:

• Only consistent benefit: less intraoperative blood loss
• No difference in functional outcomes or postoperative ROM
• Increases short-term postoperative pain (AAOS 4-star)

Tranexamic Acid (TXA):

• AAOS 4-star evidence: TXA (IV or topical) decreases postoperative blood loss and reduces transfusion requirement
• Dose: IV - 1g before tourniquet and 1g at deflation; or topical 1-3g intraarticular
• No significant increase in DVT/PE risk

DVT Prophylaxis (Postoperative):

• Both pharmacologic + mechanical compression devices recommended
• Pharmacologic options: aspirin, warfarin, LMWH, rivaroxaban, apixaban
• Duration: 14-35 days
• AAOS: Routine postoperative Doppler ultrasound for DVT NOT recommended

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POSTOPERATIVE REHABILITATION

• Rehabilitation started on DAY OF SURGERY reduces hospital length of stay
• CPM (Continuous Passive Motion): Does NOT improve outcomes - not routinely recommended
• Walking with walking frame or crutches from day 1
• Goal: 0-90° ROM in first 6 weeks (0-120° by 3 months)
• Postoperative flexion contracture: Caused by hamstring tightness - treat with therapy (no pillows under knee)
• Discharge: day 2-4 (newer enhanced recovery protocols: POD1)

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COMPLICATIONS OF TKA

EARLY COMPLICATIONS

1. Venous Thromboembolism (VTE/DVT/PE)

• Most common serious early complication
• DVT rate without prophylaxis: 40-60%; PE rate: 1-5%
• Prevention: pharmacologic + mechanical (compression stockings, pneumatic compression)
• Diagnosis: Doppler ultrasound (NOT routinely done post-TKA per AAOS)

2. Wound Complications

• Superficial wound dehiscence - local wound care
• Deep infection (see below)
• Skin necrosis (from excessive soft tissue tension, poor blood supply)

3. Stiffness (Arthrofibrosis)

• Painful limited ROM (typically <90° flexion)
• Early: Manipulation Under Anaesthesia (MUA) within 3 months (before fibrosis matures)
• Late (>3 months): arthroscopic lysis of adhesions (arthrofibrosis release)
• Higher rate after TKA following failed ORIF for tibial fractures

4. Vascular Injury

• Popliteal artery injury (rare but serious)
• Risk during posterior capsule manipulation

5. Nerve Injury

• Common peroneal nerve (risk in valgus knees - overcorrection of valgus)
• Symptoms: foot drop, lateral leg numbness
• Management: flex knee to 30° to relieve traction, splint in dorsiflexion

LATE COMPLICATIONS

6. Periprosthetic Joint Infection (PJI) - Most devastating complication

• Elevated ESR + CRP
• Elevated synovial WBC and PMN%
• Positive cultures
• Positive histology (>5 neutrophils/HPF)
• Positive alpha-defensin (highly specific)

• Early (<3 months): usually Staphylococcus aureus, direct inoculation
• Delayed (3-24 months): usually coagulase-negative Staphylococcus (low virulence, biofilm)
• Late (>24 months): haematogenous seeding

• Early acute (<3 weeks from onset): DAIR (Debridement, Antibiotics, Implant Retention) with poly exchange
• Established/chronic: Two-stage revision (remove all hardware, antibiotic spacer, 6 weeks IV antibiotics, then reimplant)
• High-risk/immunocompromised: Suppressive antibiotics only

7. Aseptic Loosening

• Most common late complication
• Osteolysis around implant from PE wear particles
• Inflammatory osteolysis → bone resorption → mechanical loosening
• Diagnosis: serial X-rays (radiolucent lines > 2mm around implant)
• Treatment: revision TKA

8. Polyethylene (PE) Wear

• Mechanism: adhesive and abrasive wear, delamination, oxidative degradation
• "Catastrophic wear" - severe wear causing implant failure:
  • Tibial post fracture (in PS TKA - especially with malalignment)
  • PE delamination and breakage
  • Accelerated by: malalignment, obesity, high activity, older PE manufacturing (gamma-in-air sterilization)
• Prevention: modern cross-linked PE, correct alignment, appropriate activity

9. Instability

• Flexion instability: PCL sacrificed but post-cam inadequate; excessive posterior tibial slope
• Extension instability: Flexion-extension gap mismatch (flexion gap > extension gap)
• Global instability: Complete MCL/LCL deficiency
• Management: depends on type - PE exchange, constrained revision, or hinged revision

