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04 Siying's Complete Orthopedics
04 Siying's Complete Orthopedics
COMPLETE
ORTHOPEDICS
With
reference
from:
1) Y&Z
Orthopedics
2) Jo
&
Li
(edited
by
Wai
Wai)
3) Orthopedia
1
Contents
Page
General Orthopedics
•Physical
Examination
•History
Taking
•Principles
of
Fractures
and
Dislocations
•Polytrauma
•Open
Fractures
•Limb
threatening
conditions
Regional Orthopedics
•Shoulder
•Humerus
•Elbow
and
Forearm
•Wrist
and
Hand
•Pelvis
•Hip
and
femur
•Knee
•Tibia
and
Fibula
•Foot
and
Ankle
•Spine
Orthopedic Conditions
•Osteoarthritis
•Rheumatic
Diseases
•Crystal
deposition
diseases
•Metabolic
Diseases
•Genetic
Disorders
•Osteochondritis
•Bone
Tumours
•Diabetic
Foot
•Paediatric
•Conditions
•Trauma
•Bone
and
Joint
Infections
2
Chapter
1:
Orthopedics
Physical
Examination
BASIC OF CLINICAL EXAMINATION
LOOK
• Skin: scar, colour changes, abnormal creases, swelling
(soft
tissue
or
bony),
sinuses,
discoloration
• Muscle:
wasting,
fixed
deformities
• Bone:
deformity,
alignment,
swelling
FEEL
• Skin: Temperature
• Bone/ joints: outlines normal/ synovium thickened/ excessive fluid in joint
• Tenderness : distribution (Ligaments,
tendons,
muscles,
Bony
landmarks)
• Wasting
(with
measurement)
MOVE
• Active: to test power
• Passive: to test ROM, painful, crepitus
• Abnormal movement: unstable joint
SPECIAL TESTS
3
Chapter
2:
History
Taking
for
Orthopaedic
Conditions
Biodata: Name, Age, Race, Gender, Occupation Deformities
PRESENTING COMPLAINTS & ASSOCIATED SYMPTOMS • Normal variation
o Associated symptoms • Pathological
§ General o Bow legs- genu varum/ varus (part distal to joint displaced
• Swelling –esp in hip, knee, ankles towards the midline)
o Permanent or acute(after injury) o Knock-knees- genu vagum/ vagus (part distal to jt away
• Suspect spine pathology: back/neck pain, from midline)
paresthesia/numbess o Kyphosis/ lordosis
§ Shoulder: weakness, cervical spine o Scoliosis
§ Hand: crepitus, cervical spine o Bony lumps
§ Hip: lumbar spine o Fixed deformity- particular movement cannot be completed
§ Knee: giving way, locking, crepitus, lumbar spine § In spine: structural deformity (others: postural
§ Foot: giving way, lumbar spine deformity)
§ Other medical illness: RA, AS, Down’s syndrome • 6 causes of bone deformity
o Congenital
Pain (SOCRATES) o Rickets/ osteomalasia
o Bone dysplasia
• Site: location and referred location – back pain only? Or radiation
o Physeal injury
to thigh and feet (ask specific sitesà dermatomal/peripheral
o Fracture malunion
nerve distribution)
o Paget’s dx
• Character: shooting (nerve), cramping
• 6 causes of joint deformity
• Timing:
o Skin contracture- burn
o Early morning pain- inflammation
o Fascial contracture- Dupuytren;s
o Relieved at night- mechanical in nature
o Muscle contracture – Volkmann;s
o Night pain- implies severity, malignancy, infx
o Muscle imbalance
• Relieving factor:
o Joint instability
o Medications (include analgesics and TCM), posture
o Joint destruction
• Aggravating factor Weakness
o History of trauma
• Ddxneuro causes
o RTA
§ If fell: able to get up? How did you come to Change in sensibility
hospital • Establish the exact distribution → identify the faulty source
§ Motorcyclist: able to get up aft injury • Tingling / numbness →
§ car: seat belt was on? o Pressure from neighbouring structure- prolapsed disc
• Duration o Local ischemia
o How long each time, when the pain appears o Peripheral neuropathy
o Similar previous episode or pain? Specific to region
• Previous treatment done (ask from the least invasive • HIP
o Medication : glucosamine, NSAID, TCM, acupuncture, o Whether pt can take care of their feet/ pedicure
hyaluronic acid, analgesic • KNEE
o Others : osteotomy, TKR , other sx o Locking: implies mechanical block/ meniscus tear
o Previous x ray § Any pain on walking down stairs ?
• Severity: o Giving way/ jumps out- ligamentous deficiency, recurrent
o How far can you walk before resting subluxation,patellofemoral problem)
o When rest how long is needed before walking o Pain at one point at the joint (meniscus tear) or pain along
o Any pain at rest? joint line (OA)
Swelling o Problem climbing stairs (patellofemoral joint) or pain on
• From ST/joint/ bone?Appear immediately after injury- hematoma standing (patellotibial joint)
• Appear slowly- inflammation, joint effusion o Stiffness
• Painful – inflammation/ infection/ CA § Morning (OA) relieved during the day
Stiffness § Inflammatory arthritis: constant pain
o Swollen now? Before this?
• By features o Any noise along the joint ?crepitus
o Generalised – RA/AS or localised o Can walk? Climb stairs? Squat down?
o Early morning + involve many joints – RA
• LUMBAR SPINE
o Transient (esp after activity) + involve a few joints- OA
in sciatica –compression / injury to sciatic nerve→ pain, altered
• By grades of joint stiffness
sensation (along L4/L5,S1,2,3), loss ankle jerk, if severe muscle
o All movements absent:
§ surgical fusion (anthrodesis) power loss along distrubtion of nerve
§ pathological fusion(ankylosis) o Pain: Radiation (look for dermatomal distribution)
• Acute suppurative arthritis- bony ankylosis o History of injury
• Tuberculous arthritis- fibrous ankylosis o Ask features of neurogenic claudication (spinal stenosis)
o All movements limited § Sleep at night?
§ Non infective arthritis- usually due to synovial o Weakness in muscle innervated by sciatic nerve
swelling/ capsular fibrosis ankle flexion, extension, inversion and eversion, great
o One or two movements limited toe extension
§ Mechanical or joint contracture o Radiation (dermatomal distribution) and neuro deficit)
Lax joints § Neurological symptoms (numbness/ paresthesia)
• Generalised hypermobility- in 5% of population; Marfan’s & distribution
syndrome, osteogensisimperfecta (brittle bone disease with blue o Relate to hx: Common due to herniated IVD (young ) or
scelra) spinal canal/ root canal stenosis (elderly)
4
o Cauda equina: sphincter disturbance (bladder and bowel FUNCTION
symptoms, saddle anaesthesia, lower limb weakness) Loss of function
o Red flags: • LL
§ Suggestive of infection/ cancer o How does it affect function: walking distance, use of stairs
• Non-mechanical pain: Night pain (wakes o Factor affecting living: lift landing, walking aid
one up, cannot sleep), rest pain, night • UL
sweats o How does it affect function: washing, dressing, combing,
• Constitutional symptoms: Fever, feeding, writing, use of chopsticks (fine motor skill)
unexplained LOW (>10kg in 6 months), o Factor affecting living: hand dominance
LOA • ADL dependence vs pre-morbid status
• Medical history: Cancer, recent bacterial o DEATHS: dressing, eating, ambulating, toileting, hygiene,
infection swallowing
• Age of onset: <20years, >55years Lower limb • Walking distance
• Obvious deformities • Going to shops
• Hx of TB • Use of stairs
§ Suggestive of spinal fracture: Trauma, • Use of walking aids (community ambulance)
osteoporosis, obvious deformities
• Hip: ability to put on socks/ clip toenails
§ Suggestive of serious injuries
Upper limb • Hand dominance
• Cauda equina: saddle anaesthesia,
• Washing, dressing (hook bra), combing, feeding,
bladder or bowel incontinence, disturbed
gait writing
• Neurological deficits • Fine motor skills: chopsticks, reading newspapers,
driving, using handphones
• Pain for >4-6weeks
• Failure to improve with therapy
§ Suggestive of high risk of permanent damage to FAMILY HISTORY
nerve
• Significant muscle wasting/weakness PAST MEDICAL HISTORY
• Loss of tendon reflexes • Medical history
• Positive Babinski reflex • Past treatment
§ Progressive o Analgesic
§ Thoracic back pain o Warfarin, aspirin, blood thinner → assess fitness for
§ Hairy patch/ café-au-lait spots (esp in kids) operation
o Scoliosis o TCM and acupuncture
§ When was the deformity first noted o glucosamine, NSAID, TCM, acupuncture, hyaluronic acid
§ Manner it was noted- health screening, family, o surgery done: osteotomy, TKR , other sx
doctor? • Personal- comorbidities (fitness for op/ RF), medication history
§ Perinatal history (current medication, previous medication, TCM, drug allergies),
§ Development milestones previous surgery/ admissions/ illness/accidents
§ Family history of scoliosis and dx that may aff M/S • Family- musculoskeletal disorders within fx
system
§ Women with scoliosis has 1% higher risk of giving SOCIAL HISTORY (ASSTOSsED)
birth to child with scoliosis, hence scree n kid
• Alcohol, smoking, support, travel, occupation/past jobs, similar
• FEET
symptoms, exercise, diet
o Referred pain: back pain
• Functional Asessemnt of disability
o Pins and needle ( lumbar spine patho/ nerve entrapment/
o Walking aids? Ambulant? ADLS, how far can she walk?
peripheral neuropathy)
o Work, travek, recreation, home, level of support from fx and
o Footwear
friends
Constitutional symptoms: Fever, night sweats, LOW, LOA
o Previous status and current disability
• Caregiver after surgery!
SYSTEMIC REVIEW
• Usual systemic review
• Recent history of trauma/ falls
• Rule out extra-articular manifestations of certain diseases (eg RA)
5
Chapter 3: Principles of Fractures o angulation, rotation & axial compression #: consist of an
oblique component caused by compression and a
GENERAL PRINCIPLES transverse component caused by angulation à oblique #
History Metaphysial vs Diaphyseal Fractures
Causes • Metaphyseal
o Healing: not by callus, but by ingrowth (as little
Mechanism movement)
Assessing injury o Movement: Little because usually compaction fracture
Fracture Emergencies (stable) as lots of cancellous bone in metaphyses
Metaphyseal vs Diaphyseal Fractures o Rapid repair: Consolidate within 3 weeks
Joint Injuries o Management
§ Minimal displacement, extra-articular: Simply cast
Imaging and allow healing by ingrowth
Radiographic Description of fractures § Displacement, intra-articular: Once reduced will
Stability of Fractures become unstable, hence must stabilize; might
Healing even need to fill with bone graft to fill gaps from
disimpaction (put in cast)
ASSESSING COMPLICATIONS OF FRACTURE • Diaphyseal
MANAGEMENT o Healing: by callus
Initial management o Movement: Lots of motion
Definitive management Fracture Emergencies
PRINCIPLES OF MX OF DISLOCATIONS • Open fractures
• Compartment syndrome (tibia, forearm, femur, foot, hand –
TABLE SUMMARY OF #S AND DISLOCATIONS
areas with myocutaneous or myofascial compartments)
GENERAL PRINCIPLES • Neurovascular compromise
History • Very bad fractures with haemodynamic instability: Unstable
• Clinical Features pelvic fractures - Openbook pelvic fractures
o Pain and tenderness • Spine
o Deformity & abnormal resting position • Multiply injured
o Swelling • Fracture-dislocations – skin or soft tissue compromise (closed
o Loss of function: inability to weight bear, abnormal FD can become open if not reduced)
mobility and crepitus (avoid) Joint Injuries
o Neurovascular compromise (impt to document)
• Ligament Injuries
§ Concomitant injuries
o Types
• High vs Low velocity
§ Sprain: Painful twisting without actual tearing of
o Indication of injury severity (concomitant injuries) ligaments or capsule
o Pathological fractures § Strain: May involve tearing of some fibers
• Mechanism of injury § Tear/Ruptured ligament: Partial/ complete rupture
Causes o Management
• Trauma: direct and indirect trauma § Conservative: Splint à Physiotherapy à Replace
• Stress Fractures (repetitive mechanical loading): Normal bone; splint with functional brace
abnormal stress § Surgical reconstruction: Symptomatic instability or
o Common sites avulsion of large enough bone fragment
§ Metatarsal (esp 2nd) • Articular Injuries
§ Femoral Neck o Types
§ Tibia § Dislocation: Complete loss of articulation at joint
§ Others: Shaft of humerus, Pars interarticularis of 5th • Associated with
lumbar vertebra, pubic rami, femoral shaft, patella, o Shaft #s often require open reduction
calcaneum, navicular, fibula o Peri-articular fracture may increase
• Pathological Fractures: (OMIT) Abnormal bone; normal stress instability (eg. Hill-sachs lesion)
o Osteopenia/osteoporosis • Anatomy
o Metabolic bone disease (hyperPTH, hyperthyroidism, • Ligamentous laxity (especially for
osteoporosis, osteogenesis imperfect, rickets) recurrent dislocations)
o Infection
• Common: Shoulder (commonest), knee
o Tumour
(2nd commonest) – stability of knee
• Periprosthetic
depends on ligaments, hip, elbow
Mechanism § Subluxation: Partial loss of articulation at joint
• Direct trauma o Management
o Tapping fracture; occur when a force is applied over small § Reduction as soon as possible (usually with
area, usually transverse fracture line (eg nightstick fracture) anesthesia and muscle relaxant)
o crush fracture: with extensive soft tissue damage, Imaging
extensive comminution • X-ray: rule of 2s
o penetrating fracture: produced by projectiles, gunshot o 2 views (orthogonal views; AP and lateral)
• Indirect trauma o 2 joints (above and below site of injury)
o avulsion or tension #: # line is perpendicular to line of force; o 2 sides (for paediatric cases)
happen to the patella or olecranon when the knee or elbow o 2 times (before and after reduction)
is forcibly flexed while extensor muscles are contracting o 2 opinions
o angulation #: transverse #, may form butterfly fragment • MRI: Soft tissue injury, Occult fractures
o rotation fracture ; when a piece of chalk is twisted until it
• CT: Image bone surface (often for complicated fractures)
breaks, a characteristic spiral fracture line is produced
• Bone scan (radioisotope scanning): only +ve abt a week after #
o compression fracture ; T- or Y-shaped fracture (e.g. at the
o Stress fractures
lower end of the humerus or femur)
o Undisplaced fractures
6
Description (on Xray) (ACS MAAD) Stability of Fractures
• Identify view + date + patient identification (“This is an AP X-ray • Stable: When upon reduction, it remains reduced with simple
view of the knee joint taken on 1/12/10 for Mdm Gee”) splintage and normal movement
• Anatomy o Inferred by x-rays and clinical examination (eg. can move
o What – Which bone >50% of normal range)
o Where – Diaphysis / Metaphysis / Epiphysis • Types of fractures
§ If diaphyseal, describe by thirds (prox/ middle/ distal) o Oblique/spiral – Unstable
• Complete vs Incomplete § Translational/rotational displacement hence need
• Simple vs Comminuted complex splint to reduce and hold
• Fracture Morphology o Avulsion – Unstable
§ Muscle pull keeps fragments apart
o Complete transverse translation – Unstable
§ Periosteal stripping circumferentially
o Intra-articular
• Acceptable displacement – if deemed acceptable, can just
immobilize in that position
o Bone union requires >50% of bone contact
o Angulation can accept up to 20 deg for long bones (in
children) – but in adults may accept lower because of
poorer remodeling capacity
Healing
• Purpose of splinting
o Alleviate pain
o Ensure union takes place in good position
o Permit early movement and return to function
• General stages in normal healing process
o 0h: Haematoma formation
o Transverse # o Within 8h: Inflammation and cellular proliferation under
§ Mechanism: 3 point bend; direct force, high energy periosteum and within the medullary cana
§ Stability: § Macrophages, undifferentiated stem cells and
• Usually remain in place after reduction platelets surround fracture site
• But may be unstable in upper limb (due to § Granulation tissue
lateral motion as opposed to lower limb where § Involve osteoclasts hence fracture gap accentuated
axial loading stabilizes #) within first few weeks
o Oblique # o 3-12 weeks: callus proliferation (formation & calcification)
§ Mechanism: unequal force distribution of 3 point § 3-6 weeks: osteoclasts remove sharp edges (thus #
bend; angular and rotational force more visible on radiographs); fibrocartilage callus
§ Stability: Tendency to slip/displace forms within hematoma
o Spiral # (# line > 2x bone width) • Soft callus - cartilage
§ Mechanism: Torsion; rotational force, low energy § 6-12 weeks: bone forms within the callus
§ Stability: Tendency to slip/displace (endochondral calcification of cartilage), bridging
o Comminuted # (>2 pieces) vs Simple # fragments; forming woven bone
§ Mechanism: Often complicated; direct force, high • Hard callus – calcified cartilage: # union
energy o 6-12 months: Consolidation
§ Stability: Often unstable § Woven bone replaced by lamellar bone
o Butterfly # (2 lines break out obliquely from point of contact o 1-2 years: normal architecture achieved thru remodeling
of blow, producing a free-floating butterfly fragment) § Takes years
§ Mechanism: low velocity injuries due to 3 point bend • 2 main ways
o Avulsion #: strong muscle inserting into small bone
o Callus formation
§ Eg. quads to patella, triceps to olecranon, peroneus
§ In response to movement
tertius to 5th MT head
§ Main advantage: Stronger
o Compression #
o Gap healing: In response to absolute immobilization
• Intra vs Extra Articular
• Shape of fracture affects rate of healing
o Extra-articular: diaphysis or metaphysis
o Spiral heal faster than transverse fracture due to larger
o Intra-articular: salter-harris classification (for children)
area of contact
• Associated structures (aka soft tissue):
• XR evaluation of healing: trabeculae cross # site, visible callus
o Calcification, gas, foreign bodies
bridging site
• Displacement (Type and plane): only comment w 2 views!
• Union vs Consolidation
o Translation/ apposition (% displacement)
Union Consolidation
§ Shifting of fragments (sideways, forwards,
Fracture line Fracture line visible Fracture line almost
backwards etc) resulting in loss of contact between
obliterated and crossed
fragments à any shortening? (ie. Bayonet #)
by bone trabeculae
o Angulation/deformity
§ With respect to apex (eg. volar apex angulation – State of callus Ensheathing callus Calcified callus ossified
apex of angulation pointing volar) calcified
§ Angle Tenderness Fracture site tender Fracture site non-tender
o Rotation: Rotation on its longitudinal axis to palpation or
o Altered length angulation stress
§ Fragment distraction and separation Completion Incomplete repair: Complete repair
§ Fragment overlap Unsafe to subject bone
• Open vs Closed to stress
• State of bone (any underlying pathology?)
7
ASSESSING COMPLICATIONS OF FRACTURES
Local Early Soft Tissue Injury 1. Nerve injury: neuropraxia, axonometsis, neurotmesis (REFER to hand injuries)
2. Vascular Injury
3. Visceral Injury
4. Fracture blisters (refer to Cx of open #)
Swelling related 1. Compartment syndrome (refer to Cx of open #)
2. Haemarthrosis
Infection Gas gangrene, osteomyelitis
Late Union-related • Delayed union
(refer to Cx of open #) • Non-union: atrophic, hypertrophic, infected
• Malunion
Avascular necrosis • Common sites: Head of femur, proximal scaphoid, lunate, neck of talus
(refer to Cx of open #)
Growth disturbance
Joint related • Joint instability
• Osteoarthritis
• Joint stiffness
Complex regional pain • Chronic progressive disease characterized by severe pain, swelling, skin changes due to
syndrome dysregulation of ANS post trauma
Soft tissue related • Heterotrophic ossification
• Muscle contracture
• Tendon rupture
• Nerve compression or entrapment
Systemic • Fat embolism syndrome (long bones) à refer to Cx of open #
• Hemorrhagic shock
• ARDS, MODS
• DVT/PE
• Sepsis
MANAGEMENT
Principles of management FRIAR: First aid à Reduction à Immobilisation à Active Rehabilitation
Initial management: refer to “open fractures - emergency care”
o General Mx of #
§ ABCDE
• Assess neurovascular status, beware of compartment syndrome
• If hypovolemic à IV fluids, packed cells, whole blood
§ Analgesics
§ Preliminary skin traction à relieve pain, minimize further displacement
§ How to determine if # is displaced or not: compare continuity of trabeculae lines
Definitive Management – Steps: 1) reduce 2) stabilize 3) rehabilitate
o Concepts:
§ Operative vs Non-Operative
• Non-operative: Analgesia, splint/protect, restore function
• Operative: Reduction, fixation, others (arthroplasty, amputation)
o Contraindications: severe osteoporosis, active infection or osteomyelitis, severe comminution that cannot be
reduced, severe soft injury, poor general condition, nondisplaced fracture
§ Broad principles:
• Reduce: Restore articular surface and normal alignment
• Stabilise: Allow healing and minimize pain
o Indications for # fixation
§ To save life or limb
§ To reconstruct displaced articular fractures
§ To prevent deformity
§ To promote union when it is delayed
§ Improved function following early motion
• Rehab: Restore function
§ Objectives: Restore function, Prevent OA
o Reduction
§ Objective: adequate (not perfect) apposition and normal alignment (except for intra-articular #s where anatomic reduction is
mandatory to restore joint congruency with absolute stability as irregularity will predispose to OA)
• Imperfect apposition may be acceptable while imperfect alignment is rarely acceptable
• Attempt closed reduction as much as possible
o If successful: then stabilize
o If unsuccessful: open reduction, then stabilize (usually internal fixation)
§ Contraindications
• Little or no displacement (i.e reduce when amt of displacement is unacceptable)
• When displacement does not matter – eg. clavicle, fibula
• When reduction unlikely to succeed – eg. compression # of vertebrae
§ 3 Methods: 1) Manipulation 2) Mechanical Traction 3) Open Reduction
• Closed Reduction
o Principles:
8
§ Minimse damage to BS
§ Rely on soft tissue attachments
§ Rarely adequate for intra-articular #
§ Difficult in babies whose bones cannot be seen in XR
o Manipulation
§ Indications
• Minimally displaced #
• Most fractures in children
• Initial management for unstable fractures (prior to definitive mechanical fixation)
§ Method
• Distal part of limb pulled in line of the bone
• Repositioning of disengaged fragments
• Alignment adjusted in each plane
o Mechanical Traction: Indications: When manipulation difficult due to powerful muscle pull
• Open Reduction (Operation)
o Indications: NO CAST
§ N – Non-union
§ O – Open fracture
§ C – neurovascular Compromise (associated injuries)
§ A – intra- Articular fractures (where there is large articular fragment that needs accurate positioning; require
anatomic reduction)
§ S – Salter-Harris 3, 4, 5 and/or special situations depending on Site
• Cannot cast or apply traction due to site (eg. hip fracture)
§ T – polyTrauma
§ Others:
• Failure of closed reduction (soft tissue interposition/difficulty controlling fragments)
• Avulsion fractures (fragments held apart by muscle pull)
• Pathological fractures
• When internal fixation needed (unstable fractures like fracture dislocations)
• Fracture in paraplegics for nursing access
• Potential for improved function w ORIF
• Infection
• New fracture thru screw holes
• Implant failure
• Stabilisation
o Principle: Stabilize the fracture site but do not completely immobilize the limb if possible; maintain till united; jt above & below for shaft #
o Principles of # fixation: Translational stability (3 point contact) + Rotational stability (engaging e metaphysis) + Axial stability
(quality/strength of implant)
External stabilization
1. splints/tape Non-rigid fixation – risk of loss of reduction
2. casts but stimulate rapid callus formation
3. traction
4. external fixator
Internal fixation Rigid fixation – immediate
1. percutaneous pinning (Kirschner or K-wires) loading but does not
2. extramedullary fixation (screws, plates, wires) stimulate callus formation
3. intramedullary fixation (rods) - biomechanically advantageous
o Sustained traction
§ Principles
• Line of pull in alignment with long axis of bone
• Continuous traction maintained
• No interruption with line of pull
• Adequate counter traction
§ Mechanism: Traction can be skin or skeletal
• Gravity
• Skin: Works by friction
• Skeletal: Works by tension
o Skeletal traction can be with Thomas’s splint or pulley frame or both
o Sites of Steinmenn pin insertion: tibia, distal femur, skull – as deep as inner table, calcaneum
§ Types: Fixed, Balanced, Combined
§ Complications:
• Circulatory embarrassment
• Nerve injury (Common peroneal palsy à weakness of dorsi flexion à foot drop)
• Skin: Pin-site infection, blisters, ulcers, pressure sores (Buttocks, Tendo Achilles, under heel)
• Problems with immobilization: DVT, pneumonia, bed sores, UTI
• Loosening of Steinmann pin
• Ring pressure (Thomas’s splint)
§ Traction care
§ Specific Examples (refer to traction slides)
• Straight leg traction (Buck’s traction): 10% of body weight
• Hamilton Russell: Vertical and horizontal line of pull to create a diagonal vector pull that is in line with the femur
9
o Usually for proximal femur fractures
• Thomas Splint with Traction: Subtrochanteric/Femoral shaft fractures
• Bryant’s traction: position BrYant’s traction: Bent Y
o Patient’s body is the stem of the Y lying on the bed, and legs are the ends of the Y up in the air
• Pearson knee piece: Distal femur or femoral shaft fractures where gastrocnemius needs to be relaxed
o Cast splintage – Need to cover joint above and below
§ Principles
• One joint above and below the #
• Cast is well molded with no pressure points
• Padding at bony prominences
• Backslab instead of full cast in acute setting as swelling likely to occur
• Always place a backslab/ U slab even if patient if just admitted for pain control
• Elevation to prevent swelling
• All hand fractures have a standard functional hand position cast
§ Indications
• Fractures that can be reduced and stably maintained
• No major soft tissue injury
• No suspicion of compartment syndrome
• No vascular compromise
§ Complications
• Immobility: Stiffness
• Pressure
o Vascular compression (tight cast): Compartment syndrome
o Pressure sores – if cast not applied smoothly
o Skin abrasion or laceration (during removing plaster)
• Looseness: Delayed union (fracture not held due to loose cast)
§ Types of plaster casting
• Forearm U slab: forearm #
• Shoulder U and O slab: proximal an midshaft humeral #
• Intrinsic plus hand slab: hand # Figure
1:
Air
Cast
• Above knee cylinder slab: knee injuries
• Above knee slab: tibia/fibular #
• Below knee slab: ankle #
• Air cast - Advantages: can remove (more hygienic), can weight bear
o Functional bracing
§ Mechanism: Segments of a cast are applied only over the shafts of the bones leaving the joints free; cast segments connected
by hinges allowing movements in one plane
§ Use
• Usually used after 3-6 weeks of traction or conventional plaster
• Commonly used for humerus and tibia
o Internal fixation
§ Indications
• Fractures that cannot be reduced except by operation
• Inherently unstable #s – eg. dislocation fracture
• #s that unite poorly (NOF fracture)
• Pathological #s – where bone disease may prevent healing
• Multiple #s
• #s in patients with severe nursing difficulties
§ Types
• Screws (have screw head and screw tract)
o Reducing single fragments onto main shaft of tubular bone
o Fitting together fragments of metaphyseal fracture
• Wires (Kirschner wires) – Used when fracture healing is predictably quick
o Children fractures
o Distal radius fractures
o Tension band wiring for patellar fracutres
• Plates and Screws
o Metaphyseal fractures of long bones
o Diaphyseal fractures of radius and ulna
o Intra-articular
• Intramedullary nail
o Used for long bones: Femur, tibia, humerus
o Have holes for interlocking screws
§ Complications of Internal Fixation / Prosthesis
• Immediate
o Surgery Related: Blood loss, Infection, Neurovascular compromise
o GA Related: Cardiovascular, allergy, paralysis, AMI, stroke
o Prosthesis related: Peri-prosthetic fracture
• Late
o Systemic: DVT – for lower limb (thus importance of early mobilization!!!! à fixation construct is stable enough
to allow postopersative functional care)
10
o Local
§ Peri-prosthetic fracture
§ Implant failure – wear and tear
§ Non-union
§ Re-fracture
o External fixation: Bone is transfixed above and below the fracture with screws or pins or tensioned wires and then connected to each
other by rigid bars
§ Rationale: Achieve immediate stability without traumatizing periosteum and endosteum further
§ Role: Usually used as a temporary measure when difficult for definitive fixation initially; often replaced by other forms of fixation
as soon as soft tissue lesions have healed
§ Indications
• Fractures with severe soft tissue damage (where wound indicated to be left open for inspection) or swelling – need to
wait for swelling to subside for definitive management
• Severely comminuted and unstable fractures
• Unstable joints
• Haemodynamically unstable patients
• Fractures of pelvis (which cannot be controlled by other method)
• Infected fractures – Internal fixation not suitable (external fixator can be easily removed in event when biofilm is formed)
• Severe multiple injuries/Poly trauma – Early stabilization reduces risk of serious complications
§ Parts of external fixator: Schanz pins + Trans-fixation bar + Pin bar clamp
§ Methods to increase stability of external fixator
• Multifixator: Fix in multiple planes
• More bars and more pins
• Position: 2 outer (as far apart) and 2 inner (as close as possible)
§ Advantages and disadvantages
• Advantages
o No foreign material in wound
o Minimal further soft tissue damage
o Provides easy access to wound
o Can be removed easily (if infected or need further debridement)
• Disadvantages
o Potential for pins to injure neurovascular structures
o Pin loosening
o Pin-track infections
• Rehabilitation
o Prevention of edema: Elevation
o Exercise: Active exercise + Assisted movement à avoid joint stiffness + regain strength and function
§ Isometric exercises to avoid muscle atrophy
§ ROM for adjacent joints
§ Continuous passive motion (CPM) following rigid fixation of fracture allows joint motion to prevent stiffness for intra-articular
fractures
§ After cast/splint removed and # healed à resistive muscle strengthening
§ Evaluate bone healing (clinical + XR)
o Functional activity
• Alternative management: Arthroplasty, Amputation
11
Table summary of fracture and dislocations
Radial head trauma: MUA (supination, direct Monteggia #, PI Nerve
Upper limb fractures dislocations by Lee Yizhi dislocation pressure), cast 6/52 inj
Fracture Method Remarks
Clavicle Sling 3/52 Malunion in adults
Physio Excellent remodeling
in children Pulled elbow Sling 3/7 or Pain, lateral
Scapula body: Sling & physio Associated with 1)rib # Supinate + flex elbow tenderness, refusal to
Scapula neck: ORIF if # dislocatn 2)lung contusion move arm
3)hemo/pneumothorax 9m-6yrs
Body # by crushing No X-ray findings
force Radial head slips out
AC subluxatn: Sling ~1/52 & physio Partial dislocatn: AC of annular lig
AC dislocatn: young and active : Arthrodesis, ligaments torn Radius and ulnar Compartment sx, PIN/
3/52 rest, physio Complete dislocation: in adults: ORIF (plates/screws/rods) AIN inj,
Inactive: Sling & physio CC ligaments torn in children: Long arm cast 6/52, check x-ray at delayed/non/mal-
Late OA: excision outer 1/3 clavicle (conoid & trapezoid) 2/52 union, PIN
Tenting of skin may
cause necrosis Single forearm ORIF or long arm cast 12/52 Non-union!
Sternoclavicular Anterior: conservative Post dislocatn: bone Cross-union
dislocatn Posterior: ORIF Tracheal and vascular Monteggia’s: ORIF (ulnar plating, reduce radial Radial/ PIN palsy
compressn head), long arm cast 90o flexion, (Mont), ECU & EDM
Anterior dislocatn: Reduction under GA X-ray to exclude # partial supinatn inj (Gal) myositis
Hippocrates/Kocher’s Axillary n often Galeazzi’s: ORIF (radial plating, reduce ulnar Ossificans, non-union,
Sling 3/52 damaged head), long arm cast in supination missed dislocation
Physio 95% of shoulder 6-8/52
# prox humerus: ORIF dislocatns Both in children: Reduction under GA, immobilisatn
Recurrent: Surgery 6/52
Posterior GA Reductn Commonly missed! Colles’ Undisplaced: Splintage in plaster EPL rupture, malunion,
dislocatn: Same as ant dislocatn 4% of shoulder slab median n
dislocatns Displaced: MUA (Bier’s/ hematoma compression,
Prox humerus: Neers 1: Sling 6/52 Usually seen in block), below elbow backslab 6/52 Sudeck’s atrophy,
Neers 2: Collar cuff 6/52 osteoporotic pple >50y in neutral or slight flexion, xray @ DRUJ subluxatn, hand
Neers 3: ORIF/HemiA Try to conserve head 2/52 shoulder stiffness
Neers 4: HemiA in young pts even with Smith’s (reverse As for Colles’ but with wrist
All followed by physio Neers 3/4 Colles’) extension
Shaft of humerus U-slab 3-6/52 + sling Suspect mets in Barton’s ORIF with buttress plate
If very unstable, plate/nail elderly! Radial styloid/ Percut K-wire/ lag screw A/w lunate dislocatn
Chauffeur’s
Supracondylar Closed reductn ASAP Cx: Shortening,
Undisplaced Below elbow cast (exclude PIPJ) AVN, non-union,
C&C 3/52 then sling 3/52 angular deformity
scaphoid 10/52 scaphoid collapse, OA
ORIF (dbl plating) in adult for early (gunstock), ↓ROM
f(x) Acute: Brachial A inj, Displaced ORIF, cast 3/52
GENTLE physio compartment sx, scaphoid
volkmann’s ischaemia Trans-scaphoid Chronic carpal
Myositis ossificans perilunate instability
Lateral condyle Undisplaced: C&C 3/52 Cubitus valgus, tardy dislocation
Displaced: ORIF (Kwire) ulnar palsy: corrective
osteotomy Peri-lunate Closed reduction, cast 6/52 Median n compression
Proximal radius Mason 1: C&C 3/52, gentle physio dislocation If irreducible, OR with IF of Lunate AVN leading to
in adults: Mason 2: ORIF plate & screw scaphoid # if present, CTR and OA
Mason 3: Excision in 48hrs ligamental + capsular repair
Mason 3 with Essex L: Prosthesis, Metacarpal Undisplaced: Crepe bandage 3/52 Rotational malunion,
splint 2/52, physio and finger exercises stiffness
<20o: C&C 2/52 Displaced: Closed reduction,
>20o: MUA, if fail OR. If unstable, IF plaster slab 3/52, finger exercises
In children: (K-wire) Displaced + unstable: ORIF with K-
Olecranon Stable & undisplaced (<2mm + no wire
change in flexion + extend against Bennet’s (intra- CRIF with precut kwires
grav): C&C 3/52 art # dislocation
Displaced: tension band wiring @ base of CMCJ
Displaced + comminuted: plate & of thumb)
screw Phalangeal Undisplaced: buddy splintage 3/52 Treat open wounds
Elbow dislocation MUA (tractn, flexion, push Posterolateral most Displaced: MUA, plasterslab 3/52 first!!
olecranon) then C&C 3/52 or above common or IF with Kwires
elbow backslab Cx= brachial A, Mallet finger Splinting in extension 6/52
median (AIN)/ulnar,
Game-keeper’s Partial tear: short arm cast w thumb
stiffness, myositis
thumb spica
ossificans, associated
Gross instability: ligamental repair
#s
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Impt Hip & Lower Limb #s and Ds (plus impt tendon ruptures)
Type Treatment Remarks & specific Cxs
Acetabulum, # o minimal displc/ highly frag à Traction, Hamilton-Russell Cxs
o main part intact, fem head displc à ORIF w cancellous o Hemorrhage > 5L
screws & plates o Ruptured urethra, bladder
o Bowel injury
Hip, post. D o Muscle relaxant + Reduce, flex knee, hip 900, correct add Cxs
-- Hip is flexed, add & int rot & int rot, lift fem head into acetabulum o Irreducible due to in-turned labrum
o OR if irreducible or bony frags in acetabulum
o ORIF if a/w #s elsewhere o # (fem head, NOF, patellar, fem
Hip, ant. D shaft)
-- Hip is abd, ext rot o Sciatic nerve palsy
o Muscle relaxant + Reduce, flex knee, hip 900, correct abd o AVN due to tearing of capsule
& ext rot, push down, convert to post. D, lift fem head into o 20 OA
acetabulum o Recurrent D
o Myositis Ossifcans (post
exploration or D a/w head injury)
Fem epiphysis, slipped o IF w screws + Manipulate if slip > 30% + epiphyseal
o AVN
-- fem shaft move up & ext rot on epiphysis closure
o Involvement of Other Hip
o Subtroch Osteotomy if epiphysis closed (chronic)
Neck of Fem (intracap) #
-- shortened, ext rot Tx principles
-- 1. subcapital, 2. transcervical o Young (< 50 y.o.) à CRIF
o Undisplc --> CRIF
-- osteoporosis impt factor o Elderly --> arthroplasty
o Displc --> Arthroplasty
Garden Classification o unfit for multiple Sx or badly displc, typ 4, avn & non-union
o Typ 1: incomplete #, trabeculae angulated likely --> Hemiarthroplasty/ Total hip replacement w/o Cxs
o Typ 2: complete #, trabeculae disrupted tryring CRIF o AVN à disruption of arterial ring
but NOT angulated @ base of neck
o Typ 3: complete #, fem head rotated, o Non-union à typ 3 & 4, bone
trabeculae disturbed, displc graft (young), arthroplasty (elderly)
o Typ 4: complete #, totally displc
Neck of fem, basal (extracap) # o Displc/ Undisplc --> ORIF w DHS or Gamma Nail, fixation Cxs
-- shortened, ext rot not removed unless pat < 45 y.o or pain o AVN & non-union NOT common
Intertroch # o Stable, little frag à DHS w long plate
-- shortened, ext rot o Unstable à DHS w long plate or Gamma Nail, then non- Cxs
Types: weight bear crutches after 48 hrs to 16 weeks o Failure of fixation (cutting out of
o Alt -->Traction +/- Thomas’s splint fixation device) à coxa vara*
1) # line thru mass of Great Troch,
2) (1) + separation of Less Troch,
3) separation of Great & Less Troch, *if early, bedrest & skeletal traction
4) 4. w a spiral # down prox fem shaft
Fem shaft # o Traction to overcome pull of quads & hams
-- leg is shortened, ext rot, abd à due to pull o Intramed Nail
of quds & hams o Alt --> Traction, EF (Ilizarov), Plating
Cxs
o Fem & Tib # à Cx rate high, early mobilisation by o Hypovolemic shock
Intramed Nail o Fat embolism
o Metastatic # à Intramed Nail + packed cement to o Delayed Union, Non-union à
relieve pain & give support esp. conservative
o Fem shaft # w nerve palsy à exploration w repair + IF o Mal-union àlat. Angulation à Tx
o Fem neck & prox shaft # àDHS + long Plate = osteotomy
o Fem shaft & patellar # à close nailing for both, mobilise o Limb Shortening
knee early o Knee stiffness à due to quads
o Open # àderibement + IF tethering, knee jt invovlement or
o Open #, IIIB,C àconservative or EF prolonged immobilisation
Fem Supra, Uni, T & Y condylar # o Child supracondylar à plaster o Infection
o Others à IF for good reduction & permit early
mobilisation
o If displc, grossly comminuted à conservative w traction
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Patellar D o CR, plaster backslab x 3/52, knee exercise Remarks
Patellar # o vertical # --> cylinder cast 6/52 w crutches during first Injuries to patellar & extensor apparatus of
2/52, physio after cast removal knee
o horizontal, undisplc # --> as of above (patellar #, rupture of quads tendon, rupture
o horizontal, displc # --> 1. sight communition: ORIF, 2. of patellar ligament, avulsion of tibial
limited damage to patellar: partial patellectomy, 3. tubercle) due to:
major damage: patellectomy, repair quads insertion &
1) direct force on knee
lateral expansions
2) violent contraction of quads
Every knee injury, exclude:
Tibial tubercle, avulsion o CRIF (w screw)
o ORIF (risk of premature epiphyseal fusion in child) o damage to extensor apparatus
o lateral D of patellar w spontaneous
Quads tendon, rupture o Tendon reattachment, plaster cast, quads exercises at reduction
2nd week, weight bear at 4th week, felxion at 6th week o torn ligaments
Patellar ligament, rupture o As of above o torn mensici
Tibial plateau, # o minimally displc --> aspirate hemarthrosis, compression
o all involve articular surface bandage, CPM & active exercise, weight bear after 6/52 Cxs
o key is to get knee f(x) vs pretty x-ray o comminuted--> aspirate, compression bandage, sk o Compartment syndrome
o knee exercises ASAP traction, CPM & exercise crutches after 6/52 o Valgus deformity
o “bumper #” o depressed # --> CR or ORIF, active exercises ASAP, o Joint stiffness
o commonly lat. tibial condyle cast-brace after 2/52
Tibia & Fibula, # o closed, minimally displc --> full cast x 12/52 (upper thigh Cxs
o Usu. # both, esp. adult to MT necks, knee slight flexion, ankle at 900), exercise
foot, ankle, knee ASAP o Infection
o commonly open
o closed, displc --> MUA (IF when CR fails), full cast x o Vascular injury (prox # damage pop
o usu. spiral # artery)
12/52, exercise ASAP
o comminuted --> EF x 6/52 + partial weight-bear, then o Compartment Syndrome
f(x)al brace o Delayed, Non-union --> Intramed Nail +
o open --> Ab ASAP, debride, clean, leave open (above bone graft indicated
grd II), EF to stabilise, WI, suture or graft when granulate o Malunion --> angulated --> osteotomy
Ankle, ligament injury o partial --> crepe bandage, activity ASAP
o partial/ complete tear of lateral o complete --> plaster immobilisation or operative repair
ligament Cxs
o bruising, swelling, tenderness o Adhesions
o painful passive inversion o Recurrent subluxation
o complete tear --> excessive
movement
Ankle # o 1 mall # --> reduce, cast x 6/52 (below knee), IF with Tx principles
o normally talus seated in mortise screw if frag large o reduce to restore shape of mortise
o one or both mall can be # o 2 mall #, below tibiofibular jt --> CR, +/- IF ,cast o plaster x 8/52
o eversion + ext rot = oblique # of lat o 2 mall #, above tibiofibular jt --> unstable, IF with screw
mall (pushed off), transverse # of for frag & plate for fibula, +/- transverse screws between Cxs
med mall (pulled off); vice-versa for tibia & fibula
o Joint stiffness
inversion o OA (not common)
Distal tibial & fibular epiphyses, #- o Salter-Harris 1,2 --> MUA, full cast x 3/52, below knee Cxs
separation cast x next 3/52
o Mal-union (valgus)
o physeal injury o Salter-Harris 3,4 (undisplc) --> as above, re x-ray 5d
o Asymmetrical growth (# thru epiphysis
after to ensure good reduction
may cause fusion of physis)
o Salter-Harris 3,4 (displc) --> ORIF, below knee cast x
o Shortening of leg
6/52
Calcaneum # o undisplc --> exercise ASAP, bandage after swell Tx principles
o fall from height subside, nwb crutches x 6/52 o elevate leg + ice packs --> decrease
o calcaneum driven up against talus o displc, avulsed tuberosity --> CRIF, immobilise in swelling
o flattened Bohler’s angle equinus (relieve tension of tendon Ach), wb after 6/52 o x-rays, CT scans (better views)
o check hip, pelvis, spine for # o displc, intra-art --> ORIF + bone grafts, splint & elevate,
o extra-art --> involve posterior part, exercises ASAP, nwb crutches after 3/52, wb after 12/52 Cxs
calcaneal processes o Broadening of foot
o intra-art --> oblique # line, run to o Talocalcaneal stiffness --> subtalar
superior articular surface arthrodesis or triple arthrodesis
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Chapter 4: Polytrauma
KEY CONCEPTS
Definition, death, types
LIFE THREATENING CONDITIONS
PRINCIPLES OF MANAGEMENT
SCORING SYSTEMS
LATE COMPLICATIONS
PHYSIOLOGIC RESPONSE TO POLYTRAUMA
Key concepts
Definition of polytrauma
• ????presence of 2 long bones# plus 1 visceral injury OR 2
visceral injuries OR ≥ 3 #
• Injury to >1 physical regions or organ systems where at least 1
injury or a combi of several injuries is life threatening
o In polytrauma patients, limb injuries are the commonest and
this can take the form of long bone # or soft tissue injuries.
