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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