10. Femoral Notching

• Occurs when anterior femoral cut accidentally notches the femoral cortex
• Predisposes to periprosthetic distal femur fracture
• Prevention: ensure 4-in-1 cutting block not placed too posterior on distal femur

11. Periprosthetic Distal Femur Fracture (PDFFx)

• Rule 1: If implant loose/unstable → Revision TKA is part of answer
• Rule 2: PS femoral component = "closed box" → CANNOT use retrograde IM nail (rIMN)
• Rule 3: Elderly patient (≥75 years) + osteoporosis + comminuted fracture → Distal Femoral Replacement (DFR) preferred
• Rule 4: Nonoperative treatment = poor outcomes, never preferred answer

• Type I: Non-displaced, stable implant → ORIF (locking plate preferred)
• Type II: Displaced, stable implant → ORIF (locking plate or rIMN if CR design)
• Type III: Any fracture + loose implant → Revision TKA

12. Patellar Fracture

• Patellofemoral maltracking (bone overload → fatigue fracture)
• Direct trauma
• Loose patellar implant (late - cement fatigue → abrasion → fracture)

• Minimal lag (≤10°) + stable TKA + well-fixed patella → non-surgical (cast/brace, NO therapy)
• Significant lag (≥10°) + stable TKA → open extensor repair
• Significant lag + unstable TKA → Revision TKA + extensor repair
• Loose patellar implant + adequate bone → component revision
• Loose implant + inadequate bone → component removal + patelloplasty or patellectomy

13. Patellofemoral Complications

• Patellar maltracking - most common: lateral tilt and subluxation
• Anterior knee pain (most common cause of patient dissatisfaction)
• Patellar clunk syndrome (soft tissue nodule in PS TKA catches in intercondylar notch at ~30-40° flexion)
• Patellar tendon rupture (catastrophic - requires reconstruction)

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RESULTS OF TKA

• 10-year survival: >90-95%
• 20-year survival: >85% with modern implants and techniques
• Pain relief: excellent in 85-90% of patients
• ROM improvement: average increase of 10-15°
• Patient satisfaction: 82-89% (10-15% are not fully satisfied - most common reason: anterior knee pain, stiffness, residual pain)

• Unrealistic preoperative expectations
• Residual anterior knee pain
• Persistent stiffness
• Instability feeling
• Psychological factors

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HIGH-YIELD EXAM POINTS (Quick Revision)

1. Primary indication = debilitating pain affecting ADL NOT controlled by conservative treatment
2. Avoid intraarticular steroid injection within 2 weeks of TKA (infection risk)
3. Standard approach = medial parapatellar (most common); lateral parapatellar for severe valgus
4. Valgus cut angle = 5-7° (angle between anatomic and mechanical femoral axis)
5. Femoral rotation reference = Transepicondylar Axis (TEA) is gold standard
6. Gap balancing = flexion gap must equal extension gap (rectangular)
7. Most common cause of patellar maltracking = femoral component malrotation (internal rotation)
8. "No-thumb test" = assess patellar tracking without manual guidance
9. Tibial component rotation = aligned to medial 1/3 of tibial tubercle (anterior) or directed toward 2nd metatarsal head
10. PCL retained in CR design; PCL sacrificed, cam-post used in PS design
11. AAOS 4-star: No difference between CR vs PS design outcomes
12. AAOS 4-star: TXA reduces blood loss - use it
13. AAOS 4-star: No drain needed
14. AAOS 4-star: CPM does NOT improve outcomes
15. AAOS 4-star: Start rehab on day of surgery
16. ACB + iPACK = best pain management combination (preserves quadriceps function)
17. FNB = fall risk (quad weakness) - needs knee immobilizer
18. PS TKA = closed box = no retrograde IM nail for periprosthetic fracture
19. MUA within 3 months for stiffness (before fibrosis matures)
20. Most common late complication = aseptic loosening (PE wear → osteolysis)
21. Most devastating complication = PJI - two-stage revision for chronic infection
22. Femoral notch = predisposes to periprosthetic distal femur fracture
23. All-polyethylene tibia = no difference in outcomes vs. modular metal-backed
24. Kinematic alignment = maintain native axis (no balancing needed); Mechanical alignment = neutral mechanical axis (balancing required)
25. 10-year survival >90-95%; 20-year >85%

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• Miller's Review of Orthopaedics, 9th Ed - Sections 13-17 (TKA comprehensive)
• Campbell's Operative Orthopaedics, 15th Ed 2026 - TKA, Revision TKA, Complications
• Morgan and Mikhail's Clinical Anesthesiology, 7th Ed - TKA anaesthesia considerations