However it is the head and visceral injuries that are most lethal.
• Different from multipled injuries – not life threatening – or a severe life-threatening single injury (barytrauma)
Death
• Trimodal pattern
o 1st hr: Cerebral, cardiovascular injury, airway obstruction, external bleeding à most patients die
o 1-4 hs after injury (golden hour – deaths avertable): Hypoxia, hypovoemic shock (uncompensated blood loss)
o Days or weeks after (ICU): Complications of trauma and multiple organ failure à attributed to initial Mx of injury
Types of trauma
• Examples: deceleration trauma, being run over, crush trauma, avulsion trauma, penetrating injury, explosion injury, thermal injury, chemical
injury, radiation injury
Principles of management
General principles in management of orthopaedic injuries in polytrauma
• Management: Primary survey + Secondary survey
• 4 different periods in orthopaedic management of trauma injuries
o Acute or resuscitation period (1-3 hrs after trauma)
§ Decompression of organ cavities (tension pnemothorax, cardiac tamponade)
§ Haemorrhage control
§ If pelvis is fractured, early stabilisation with pelvic clamp is crucial
o Primary or stabilization (of #) period (<24hrs)
§ Decision on temporary and definitive fixation of fractures
§ Limb salvage v.s. amputation (many scoring systems i.e. mangled extremity scores/Hannover fracture scale)
§ Optimal timing of long bone # stabilization in trauma patients in the primary period - Divided into 3 groups of patients:
• 1. Polytrauma without brain and chest injury
o Early stabilization (within 48hrs) does not improve survival but it will benefit some patients (eg. reduces no. of
days of mechanical ventilation etc.) à ?improves morbidity
o Thus it is preferable to perform long bone stabilisation in polytrauma patients
• 2. Brain injury 3. Chest injury
o No evidence that early long bone stabilisation (within 48hrs) improves survival/ morbidity or decreases Cx
compared to late stabilisation
§ All polytrauma patients should preferably undergo early long bone stabilisation (Class II evidence) in the primary period
o Secondary or regeneration period (3-8 days)
§ Continued haemodynamic and resp stability
§ Debridement of soft tissue necrosis
§ Eliminate septic foci
§ Wound closure
§ Joint reconstruction
§ In definitive treatment of #, in order to preserve normal function, there should be
• articular congruity
• stable fixation
• axial alignment with the rest of the extremity
• restoration of full range of motion
o Tertiary or rehabilitation period (>8 days)
§ Patient weaned off intensive care
§ Physiotherapy initiated
§ If patient has developed multiple organ failure, no further operative procedures can be considered at this stage.
16
• Special considerations
o Pelvic #
§ Ensure that there’s no need for general surgical intervention e.g. intra-abdominal or retroperitoneal haemorrhage
§ Haemorrhage control with pelvic packing and temporary stabilisation with ext fixators and pelvic-clamps
o Spine #
§ Urgent spinal stabilisation is required (urgent = within 24 hrs of the injury)
o Long bones #
§ Pts with # shaft of femur can lose up to 1 l of blood. Femoral shaft fractures should undergo immediate stabilization of the
fracture within 24 hours of injury
§ Immediate stabilization of long bone fractures has many advantages in the multiply injured patient, such as improved long-term
function, prevention of DVT and decubitus ulcer, decreased need for analgesia, and reduction in the incidence of adult
respiratory distress syndrome and fat emboli
§ Recommendations for staged treatment of femoral shaft fractures
18
• Tscherne classification for closed fractures and soft tissue injury
o Grade C0: Little or no soft-tissue injury.
o Grade CI: Superficial abrasion (shaded area) and mild to moderately severe fracture configuration.
o Grade CII: Deep, contaminated abrasion with local contusional damage to skin or muscle (shaded area) and moderately severe
fracture configuration.
o Grade CIII: Extensive skin contusion or crushing or muscle destruction (shaded area) and severe fracture.
20
Chapter 5: Open Fractures à EMERGENCY!
DEFINITION: A fracture or its haematoma that communicates with the environment (may not be obvious! Eg. communication w bladder cavity)
Diagnosis
• See bone
• Marrow bleed – fat globules
• When apply pressure
o Skin or subcutaneous bleed will stop for awhile
o Bone bleed will not stop
CLASSIFICATION: Gustilo Anderson (for prognostication and management)
Types Features
Type I Size: Small (<1cm)
Soft tissue injury: Minimal damage, no crush
Contamination: Mild (will not be the case if environment of injury dirty – eg football field); clean puncture (compound from within)
Usually low impact: simple fracture à transverse, short oblique, little comminution
Risk of amputation: 5%
Type II Size: Medium (1-10cm)
Soft tissue injury: Moderate crushing, no flap/avulsion
Contamination: Moderate
Usually low impact: Moderate comminution (eg. butterfly fragment)
Risk of amputation: 10%
Type III Size: >10cm
Soft tissue injury: extensive damage to skin, muscle and neurovasculature
Contamination: Significant
Usually high impact: extensive comminution and instability
IIIA: Adequate soft tissue coverage of bone (muscular coverage adequate; NOT SKIN) despite extensive lacerations/ flaps
Segmental # (# at 2 levels)
Eg. Farm injuries / any injury occurring in a highly-contaminated environment, GSW
Risk of amputation: 20%
IIIB: 1) Inadequate soft tissue coverage 2) Periosteal stripping and exposure of bone 3) Severe comminution
Risk of amputation: 30%
IIIC: Arterial injury which needs repair (major artery) regardless of wound size/soft tissue injury
Prophylactic fasciotomy always done to prevent post-op compartment syndrome
Risk of amputation: >40%
*Note: can only differentiate Grade 3 into a, b and c after formal debridement has been done
EMERGENCY CARE
Approx 30% of patients w open # are polytrauma patients who have suffered damage to 2 or more systems. Manage according to ATLS. Only
manage the # when the patient is stable (In red: for open #s)
1. Primary Survey
a. Stabilise Patient: ABCDE
b. Assess neurovascular status of the limbs (above and below)
i. Control any hemorrhage w direct pressure. Set IV line and start IV fluids
ii. Don’t reduce any # unless there is an apparent neurovascular compromise from the position of #
iii. Dressings and splints that might have been put on at the accident site shld be removed partialy to assess soft tissue conditions
and neuromuscular function. All sterile wound dressings shld be left in place because redressing wounds in the emergency
room increases the infection rate
c. Rule out any other fractures (esp joint above and below) and injuries (visceral, c-spine etc) – remove gross debris (ie. Turf, rocks)
d. Rule out open fracture
i. Closed Fractures: Reduce + Stabilise + Exercise
2. Early Management (Make patient comfortable)
a. Analgesia: 75mg I/M pethidine
b. Splint fracture (one joint above and one joint below): to decrease pain, progression of soft tissue injury, blood loss
3. Proceed with finding out more: Take an AMPLE history + Imaging (XR) + Take photograph (for documentation)
4. Prepare for EOT
a. Start IV Abx (after wound c/s samples are taken) in all open # during the first 3-5 days (empirical NOT prophylactic!)
i. Use broad spectrum Abx: usually Benzylpenicillin + flucloxacillin or 1st gen Cephalosporin
ii. If wound heavily infected (esp GA type 3), add gentamycin +/- metronidazole (flagyl) to cover gram negative and anaerobes,
and monitor for toxicity
b. Tetanus toxoid booster (TTB): 0.5ml
Human anti-tetanus immunoglobulin (HATI): 250 units
Simple wound Tetanus-prone wound
Full course + booster within 10yrs - TTB
Full course + booster 10yrs ago TTB TTB + HATI
Non-immunised / unknown TTB TTB + HATI
c. NBM
d. Must get into OT within 6hrs (golden hrs) since risk of infx increases after this time à done under LA/GA
e. Sterile scrub: use scrubbing brush and scrub the site to debride all necrotic tissues (dead muscle/ fat/ other tissues)
4Cs Dead muscle Live muscle
Consistency Mushy Turgid
Colour Pale pink/ purple Pink/bright red
Contraction when stimulated (most impt) Absent Present
Capillary No bleed when cut Bleeding
21
IRRIGATION AND DEBRIDEMENT (most important steps in treatment of open #)
• Principles of Treatment
o Only now are all the splints and bandages removed à reexamine thoroughly for neurovascular function.
o Wound Debridement (under regional or GA): Remove foreign material and dead tissue, leaving a good blood supply (within
golden period of 6 hours, otherwise the wound is considered infected)
§ Wound margin excision: Just enough to leave healthy skin edges
§ Wound extension: Ensure adequate exposure (including the joint) for inspection of wound site and thorough cleansing (but
must take into account possible need for skin flap)
§ Removal of devitalized tissue: Devitalised tissue provides a nutrient medium for bacteria
• All non-viable, mutilated or macerated skin removed: no bleed when cut, dusky colour
• Fascia is expendable so it can be safely removed without fear of functional deficit.
• Free fragments of bone removed; #ed bone ends must be exposed so they can be cleaned w brushes or removed
§ Nerves and tendons: Leave cut nerves and tendons alone unless wound is clean + no dissection required and necessary
expertise available
• Exposed tendon will not survive for long: early skin coverage, skin grafting or a muscle/skin flap may be necessary to
preserve its viability
o Wound cleansing: Irrigation with saline and removal of foreign material, blood clots and tissue debris
§ Fluids delivered under pressure and under a pulsed system à Repeat irrigation at regular intervals as there is a higher
chance of removing contaminated material
§ Dilute bacterial contamination
o Take wound cultures
22
5. 48hr later
a. “Relook operation”: see if repeat I&D necessary
b. Ensure soft tissue coverage over exposed area by 48th hr – exposed tendon will not survive for long…NEED FLAP!!
WOUND COVERAGE
• Primary closure w immediate suturing: Small, uncontaminated type I wound that is free from contusion
• Leave open for 2 days until dangers of tension & infection have passed (for all other open #) – ideally wound cover w/i 3-5 days
o Principles:
§ Keep moist meanwhile
§ Once wound is clean and tissues are viable, delayed primary closure or skin grafts can be done.
§ Aims of covering wound: 1) Achieve a safe early closure 2) Avoid nosocomial infx 3) Obliterate dead space 4) Facilitate
future reconstruction
o Suture
o Skin graft (no BS): has to achieve a new BS within 2-3 days to ensure viability (graft requires the bed to have good BS)
§ Often used as in intermediary measure before a flap
§ 2 types:
• Split thickness skin graft
o Features
§ Consists of epidermis and part of dermis
§ Taken from inner thigh or lateral buttocks
o Advantages
§ Good for large defects
§ Can tolerate less ideal conditions and less vascularity than full thickness skin graft
§ Multiple grafts may be obtained from same site
o Disadvantages
§ Grafts contract
§ Have poor growth in children
§ Abnormal pigmentation
• Full thickness skin graft
o Features
§ Composed of full thickness of skin
§ Acquired from groin, postauricular, supraclavicular areas
o Advantages: for fresh, small, uncontaminated wounds
o Flap (has own blood supply)
§ Principles:
• Choice of flap coverage must take into account age and needs of patient, location, size and condition of the defect,
likelihood of subsequent reconstructive surgery and associated zone of injury, tissues available for the flap
§ Advantage: Can be used to reconstruct skin and soft tissue defects regardless of their vascularity (but delayed bone or
soft tissue reconstruction is proposed, especially if bone graft or tendon transfer are being planned)
o Eg. Tibia (Common site for open fractures, and has a poor vascular bed)
§ Prox tibia: Gastrocnemius flap
§ Middle tibia: Soleus flap
§ Distal tibia: Free flap, soleus flap
§ 4 types: skin, fasciocutaneous, muscle, musculocutaneous
• 2 kinds of skin grafts:
o Free: tissue with blood supply detached from original location
§ Free microvascular flap is used for large defect.
• Helps prevent multiple reoperations. Provide durable coverage of the # site, diminishes the
infection rate and shortens the healing time. Eg. latissimus dorsi and vertical rectus abdominis.
o Pedicled/ local: tissue left attached to donor site & transposed to new location keeping pedicle intact as a
conduit for blood supply
§ Eg. 1 of the 2 heads of the gastocnemius is used and there must be a functional soleus for lesions
around the knee and proximal third of the tibia
§ Distant vs Regional
• Vacuum Assisted Closure (VAC) Dressing / Negative pressure wound therapy
o Mechanisms
§ Stimulate angiogenesis by stimulating granulation tissue
§ Reduce edema and fluid – expedite healing
§ Reduce size of wound
§ Reduce bacterial count (remove some bacteria, reduce oxygen levels)
o Indications: Diabetic foot, open fractures (act as sterile dressing) large wounds)
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6. 4-6weeks later: bone graft/ transport
MANAGEMENT OF BONE LOSS
• Bone Loss
o Mechanism: Either from initial direct injury or from subsequent repeated debridements
o Any bone replacement methods should only be done after adequate soft tissue coverage and revascularization
o Bone graft
§ Mechanisms
• Osteoinduction (most impt): Undeveloped tissue transformed to bone by inducing agent
• Osteoconduction: Transferred bone acts as scaffold for new bone to grow (+ neovascularization)
• Osteogenesis: New bone formed from live osteoblasts in transplanted autograft
§ Principles
• Cancellous grafts incorporated more quickly and more completely than cortical grafts
• Vascularised grafts are ideal (but technique consuming and requires microsurgery) – lower rate of necrosis
• Autografts > allografts > xenografts
• Reduction of antigenicity in allografts: Freezing, freeze drying, ionizing radiation, demineralization, impregnation of
graft with host marrow
§ Applications
• Vascularised grafts: Exceptional circumstances such as congenital pseudoarthrosis of tibia, non-union of NOF #
• Cortical graft (can fill large gaps): Bone loss due to trauma or tumour
• Cancellous grafts (wide variety of uses): filling cavities, filling spaces due to fracture etc (MANY MANY USES)
o Bone transport: Used for large gaps
§ Ilizarov’s principle of distraction osteogenesis: Controlled gradual distraction gives rise to neovascularisation and new
bone formation between bone surfaces
• Callostasis: Corticotomy or osteotomy to create segment of bone in one of the fracture fragments; fragment moved
gradually (1mm a day) by wires and new bone forms in the gap
o Free composite tissue transfer
§ Example: fibula, which is mainly a cortical bone that provides excellent strength and length for large segmental bony
defects. It is used together with muscle and skin with its pedicle.
7. Then SKIN GRAFT: after swelling subsides; if not, compartment syndrome may occur after grafting
24
§ Infection resulting in infected non-union
• Infected pseudoarthrosis
• Infx especially likely with tissue necrosis (vascular compromise) which acts as a nidus for infection
o Types:
§ A2: torsion wedge, intermediate fragment
§ B2: comminuted, necrotic intermediate fragment
§ C2: defect, loss of fragment of the diaphysis
§ D: atrophic pattern, scar tissue with no osteogenic potential
is replacing the missing fragment)
• Appearance: Penciling of ends, round edges
o Management: Bone graft, open decortications, bone transport or
free composite tissue transfer.
o AVASCULAR NECROSIS *** (refer to “hip”)
• Regional: neurovascular injury, soft tissue blisters, CRPS, heterotrophic ossification, joint stiffness, compartment syndrome
o Neurovascular injury
o Fracture blisters (Soft tissue blisters):
§ Types: hemorrhagic and non-hemorrhagic
• Usually hemorrhagic – indicate deep soft tissue damage
§ Mechanisms of injury: shearing of skin (may become infected if operated on), delamination due to ischemia (can be due to
compartment syndrome)
• Blisters commonly appear in compartment syndrome (but often serous instead of hemorrhagic)
o Complex regional pain syndrome:
§ A chronic pain state induced by
• Soft tissue/ bone injury: CRPS 1 aka reflex sympathetic dystrophy aka Sudeck’s dystrophy
• Nerve injury: CRPS 2 aka causalgia
§ Pathophys: pain is a/w autonomic changes (eg. sweating or vasomotor abnormalities), and/or trophic changes (eg. skin/bone
atrophy, skin loss, joint contractures)
§ Aetiology unknown
§ Rx: no cure; pain relief only
o Heterotrophic ossification
o Joint stiffness
o COMPARTMENT SYNDROME ************ (Orthopaedic emergency!!)
§ Pathology: Increased intracompartmental (muscle and tissue bounded by fascia and bone with little room for expansion like in
forearm, calf) pressure sufficient to occlude microvascular circulation causing ischemia and tissue necrosis
subsequently (most commonly deep posterior)
§ Pathophysiology à decreased blood inflow + outflow
• Tissue injury results in bleeding and edema
• Increased intracompartmental pressure disrupts Starling’s forces
• Compromised perfusion results in further tissue damage
• Further edema and perfusion compromise
• Order of collapse: capillaries à venules à arterioles (last to
collapse because have muscles)
§ Significance:
• Muscle will die within 4-6 hours of ischemia
• May lead to rhabdomyolysis and kidney failure if untreated
• Nerve then undergoes necrosis later
§ Complications
• Volksmann ischemic contracture
• Permanent functional impairment
• Renal failure from release of myoglobin from muscle necrosis
• Death
§ Common Sites: Leg (proximal third of tibia), forearm flexor compartment, hand, foot, elbow
§ Etiology: external restriction of compartment or internal increase in compartment volume
• Trauma – Crush injury, fracture, dislocation, soft tissue damage and muscle swelling à edema and hemorrhage
• Vascular: arterial compromise (post ischemic swelling), muscle anoxia, venous obstruction, increased venous pressure
• Iatrogenic: Tight cast, constrictive dressing, splint
§ Diagnosis
• Clinical (5Ps)
o Lack of oxygenated blood and lack of waste product removal results in pain and decreased peripheral sensation
secondary to nerve irritation
o Early: Pain, Paresthesias, Pallor, Palpable tense swollen compartment, blistering
§ Most important feature is PAIN out of proportion to injury (Other signs are ‘late signs’)
• Not relieved by analgesics
• Increase w passive stretch (stretching of muscles traversing compartment): dorsiflexion of toe for leg
o Late signs: Pulselessness (pulses are usually still present; CRT normal), Paralysis
Anterior leg Volar forearm
Fracture Type Tibial fracture Supracondylar (humerus)
Weakness Toe, foot extension Finger, wrist flexion
Pain Toe, foot flexion Finger, wrist extension
Sensory 1st dorsal web space Volar aspect of fingers
25
• Investigation
o Split Catheter (Compartment pressure monitor): perfusion pressure (difference between diastolic pressure and
intracompartmental pressure) <30mmHg or absolute pressure of >30mmHg
§ Role: Unresponsive patients
§ Normal tissue pressure is abt 0 mmHg
§ Management
• Remove: Cast, constrictive dressings
• Place limb at level of heart
• Bivalve casts down to skin and spread open
• Fasciotomy – Open all 4 compartments with medial and lateral incisions in leg
o Usually indicated when the perfusion pressure falls to <30mmHg (inadequate perfusion and/or ischemia begins) in
a patient who has any signs or symptoms of a compartment syndrome - even if distal pulses still present
o Or indicated if unable to monitor and there is no improvement in clinical signs after 2hrs of splitting the dressings
(examine at 15mins interval)
• Systemic:
o Hypovolemic shock
o Fat embolism
§ Pulmonary: SOB, hypoxemia
§ Neurological: Agitation, delirium, coma
§ Dermatological: Petechial rash (esp chest)
§ Haematological: Anaemia, low platelets
o Venous thromboembolism (DVT/PE) from immobility
o MODS
o ARDS (esp in polytrauma patients)
• Classification by early and late Cx
Early Late
Local Neurovascular injury Malunion
Swelling Nonunion
Compartment syndrome AVN
Infx Post-traumatic arthritis
Implant failure Osteomyelitis
Soft tissue blisters (à infx) Heterotrophic ossification
Growth disturbance in children
Joint instability
Joint stiffness
Nerve compression/ entrapment
Reflex sympathetic dystrophy (RSD)
Systemic Hemorrhagic shock MODS
Sepsis Renal failure
Fat embolism Shocked lung
DVT/PE PTSD, depression
ARDS
26
Chapter 6: Limb threatening conditions
• Vascular Impairment
o Haemorrhage: visible or occult
o Ischaemia: acute interruption of BF to a limb/organ à anaerobic respiration predominates à leading to lactic acidosis and
eventually cell death
o Causes: Dislocations or fractures
o Arteries involved: Axillary, brachial, femoral, popliteal
• Mangled Extremity (refer to “Polytrauma)
• Acute Compartment Syndrome (refer to “Complications of Open fractures)
• Necrotizing Fasciitis
o Insidious soft tissue infection characterized by tissue necrosis
o Organisms spread from subcutaneous tissue along superficial and deep tissue planes, of which the latter causes vascular occlusion,
ischaemia and tissue necrosis.
o Less seen in multiple trauma
o 3 types of NF: Type 1 – Polymicrobial NF
Type 2 – Grp A Strep NF (Flesh-eating bacterial infection)
Type 3 – Gas gangrene
o Presents with fever, chills, erythema and painless bullae formation
o Treatment: antibiotics and surgical debridement
• Gas Gangrene
o Onset: 12-24hrs after injury
o Commonly Clostridial infection, but may be caused by other organisms
o Decreased oxidation reduction potential promotes advance of a highly lethal condition
o Less seen in multiple trauma
o S/S:
§ Present with intense pain and swelling around the wound
§ Associated with a brownish discharge and bronze discolouration of wound
§ Gas (with a musty odour) formation usually not marked
o Important to distinguish from anaerobic cellulitis, which presents with abundant gas formation that is foul smelling in nature
§ Distinction between the two can be made by doing a Gram stain of the exudate
o Management: fluid & electrolyte replacement, antibiotics, multiple incisions & fasciotomy, hyperbaric oxygen
• Osteomyelitis (refer to “Bone and Joint Infections”)
o Infection of bone and bone marrow
o Difficult to treat, can be life threatening as well due to septicaemia
o Routes of spread: haematogenous, contiguous from a focus of infection
o Bacteria can be inoculated at the time of trauma
o Present with fever, headache, vomiting, severe bone pain
o Treatment: antibiotics and extensive debridement of necrotic tissue
27
Shoulder
Atraumatic Traumatic
Fractures
•Clavicle
Frozen
Shoulder
•Scapula
Biceps
•Tendinitis
•Tendon
rupture
Shoulder
Joint
•TB
•OA
•RA
•Milwaukee
Shoulder
Scapula
•Congenital
Elevation
•Klippel-‐Feil
Syndrome
•Winged
Scapula
28
Examination of the Shoulder 2. Power of rotator cuff muscles (0-5):
The preliminaries: Introduce yourself to patient, ask for permission to - Abduction (supraspinatus): lift up arms 90deg in abduction,
forward 30deg in plane of scapula, internal rotate (completely
examine. Ensure adequate exposure (remove shirt; expose shoulders
pronate) both arms, resist downward movement
up to and including scapula) but consider patient modesty also. - Internal rotation (subscapularis) – Gerber’s lift-off test: get
Ensure good lighting, and good positioning of bed. patient to place hands behind back, then examiner presses the
hand against the patient’s back while patient attempts to lift his
4 main parts of shoulder girdle: sternoclavicular joint, hand off. If patient is unable to place hands behind back due to
acromioclavicular jt, glenohumeral jt, scapulothoracic articulation restricted ROM, perform the belly press test, Pt presses palms
against abdomen and keep elbows forward (if there is any
weakness if the subscapularis, the elbow will fall backwards),
LOOK—Front, Side, Back X2
examiner attempts to pull the hand off the abdomen.
1. General appearance and vitals – pallor, BP, and HR. - External rotation (infraspinatus and teres minor) arms tucked at
2. Scars/ sinuses: shoulder, in axilla- ask patient to lift arms the side, actively external rotate arms, push out against
3. Swelling resistance
- Bump(s) over sternoclavicular jt, clavicle, ***Release suddenly to check for counter action (test for muscle tear)
acromioclavicular jt
- Effusion points in the axilla – remember to look
4. Deformity – asymmetry between two shoulders SPECIAL TESTS
- Foreshortening of the shoulder joint indicates previous Supraspinatus impingment tests:
clavicular fracture, acromioclavicular joint problem 1. Neer’s Test: stabilise the scapula/shoulder, pronate/internally
5. Discolouration – redness, bruising, etc rotate arm and passively flex the arm 90deg (holding the
6. Muscle wasting – squaring of shoulders (deltoids); forearm distal to elbow) and look for expression of pain
hollowing of supra- or infraspinous fossa; trapezius 2. Painful arc (between 60 to 120 degrees of passive abduction
classically, greater tuberosity hits acromion & the
FEEL supraspinatus is caught in btwn).
1. Warmth 3. Hawkin’s test – passively flex shoulder and elbow to 90
2. Tenderness and deformities—Palpate in a U-shape degrees then internally rotate the arm; look for expression of
- Start fr SC jt, ballot SC jt, go along clavicle to AC joint, pain
then ballot AC joint Supraspinatus tendonitis:
- Follow back to spine of scapula, and palpate in 1. Jobe’s test (or beer can test) – with arm abducted 90 degrees
supraspinous and infraspinous fossae for tenderness and in neutral rotation, internally rotate the arm, like inverting
- Locate coracoid process anteriorly, palpate that (short a beer can held in the hand.
head of biceps, coracobrachialis) Supraspinatus tear:
- Head of humerus 1. Abduction paradox & Drop-off sign – unable to initiate
- Greater tuberosity (particularly supra/infra-spinatus abduction but passively abducted to more than 90 degrees,
insertion) abduction proceeds by deltoid action. Less than 90 degrees
- Bicipital groove (gently rotate forearm & feel for cord-like of abduction, arm will fall to pt’s side, unable to maintain
structure)– tendon of long head of biceps abduction.
2. Rotator cuff tear: complete and large tear, patient cannot
MOVE actively abduct shoulder but may be able to do so passively
1. Range of movements: w positive drop arm sign when allowed to return to neutral
- Active first; if restriction in ROM, assess passive range – position
differentiates between pain, joint stiffness or muscle Biceps tendinitis (tendon of long head of biceps)
weakness. 1. Speed’s test – with elbow fully extended and forearm
In supraspinatus impingement or tear, passive range is greater supinated, the patient flexes his shoulder against resistance
than active range as active range is limited by pain and/or on the arm; test is positive when there is pain localised to the
bicipital groove.
weakness; limitation is usually only in one movement e.g.
2. Yegarson’s test – with elbow flexed to 90 degrees and
abduction. forearm pronated, patient attempts to supinate forearm
In frozen shoulder, passive and active ROM are equally restricted, against resistance; test is positive when there is pain
and usually in more than one type of movement. localised to the bicipital groove
NOTE: for abduction and flexion, important to fix the scapula. note 3. Popeye’s sign (degenerative rupture of long head of biceps):
the glenohumeral joint mvment; scapulothoracic mvment actively flex elbow to 90deg and resist flexion; look at
compensate for decreased mobility at the glenohumeral joint. prominent muscle belly of biceps muscle.
Stability (glenohumeral joint)
a. Abduction (normal passive: 0-180) (raise both arms to
meet above the head) – also assess “painful arc” of 60 to 1. Anterior apprehension test (anterior dislocation; done for
120 degrees for supraspinatus impingement. suspected cases of shoulder instability) patient seated, stand
b. Adduction (normal P: 0-45) (cross-shoulder – get patient to behind patient and passively abduct shoulder to 90deg and
touch other shoulder with hand, observe how far the hand external rotate the arm, thumb apply pressure anteriorly
can reach). against humerus head and look at patient’s face for
c. Flexion (normal P: 0-180) and extension (normal: 0-?). apprehension or guarding.
d. Internal rotation (normal P: thumb at T4) (place hands Laxity
behind back and see how which level the patient’s 1. Sulcus Sign (inferior glenohumeral instability) patient
extended thumb can reach e.g. inf angle of scapula – T7). standing, grasp arm and pull downwards, depression
e. External rotation (normal P: 0-45) (with elbows tucked between acromion and humeral head.
close to sides and flexed 90 degrees, rotate outwards). Labrum Tear (not necessary)
1. O’Brien’s Test with thumbs down, flex shoulder to 90°, adduct
to 20°. Press and resist should be painful. Thumbs up is
relieving.
FINISH with assessment of neurovascular status of the upper
limb, and examine the cervical spine.
29
IMPORTANT HISTORY TO TAKE FOR SHOULDER PAIN Important features to look out for on shoulder X-ray:
- Duration (time course of frozen shoulder – pain and stiffness for - Narrowing of subacromial space
first 6 months, less pain but persistent stiffness for next 6 to 12 - Bony spur on inferior aspect of acromion or acromioclavicular joint
months, and recovery of joint mobility 18 months after start of - Calcification of supraspinatus tendon (acute calcific tendinitis)
symptoms). - Narrowing of joint spaces esp. glenohumeral joint
- Any preceding trauma (frozen shoulder and rotator cuff tear often - Osseous lesion(s) if any
follow minor precending injury). - Subluxation/dislocation
- Neck vs shoulder pain – shoulder pain may be due to cervical - Bone erosions
pathology; shoulder pain is typically located over the deltoid
insertion and tip of shoulder, not along the trapezius or neck. CAUSES OF SHOULDER PAIN
o Pain on top of shoulder suggests AC or C-spine pathology
- Shooting pains travelling down arm, numbness and/or weakness Tendon (rotator Tendinitis
of hand – indicative of cervical spine pathology or nerve problem. cuff disorders) Rupture
- Pain on lying on shoulder while sleeping. Frozen shoulder
- Function of shoulder (see below). Joint disorders Glenohumeral arthritis
- Diabetes (very important as diabetes is a cause of idiopathic Acromioclavicular arthritis
frozen shoulder). Other structures in jt:
- Heart disease – may result in referred pain to shoulder. subacromial bursitis etc
- Red flags – night pain, worsening pain, constitutional symptoms Referred pain Cervical spondylosis
Cardiac ischaemia
FUNCTIONAL ASSESSMENT IN SHOULDER PROBLEMS Mediastinal pathology
- Ability to reach for objects placed in overhead positions Instability Dislocation
- Ability to comb hair Instability
- Ability to touch opposite shoulder and back (for personal hygiene) Bone lesions Infection
- Ability to wear top e.g. shirt, T-shirt, blouse Neoplasm
Nerve lesions Suprascapular nerve
INVESTIGATIONS: entrapment
- No blood investigations are required usually
- Shoulder X-ray is the most useful invx: need >/= 2 views Think 4 Ss for Shoulder:
o AP, axillary (w arm abducted to see relation of humeral Stiffness: Frozen Shoulder, Post-traumatic/post-surgical stiff shoulder.
head to glenoid) Strength: Rotator cuff tear
- Other Ix: double contrast arthrography, U/S, CT/MRI Stability: TUBS vs AMBRII
Smoothness: Subacromial abrasion Primary degenerative joint
disease, AVNs, Recurrent dislocations, post-surgery arthritis, RA.
CHRONIC TENDINITIS
• Pathology: Chronic vascular response in tendon in response to 1) overuse 2) minor tears 3) impingement (factors above)
• Risk Factors: Adult (40-60)
• Symptoms
o Pain
§ Site: In shoulder and over deltoid
§ Exacerbating: Certain movements/ demanding activities
§ Relieving: NSAIDs and rest
§ Time course: characteristically worse at night; cannot lie on affected side
§ May have Hx of recurrent attacks of subacute tendinitis
§ Pain and stiffness may restrict daily activities
• Signs
o As above in acute tendinitis
o In long standing: Muscle wasting, power loss, restricted movement
• Complications
o Chronic cuff pathology à Subluxation of humeral head upwards à joint incongruity à Osteoarthritis à decreased ROM
o Rotator cuff tears
• Management
31
o Conservative: refer to Mx of acute tendinitis
o Surgical (usually arthroscopic acromioplasty)
§ Subacromial decompression: Excision of coracoacromial ligament and antero-inferior part of acromion
§ Osteotomy of subacromial osteophytes
On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left / right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.
On palpation the clavicle is (non-tender / tender) and there (is / is no) step deformity noted.
The acromioclavicular joint is (non-tender / tender) , the area just anterior to the acromion is also (non-tender / tender) . There is no tenderness
over the bicipital groove.
Active ROM for shoulder flexion is ___ degrees, shoulder extension is ___ degrees.
Patient is unable to initiate abduction of the shoulder but was able to __________________. OR
Patient is able to abduct shoulder from ___ to ___ degrees but this was subsequently limited by pain.
External rotation was ___ degress and patient is able to reach up to T__ with his thumb.
(when testing passive abduction, push on shoulder to prevent scapula from rotating)
I would like to move on to assess the power of the rotator cuff muscle.
There (is / is no) weakness of the (supraspinatus / infraspinatus / teres minor or subscapularis) .
Impingement tests namely Neers and Hawkins tests are (negative / positive) .
My diagnosis is (left / right) (supraspinatus tendonitis / OA of AC joint / partial rotator cuff tear) .
32
• Clinical features
o Patient aged 40-60 years
o Symptoms
§ Aching in the arms and shoulder after trauma, often trivial
§ Pain gradually increases in severity and prevents sleeping on the affected side
§ Subsides after several months with increasing stiffness that continues for 6-12 months
§ Movement is regained gradually but may not return to normal
o Signs: Shoulder appears normal w no/slight wasting; most marked feature is decreased active & passive movement in all directions
Stage 1 (freezing) Pain á with movement, worse at night
2 – 9 months Surgical release contraindicated in this stage – will get recurrence from ongoing inflammation
Stage 2 (frozen) Pain â, with ROM â 50% less (stiffness)
4 – 12 months Surgical release indicated (MUA not recommended, may cause # or labral & cuff tears)
Stage 3 (thawing) Resolution
12 – 18 months
• Differentials (for shoulder stiffness)
o Post traumatic stiffness (stiffness max at start then lessen; without much pain)
o Disuse stiffness
o Regional pain syndrome aka reflex sympathetic dystrophy. Either post acute trauma, MI or stroke.
o Infection
• Investigations
o X-ray:
§ Usually normal (may have decreased bone density in humerus)
§ Useful in excluding ddx of painful shoulder, such as glenohumeral arthritis, infection, post-traumatic stiffness, diffuse stiffness
(eg. due to overly cautious nursing) and reflex sympathetic dystrophy (pain pattern is different anyway)
o Arthrography: contracted joint
• Management
o Conservative: Analgesia (NSAIDs), corticosteroid injections, local heat, exercise
§ Aim of conservative treatment is to relieve pain and prevent further stiffening while waiting for recovery (since natural course is
recovery in 12-18 months)
§ Physiotherapy:
• Repeated circular movement of shoulder
• Assisted abduction – use towel or rope, loop it over an overhead bar like a pulley system, and hold on to each end with
one hand. Patient uses downward pull of normal arm to passively abduct painful arm overhead.
• Assisted internal rotation – both hands gripping either end of a towel slung across the patient’s back diagonally; the hand
on the painful side holds the lower end while the hand on the normal side holds the end above the shoulder. Patient uses
hand on normal side to pull upwards on towel, passively internally rotating the painful shoulder.
• Wall-crawling – patient uses fingers to “crawl” up a wall slowly, increasing flexion movement.
o Surgical:
§ Poorly defined role, only for patients who fail conservative management (no progress for 12 weeks)
§ Manipulation under anesthesia (MUA; gold standard – but not for diabetics, osteoporotics)
• Passive stretching of e capsule while patient is under anaesthesia, but be careful of causing #s especially in the elderly
• Followed immediately by active exercises
§ Arthrosopic capsular release: division of interval between supraspinatus and infraspinatus
• May dramatically improve ROM; must be followed by aggressive physiotherapy post-op
§ Distend the joint by injecting a large volume of sterile saline under pressure
• Prognosis:
o Better in younger patients with post-traumatic frozen shoulder
o Idiopathic frozen shoulders that occur in diabetics tend to recur and not improve.
On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left / right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.
On palpation the clavicle is (non-tender / tender) and there (is / is no) step deformity noted.
The acromioclavicular joint is (non-tender / tender) , the area anterior to the acromion is also (non-tender / tender) . There is no tenderness over
the bicipital groove.
Active ROM for shoulder flexion is ___ degrees, shoulder extension is ___ degrees.
Rom for abduction is ___ and adduction is ___. (limited by pain)
External rotation was ___ degrees and paitnet is able to reach up to T__ with his thumb.
(ER and IR limited in frozen shoulder)
(when testing passive abduction, push on shoulder to prevent scapula from rotating –movment at scapulo thoracic joint vs glenohumeral joint)
Passive ROM was also limited for the above actions.
33
3. Biceps
BICIPITAL TENDINITIS
• Pathology: Inflammation of biceps tendon secondary to rotator cuff impingement due to its proximity to rotator cuffs
o Rarely, presents as an isolated problem in young individuals after a shoulder strain
• Risk Factors
o Young: unaccustomed shoulder strain
o But still commoner in elderly
• Symptoms: Pain and tenderness sharply localized to bicipital groove
• Signs: Speed’s/Yergason’sà pain in bicipital groove
• Management
o Conservative: Rest, heat treatment
o H&L injection if healing is delayed
o Surgery for refractory case or if a/w cuff lesions: anterior acromioplasty
On general inspection, I note a ___ by ___ cm hemispherical swelling over the (left / right) arm. There is no overlying scar or skin changes.
I would like to move on to palpate the lump. (ask pt for any pain first)
The surface of the swelling is smooth, the edges are well defined and it is firm in consistency. It is non-tender and not warm. The overlying skin is
freely mobile.
(attempt resisted biceps flexion)
The lump becomes more prominent with resisted elbow flexion à popeye bulge
Slip sign is negative.
34
• Joint stability
o Rotator cuffs (mainly)
o Glenoid labrum: deepens socket
o Ligaments (weak)
§ Glenohumeral ligaments – inferior, middle, superior (*note that the inferior ligament prevents anterior dislocation of humerus)
§ Transverse humeral ligament, coracohumeral ligament
o Capsule
o à Least supported part of the jt lies in the inferior location where it is unprotected by the muscles
• NOTE: Shoulder laxity is not equivalent to instability!!!
• Recurrent shoulder instability classification
o TUBS: Traumatic, Unilateral (& directional), Bankart lesion (tear in glenoid labrum), Sx
§ Less trauma associated w higher likelihood fo recurrence
o AMBRII: Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior capsular shift, Interval closure
§ Patients have excessive shoulder laxity (capsular & ligamentous) bilaterally (thus instability usually responds to a rehab program)
à often able to voluntarily dislocate and relocate joint (habitual dislocation) + sulcus sign
§ Surgery: rarely indicated; but if necessary it involves tightening of inferior capsule (via inferior capsular shift or interval closure)
• X-Ray views
35
§ Kocher’s method: elbow flexed 90deg ad close to body à arm slowly rotated 75deg laterally à elbow lifted forwards and
adducted à rotate arm medially
• Not recommended due to risk of nerve, vessel and bone injury
o X-ray post-reduction to confirm reduction and exclude fracture
o Check muscle + neurovascular status: Test abduction to rule out axillary nerve injury (deltoid) or rotator cuff tear. Also rule out median,
radial, ulnar and musculocutaneous nerve injuries.
o Arm rested in sling for 1-2 weeks (shorter period for >30yo due to risk of stiffness)
o Abduction and lateral rotation avoided for 3 weeks
ANTERIOR INSTABILITY
• Pathology: Recurrent dislocations or subluxations post acute anterior dislocation w detached/stretched labrum or capsule (50% of patients
<25yo have recurrent dislocation following acute anterior dislocation)
o Most common type of instability (95%)
• Symptoms
o Recurrent dislocations during relatively trivial actions (w increasing ease) esp over arm movements (abduction, extension, external
rotation) such as swimming, dressing, reaching back or upwards à can often reduce the dislocation himself
o Recurrent subluxation: ‘Catching’ sensation followed by numbness or weakness (dead arm syndrome) when attempting to throw a
ball
o ROM full btw episodes of dislocation
• Signs
o Check for generalised ligamentous laxity (treat more aggressively): sulcus sign
o Anterior apprehension sign: examiner lifts the arm into abduction, external rotation and
extension, patient’s body tautens in apprehension when he senses that the humeral head is abt
to slip anteriorly. Repeat test by applying pressure to the front of the shoulder at the same time,
patient will feel more secure now
o Drawer test: scapula is stabilised with one hand while examiner grasps the upper arm with the
other hand to manipulate the head of the humerus forwards and backwards with the patient
supine
o Fulcrum test: patient lies supine and examiner places one hand behind the patient’s shoulder to
lever the humeral head forward by extending and laterally rotating the arm, patient becomes
apprehensive
• Investigations Hill-‐Sachs
Lesion
o X-Ray: AP, lateral, axillary views
§ Hill-Sachs lesion: Depression in posterosuperolateral part of humeral head due to
repeated impact with anterior rim of glenoid (impaction fracture) à May destabilize joint and predispose to further dislocation
• Best seen in AP (w arm internal rotated)
§ Axillary view: subluxation of humeral head toward anterior lip of glenoid
o MR Arthrogram (galodinium dye injected into joint to detect fine cuts)
§ Bankart lesion: Avulsion of anteroinferior glenoid labrum at its attachment to inferior glenohumeral ligament complex
• Management
o Surgery
§ Indications:
• Frequent dislocations (esp if painful)
• Fear of dislocation/subluxation that prevents participation in daily
activity
§ Types:
• Bankart (gold standard) – Repair/ re-attachment of glenoid labrum
• Putti-platt: shorten and tighten anterior capsule and muscles
• Bristow – Reinforcement of anterior-inferior capsule using adjacent
muscles
On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left
/ right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.
This patient has (left / right) shoulder instability that is not complicated by axillary nerve palsy.
I would like to complete the rest of the shoulder examination.
36
o Trauma: direct blow to front of shoulder, fall on flexed and adducted arm, fall on outstretched hand
o Typically a fracture-subluxation instead of a complete dislocation
• Signs
o Arm locked in medial rotation
o Front of shoulder flat; prominent coracoid
• Complications
o Recurrent dislocations (posterior instability)
o Unreduced dislocations: OR in injuries up to 8week old in young
• Investigations
o Xray
§ Axillary view (BEST): can also best see reverse hill sach and posterior labrum tear
§ AP view
• NOTE: may miss dislocation coz humeral head may seem in contact w glenoid
• Possible empty glenoid sign: humeral head appear “away” from glenoid fossa
• Classic electric light bulb appearance (medially rotated humeral head looks
globular/symmetrically bulbous)
§ Lateral view
• Shows posterior subluxation
• Sometimes shows indentation on anterior humeral head
• May have accompanying #s of humeral neck, posterior glenoid rim or lesser
tuberosity
• Management
o Manipulation and reduction: Arm pulled and laterally rotated while head of humerus pushed
forward
o Rest of management as for anterior dislocation Light
bulb
sign
INFERIOR DISLOCATION
• Mechanism of Injury: Humeral head is levered out of its socket (when arm is hyperabducted) and pokes into axilla
• Symptoms: Arm locked in abduction
• Signs: Humeral head may be felt in or below axilla
• Complications
o Severe soft tissue injury
o Avulsion of capsule and surrounding tendons
o Muscle rupture
o Fracture of glenoid or proximal humerus
o Neurovascular injury: Brachial plexus or axillary artery
• Investigations: X-ray à humeral shaft points upwards w head sitting below glenoid
• Management:
o M&R: pull upwards in the line of the abducted arm w counter-traction
downwards over the top of the shoulder
§ Examine for neurovascular damage post-reduction
§ Rest arm in sling for 3 weeks
o Open reduction if above doesn’t work
5. Acromioclavicular Dislocation/Instability
• General Information
o ACJ is the only point of ligamentous attachment to the clavicle and thorax
o Scapula is fixed to clavicle by ACJ and coracoclavicular ligaments
• Mechanism of Injury
o Fall on shoulder à tear ligaments à upward subluxation of clavicle
o Tear of acromioclavicular ligaments (subluxation)
o Accompanying tear of coracoclavicular ligaments (complete
dislocation)
• Symptoms: Pain
• Signs
o Tenderness isolated to site
37
o Prominent ‘step’ deformity (indicative of complete dislocation; absent in subluxation)
– AC ballotment
o Scarf test: Place hand over opposite shoulder and move up; pain localized over AC
joint
• Classification (Rockwood): 5 types depending on ligament, capsule and fracture
involvement
• Complications
o AC Instability: Discomfort and weakness (if unreduced) esp with strenuous
overhead activity
o Rotator cuff tendinitis
o Secondary OA (due to subluxation)
• Investigations
o X-Ray
§ AP, axillary, cephalic tilt views
§ Stress view (stand + hold 5kg weight in each hand): Diff subluxation from dislocation
• Management
o Subluxation: Armsling till pain subsidesà shoulder exercises
o Dislocation (in young with a)prominent clavicle, b)inferior or posterior clavicular dislocation)
§ ORIF + repair torn ligaments (screw inserted downward from clavicle into coracoid process and left for 8 weeks)
On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left / right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also note a step deformity at the AC joint.
On palpation the clavicle is (non-tender / tender) and there (is / is no) step deformity noted.
The acromioclavicular joint is slightly tender with a palpable step deformity, the area just anterior to the acromion is also (tender / non-tender) to
palpation.
There is no tenderness over the bicipital groove.
Diagnosis is that of AC joint dislocation, I would like to complete the rest of the shoulder examination:
Active ROM for shoulder flexion is ___ degrees, shoulder extension is ___ degrees.
Patient is unable to initiate abduction of the shoulder but was able to __________________. OR
Patient is able to abduct shoulder from ___ to ___ degrees but this was subsequently limited by pain.
External rotation was ___ degress and patient is able to reach up to T__ with his thumb.
(when testing passive abduction, push on shoulder to prevent scapula from rotating)
I would like to move on to assess the power of the rotator cuff muscle.
There (is / is no) weakness of the (supraspinatus / infraspinatus / teres minor or subscapularis) .
Impingement tests namely Neers and Hawkins tests are (negative / positive) .
AC JOINT OSTEOARTHRITIS
• Risk factors:
o Middle aged/ elderly
o Trauma or occupational stress
• Symptoms: pain
• Signs
o Tenderness at ACJ
o Pain at extremes of abduction and flexion (shoulder movements unaffected unless shoulder involved)
• Management
o Conservative
o Surgery: excision of lateral end of clavicle
38
CLAVICLE FRACTURES
• Generally heal with minimal treatment; but recent studies show up to 15% don’t heal well
• Site: Usually at junction between middle and lateral third
o Bone transits from tube to flat area
o Lack of muscle attachment (medial has SCM, lateral has deltoid)
o Little cancellous bone
• Surgery is indicated if
o Neurovascular compromise
§ Subclavian artery
§ Brachial plexus
o Open fractures
o Risk of open fractures (eg tented skin –impending perforation of soft tissue)
o Multiple fractures/injuries
§ Easier for nursing and rehab (eg femur fracture hard to use crutches if clavicle fracture)
o Polytrauma
o Failure of conservative management
o Mal/nonunion
o Floating shoulder (unhingement of shoulder from axial skeleton)
§ Scapula fracture + clavicle fracture
o Significant displacement/shortening/ angulation > 20 degrees
o Lateral third fractures (weight of arm + possible tears of coracoclavicular ligaments cause certain degree of displacement à affect
function)
• Management
o Conservative: Arm sling, clavicle brace
o Surgery (internal fixation)
§ May damage supraclavicular nerve (numbness or neuromas) in openly invasive techniques
§ Hook plate (for distal third #): Hook placed under acromion to hold fragment down à must eventually remove due to
impingement
• Complications
o Early (rare)
§ Damage to vital structures – pneumothorax, subclavian arteries, brachial plexus
o Late
§ Non-union (often in displaced lateral 3rd fractures)
§ Malunion (lump often disappears with time)
§ Shoulder stiffness
STERNOCLAVICULAR DISLOCATIONS
• High risk injury because (IMPINGEMENT ON MEDIASTINAL FRACTURES)
o Trachea, Esophagus, aorta
• Side impact (because of obliquity of joint)
• Management
o Push shoulders out (reduction) OR
o Clamp clavicle and pull it out
ACROMIOCLAVICULAR BURSA
On inspection, I note a ___ by ___ cm hemispherical swelling over the (left / right) shoulder.
There is no overlying scar or skin changes.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.
I would like to move on to palpate the lump. (ask pt for any pain first)
(determine if mass is arising from AC joint with palpation)
The mass seems to be arising from the AC joint. The surface of the swelling is smooth, the edges are well defined and it is tense. It is non-
tender and not warm. The overlying skin is freely mobile and it is superficial to the muscle.
The swelling (is / is not) transilluminable and it is slightly compressible and fluctuant. There is no punctum seen.
39
Humerus
Fractures
Proximal Humerus
40
1. Proximal Humerus***
• MOI: FOOSH resulting in fracture of surgical neck +/- one or both tuberosities
o Usually occurs after middle age: most common in osteoporotic post-
menopausal women
§ In elderly:
• Transverse fracture extend across surgical neck often with
greater tuberosity involvement
• Shaft usually impacted into head in abducted position
§ In young: FOOSH usually causes dislocation in younger patients
but proximal end may be broken into several pieces
o Proximal humerus fractures in children
§ In children, the physis can separate or there can be metaphyseal
fractures, considerable displacement and angulation is acceptable
§ Fractures may be pathological as proximal humerus is a common
site of bone cysts and tumors in children
• Fractures due to bone cyst: rest the arm in a sling for 4-6 wks
• Risk Factors: Adult (after middle age), Osteoporosis
• Symptoms: Pain (may not be severe as fracture firmly impacted), Large bruise in upper arm
• Complications
o Immediate:
§ Neurovascular injury:
• Axillary nerve (most common)– Test regimental badge area as testing deltoids might be painful
• Bachial plexus injury
• Brachial artery injury
§ Shoulder dislocation
o Late: Stiffness, AVN of humeral head associated with anatomical neck fractures (10% of 3-part #; 20% of 4-part #), Malunion w loss
of rotation
• Investigations: X-rays
o AP: Single impacted fracture extending across surgical neck in elderly, fragments more clearly separated in younger patients
o Obtain axillary and Y-scapular lateral views to exclude shoulder dislocation
o Inf subluxation of the femoral head as fracture heals
• Management
o GENERALLY DON’T NEED OPERATION
§ Reasons: Extra-articular + Healing good at humerus as in plane of movement
§ Recommended management (conservative)
• Send patient home with collar and cuff (not arm sling) and analgesia
• Allow gravity to assist reduction of fragments (will gradually occur as patient relaxes fr initial holding of arm close to body)
§ M&R often don’t work well as patient holds arm close to body
o Based on Neer’s classification (distinguishes btw no of displaced fragments which is defined as >45deg angulation or 1cm separation)
*Note: Number of parts refer to number of significant parts (i.e shaft, head, lesser and greater tub) and not gross number of parts
One part No matter how many fracture Rest with arm in collar and cuff (6 weeks)
lines there are, as long as they Active exercises once fracture unites (usu aft 6wks)
are undisplaced or firmly Cause few problems
impacted, considered as 1 part
Two part 1 fragment displaced (surgical - Closed reduction, collar and cuff for 4wks
neck/greater - IF if reduction fails or fracture unstable after reduction
tuberosity/anatomical neck) - Anatomical neck: in young patients, M&R with screw fixation; in older patients,
hemiarthroplasty due to risk of AVN of humeral head (rare)
- Surgical neck or greater tuberosity fractures: M&R à arm bandaged to chest (3-4
weeks) à active exercises
- For 2-part fracture dislocations, closed reduction usu possible
- Fracture of the greater tuberosity may be a/w ant dislocation of shoulder while
fracture of the lesser tuberosity a/w post dislocation
Three part 2 fragments are displaced, usu - Young: ORIF with plates and screws
head (# along surgical neck) and - Elderly (with osteoporosis): M&R à physiotherapy
greater tuberosity - 3 part fracture dislocation requires ORIF, at risk of brachial plexus injury
Four part All the major parts are displaced - A/w poor outcome, high risk of vascular injury, brachial plexus damage, injuries of
(surgical neck + both chest wall
tuberosities) - Usu needs Prosthetic replacement (reserved for elderly) - Hemiarthroplasty (esp
in elderly) due to risks of incomplete reduction, non-union, AVN of humeral head
Fracture- 2-part, 3-part or 4-part fracture- Treat as above according to number of parts
dislocation dislocation
41
2. Shaft of Humerus***
• Mechanism of Injury
o FOOSH twisting humerus causing spiral fracture
o RTA: Fall on elbow with arm abducted, hinging the bone à oblique or transverse fracture
o Direct blow to arm causing transverse or comminuted fracture
o NOTE: in elderly, fracture may be due to mets
• Symptoms: Pain, Bruise, Swelling
• Signs: Displacement of fragments depends on relation of site of fracture to insertion of deltoid
o If # line proximal to deltoid insertion, prox fragment adducted by pec major, lats dorsi, teres major while distal fragment abducted by
deltoids
o If # line distal to deltoid insertion, prox fragment abducted by deltoid and distal fragment pulled proximally by biceps and triceps
• Complications
o Immediate:
§ Brachial artery injury (dx w arteriography)
§ Radial nerve injury in spiral groove on posterior surface of humerus under the cover of the
triceps (nerve seldom divided in closed injuries hence to rush to operate; usually heals in 3mths)
• Patient presents with wrist drop and paralysis of the MCP extensors; common with oblique
fractures at the junction of the middle and distal 1/3 of bones
o Common in Holstein Lewis fracture (oblique) where nerve may become
entrapped in fracture site if attempt to reduce (hence must do open reduction) –
lateral sided spike; lower third #
• Function can be restored by tendon transfer in neurotmesis
• Test nerve before and after treatment: MCPJ extension, wrist extension (ECRL may be
supplied by branch prox to fracture)
o Late:
§ Delayed/Non/Mal-union: common in conservatively managed patients
§ Joint stiffness
• Investigations: XR to look for tumours in elderly as fractures may be pathological
• Management: Usually conservative Holstein
Lewis
Fracture
o Conservative normally: U-slab (over tip of shoulder) or functional brace + collar and cuff + exercises
(but avoid abduction until fracture heals)
§ Most heal readily; weight of arm with external cast enough to pull fragments together. Hanging cast is applied from shoulder to
wrist with elbow flexed and forearm is suspended by a sling ard patient’s neck
§ Spiral fractures unite in abt 6wks while other fractures take 4-6wks longer
o ORIF with plate and screws or intramedullary nail with locking screws
§ Indications: Pathological #s, open #, polytrauma, segmental #, floating elbow (radius and ulnar + humerus fractures), vascular
injuries, radial nerve palsy after M&R, non-union, displaced intra-articular extension
§ Cx rate after IF of humerus high (compression plate, screws, intramedullary nail, external fixation)
o External fixation for open fractures
SUPRACONDYLAR FRACTURE **
• Fractures in distal 1/3 of humerus proximal to trochlea and capitulum
• Background:
o “In Singapore, the typical child who has a supracondylar # is a 7yo falling
off a monkey bar with his non-dominant hand”
o One of the commonest # in children; Most common # in KKH requiring Sx
o Mechanism of Injury
§ Hyperextension injury due to FOOSH: Posterior displacement and
inward twist of distal fragment as forearm usually in pronation
(most common) à proximal fragment can poke into the soft tissue
anteriorly, injuring the brachial artery or median nerve
§ Ant displacement of dist fragment (rare): Due to over-reduction of
post displacement or due to direct trauma w joint in flexion
§ Weakest point in olecranon fossa
• Symptoms: Pain over elbow
• Signs: Elbow swelling, S-deformity of elbow (in posterior displacement)
o Assess neurovascular status
• DDx: elbow dislocation (equilateral triangle by epicondyles and olecranon is disrupted)
• Complications
o Early
§ Median nerve injury, esp anterior interosseous branch (loss of function usually temporary; recovery expected in 6-8/52)
§ Arterial obstruction: Brachial artery injury/ kinking by proximal fragment è compartment syndrome, Volkmann’s ischemic
contracture (irreversible contracture of flexor muscles of the hand due to ischemic processes in the forearm)
• Symptoms 5Ps: pain, pallor, paresthesia, paralysis, perishingly cold, swelling, bruising
§ Compartment syndrome: pain + 1 positive sign [pain on passive extension of the fingers, tense and tender forearn,
pulselessness, blunted sensation, increased capillary refill time], KIV angiography, vessel graft, forearm fasciotomy
§ Ulnar nerve: damaged by careless pinning
o Late
§ Malunion: uncorrected angulation and internal rotation of distal
fragment may lead to cubitus varus deformity (gunstock deformity;
may cause ulnar tunnel syndrome); rarely valgus (may cause late ulnar
n. palsy)
• Disability is slight: increased extension but reduced flexion
• Conservative Rx OR supracondylar corrective osteotomy for jt
malalignment
§ Stiffness of elbow joint
§ Myositis ossificans
• Investigations
o X-ray: AP + lat (# best seen on lateral view)
§ # line across distal humerus, posterior tilt/displacement of distal
fragment +/- medial or lateral displacement
§ Fat pad sign in undisplaced fracture: elevated anterior lucency/ visible posterior Fat
Pad
Sign
3 Completely displaced w no cortical Closed reduction and percutaneous pinning (CRPP): Fixation:
contact à increased risk of M&R under GA + held by percutaneous K wires - Fix w elbow at greatest angle of
neurovascular injury or circulatory Indications for open reduction: flexion possible w/o
compromise due to swelling (i) closed reduction fails compromising circulation
• Brachial artery (pulseless (ii) open fracture (check radial pulse)
hand) and median nerve (iii) vascular damage present - Never apply a complete plaster
may kink (NOT rupture) OR due to risk of swelling
• Presents as a pulseless Continuous traction through a screw in the olecranon Remanipulation if reduction is poor
hand or skin traction with the elbow almost straight and - No more than 2
• Ulnar n usually not affected the arm in a small Thomas splint (Dunlop traction) remanipulations due to risk of
(if affected, usually • Indications for continuous traction swelling. Employ continuous
iatrogenic) o Fracture severely displaced and cannot traction instead
be reduced by manipulation - K-wires and plaster backslab
o Severe injuries / multiple injuries may be used for unstable #s
o With elbow flexed at 100deg pulse
obliterated
+
Support: collar and cuff for 3weeks + sling for
another 3 wks to avoid extension, but flexion allowed
Rx Undisplaced #
ORIF Posterior slab with elbow flexed almost 90 deg
Check x-rays 1/52 after injury
Displaced#
ORIF, elbow held at 90 deg with arm in a sling, healing occurs by 12wks
Skeletal traction may be considered for severely comminuted #
Elbow replacement in the elderly
Complications
Early-1.Vascular injury
2.Median n. or ulnar n. damage
Late- 1. Elbow stiffness
2. Heterotopic ossification
Fractures
(Proximal)
• Radial
head
/
neck
• Olecranon
Process
• Radius
and
Ulna
• Radius
OR
ulna
• Monteggia
fracture
• Galeazzi
fracture
Fractures
(Distal)
• Colles'
fracture
• Smith's
fracture
• Radial
styloid
process
• Barton's
fracture
• Comminuted
intra-‐articular
fractures
in
young
adutls
• Distal
forearm
fractures
in
children
46
Examination of the elbow Ligaments:
The preliminaries: Introduce yourself to patient, ask for permission to Lateral collateral lig attached by apex to the lateral epicondyle and
examine. Ensure adequate exposure of entire UL, remove all base to annular lig of radius
accessories. Medial collateral lig attached to medial epicondyle to medial margins of
LOOK: olecranon and coronoid process
1. Ask patient to flex shoulders and extend elbows to look for obvious
deformities: eg. cubitus varus/valgus; comment on carrying angle if no Nerve supply: branch from median, ulnar, musculocutaneous, radial n.
deformity
2. Ask patient to flex elbows to look at region of olecranon: obvious Movements:
deformities, lumps & bumps Flexionàbrachialis, biceps brachii, brachioradialis, pronator teres; in
PALPATION: flexion, the bony points form the boundaries of an equilateral triangle
1. Feel for lateral epicondyle and palpate for tenderness (MUST do for Extensionà triceps, anconeus; in extension, the med and lat
tennis elbow) epicodyles and top of the olecranon are in a straight line
2. Feel for radial head (can be located by gently supinating and
pronating the forearm as it moves under the palpating fingers) Relations:
3. Feel for medial epicondyle and along cubital tunnel (where ulnar Antà brachialis, biceps tendon, median n., brachial artery
nerve is) Postà triceps, small bursa
4. Feel olecranon for any obvious swelling, bursa, gouty tophi Medàulnar n. passes behind the med epicondyle and crosses medial
ligament of the jt
MOVE: move both arms tgt to allow comparison Latà common extensor tendon, supinator
1. Flexion & Extension
2. Supination Forearm normally slightly in valgus in relation to the upper arm,
3. Pronation average carrying angle in children being abt 15 degrees.
In children, the secondary ossific centres can be seen on x-rays. The
SPECIAL TESTS average ages at which the ossific centres appear are ‘CRITOE’
1. Provocative tests for lateral epicondylitis: fully extend elbow, C apitulum-2yrs
pronate forearm and actively extend wrist against resistance à pain R adial head- 4yrs
at lateral epicondyle shld be increased I nternal(medial) epicondyle-6yrs
2. Provocative tests for medial epicondylitis: fully extend elbow, Trochlea-8yrs
supinate forearm and actively flex wrist against resistance à pain at O lecranon-10yrs
medial epicondyle shld be increased E xternal(lateral) epicondyle-12yrs
47
1. Atraumatic
TENNIS ELBOW (LATERAL EPICONDYLITIS/ GOLFER’S ELBOW (MEDIAL EPICONDYLITIS)
• Pathology:
o Tennis elbow: minor trauma or repetitive strain on common tendon of origin of wrist extensors attached to lateral humeral epicondyle/
chronic tendinitis and fibrosis of origin of ECRB
o Golfer’s elbow: minor trauma or repetitive strain on common tendon of origin of wrist flexors attached to medial humeral epicondyle
• Risk Factors: Occupational stress/ unaccustomed activity (painter, carpenter, cook etc)
• Symptoms
o Pain
§ Site: latera/medial epicondylar pain (radiates widely in severe cases)
§ Aggravated by shaking hands, pouring tea, opening doors
§ Pain on active wrist extension w a straight elbow (tennis elbow)
o NORMAL ROM
• Signs
o Elbow looks normal, full and painless flexion and extension
o Tenderness
§ Tennis elbow
• Just below lateral epicondyle
• Pain reproduced by
o Actively extending wrist against resistance
o Passively flexing wrist (stretch common extensor tendon)
§ Golfer’s elbow
• Just below medial epicondyle
• Pain reproduced by passive extension of wrist
• Management
o Mild: rest, exercise (straighten elbow and flex wrist), lifestyle modification
o Moderate: Corticosteroid and local anaesthetic (H&L)
o Severe (symptoms recur): Surgery to detach common tendon on lateral side of elbow from origin at humeral epicondyle, lengthen
tendon (ECRB), excision of fibrous mass, extra-corporal shockwave
CUBITUS VALGUS
• Cause: non-union of # lateral condyle (a/w bony knob on medial elbow)
o Results ∵ medial condyle grows more than lateral condyle
• Mx:
o Undisplaced – backslab
o Moderate displacement – closed reduction and backslab
o Unstable – K-wire and cast
o Rotated – Open reduction and K-wire
o X-ray weekly to detect slipping
• Treat early if getting more and more valgus. If the child is asymptomatic, elbow not worse, monitor and watch.
• Cx: Tardy ulnar nerve palsy – manage by transposing ulnar nerve anterior to elbow (so that no longer tented up) or osteotomy
OLECRANON BURSITIS
• Causes: pressure, friction, infxn, gout (a/w tophi), RA (a/w polyarthritis & SQ nodules over the olecranon)
Olecranon bursa
There is a __ x __ cm hemispherical mass over the olecranon. The overlying skin is thickened, shiny, white and cracked (from repeated rubbing).
There are no signs of erythema or any scars noted.
I would like to move on to palpate the mass. (ask pt for any pain first)
The mass is smooth, with an indistinct edge and a soft and spongy consistency. It is neither warm nor tender.
It is fluctuant and transilluminates (may not if wall of bursa is thick or there is small amt of fluid).
It is immobile and fixed to the underlying structure + / - fixed to the overlying skin.
There may be underlying skeletal abnormality (e.g. exostosis, deformed joint), thus bursa develop to ease movement of skin over the skeletal
abnormality. I would like to complete the examination by examining the contralateral limb for symmetrical lesions, the joint for joint disease and
skeletal abnormalities.
DDx: olecranon bursa / synovitis / RA nodule / gout
Cx: bursitis (inflamed from repeated trauma / RA / gout / haematogenous infection)
48
2. Dislocations
ELBOW DISLOCATION (commoner in adults)
• Mechanism of Injury:
o (90%) FOOSH w elbow in extension à forearm bones dislocated posteriorly or posteolaterally (lateral shift may occur)
o (10%) Side swipe injury (driver w elbow out of the window) causes forward dislocation usu a/w # and severe soft tissue damage
• Symptoms: Pain and swelling (marked if very severe)
• Signs
o Deformity; displacement of bony landmarks
o Patient supports forearm with elbow in slight flexion
• Complications
o Early: considerable soft tissue disruption and possible neurovascular injury
§ Vascular injury: brachial artery (emergency)
§ Nerve injury: median, ulnar nerves (spontaneous recovery in 6-8weeks usually)
o Late
§ Recurrent dislocation if there is a large coronoid #, radial head # or olecranon process #
• Reduction usually stable and recurrent dislocation unlikely if there are no associated #
§ Elbow stiffness
§ Unreduced dislocation: can attempt M&R till 3weeks after injury
§ Heterotopic ossification, myositis ossificans (soft tissue ossification)
• Associated with forceful reduction and excess passive movement of elbow
• Signs: excessive pain, tenderness, tardy recovery of active movements
• Management: splint until pain subsides, then resume movements; NSAIDs; excise bone once it is mature if bone mass
markedly restricts movement
§ Secondary osteoarthritis
• Investigations: X-Ray to confirm dislocation and exclude fracture (esp medial epicondyle, lat condyle, coronoid, radial head and neck,
olecranon process in rare ant dislocations)
• Management
o For uncomplicated dislocation: M&R under anaesthesia
§ Administer anaesthesiaà slightly flex elbow and apply traction on forearm to correct lateral displacementà further flex elbow
and push olecranon forward à check neurovascular status à check XR
§ Week 0: Arm rested in light cast with elbow flexed just above 90deg and wrist supported in collar and cuff
Week 1: Cast is removed, gentle exercises
Week 3: collar and cuff removed
o For fracture dislocation
§ Internal fixation
§ Side swipe injuries: repair vascular damage, skeletal stabilisation
§ Hinged external fixator used if elbow remains unstable after anatomical restoration to maintain mobility while tissues heal
PULLED ELBOW
• MOI: pull on the arm with forearm pronated, causing subluxation of annular ligament over head of radius into radiocapitella joint.
o Usually affects a child btw 2-3yrs
• No x-ray findings
• Treatment: Supinate then flex the elbow, ligament pops back in place
OLECRANON FRACTURE
• Mechanism of Injury:
o Direct blow or fall on elbow à comminuted fracture
o Avulsion by contraction of triceps when patient falls on hand à clean transverse fracture
• Signs and symptoms
o Comminuted fracture: graze, bruise
o Transverse fracture: palpable gap, inability to extend elbow against gravity
49
• Investigations: X-ray (lateral view) à check position of radial head as it may be dislocated
• Management
o For comminuted fracture (commonly in elderly): treat as bruise and rest in sling for 1/52 as immobilization can lead to
stiffness in elderly; review XR
o For undisplaced transverse fracture: immobilize at 60deg in cast for 2-3/52
o For displaced transverse fracture: ORIF w cancellous screw fixation/ tension band wiring
• Complications
o Early: transient ulnar nerve palsy
o Late:
§ Joint stiffness, secondary OA
§ Non-union (treat via internal fixation and bone graft)
Fracture Management
Undisplaced (hairline/ marginal): vertical split in -Support elbow in collar and cuff or light compression bandage and
the radial head sling (+ backslab if pain severe) for 3 weeks
-Encourage active movements
-LA injection and aspiration of hematoma
Fracture dislocation Reduction and fixation; need to restore radial pillar à then treat
according to Type II or Type III
50
o Children (radial neck fracture)
Fracture Management
Radial head tilt of <30deg and up to 3mm -Rest in collar and cuff
transverse displacement -Exercises after 1 week
Radial head displacement >30deg -M&R + K-wire if unstable: Extend elbow and apply traction and varus
(>20deg in adults) force (or pronate and supinate and apply pressure when prominent part of
radial head presents) à push radial fragment into position
-(if above fails) Open reduction (no int fixation) then splint in 90deg flexion
for 1-2 weeksà then encourage movements
***NOTE: never excise radial head in children, will interfere with
synchronous growth of radius and ulna
Seen 1 week after injury -Untreated/ only with light splintage
51
• Complications: below Cx + common Cx above
o Neurovascular injuries: Radial nerve, median nerve, tardy ulnar nerve palsy (Rx: transposition of ulnar nerve), brachial artery
o Unreduced dislocation (diagnosis missed or dislocation imperfectly reduced)
§ Radial head remains dislocated, limiting elbow flexion
§ Children: no treatment until end of growth
§ Adults: operative reduction, or radial head excision
• Investigations: X-Ray (lateral)
o Fractured prox 3rd of ulna
o Radial head lies in a plane anterior to capitulum (normally radial head points directly to capitulum)
• Management (principle: restore length of fractured bone then reduce dislocation)
o Children: M&R + plaster cast (good remodeling potential)
o Adults/ children with displaced fractures:
§ Try M&R (reduce ulnar # by pulling along longitudinal axis of forearm and pushing radial head back into joint and fixed w plate
and screws)à radial head usually reduces after ulna is fixedà open reduction if radial head doesn’t reduce, or unstable.
§ Plaster cast in 90deg flexion and supination
§ If elbow is stable, mobilize in 10days; if unsure, immobilize arm in plaster with elbow flexed for 6 weeks
o Malunion and non-union
52
• Bier’s block: exsanguinationà pneumatic tourniquets to retain agentà inject IV lignocaine à tourniquet is
depressurized to restore circulation
o Need to have: monitoring equipment for lignocaine toxicity, assistant, and cast trolley with cast prepared
• Axillary block: inject local anaesthesia in close proximity to brachial plexus
• Or GA
2. Manipulation and reduction
• Indications: displaced, deformity or angulation present, joint line in lateral XR
tilted >/=10deg posteriorly
• Method:
o Exaggerate deformity (disimpact and address dorsal translation):
apply traction in line of forearm w countertractiion applied by assistant to
flexed elbow
o Traction (address shortening): maintain traction w elbow extended
o Volar tilt (address dorsal angulation)
o Ulnar tilt (address radial deviation)
• Post-manipulation:
o X-ray to check position
o Check circulation and assess swelling à complete plaster if swelling is
minimal
3. Dorsal plaster slab from just below elbow to metacarpal necks, 2/3 around
circumference of wristà held by crepe bandage: Wrist in pronation, slight ulnar
deviation, slight palmar flexion à final moulding w pressure over posteriorlat
aspect of distal fragment
4. Post reduction:
• Elevate arm for 1-2days and start shoulder, elbow and finger exercises asap
• X-ray 10days later to check reduction
• Remove back-slab after 5 weeks and begin exercises
o Comminuted and unstable Colles’ fracture
§ Same as above but with percutaneous K-wire fixationà remove plaster and wires after 5 weeks and begin exercises
§ For very unstable fractures: external fixation (prox pins through radius, distal pins through shaft of 2nd metacarpal)
• Complications
o Early
§ Circulatory impairment
§ Carpal tunnel syndrome from swelling in carpal tunnel: most common Cx
§ TFCC injury from RUJ subluxation
§ Associated scaphoid #
§ Comminution of radial fragment
o Late
§ Malunion (treatment not necessary but can be corrected by osteotomy): radial drift of distal fragment
§ Ligament injuries around wrist: pain and weakness persist even after fracture healed
§ Tendon injury: frayed EPL may rupture weeks after (require tendon transfer with an extensor tendon of index finger)
§ Joint stiffness: shoulders and fingers
§ Complex regional pain syndrome: Pain, tenderness, trophic skin changes, vasomotor instability & osteoporosis of finger joints
if exercises are neglected, due to sympathetic overactivity - swelling, erythema, warmth, changing to cyanosis with blotchy, cold
& sweaty skin, stiff hand
• Mx: physioRx, rest & splintage for pain, chemical sympathetic blockade if severe
53
DISTAL FOREARM FRACTURES IN CHILDREN (JUVENILE COLLE’S #)
• Mechanism of injury: FOOSH with wrist in extension, resulting in distal radial physis fracture or metaphyseal greenstick/buckle fracture +
dorsal displacement of distal fragment
• Symptoms: Pain and swelling around wrist
• Signs: Dinner fork deformity
• Complications
o Early
§ Compartment syndrome: hence avoid over-forceful or repeated manipulations, split plaster, elevate arm for 1-2days, encourage
exercise
o Late
§ Malunion: uncommon in children <10yrs old; deformity up to 30deg will straighten with remodeling over next 5 yrs
§ Radioulnar discrepancy: premature fusion of radial epiphysisà bone length discrepancy
• Investigations
o X-ray
§ Physeal injuries: Salter-Harris 1 or 2 with dorsal and radial displacement and angulation of epiphysis
§ Metaphyseal injuries: 3 types
1. Buckling of cortex
2. Greenstick fractures with angulation
3. Complete fractures with displacement and shortening
§ NOTE: ulnar may be bent though not fractured if only radius is fractured
• Management
Fracture Management
Physeal -M&R under anaesthesia
-Immobilize with full length cast with wrist slightly flexed and ulnar deviated
and elbow at 90deg for 4 weeks
NIGHTSTICK INJURY
• Isolated fracture of the ulnar with minimal displacement.
• MOI: Holding up arm to protect face from blow
• Rule out fracture clinically and radiographically
• Rx: Below elbow cast for 6 wks for distal one-third #. If angulation of proximal two-thirds severe, consider ORIF.
54
Wrist
&
Hand
Atraumatic
Traumatic
Nerve
Fractures
• Median
• Scaphoid
• Ulnar
• Ulnar
side
wrist
injuries
• Radial
• Metacarpals
• Bennett's
fracture-‐subluxation
• Phalanges
Acute Infection
55
APPROACH TO THE HAND EXAMINATION: LOOK (forearm, wrist, hand)
Start off with a quick screen – expose both hands up to elbow, look at Observe hands palmar & dorsal surfaces
the plantar aspect with hands open, then ask patient to close hand, 1. Scars
then look at the dorsal aspect 2. Swellings: Lumps and bumps on the hand
- Tenderness (infx/inflamm; neuromas may feel
uncomfortable)
By this time you should have ascertained the problem:
- Site, size, shape, borders, surface
1. A lump - Overlying skin changes (eg. red & indurated in inflamm,
2. Deformity – arthritis hyperpigmentation may be due to previous therapeutic
3. Nerve palsy procedures like steroid injection)
- Consistency: 3 types
Approach to nerve palsies: • Soft may indicate soft tissue origin like lipoma or
1. Which nerve is involved? nerve tumours
2. What level is the nerve involved? • Firm may indicate cystic or fluid filled lump
3. What is the cause? which has undergone solidification
• Hard may indicate chronic inflamm like
Ulnar nerve dequervian tenosynovitis where tendon sheath
Look: Claw hand underwent changes or origin from bone)
Wasting of the first dorsal interosseous, guttering - Fluctuance (fluid filled lumps; test by holding lump w thumb
Test: Abduction of index finger (first dorsal interosseous) and index finger and use other finger to press lump
perpendicularly; positive if examining thumb and index
Adduction (cross the first two fingers)
fingers are displaced outwards)
FDP of the little finger - Slip sign (to test if lump is isolated and mobile)
Froment’s sign - Compressability (for soft or firm lumps; lump flattens and is
Sensation to little finger, hypothenar eminence restored upon release of pressure)
Site of lesion: FDP and sensation to hypothenar lost in elbow - Blanching of hyperpigmented area on compression and
lesion, preserved in lesion at wrist refilling when pressure is released indicates that swelling is
Cause: Carrying angle of elbow vascular in origin
- Transilluminability (requires torch to be in contact w the
Lacerations over medial aspect of elbow
lump; fluid or other light-porous contents; negative despite
Thickened ulnar nerve initial suspicion if content replaced by hematoma, bleeding
Ulnar nerve subluxation into ganglion cyst or other non light porous contents)
- Mobility (if lump is attached to tendon, moves along tendon
Median nerve course in active movement and can move perpendicular to
Look: Wasting of thenar eminence the course passively)
Test: FPB (abducting thumb) - Increase (superficial to muscle) or decrease (intramuscular
lump) in size with flexion (muscle contraction)
FDP and FPL (making OK sign)
- Attachment to overlying skin and surrounding structures
FDS (flexion of PIPJ) - Tinnels sign elicted from lump (neuromas; sensation of
Sensation to index finger, thenar eminence tingling distal to lump and in the area of distribution of the
Site of lesion: Carpal tunnel spares thenar sensation, FDP, FPL, sensory nerve)
FDS but affects FPB; AIN lesion hits FDP, FPL; - Common DDx of any lump: ganglion (most common lump of
high lesion loses all hand/wrist), PVNS (2nd most common), implantation dermoid,
pyogenic granuloma
Cause: Tinel’s and Phalen’s at carpal tunnel
- Common sites for ganglions: dorsal radial wrist, dorsal distal
IP jt, volar radial wrist, volar distal thumb (A1 pulleys of
Radial nerve fingers)
Look: Finger drop with or without wrist drop - Common sites for PVNS: synovial line tissues (over finger jts,
Test: EPL (retropulsion of thumb) hand tendons)
Extension of fingers (ED) 3. Sinuses
Extension of wrist (ECR, ECU) 4. Deformity (elbow, wrist, fingers, distal radioulnar jt)
Loss of hand cascade (little finger is most flexed, index finger
Extension of elbow (triceps brachii)
least flexed, in resting position of hand)
Sensation over first web space
- Joint contractures if any
Site of lesion: PIN lesion will cause finger drop but not wrist drop
- Dinner fork deformity
and no sensory loss; spiral groove injury will cause - Rheumatoid features:
wrist drop and sensory loss • Elbow: swelling, deformity, subluxation of radius
Cause: Humeral neck fracture most common • Wrist: synovial/bony swelling, prominenece of
ulnar head, volar subluxation of carpus,
Examination of the Hand radial/ulnar deviation of wrist à Any deformity
at wrist must be tested to see if reducible
The preliminaries: Introduce yourself to patient, ask for permission to
§ Caput ulnar syndrome has prominent
examine. Ensure adequate exposure beyond elbows, remove all ulnar head: piano key sign done by
accessories. Ensure good lighting, and good positioning by placing supporting distal radius and using
patient’s hands on a pillow. thumb to depress ulnar head à +ve
The focus of hand examination is the 5 different tissues in the when ulnar head reduced on
pressure and returns to a dorsally
hand – (1) Skin and subcutaneous tissue; (2) Muscle and
subluxed position when pressure
tendon; (3) Blood vessels; (4) Nerves; and (5) Bones and joints. released
Note which tissue(s) the pathology lies in. • MPJs: MP jt ulnar deviation, synovial/bony
swelling, MP volar subluxation/dislocation
(proximal phalanx volar to MP heads) à ulnar
56
deviation may be chronic and must test if – assesses proximal and distal radioulnar joint, and biceps
reduction can be achieved action. Flex elbows to look at elbow and dorsum of forearm.
• Fingers: boutonneire or swan-neck deformity 2. Quick Nerve Screening
• Thumb: carpometacarpal jt swelling or - Median: Oppose thumb to little finger
subluxation, Z deformity (boutonneire or swan- - Ulnar: Cross index & middle finger
neck type) - Radial: Thumbs up sign
• Movement: full flexion of fingers (decreased 3. Assessment of active and passive range of movements
ROM, subluxation of extensor tendons where - If active range of movements < passive range of movements,
tendons appear on ulnar aspect of MP jt), pinch there is muscle weakness (nerve palsy), tendon rupture, or
fingertips, extend fingers (extension lag may be tendon adhesion to surrounding tissue.
due to loss of tendon function like rupture of - If passive range of movement is restricted, there is joint
extensor tendon, contracture of MP jt, contracture.
subluxation/ dislocation of MP jt) - Symmetry of movements is a useful guide to whether there is
• Synovitis common on wrist which appears as abnormality.
soft to firm lump that is not well defined NERVE TESTING: median + ulnar + radial
• Offer to examine rest of MSK, including 3 impt functions: SENSORY, MOTOR, and AUTONOMIC
shoulder, hip & knees esp C-spine (esp impt if - Sensory: pinprick sensation over area supplied by nerve; most
planning for sx) sensitive testing is using 2 point discrimination.
• Look for assoc nerve pathology: wasting of - Motor: Power of muscle(s) supplied by nerve.
muscles due to nerve pathologies (w typical - Autonomic: Skin warmth, dryness. Use a plastic pen and rub over
pattern of deficits) or due to disuse atrophy finger supplied by that nerve; normally there should be feeling of
- OA features (elbow, wrist, MP jts usually not significantly friction, but if autonomic supply is lost the pen will slide smoothly
involved): over the skin.
• PIP jts: radial/ulnar deviation, bouchard nodes
• DIP jts: Heberdens nodes, mallet deformities VASCULAR EXAMINATION
(due to laxity of extensor tendons), radial/ulnar - Colour of the skin (pink, or dusky, or pale)
deviation - Pulses
• Thumb: swelling and subluxation of - Capillary refill (should be <2 seconds)
carpometacarpal jts (do standard PE for every - Temperature
swelling found), laxity of carpometacarpal jt, - Tissue turgor
grinding test (may elicit pain) - Allen’s test (hand; test patency of palmar arch which is the
• Movement: Fully extend and flex fingers communication btw radial and ulnar artery): Get patient to clench
(decreased ROM with or without pain in fist tightly, place fingers of each hand on radial and ulnar arteries
extremes of motion) respectively, then get patient to squeeze hand 5-6 times to drain
- Tendinopathy: venous blood, then get patient to open hand and examiner
• Trigger digits releases one hand, noting the time that is required for the hand to
• DeQuervain tenosynovitis: Tenderness and hard turn pink. Then release the other side to allow hand to reperfuse,
swelling over first dorsal compartment of wrist and repeat for the other artery.
5. Discolouration, skin changes - Allen’s test (finger): Bend finger tightly. Same concept.
6. Muscle wasting
- Forearm OTHER TESTS (consider wrist examination steps)
- Thenar eminence, hypothenar eminence Finklestein’s test – for DeQuervain’s tenosynovitis
- Wasting of the interossei à guttering - Pt closes fist with thumb tucked into clenched fingers.
FEEL - Holding arm outstretched with forearm in neutral rotation i.e. thumb
1. Temperature facing upwards, patient is told to ulnar deviate the wrist.
2. Tenderness over: - Positive test is when there is pain localised to the radial styloid
- Anatomical snuffbox – base (scaphoid); borders (EPL, APL, region (1st dorsal compartment)
EPB) - Finklestein’s is a very sensitive test for DeQuervain’s.
- Distal radio-ulnar joint – check for subluxation (piano-key - Tinel’s test: tap on radial nerve along its course (anterior forearm
sign) up to spiral groove) à +ve when there are shooting pains along
- Lister’s tubercle on dorsum of distal radius - scapholunate course of radial nerve (up to the sensory ss of the hand)
junction is just distal to this landmark
- Radial and ulnar styloids FINISH with examination of the cervical spine.
3. Feel joints of hands for:
- Tenderness
- Nodules
- Joint line irregularity
- Subluxation
MOVEMENTS
1. Quick screening tests
- With forearm supinated (palms face-up), get patient to fully
flex fingers and extend – tests patency of flexor tendons
and nerves. à median nerve (eg. Benediction sign), trigger
fingers, jt pathology that prevents full ROM etc
- With forearm pronated (dorsum face-up) and wrist
extended, observe for any wrist and/or finger drop, then get
patient to fully flex fingers and extend – tests patency of
ECRB, ECRL and ECU for wrist, EDC for the MCP joints,
intrinsics for the PIP and DIP joints. à radial nerve
- With elbows tucked in close to patient’s sides, get patient
to pronate and supinate forearm to check range of movement
57
General Information
• 6 Tissues of Hand: Skin, Joints, Bone, Nerve, Vessel, Muscle/Tendon
Lumps § Ganglion § Haemangiomas
§ Pigmented villonodular synovitis (PVNS) § Pseudoaneurysms
§ Implantation dermoid cyst § SCC
§ OA – Heberden’s & Bouchard’s nodes § Glomus tumours
Joint § RA hands § OA hands
Vascular § Hemangiomas
Nerve § Ulnar n palsy § Radiculopathies
§ Median n palsy § Erb’s palsy (C5-6)
§ Radial n palsy § Klumpke palsy (C8-T1)
§ Carpal tunnel syndrome
Muscle / § de Quervain’s dz § Trigger finger
tendon § Tenosynovitis § Dupuytren’s contracture
§ RA – Swan neck & Boutonniere deformities, tendon rupture § Mallet finger
Bones § Colles’ # § Boxer’s #
§ Smith’s # § Scaphoid dislocation
§ Scarphoid # § Lunate dislocation
§ Bennett’s # § Gamekeeper’s thumb
Painful Wrist Painful Hand
Referred Cervical spondylosis Neck
Shoulder
Mediastinum
Joint RA RA
OA OA
Infection
Periarticular De Quervain Carpal tunnel
Tenosynovitis Tenosynovitis
Instability Infection
• Pathology: Trauma, Infection, Inflammation, Degeneration, Tumour
• Anatomy of Finger Tip
o Nail bed + Nail plate
§ Sterile matrix (pink part)
§ Germinal matrix (small white area): where nail growth primarily takes place
o Terminology
§ Eponychium – proximal fold
§ Paronychium – lateral nail fold (border tissue around nail)
§ Hyponychium – epithelium beneath nail btwn free edge of skin nail and skin
§ Lunula – white semicircle
• Dorsal vs Palmar skin
o Palmar:
§ No pilosebaceous system
§ Exocrine sweat glands
§ Thick dermis
§ Tough and resistant to pressure
§ Anchored to fascia by fibrous tracts
o Dorsal:
§ Pilosebaceous system
§ Thin epidermis, dermis
§ Loose connection with deeper planes: supple, mobile, stretchable
§ Hence all swellings shows up on dorsal hand 1st (even if problem on volar side)
• Flexor tendon sheath
o 5 annular pulleys
o 3 cruciate pulleys
o Palmar aponeurosis
o Thumb = 2A + oblique pulley
o A2 and 4 most important
o A1 in trigger finger
• X-ray
o AP View: alignment of carpal bones in Gilula lines (carpal arc)
§ Some lovers try positions that they cannot handle: (lateral to medial)
scaphoid lunate triquetrium pisiform trapezium trapezoid capitate hamate
o Lateral view: Radius, lunate, capitate, 3rd metacarpal in one straight line
• Other Imaging Modalities
o CT: Articular and carpal bone #s, Tumours
o MRI: Soft tissue injury, Kienbocks’ disease, scaphoid #, tumours
o Arthroscopy: Wrist (carpal instability, TFCC tears)
• Position for Immobilisation: Intrinsic plus position (MCPJ in flexion & PIPJ in extension)
o Stretch collateral ligaments for MCPJ
o Stretch fibrous part of volar plate of IPJ
• Congenital Deficiency: Too little (absence and hypoplasia), Too many (duplications), Undifferentiated (syndactyly)
58
• H&L (hydrocortisone and lignocaine) injections:
o Common hand indications (ReaCTeD): RA, CTS, Trigger finger, De Quervain’s tenosynovitis
o Up to 2 injections on the same digit (interval of >/= 3 months)
o General notes on H&L:
§ Can H&L everything except plantar fascitis and archilles tendonitis
§ SEs of H&L include:
• Hypopigmentation of the skin } particularly if too much steroid
• Depression in the skin due to lipoatrophy } injected into space and spills over
• Infx: generally takes quite long for the onset (at least a few weeks compared to after other procedures) because steroid
is anti-inflammatory and hence body takes very long to mount a response against the infx. One common cause of infx is
from introduction of skin micro-organisms and hence good skin preparation is required.
• Tendon rupture: steroids can weaken the tendon. This SE is not so common
except if the doctor moves in and out of the tendon too much and damage the
tendon. This is also a SE only related more commonly to multiple injections.
• Can hit the nerve: in the case of De Quervain’s disease, can get neuroma. This
is because the radial nerve here is purely sensory and no motor components
and hence no radial nerve palsy will be seen. The neuroma is painful and feels
like a electric shock when touched.
• Zones of the hand:
o Zone 2 is no man’s land
o Return of function is difficult in Zone 1 due to short stump of FDP
• Wallerian degeneration: degeneration of axons distal to site of transection (resorbed by phagocytes)
• Seddon’s classification
o Neuropraxia (mildest form of nerve injury)
§ Mechanism: Mechanical pressure causing segmental demyelination (interruption in
conduction of impulse down nerve fiber w axonal continuity conserved) à
likely a biochemical lesion caused by concussion/ shock-like injuries to e
fibres
§ Effect:
• Recovery takes place w/o Wallerian degeneration
• Temporary loss of function reversible within hrs to mths of the injury
(mean is 6-8wks; not the 1mm/day rule)
• Often greater involvement of motor than sensory w autonomic fx retained
§ Recovery: Within few days or weeks
§ Example: Saturday night palsy
o Axonotmesis
§ Mechanism: loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue
framework of the nerve à usually the result of a more severe crush or contusion than neuropraxia
§ Effect:
• Loss in both motor and sensory
fx is more complete than in
neuropraxia
• Small extent of wallerian degen
§ Recovery:
• Axonal regeneration begins
within hours of nerve damage
• Eventually axonal processes join
to end organs in weeks,
resuming function
§ Example: Nerve injury after closed #s
or dislocations
o Neurotmesis
§ Mechanism: Destruction of endoneural
tubes with subsequent scarring
impairing regenerating axons from
entering distal segment to reach target
organs à occurs on severe
contusions, stretch, lacerations
§ Recovery:
• Regenerating fibers mingle with proliferating Schwann cells and fibroblasts to form a neuroma at site of injury
• New axons fail to reach target audience or fail to become myelinated, hence function impaired
• Surgical repair essential and quality of recovery always imperfect.
§ For neurotmesis is better to use a new, more complete Sunderland system
• Sunderland system
o First-degree: "Seddon’s neuropraxia"
o Second-degree: "Seddon’s axonotmesis"
o Third-degree: endoneurium disruptured, epineurium & perineurium intact
§ Thus, when the axons regenerate, they may enter an incorrect nerve sheath, resulting in abnormal regeneration.
§ Accompanying e loss of e nerve sheath is intraneural scarring, which further obstructs axonal regrowth thru the site of injury.
§ Recovery may range from poor to complete and depends on degree of intrafascicular fibrosis;
o Fourth-degree: interruption of all neural and supporting elements; epineurium intact; the nerve is usually enlarged.
o Fifth-degree: complete transection with loss of continuity. Grade V corresponds to Seddon's classification of a neurotmesis lesion
59
1. Nerve
GENERAL INFORMATION
• Assess the following components • Extrinsic: ganglion
o Neurological: Sensory, Motor, Autonomic o Metabolic: Diabetes – peripheral neuropathy
o Muscle wasting o Degenerative: OA around elbow (cubital tunnel
o Deformities impingement)
o Special Tests • Investigations
• Quick screen o Nerve conduction study
o Sensory o EMG (electromyography) – inclusive of neuromuscular
§ Radial – Over dorsum of first web space junction
§ Ulnar – Over tip of little finger o X-ray (previous injuries may lead to nerve lesions)
§ Median – Over tip of thumb
o Motor
§ Radial – Thumbs up
§ Ulnar – Criss cross fingers
§ Median – Abduction of thumb
§ AIN – O sign
• After determining neurological problem, move on to make
pathological diagnosis:
o Inspect: Scars, injuries, deformities (valgus)
o Palpate along course of nerve Nerve Site of entrapment Provocative test
§ Thickened nerve Brachial Supra/infra- Arm elevation
§ Lump plexus clavicular Pressure btw scalene muscles
o Move Radial Distal forearm Forearm pronation + wrist ulnar
§ Range of motion: may be affected in OA nerve deviation
§ Eg. Look for subluxation of ulnar nerve during Pressure over tendinous junction of
movement ECT and brachioradialis
o Provocative Tests: Eg. Phalen’s Ulnar Cubital tunnel Elbow flexion + pressure on cubital
• Causes of nerve lesions nerve tunnel region
o Trauma Guyon canal Pressure at guyons canal
§ Acute – fracture, dislocation Median Proximal forearm Forearm supination + pressure on
§ Chronic – Tardy ulnar nerve (cubitus valgus) nerve pronator teres
o Infection – leprosy (thickening of nerves) Carpal tunnel Wrist flexion and/or extension w
o Compression pressure proximal to carpal tunnel
§ Tumour
• Intrinsic: neurileimoma (schwanomma)
MEDIAN NERVE
• Sensory supply:
o Palmar surface of radial 3½ digits and corresponding area
of palm, over thenar eminence
o Palmar cutaneous branch to thenar eminence is given off
before carpal tunnel, thus no loss of sensation over the
thenar eminence. Unless high median nerve palsy.
o Test tip of index and middle fingers and thumb, and thenar
eminence
• Motor supply:
o AIN (2 ½): FPL, PQ, radial ½ of FDP
o Median nerve proper (5 ½): FDS, PT, FCR, PL, L1, L2
o Recurrent motor branch (3): thenar muscles (APB, OP,
FPB)
o General steps: clench fist & test power of FPL (benediction
sign) à Test FDS à Test radial 3 FDP à OK
o Intrinsics –Test abductor pollicis brevis (APB) by fixing 4
digits to the table and getting patient to abduct thumb (in a
plane perpendicular to the plane of the palm) against
resistance à elicit abduction and look for belly of APB.
The APB is the thenar muscle that is solely supplied by the
median n. 99% of the time; the other two muscles may
receive cross-supply from the ulnar n.
o Anterior interosseous nerve supplies FPL, pronator
quadratus and radial half of FDP
§ Testing FDP: Fix middle phalanx of index finger and
get patient to flex the DIPJ
§ Testing FPL: Flexion of the IP joint of the thumb
while fixing the proximal phalanx
§ OK sign: Ask patient to make an “OK” sign by
forming a circle with the thumb and index finger; this
action involves flexion of DIPJ of index finger and IPJ
of thumb, so if there is anterior interosseous nerve
palsy these two joints are extended (like holding a
60
needle) and the OK sign cannot be made properly. The FDS is still intact, however, since the patient is able to flex his PIPJ of
the index finger.
o Testing the FDS and its tendons (supplied by median nerve proper): Fix the distal phalanges of the fingers adjacent to the finger
being tested, and get patient to flex the PIP joint of the finger being tested.
• Others
o Tinel’s sign: tap over proximal edge of the palm (carpal tunnel). Positive sign is when there is shooting pain and numbness radiating
towards the radial 3.5 digits.
o Compression test: apply direct pressure over carpel tunnel w thumb up to 1 min (numbness can be elicited after 30s in severe
cases). +ve when numbness over radial 3.5 digits is reproduced by this test.
o Phalen’s test: examiner’s thumb is placed over the carpal tunnel and patient’s wrist is flexed for up to 1 min (numbness can be
elicited after 30s in severe cases) or ask patient to put dorsal surfaces of hands together and fully flex wrist. Positive when numbness
over radial 3.5 digits is reproduced by this test.
• High lesion (pronator tunnel syndrome, forearm fractures, elbow dislocation, elbow – ligament of Struthers)
o Carpal tunnel (carpal tunnel syndrome, #, dislocations abt the wrist)
o Deformity/ sign: Benediction sign (or median claw) on flexion; *note: middle finger can still flex slightly despite lack of median
innervation because small, ring and middle finger share a common FDP body
o Posture: Loss of thumb abduction
o Wasting of flexor pronator mass, thenar eminence
o Motor:
§ Long Flexors: Paralysis of long flexors to thumb, index, middle finger (both FDS and FDP knocked out)
§ Intrinsics: Loss of opposition and abduction of thumb
o Sensory: lateral 3.5 fingers, over thenar eminence
• Anterior interosseous nerve lesion (trauma at elbow or forearm, usually at origin of deep head of pronator teres)
o Motor: flexor pollicis longus, pronator quadratus, radial half of FDP
o Deformity/sign:
§ Benediction Sign: Usually partial (some flexion of index; but still absence of flexion at thumb IPJ)
§ Inability to produce O sign (inability to flex DIPJ of index and IPJ of thumb)
• NOTE: In median high lesions, failure of producing O sign is even greater due to loss of thumb abd (not affected in AIN)
o Sensory loss: none (AIN has no cutaneous innervation but has articular proprioception)
• Low Lesions (Carpal tunnel syndrome, cut at wrist, carpal dislocations)
o Wasting of thenar eminence (Opponens pollicis, abductor pollicis brevis, flexor pollicis brevis)
o Posture: Loss of thumb abduction
o Motor: lack of ability to abduct and oppose thumb
o Sensory loss: lateral 3.5 fingers on volar aspect up till nail bed (skin over thenar eminence not affected as palmar cutaneous
branch spared)
o Special tests:
§ Tinel’s test
§ Compression test
§ Phalen’s test
§ Strength testing of abductor pollicis brevis (palmar abduction)
• Muscles supplied by median nerve (flexors of forearm less FCU and ulnar 2 FDP + LOAF): pronator teres, flexor carpi radialis, palmaris
longus, FDS, lateral 2 FDP, flexor pollicis longus, pronator quadratus, thenar muscles, 1st and 2nd lumbricals
61
• History
o Presentation
§ Sensory
• Burning pain & Parasthesia over lateral 3.5 fingers (often on flexion): GRASPING ACTIVITY like reading newspaper,
driving, on phone
• Usually night pain that wakes patient from sleep and relieved by hanging arm over side of bed or shaking arm
§ Motor: Weakness: Incoordination of finger movement, poor grip
o Associated Conditions
o Ruling out differentials: Neck pain
• Physical Examination: Refer above for signs
o Look: Thenar wasting, Loss of abduction posture of thumb (autonomic innervations by median nerve)
o Feel: Dryness region of supply, sensory test
o Move: Test thumb abduction (APB), FDS and FDP (working), wrist extension (rule out C6)
o Special tests: Phalen’s, Compression/Durkan’s test (more specific but less sensitive), Tinel’s test
• Investigation: Nerve conduction studies (TRO other differentials), EMG
• Differentials
o Cervical nerve root lesion (neck pain, other suggestive neurological deficits; cervical spondylosis of C6-7 lvls or secondary to cervical
disc herniation)
o Thoracic outlet syndrome
§ Background:
• Lower trunk of brachial plexus n subclavian artery pass btw the ant n middle scalene muscles and over the 1st rib.
• Compression maybe due to cervical rib (rare), fibrous bands or abnormalities of scalene attachments, pancoast tumour
§ S/S
• Typically woman in her 30s complains of pain n paresthesia extending down from her shoulder down the ulnar aspect of
her arm to the medial two fingers
• Worse at night, agg by bracing shoulders or raising arms above shoulder height
• Symptoms increase with increasing age as shoulders sag
o AIN syndrome: entrapment usually at the origin of the deep head of pronator teres; ss FPL, pronator quadratus and radial side of
FDP à inability to make OK sign but sensory INTACT
o Pronator syndrome: compression of median n by ligament of Struthers (fibrous band arising from medial epicondyle of humerus,
attaches to supratrochlear spur on the lower anterior humerus), pronator teres muscle or proximal arch of FDS
• Management
o Conservative
§ Lifestyle modification: Reduce repetitive activity
§ Occupational therapy: Splint wrist in neutral position (esp at night; help with night pain or pregnancy related symptoms)
§ Supplements: Vitamin B complex
§ Pharmacological: NSAIDs
o H&L injection just proximal to carpal tunnel
o Surgery (Carpal Tunnel Release) – Division of transverse carpal ligament
§ Open/ Endoscopic
§ Complications
• Scar –hypertrophic/ keloid, scar tenderness
• Failure of relief – Incomplete division of flexor retinaculum
• Nerve injury – palmar cut branch of median n (lies supf to flexor retinaculum) and motor branch of thenar (usually leaves
the radial side of median n towards distal extent of the standard incision) à risk of nerve injury can be decreased by
making the skin incision on the ulnar side of the palmar crease
Patient is a (age) (gentleman / lady) . Sensation was intact over the radial side of the left palm but decreased
On inspection, both hands are in the normal resting position with the over the radial 3 ½ digits.
forearm supinated and the wrist extended. The MCP and IP joints are
flexed, more pronounced in the little finger and less in the index finger. Tinel’s was positive over the ventral aspect of the proximal wrist.
I note wasting of the thenar eminence of the left hand, in addition there My diagnosis will be a severe left median nerve palsy secondary to
is a ___ cm scar over the transverse carpal ligament of the right hand carpal tunnel syndrome. I would like to complete the examination by
signifying possible previous carpal tunnel release of the right hand. doing a neck examination to rule out cervical spondylosis which could
have resulted in radiculopathy that may mimic the symptoms of CTS.
Abduction of the left thumb was weak (power: ___) but power of the
long flexors of the thumb and index finger was full on testing of flexion
of the DIP joint of the index finger.
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ULNAR NERVE
• Sensory supply
o Dorsal and palmar surfaces of ulnar 1½ fingers and
corresponding areas of palm and dorsum of hand
o Cutaneous branch to the dorsum of the hand is given
off before the wrist, so there is sparing of sensation
over that area in an ulnar nerve lesion at the wrist.
o Test the little finger, over the hypothenar eminence,
and over medial side of the dorsum.
• Motor supply
o Ulnar nerve proper (1 ½): FDP, FCU
§ Loss leads to wasting on medial side
o Deep motor branch (15 ½): hypothenar muscles
(AbDM, FDMB, ODM), interossei, 2 medial lumbricals,
adductor pollicis, deep head of FPB
§ 1st sign of loss in hand is usually wasting of the
1st dorsal interossesous muscle (hollowing of 1st
web space)
o Intrinsics
§ Test palmar interossei – cross index & middle
§ Test dorsal interosseous – abduction of the
index finger against resistance. (Not necessary)
§ Test Abductor Digiti Minimi (ADM) – Abduct
fingers and push both little fingers to each other
§ Froment’s sign – get pt to hold a piece of paper
between thumb and radial border of the hand.
This tests action of adductor pollicis. Pt with
paralysis of this muscle the will compensate by
flexing the thumb (FPL median n). Compare to
normal side.
§ Wartenburg sign – ask patient to hold fingers
adducted & extended; the little finger will
become abducted as the adduction ability of the
intrinsics is lost, and the extension action of the
extensor digiti minimi (EDM) pulls the little finger
into abduction.
o FDP of the ring and little finger: hold middle phalanx of
finger and get patient to flex the DIP joint of the finger.
• Other tests:
o Tinel’s sign: tap along the course of the ulnar nerve as
it runs behind medial epicondyle; if patient has had
operation to anteriorly transpose ulnar nerve, then tap anterior to the medial epicondyle. Positive when there are shooting pains
along the course of the ulnar nerve.
o Ulnar nerve subluxation: place a finger on the ulnar nerve and slowly passively flex patient’s elbow, feeling for anterior subluxation
of the ulnar nerve; may fully flex elbow and leave finger on ulnar nerve for 30-60s to test if there is an increase in numbness
• High lesion – Majority
o Common sites of lesion: Cubital tunnel, elbow #s, ulnar subluxation, medial epicondyle (ulnar neuritis from local friction, pressure
or stretching (eg. cubitus valgus), distal to elbow (compression as it passes btw 2 heads of FCU), brachial plexus (trauma, tumour)
o Ulnar tunnel syndrome (ganglion, hook of hamate fracture)
o Wasting: guttering btwn metacarpals, 1st dorsal interossei wasting, hypothenar eminence, adductor pollicis
§ & hypothenar + 1st dorsal interosseous wasting + guttering btw MP & valgus/varus deformity of elbow
o Motor: poor finger abduction, inability to cross fingers (Earle and Vlastou’s), weak FDP of little and ring finger
o Sensory loss: volar and dorsal aspect of medial 1.5 fingers
o Tinel’s + posterior to medial epicondyle
o Deformity/Sign:
§ Minimal clawing: Less clawing as medial half of FDP no longer working to facilitate clawing
§ Wartenberg sign: Ulnar deviation of little finger in extension due to unopposed action of extensor digiti minimi which insertion
is slightly medial(only in extension; must ask patient to keep fingers together)
§ Radial deviation of wrist on flexion (Unopposed FCR)
o Management
§ Anterotransposition
§ Cubital tunnel release (if compression at cubital tunnel)
o History: Repetitive activity (gym), osteoarthritis, history of #
• Low lesion
o Common site of lesion: Wrist (lacerations, occupational trauma, guyon’s canal, pressure from deep ganglion)
o Wasting: intrinsic muscle wasting (as above)
o Motor: Medial FDP function normal, but poor finger abduction and poor thumb adduction (difficult to pinch)
o Sensory loss: volar 1.5 fingers (@ level 5cm prox to guyon’s canal, dorsal branch of ulnar nerve)
o Deformity:
§ Clawing (hyperextension of MCP of little and ring fingers, flexion of IPJ of little and ring fingers)
• Unopposed FDS and FDP (flexion of MCP)
• Loss of 3rd and 4th lumbrical + interossei function which normally flex MCP and extend IPJs
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• Middle and index finger not flexed because lateral lumbricals supplied by median nerve
§ Wartenburg sign: Ulnar deviation of little finger
o Special Tests
§ Froment’s sign: Must keep palms together
o History: Trauma (ulnar hammer), fractures, tumour, ulnar artery thrombosis
• Muscles
o In forearm: flexor carpi ulnaris, medial half of FDP
o In hand (all except LOAF): hypothenar (opponens digiti minimi, abductor digiti minimi, flexor digiti minimi), 3rd and 4th lumbricals,
dorsal and palmar interossei, adductor pollicis
Patient is a (age) (gentleman / lady) . Froment’s test was also positive with flexion of the IP joint of the thumb
On inspection, I note the presence of clawing of the left hand with signifying weakness of the adductor polliciis.
hyperextension of the 4th and 5th MCP joints and flexion of the proximal There was also weakness of the long flexors of the ring finger (FDP).
(and distal in low lesion) IP joints of the ring and little finger. Sensation was decreased over the ulnar 1 ½ fingers and the dorsum
and palmar aspect of the ulnar side of the hand.
There is also wasting of the hypothenar eminence of the left hand and
the dorsal interossei muscle signified by hollowing of the first web Further examination of the upper limb revealed cubitus valgus
space. There are no scars noted over the wrist, forearm or medial deformity of the left elbow.
epicondyle. Tinel’s was negative over the medial epicondyle and the left forearm.
On examination, finger abduction of the left hand was weak (power: _). My diagnosis will be a high ulnar nerve lesion secondary to a malunion
of left supracondylar #.
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RADIAL NERVE
• Sensory supply:
o Numbness classically over dorsal surface of radial 3½ digits
and corresponding area of dorsum of hand (esp base of
thumb extending to first web space; anatomical snuff box)
o Test the dorsal aspect of the first web space.
• Motor supply:
o Posterior interosseous nerve (9): ECRB, supinator, EDC,
EDM, extensor indicis, ECU, APB, EPL, EPB
o Radial nerve proper (4): triceps, brachialis, brachioradialis,
ECRL
o General steps: pronate à clench fist à extend wrists (high
radial nerve)à wrist to neutral position à claw hand
(extend MP and flex IPs; lower radial nerve) à put palms
flat against table & extend thumb
o The most distal extensor muscle supplied by the posterior
interosseous nerve is the extensor indicis propius (EIP) but
this cannot be tested accurately due to the tendon slip from
EDC to the index finger.
o Instead, the next most distal muscle, the extensor policis
longus (EPL), is tested instead – place the hand flat on a
table and get the patient to lift his thumb off the table
(tendons are well demarcated showing retropulsion of the
thumb). If EPL function is intact all other muscles supplied
by radial nerve should be intact.
o Extensor Digitorum (Communis) ED(C) testing – get
patient to extend MCP joints and flex the PIP and DIP joints
(like making a claw) to isolate action of the ED(C). Or simply
test finger extension against resistance à posterior
interosseus nerve
o Higher lesions e.g. shaft of humerus fracture result in
paralysis of the wrist extensors (ECRL, ECRB, ECU) and
wrist-drop results i.e. low lesions of radial nerve do not
result in wrist-drop, so be careful.
o Elbow extension. Triceps function is usually preserved
unless lesion is very high up; shaft of humerus # usually
does not result in triceps paralysis.
• Very high
o Common sites affected:
§ Axilla: Saturday night palsy (back of a chair), crutch palsy
§ Mid-humeral lvl (spiral groove during humerus shaft fracture, tourniquet palsy)
§ At or below elbow (elbow dislocations, monteggia fractures, ganglions, surgical trauma)
o Motor: inability to extend 1)fingers, 2)thumb, 3)wrist (test with cogged wrist)
o Muscle wasting: forearm extensor compartment, triceps (only for very high injuries)
o Sensory loss: over anatomical snuffbox, base of thumb extending to first webspace, dorsum of lateral 3.5 fingers short of nail beds
o Deformity/sign: wrist drop + finger drop
• Radial tunnel syndrome (at level of epicondyles)
• Low lesion (fracture/dislocation at elbow injuring posterior interosseous nerve – around level of elbow; given out btwn 2 heads of
supinator)
o Motor: inability to extend MCP joints (NOT IPJ – Intrinsics) and extend thumb
o Deformity: Radial deviation (extensor carpi ulnaris knocked out), Finger drop
o Sensory loss: none (except for articular proprioception)
• Muscles
o Direct branches from radial n: triceps, anconeus, brachioradialis, extensor carpi radialis longus
o Deep branch of radial n: extensor carpi radialis brevis, supinator
o Posterior interosseous nerve: extensor digitorum, digiti minimi, carpi ulnaris, pollicis brevis, pollicis longus, indicis, abductor pollicis
longus
Patient is a (age) (gentleman / lady) . On examination, power of left wrist extension was ___ and extension of
On inspection, both hands are in the normal resting position with the the left MCP joints was ___.
forearm supinated and the wrist extended. Power was full on extension of the left PIP joints. Power of elbow
The MCP and IP joints are flexed, more pronounced in the little finger extension is ___.
and less in the index finger. Sensation was decreased over the 1st dorsal web space of the hand
I do not note any wasting of the thenar or hypothenar eminences or and the dorsum of the forearm.
intrinsic muscles of the hands. Further examination of the upper limb revealed a ___ cm scar over the
There are no scars noted on the hands. Wrist drop and finger drop of arm.
the left hand was noted.
My diagnosis will be a left radial nerve palsy at the level of the arm
possibly secondary to a previous # of mid shaft of humerus.
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OTHERS
• Complete claw / Simian hand (with thumb involvement – unable to oppose)
o T1 root, combined median and ulnar palsy
• Axillary nerve
o Motor: Deltoid
o Sensory: Lateral cutaneous nerve of arm
• Musculocutaneous nerve
o Motor: Flexors of arm
o Sensory: Lateral cutaneous nerve of forearm
• Spinal accessory nerve
o Motor: Trapezius
o Injury due to: Lymph node biopsy, stab injury
• Long thoracic nerve
o Motor: Serratus anterior (winging of scapula)
o Roots: C5-7
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2. Lumps and Bumps
GENERAL INFORMATION
• 6 S: Site, Shape, Size, Surface, Skin, Slip sign
• 3 C: Consistency, Color, Compressibility
• 2 F: Fluctuance, Fixity (mobility)
• 3 T: Tenderness, Transillumination, Tinel’s
Based on consistency
• Cystic and soft: Ganglions, lipoma, vascular malformation
• Firm: PVNS< neuroma, fibroma
• Hard: Osteochondroma, bone tumours
Characteristics of a lump There is a ___ x ___ cm, (shape: hemispherical / elliptical / fusiform) swelling over the
(site: dorsum / volar / plantar aspect of the forefoot / midfoot / hindfoot / finger / palm /
S4 Size, shape, site, surface wrist) , with a ___________ surface, well-defined edge and is soft to firm in consistency.
E Edge It is non-tender and not warm to touch.
C2 Consistency, colour (& skin) The overlying skin is (normal / has a punctum / coloured) and the lump (is / is not)
T3 Tenderness, temperature, mobile from side to side, and (is / is not) attached to the skin or underlying structures
transilluminable such as (muscle / tendon / bone) . The lump moves upon flexion of the fingers
suggestive of tendon attachment / the lump deceases in size with elevation of the lump.
O Others:
Mobility, fluctuance, pulsatile The lump (is / is not) (fluctuant / compressible/ pulsatile / transilluminable) .
Slip sign is/ is not positive. Tinel’s (is / is not) positive.
R Relations / related signs
GANGLION***
• Definition: Mucinous cyst of unknown cause (possibly due to cystic degeneration in joint capsule or tendon sheath)
• Theories for pathogenesis
o Myxomatous cycstic degeneration
o One way check valve communication with synovial body (eg.
tendon sheath, synovial joint)
• Features
o Shape: Spherical; may be multi locular
o Sites (IMPORTANT DETERMINANT): fr most to least common
§ Dorsal wrist (scapholunate junction)
§ Volar wrist (radial aspect – scapholunate, scapho-trapezio-
trapezoid)
§ Volar MCP joint
§ Dorsum of DIPJ (digital mucus cyst) – OA due to
osteophyte
§ Proximal digital crease (flexor sheath ganglion)
§ NOTE: Big ganglion cyst in GH joint almost always a/w rotator cuff tear
o Well-defined, cystic, smooth, firm
o Tenderness: usually non-tender; may be so for flexor sheath ganglia
o Attachments:
§ Attached to underlying fibrous tissue
§ Usually not attached to skin
§ If attached to joint capsule, tendon sheath, or IM spetum, ganglion becomes less mobiles when structures made tense
o Transilluminable – unless bleeding or infection (pus)
o Flunctuance: Positive
o Content: Glairy fluid (uncooked egg white colour and consistency)
• Types:
o Simple
o Compound: chronic inflammation distends tendon sheath above and below the flexor retinaculum (a/w TB, RA)
o Occult
o Interosseous
• Treatment
o Unnecessary –usually resolves spontaneously after some months
o Surgery (if compressing nerve etc)
§ Aspiration: high recurrence in 6-12 months (10-15%)
§ Excision if recurrence: cosmesis or if ganglion is causing pain (recurs in 20-30%)
PIGMENTED VILO NODULAR SYNOVITIS (AKA GIANT CELL TUMOUR OF TENDON SHEATH)***
• COMMONEST hand lump disorder esp in patients 20-50yo
• Definition: benign proliferative disorder of synovial lining of joint, bursa and tendon sheaths, producing localized/ diffuse inflammation and
nodular thickening of the synovial membrane
o PVNS is a histological diagnosis: Pigmented (haemosiderin) vilonodular (multilobulated) synovitis (affecting joints and tendon
sheath); multinucleate giant cells present
o 2 types (+ sites)
§ Diffuse form – affects entire synovial lining of a joint, bursa or tendon sheath
• Affects large joints (knee > hip > ankle, shoulder)
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§ Localized/nodular form – affects tendon sheaths around small jts of hands & feet (termed nodular tenosynovitis)
• Appears in the form of a localised nodule or mass in a synovium, and the surrounding synovium is generally normal
• Features:
o Insidious onset of a solitary, well circumscribed, multilobulated, tan coloured (sometimes has pale yellow regions of lipid
deposition) nodular/ diffuse joint swelling that is accompanied by a dull aching joint pain.
o Site: Most commonly on volar aspect near DIPJ (often index and middle digit)
o Consistency: Firm to soft rubbery
o Fixity: Attached to tendon sheath or IPJ
o Does not transilluminate
o Tenderness: Absent
o May have decreased ROM and locking of joint
• XR: joint swelling, periarticular erosions (saucerisations), joint space narrowing, sub chondral cyst, osteophytes formation (secondary OA
changes)
• Treatment: Synovectomy
o However, diffuse lesions have a high rate of recurrence (>50%) unless synovectomy complete
o If refractory to repeated Sx, may be managed with low-dose radiotherapy
LIPOMA
• Definition: Cluster of fat cells that have become over-active and distended with fat that they have become palpable lumps
• Features
o Surface: Lobulated (more prominent with firm pressure)
o Edges: Well circumscribed
o Consistency: soft
o Attachment to neighbouring structures: possible
o Slip sign: Not very useful diagnostic feature
o Fluctuance: Yield to pressure but do not fluctuate
o Non-tender
o Transillumination: Negative
• Treatment -- Surgical: marginal excision (pre-op staging and biopsy for liposarcoma if atypical)
IMPLANTATION DERMOID
• Definition: Cyst that develops as a result of implantation of epidermal fragment into dermis by a penetrating injury; epidermis continues to
grow and forms a cyst lined by stratified squamous epithelium and filled with keratin
• Features
o Site: Sites commonly subjected to injury (eg. volar surfaces of fingers and palms)
o Consistency: Hard and tense
o a/w trama to overlying skin: May have scar
• Most diagnostic feature is previous injury at site and presence of scar
NERVE SWELLINGS
• Neuroma: general term for tumor of any component of a nerve bundle
o Type: Usually neurilemmoma/schwanomma
§ Benign nerve sheath tumour composed of Schwann cells
o Features:
§ Along nerve route
§ Positive Tinel’s sign
§ Homogeneous texture
• Neurofibroma (benign neoplasms derived from the myelin sheath of peripheral nerves; schwannoma has mostly just schwann cells in it,
whereas a neurofibroma has a bunch of other cell types, like fibroblasts, endothelial cells, and mast cells)
o Localized to digit and part of hand
o 4-5cm, irregular and wrinkled skin, soft, mobile w skin, a/w café au lait spots
VASCULAR MALFORMATIONS
• Types: Usually venous, or AV malformations
• Features: Compressible, Posture dependent, Discoloration, may have thrills and bruits
OTHERS
• Gouty Tophi
o Relatively immobile, stuck to tendon/ joint, firm (can be soft), whitish, not transilluminant, tender in acute cases
o Site: ear, ankle, elbow, finger
o Cx: skin ulcerations
o DDx: PVNS
• Squamous cell CA
o Due to burns, sunburn, Arsenic
o Spread by lymphatics
• Glomus tumours (AKA glomangioma, or nonchromaffin paraganglioma)
o Rare benign neoplasm that is a specialized arteriovenous anastamosis and is usually found in the skin of the extremities
o It arises from the glomus body (Component of the dermis layer of skin, involved in body temperature regulation), which consists of an
AV shunt surrounded by a capsule of connective tissue
§ Glomus bodies are most numerous in the fingers and toes
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§ The role of the glomus body is to shunt blood away from the skin surface when exposed to cold temperature, thus preventing
heat loss, and allowing maximum heat flow to the skin in warm weather to allow heat to dissipate.
o Small, vascular & tender swelling, usually occurs at the region of the nail beds.
o Treatment: Radiotherapy and Surgery
• Pyogenic Granuloma
o Relatively common benign vascular lesion of skin and mucosa. Exact cause unknown
o Usually occurs in children and young adults as a solitary, glistening, friable, polypoid bright red papule or nodule. Prone to bleeding
and ulceration.
o Ranges from few mm to several cm in size.
o Regressing lesions: Appear as soft fibroma. Normally occurs at Head and Neck and distal extremities.
o Typically evolves rapidly over a period of a few weeks.
o Usually Hx of trauma preceding the onset of lesion may be elicited
o Untreated lesions eventually atrophy, fibrose and slowly regress.
• Enchondroma
o Commonest primary bone tumour of hand
o Hard, irregular, fixed swelling
• Malignant melanoma
• Giant cell tumour
• Osteochondroma
3. Deformities
DUPUTREN’S CONTRACTURE
• Epidemiology: Often in middle-aged, Caucasian male
• Definition: Nodular hypertrophy & contracture of palmar aponeurosis, resulting in tendons attached to finger not being able to move
properly
• Pathogenesis: Local microvessel ischemia à Increase xanthine oxidase activity à Superoxide free radical production à Stimulate
myofibroblast proliferation and type III collagen formation (specific platelet-derived and fibroblast GF also play a role in etiology)
o Allopurinol may help to reduce symptoms (XO inhibitor)
o The process of chronic inflammation is thought to be essential to the subsequent fibrosis
• Examination
o Look (usually ring and little finger affected) @ BOTH HANDS
§ Scar from previous Sx
§ Visible cords
§ Pitting/tethering of skin on palmar aspect of hands
§ Flexion deformities – MCPJ and PIPJ
§ Garrod’s pads at dorsum of PiPJ (thickening of s/c tissue)
§ Involvement of thumb and 1st web space is a sign of more aggressive disease
o Feel: swellings are fixated to skin
o Move
§ Assess ROM (active and passive)
§ Table top test
o Offer:
§ Enquire abt causes and associations
§ Assess function – writing, dressing, fine movement etc
§ Look for other features of diffuse fibromatosis
• Differentials: Skin contracture (look for scar from previous wound), tendon contracture (thickened area or cord moves on passive flexion of
involved finger), congenital contracture of little finger (affects PIPJ), ulnar claw
• Associated Conditions (DEAFEST PAIL): DM, Epilepsy, Age, Family history (AD)/ fibromatoses, Epileptic medication (eg. phenobarbitone),
Smoking, Trauma & heavy manual labour, Peyronie’s disease (fibrosis of corpus cavernosum; seen in 3% of patients w Dupuytrens
contracture), AIDS, Idiopathic, Liver disease (secondary to alcohol)
• Sx Rx: indicated when deformity interferes with function or is rapidly progressive (ie. When MCPJ or PIPJ contracture >30deg)
o Fasciotomy: for prominent bands
o Partial fasciectomy (w Z-plasty) to length wound: in conjuction w post-op physioRx (early active flexion ROM exercses for grip strength)
and night-time splintage in extension
o Dermofasciectomy (w full-thickness skin grafting): a/w lowest risk of recurrence
o Arthrodesis/ amputation: for late presentations and repeated recurrences
SKIN CONTRACTURES
- Cuts and burns are liable to heal with contractures, causing puckering of the palm or fixed flexion deformities. Surgery incisions should never
cross flexor creases.
- Rx: Established contractures may require excision of the scar and Z–plasty of the overlying skin.
OTHERS
Ruptured extensor pollicis longus
• Injury to long thumb extensor after fraying
• Secondary to colle’s fracture, rheumatoid arthritis
• Treatment: Tendon transfer usually required
Dropped finger
• Rupture of extensor tendon
• Patient unable to hold finger at extension at MCP joint
• Treatment: (1) direct repair (2) distal portion of the tendon attached to adjacent finger extensor
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Boutonneire
• Flexion deformity of PIP joint due to interruption of central slip of extensor tendon
• Lateral slips separate and head of proximal phalanx pops up in between the lateral slips
• Treatment: post traumatic usually repairable. Chronic deformity (in RA) usually cannot be repaired
Swan neck deformity
• Reverse of Boutonniere – PIP hyperextended, DIP flexed
• Due to imbalance of extensor vs flexor action in finger (commonly in rheumatoid arthritis)
• Treatment: tendon rebalancing and joint stabilisation
Polydactyly: Post-Axial associated w renal failure
MUSCLE CONTRACTURE
Forearm § Ischaemic contracture of forearm muscles, commonly caused by:
o Volkmann’s ischaemic contracture: # causing compartment syndrome resulting in muscle ischaemia & necrosis. Infracted
muscles replaced by fibrous tissues. Usually follows circulatory insufficiency due to injuries at or below the elbow.
o Tight plaster cast & limb swelling
§ Shortening of long flexors causing flexion deformity of fingers which is only correctable on wrist flexion (tendodesis effect)
§ May be a/w ulnar and/or median nerve palsies
§ Treatment: If marked disability: muscle release, Excise dead muscle or tendon transfer
Intrinsic § MCPJ flexion, IPJ extension & thumb adduction
muscles § Causes: spasticity (eg CP), scarring (trauma and infection)
§ Treatment: muscle release
§ Aka intrinsic plus. Intinsic minus is used to describe Ulnar claw due to paralysis of the intrinsic muscles.
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§ Complications
• Infection
• Radial nerve palsy – Superficial radial nerve
• Snapping of extensor tendon (due to extreme radial release of extensor retinaculum)
• APL and EPB adherence (will limit thumb movements)
• Differentials for radial sided wrist pain (proximal to distal)
o Intersection syndrome: Inflammation at intersection where 1st dorsal compartment (APL, EPB) muscle bellies cross over 2nd
compartment (ECRL, ECRB) muscle bellies
o De Quervain’s disease
o Wartenberg’s syndrome: Irritation/compression of superficial branch of radial nerve
o Scaphoid fracture: Pain over anatomical snuffbox
o Scapholunate instability
o 1st CMC joint OA
• Other sites of extensor tenosynovitis
o ECRB (most powerful extensor of the wrist; 2nd Compartment): Pain and point of tenderness just medial to anatomical snuff box
o Extensor Carpi Ulnaris (6th compartment): Pain and point of tenderness immediately distal to head of ulnar
o Treatment: Splintage and H&L injections usually effective.
On inspection, both hands are in the normal resting position with the forearm supinated and the wrist extended. The MCP and IP joints are flexed,
more pronounced in the little finger and less in the index finger.
I do not note any obvious deformities. However, I note slight swelling over the radial side of the wrist.
The overlying skin is not erythematous. I do not note any scars in the surrounding skin.
I would like to proceed to palpate the patient’s wrist. (ask pt for any pain first)
The overlying skin of the wrist joint does not feel warm. I note tenderness at the tip of the radial styloid.
ROM of flexion and extension of bilateral wrist is full at 80 degrees.
Ulnar deviation of both wrist is 40 degrees. Radial deviation of both wrists is 15 degrees.
Supination and pronation of both wrists is full at 90 degrees.
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o Injection
§ H&L into tendon sheath – Triamcinolone and lignocaine: approx 70% success rate but not administered more than twice due to
lowered efficacy and risk of tendon rupture (other side effects: infection, hypopigmentation over area of injection, steroid flare, fat
necrosis, periarticular osteoporosis)
• Higher rate of success in female patients, with short duration of symptoms (<4months), for discrete palpale nodule, single
digit involvement, no associated conditions (eg. DM, RA)
o Surgery
§ Procedure: Division of A1 pulley in the midline (tendon sheath), then ask patient to actively move digit to confirm full release
(motion encouraged immediately following the procedure)
§ Indications: Stage 4 or failed injection therapy
§ Complications: May cut on A2 pulley causing bowstringing
On inspection, I note an abnormal resting position of the (L / R) hand. I feel a nodule in the palm just proximal to the (index / middle / ring /
The (index / middle / ring / little) finger is flexed at the PIP joint. little) finger at the level of the distal transverse palmar crease. The
Resting position of the (left / right) hand is normal. surface is smooth, edges distinct and it feels firm. It is tender and not
I do not note any skin changes or scars on the hands. I also do not warm to touch. The overlying skin is mobile.
note any wasting of the intrinsic muscles.
He / she is able to actively extend his / her finger.
I would like to move on to palpate the hand. (ask pt for any pain first) My diagnosis is grade (1 / 2 / 3 / 4) trigger finger of the (left / right)
(index / middle / ring / little) finger.
5. Infections
BACKGROUND
• Most commonly due to implanted staph aureus
• Pathology: inflammation and suppuration in small closed compartmentsà increased pressures may
reach levels that threaten local blood supplyà MAY LEAD TO tissue necrosis or a stiff and uselss
hand
• Clinical features:
o Usually a hx of trauma, may be unnoticed
o Local: pain (may become throbbing pain), swelling, tenderness, red and tense tissues with decreased ROM
o Systemic: fever
• Principles of treatment
o Antibiotics:
§ Prophylactic: usually flucloxacillin; (in severe cases) fusidic acid or cephalosporin
§ Altered when bacterial sensitivity known
o Rest and elevation: sling; roller towel
o Analgesics
o Drainage: drain pus when there’s signs of abscess (throbbing pain, marked tenderness, toxaemia)
§ Tourniquet + GA/LA
§ Incision never across a skin crease/ interdigital web as healing will result in soft-tissue contracture across crease
§ Excise necrotic tissue + thoroughly cleanse area
§ Either leave wound open/ sutureà cover with non-stick dressings
§ Send pus for microbiological investigation
o Splintage: In position of safe immobilization (wrist slightly extended, MCPJ flexed, IPJ extended, thumb abducted) as ligaments are at
greatest lengthà reduce likelihood of stiffness
o Physiotherapy
• Possible compartments:
o 1) nailfold (paronychia)
o 2) pulp space (whitlow, felon): usually prick or splinter of finger tip
o 3) subcutaneous tissues
o 4) tendon sheath (suppurative tenosynovitis)
§ Uncommon but dangerous- risk of tendon necrosis and patient may end up
w useless hand
§ Clinical features: Affected digit swollen, painful, held bent, tender, no active
/passive movement
§ Treatment:
• IV antibiotics
• Surgical drainage if no improvement after 24hrs
72
o 2 incisions (proximal end + distal end of sheath)à irrigate sheath with saline or Ringer’s lactate solution using a
fine catheterà leave for postoperative irrigation for 2 daysà dressing and splinting
o Tendon-sheath infection in thumb/ little finger may spread prox to synovial bursaà drain via incision above wrist
o 5) deep fascial spaces: Spread from infection of web space/ tendon sheathà palm is ballooned and normal concavity lost, w whole
hand held stillà Rx is I&D
o 6) joint infx
§ Clinically hard to distinguish from Acute Gout. So Aspirate joint
§ Can be infected directly or indirectly.
§ Rx: IV antibiotics and splint. If no improvement in 24 hrs à open drainage
o Others:
§ Bites
• Animal bites pathogens: Staph and strep, (consider rabies)
• Human bites pathogens: Staph aureus, Strep A, Eikenlla corrodens, anaerobes
• XR done to exclude fracture or foreign body
• Mx:
o Fresh wound: Examined in OT. Swab for c/s. Explore for foreign bodies such as tooth. Splint elevate and start
prophylactic antibiotics
o Infected Bites: debridement and washout. Start IV antibiotics—Broad sprectrum penicillin and cephalosporin.
o Post op: Physiotherapy. Deal with tendon lacerations when tissues are completely healed
§ Chronic
• TB: May present with compound palmar ganglion (above and below the carpal tunnel)
• Leprosy (Hansen’s Disease): Cause auto-resorption
6. Fractures
• NOTE 1: commonest Cx of hand # is tendon adhesion
• NOTE 2: Complications of wrist #
O Most common complications are poor grip strength, stiffness and radial shortening
O 80% have normal function in 6-12 months
O Early Cx:
§ Difficult reduction +/- Loss of reduction
§ Compartment syndrome
§ EPL tendon rupture
§ Acute carpal tunnel syndrome
§ Finger swelling with venous or lymphatic block
O Late:
§ Malunion, radial shortening
§ Painful wrist sec to ulnar prominence
§ Frozen shoulder (shoulder-hand syndrome; aetiology unknown)
§ Post-traumatic arthritis
§ Carpal Tunnel Syndrome
§ Reflex sympathetic dystrophy
• NOTE 3: deformity in hand # is due to MALunion
SCAPHOID FRACTURE *** (most commonly fractured carpal bone – 75% of wrist #s)
• Mechanism of Injury: ALWAYS INTRA-ARTICULAR
o FOOSH with wrist extended
o Combination of dorsiflexion and radial deviation results in force passing between 2 rows of carpal bones, resulting in scaphoid
fracturing transversely across its waist (as it lies btwn both rows)
o May have accompanied disruption of scapholunate ligaments
• Risk Factors: Rare in children and elderly
• Symptoms
o Pain (over anatomical snuffbox)*** & over scaphoid tubercle (following course of FCR)
o Swelling (over anatomical snuffbox)
o Restriction of thumb movement (not so much of wrist movement)
• Signs: painful motion of wrist joint; distraction & axial loading of e 1st MC can increase the pain
• Classification
o # of scaphoid tubercle
o Undisplaced # of waist
o Displaced # of waist
• Investigations
o X-ray: often hard to see
§ 5 Views: AP, lateral, SCAPHOID VIEW, 2 oblique (semi-pronated and semi-supinated)
§ X-ray again in 2 weeks later if unsure as fracture may not be seen in first few days
§ Usually # is thru narrowest part of the bone (waist); other potential # sites include tubercle and proximal pole
o MRI: useful in diagnosing occult scaphoid # and showing AVN of bone
o Not CT (for articular #s)
73
• Management
o Initial (in the event that fracture not seen on x-ray):
§ Scaphoid plaster & sling: hand pronated, wrist dorsiflexed & radial deviated & thumb forwards in ‘glass holding’ position
§ Plaster to extend from below elbow to just below MCP and IPJ of thumb; incorporate proximal phalanx of thumb
o # of scaphoid tubercle: don’t need splintage; crepe bandage and movement encouraged (treated as sprain)
o Undisplaced # of waist
§ No need reduction
§ Scaphoid plaster for 6-12 weeks (union is slow): 90% should heal
§ Internal fixation and bone graft if delayed/non-union signs at 12 weeks
o Displaced or unstable #, or delayed/non-union:
§ ORIF with scaphoid compression screw
§ Acute #: favours percutaneous fixation and arthroscopy assisted
§ Non-union: favours open fixation w bone grafting
• Vascularized bone grafting when there is AVN
• Complications
o Avascular necrosis of proximal pole (blood supply diminishes proximally – supplied by dorsal and volar branches of radial artery)
§ Can cause secondary radiocarpal OA (excise scaphoid and consider arthrodesis of proximal to distal row of carpal bones)
§ Diagnosed by increased density of prox fragment on X-ray after 2-3 months
§ Occurrence
• 1% of distal third fractures
• 20% of middle third
• 40% of proximal third
§ Management
• Remove entire proximal row of carpal bones (carpectomy)
• Remove scaphoid and fuse the proximal to distal row (4 corner fusion: capitate-hamate-triquetrum-lunate)
o Non-Union v common (union may be slow <months> due to poor BS at prox part of scaphoid) à chronic pain on motion and loading
§ Management: plaster fixation, internal fixation and Bone graft (or same as for AVN)
o Osteoarthritis
§ Excision of radial styloid if arthritis confined to distal pole
§ Salvage procedures: intercarpal and radiocarpal fusion
BOXER’S FRACTURE
• Transverse # of 5th metacarpal neck
• Dropped knuckle deformity permanent
• Indications for surgery: Usually severe angulation (>30degrees)
BENNETT’S FRACTURE-SUBLUXATION
• Fracture of 1st metacarpal base extending to CMCJ
• XR: small medial fragment of bone seen. Proximal and lateral subluxation of 1st MC present
• Management: M&R + 4 weeks in plaster cast
ROLANDO’S FRACTURE
• Comminuted fracture of 1st metacarpal base extending to CMCJ
• Management: Fixation (K-wires)
MALLET FINGER
• Rupture of extensor tendon of terminal phalanx as fingertip forcibly bent during active extension
• Loss of active extension of DIPJ, normal passive extension of DIPJ
• Rx:
o If soft tissue injury (muscle imbalance): treat conservatively w mallet splint for 8weeks if pure soft-tissue injury
§ For cases with hyperextensible PIP, splint with DIPJ extension & PIPJ flexion, using a skintight cast.
o If avulsion #
§ Extra-articular or involving <2/3 of joint: conservative Rx (splint for 6weeks if large flake of bone avulsed)
§ Intra-articular or involving >/= 2/3 of joint: surgical reduction
RUGGER-JERSEY FINGER
• Opposite MOI from mallet finger: rupture of FDP as fingertip forcibly extended during active flexion (eg. player grasping jersey of
opponent during tackling)
o Tendon may rupture directly fr its insertion into the bone or it may avulse bone fragment from base of distal phalanx
o Commonly affects 4th finger (75%)
• Usually present late (pain, tenderness over volar distal finger, swelling, finger in slight extension relative to other fingers in resting
position, bruising absent, X-rays negative usually)
• Management: Repairà tendon graftingà arthrodesis of DIPJ
74
METACARPAL SHAFT FRACTURE
• Mostly stable and undisplaced.
• If displaced, need ORIF with plates or K-wire. Make sure no rotational deformity. Otherwise will have scissoring of fingers on flexion.
7. Dislocations
LUNATE AND PERILUNATE DISLOCATIONS
• Mechanism of Injury: Fall w hand forced into dorsiflexion may tear ligaments that normally bind carpal
bones
o Types of injury:
§ Lesser arc injury: lunate and periluante dx (no fracture)
• Perilunate dislocation (most common): Lunate remains attached to radius while
rest of carpus displaced backwards
• Lunate dislocation: Hand usually immediately snaps forwards again, but in the
process, lunate may be levered out of position to be displaced anteriorly
§ Greater arc injury: trans-scapho perilunate # dislocation (w scaphoid #)
• Trans-scaphoid perilunate dislocation: Sometimes scaphoid remains attached to
radius and force of perilunar dislocation causes it to fracture through waist
• Symptoms
o Wrist is painful and swollen
o Wrist held immobile
o May have symptoms of carpal tunnel compression – parasthesia, blunting sensation over median
nerve territory + weakness of palmar abduction of thumb
• Complications
o Delay may result in difficulty in reduction and AVN and secondary OAà Partial arthrodesis Perilunate
Dislocation
considered if symptomatic (stiff and painful)
o Carpal tunnel compression
o Improper reduction of perilunate dx may result in secondary lunate dx
o Sudeck’s atrophy
• Investigations
o X-ray
§ Perilunate dislocation
• PA view: disruption of carpal anatomy (using Gilula lines)
o Carpus diminished in height
o Bone shadows overlap abnormally
o May have accompanying scaphoid fracture
• Lateral view: disruption of carpal anatomy (using multiple stack of C lines)
o Lunate not displaced forward
o Capitate displaced backwards
§ Lunate dislocation:
• AP view: Lunate appears triangular instead of quadrilateral (crescent moon shape
of bone becomes obvious)
• Lateral view: Dislocated lunate tilted forwards and displaced in front of radius, while
capitate and metacarpal bones line in line with radius
• Management Lunate
Dislocation
o Closed reduction
§ Reduce: Pull hand with wrist in extension and apply thumb pressure to displaced bones
§ Plaster slab applied holding wrist neutral
§ Percutaneous K wires may be needed to reduction
o Open reduction
§ If closed reduction fails
§ Carpus exposed by anterior approach (concomitant decompression of carpal tunnel)
§ Hand pulled and lunate levered into place
§ Held in place by K wire
SCAPHOLUNATE DISSOCIATION
• Mechanism of Injury: Subluxation of scaphoid and disruption of ligaments between scaphoid and lunate
• X-ray:
o Foreshortening of scaphoid and appearance of large gap between scaphoid and lunate
o Ring sign: rotation of scaphoid cause it to be viewed end on in PA view
SCAPHOID DISLOCATION
• Displacement is usually anterior
• Rx: closed reduction + plaster fixation in stable position. If instability is present, fix with K-wires
75
8. Joint Disorders
CHRONIC CARPAL INSTABILITY
• Causes: Injury, Arthritis, Kienböck’s disease (patchy lunate AVN after trauma)
• Features: Pain, Weakness, Clicking on movement
• Commonest type: Scapholunate dissociation – X-ray shows Terry Thomas sign (abnormal gap between scaphoid & lunate)
• Rx:
o Acute: reduction & fixation with plaster or K-wires
o Chronic: splintage, analgesics, H&L injections, arthrodesis
KIENBOCK’S DISEASE
• Patchy AVN secondary to post-stress/injury of the lunate.
• Predisposing factor: relative shortening of ulna à excessive stress on lunate
• Presentation: ache and stiffness, localised to centre of dorsal wrist. Possible limitation of wrist extension
• Imaging: Earliest signs of osteonecrosis only detected by MRI. XRay – increased density, later irregularity and flattening of bone. Eventually
OA features.
• Treatment:
o Osteotomy of distal end of radius (reduce pressure on lunate)
o Microrevascularisation of bone if expertise available
o Partial arthodesis in late cases.
76
Pelvis
Fractures
General
Principles
of
Pelvic
Fractures
Isolated
Fractures
Fractures
of
Pelvic
Ring
Fractures
of
Acetabulum
Injuries
of
Sacrum
and
Coccyx
77
1. General Principles of Pelvic Fractures
• Most common fracture involves pubic rami, followed by ilial, ischial, acetabular, coccygeal and sacral bones
• Tile’s Classification of pelvic fractures
Type
A
Type
B
Type
C
o Type A: stable, minimally displaced, includes avulsion fractures and fractures not involving pelvic ring, e.g. rami fracture
o Type B: partially unstable, rotationally unstable, but vertically stable, e.g. “open book” fracture from external rotational force to pelvis
o Type C: unstable, rotationally and vertically unstable, associated with rupture of ipsilateral ligaments, e.g. vertical shear fracture
• Diagnosis
o History of injury, high energy trauma
o Examination reveals local swelling, tenderness; if unstable, may have deformity of the hips and instability of pelvis with palpation
o MCQ à trendelenberg test is a test of stability of pelvis on femur
• General Treatment
o ABCs
o Assess genitourinary injury (rectal exam/vaginal exam mandatory)
o Type A - bedrest and mobilization with walking aids
o Type B/C - external or internal fixation
• General Complications
o Hemorrhage - life threatening
o Fat embolism
o Bladder/bowel injuries
o Neurological damage
o Obstetrical difficulties
o Persistent sacro-iliac (SI) joint pain
o Post-traumatic arthritis of the hip with acetabular fractures
2. Isolated Fractures
Avulsion Fractures
• Mechanism of Injury: Piece of bone pulled off by violent
muscle contraction (sportsmen)
• Examples
o Sartorius pull off ASIS
o Rectus femoris pull off AIIS
o Adductor longus pull off piece of pubis
o Hamstrings pull off part of ischium
• Management: Rest
Direct Fractures
• Mechanism of Injury: Direct blow to pelvis (usually fall from
height) may fracture ischium or iliac blade
Stress Fractures
• Often affects pubic rami in osteoporotic or osteomalacic
patients
4. Fractures of Acetabulum
• Mechanism of Injury
o Head of femur driven into pelvis
o Due to:
§ Blow on side (fall from height)
§ Blow on front of knee (dashboard injury)
o Usually due to severe injury, hence suspect other injuries/fractures
• Patterns of Fracture
o Acetabular wall
§ Fractures of acetabular wall affect depth of socket
§ May lead to hip instability (unless properly reduced and fixed)
o Anterior column
§ # Separates a segment btwn AIIS and obturator foramen
§ Uncommon
§ Good prognosis (does not involve weight bearing area)
o Posterior column
§ # runs upwards from obturator foramen into sciatic notch separating the
posterior ischiopubic column of bone and breaking the weight bearing part of
the acetabulum
§ Associated with posterior dislocation of hip
§ May injure sciatic nerve
§ Usually treated urgently with internal fixation
o Floor of acetabulum (uncomminuted transverse #)
§ # separates iliac portion above from pubic and ischial portions below
§ Sometimes there is also a vertical split into obturator foramen (T-fracture)
§ Easy to reduce and hold
79
o Complex fractures (combinations of above)
§ Damage various portions of acetabulum
§ Require ORIF
• Tile’s classification of acetabular fracture
o a,b: Simple fractures involving either anterior or
posterior wall or column
o c: Transverse fractures
o d: T-type fractures involving two columns
• X-rays (i.e. AP, inlet, and outlet views) judet view for
acetabular fractures
o 6 lines to look for in a pelvic X-ray specifically
looking for acetabular fracture
§ Iliopectinael line – anterior column of pelvis
§ Ilioischial line – posterior column
§ Acetabular teardrop – should be in line w ilioischial line
§ Dome – superior weight bearing area costing of both ant and post column
§ Ant wall of acetabulum
§ Post wall of acetabulum
• Complications
o Nerve injury: Sciatic nerve (posterior fractures) – but nerve usually not severed hence
good chance for recovery
o Avascular necrosis of femoral head
o Heterotopic bone formation (prevented with prophylactic indomethacin)
o Osteoarthritis (especially if weight bearing surface involved)
• Management
o Initial
§ Manage shock
§ Reduce dislocation
§ Definitive fracture management delayed until patient fit (not >7 days)
o Conservative: For undisplaced fractures and simple fractures which do not involve
weight bearing portion – (roof)
§ Maintain traction for 6-8 weeks
o Operative:
§ Indications (in young as likelihood for OA is great hence ORIF is justified)
• Unstable fractures
• Fractures resulting in significant distortion of ball and socket congruence
• Associated fractures of femoral head
• Retained bone fragments in joint
§ Aim: Perfect anatomical reduction
80
Hip
and
femur
Atraumatic
Traumatic
Age
0
yrs
Dislocations
• DDH/CDH
• Hip
dislocation
Others
• Acetabular
dysplasia
and
subluxation
of
hip
• Protrusio
Acetabuli
• Coxa
Vara
• Femoral
anteversion
81
Examination of the Hip Bryant’s triangle
The preliminaries: Introduce yourself to patient, ask for permission to - This is constructed with the patient supine as a rough means of
examine. Ensure adequate exposure til underwear but consider patient detecting disturbance of the normal anatomy of the femoral
modesty also. Ensure good lighting, good positioning of bed. head and neck. It is a right-angled triangle, with the following sides
(assuming patient is lying down):
- If shortening is in the femur, it is important to assess if the
With patient standing: shortening is above or below the greater trochanter
LOOK: front, side, back - Shortening of the horizontal line on one side as compared to the
1. Posture and Deformities other indicates shortening above the greater trochanter
2. Swelling
3. Scars, Sinuses – in e gluteal folds, make sure to check
4. Discolouration – redness, bruising, etc
5. Muscle wasting – gluteal muscles
GAIT AND RELATED TESTS
1. Get patient to walk a distance – notice if there is any obvious
antalgic or Trendelenburg gait, of if one of e limbs appear shorter
than e other
2. Trendelenburg test: SSS (sound side sags)
- Get patient to stand in front of you and place both hands on top
of your own (palms down on your palms up)
- Then make patient stand on one foot at a time, lifting the other
hip off the floor
- If the side that the patient is supporting his weight on has a
pathology, there will be dipping of the contralateral hemipelvis
and his hand will press harder on that side to lever himself
Causes of positive Trendelenburg test: - Bryant’s triangle is formed by a line joining the ASIS and the greater
- Fulcrum problems e.g. hip OA, AVN trochanter, a line dropped vertically from the ASIS, and a line
- Lever arm problems e.g. NOF#, coxa vara running horizontally across from the greater trochanter
- Effort problems e.g. weak abductors - The length of C is gauged on each side, and the sides compared.
- Nerve problems e.g. Superior Gluteal N or L5 Pathology of the femoral head or neck which displaces the greater
- Others: legg perthes dz, DDH, slipped capital epiphysis trochanter will tend to shorten this side of the triangle
With patient lying supine, knees fully extended: observe attitude of hip, MOVE
knee and ankle jt when patient climbs up the bed 1. Thomas’ Test for fixed flexion deformity of the hip
LOOK - Place patient’s legs at 90 degree knee flexion
1. Deformity of the hip – fixed adduction or abduction deformities; - Then place your hand under patient’s lumbar region
asymmetry in attitude of the limb - Get patient to flex one leg at the hip until the lumbar lordosis is
2. Obvious swelling(s) -- Hernia can cause hip pain obliterated (back pressing your hand to the bed) and then ask
FEEL patient to hold on to the flexed leg at the knee
- Ask patient to fully extend the other leg to see if there is any
o Feel for temperature – any increased warmth
fixed flexion of the hip à measure w goniometer if there is fixed
o Palpate bony landmarks of the hip and note any tenderness:
flexion
ASIS à down inguinal ligament à pubic tubercle à hip jt
- Repeat with the other side
(2cm below and lateral to midpoint of inguinal ligament) à
- Be consistent in performing the test – amount of pressure of
gluteus medius à greater trochanter
lumbar region on the hand should be equal when testing either
LIMB LENGTH MEASUREMENT
side
Relative/Apparent limb length (eg. scoliosis, contractures)
- For measurement of relative limb length just ask patient to adopt the NOTE: if patient has a knee contracture, shift him such that
most comfortable position: “shoulders above hip above feet”; ensure
his knee joint lies over the edge of the bed, to accurately
both limbs are parallel; pelvis needn’t be squared
- Locate xiphisternum and then measure from that point to the medial assess for FFD of the hip
malleolus on either side
Contractures and apparent length discrepancy 2. Range of movements:
- Adduction deformity results in shortening of the abnormal side - Hip movements are mostly assessed passively
- Abduction deformity results in lengthening of the abnormal - While during Thomas’ test, also assess degree of full hip flexion
side on either side (normal is 140 degrees flexion)
True length: - Abduction and adduction – place hand on the ASIS to assess
Square the pelvis for true length measurement; ensure axes of both movement of the hip joint when the pelvis is not moving;
measure angle when the resting hand on ASIS detects
lower limbs are at right angles to the line joining the two ASIS (both ASIS
movement (normal range is 45 degrees abduction and 25-30
to be made level). If not possible to square pelvis due to contracture on degrees adduction)
one side then arrange the other limb in the same position when measuring - External and internal rotation – flex hip and knee to 90 degrees
true length for that limb. each, place left hand on knee pressing downwards to fix pelvis
- Locate ASIS by feeling laterally from the pubic tubercle; the ASIS is (normal is 45 degrees external rotation, 45 degrees internal
the first bony prominence that the hand feels rotation; if hip is extended flat on bed, measure angle by
- Measure from ASIS to medial malleolus (use the same relative point drawing imaginary axis thru patella and compare it to the 90deg
on the malleolus on either side e.g. superior border, midpoint, etc) sagittal plane)
- If one side has an abduction contracture, then place the other leg in
the same relative position when measuring true length; same for other NOTE: If patient cannot flex hip due to pain, internal and
deformities external rotation of the hip can be assess with patient in
Galeazzi’s test (done when there is a true length discrepancy) prone position and the knee flexed
- Place the hips 45deg and knees 90deg and ensure both heels are - Turn patient to the prone position to assess extension of the hip
tgt with both malleoli touching. Look at knee from side to side. If
knee of affected side is proximal, then there is femoral shorterning
FINISH with examination of the neurovascular status of the lower limb
or hip dx. If knee of affected side is distal, then there is tibial
shortening. (distal pulses, “tip-toe” and “stand on heel”, examination of the spine and
- This screening test helps to assess the segment shortening the knee joints & SLR.
affected limb (if the shortening is due to femur or tibia or both)
82
Approach to Hip Pain
• Causes of painful hip
Referred pain § Discogenic dz § True hip pain referred to knee: anterior obturator nerve
Joint disorders § Infection § Perthes’ dz § Slipped capital femoral epiphysis
§ OA § RA § Osteonecrosis
Periarticular disorders § Hernia § Tendinitis § Bursitis / synovitis
• History and PE
o Site of pathology
§ Hip pain (anterior) — usually at groin
§ Pain at gluteal region (posterior) — usually lumbar pathology
• Most sensitive hip test which can be used for quick screening of hip: internal rotate (capsule in spiral fashion)
o Impingement test: Flexion, adduction, int rotation
• Caveat: acetabular pathology may present only as gluteal pain
• Other conditions presenting w “hip” pain: trochanteric bursitis, IT pathology (snapping, tendinitis), gluteal muscle strain,
referred pain from spine, SI pathology, non-ortho pathology (hernia, LN, pelvic inflammatory dz)
o Cause of pathology
§ Vascular: Perthes’ disease, AVN
§ Infection: OM, septic arthritis, TB, Transient synovitis
§ Trauma: OA (degenerative), dislocation, fracture
§ Autoimmune: RA
§ Metabolic
§ Iatrogenic
§ Neoplastic
§ Congenital: SCFE, DDH
o Look for predisposing factors e.g. Osteoporosis and fall risk
o Look for complications of pathology
o Assess premorbid status (goal for mgmt is to regain premorbid status)
o Assess carer support
• Special Ix: MR arthrogram (if other radiological modalities all negative)
Gait analysis
• Normal Gait
o Stance phase—heel strike + mid stance + push off
o Swing phase—Acceleration + initial swing + midswing + deceleration
Type of gait Notes Causes
Antalgic Short stance phase, increased swing phase Pain (infection, inflammation, transient synovitis)
Short limb Ipsilateral hip drops when weight on short leg Previous fracture
Congenital shortening
Hand-to-knee Patient places hand on thigh to keep knee Commonly due to diabetic neuropathy affecting femoral nerve
extended due to weak quadriceps
Trendelenburg Sound side sagsà sideways lurch of trunk to Abductor weakness
bring patient’s body weight over affected limb 1) Bone (shortened contraction length causing
Gluteal/abductor Patient tilts toward side of problem to prevent weakness) –hip dislocation/ subluxation, short NOF,
lurch jamming of femur into acetebulum by gluteal coxa vara, flattened femoral head
muscle 2) Muscle –myositis
3) Neuro –poliomyelitis, L5, sup gluteal nerve
83
Hip pain –OA, AVN, Perthes disease
Adductor lurch Hip dysplasia
Cerebral palsy
Toe to heel Cerebral palsy
Club foot
Idiopathic
High stepping Foot lands flat or on ball Proprioception loss
Circumduction gait Foot drop (L5 injury/ common
Foot slap Due to partial paralysis of peroneal n Commonly due to peroneal nerve or sciatic nerve
(weakness) mononeuritis multiplex palsy)
Hip-hike gait Due to knee stiffness
Ataxic Broad based Cerebellar lesions
Parkinsonian/ Shuffling Parkinson’s disease
festinant
Scissoring (spastic) Jerky, feet in quinus, hips adducted UMN lesion (cord compression, multiple sclerosis, cerebral palsy)
FOOT DROP
1. Expose patient adequately, roll up pants
2. Observe face (eye / facial asymmetry / skin) + ULs
3. Observe LL for wasting / abnormal posture / skin lesions à note unilateral foot drop
4. Walk the patient à high stepping gait
5. Ask pt to stand on heels to confirm
Neurological Examination
6. Test for fasciculations
7. Tone (+ clonus)
8. Reflexes (brisk = cortical foot drop; absent = sciatic nerve lesion)
9. Power
• Hip internal rotation (normal à sciatic nerve lesion; weak à consider L5 root or lumbosacral trunk lesion)
• Knee flexion & extension
Common Peroneal Nerve:
• Ankle dorsiflexion (weak) and plantar flexion (weak if tibial nerve is involved) • Part of sciatic nerve (L4, L5, S1, S2)
• Eversion & inversion of foot (weak if tibial nerve is involved) • Supplies short head of biceps femoris
Common peroneal in thigh, crosses post to lat head of
Sciatic nerve L5 radiculopathy Cortical lesion
nerve gastrocnemius and becomes
Ankle dorsiflexion Weak Weak Weak Weak subcutaneous behind head of fibula
Ankle • Divides into superficial & deep
Strong Weak peroneal nerves
plantarflexion
• Gives off lateral sural cutaneous
Foot inversion Strong Weak Weak branch which joins with medial sural
Foot eversion Weak Weak Weak Weak cutaneous nerve à sural nerve
Hip internal
Strong Weak
rotation
Hip abduction Strong Weak
Ankle DTR Present Absent
10. Sensation
• Loss over L5 dermatome à L5 radiculopathy
• Numb over whole limb à sciatic nerve
• Glove & stocking distribution à peripheral neuropathy
CAUSES
Cortical foot drop Stroke, SOL
L5 PID, lumbar spondylosis
Sciatic Nerve Pelvic / hip #, hip posterior dislocation, nerve tumours
Common peroneal External pressure (casts)
nerve Trauma (tibia / fibula #, dislocation of knee, surgery)
Masses (ganglion, popliteal cysts, tumours)
Entrapment in fibular tunnel
DM, Leprosy
Bilateral foot drop Peripheral neuropathy
Bilateral L5 radiculopathy
Cauda equina syndrome
Motor neurone disease
Spastic paraplegia
MANAGEMENT
• Avoid further compression
• Identify & treat underlying cause
• Surgical exploration if progressive or no identifiable cause
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Approach to limping child
• Presentation: limping child/ delayed walking/ abnormal gait
• Things to consider: Site, Painful or painless, Age (rmber that regardless of age, must always include red flags (tumour, trauma & infx
<septic arthritis, OM, synovitis>) under painful cases)
Age Painful Painless
<3yo Most commonly due to infx Limb length discrepancies
Trauma (exclude NAI) - Bone: femur vs tibial shortening
- Toddler’s # (1-4yo): distal tibial # - Joint: commonly DDH
3yo to 7yo Transient synovitis (3-10yo; boys) - Generalized:
schoolgoing - Diagnosis of exclusion!!! o Muscle hypertrophy on one side
- COMMONEST cause of irritable hip § Causes: nerve (NF), vessels (hemangiomas)
Inflammatory arthritis o Polio infx
Growing pain - Physiological:
- Diagnosis of exclusion!!! o Metatarsal adductors
- Usually btw 4-5yo and during puberty o Tibial torsion
- Bone growth rate faster than rate of increase in length o Femoral anteversion
of muscle and tendon o Flat foot
- Pain occurs usually at the end of the day, often Biggest concern: undiagnosed DDH
relieved w massage/ after a good night’s rest
Leukaemia (4-10yo)
7-10yo Perthe’s disease (4-8yo)
Transient synovitis
Adolescents SCFE (~15yo)
>10yo Growing pains
1. Age 0yrs
DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)/ CONGENITAL DISLOCATION OF THE HIP (CDH)
• Epidemiology
o Incidence
§ 1 in 1000 live births; common enough for condition to be screened by neonatologists
§ Girls > boys; Left hip > right hip (bilateral in 20%)
o Risk factors
§ Family history: generalized joint laxity or shallow acetabulum
§ Intrauterine malposition/ crowding: multiple pregnancies, oligohydramnios, fibroids, large baby, small mother, extended
breech delivery
§ Postnatal posture: carrying babies with hips and knees fully extended
• Pathology
o Acetabulum unusually shallow and roof slopes upward too steeply; includes
§ frank dislocation, subluxation or partial displacement of hip OR
§ acetabular dysplasia without actual displacement
o Usually femoral head displaced posteriorly and superiorly
o Reduction impeded by joint capsule which folds inward and by fibrocartilaginous labrum
o Maturation of acetabulum and femoral epiphysis is retardedà femoral neck anteverted
o **Circular head needs to be in constant contact with acetabulum to ensure that
it remains spherical, concentric and well covered, ensuring proper Distribution
of body weight (prevent OA) + ROM
o Other contributing factors: tight iliopsoas, hypertrophic ligamentum teres,
hourglass capsule, fibrous tissue in acetabulum
• Diagnosis
o Newborn: Positive Barlows and Ortolani
o High risk cases (hip laxity or hip clicks): Ultrasound at 4-6 weeks
o Beyond 3 months (clinical signs) + X-ray
§ Reduced hip abduction
§ Assymetrical thigh skin creases
§ Galleazi test – femur shortening
§ Trendelenberg/waddling gait
• Symptoms
o Delayed walking, limping, hip clicks
o Unilateral dislocation: skin creases asymmetrical, hip abduction limited,
leg slightly short and internally rotated
o Bilateral dislocation: perineal gap abnormally wide, hip abduction limited,
waddling gait may be mistaken for normal toddling
• Signs
o Ortolani’s test (tests reducibility) - ABDUCT
§ Passively flex hips to 90deg and abductà on impeded hip abduction
apply pressure on greater trochanterà feel clunk as dislocation
reduces and hip abducts fully
§ Normally smooth abduction to 90deg
o Barlow’s test (tests dislocatability) - ADDUCT
§ Dislocate the hip by flexing the hip jt and adducting it followed by posterior force in the line of the shaft of femur
o Trendenlenburg’s test positive
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• Investigations
o NOTE: DX IS CLINICAL (US and XR are both not used to diagnose at birth)
§ U/s not done at birth due to laxity of hip joint (due to maternal hormones; for baby to
come out of birth canal) and thus inaccuracy of reading à earliest u/s at 6 weeks
§ X-ray has radiation + hip not ossified
o Ultrasonography (<3 months):
§ Indications:
• Screen for high-risk cases (above RF, hip laxity, hip clicks): US at 6weeks to
look at acetabular alpha/beta angles
• To ensure concentric stable reduction after treatment
• Weekly after w splint to ensure reduction & correct application of splints
• Every 6 weeks after once hip reduced
• Most effective <3months old (3 months onwards: XR)
§ Abnormal acetabular shape and femoral head position
§ Big alpha angle means hip held well
o X-rays in older children (>3months old)
§ Acetabulum: shallow + roof slopes upward too steeply
§ Femoral head: small + ossific centre of femoral head underdeveloped +
displacement superiorly and posteriorly
§ Shenton’s line: line fr inf border of femoral neck to inf border of pubic ramus broken
§ Perkin’s line: vertical line drawn along lateral most aspect of acetabular roof à Normally epiphysis should lie medial
§ Hilgenreiner’s line: horizontal line drawn thru superior aspect of triradiate cartilages à Normally epiphysis should lie below
§ Acetabular roof angle (Acetabular index): Normally 30deg or less
§ Von Rosen’s lines: hips abducted 45degà femoral shafts should point toward acetabula.
§ Medial gap: Greater the gap, greater possibility of dislocation
• Management:
o Goal of management is to achieve concentrically reduced and stable hips with good acetabular cover (to avoid early OA)
§ NOTE: the earlier the treatment the likelier the child will develop a normal hip.
§ If treatment started at 1yr, only <50% chance of absence of hip trouble in future
o 0-6 months (diagnosis at birth or from ultrasound followup)
§ Wait and see: watch instead of intervening if unsure of diagnosis
• Just observe if: hip laxity ONLY or hip clicks
• Repeat US at 4-6 weeks:
o If hips reduced and stable à no further Rx
o Otherwise treat as DDH
§ Reducible – Pavlik harness or abduction splint (old method) for 6wks – 3-4 months
• Details about abduction splint
o Double napkins/ abduction pillows for newborn
o Pavlik harness for larger infants
§ Human position: Hips 100deg flexed and 50deg abducted; allow
some movement in splint
§ AVOID: Frog position w hip abducted at 90deg- can cause AVN
(femoral head v sensitive to tension)
o U/S to ensure hip reduction before splinting à repeat US IN HARNESS after
1/52 to check position
• Repeat U/S OUT OF HARNESS after 6/52
o If stable on reexamination, observe for 6 mths (U/S every 6 weekly until 1st XR at 3months, then 6months)
o If unstable on reexamination, apply abduction splintage until hip is stable and acetabular roof developing
satisfactorily (usually 3-6months)
• OR wear for at least 3 mths till 1st XR: if XR shows concentric hips w good acetabular cover, then wean off splints
§ Irreducible carry out: Adductor tenotomy; Closed reduction + hip spica (Change cast every 6 weeks)
o 6-18 months (persistent/ missed dislocation, failed pavlik, failed tenotomy, persistent irreducibility)
§ Closed reduction can still be attempted but more difficult to achieve stability
• Blocks to reduction (hence hard to do adductor tenotomy)
o Extra-articular: adductors, iliopsoas
o Intra-articular: tight hour glass capsule, transverse ligament, pulvinar
• M&R under anaesthesia (gradually to prevent femoral head necrosis)
o Traction + gradual increase in abduction for 3 weeks
§ Arthrography to check reduction (medial pool of dye = unreduced)
• If reduced, apply plaster spica at 60deg flexion, 40deg abduction, 20deg int rotationà after 6 wks replace w abduction
splint that prevents adduction but allows movement à regular XR (6monthly) à discard if XR show concentric femoral
head w normal acetabular roof
• If unreduced, perform open reduction (usualy involves femoral derotation and shortening)à apply plaster spica for
3mths
o Beyond 18 months: Salter osteotomy + open reduction
§ Less potential for acetabular remodeling à both acetabular and proximal femoral Sx will be required
• Acetabular Sx (Salter osteotomy): Innominate osteotomy (bring acetabulum down to provide acetabular cover)
o Done at 2yo
o The entire acetabulum, tgt w the pubis and ischium, is rotated anteriorly and laterally as a unit, w the symphysis
pubis acting as a hinge. The osteotomy is held open anterolaterally by a wedge of full thickness bone graft, usually
taken from the anterior part of the iliac crest
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o Osteotomy redirects the entire acetabulum so that its roof covers femoral head both anteriorly and superiorly
o In young children, the acetabular deficiency is usually anterior, and thus the
Salter Osteotomy is designed to provide coverage anteriorly at the expense
of posterior coverage
o Success of procedure depends to some extent on the flexibility of the
symphysis pubis (which decreases w age), thus the importance of
screening so as to intervene earlier
§ Open reduction
o Chronic neglected dislocations (rare) usually not reduced if:
§ >8 yrs for unilateral (no more remodeling past 8 yrs so reduction would cause OA)
§ >5 years for bilateral
• Prognosis: *All will walk assuming muscles and nerves are functional
o Good results if treated <6yo if unilat
o Consequences of not reducing
§ Partial dislocation (formation of false joint): progressive deformity, disability and
secondary hip OA
§ Complete dislocation: Trendelenburg gaità scoliosis
§ Bilat: waddling gait (hips dislocated behind so nothing to hold pelvis in btw)à lordosis
2. Age 0-5yrs
TRANSIENT SYNOVITIS
• Incidence
o Commonest cause of hip pain in children (3-10yrs old)
o Boys 2X more than girls
• Pathology: inflammation of the synovium of the hip joint, postulated due to URTI/ pharyngitis/ bronchitis/ otitis media or trauma (weak link)
à no definite cause known
• Diagnosis: of exclusion.
• Symptoms (last for 1-2weeks)
o Unilateral groin/ hip pain; inability to bear weight
o V young children may have no symptoms other than crying at night
o Recent Hx of above illnesses (in >50% of cases)
• Signs
o Log roll (most sensitive test): detect involuntary muscle guarding of one side
o Antalgic gait
o Tenderness on palpation even during passive movement
o Mild restriction of ROM (2/3 of patients)
• Investigations
o U/S: joint effusion
o X-ray: no changes
• Management (non-operative)
o Heat, massage, bed rest for 7-10days in a position of comfort
o Medications: NSAIDs (naproxen/ ibuprofen)
• Important to rule out RED FLAGS
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• Oral Abs also acceptable: provided adequate blood lvls of Abx are demonstrated, parents are reliable, and Abx does not
cause GI disturbances that would interfere with absorption
• NOTE: Consider septic joint to be a closed abscess (don’t expect Abs alone to work à Sx!)
o Surgical
§ Perform repeated percutaneous joint aspirations
• Only if easily accessible peripheral joint, clinical course <6days, no OM, no immune deficiency or chronic illness
§ If condition fails to improve, perform open drainage in OT
• Indications:
o Hip and shoulder joints
o Peripheral joints that do not respond to percutaneous aspiration
o Patients who are systemically ill
o Suspected organism (S.aureus/gram-) produce cartilage-damaging enzymes
§ Gonococaal arthritis less likely to rapidly damage a joint thus may be managed w repeated aspirations if
the joints involved are peripheral. Open drainage should stil be done for gonococcal arthritis of hip
§ Apply traction on hip / splint in abduction until infection resolves; if instability is suspected (esp if Rx was delayed and
substantial capsular damage may have occurred), immobilize patient for a longer period
• Neglected septic hip with radiographic instability requires spica cast; Unstable shoulder requires a sling and swathe
o Follow up (at least up to 1yr after surgery)
§ Assess joint function
§ X-ray: ensure no radiographic evidence of loss of joint space, AVN of epiphysis, joint instability, damage to growth plate
3. 5-10yrs
PERTHES’ DISEASE (COXA PLANA)
• Epidemiology
o 1 in 10 000
o Children aged 4-8yrs old
o Boys 4X affected compared to girls
o R=L; Bilateral 10-15%
• Normal BS of femoral head:
o 0-4months: femoral head supplied by
§ 1) Metaphyseal vessels,
§ 2) Lateral epiphyseal vessels in retinacula (from medial &
lateral femoral circumflex from profunda femoris),
§ 3) Scanty vessels in ligamentum teres (from obturator)
o By 4yrs: metaphyseal supply disappeared
o By 7yrs: vessels in ligamentum teres developed
o 4-7yrs: femoral head blood supply mostly fr lateral epiphyseal vessels
• Pathology
o Trauma/ non-specific synovitis results in effusion in hip jointà increased pressure on lateral epiphyseal vessels in retinacula
disturbs blood supplyà avascular necrosis of femoral head à collapse & fragmentation, healing & remodeling à can cause
progressive deformity of hip jt & eventually early degenerative disease
• Pathological stages (similar to AVN)
Stage Process X-ray
1 Ischemia causing death of part of femoral head Normal (femoral head stops enlarging)
2 Revascularisation and repair - Epiphysis flat and sclerosed (new bone is laid; healing and
- If only part of epiphysis involved and repair process rapid reossification à small dense capital epiphysis)
- Bony architecture completely restored - Apparent widening of joint space
3 Distortion and remodeling - Epiphysis:
- If large part of epiphysis involved or repair process slow • Coxa plana (flattened)
- Epiphysis may collapseà subsequent distorted growth of • Coxa magna (enlarged)
head and neck • Fragmentation (collapse)
• Lateral displacement
- Metaphysis: Rarefaction, Broadened
- Femoral head incompletely covered by acetabulum
• DDx: non-specific transient synovitis
• Symptoms
o Hip pain and irritation; referred pain to knee
o Limp; Shortened leg
• Signs
o Early: all ROM limited and extremes painful
o Late: abduction and internal rotation often limited
• Investigations
o X-ray (described above)
o Radioisotope scanning: ischaemic area appears as a ‘void’ even before X-ray changes appear
• Prognostic grading (Catterall grading: according to degree of femoral head involvement)
Grade Severity Prognosis
1 Involves anterior portion of epiphysis only Revascularisation may be complete
No collapse or sequestrum w/o bone collapse
2 ≤50% epiphyseal involvement with a sequestrum Bony collapse inevitable
3 ~75% epiphyseal involvement with collapse and sequestrum Bony collapse inevitable
4 Whole epiphyseal involvement Poor prognosis
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o Natural Hx: 75% have eventual healing and revascularization of the necrotic femoral head within 2-3 years
o Age: Younger better – as head can regrow
o ROM – less impaired better
o Disease severity/head involvement – the lesser the involvement the better
• Management: Aim for resolution of symptoms, and a spherical, well covered femoral head
1) Initially: skin traction on affected leg until pain subsides (~3 weeks)
2) Definitive: depending on prognosis Treatment
Favourable prognostic signs No active treatment
• Onset <6yo (Maintain/Improve ROM with activity modification)
• <50% femoral head involvement
• No stiffness or shortening on examination
• Absence of metaphyseal rarefraction
• Normal femoral head shape
Unfavourable prognostic signs Containment of femoral head (1 of 3 ways)
• Onset >6yo 1. Abduction splint (for a year, for bone changes to
• Involvement of >50% femoral head run their course)à unpopular
• Significant stiffness or shortening on examination 2. Varus osteotomy of femur
• Severe metaphyseal rarefraction 3. Innominate osteotomy of pelvis
• Lateral displacement of femoral head
4. 10-20yrs
SLIPPED CAPITAL FEMORAL EPIPHYSIS (EPIPHYSIOLYSIS)
• Commonest cause of hip pain in adolescence (11-15yo)
• Risk factors
o Associations: fat pubertal children, family Hx, precocious puberty, rickets, down’s
o Think of endocrinopathies in Bilateral SCFE: hypogonadism, hypothyroidism, hypopituitarism,
growth hormone deficiencies
o +/- history of trauma (30%)
o 2M: 1F
• Pathology: Insufficiency/stress fracture through hypertrophic zone of cartilaginous growth plate à
femoral neck glides upwards (head stays in place) à limb shortens and externally rotates (may
become fixed) à stiffness of hip à AVN à chrondrolysis (early onset OA)
o Excessive weight on predisposed hip
o Possibly due to imbalance btwn growth hormone (for bone growth) and gonadal hormone (physeal fusion)à immature physis too
weak to resist stress imposed by increased body weight
o Hence impt to rule out endocrine problems: pituitary, growth, thyroid, parathyroid, gonadal
• Symptoms
o Pain in groin +/- radiation to ant part of thigh or knee (referred pain; thus diagnosis delayed coz they
can present w knee pain)
§ Painful = unstable (weight bearing not possible)
o Limp
o Bilateral SCFE in 1/3 of cases
• Signs
o Pain on movement (for acute slip)
o Coxa vara deformity
o Leg 1-2cm short; externally rotated and flexed
o Limited abduction and internal rotation
• Investigations
o X-ray
§ AP view:
• Epiphyseal plate appears too wide and woolly
• Trethowan’s sign: Kline’s line drawn along
superior surface of neck remains superior to
head instead of passing through it (“ice cream
falling off cone”)
§ Lateral view:
• Femoral epiphysis tilted backward
• Detect tilt by measuring angle btwn epiphyseal
base and middle of femoral neck
o If angle is <90deg, epiphysis has
slipped posteriorly
• Prognosis depends on severity and stability of slip
• Complications
o AVN (may also be seen after reduction or pinning of slip)
o Coxa vara deformity: If displacement not reduced and epiphysis fuses in deformed positionà may need correction by osteotomy to
prevent secondary OA
o Secondary OA: In unreduced displacement and AVN
• Management: ONE GOOD SCREW (cannulated screw inserted percutaneously; always need Sx to stop progression)
NOTE: (manipulation is contraindicated)
o Displacement <1/3 epiphyseal width: Accept position, Epiphyseal fixation with pins
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o Displacement of 1/3 – ½ epiphyseal width
§ Epiphyseal fixation with pins +/- compensatory osteotomy (if residual deformity present even after remodeling)
o Displacement > ½ epiphyseal width
§ Surgery (2 choices)
1) Epiphyseal replacement with piece of femoral neck + fixation with pins
2) Epiphyseal fixation with pins +/- compensatory osteotomy
o Femur divided just below greater trochanterà distal fragment repositioned in valgus, flexion and internal rotation
90
• Ficat Arlet Staging + Management
o Extent of disease for stage 1,2,3 à A: <15%, B: 15-30%, C: >30%
Stage Processes & X-ray (Ficat-arlet staging) Radiographs Management (ELIMINATE
Clinical features CAUSE!!)
0: preclinical Hip at risk -Normal; may have signs of
à Preclinical phase previous trauma
of ischemia &
necrosis; no pain
1: pre- - Bone death -CT scan and X-ray normal Conservative: for early stage
radiographic (Marrow necrosis & (XR may be normal for disease or in medically unfit à
cell death within months after symptoms begin) ineffective at halting progression;
48hours) w/o -MRI: edema prevent bony collapse with
structural change -Bone scan: increased uptake - bed rest
à pain, typically in - weight relief (crutches)
groin - splintage
- NSAIDs/ other analgesics
- Bisphosphonates (slows resorption
of necrotic bone)
- PhysioRx
- Control RF
Coronal T1-weighted MRI in a patient with AVN
shows decreased signal within the femoral head Surgical: Core decompression +/-
(arrow), representing edema bone grafting
2: pre- - Repair and early X-ray • used if venous stasis or marrow
collapse structural failure - Earliest findings are mild edema
- Small # appear in density changes: Subarticular • Centre of head of femur
dead bone segment of increased bone excavated
- Days/weeks after density due to increased • Fibular/other graft to fill up cavity
infarction, new bone sclerosis/ cyst formation • Used in young active pts (best
laid down upon (reactive new bone formation chance of preserving femoral
dead trabeculae in the surrounding living tissue head)
which increases the total mass
à Pain & stiffness of calcified bone)
- Normal bone contour
- Osteopenia T2 weighted: AVN of bilateral femoral heads
- NO collapse -reparative border appear hypo/hyperintense
(double rim sign) on right side indicating granulation
MRI: geographic defect and sclerosis respectively.
Bone scan: increased uptake -Dark line bordering the AVN focus on left side
represents sclerosis.
-Normal cartilage and acetabulum
3: collapse - Major structural - Radiographic changes Surgical: (bone collapse alr
failure obvious occurred!!)
- Necrotic portion - Step-off in contour of - Femoral head resurfacing
crumbles subchondral bone - Hemiarthroplasty
- Bony outline - Pathognomonic crescent - Sugioka transtrochanteric rotational
distorted sign: subchondral lucency osteotomy
(evidence of subchondral - Realignment osteotomy: angular
à Painful & collapse; indicate early osteotomy
stiffness, limping flattening of femoral head) • redistributes weight-bearing
- Acetabulum intact forces to undamaged articular
cartilage supported by healthy
MRI: crescent sign and bone and may relieve pain and
cortical collapse prevent further bone distortion.
• also for late stage 2 disease with
cyst formation
He / she presents with a (duration) history of bilateral progressive groin pain (right > left / left > right) that has:
1. Failed to improve with conservative management
2. Gotten progressively disabling over the years
3. Resulting in marked loss of functioning
The pain is associated with:
1. Morning stiffness in the hip / stiffness after resting
2. Progressive shortening of 1 limb
The knee pain started (duration) years ago and has gotten progressively worst.
He / she describes the pain as (nature: sharp / dull / aching) . It is mechanical in nature, aggravated by movement when he / she does (type of
activity) and relieved by rest. It is also worst at the end of the day.
The pain is felt in the groin with radiation to the knee.
His / her current pain score is ___ and the pain (severity: affects sleep / requires frequent use of painkillers) .
In addition, he / she experiences stiffness in the hip after a period of rest.
Over the years, he / she noted that her (left / right) limb has shortened in length.
Functional Status
He / she suffers marked functional impairment from his / her condition. He / she walks with a limp. (if any)
His / her walking distance is limited to ______ from ______ previously, (with / without) a walking aid.
He / she (has / has no) difficulty putting on her socks & shoes and tying her shoelaces / wearing pants.
Currently, he / she is (able / unable) to climb the stairs, with (2 feet per stair / alternate foot per stair) .
He / she is (able to / not able to) sit cross legged.
He / she is (able to / unable to) squat / use a squatting toilet since (duration) years ago.
Systemic Review
There are no symptoms suggestive of referred pain such as back pain or neurological symptoms like weakness or numbness of the lower limbs.
Although pain radiated to the knee, it did not radiate to the calf or the foot.
He / she (has / does not have) any previous trauma or childhood injury to his / her hip. (+ details)
There is no involvement of other joints in the body. He / she also does not have a history of joint infection.
There is no fever, night pain or constitutional symptoms like loss of weight or loss of appetite.
Family History
There is no family history of blood disorders or similar joint problems (sickle cell disease or Gaucher’s disease).
Drug History
He / she has NKDA and is currently on: (esp. long-term steroid use) for her medical condition(s): ___________.
He / she has been taking TCM (details) for (medical condition) for (duration) .
Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a ________.
He / she (has / has never) engaged in deep sea diving or worked in compressed air environment.
He / she lives with his / her _________. His / her main caregiver is his / her ______________.
He / she lives in a residential (with / without) lift landing. There (is / is no) squatting toilet in the house.
Currently, the family (does not have any financial issues / is receiving financial aid from ) .
In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with a significant past medical history of _______ on long term steroids and
________ / previously a heavy drinker, presenting with bilateral progressive groin pain for (duration) , worst on the (left / right) associated with
stiffness and progressive shortening of the limb that has failed conservative management and is currently admitted for hip replacement surgery.
My provisional diagnosis will be that of avascular necrosis of the (left /right) hip secondary to _________.
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PHYSICAL EXAMINATION
Examination of the upper limbs did not reveal any Herberden’s nodes or Bouchards nodes, gouty tophi or rheumatoid nodules.
Apparent limb length is ______ cm while true limb length is ______ cm.
There was no tenderness on palpation of the greater trochanter.
Thomas’ test for fixed flexion deformity was positive for the (left / right) limb.
Range of motion was severely limited over the (left / right) hip.
Internal rotation ___, external rotation ___, abduction ___, adduction ___. Flexion of the hip ranged from ____.
There is / is no fixed external rotation deformity or fixed flexion deformity of the hip.
Screening of the knee joint and the back did not reveal any abnormalities.
Popliteal, posterior tibial and dorsalis pedis pulses were well felt in both lower limbs.
Neurologically, power of bilateral lower limbs is full and sensation is intact bilaterally.
In summary, Mr / Mdm XXX has bilateral osteoarthritis of the hip likely secondary to avascular necrosis from (long term steroid use as evidenced
by the cushingoid features noted on general inspection / heavy alcohol consumption / SLE) . He / she has an (antalgic / Trendelenburg gait) and
the Trendelenburg test was also positive over the (left / right) . Marked gluteal wasting was noted, he / she also has a fixed flexion deformity of the
hip and apparent as well as true limb length shortening. Range of motion of the hip: (internal rotation / external rotation / abduction / adduction /
flexion / extension) were severely limited at ____ degrees.
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6. Hip dislocations
GENERAL PRINCIPLES
Cause X-ray Management
Septic arthritis Absent femoral head (surviving area too -Traction
- Partial/complete dissolution of femoral head osteoporotic to be seen) - (if above fails), open reduction with greater
trochanter in acetabulum + varus osteotomy of
femur
Muscle imbalance - Improper greater trochanter - As for DDH + muscle rebalancing operation
- Cerebral palsy, myelomeningocele, polio - Valgus femoral head
Trauma - Look for associated acetabular rim # - Reduction (ORIF if rim # is present)
After total hip arthroplasty (main cause)
- 1-4% in primary THA, 16% in revision cases
- 74% Posterior > 16% anterior > 8% central
- THA unstable in flexion & int rotation
Mechanism of - Dashboard injuryà femur thrust upward and femoral head Fall on side/ blow
injury forced out of socket; often a piece of bone at back of over greater
acetabulum sheared off trochanterà femoral
Associated injuries head forced
1. PCL injury medially, fracturing
2. Posterior wall acetabulum # acetabulum
3. Femur # (distal, neck, head)
4. Sciatic nerve
Signs - Shortened limb - Abduction, external rotation
- Adduction, internal rotation - Slight flexion
- Slight flexion
Investigations AP film: (NOTE: AVN is a distinct possibility!) AP film:
(X-ray) - Femoral head above acetabulum - Occasionally head directly ant to
- Femoral head smaller, trochanter less prominent (due to normal positionà confirm with lateral
adduction + int rotation) film
Multiple views (or CT):
- Exclude acetabular rim/ femoral neck fracture
Management M&R (Bigelow’s manoeuvre) M&R (Barlow’s equivalent)
- Relax muscles: conscious sedation (IV fentanyl)/ spinal/ GA - Muscle relaxation
- Assistant stabilizes pelvis - Assistant stabilizes pelvis
- Fully flex hip (by simply hooking leg and stand up over - Fully flex hip + adduct + int rotate
patient) & apply upward traction + abduct + ext rotate + downward pressure on femur
- X-ray
- Maintain via traction until pain free (~2 weeks)
- After 3 weeks walk with crutches
Complications Early:
• Fractures (femoral head, neck, shaft)
• Vascular injury: femoral veinà thrombosis & embolism
Late:
• Myositis ossificans
• Coxa magna (in up to 50% of children after hip dislocation)
• Recurrent dislocation
• Secondary OA (due to cartilage injury or intra-articular loose bodies)
Early: AVN of femoral head
• Nerve injury: Sciatic nerve (damaged in 10-20% but • If necrotic segment small, carry
usually recovers within months; occurs esp when rim # out realignment osteotomy
is present)à splint ankle (ankle foot orthosis) to • Younger patients:
overcome footdrop hemiarthroplasty of femoral
Late: head or hip arthrodesis
• AVN of femoral head: 10% occurrence; increases to • Patients >50yr: total hip
40% if reduction delayed by a few hours replacement
• Post-traumatic OA
o Due to 1) cartilage damage, 2) retained fragments
in joint (loose bodies), 3) femoral head ischemic
necrosis
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7. Fractures of proximal femur
GENERAL INFORMATION
• DDx of hip #: pubic ramus #, acetabular #, isolated # of greater trochanter, trochanteric bursitis/ contusion
• Female to male ratio is 2:1
• Type of fractures
Location Capsule Type Note Incidence
Neck of femur Intracapsular Subcapital -Tardy healing - Seen in same
Transcervical frequency
Extracapsular Basal -Treated like intertrochanteric #
Intertrochanteric Extracapsular -Unite very easily
Pertrochanteric (trochanter #ed) -Seldom cause AVN
Subtrochanteric Extracapsular -Blood loss greater than - Rarest
intertrochanteric/ NOF fractures
• Risk factors
Non- • Old age Modifiable Causes of increased risk of falls
Modifiable • Female sex • Poor vision, vestibular dysfunction
• Early menopause • Lower limb weakness
• Nulliparity • Co-morbidities (CCF, CVA)
• Family/ personal history of • Hazards at home
fractures Reduction of bone strength
• Caucasian • Osteoporosis, low Ca intake
• Steroids, alcohol, smoking, increased/decreased T4
• Physical immobility
• Pathological bone conditions
• Chronic liver and renal failure
• WHO fracture risk assessment tool (FRAX)
o Gives 10-year probability of hip # and 10yr probability of a major osteoporotic # (spine, forearm, hip, shoulder)
§ For local chinese: use Hong Kong chinese
§ For local Indians: use US (Asian)
o Disadvantges:
§ Cannot calculate for patients <40yo
§ Does not take into account type of #, number of #
§ Does not tell u who to treat; still rely on clinical judgement
o Risk factors used: age, sex, weight, height, previous # (spontaneous or from low impact trauma), present fractured hip, current
smoking, steroids (>3 months of 5mg daily), RA, secondary osteoporosis (eg. type 1 DM, osteogenesis imperfecta, untreated long
standing hyperthyroidism, hypogonadism or premature menopause [<45yo]), chronic malnutrition, malabsorption and chronic liver
disease), alcohol >/=3 units a day, bone mineral density
• History
o Fall: how patient fell, pain/ tenderness/ deformity, can walk?
o What happened before fall: hazards at home, LOC?
o Predisposing fx to #: modifiable and non-modifiable
o Comorbidities
o Premorbid functional status
o Osteoporotic RF
• Symptoms
o Painful limited hip movements +/- Bruising (suggestive of extra-capsular fracture)
• Signs
o Shortened, externally rotated
o Fracture of proximal half: Flexed, abducted
o Bruising suggest extra capsular #
o Tenderness over femoral neck
o Painful limited hip movements
• Investigations: confirm Dx + determine severity + pre-op Ix
o Radiological
§ AP pelvis (not hip)
§ Lateral x-ray of affected hip
o Pre-op
§ Haemotological: FBC, PT, aPTT, GXM (group and cross match)
§ Renal panel: U/E/Cr, urinanalysis
§ Liver panel
§ Chest x-ray
§ ECG
• Initial management
o Analgesia
o Antibiotics if infection suspected
o Pre-op traction for pain relief and to ensure union takes place in good position
o Thromboembolism prophylaxis (SC heparin 5000units BD)
• General principles of management
o Conservative: if undisplaced, clinically stable & ROM is full and painless
o THR indications: OA hips, Pathological #, Acetabular involvement, Revision hip
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• After care:
o Weight bearing
o Physiotherapy (preserve joint movement, restore muscle power, access type of mobility aids needed)
o Treat osteoporosis and comorbidities
• Cx of femoral #s:
o Non-union in 30%; also delayed union and malunion (coxa vera) à OA
o Redisplacement
o Erosion of femoral head in unstable IT # causing coxa vera
o AVN in intracapsular NOF #, rarely in intertrochanteric
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o Children until 10yo
§ Traction (3-4weeks)
• Gallow’s traction for children <12kg
• Thomas’ splint with pearson knee attachment for older children
§ Spica (another 6weeks)
o Teenagers
§ Longer time in traction and spica
§ ORIF with plate and screws if reduction unsatisfactory
• Complications
o Prognosis: high morbidity/ mortality; often need blood replacement
§ General Cx (from high-energy injuries): Haemorrhage, shock, fat embolism, ARDS, DIVC, MODS
o Early
§ Vascular injury (to be repaired or grafted immediately) – Femoral artery
§ Neurological: Sciatic nerve
o Late
§ Thromboembolism
§ Fat embolism
§ Infection (from open injuries or internal fixation)
§ Delayed union/ non-union: If #ed femur doesn’t unite in 100 +/- 20days, do exchange nailing w larger nail +/-bone-grafting
§ Malunion: Esp fractures treated by traction and bracing
§ Joint stiffness of knee: From joint injury at same time or due to soft-tissue adhesions during treatment
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9. Hip arthroplasty
Bipolar arthroplasty
Hemi-arthroplasty (only
femoral component)
Unipolar arthroplasty
Hip arthroplasty -Moore's &
Thompson
Total Hip Replacement (femoral +
acetabular components)
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Knee
Atraumatic
Traumatic
Deformities
Fractures
• Genu
Valgus
• Tibial
Plateau
Fractures
• Genu
Varum
• Patella
Fractures
Dislocation
• Patella
Dislocation
Osteochondritis
• Knee
Dislocation
Dissecans
Meniscal
Lesions
Patellofemoral
Overload/
Chondromalacia
Patellae/
Patella
Pain
syndrome
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Examination of the Knee MOVE
The preliminaries: Intro urself to patient, ask permission to examine. 1. Active range of movements:
Ensure adequate exposure (underwear) but consider patient modesty - Get pt to flex knee all the way and then extend, look for
also (midthigh). Ensure good lighting, and good positioning of bed. any restriction of full flexion or extension (compare both
sides and measure difference if unequal)
With pt standing. Ask pt to stand with feet side by side:
- Fixed flexion deformity of the knee---Ask patient to push
down on examiner’s hand placed in the popliteal fossa to
LOOK— Inspect knee and LL fr Front à Side à Back à Side see if patient is able to press hand against bed (or
1. General appearance and vitals – pallor, BP, and HR. obliteration of space under popliteal fossa). (N: 0-135°) à
2. Limb alignment & Deformity: varus (normal M 7° F 9°)/ valgus if there is residual deformity, patient has some degree of
- measure intercondylar distance (normal <5cm) and extensor lag à measure extent of deformity with
intermalleolar distance (normal < 2cm) goniometer
- Fixed flexion deformity (fr side) 2. Passive range of movements:
- Pelvic tilt (best fr back) - Passive extension: Ask patient to relax and assess for
3. Scars over anterior and posterior aspect of knee fixed flexion deformity by raising leg at the ankle à
4. Swelling measure angle if present
- effusion w/ obliteratn of medial parapatellar fossa - Passive flexion: flex patient’s knee and ensure no pain,
- cyst e.g. Baker’s cyst over popliteal fossa then measure angle at maximal flexion
5. Sinuses - If patient has restricted ROM, need to differentiate fixed
6. Discolouration – redness, bruising, etc flexion deformity from extensor lag by assessing if there
7. Muscle wasting – quadriceps is a joint contracture or muscle weakness
WALK +SQUAT: assess gait especially looking for antalgic gait 3. Crepitus: Feel with hand over patella during passive movement
With patient lying supine, knees fully extended:
SPECIAL TESTS
LOOK AND FEEL With legs placed in 90 deg flexion & aligned (heels in the same line):
1. Feel for temperature gradient over the knee joint (proximal to 1. Posterior sag sign (MAKE SURE DONE 1ST)
distal), and any temp diff compared to the other knee - Flex both knees to 90deg and view knees from side
2. Effusion – obliteration of medial parapatellar fossa looking for posterior sag of tibial tuberosity on the
- Fluid shift/ bulge test (10-20cc) (sensitive for small femoral condyles à posterior cruciate injury
amounts) – milk fluid from suprapatellar pouch, stroke 2. Posterior drawer test
medial parapatellar fossa to empty it, then swipe the lateral 3. Anterior drawer test à ensure not false +ve
side and look for refilling of the medial fossa (bulge) - Sit on patient’s feet, use both hands to splint the
- Cross-fluctuance (30-50 cc): milk fluid from suprapatellar hamstrings (ensure they are relaxed), with thumbs on the
pouch w L hand and apply pressure on medial aspect of joint line, and pull towards you. Compare both knees
knee and feel for cross-fluctuance on lateral aspect of knee - In ACL tear, there will be no end-point on pulling forward
- Patellar tap/ ballotment test (>60cc) – milk fluid from 4. Lachman’s test
suprapatellar pouch downwards w L hand, use index & - With knee in 20-30 degrees flexion, place left hand on
middle fingers of R hand to press down on patellar to feel thigh pressing downwards to stabilize femur, and right
for ballotment; positive when patellar hits femur w a tap hand under the proximal calf with thumb over the joint
3. Feel the articular surface of the patella for tenderness, line pulling the tibia towards you
osteophytes. - Also testing for ACL, but more sensitive test
4. Muscle wasting over quadriceps (esp vastus medialis) & 5. Pivot shift for ACL
hamstring - Lift leg up and with lower limb adducted and knee
- Measure circumference of quadriceps 10-15cm (or 4 extended, patient is told to relax and the leg is internally
fingerbreadths; 15cm safer to avoid the patella and rotated with valgus force applied to the knee, and then
suprapatellar pouch) proximal to superior border of the flexed; positive when tibia suddenly shifts forward on
patella) – “objective assessment of wasting”; significant if femur with a click sound
difference is >2 cm. 6. Collateral ligaments (varus and valgus stress test)
5. Other swellings eg. cysts arnd knee, osteophytes in OA knee - test in full extension (where capsular elements and
6. Feel medial & lateral patella facet: use fingers to gently cruciates are also taut and restrict displacement) and in
sublux patella medially/laterally to palpate the facets 30 degrees flexion (where only the MCL and LCL are
7. Patella grinding test (damn pain): apply downward pressure responsible for preventing displacement
on patella and observe patient’s face for any pain à PFOA 7. Other special tests that can be done:
8. Patellar apprehension test for recurrent patellar dislocation – - Quadriceps active test for PCL – with patient’s knee
apply lateral force on patella and attempt to sublux the patella joint in 90 degree flexion and examiner sitting on
laterally and look for apprehension on patients face or do it patient’s foot, get patient to contract quadriceps
while flexing and extending the knee joint; positive when muscle; positive when tibia shifts forward eliminating
patient feels like patella is about to dislocate the posterior sag appearance
With knee flexed to 90 degrees: - McMurray’s test (NOTE: test is painful, thus don’t do it
1. Palpate for tenderness with one thumb: during exam): start pain=post horn; end pain= ant horn
- Tibial tuberosity • Insensitive test; better for big tears/ bucket handle
- Patellar tendon • Start with knee in full flexion, and place thumb and
- Around either side of e patella (retropatellar tenderness) fingers on jt line
- Quadriceps tendon arnd e superior border of the patella • To test medial meniscus, externally rotate tibia w
- Medial and lateral joint lines, one at a time your R hand at e ankle, and apply valgus force at
- Femoral condyles the knee with your left hand, then extend the knee
- Gerdy’s tubercle: insertion of IT band • To test lateral meniscus, internally rotate tibia and
- Lateral collateral ligament: start at prominence of head of apply varus force at the knee, then extend
fibula and palpate upwards towards lateral epicondyle • Repeat the test, looking out for palpable or audible
- Medial collateral ligament: feel medial epicondyle and click in the knee during extension, or for pain
palpate downwards - Check Q-Angle of knee
FINISH with assessment of neurovascular status of the lower
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limb (palpate distal pulses, “tip-toe” and “heel-step”, and
examine the back, hip and ankle joints for any pathology.
Approach to Knee Conditions
Symptoms o Non-Mechanical
• Pain § Constitutional features
o Referred Pain: Always examine hip if knee is normal – § Constant/ night pain
obturator nerve crosses both joints § Morning stiffness (>1 hr for >/=6 weeks)
o Generalized: arthritis (OA, RA) § Progressive deterioration
o Localized (mechanical disorders) § Panarthritis
§ PF disorders: patellar instability, PF overload, o Mechanical
PFOA, osteochondral injury, chondromalacia § Local symptoms
patellae § Progressive (very gradual)
§ Jt disorder: osteochondritis dessicans, loose body, § Specific mechanical correlation (arthritis of specific
synovial chondromatosis, ligament tears, meniscal area)
tears Examination & Ix
§ Periarticular disorders: patellar tenditnitis, patellar • Suspect systemic
ligament strain, bursitis, OSD o General examination
• Swelling • Suspect local
o Anterior knee lump: OSD, housmaid’s knee, clergyman’s o Knee examination
knee § Effusion
o Posterior: baker’s cyst, popliteal cyst, popliteal aneurysm • Very turbid – Gout, Infection (eg. TB)
o Lateral: meniscus cyst • Straw coloured - RA
o Traumatic knee swelling: • Clear – OA (Mechanical)
§ Effusion, usually represents hemarthrosis (swelling • Purpose of arthroscopy:
instantly) o Establish or refine accurary of Dx
§ Ligamentous injury w hemarthrosis o Help decide whether to operate; plan Sx approach w
§ Meniscal injury (swelling after hrs) more precision
§ Traumatic synovitis o Record progress of knee disorder
o Non-traumatic knee swelling o Perform Sx procedures
§ Septic or crystal induced arthritis • XR:
§ Seronegative arthritis (P-A-I-R: psoriatic, AS, IBD, o AP weight bearing, lateral
Reiter’s) o Skyline view (knee flexed and beam aimed from anterior
§ Seropositive arthritis (RA, SLE) tibia to ant femur): PFJ
§ Avascular necrosis (rare) o Tunnel view: knee bent, can see the hollow btw 2
§ Sickle cell dsease articular surfaces
§ Synovitis o Oblique: for intra-articular #
• Stiffness o Erect-leg full-length view:
o Early morning: inflammatory § Radiograph from hip to foot w patient standing
o After periods of inactivity: OA § Useful in evaluating limb length discrepencies and
• Weakness genu varus/valgus
• Locking – spontaneous block to full extension àtorn meniscus, o Rosemberg view:
loose body (jammed btw articular surfaces) § 30-40deg flexed weight bearing view w the XR
• Pseudo-locking: restricted ROM without mechanical block beam tilted caudal to profile the jt line
o Arthritis (effusion, pain), muscle spasm following injury § Best view to visualize loss of medial jt space
• Instabilitity (giving out) • Other Ix: Aspiration (colour, uric acid crystals, c/s), MRI, bone
o Ligamentous instability: ACL, PCL, LCL, MCL scan, bloods (FBC, ESR, CRP, uric acid, RA profile….)
o Recurrent dislocation of patella/ patellar subluxation Problem Based Approach
o Torn meniscus, loose body • Serious
o OCD o Presentation usually non mechanical in nature
o RA o Diagnosis: Infection, Tumour, Inflammation
o Muscle weakness • Disabling
• Function impairment – Limping (could be due to pain, o Usually mechanical in nature
weakness, locking etc) o Diagnosis: Ligament injury, meniscal injury,
• Deformities: osteochondritis dissecans, osteoarthritis
o RA, TB, genu varum/valgum, charcot joint • Bothersome: causes concern and requires care/reassurance
Epidemiology but precise dx may not be necessary
• Age o Evaluation reveals it is not serious or disabling: tendinitis,
o Children – Often developmental Conditions OSD à explain, reassure, rehab
§ DDH Pitfalls
§ Discoid meniscus (prone to tear) • Malingering – Dangerous diagnosis to make
§ Patellar dislocation (not developmental) o When evaluation exhausted, seek or ask patient to seek
o Adolescents/Adults – Trauma Conditions (meniscus, second opinion
ligament) § Eg. Stress fractures may not appear on xrays;
o Elderly – Degenerative early infx like necrotizing fasciitis
• At all Ages • Major knee trauma
o Infection (eg. septic arthritis, TB) o Xray may look alright after reduction; but important to
o Inflammation assess neurovascular status; monitor and manage
§ Young - Still’s Random
§ Older - SLE, RA • 80% of haemarthrosis due to ACL Injury
o Tumour (osteogenic sarcoma) • Septic arthritis and gout have acute onset
History • White count raised in gout but not in RA
• Mechanical vs Non-Mechanical
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1. Lower limb malalignment (intoeing due to malalignment of hip, knee, ankle or foot)
General Information
• Deformity gauged by observation with patient standing and weight bearing
• Foot progression angle – angle that the axis of foot makes with midline
o Normal – 6-10 degrees external rotated
o Intoeing – negative 20-30 degrees
• Knee deformities:
o Genu varum: Measure distance between knees with legs straight and medial malleoli just touching (should be <6cm)
o Genu valgum: Measure distance between medial malleoli when knees held touching with patellae facing forwards (should be <8cm)
• Deformities common in children and most correct spontaneously by 10-12, hence no need to treat but just follow up every 6 months
• Physiologic evolution of leg alignment at various ages (2, 4, 6yo are milestones!)
o 0-18months/2yrs: genu varus (tibial intortion)
o 2-6yo: genu valgus due to laxity of ligaments (valgus maximal at 4yo)
§ Reassure parents; monitor child’s inter-malleolar distance every 6 mths to record progress
o 6-7yo: ligaments tighten and deformity starts to straighten out
§ Operative correction shld be advised if a marked deformity persist past 10yo
o Normal adults/teens: slight valgus (5-7deg)
• Etiology of malalignments
o Trauma to growth plate à growth arrest
o Infection (neonatal period)
o Tumour (osteochondromas)
o Bone dysplasias: multiple epiphyseal dysplasia (Rx: hemiepiphysiodesis) etc
o Rickets
§ Pathology: Failure of mineralization of physes or bone due to Vit D deficiency
§ Causes: nutritional deficiency, GI absorption, renal tubular defects etc
§ Investigations
• X-ray: Epiphysial flaring – prominent physes
• Bloods: Reduced calcium and phosphate, increased ALP
§ Management: Correct cause + Correct deformity
o Blount’s disease (infantile)
§ Pathology:
• Growth disorder: Idiopathic arrest of growth plate on medial side of tibia
• Progressive genu varum due to abnormal growth of posteromedial part of proximal tibia à varus angulation of
proximal tibia and medial rotation of tibia
• Often bilateral
• Rotational element often present
§ Epidemiology:
• Overweight children
• Children who start walking early
• Female
§ X-ray:
• Sloping of medial half of epiphysis
• Abnormal flattening
• Metaphyseal-diaphyseal angle: Abnormal if >11 degrees
§ Management:
• </=3yo: circumferential brace/ AFO
• >3yo: high tibial osteotomy
• Mechanism of malalignment/ intoeing
Child HIP: medial femoral torsion (femoral anteversion; Twisted thighbone)
- Excessive internal rotation due to femoral anteversion
- Usually bilateral
- History of ‘W-sitting’
- Management
§ Cross legged sitting
§ Surgery only indicated if intoeing interferes with walking/running
§ Derotational osteotomy
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Toddler LEG: medial tibial torsion (Twisted shin)
- Commonest cause of bow-leggedness in 1yos
- Negative thigh foot angle (refer to photo) indicative of tibial torsion
- Thigh foot angle
§ Normal: 15 deg
§ Negative angle
• Management:
o Importance of aligning early
§ Genu valgus:
• Accept valgus till about 5-7yo
• If valgus >7yo, mechanical axis will be lateral (ie. Pressure at lateral portion of growth plate) à inhibition of lateral growth
plate compared to medial à OA of lateral compartment (abt 30-40yo)
§ Callosities may form in intoeing
o Surgery for knee deformities
§ Indications: Marked deformity and instability
§ Procedures
• Epiphyseodesis (in young): Stapling of one side of physis to slow growth on that side
• Osteotomy
o Valgus: Supracondylar femoral
o Varus: High tibial
• Joint reconstruction
• Adult onset knee deformities:
o Rheumatoid arthritis – Usually valgus
o Osteoarthritis – Usually varus
2. Osteochondritis Dissecans
• Pathology: Avascular necrosis of a fragment of subchondral bone predisposes overlying cartilage and subchondral bone itself to
fragmentation; osteochondral fragments (loose bodies) within joint space causes further pain and damage
o Usually affected lateral part of medial femoral condyle
o NOTE: unlike AVN of femur – dome of femoral condyle
• Risk Factors
o Male (15-20yo)
o Trauma:
§ Single impact with edge of patella
§ Repeated contact with adjacent tibia ridge
• Symptoms (bilateral in 25%)
o Intermittent ache or swelling
o Giving way
o Locking
• Signs
o Diagnostic Signs
§ Tenderness localized to one femoral condyle
§ Wilson’s sign
• Pain felt when knee flexed to 90 deg, rotated medially and gradually straightened
• Absence of pain when test repeated with lateral rotation
o Quadricep wasting, Joint effusion
• Investigations
o X-ray (intercondylar/tunnel view)
§ Line of demarcation around lesion
§ Empty hollow and possibly a loose body elsewhere (once fragment detaches)
o Radionuclide scans: Increased activity around lesion
o MRI: Area of low signal intensity in T1-weighted images
• Management
o Conservative – During early stage when cartilage intact and lesion is stable
§ Lifestyle modification: Curtail activity for 6-12 months; small lesions often heal spontaneously
o Surgery – Unstable fragments (detachment)
§ Small, ill-fitting fragment: Arthroscopic removal and the base drilled and eventually covered by fibrocartilage
§ Large fragment >1cm diameter: In situ fixation with pins or Herbert screws
§ Cartilage transplantation
§ After Sx, knee casted for 6 weeks thereafter movement encouraged but weight bearing deferred until x-ray shows healing
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• NOTE: Other causes of loose body in knee
o Injury (chip of bone, cartilage, meniscus)
o OA (pieces of cartilage or osteophyte)
o Synovial chondromatosis: cartilage metaplasia in synovium à sometimes produce 100s of loose bodies
o Charcot’s joint (large osteochondral bodies separated by repeated trauma in insensate joint)
§ Jt that has lost protective sensation thus progressively deforms as it suffers repeated trauma
§ Causes: DM, peripheral neuropathy, tertiary syphilis, tabes dorsalis, syringomyelia, myeomeningocele, cauda equina
§ S/S:
• Rapidly progressive OA
• Gross jt deformity but painless
• Unstable joint, effusion, no warmth
§ Rx:
• Rest and immobilize
• Stabilize w cast/calipers
• Surgical arthrodesis
o S/S of LB: sudden locking (ranging positions of getting stuck), swollen jt (synovitis), palpable LB (sometimes like a joint mouse)
o Rx: if symptomatic, remove LB unless joint is severly osteoarthritic (?TKR)
I would like to move on to palpate this swelling. (ask pt for any pain first)
The swelling has well defined edges and the surface is smooth. It is firm in consistency.
There is slight tenderness on palpation but it does not feel warm. It is not attached to the overlying skin.
The swelling is not transilluminable nor is it compressible. It is fluctuant in nature.
I will like to complete the examination by completing the rest of the knee examination.
105
ACUTE SWELLING OF ENTIRE JOINT
• Haemarthrosis
o Post-traumatic
§ Signs and Symptoms
• Immediate swelling after injury
• Painful, warm, tense
• Restricted movement
• Later may feel doughy
§ Etiology
• Fracture (Patellar, femoral condyle)
• Ligament (ACL) tear
o Non-traumatic
§ Pathology: Acute bleed into knee (most common site) in patients with clotting disorders
§ Aspirate + splint + infuse CF
• Acute septic arthritis
o Signs and symptoms
§ Signs of inflammation – tenderness, redness, warmth, swelling
§ Investigations
• Raised white cell count and ESR
• Aspiration reveals pus in joint à c/s
§ Common pathogens: Staph aureus, strep gonorrhea (in adults)
§ Management: IV antibiotics, drainage of joint
• Synovitis
o Traumatic
§ Pathology: Injury stimulates a reactive synovitis
§ Signs and Symptoms
• Swelling appearing after some hours (unlike haemarthrosis) and subsides spontaneously over a few days
• Quadriceps wasting (due to inhibition of quadriceps action)
• Decreased ROM
§ Management: Aspiration (if fluid amount considerable; hastns recovery)
o Aseptic non-traumatic
§ Etiology: Gout or pseudogout
§ Content: Turbid fluid
§ Investigation: Microscopy reveals crystals
§ Management: NSAIDs
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Nerve Neuroma Eg. tibial nerve
Enlarged -‐ Above the joint line
bursae -‐ Painless, slightly medial and most prominent w knee extended
-‐ Lump fluctuant and transilluminates
-‐ a/w semimembranosus and medial head of gastrocnemius medially and w poplitues and lateral
head of gastroc laterally
-‐ spontaneously resolves even if aching
Cysts Baker’s cyst -‐ Below jt line and deep to gastroc
-‐ a/w degerneative changes in knee jt
Popliteal cyst -‐ enlargement of popliteal bursa
-‐ knee jt is normal
• Semimembranosus bursa
o Pathology: Enlargement of bursa between semimembranosus and medial head of gastrocnemius
o S/S: Painless, fluctuant and transilluminable swelling in medial part of popliteal fossa (most conspicuous with knee straight)
o Management: Waiting (as usually disappears); excision if symptomatic (pain)
• Baker’s cyst
o Pathology:
§ Posterior herniation of knee jt capsule
§ Leading to escape of synovial fluid into the posterior bursa, stiffness and knee swelling (fluid distension of the gastrocnemio-
semimembranosus bursa)
§ Common in children, occurring more often in boys
§ Often a/w OA, RA and Charcot’s joint
§ Impt TRO DVT, but the 2 can co-exist
o Signs and Symptoms
§ Swelling usually below the joint
• Fluctuant, may be transilluminable, non-tender, positive slip sign (it is a deep structure)
• Reducible only if connected to knee jts which not all baker’s cysts are (esp in children)
§ If cyst ruptures & synovial contents spill into muscle planes, pain & swelling experienced in calf (may be mistaken for DVT)
o Cx:
§ Due to their anatomic location, Baker’s cysts can increase risk of DVT
• Most commonly, the baker’s cyst is located btw tendons of the medial head of gastroc and the semimembranosus bursa
• BUT sometimes, the cyst can be found btw the heads fo the gastroc muscles à can result in a lateral deviation of the
popliteal vein à compression of the popliteal vein à predisposes to venous stasis and DVT
o Ix: U/S: fluid btw semimembranosus & medial gastroc tendons in communication with posterior knee cyst (100% accuracy)
o Management
§ Children: Sx excision of cysts rarely indicated
• Usually spontaneous resolution of cysts in 10-20 months thus a prolonged period of observation is strongly recommended
before surgical excision is considered
• In protracted cases, cysts may respond to aspiration and steroid injection
o NOTE: unlike in adults, cysts in children may not be intra-articular and thus may respond to aspiration
§ Adults: Excision not advised as recurrence likely unless underlying condition treated
• Popliteal cyst
o Pathology: cyst located on the medial side of popliteal fossa, just distal to flexion crease of the knee, under medial head of gastroc
o Epidemiology:
§ Found n children and young adults
§ 2x more common in boys
§ Usually unilateral
o Signs:
§ More prominent during knee extension and vice versa
§ If cyst is not found in medial part of popliteal fossa or has a solid component (on US), rule out tumour with CT/MRI
o Rx: Conservative unless symptomatic; may spontaneously remit
On inspection, do not note any skin discolouration, scars, sinus or any obvious swellings anteriorly.
There is no muscle wasting, genu varum or genu valgum deformity.
There is no fixed flexion deformity of the knee.
Semimembranosus Bursa Popliteal Cyst
There is a ___ x ___ cm hemispherical lump in the popliteal fossa, it There is a ___ x ___ cm hemispherical lump in the popliteal fossa, it
lies above the level of the joint line, slightly to the medial side of the lies below the level of the joint line, deep to / bulging out between
fossa. It appears well-defined. There are no overlying skin changes the 2 heads of the gastrocnemius. It appears well-defined. There are
or scars. There is no wasting of the quadriceps muscles. no overlying skin changes or scars. There is no wasting of the
quadriceps muscles.
I would like to move on to palpate the swelling. I would like to move on to palpate the swelling.
(ask pt for any pain first) (ask pt for any pain first)
(palpate with knee flexed – mass becomes soft, fluctuant & mobile) (palpate with knee flexed – mass becomes soft, fluctuant & mobile)
The lump is non-tender and not warm. The surface is smooth, the The lump is non-tender and not warm. The surface is smooth, the
edge is regular and it is firm in consistency. It fluctuates, but is non edge is regular and it is firm in consistency. It fluctuates, but is non
pulsatile, not compressible and slip sign is negative. pulsatile, not compressible, and slip sign is negative.
I would like to move on to transilluminate the mass. I would like to move on to transilluminate the mass.
The mass transilluminates. The mass does not transilluminate (muscle covers it).
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Bend the knee to see if it empties into the knee joint (empties = popliteal cyst; does not empty = semimembranosus cyst).
Differentials include:
• Skin and subcutaneous tissue lumps (lipoma, sebaceous cyst)
• Artery (popliteal artery aneurysm)
• Vein (saphena varix, DVT)
• Nerve (neuromas)
• Bursa (semi-membranosus bursa – bursa between the SM and the medial head of the gastrocnemius)
• Cyst (popliteal cyst – bulging of the posterior capsule & synovial herniation, often 2° to OA / RA)
I would like to complete the examination by completing the rest of the knee examination. (for OA / RA / effusion)
I would like to perform a neurological and peripheral vascular examination, including feeling for peripheral pulses.
I would like to examine the hip and ankle as well.
4. Patellofemoral Overload
Patellofemoral Overload / Patellar Pain Syndrome / Chondromalacia of Patella
• Pathology: Softening and fibrillation of articular surface of patella due to repetitive
mechanical overload of patellofemoral joint due to:
o Malcongruence of patellofemoral surfaces (because of abnormal shape of patella or
intercondylar groove) OR
o Malalignment of extensor mechanism or relative weakness of vastus medialis
which causes patella to tilt, subluxate or bear more heavily on one facet during
flexion and extension (PATELLA MALTRACKING)
• Risk factors for patella maltracking:
o Lateral patella tilt (due to malalignment of extensor mechanism or relative weakness
of vastus medialis)
o Tightness of lateral side
§ Attachment to ITB
§ Lateral retinaculum tighter than medial
o Weakness of VMO
o Large Q angle: ASIS à Center of patella à tibial tubercle
§ Measure of how lateral the quadriceps pull is
§ Q angle is the angle formed by a line drawn from the ASIS to the central patella and a
second line drawn from the central patella to the tibial tubercle.
§ An increased Q angle is a risk factor for patellar subluxation.
§ Normally Q angle is <18 deg for males and <22 deg for females with knee in full
extension; and <8 deg for males and <9 deg for females w knee in 90 deg extension.
§ Biomechanics of PF joint are effected by patellar tendon length & the Q angle.
§ Q angle is increased by:
• genu valgum
• Increased femoral anteversion
• External tibial torsion
• laterally positioned tibial tuberosity
• tight lateral retinaculum
• Larger pelvis (hence maltracking more common in females)
§ Note: The Q angle may not be accurate in extension, since a laterally dislocated
patella may give the false impression that the Q angle is normal; In flexion, this is not a
problem since the patella is well seated in the trochlear groove
o Valgus knee
o Internal femoral torsion
o Abnormal patella: High or small
• Epidemiology: Teenage girls, Athletic young adults
• Symptoms: Anterior knee pain (beneath patella): Aggravated by activity (climbing stairs, standing after prolonged sitting)
• Signs
o LOOK: Quadriceps wasting, small effusion
o FEEL: retropatellar tenderness
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o MOVE: Crepitus
o Patella grind test: Pain when pressing on patella against femur + contract quads (central + medial + lateral pressure)
• Cx: assoc w dvlpment of PFOA
• Investigations
o X-ray
§ Skyline view: Show abnormal tilting or subluxation (LATERAL CONDYLE HIGHER)
§ Lateral view (with knee partly flexed): See if patella is high or small
o CT/MRI – with knees in full extension and varying degrees of flexion
§ Measure patellofemoral malposition most accurately
o Arthroscopy: Exclude other causes of knee pain
• Management
o Conservative à most patients recover
§ Lifestyle modification
§ Physiotherapy: Strengthen vastus medialis obliques to counterbalance tendency for lateral tilting or subluxation of patella
§ Analgesics
o Surgery – If symptoms persist
§ Arthroscopy lavage & shaving of fibrillated cartilage
§ Lateral release +/- patellar realignment (if patella unstable)
§ Drill exposed subchondral bone: revascularization may help repair w fibrocartilage
§ Patellectomy
• Differentials (other causes for anterior knee pain)
o Patella tendinosis (Jumper’s knee): Pain at inferior pole of patella or along tendon due to overuse of extensor mechanism
o Patella subluxation
o Osgood Schlatters
o Plica syndrome: Plica (an extension of the protective synovial capsule of the knee) becomes irritated due to catching onto femur, or
pinching between femur and patella
o Hoffa syndrome: Impingement of fat pad between femoral condyle and patella
5. Fractures
TIBIAL PLATEAU FRACTURES
• Mechanism of Injury: Crushing or splitting of one or both tibial condyles by opposing
femoral condyle due to strong bending forces combined with axial loads (eg. car
striking pedestrian on side of knee - bumper fracture) or fall from a height in which
knee is forced into valgus or varus
o Lateral > medial
• Signs and Symptoms:
o Joint swelling (may have hemathrosis)
o Diffuse tenderness on side of fracture
o Tenderness on opposite side indicates ligament injury
• Associated injuries/ complications
o Compartment syndrome (esp Types 5 and 6)
o Popliteal artery injury
o Ligament/meniscal tear (esp contralateral side)
o Malunion
o Joint stiffness (minimize by early ROM)
o Secondary OA: esp with marked plateau depression, deformity (valgus or varus)
and ligamentous instability
• Classification (Schatzker’s Classification)
Type Description
1 Simple split of lateral condyle
2 Split of lateral condyle with more central area of depression (the force may have been greater or
underlying bone may be osteoporotic and unable to resist depression)
3 Depression of lateral condyle with intact rim
4 Fracture of medial condyle
5 Fractures of both condyles but central portion of metaphysis still connected to tibial shaft
6 Combined condylar and subcondylar fractures (split extends to metadiaphysis)
• Ix: XR multiple view and sometimes tomography to shoe the true extent of fracture
• Management by fracture type
Fracture Management
Lateral condylar #: Conservative
Undisplaced/minimally Aspirate haemarthrosis, compression bandageà hinged cast-brace + knee
displaced # movements when pain and swelling subsidesà avoid weight bearing for 3wks
- Acute pain and swelling often subsides in 1 wk
Lateral condylar #: ORIF (lag screws and buttress plate)
Markedly displaced/
comminuted
Medial condylar # ORIF +/- lateral ligament repair
Bicondylar # ORIF
Osteoporotic condylar # ORIF or TKR (if # pattern permits)
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• Management by extent of depression
o Fracture displacement ranging from 4-10mm can be treated non-operatively
§ If depression is <3mm: traction + mobilization (Sarmiento program of functional cast bracing + NWB for 2 months; # requires abt
2-3 months to heal)
§ If depression >3mm, displaced or comminuted; or if there is doubt abt degree of displacement:
• ORIF +/- bone graft to elevate fragment
• Indications for Sx
o Absolute indications for Sx:
§ Open plateau #
§ # with an associated compartment syndrome
§ # assoc w a vascular injury
o Relative indications for Sx:
§ Most displaced bicondylar #
§ Displaced medial condylar # (coz medial # are more complex)
§ Lateral plateau # that result in joint instability
o Contraindications to Sx
§ Presence of a compromised soft-tissue envelope (for immediate open reduction)
§ # that do not result in joint instability or deformity and can therefore be treated w non-operative modalities
PATELLAR FRACTURES
• Mechanism of Injury
Type Mechanism
Undisplaced crack Direct blow
Comminuted/Stellate Fall or direct blow on front of knee
Transverse fracture with gap Indirect traction injury due to forced, passive flexion of the knee while the quads muscle is contracted
between fragments (entire extensor mechanism is torn across and active knee extension is impossible)
• Symptoms
o Pain
o Swelling (haemarthrosis)
o Inability to extend knee (esp in transverse #; affects treatment)
• Signs
o Bruising of knee jt w or w/o abrasions
o Patellar deformity; Gap may be felt
o Tenderness over patella
o Proximal displacement of patella (esp in transverse #)
• X-ray (AP, lateral, skyline)
o Note: Don’t confuse with congenital bipartite patella (common congenital
fragmentation of patella à Type I: inf pole of patella, Type II: lat. margin, Type
III: smooth line extends obliquely across superolateral angle of bone)
• Complications: PFOA
• Management (depends on state of extensor mechanism): all require PhysioRx after initial Rx
o General indications for Sx:
§ Significant articular step-off >2mm
§ Loss of extensor mechanism with displacement >3mm
§ Open fracture
o Undisplaced or minimally displaced crack: CONSERVATIVE
§ Aspirate haemarthrosis (if present)
§ Protection with plaster cylinder holding knee straight (4-6/52) if extensor mechanism intact + early ROM to preserve mobility
o Comminuted (stellate) fracture:
§ Acceptable displacement: Backslab + early ROM
§ Severe displacement: complete or partial patellectomy (depending on severity of displacement) to avoid damage to
patellofemoral joint predisposed by irregular undersurface of patella
o Displaced transverse fracture:
§ Internal fixation (tension band wiring + 2K-wires)
§ Extensor expansions repaired if torn
§ Plaster backslab worn until active extension of knee regained
6. Dislocation
PATELLAR DISLOCATION (FIRST TIME)
• Mechanism of Injury
o Normal anatomical predisposition: Knee angled in slight valgus hence tendency for patella to pull towards lateral side when quads
contract (medial retinacular fibers may be torn)
o Precipitation: Sudden contraction of quadriceps while knee is stretched in valgus and external rotation
• Symptoms
o Tearing sensation
o Feeling that knee has gone ‘out of joint’
o Often patella reduces spontaneously
o Joint may be swollen (blood stained effusion)
• Signs
o If patella does not reduce spontaneously, uncovered medial femoral condyle is prominent
(may be mistaken for patella)
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o Tenderness on medial joint + swollen knee
o Active and passive movement not possible
• X-ray
o If unreduced, patella seen to be laterally displaced (and tilted or rotated)
o May have associated osteochondral fracture
• Management: Reduction + Backslab + PhysioRx
o Plaster cylinder/splint for 2-3/52 + walk w crutches
• Complications: Recurrent dislocation/subluxation (non-operative treatment for 1st time dislocation has 15-20% recurrence chance)
KNEE DISLOCATION
• Mechanism of Injury
o Significant trauma (eg. RTA) where cruciate ligaments and one/both collaterals are torn
o Can be anterior (most common), posterior, rotatory or lateral
• Symptoms: Bruising + Swelling + Gross deformity
• Complications
o Early
§ Vascular injury (35-50%) and ischemia: Popliteal artery (tethered to knee joint: geniculate arteries and ant tibial artery goes
thru hiatus in interosseous membrane) – may have an intimal tear which may bleed insidiously or a disruption
• If merely kinked, pulse should return post reduction
• If tear:
o Full tear: Pulse wont return
o Intimal tear: Weak pulse returns
• If weak pulse/no pulse, investigate with arteriogram
§ Nerve injury: Posterior tibial, common peroneal nerves
§ Capsular/ ligament/ meniscal injuries
§ Compartment syndrome
o Late
§ Reperfusion injury
§ Joint instability (AP glide, lateral wobble)
§ Joint stiffness
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• Investigations
o X-ray: Rule out tibial spine fracture due to cruciate ligament avulsion
o Arteriogram/ doppler: If have doubts about circulation
• Management
o Reduction + Backslab in 15 deg flexion (dangerous to use cylinder plaster due to swelling)
§ If unstable or if vascular repair – external fixator
§ If open wound/ vascular damage (need to operate anyway), take opportunity to repair ligaments and capsule
o Above knee cast applied after swelling subsides (for 4-12 weeks)
o Quadriceps muscle exercises
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ACL INJURY (more common than PCL injury)
• Attachments
o Medial aspect of lateral femoral condyle
o Intercondyloid eminence of tibia
• Function
o Prevent anterior translation
o Prevent internal rotation of tibia
• Components
o Anteromedial – taut in flexion
o Posterolateral – taut in extension
• Mechanism of Injury
o Internal rotation on hyperextended knee
o Indirect varus blow to knee
o à patients w greater Q-angle got greater chance of ACL tear
• Hx:
o Audible pop
o Giving way à knee instability à inability to continue activity
o Immediate swelling if hemarthrosis
• Signs
o Anterior drawer + Lachman’s + Pivot shift + Apleys distraction test
o Note false +ve in PCL tears
• ACL does not have ability to heal:
o Synovial fluid keeps 2 ends apart
o Synovial fluid produces proteolytic enzymes which exacerbates damage
o Synovial fluid prevents formation of a fibrin platelet clot at wound site
• Blood supply: Medial geniculate artery (ruptured in ACL tear)
Inspect for skin changes / scars / wasting / deformities / swelling (if present à do effusion test)
If no specific instructions: “At this point of time, I would like to proceed to test the ligaments first”
Flex knee to look for posterior sag Flex knee to look for posterior sag
à There is no posterior sag of the knee à There is posterior sag of the knee
(Warn patient about sitting on feet) (Warn patient about sitting on feet)
(Compare both sides when examining the ligaments) (Compare both sides when examining the ligaments)
Posterior drawer à Posterior drawer is negative Posterior drawer à Posterior drawer is positive
Anterior drawer à Anterior drawer is positive Anterior drawer à Anterior drawer is negative
Lachman test à Lachman test is positive (false positive anterior drawer / Lachman test)
My diagnosis is a (left / right) ACL tear. My diagnosis is a (left / right) PCL tear.
I would like to test for the integrity of the collateral ligaments.
Varus & valgus stress test at 30 degrees and knee in full extension à The collateral ligamants are intact.
I would like to look for associated meniscal injuries by palpating the joint line.
PCL INJURY
• Mechanism of Injury
o Dashboard injury (hit ant tibia on dashboard and tibia forced backwards)
o Hyperflexion or hyperextension w anterior tibial force
o Fall onto flexed knee w plantarflexed foot
• Attachments: Medial condyle of femur, Posterior intercondylar area of tibia
• Signs: Posterior sag + Posterior drawer + Reversed pivot shift + apleys distraction test
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8. Meniscus Tears
• Role of menisci
o Increase stability of knee (screw home mechanism)
o Control complex rolling and gliding actions of joint
o Distribute load during movement
• Mechanism of Injury: Meniscus split in its length by force grinding it between femur and tibia
o In young: Weight taken on flexed knee with twisting strain à usually during sports (esp football)
o Older (>40): Relatively little force needed as fibrosis restricts mobility of meniscus
§ May not have a notable initial injury and main compliant is of recurrent giving away or locking
• Anatomy
o Semilunar shaped fibrocartilaginous wedges
o Medial: larger, kidney shaped
o Vasculature: Periphery supplied by radial branches of geniculate arteries while majority is avascular and obtain nutrition from
synovial diffusion
• Pathology
o Medial meniscus affected more because:
§ Attachment to medial collateral ligament make it less mobile
§ Absence of popliteus muscle insertions which can pull meniscus into more favorable position during sudden movements (as
with lateral meniscus)
o Types of Tears
§ Bucket handle tears
• Split is vertical but runs along part of circumference of meniscus creating a loose sliver still attached anteriorly and
posteriorly
• Loose sliver may displace toward center of joint and jam between femur and tibia causing locking (block to extension)
§ Horizontal tears
• Usually degenerative or due to repeated minor trauma
• Some are associated w meniscal cysts
o Most of meniscus is avascular and does not repair (except outer third which is vascularised from capsule)
o Loose tag à mechanical irritant à synovial effusion à secondary OA
• Symptoms
o Severe pain (over joint line) post trauma (hence further activity avoided)
o Knee may be locked in partial flexion (torn part jammed btw tibia and femur, blocking extension)
§ Locking suggestive of bucket handle tear
§ Patients may learn to ‘unlock’ knee by bending it fully or by twisting it from side to side
o Swelling (hours later or next day; unlike in ligament tear)
o Initial symptoms subside with rest but recur with trivial twists and strains or even give way spontaneously (followed by pain and
swelling)
• Cx: recurrent synovial effusion and articular cartilage damage due to loose meniscal tag à swelling, secondary OA
• Signs
o Tenderness localized to joint line (usually medial)
o McMurray’s test
o Apley’s grinding test
o Joint may be held slightly flexed; may have limited extension
o Effusion
o Quadriceps wasting (in late presentation)
• Investigations
o MRI
o Arthroscopy: If lesion identified can be treated at same time
• Management: Meniscus preservation if possible
o Arthroscopic surgery (subtotal or total menisectomy)
§ Outer 1/3: good vascular ss (fr capsule), good healing à attempt repair
§ Mid 1/3: intermediate vascular ss and healing
§ Inner 1/3: avascular and poor healing à total or subtotal (displaced portion) excision
o Postoperative physiotherapy
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Tibia
and
Fibula
Fractures
Fractures
Tibia
and
Fibula
Fractures
Tibial
Diaphysis
Fracture
Tibial
plateau
fractures
(refer
to
knee)
Pilon
fracture
of
Distal
Tibia
(refer
to
ankle)
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1. Tibia and Fibula Fractures
• Mechanism of Injury:
o Forces
§ Twisting force: Spiral fracture of both leg bones at different levels
§ Angulatory force: Short oblique fractures; usually with separate triangular butterfly fragment
o Subcutaneous position predisposes to open fractures
§ Direct injury (eg. motorcycle accident): May crush or split overlying skin (out à in)
§ Indirect injury (spiral or oblique): Bone fragment pierces skin from within (in à out)
• Management
o Objectives
§ Limit soft tissue damage and preserve skin cover
§ Obtain and hold fracture alignment
§ Recognise compartment syndrome
§ Start early weight bearing (loading promotes healing)
§ Start joint movements ASAP
o Low Energy Fractures
§ Undisplaced # (or minimally displaced): Cast from thigh to metatarsal neck
§ Displaced #: Reduction under GA + Cast application
§ Skeletal Fixation (can be done where appropriate skills and facilities available)
• Locked intramedullary nailing (diaphyseal fractures)
• Plate fixation: Metaphyseal fractures
• External fixation: Metaphyseal and shaft fractures
o High Energy Fractures
§ External fixation: Inflicts little damage to badly injured limb
o Open Fractures
§ Antibiotics
• Gustilo I-IIIA: Broad spectrum cephalosporin
• Gustillo IIIB-C: Additional Aminoglycoside (gentamicin) + Metronidazole (soil contamination)
§ Debridement
§ Stabilisation: External fixation favoured for more severe injuries
§ Soft tissue cover
§ Rehabilitation
• Complications
o Vascular injuries: Popliteal artery
o Compartment syndrome
o Infection
o Malunion à Predispose to early OA
o Delayed-union/Non-union: Due to poor muscle cover hence poor blood supply
o Joint stiffness
o Algodystrophy (complex regional pain syndrome)
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Foot
and
ankle
Atraumatic Traumatic
117
Examination of the Foot and Ankle • Isolate and test ROM of Subtalar jt: maximal dorsiflexion to lock
The preliminaries: Introduce yourself to patient, ask for permission to talus in ankle mortis (isolate talus and cup heel) and isolates
examine. Ensure adequate exposure (midthigh downwards w shoes inversion and eversion; compare both sides.
removed) but consider patient modesty also. Ensure good lighting & good • Isolate and test ROM of Midfoot jt: neutral flexion, immobilise
hindfoot w opposite hand (isolate with thumb on talar neck) and
positioning of bed.
test isolated movement of midfoot
SPECIAL TESTS
With patient standing: Ankle instability
LOOK – Front, Medial Back, Lateral With ankle in 10° plantarflexion
1. General appearance and vitals – any pallor, BP, HR etc. 1. Valgus and varus test
2. Posture: Knee and Foot alignment 2. Anterior Drawer test for insufficiency/ laxity of anterior
3. Foot and soles: Scars, Sinuses, Swelling, Lumps, Hair Loss, talofibular ligament (ATFL) – stabilise/immobilise tibia with L
Trophic changes, ulcerations, callosities hand, cup heel with R, keep ankle in abt 10deg plantar flexion
4. Forefoot: and apply anteriorly directed force on heel; compare amt of
Ø Toe defotmities, splaying laxity w other side
Ø Halux Valgus 3. Talar tilt – inversion and eversion force
Ø Crossed toes ** look out for generalised ligament laxity
Ø Hammer toes
Simmond’s test: for integrity of tendo archilles: prone position, foot
Ø Claw toes
5. Mid foot: overhanging the bed so that it is free to move; cup and squeeze calf
Ø Pes Planus or Pes Cavus muscles and observe for plantarflexion; likely that tendo archilles is torn if
6. Hind foot: plantarflexion doesn’t occur
Ø Achilles Tendon (swellings?) Coleman Block Test
Ø Heel alignment - Used to evaluates hindfoot flexibility and pronation of forefoot;
Ø Hindfoot Valgus/varus - initial deformity is in the forefoot followed by subsequent
Ø Hindfoot swelling changes in the hindfoot;
Ø Too many toes sign - test is performed by placing the patient's foot on wood block,
7. Clues 2.5 to 4 cm thick, with the heel and lateral border of foot on the
Ø Walking aid, shoes (patterns of abnormal/ block and bearing full weight while the first, second, & 3rd
asymmetric wear in the soles), orthosis. metatarsals are allowed to hang freely into plantar flexion and
8. Ask patient to tip-toe: pronation;
Ø Look at heel alignment: Valgus vs Varus - Interpretation:
(protection vs predisposition to sprains) o test is based on premise that there is fixed flexion of
i. Neurological cause—CP, SB, SCI 1st metatarsal;
ii. Muscular—Disuse, CMT, MD o this test negates effect that forefoot (first metatarsal
iii. Tendinous-- PTTD in plantar flexion) may have on the hindfoot in
Ø Look at calf contraction stance;
9. Quick inspection of knee (gross abnormalities) o if heel varus corrects while the patient is standing on
10. Squat the block, hindfoot is considered flexible;
11. Gait: Foot drop, stiff ankle, fixed equinus o if subtalar joint is supple & correct w/ block test,
then surgical procedures may be directed
With patient sitting down or lying supine to correcting forefoot pronation, which is usually due
LOOK to plantar flexion of 1st metatarsal;
1. Deformities of the Sole—Corns, callousities, Ulcers o if hindfoot is rigid, then surgical correction of both
2. Restng position of the foot: normally equinovarus forefoot & hindfoot are required;
FEEL Specific Conditions
ASK FOR PAIN 1. Posterior Tibial Tendon Dysfunction
1. General palpation: begin post to med malleolus (post tibial Inflammation of the posterior tibial tendon – acquired flat foot
tendon), over bony medial malleolus, along medial jt line, along (most common cause in adults). Progressive flattening of arch
ant jt line, over lateral jt line, bony lateral malleolus, post to a/w pain. May lead to OA
lateral malleolus (peroneal tendons), archilles tendon § Examine tibial posterior (tenderness)
(tenderness or gaps in tendon) § Perform Jack’s test
- Bone: metatarsal head, sesamoid bones § Check Tendo Achilles tightness
- Tendon: extensor digitorium brevis (top of foot), 2. Hallux Valgus
tibialis posterior (posterior to medial malleolus), § MTPJ dorsal osteophyte, pain with extension
peroneals (lateral malleolus), ATFL (lateral § Test PROM, sesamoiditis, 1st TMTJ laxity
malleolus), plantar fascia 3. Pes Cavus (think Charcot Marie Tooth)
- Ankle joint line § Claw toes
2. Increased warmth: suggestive of inflammation – RA/Gout § Test tibialis anterior & peroneii
3. Tenderness: § Test sensation & deep tendon reflexes
- Along the bone à Osteomyelitis (missing/decreased in CMT)
- Along joint lines à Septic Arthritis § Champagne bottle legs
4. Joint Effusion § Intrinsic Muscle wasting
5. Lumps: document in detail with layer of attachment § Hand involvement
6. Jack’s test/Hubscher manoeuvre: in pes planus – extension § Marionette Gait
of the big toe with weight bearing FINISH with examination of neurovascular status of foot and ankle.
- Arch formation (+ve): flexible flat foot Esp polio (sensory is normal) or CMT/ Pes cavus. Offer to examine the
- No arch (-ve): rigid flat foot knee.
MOVE
1. Peripheral pulses, Capillary Refill
Active ROM (combined movements), then Passive ROM (isolate and test 2. 5 Nerves that ss foot and ankle:
ROM of subtalar jt and midfoot jt) - Superficial peroneal nerve over dorsum of foot
• Active Dorsiflexion & Plantarflexion –observe from side and - Deep peroneal nerve in first web space
compare both sides - Saphenous nerve on medial border foot
• Active pronation and supination - Sural nerve on lateral border of foot
- Tibial nerve in sole
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General information
• Foot has a transverse arch and 2 longitudinal arches
o Medial arch: calcaneum, talus (apex), navicular, 3 cuneiforms, 3 medial metatarsals
o Lateral arch: calcaneum, cuboid, lateral 2 metatarsals
• Arches are maintained by
o Ligaments
§ Spring ligament- from sustentaculum tali of calcaneum to navicular tuberosity
§ Short plantar ligament- from calcaneum to cuboid
§ Long plantar ligament- from calcaneum to 2/3/4 metatarsals
o Muscle tendons
§ Medial arch by: tibialis posterior, tibialis anterior
§ Lateral arch by: peroneus longus
• Movements
o Plantarflexion and dorsiflexion at ankle joint
o Pronation and supination at intertarsal and tarsometatarsal joints
§ around axis through 2nd metatarsal
§ pronation – sole turns laterally; supination –sole turns medially
o Abduction and adduction by rotation of leg below the knee
§ toes turn toward or away from midline
§ forced abduction or adduction may disrupt mortise by
1. diastasis of tibiofibular joint
2. tearing of collateral ligaments
3. fracturing of malleoli
o Inversion = plantarflexion + adduction + supination
Eversion = dorsiflexion + abduction + pronation
• Positions
o Equinus: downward pointing foot
o Calcaneus: upward pointing foot
o Plantaris: only forefoot pointing downward
o Pes valgus: pronation with abduction
o Pes varus: supination with adduction
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1. Deformities
IDIOPATHIC CLUB FOOT (CONGENITAL TALIPES EQUINOVARUS)
• Incidence:
o 1 or 2 per 1000births: screened at birth by neonatologists
o Boys affected 2X of girls
o Bilateral in 1/3 of cases
o Also seen in neurological conditions (myelomeningocele, arthrogryposis)
§ Arthrogryposis: non-progressive condition characterized by multiple
joint contractures found throughout the body at birth
• Note difference between flexible/positional VS structural
o Flexible/positional –
§ Able to dorsiflex foot; foot can be passively externally rotated
and has a full ROM
§ Due to position in womb
§ Rx: easily correctable PhysioRx and stretching
o Structural à requires intervention
§ Idiopathic (mainly)
§ Neuromuscular/paralytic (eg. hemiplegia CP, spina bifida;
peroneals <S1> not working, resulting in muscle imbalance)
§ Syndromic (eg. distal type arthrogryphosis)
• Typical Signs: CAVE
o Midfoot Cavus
o Forefoot adducted (metatarsus) and supinated
o Hindfoot in varus
o Heel in equinus
• Clinical features
o Heel unusually small and high
o Normally foot can be dorsiflexed and everted until toes almost touch front of leg; in club-foot,
manoeuvre meets varying degrees of resistance
o Signs of severity:
§ Deep creases appear posteriorly and medially
§ Atrophic calf muscles
• Complications if untreated
o Secondary growth changes in bone (as skin and soft tissues of calf and medial side of foot are short and underdeveloped)
• Management: Painless, plantigrade, function (note: foot will always remain small due to tight ligaments)
o Principles: Correct early, fully and maintain correction
o Rule out associated disorders (DDH, spina bifida)
o Conservative (w/i 1 or 2 days of birth): manipulation & serial casting (up to 4wks) THEN Abduction orthoses
§ Repeated manipulation: 4-6 manipulations wkly to fortnightly until external rotation of 60 degrees achieved
• Ponsetti Casting: Toe to groin casting with Plaster of Paris
• Order of manipulation (Distal to proximal – CAVE)
o Cavus – Dorsiflex first ray to correct cavus
o Metatarsus adductus – Reduce talus with counter pressure on medial distal tibia
o Hindfoot varus: Forefoot abducted in supination
o Equinus: not manipulated (forced dorsiflexion will cause vertical talus and rocker bottom foot)
à if equinus persists after forefoot correction, treat w surgical release of achilles tendon by percutaneous
tenotomy
§ Foot abduction orthosis: maintenance of correction & prevent relapses!
• Dennis Browne boots: for infants
o 23 hrs/day for 3 months, then wean till child begin to cruise
o Then night and nap until 4 years old
• Moulded ankle-foot orthoses (for older children)
o Operative (for resistant cases) – SELDOM DONE
1. a)release capsular and ligamentous contractures and fibrotic bands
2. b)lengthen tendons to reposition foot
3. Hold with cast +/- K wires for 6-8 weeks
4. Maintain using Dennis Browne boots or customized orthosis for older
children
o For late or relapsed club foot:
§ Revision of soft-tissue releases +/- shortening of lateral side of foot by calcaneocuboid fusion or
cuboid enucleation
§ OR Gradual correction by circular external fixator (Ilizarov method)
o In adolescence: corrective osteotomies and fusions
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FLAT FLOOT (PES PLANUS)
• Definition: condition whereby arch of foot collapses w the entire sole of the foot coming into
complete/ near complete contact w the ground
• Examination
o Look
§ In weight bearing position:
• Hindfoot: ankle neutral, subtalar joint in valgus
• Midfoot: planus
• Forefoot: pronation
• Foot: abduction
§ Too many toes sign (in normal foot, only 5th and part of 4th toe seen; in flat foot more than Rocker
b ottom
deformity
that are visible)
o Move
§ Tip toe/ dorsiflex – does medial longitudinal arch re-form (if re-forms, indicative of
flexible flatfoot)
§ Jack’s test – great toe passive extension
o Special: Ligament laxity (if score 4 or more, indicative of ligament laxity)
• General principles of Rx:
o Indications for Rx:
§ Rigit flatfeet
§ Associated foot or lower leg pain
§ Condition affects knees or lower back
o Use of orthotics: arch support (to be used for the rest of patient’s life) + exercises
recommended by podiatrist
o Sx as last resort: usually time-consuing and costly
• Infantile flat-foot (congenital vertical talus)
o Incidence: rare; usually bilateral
o Signs
§ Midfoot: Rocker-bottom foot (medial arch not only flat but curves opp way from normal)
§ Foot: valgus
o Investigations
§ X-ray:
• Calcaneum in equinus
• Talus points into sole of foot
• Navicular dislocated dorsally onto neck of talus
o Management
§ Operation ideally before 2 years (no passive correction as tendons and
ligaments on dorsolateral side of foot usually shortened)
• Flat-foot in children and adolescence
o Note: 90% of children less than 2 have flat foot
o Signs: when weight bearing, foot pronated, medial border of foot in contact
with ground, heel becomes valgus
1. Flexible flat foot (dynamic)
§ Causes: rmber to check for laxity and tight TA
• Generalized ligamentous laxity
o All children have ligament laxity till abt 7
o Normal dvlpmental stage in toddlers à usually
disappears in a few yrs
• Tight tendoachilles: growth spurts creates muscle tightness
esp TA due to imbalance of muscle and bone growth
o Patient accommodates by everting foot causing arch to eventually
Beighton
score
for
ligamentous
laxity
collapse
• Collagen tissue disorders: eg. Marfans Talocalcaneal
bar
(coalition)
§ Symptoms: NIL
§ Signs:
• Jack’s Test: Great-toe extension test (arch restored by dorsiflexing
great toe as plantar fascia tightens)
• Tip toe: heels invert and arch forms in flexible flat foot
§ Management: If TA tight, stretching, good shoes, medial arch support
§ Investigations unnecessary
2. Rigid flat foot/ spasmodic flatfoot (fixed)
§ Cannot be corrected passively
§ Causes (bone, ligament, muscular):
• Tarsal coalition (abnormal bar of bone connecting calcaneum to
talus/navicular) w or w/o peroneal spasm (Peroneal and extensor tendons
appear to be in spasm)
o Calcaneo navicular (9-12yo): do an oblique XR
o Talo-calcaneum (12-15yo): 50% bilateral; do CT
• Inflammatory joint condition
• Neuromuscular disorder – cerebral palsy
• Ligament – Marfan’s, Ehler Danlos
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• Idiopathic
§ Symptoms: pain
§ Investigations:
• X-ray (AP, lateral, oblique): identify underlying disorders
• CT to demonstrate tarsal coalitions
§ Management
• If due to underlying disorder (polio): splintage or operation + muscle rebalancing
• Spasmodic flatfoot: treat underlying problem; usually needs Sx
o Rest in cast or splint; remove bony irregularity; triple arthrodesis if pain intolerable
o Treat tarsal coalition if <30% involved, w soft tissue interposition (fat and EDB)
• Flat foot in adults
o Possible causes
§ Constitutional flat-feet (asymptomatic for many years) causing pain after change in daily activities
§ Recent onset:
• Underlying disorder (RA, general muscular weakness)
• Tibialis posterior tendon dysfunction (tendon inflamed or torn): Tibialis post. synovitis or rupture (esp unilateral
flatfoot) – may be due to trauma or repetitive impact (sports)
o Management
§ For painful rigid flatfeet: footwear and arch supports
§ For underlying disorder: treat disorder
§ For tibialis post rupture: operative repair/ tendon replacement
o Signs
§ Forefoot: pronated
§ Midfoot: medial arches dropped, tuberosity of navicular prominent
§ Hindfoot: heels in valgus, too many toes sign
o Investigations: X-ray
§ Talometartarsal angle (line bisecting talus vs line through shaft of metatarsal
on lateral view: normal is 0)
This is a young boy with bilateral pes planus of the feet as evidenced
by a loss of medial arch of the foot. The foot also appears to be There (is / is no) tenderness of the foot over the ___________ on
pronated and the heels are in valgus with toes visible lateral to the palpation.
outer edge of the heel. (too many toes sign)
ROM was ___ for ankle dorsiflexion, ___ for ankle plantarflexion. OR
(ask pt to go on tip toes) Ankle dorsiflexion was limited to ___ due to a tight Achilles tendon
The pes planus is flexible as evidenced by inversion of the heels on tip (compensatory flat foot) while ankle plantarflexion was ___.
toeing and restoration of the arch on dorsiflexion fo the big toe. OR The Inversion was ___ and eversion was ___ at the subtalar joint.
pes planus is rigid as evidenced by failure of the heels to invert on tip Rotation at midtarsal joint was ___.
toeing.
There are no other deformities of the foot noted. There are no signs of joint hypermobility at the __________ joints.
The extensor and peroneal tendons (appear / did not appear) to be There are also no signs of neuromuscular abnormalities.
in spasm.
There (is / is no) wasting of the muscles in the foot. I would like to end my examination by screening the spine, hip and
There are no scars / swelling / erythema of the overlying skin. knees for any abnormalities.
Thi is a patient with bilateral pes cavus deformity of the feet / pes cavus
deformity of the (left / right) foot as evidenced by an accentuated There is tenderness over the IP joints of the clawed toes as well as the
longitudinal arch of the (feet / left foot / right foot) . metatarsal heads of the foot.
I also note that the (left / right) heel is inverted. The claw toe deformity is (mobile / fixed) as the patient is (able /
unable) to straighten the toes on both active and passive movement of
There is associated clawing of the _____ toes of the (left / right) foot the IP joints.
with flexion of the POP joints and DIP joints and hyperextension of the
MTP joints. The MTP joints are (subluxed / dislocated) . I would like to move on to do a neuro exam of the foot to look for
peripheral neuropathy which can present with pes cavus.
I also note the presence of callosities / ulcers on the dorsal aspect of
the POP joints of the toes as well as on the plantar surface of the foot I would like to complete the examination by:
over the heads of the metatarsal bones which are the pressure points. • Walking the patient to look for antalgic gait / foot drop / varus
deformity
In addition, I note that there is wasting of the intrinsic muscles of the • Examining the shoes for signs of abnormal wear
feet and the _____ muscles of the ______. • Enquiring about the effect of the condition on his / her life
Otherwise, there is no other skin changes / swelling / scars noted.
HALLUX VALGUS
• Incidence: commonest foot deformity
o Usually bilateral
• Risk factors: Idiopathic, hereditary, loss of muscle tone, RA, wearing enclosed footwear (narrow toe box with heels)
• Associated deformities: inflamed bunion, hammer toe, metatarsalgia, secondary OA of 1st MTPJ, callosities, pes planus
• Signs
o Lateral deviation and rotation of hallux
o a/w Bunion from hypertrophy of medial part of metatarsal head and
overlying bursa
• Symptoms
o +/- pain from
§ Shoe pressure on inflamed bunion
§ splaying of forefoot and muscle strain (metatarsalgia)
§ associated lesser toe deformities
§ secondary OA of 1st MTP joint
• Investigations: weight-bearing X-ray to assess
o Degree of metatarsal and hallux angulation
o Presence of OA of 1st MTPJ
• Management
o Adolescents
1. Conservative: footwear modifications (deep toe-boxes, soft uppers and low heels), physiotherapy
2. Operative (~30% recurrence in adolescents): corrective osteotomy of 1st metatarsal + soft tissue rebalancing around MTPJ
o Adults
§ Operative: Indications – Pain, function, cosmesis
• Bunionectomy
• 1st metatarsal realignment osteotomy + soft-tissue rebalancing
• Keller’s procedure/ excision arthroplasty (removal of medial eminence + resection of base of prox phalanx)
• Arthrodesis if MTPJ very osteoarthritic
o Contraindications to surgery: Diabetes, PVD
1. Comment on hallux valgus (note angle) This is a patient with bilateral hallux valgus deformity of ___ degrees on
2. Comment on overriding toe if any the right foot and ___ degrees on the left foot. OR This is a patient with
3. Comment on bunion + overlying skin a hallux valgus deformity of ___ degrees noted on the (left / right) foot.
4. Look for callosities over the dorsal PIP joint of 2nd toe / plantar It (is / is not) associated with an overriding second toe.
surface I note that the big toe is rotated with the nail facing medially. / There is
5. Proceed to touch bunion no associated rotation of the big toe.
6. Move 1st MTP joint (comment on hypermobility + ROM)
7. Ask patient to stand à look for pes planus (if so, differentiate In addition, there is a bunion present on the (left / right) foot (with / with
flexible or rigid) no) erythema of the overlying skin suggestive of inflammation of the
8. Ask to look at hands + walk the patient bursa. (if transilluminable à more likely a ganglion)
9. Request to look at shoes There are also callosities noted over the plantar surface of the (left /
right) foot / dorsal aspect of the PIP joint of the 2nd toe.
The bunion is (tender / non-tender) and (felt / did not feel) warm
on palpation.
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Tenderness (was / was not)) present on palpation of the first (ask to look at pt’s hands) I note there are no deformities of the small
metatarsophalangeal joint. joints of the hands or other deformities of the toes in the feet which may
suggest presence of RA.
There (is / is no) hypermobility of the metatarsophalangeal joint
indicative of instability. (ask pt to walk) I note that patient has an antalgic gait, but no other
ROM was ___ for plantarflexion, ___ for dorsiflexion, ___ for abduction deformities of the heel and ankle. OR
and ___ for adduction. Patient does not have an antalgic gait or any other deformities of the
heel and ankle.
Patient (has / does not have) pes planus which can be associated
with hallux valgus secondary to ligamentous laxity. This is evidenced by I would like to complete my examination by:
a loss of medial arch of the foot. The foot also appears to be pronated • Assessing the ROM of the other toe joints
and the heels are in valgus with toes visible lateral to the outer edge of • Examining the shoes to look for abnormalities of weight bearing
the heel (too many toes sign). The pes planus is (flexible – normal • Enquire about the functional impairment caused by this condition
arch regained on tip-toe / rigid – failure of heels to invert on tip toeing) .
Bunions:
• Definition: localized painful swelling at the base of the big toe
o Joint is enlarged, toe is often malaligned
o Frequently assoc w inflammation
o Can be a/w degenerative joint dz (OA) or bursitis
• Epidemiology: 10x more common in women
• 2 primary causes: hereditary, shoewear
• Diagnosis and pathogenesis: a/w hallux valgus deformity
o Valgus alignment of MTPJ is aggravated by eccentric pull of EHL and intrinsics
o Secondary exostosis forms with bursa and thick skin creating the bunion
• Rx: for cosmesis or pain w shoes
o Conservative: properly fitted shoes and toe spacer
o Sx: removal of bunion w realignment of 1st MTPJ
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LESSER TOE DEFORMITIES
2. Others
DISORDERS OF TENDO ARCHILLES
• Peritendinitis
o Pathophysiology: local irritation of paratenon around tendoachilles
o Symptoms: pain and swelling around tendoachilles
o Risk factors: athletes, joggers, hikers
o Management:
§ Conservative: rest, ultrasound, heel raise
§ Operative; excision of inflamed and degenerate tissue
• Archilles tendonitis
o Chronic inflammation from running and shoe-wear (high heels)
o May dvlp heel bumps (Haglund’s deformity: prominence of the posterior superior calcaneus where the archiles tendon laterally inserts
into calcaneus)
o Diagnosis:
§ Pain, aggravated by passive stretching
§ Tenderness, swelling
§ Crepitus on plantar flexion
o Rx:
§ Rest, gentle stretching, NSAIDs
§ Proper footwear +/- orthotics
§ Don’t inject steroids!!! (prone to rupture!)
• Rupture
o Pathophysiology: when pushing off (jump, run), calf muscle contracts but contraction resisted by body weight (usually involves
eccentric loading on a dorsiflexed ankle w knee extended; soleus and gastroc on maximal stretch) à rupture of degenerate tendon
§ Rupture at musculous tendinous junction occurs most often in young ppl, but ruptures near the calcaneus also occur
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o Risk factors
§ Age >40yrs
§ Long term steroid use
o Symptoms: feeling of having been struck just above the heel, inability to tip-toe
o Signs
1. Get pt to kneel on the chair This patient likely has a ruptured (left / right) Achilles tendon as I notice that there
2. Comment on step in the tendon is a step in the tendon. I would like to proceed to confirm my diagnosis.
(Gap seen and felt 5cm above insertion of
tendon (musculotendinous junction)) There is a palpable gap in the tendon just 5cm above the point of insertion of the
tendon. Plantarflexion on the (left / right) is weak, and not a/w tautening of
3. Ask patient for any pain tendon, consistent with the diagnosis.
4. Palpate tendon
5. Weak plantarflexion without tautening of Simmond’s test is positive on the (left / right) . Hence the diagnosis is a ruptured
tendon (pt in kneeling position, ask pt to push (left / right) Achilles tendon.
sole against your hand)
6. Perform Simmond’s test
(lack of plantarflexion on squeezing calf)
o Management
§ Conservative (re-rupture rate 10%) in acute cases: 8weeks of casting heel in equinus to approximate tendon ends à 6weeks
of shoes with raised heel
§ Operative (more reliable): Operative repair to equinus + the above OR a lockable brace (allows early ankle movement but
blocks tension on repaired tendon)
PAINFUL ANKLE
• Footballer’s ankle/ anterior ankle impingement syndrome
o Definition: painful mechanical limitation of full ankle ROM secondary to an osseous or soft-tissue abnormality
o Pathophys: repeated forced dorsiflexion à tearing of anterior capsule of ankle joint à subsequent bone spur formation (osteophytes)
aka anterior exostoses of the tibia à subsequent pain + limited ROM
o Rx:
§ Acute phase:
• Conservative: NSAIDs, physioRx, orthotics, bracing
• Sx: arthroscopic excision and debridement
§ Recovery phase:
• Posterior splinting for 1/52 w supportive brace and compression stocking
• physioRx for 2/52 for strengthening, ROM, proprioception and sports-specific rehabilitation
• Tenosynovitis
o often tibialis posterior or peroneal tendons
o Signs: tenderness and swelling localised to affected tendon
o Symptoms: pain aggravated by active movement against resistance
o Management: local injection of corticosteroids
• Rupture of tibialis posterior tendon
o Symptoms: pain (arises suddenly), may have felt the tendon snap
o Signs:
§ Hindfoot: heel in valgus during weight bearing
§ Midfoot: pes planus
§ Tenderness around medial malleolus
§ Active inversion of ankle painful and weak
o Management
§ Physically active patients: operative repair or tendon transfer using FDL
§ Poorly mobile patients: splintage
• Osteochondritis dissecans of talus
o Symptoms: pain, slight limitation of movement in ankle esp in young patients
o Investigations:
§ X-ray: small osteochondral fracture of dome of talus
§ MRI, Arthroscopy
o Management
§ Articular surface in tact: restrict activities
§ Separated fragment: operative removal
• Avascular necrosis of talus
• Chronic ligamentous instability
PAINFUL HEEL
Posterior heel pain
• Traction apophysitis (pulling osteochondritis)
o Mechanism: mild traction injury
o Suspect in: young boys
o Symptoms and signs:
§ Pain and tenderness localized to tendoarchillis insertion
o Investigations: X-ray
§ Increased density or irregularity of apophysis (but painless heel often
look similar)
o Management: raise heel of shoe, restrict strenuous activities for a few weeks
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• Retrocalcaneal bursitis
o Suspect in: older girls and young women
o Symptoms: painful bumps on back of their heels
o Signs: prominent posterolateral portion of calcaneumà shoe friction causes bursitis
o Ix:
§ X-ray: look for Haglund deformity (á prominence of the posterosuperior aspect of the calcaneus)
§ U/S
o Management:
§ Conservative: Physiotherapy, Change footwear (use open back shoes to relieve pressure on the affected region, avoid shoes
with lace, pad heels by inserting heel cup in the shoe to help raise the inflamed region slightly above the shoe’s restricting heel
counter), NO STEROID INJX
§ Operative: removal of calcaneal prominence (Haglund deformity)
• If fail conservative therapy & symptoms persist
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PAIN OVER FOREFOOT
Generalised pain
• Metatarsalgia (commonest expression of foot strain)
o Conditions that give rise to faulty weight distribution (forefoot deformities, prolonged walking or standing etc)à mismatch btwn
loads applied to foot, structure on which loads are acting, muscular effort to maintain structure.
• RA: Starts off at MTPJà symmetrical and bilateral swelling and tenderness
Localised pain
• Sesamoiditis
o Inflammation of peritendinous tissues around sesamoids (esp medial)
o Causes:
§ Acute: trauma, unaccustomed stress
§ Chronic: sesamoid displacement, local infection, AVN
o Signs: pain and tenderness directly under 1st metatarsal head, aggravated by walking or passive dorsiflexion of great toe
o Management: conservativeà injection à operative removal of sesamoid
• Freiberg’s disease (crushing osteochondritis of 2nd metartarsal head)
o Suspect in: young adults esp women
o Signs
§ Tender bony lump of enlarged 2nd metatarsal head
§ Painful movement of MTPJ
o Investigations: X-ray shows 2nd metatarsal head wide and flat
o Management
§ Conservative: footwear modifications (moulded insoles)
§ Surgical: operative synovectomy, debridement and trimming of metatarsal head
• Stress fracture (2nd and 3rd metatarsal bones)
o Suspect in: young adults after unaccustomed activity, old osteoporotic patients
§ Other common sites of stress # (MCQ): head of femur, distal end of femur, tibia
o Signs: Affected metatarsal shaft feels thick and tender
o Investigations: X-ray
§ Early: normal
§ Later: fusiform callus around a fine transverse fracture
o Management: Rest
• Morton’s metatarsalgia
o Interdigital nerve compressionà secondary thickening of nerve
o Suspect in: women aged ~50yrs
o Symptoms: pain in forefoot radiating to toes, aggravated by tight-fitting shoes
o Signs:
§ tenderness over one of the intermetatarsal spaces (usually 3rd)
§ pressure just prox to interdigital web may elicit pain and tingling distally
§ Mulder’s click: painful click on squeezing metatarsal heads together
§ ‘Blocking test’: pain relieved on injecting local anaesthesia beneath transverse intermetatarsal ligament
o Management
§ Conservative: footwear modifications (protective padding and wider shoes)
§ Operative:
• Nerve compression release by dividing tight transverse intermetatarsal ligament.
• Intractable cases: excision of ‘neuroma’
TOENAIL DISORDERS
• Ingrown toenail
o Nail burrows into nail grooveà ulcerates and wall grows over nail
o Management;
§ Conservative: cut the nail square, insert pledgets of wool into nail groove, keep feet clean and dry
§ Operative excision or chemical ablation with phenol of affected portion of germinal matrix
§ Rare: remove entire nail or ablate nail bed
• Overgrown toenail (onychogryposis)
o Nail becomes hard, thick and curved
o Management: chiropodist or complete excision
• Subungual bone growth
o Nail lifted from bed by exostosis growing on dorsum of terminal phalanx
o Investigations: X-ray shows exostosis
o Management: remove exostosis
3. Ankle injuries
GENERAL INFORMATION (EVALUATION OF ANKLE COMPLAINTS)
• History: pain, swelling, mechanism of injury, effect on standing/walking
• PE
o Neurovascular status
o Look, feel, move (dorsiflexion, plantarflexion)
o Also assess tenderness at knee (Maisonneuve), lateral and medial malleoli
o Special tests: anterior drawer (for ankle), talar tilt, squeeze test, simmond’s test, Thompson test
• X-ray
o Views: AP, lateral, mortise (30deg internal rotation to give true view of talus in tibiotalar joint)
128
§ Medial & lateral jt spaces should be symmetric and <4mm w no talar tiltà disrupted space signifies ligamentous or bony injury
§ Signs of ligamentous injury:
• Widening of tibiofibular space, asymmetry of talotibial space, widening of medial joint space, tilting of talus
o When to x-ray (Ottawa ankle rules)
§ Pain in malleolar zone, AND
§ Bony tenderness over posterior aspect of distal 6cm of medial or lateral malleolus OR
§ Inability to weight bear both immediately and in the A&E for 4 steps
o Foot x-ray series only required w (Ottawa foot rules):
§ Pain in midfoot zone AND
§ bony tenderness over navicular or base of 5th metatarsal OR
inability to weight bear both immediately and at A&E for 4 steps
• Ring Principle of the Ankle
o The ankle can be thought of as a ring comprising:
§ a: lateral malleolus
§ b: medial malleolus
§ c: posterior medial malleolus
§ d: deltoid ligament
§ e: syndesmotic ligament (syndesmosis)
§ f: calcaneofibular ligament
129
§ Sport-specific or function-based trng: upon achieving full strength and pain-free ROM in the lower extremity, the athlete can be
cleared to return to sport, most often without any brace or external support
Grade Pathology Signs Treatment
I Microscopic tear -Minimal tenderness and swelling; Non-operative
of collagen fibres pain but no gift -RICE (rest, ice, compression, elevation)
II Macroscopic tear -Moderate tenderness and swelling -Treat with activity: apply bandage/ brace (usualy in
of some collagen (not as painful as grade 1; pain on dorsiflexion and eversion; individualized to patient’s
fibres motion); solid end point to gift (opens discomfort; remove when swelling disappears)à begin
up and stops); physioRx exercise immediatelyà protective weight
-Some instability bearing instituted w crutches and stopped as soon as
patient can walk (usually few days) à usually return to
play within 2-3wks
III Complete tear of -Significant tenderness and swelling Non-operative
collagen fibres (?little or no pain) -RICE
-Significant instability (no end point -Brace w a hinged knee orthosis and crutches for 1-2wks
to ligament laxity) (in past: BK cast immobilization for 6 weeks: from knee
-Talar tilt (apparent on mortise view) to toes with foot plantigrade)à physiotherapy à
Usually return to play after >/=6wks
ANKLE DISLOCATIONS
• Commonly at the subtalar joint rather than tibiotalar joint (tibiotalar joint dislocation only in fracture dislocations as mortise holds joint strongly)
• Management
o Reduction done before X-ray: Ulceration may occur if delay
Look
• Painful snapping sensation over lateral ankle • Ankle deformity
• (+/- weakness, pain) • Swelling / bruising
• Chronic lateral ankle instability • Prominence of tendon with dorsiflexion / internal
MANAGEMENT rotation
• Surgical anatomical repair of the Bankart-type lesion of the superior Feel: Tenderness posterior to lateral malleolus, Clicking
peroneal retinaculum Move
• + below-knee plaster cast with foot in equinus x 6/52 • Flex knee and ask pt to dorsi- & plantarflex
• + physiotherapy • Inversion / eversion
4. Ankle fractures
Fractures of the ankle involve
•
o ipsilateral ligamentous tears or bony avulsion
o contralateral shear fractures
• Pattern of fracture
o Determined by mechanism of injury
o Avulsion fractures are transverse
o Shear fractures are oblique if pure inversion / eversion
o Shear fractures are spiral if rotational force
MALLEOLI FRACTURES
• Mechanism of injury:
o (COMMONEST) abduction and/or lateral rotation of ankle à
§ lateral malleolus sheers off at oblique angle
§ medial side: strain may rupture deltoid ligament or produce transverse avulsion fracture of medial malleolus
o sudden adduction of ankle à
§ medial malleolus sheers off
§ lateral side: strain injury or fibular fracture
o forward lunge of tibia à posterior edge of tibia fractures against the dome of talus
o axial compression of ankle (fall from height)à shatters articular plafond of tibia
• Symptoms: Intense pain and inability to stand on leg, Swelling, deformity
• Signs: Tenderness over medial and lateral sidesà suspect double injury
130
• Classifications:
o Lauge-Hansen classification (based on adduced mechanism of injuryà reduce displaced fragments by reversing injurious forces
during manipulation of ankle): 1st word refers to position of foot & 2nd word refers to direction of movement of the talus in relation to leg
o Danis Weber classification (based on level of fibular fracture relative to syndesmosis)
Danis Weber classification Lauge-Hansen classification Prognosis (risk of
syndesmotic injury)
Type A (Infra-syndesmotic): Supination-Adduction (Supination = inversion) Low risk of
• Transverse fibular fracture below tibiofibular • Sequence of injury syndesmotic injury
syndesmosis o Supination force may rupture portions of lateral collateral and ankle instability
• Avulsion of lateral malleolus below plafond ligaments or may avulse distal fibula, resulting in transverse
or torn calcaneofibular ligament fracture below the level of intact syndesmosis;
• +/- oblique or vertical fracture of medial o Adduction forces talus against the medial side of the joint,
malleolus resulting in vertical fracture of the medial malleolus
Type B (Trans-syndesmotic) Supination-External rotation 50% risk of
• Oblique fibular fracture at syndesmosis • Most common (45-65%) syndesmotic injury and
• +/- avulsion of medial malleolus or • Supination and external rotation, resulting in oblique fracture at ankle instability
rupture of deltoid ligament the level of the sydesmosis
• +/- fracture of posterior malleolus Pronation-abduction (pronation = eversion)
• +/- disruption of anterior fibres of • Sequence of injury
tibiofibular ligament o Avulsion fracture of medial malleolus or rupture of deltoid
ligament;
Type C (Supra-syndesmotic) o Abduction force then either ruptures the syndesmosis or ~100% risk of
• Fibular fracture above syndesmosis avulses its bony attachment sites; syndesmotic injury and
• Fracture of medial malleolus OR disruption o Lateral force from talus impacts and fractures fibula at or
ankle instability
of deltoid ligament above level of syndesmosis and ruptures interosseous
• Frequently tears syndesmosis membrane
• +/- Maisonneuve fracture if at proximal Pronation-external rotation
fibula • Sequence of injury
• Torn tibiofibular ligament OR ligament o Transverse # of the medial malleolus or disruption of deltoid
avulses small piece of tibia ligament;
o External rotation then results in rupture of the anterior
tibiofibular ligament or its bony insertion;
o Oblique or spiral fracture of fibula above the level of the jt;
o Posterior injury with tibiofibular ligament rupture or avulsion
of posterior malleolus
• Fibular fracture may be proximal (i.e., Maisonneuve #, which is
a spiral # of the proximal third of the fibula a/w a tear of the
distal tibiofibular syndesmsis and the interosseous membrane)
131
*Note: Syndesmotic injury managed with a syndesmotic screw
• Management
o Reduce swelling (elevate leg +/-foot pump; may need to wait days)
o Reduction
§ Undisplaced fractures: NWB BK cast
• Type A: stable hence minimal splintage with bandage or plaster slab
• Type B: if stable, apply below-knee cast with ankle in neutralà remove in 6-8weeksà physiotherapy
• Type C: fix
§ Displaced fractures: reduce ASAP
• Type A: closed reduction + IF with screws à cast 6-8weeks
• Type B: closed reduction + IF à cast 6-8weeks
• Type C: ORIF à cast 6-8weeks
• NOTE: fix fibula with plates and screws; medial malleolus with screws
o Indications for ORIF
§ fracture-dislocations
§ type C fractures
§ trimalleolar (lateral, medial, posterior) fractures
§ talar shift or tilt
§ failure to achieve or maintain closed reduction
• Complications
o Early
§ Vascular injury in severe fracture-subluxation
§ Wound breakdown and infection (esp diabetics)
o Late
§ Incomplete reduction (common)à secondary OA
§ Non-union of medial malleolus due to flap of periosteumà prevent with ORIF
§ Joint stiffnessà prevent with mobility
§ Reflex sympathetic dystrophy (swelling and diffuse tenderness, trophic changes and osteoporosis)
§ High incidence of posttraumatic OA from malunion / incomplete reduction
o Prognosis dependent upon anatomic reduction
• Associated injuries/complications
o 30% will have ipsilateral injuries and 5-10% will have bilateral injuries
§ Compartment syndrome
§ Compression # of vertebral column, esp L1
§ Contralateral # of: os calcis, tibial plateau, pelvis, acetabulum (vertical shear injuries)
§ Vascular injuries
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• Signs: severe swelling, fracture blisters
• Investigations:
o X-ray; CT in severe injuries
o Comminuted fracture of distal end of tibia, extending into ankle joint
• Management
o Conservative
§ Pain relief + Abx prophylaxis (open #/ internal fixations) + Elevation (control soft tissue swelling) + splint (cast
immobilization if # is undisplaced)
o Surgical:
§ Primary stabilization: calcaneal traction or external fixator (due to high risk of infection) for 2-3wks +/- fibular # fixation
§ Definitive surgery after condition of soft tissues is optimized (blisters have epithelized, skin is wrinkled)
• Types: ORIF, external fixation, limited internal fixation w external fixation, percutaneous pinning
§ Indications for surgery
• Open fracture
• Displaced fracture
o Articular fragments with gap of >2mm or step of >1mm
o Rotational malalignment
• Vascular compromise
• Compartment syndrome
o Post-op: elevation, post-op physiotherapy, partial weight bearing after 6 weeks
• Complications
o Secondary OA from cartilage injury
6. Midfoot injuries
MID-TARSAL INJURIES
NOTE: Assume fractures in this region to be combination fractures or fracture-subluxations
• Symptoms
o Bruising, swelling of foot
• Signs
o Diffused tenderness across midfoot
o Deformities (medial mid-tarsal dislocation looks like ‘acute club foot’; lateral dislocation has valgus deformity, longitudinal stress
injuries have no obvious deformity)
o Exclude compartment syndrome
• Investigations
o Multiple X-ray views: ensure that all tarsal bones are clearly shown
o CT
• Management
o Ligamentous strains: Bandage until pain subsidesà mobilise
o Undisplaced fractures: Elevate footà below-knee castà limited weight bearing on crutchesà remove in 4-6weeks
o Fracture-dislocations
§ Closed reduction under GA +/- K-wiresà below knee cast for 6-8weeks (restoration in 6-8months)
134
TARSOMETATARSAL INJURIES
NOTE: Sprains are common; dislocations are rare. Suspect fracture-dislocation in pain, swelling and bruising after an accident even with no
obvious deformity.
• Investigations
o Multiple X-ray views +/- CT for full extent of injury
§ Medial edge of 2nd metatarsal should be in line with medial edge of 2nd cuneiform
§ Medial edge of 4th metatarsal should be in line with medial side of cuboid
• Management
o Undisplaced sprains: cast for 4-6weeks
o Subluxation or dislocation: M&R under GAà fix with Kwires or
screws + cast
• Lisfranc Injury
o Mechanism: Twisting force; fall onto plantarflexed foot or direct
crush injury
o Injury
§ Term used in general to describe a 2nd tarso-metatarsal
displacement injury
§ Can be used specifically for injury to the Lisfranc
ligament (between medial cuneiform and base of 2nd
metatarsal)
§ May be merely a ligament tear, dislocation
(tarsometatarsal joint) or fracture dislocation (speck
signl; shortened forefoot prominent base à ORIF)
7. Forefoot injuries
METATARSAL FRACTURES
• Anat: as with hand, 1st, 4th, 5th MT are relatively mobile while 2nd and 3rd are fixed
• Mechanism of injury: direct blow, twisting injury, avulsion fracture, repetitive stress (march fracture)
• Symptoms: pain and swelling
• Types
Fracture Mechanism Clinical Features Treatment
Avulsion of base of 5th MT Sudden inversion followed by • Oblique fracture ORIF if displaced
contraction of peroneus brevis • Tenderness at base of 5th MT
Jones Fracture (Midshaft 5 MT) Stress injury
th • Tenderness along shaft of 5th MT Non-weight bearing below
• Tends to displace due to knee (NWB BK) cast x 6/52
peroneus brevis and tilting ORIF if athlete
• Transverse fracture
• Prone to non-union as injury at
watershed area of BS
March # (below): shaft 2nd 3rd MT Stress injury
1st MT Fracture Trauma Painful 1st MT ORIF if displaced
If not: NWB BK cast x3ks then
walking cast x2wks
• Stress injury (march fracture)
o Risk factors: young adult (recruit or nurse), osteoporotics after operations that shorten big toe hence
extra stress on adjacent metatarsals
o Signs: tender shaft of 2nd/ 3rd MT & tender lump just distal to mid-shaft of metatarsal bone (usually
the 2nd)
o Investigations: X-ray normal at firstà hairline crackà mass of callus or periosteal new bone
o Management: NO reduction nor splintage (support forefoot with Elastoplast and encourage walking)
FRACTURED TOES
• Management:
o Disregard fractureà encourage walking in suitably adapted boot
o If pain is marked, buddy splint for 2-3weeks
FRACTURED SESAMOIDS
• Mechanism of injury: direct injury (landing on ball of foot), sudden traction, repetitive stress (dancers
and runners)
• Symptoms: Pain directly over sesamoid
• Signs
o Tenderness over sesamoid
o Pain exacerbated by passive hyperextension of big toe
• Management
o Often unnecessary
o Local injection of lignocaine for pain
o Immobilise in short-leg walking cast for 2-3 weeks
o Excision of offending ossicle
135
Spine
Atraumatic
Traumatic
Thoracolumbar
and
Deformity
Lumbar
Spine
• Scoliosis
• Wedge
Compression
Fracture
• Kyphosis
• Burst
Fracture
• Flexion-‐Distraction
• Fracture
Dislocation
136
Examination of the Cervical Spine o For thoracic outlet syndrome:
The preliminaries: Introduce yourself to patient, ask for permission to - Adson’s manoeuvre: palpate radial pulse, extend neck
actively and rotate it towards the side being tested and take
examine. Ensure adequate exposure (remove shirt) but consider
a deep breath. Positive is diminished pulse. (interscalene
patient modesty also. Ensure good lighting, good positioning of bed. compression of the subclavian neurovascular bundle)
- Wright’s Test: palpate radial pulse, passively abduct
LOOK (patient sitting upright, shirt off): back, side, front shoulder. Feel for diminished pulse.
1. Gait: myelopathic gait, high stepping gait
2. General appearance and vitals – any pallor, BP, and HR. NEUROLOGICAL EXAMINATION (esp. if susp myelopathy)
3. Posture: erect, splinting, tilting & cervical lordosis & symmetry
4. Deformity – namely tilting of the head (‘wry neck’) UPPER LIMB:
- Normally, head is balanced over the shoulders
1. Tone, clonus, muscle wasting
- Causes: torticollis (congenital), PID, inflamed neck glands,
2. Power (0-5): C5-T1
cerebellar dysfunction, ophthalmologic disorders, congenital
3. Reflexes (0-3+) – biceps, triceps, brachioradialis
scoliosis, atlanto-axial rotatory dislocation, etc
- C5/C6: ‘inverted supinator reflex’ (spastic finger flexors)
5. (Scars, sinuses, swellings) E.g. cervical lymph nodes
↓elbow flexion ↑finger flexion on tapping the brachioradialis
6. Tandem gait, rombergs etc
tendon; associated with hyper-reflexic triceps jerk.
- above C5: Shimizu’s sign (scapulo-humeral reflex) tap
FEEL spine of scapula, hyperactive when the scapula elevates or
Bony Landmarks: the humerus becomes abducted.
(A) Thyroid cartilage: C4 superiorly, C5 inferiorly 4. Sensory function (0-3+)– compare with chin and not chest
(B) Hyoid Bone: C3 pathology is in the cervical region and the chest belongs to
(C) Cricoid Bone: C6 thoracic dermatomes
1. Palpate for tenderness along spinous processes and 5. Proprioception – thumb
interspinous ligaments (from midline of the occiput downwards): 6. Cerebellar function – dysmetria, dysdiadochokinesia
use either the tip of the thumb or tips of the index & middle 7. Myelopathic hand:
fingers for palpation of midline and paraspinal structures (ii) Thenar atrophy
- palpate for any step deformity (high-grade listhesis), and (iii) Hoffmann’s sign
ligamentous gap (more applicable for trauma). - Hold patient’s right hand with examiner’s left hand, and
2. Move hands along shoulder: feel for tenderness and warmth ensure wrist, MP and IP jts are extended à index
3. ‘Trigger points’: Points that are extremely tender with radiation; finger of examiner on volar surface of patient’s middle
reproduces patient’s usual pain symptoms (myofascial pain finger and middle finger over dorsal surface and flicks
syndrome?). the patient’s distal phalanx downwards with thumb.
4. Palpate paravertebral muscles for spasm - Positive: flexion of the thumb and index finger
5. Sternocleidomastoid for swelling/tenderness (iv) Grip and release test
6. Lymph Nodes - 20 cycles of open-close fist in 10 seconds.
- In cervical myelopathy the movement is slow, difficult
MOVE and incomplete.
1. Flexion-extension: (v) Finger escape sign
- 50% at atlanto-occipital junction. - When patient is asked to keep fingers adducted and
- Flexion: chin touch chest extended, the ulnar two fingers drift into flexion and
- Extension: occipitomental line (chin to occipital abduction within 30 seconds.
protuberance) at least 45° to the horizontal (usually more
than 60° in young patients) LOWER LIMB
2. Lateral flexion: 1. Tone, clonus (usually increased tone in LL)
- Check symmetry of movements 2. Power (usually decreased)
- 45° both sides 3. Reflexes – Knee, ankle, plantar reflexes (usually hyper-reflexic)
3. Rotation 4. Sensation (usually decreased)
- 50% at the atlanto-axial joint (odontoid) 5. Proprioception and cerebellar function
- check for symmetry of movements on both sides - Gait is usually broad-based and clumsy, check Romberg’s.
- 80° both sides
DRE: For saddle anaesthesia, anal wink reflex, anal tone.
SPECIAL TESTS
o For cervical spondylosis:
1. Spurling’s and Davidson’s tests (provocative test to elicit
pain along nerve root for patients w pain due to
compression of nerve roots or radiculopathy)
- Spurling’s: Active extension, lateral flexion and rotation
of patient’s neck to affected side with axial pressure à
radicular symptoms reproduced
- Davidson’s: Subsequent abduction of the arm on the
affected side à relief.
2. Cervical compression and distraction
- Axial loading of the cervical spine results in radicular
symptoms
- Distraction of the neck (pull the head superiorly)
relieves the symptoms.
o For cervical myelopathy:
- Lhermitte’s sign: neck flexion à electric shock-like
sensations (centre of back to all 4 limbs).
- Ulnar drift: flex shoulder w elbows extended and palms down
à ulnar deviation of little finger away from fingers
137
Examination of the Thoracolumbosacral Spine - Make patient sit down to fix pelvis OR stabilise iliac crest,
The preliminaries: Introduce yourself to patient, ask for permission to then cross arms over chest then rotate
- Angle between line joining shoulders and line joining ASIS is
examine. Ensure adequate exposure (in underwear) but consider patient
the extent of rotation
modesty also. Ensure good lighting, good positioning of bed.
LOOK (patient standing, back and legs exposed) NERVE ROOT TENSION SIGNS
1. General appearance and vitals – any pallor, the BP, and HR. 1. Straight leg raising test (SLR)
2. Front: scars - Knee extended, raise the leg being tested, checking
3. Side: patient’s face to assess pain
• Deformity - Stop when patient complains of pain & ask what kind of
o Loss or exaggeraton of thoracic kyphosis/ lumbar lordosis pain: +ve SLR when there’s pain radiating into e lower limb
o Hyperkyphosis (protruded abdomen) – Scheuermann’s (radicular pain)
disease (adolescents) or multiple osteoporotic compression - note angle at which pain occurs
fractures in old ladies - Also assess cross-SLR – patient complains of radicular
o Gibbus deformity (angular kyphosis) – in infections like TB pain in the affected side when the normal lower limb is being
• Skin changes raised
4. Back: 2. Lasegue test/ SNST (not commonly done, beware of
• Postural: Sciatic listing (relieve impingement) variations)
- With knee and hip flexed to 90 degrees each, slowly extend
• Deformity
knee and look out for radicular pain
o Scoliosis (postural/fixed) à Adam’s fwd bend test
- OR after measuring angle of SLR, lower LL by 5deg (or till
§ Imbalance in heights of shoulders (R usually higher
no pain) & dorsiflex ankleà +ve if radicular pain reproduced
than L in idiopathic scoliosis), asymmetrical limb
- More specific than a simple SLR, because positive SLR can
waist distance, prominence of hips (R typically
be due to other causes e.g. hamstring tightness
more prominent), truncal shift (plumline from C7
3. Bowstringing test
spinous process should be in line with natal cleft;
- Hip flexed ~100°, knee flexed 80-90°: press biceps femoris
measure amt of shift of plumline w ruler)
tendon (lat side of popliteal fossa) – should be no pain.
§ Measure rib hump and lumbar hump w
- Press medial to the tendon (common peroneal nerve)
scoliometer: measure w patient bent forwards
- Positive test: pain radiates proximally and/or distally from the
o Tilting of the shoulder (one of the shoulders/scapula
point of pressure.
may be higher in thoracic scoliosis), pelvis (one of the
- Most useful confirmatory test of nerve root tension
hip or iliac crest may be prominent in lumbar or
Femoral Stretch Test: patient lies prone, hip extended and knee
thoracolumbar scoliosis), limb shortening
• Skin changes: Birthmarks, hemangioma, neuro-fibromata, cafe flexed to 90deg. Cup hand on knee and support thigh, and leg
au lait spots, hariy patches/midline dimples supported by forearm. L hand supported on hip and gently extend hip
5. Gait: walk tendem gait (myelopathy), then toes only, then heels only to 15-20deg à +ve if patient complains of anterior thigh pain.
• Recognise antalgic gait, broad based gait, high step gait etc (test femoral root compression: L2, L3, L4)
FEEL Pump handle test: flex hip and knee of involved side and bring knee
1. Palpate for across to opp shoulder
- Tenderness along spinous processes Positive if this increases pain in region of sacroiliac jt
- step deformity (high-grade listhesis) Gaenslen’s Test (test femoral root: L2,L3,L4): lie supine w legs
- ligamentous gap (more applicable for trauma)
hanging freely; flex both hips, then extend hip on involved side à
- Palpate from C7 (most prominent spinous process)
downwards à L4 (at level of imaginary line drawn btw iliac +ve if extension causes increase in pain in sacroiliac region
crest) à sacrum: use either tip of the thumb or tips of index Patrick/Faber Test
& middle fingers for palpation of midline and paraspinal - for sacroilitis – in young male, may indicate ankylosing spondylitis
structures - Flex, ABduct and Externally Rotate the hip (“4”) à L hand placed
2. Palpate paravertebral muscles for spasm/ tenderness on opposite ASIS and R hand placed on apex of “4” (knee)
3. Palpate area of sacroiliac joint: PIIS - Positive if pain elicited in sacroiliac jt region on exerting downward
4. Percuss for tenderness force on apex
- Pain on percussion à pathology in the antr vert body
(infection or tumour) NEUROVASCULAR EXAMINATION
- Do a renal punch to exclude renal pathology 1. Tone: ankle clonus
MOVE (mostly passive) 2. Reflexes (0-3+): DTR + Babinski reflex (+ve if big toe moves
NOTE: There are no “normal” range of movements in the spine, but up and small toes fan out)
assessment of ROM helps establish a baseline range that is useful for 3. Sensation by dermatome (0-3+): light touch + pain
4. Power (0-5): Particularly knee extension for L4; ankle and big
future monitoring of disease progress or efficacy of Rx
toe dorsiflexion for L5; ankle and big toe plantarflexion for S1
1. Flexion-extension: 5. Pulses
- Flexion: Schoeber’s test (“bend forward to touch your toes”) 6. PR
– mark the level of the PSIS (1st bony prominence while - Saddle anaesthesia (S3, 4, 5)
palpating the iliac crest posteriorly) and a point 10 cm above - Inspect anal orifice for tone (“crow’s feet”)
it and another pt 5cm below it– increase in distance when - Anal wink reflex – scratch perianal skin and watch for anal
bending forwards should be >5cm. wink
- Extension: normally about 30° (support the pelvis) - Put finger in rectum to assess anal tone
2. Lateral flexion:
- “Slide your hand down side of ur leg as far as u can go” FINISH by offering to examine the hip joint.
- Touching knees should be normal
3. Rotation
138
1.
Important
concepts
Anatomy
History o Positive Babinski reflex
• Pain: Mechanical vs Pathological (inflammatory, infective, • Other medical illness: RA, AS, Down’s syndrome
tumour) Investigations
• Stiffness • Imaging
• Deformity o X-ray: bony alignment
• Neurological symptoms (radiculopathy vs myelopathy vs o MRI: nerve, soft tissue
specific cord syndrome) o CT: Bony details
• Systemic Review: Note that visceral pathologies can lead to o Bone scan: Screening metastasis
spine pain as well – eg. AAA • Blood Tests
Red flags of spinal conditions o FBC (infection, tumour)
• Suggestive of infection/ cancer o Renal panel
o Non-mechanical pain: Night pain (wake up, cannot o ESR (infection, tumour, spondyloarthropathies)
sleep), pain at rest, night sweats • Infection (nerve root/facet blocks)
o Constitutional symptoms: Fever, unexplained LOW Flexion vs Extension
(>10kg in 6 months), LOA • Mechanical Pain (as above)
o Medical history: Cancer, recent bacterial infection • Neurological Deficit / Pain
o Age of onset: <20years, >55years o Flexion: Worsens PID
o Obvious deformities o Extension: Worsens neurogenic claudication (spinal
o Thoracic back pain (metastasis) stenosis)
• Suggestive of spinal fracture: Trauma, osteoporosis, obvious Sites of Pathology
deformities • Vertebrae: Fracture, Tumour, Infection
• Suggestive of serious injuries • Disc: Discogenic degeneration, PID, Infection
o Cauda equina: saddle anaesthesia, bladder or bowel • Facet Joint: Degeneration, Instability
incontinence, disturbed gait • Nerve Root: Radiculopathy
o Neurological deficits • Spinal Cord: Myelopathy
o Pain for >4-6weeks • Ligaments: Stretched, torn
o Failure to improve with therapy Spine X-ray
o Bilateral leg pain • AP View
• Suggestive of high risk of permanent damage to nerve o Opening: Which level of spine (which levels shown)
o Significant muscle wasting/weakness o General comments
o Loss of tendon reflexes § Posture: Scoliosis
139
§ Alignment: whether vertebral bodies are sit § Prevertebral space –normally
squarely above each other • <6mm at C2 (above trachea)
§ Osteopenic • <22mm or 1 vertebral body at C6 (below
o Pathology trachea)
§ Parts § Trauma
• Pedicles: ‘Owl winking’ sign • Fracture line
• Spinous processes: centered? • Displacement
§ Vertebral body § OA: LLOSS
• Vertebral body shape: Squaring? • Oblique view: defect in the pars inter-articularis (spondylolysis)
• Vertebral height à scotty dog sign
§ Disc space
• Lateral View
o Opening
o General comments
§ Posture: lordosis, kyphosis
§ Alignment:
§ Lines: Anterior vertebral, posterior vertebral,
spinolaminar, posterior spinous
§ Osteopenic?
o Pathology
§ Vertebral (loss of height, fragmentation,
displacement)
§ Disc space (increasingly larger down the levels)
• Pathology: Nerve root lesion resulting in neurological deficits of affected dermatomes and myotomes
• Causes
o PID
o Spondylosis – narrowing of neural foramen, facet joint hypertrophy, bony spurs
o Spondylolisthesis
o Other causes: CIN DVT M
• Presentation:
o Neurological defects
§ Sensory: Pain, parasthesia, sensory loss
§ Motor: Weakness, loss of reflexes
o Pattern
§ Shooting pain down e leg according to compressed n. root (radicular pain)
§ Isolation to specific dermatomes / myotomes
o PE: any test that triggers compression of nerve root will be positive (eg. SLR)
• Management
o ACDF (Anterior cervical discectomy and fusion), ACCF (Anterior cervical corpectomy and fusion)
o Anterior discectomy without fusion (artificial disc replacement)
140
• Dermatomes and Myotomes, Reflexes (Babinski’s Reflex: L5, S1, S2)
Level Motor Sensory Reflex
C4 Spontaneous respiration (diaphragm) Clavicles
Shoulder abduction
Regimental Biceps jerk/
C5 Elbow flexion (biceps, brachialis,
badge Supinator
brachiobrachialis)
jerk
C6 (radial nerve) Wrist extension (ECRL, ECRB) Thumb
C7 (median n.) Elbow extension (triceps), wrist flexion Middle finger
Triceps Jerk
C8 (ulnar nerve) Finger grip (FDP) Little finger
T1 Finger abduction/ adduction (interossei) Medial forearm
T2 Medial arm
T3 Armpit
Lvl Motor Sensory Reflex
L1 Underwear
L2 Hip flexion (iliopsoas; femoral nerve) Lateral quads
Knee extension (quads; femoral nerve)
L3 Lat & above knee Knee
Hip adduction (obturator nerve)
jerk
Ankle dorsiflexion (prominent TA tendon; deep peroneal n);
L4 Medial aspect of leg
hip abduction (superior gluteal nerve)
Big toe dorsiflexion (EHL)
L5 1st web space
Toes dorsiflexion (EDL)
Big toe plantarflexion (FHL)
Ankle plantarflexion (gastrocsoleus; tibial nerve) Sole of foot, lateral Ankle
S1
Knee flexion (sciatic n) heel jerk
Hip extension (inferior gluteal n)
S2 Posterior thigh
Mr / Mdm XXX is a __ years old (race) gentleman / lady, Past Medical History
premorbid status: (ADL independent, community ambulant – w / wo aid) , Mr / Mdm XXX has a past medical history of ___________ for (duration) .
occupation: ____________________, (note any DM & peripheral neuropathy)
with a significant PMHx of , He / she also does not have a history of peptic ulcer disease / GI bleeding.
presenting complaint: currently presents with a (duration) history of neck He / she had previous operations for ____________.
pain associated w (duration) of (numbness / weakness) in e (left / right) UL. He / she has NKDA and is currently on ___________ for her medical conditions.
The neck pain started (duration) ago and has gotten progressively worst. Family History
He / she describes the pain as (nature) . He / she (has / has no) family history of cancer or similar back pathologies.
It is mechanical in nature, aggravated by movement such as (type of activity)
and relieved by rest. Social History
The pain is localised at the (site) of the neck (and shoots down to the lateral He / she (does not smoke / smokes / is an ex-smoker and has quit XX years
aspect of the arm / forearm / thumb / fingers / with no radiation) . ago) , ( sticks/day x years).
Current pain score is ___ & the pain (affects / does not affect) his / her sleep. He / she (has / does not have) a habit of regular intake of alcoholic drinks.
There is no hx of any specific activity that precipitated e onset of e pain initially. He / she has (good / poor) social support. He / she works as a _________
and his / her condition affects her job. He / she lives with his / her ________. His
There (is / is no) associated stiffness in the back especially in the morning / her main caregiver is his / her ______________.
that does not last more than 30 mins. He / she lives in a residential (with / without) lift landing. There (is / is no)
squatting toilet in the house.
In addition, he / she experiences (numbness / weakness) over the (site) of Currently, the family (does not have any financial issues / is receiving financial
his / her upper limb that has gotten progressively worst over the last (duration) aid from ) .
. There are no associated neurological symptoms such as weakness or
numbness in the lower limb. He / she also does not complain of clumsiness or In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co-
unsteady gait. morbidities of ________________, currently presenting with chronic neck pain
Functional Status for (duration) associated with progressive (numbness / weakness) of the
Currently, his / her symptoms have limited his / her function such as (carrying (left / right) upper limb which has failed to improve with conservative
heavy objects / ability to work / drive) . management and has affected his / her daily functioning.
Systemic Review My provisional diagnosis will be that of possible ___ cervical radiculopathy
He / she does not have any red flag symptoms like changes in bowel or urinary secondary to cervical spondylosis / PID.
habits, fever, or constitutional symptoms like loss of weight or loss of appetite.
There (is / is no) history of previous trauma to the neck. PHYSICAL EXAMINATION
On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
Management so far (options tried) Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
He / she was treated conservatively with __________ for the past (duration) . ______; VAS: _____.)
However, the above have not been able to control his / her symptoms. He / she Heart: S1S2 were heard on auscultation.
is keen for operation as his / her symptoms affect his / her functioning. Lungs: Lungs are clear.
Abdo: Soft, non-tender
141
Power was:
He / she (does / does not) have wrying of the neck or other abnormal posture. ___ for shoulder abduction,
There (is / is no) wasting of the trapezius muscles noted. ___ for elbow flexion,
There (is / is no) (skin changes / previous scars / swelling) arnd e neck region. ___ for elbow extension,
___ for wrist extension,
Palpation (revealed / did not reveal) tenderness over the cervical vertebrae or ___ for finger flexion and
paravertebral muscle spasm. ___ for finger abduction
Creptius was felt on flexion of the neck. (on the left / right arm) and full in the (left / right) arm.
Flexion of the neck was ____.
Extension of the neck was ____. Sensation was decreased over e (C5 / C6 / C7 / C8 / T1) dermatome in e
Lateral flexion was ____ bilaterally and lateral rotation was ____ bilaterally. (left / right) arm and normal in all dermatomes in e (left / right) arm.
Lhermitte’s test was negative. Neurological examination of the lower limb was normal.
Spurling’s test was positive.
I would like to complete the examination with a digital rectal examination to rule
There is marked wasting of the (biceps / triceps / intrinsic muscles of the hand) out cauda equina syndrome.
noted.
Pronator drift was negative, no finger escape sign noted. In summary, Mr / Mdm XXX has signs consistent with that of a _____
Tone in the upper limbs was normal. radiculopathy in the (left / right) arm as evidenced by a decreased (biceps /
(Biceps / triceps / supinator) reflexes were (normal / absent) over the (left / triceps / supinator) jerk, loss of power in ________ and loss of sensation over
right) arm. the (C5 / C6 / C7 / C8 / T1) dermatome. Spurling’s test was positive when the
Hoffman’s reflex was negative bilaterally. neck was flexed to the (left / right) . No other abnormalities were noted on
inspection and palpation of the neck. ROM of e neck was limited to _____ / full.
MYELOPATHY
• Pathology: Compression of spinal cord (cervical or thoracic)
o C5-6 > C4-5 > C3-4 > C6-7
• Causes:
o Common: Cervical spondylosis (bony spurs and thickened ligament), PID
o Others: infection, trauma, tumours, demyelinating disorders, vascular disease
o Anatomically (applies for spinal stenosis?)
§ Anterior: protruding disc, posterior syndesmophyte, ossification of posterior longitudinal ligament (OPLL)
§ Anterolateral: jts of Luschka (uncovertebral jt)
§ Lateral: cervical facets (thickening, bony spurs)
§ Posterior: ligamentum flavum
• Presentation: think of dorsal cord vs ventral cord vs lateral cord vs total cord vs pure motor vs central cord vs CES
o Clumsiness in hands and legs (first symptom):
§ Gait disturbance (ataxic, broadbased, clumsy) – damage to ascending proprioception fibers
§ Loss of dexterity (clumsiness of fine actions) – fewer nerves supplying muscles has decreased capacity for modulation;
strength is usually normal because muscle can hypertrophy to compensate
o Neurological
§ Sensory:
• Parasthesia but usually not significant pain
• Numbness (depends on part compressed –spinothalamic/ DCML)
• Tightness, hot or cold sensations in the trunk
• Tingling in the legs
§ Autonomic: Bladder and bowel symptoms (severe cases)
o TRO malignancy: LOW, LOA, malaise…
• Signs
o Clinical picture: LMN signs at level of lesion and UMN below level of lesion
o Upper Extremity
§ Finger escape sign: patient hold out hand w fingers extended and the medial fingers drift into flexion
§ Hoffman’s
§ Lhermitte’s sign: Parasthesia down limbs on neck flexion
§ Grip and release: Less than 20 in 10s
§ Inverted brachioradialis reflex
§ Jaw jerk
§ Scapulohumeral reflex
o Lower Extremity: Hypertonia (Babinski’s sign, clonus, may have involuntary spasms in legs), hyperreflexia, Oppenheim’s sign
(dorsiflexion of big toe elicited by downward irritation of medial side of tibia)
• Investigations: EXCLUDE TUMOUR
o Plain X Ray
o CT – bony spurs and ligament ossification
o MRI – disc prolapse and cord compression
o Special tests/criterion
§ Pavlov’s ratio: Ratio of canal diameter to AP width of vertebral body (normal:
≥ 1; abnormal ≤ 0.85)
§ Sagittal diameter of midcervical canal (post surface of vert body to base of
spinous process) <11mm
• Management
o Conservative
§ Analgesics, collar, isometric exercises, gait training
§ Avoid manipulation and traction
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o Canal widening procedure (almost always requires Sx; else will worsen)
§ Anterior approach: Anterior cervical discetomy and fusion (ACDF) or anterior cervical corpectomy and fusion (ACCF)
§ Posterior approach: Laminoplasty or Laminectomy & fusion
Social History Mr / Mdm XXX has a (broad based / spastic) gait on walking.
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years Rhomberg’s test is (positive / negative) .
ago) , ( sticks/day x years). He / she (is / is unable) to perform tandem gait.
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a _________ I would like to complete the examination with a digital rectal examination to rule
and his / her condition affects her job. He / she lives with his / her ________. His out cauda equina syndrome.
/ her main caregiver is his / her ______________.
He / she lives in a residential (with / without) lift landing. There (is / is no) In summary, Mr / Mdm XXX has signs consistent with that of a _____
squatting toilet in the house. myelopathy as evidenced by a positive Lhermitte’s test, spastic broad based
Currently, the family (does not have any financial issues / is receiving financial gait, inability to perform tandem gait and signs consistent with a UMN lesion as
aid from ) . evidenced by presence of clonus, hyperreflexia, generalised weakness in the
lower limbs and presence of finger escape sign, positive Hoffman’s reflex,
In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co- hyperreflexia of the triceps & biceps jerk and weakness in the upper limbs. In
morbidities of ________________, currently presenting with chronic neck pain addition, he / she has loss of pin prick sensation, proprioception and vibratory
for (duration) associated with progressive (numbness / weakness) of the sensation in the lower limbs and loss of pin prick sensation over the (C5 / C6 /
(left / right) (upper / lower) limbs and unsteadiness in gait which has failed to C7 / C8 / T1) dermatomes in the upper limbs. Examination of the neck also
improve with conservative management and has affected his / her daily revealed creptius with restriction of lateral flexion and rotation.
functioning.
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SPINAL STENOSIS
• Pathology: Narrowing of spinal canal resulting in compression of spinal cord (if cervical) or cauda equina (because spinal cord ends at
L1/2 and spinal stenosis often at L4,5, S1 level)
• Causes
o Spondylosis leading to bony spurs and hypertrophy of facet joint
o Spondylolisthesis (usually degenerative; spondylolytic too)
o PID
• Presentation: root canal vs central canal stenosis (signs are variable depending on site & severity of stenosis)
o Neurogenic claudication – during walking, nerves require greater blood supply; hence demand outstrips supply; also due to epidural
venous congestion
§ Posterior thigh, calf or buttocks cramping pain (travel down leg), weakness, numbness or parasthesia after standing
upright/walking (note: leg pain >>>>> back pain, unless back pain due to underlying pathology)
§ Relieved by flexion (decrease stenosis) – pain worse when extends à patient often stands in slight flexion
§ Segmental sensory deficits, decrease power, decrease reflexes
o NOTE: diagnosis mainly made w Hx; PE usually unremarkable
Mr / Mdm XXX is a __ years old (race) gentleman / lady, He / she also does not have a history of peptic ulcer disease / GI bleeding.
premorbid status: (ADL independent, community ambulant – w / wo aid) , He / she had previous operations for ______________.
occupation: ____________________, He / she has NKDA and is currently on __________ for her medical conditions.
with a significant PMHx of ___________________,
presenting complaint: currently presents with a (duration) history of low Family History
back pain associated with (duration) history of (bilateral / left / right) leg He / she (has / has no) family history of cancer or similar back pathologies.
pain on walking.
Social History
The low back pain is (nature) , with a pain score of ___, shooting down the He / she (does not smoke / smokes / is an ex-smoker and has quit XX years
(anterior / lateral / posterior) aspect of the thigh(s) and the (anterior / lateral / ago) , ( sticks/day x years).
posterior) side of the leg(s) to the (dorsum / sole) of the feet bilaterally (right He / she (has / does not have) a habit of regular intake of alcoholic drinks.
> left / left > right) upon walking (distance) or even when he / she is He / she has (good / poor) social support. He / she works as a _________
standing. and his / her condition affects her job.
He / she lives with his / her ________. His / her main caregiver is his / her
The leg pain is aggravated by standing upright and walking up slope, but ______________.
persists even when he / she stops walking. It is only relieved by (flexion of the He / she lives in a residential (with / without) lift landing. There (is / is no)
back / sitting down / walking down slope) . There is no associated rest pain in squatting toilet in the house.
the lower limbs. Currently, the family (does not have any financial issues / is receiving financial
aid from ) .
In addition, he / she experiences (progressive / non-progressive) weakness of
the (left / right) lower limb and associated numbness over the (site) of her In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co-
(L/ R) LL for the past (duration) , usually after standing upright or walking. morbidities of ________________, currently presenting with symptoms
suggestive of mechanical axial back pain and neurogenic claudication,
There (is / is no) associated stiffness in the back especially in the morning associated with a ______ radicular pain, evidenced by a low back pain that
that does not last more than 30 mins. shoots down the ______ that is associated with weakness of the lower limb and
numbness over the ____ dermatome.
Functional Status
Currently, his / her symptoms have limited his / her daily function. My provisional diagnosis will be that of spinal stenosis.
His / her walking distance is limited to ______ from ______ previously, (with /
without) a walking aid. PHYSICAL EXAMINATION
Systemic Review On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
He / she does not have any red flag symptoms such as changes in bowel or Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
urinary habits, history of night pain, fever or constitutional symptoms like loss of ______; VAS: _____.)
weight or loss of appetite. There is also no hx of previous trauma to the back. Heart: S1S2 were heard on auscultation.
Lungs: Lungs are clear.
Management so far (options tried) Abdo: Soft, non-tender
His / her symptoms have failed to improve with conservative management such
as _________ for the past (duration) . Mr / Mdm XXX gait is ____________________.
He / she stands in slight forward flexion, has a list to the (left / right) and there
Past Medical History is reduced lumbar lordosis on inspection. There were no other deformities of the
Mr / Mdm XXX has a past medical history of _____________ for (duration) .
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spine. There are no scars, no sinuses, no swelling and no other skin changes ___ for plantar flexion.
over the spine. Sensation was decreased over the ____ dermatome in the (left / right) leg and
normal in all dermatomes in the other leg as well as both upper limbs.
There is tenderness on palpation over the lumbar vertebrae. Paravertebral
muscle spasm was noted over the (left / right) side of the lumbar spine. There Pulses in the lower limb were well felt.
is no step deformity noted.
Lumbar excursion is _____ cm. (Schober’s test) I would like to complete the examination with an abdominal examination to
Extension of the spine is _____. check for a palpable bladder, to rule out retroperitoneal pathology and perform a
His / her fingers are able to reach ______ bilaterally on lateral flexion of e spine. digital rectal examination to check for saddle anaesthesia and the anal tone to
Lateral rotation of the spine was ________ bilaterally. rule out cauda equina syndrome.
Straight leg raise was ____ degrees on the right and ____ degrees on the left In summary, Mr / Mdm XXX has signs consistent with that of a _____
lower limb, associated with a positive Bowstring test / Lasegue sign. FABERE’s radiculopathy in the (left / right) lower limb, likely secondary to a ______
test was negative bilaterally. lateral recess stensosis, as evidenced by a decreased (knee / ankle) jerk
reflex, loss of power in _________, loss of sensation over the ____ dermatome,
Neurological examination of the LL did not reveal any wasting or deformities. as well as a positive straight leg raise in the (left /right) lower limb to _____
Tone in the lower limbs was normal. degrees with a positive Bowstring and Lasegue test. I also note a slight forward
(Knee / ankle) reflex was absent over the (left / right) leg, reflexes over the flexion and sciatic list on inspection associated with paravertebral spasm on the
other leg was normal. OR (left / right) side of the lumbar spine, reduced lumbar lordosis and tenderness
(Knee / ankle) reflex was absent bilaterally. on palpation of the lumbar vertebrae. Excursion of spine was severely limited
Plantar reflexes were down going bilaterally. due to pain.
Power:
___ for hip flexion, In summary, Mr / Mdm XXX has signs suggestive of a central canal stenosis as
___ for knee flexion, evidenced by bilateral lower limb involvement, with no distinct signs of a
___ for knee extension, particular nerve root involvement suggestive of a lateral recess stenosis.
___ for ankle dorsiflexion and
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3. Causes of Neurological Deficit
PROLAPSED INTERVERTEBRAL DISC
• Pathology: ACUTE posterior or postero-lateral herniation of nucleus pulposus through annulus fibrosis;
nucleus pulposus (accompanied by local edema due to inflammation) then compresses on neural structures
o Extents of herniation: Sequestration (separation of herniated segment from rest of nucleus pulposus),
Protrusion (nucleus pulposus herniates through large tear), Extrusion (nucleus pulposus herniates
through small tear), Bulge
• Background:
o Commonly in adults 25-40yrs
o Causes: precipitating event of a local strain or injury (weight lifting, stooping) – usually predisposing
defect present (degenerate disc)
o Common levels affected:
§ Cervical: immediately above/below C6 vert, hence nerve root of C6/7 affected
§ Lumbar: L4/5 commonest then L5/S1
o Postero-lateral vs Central disc prolapse
§ Central disc prolapse
• May only present with back pain
• Often no leg pain (especially if lower level as other lumbar nerve roots supplying leg
sensation have exited)
• May present w bilateral radiculopathy if prolapse is significant
§ Postero-lateral prolapse: Usually compresses traversing nerve (radicular symptoms)
o Cervical (exit canal) vs Lumbar (root canal) PID (refer to diagram on the right)
§ For usual posterior/postero-lateral herniation: Exiting cervical nerve root while traversing lumbar nerve root affected
§ But for both, it is always the lower level affected (btwn C1 and C2 its C2, and between L1 and L2 is L2 affected)
§ Occurs as such because of course of the nerve: At cervical level the nerve travels horizontally to exit out (no concept of
traversing nerve) while at lumbar level, exiting nerve exits early at the neural foramen while the traversing nerve travels down
across the level of compression
• Presentation
o Neurological Conditions
§ Radiculopathy (posterolateral compression of nerve root when exiting) è radicular pain
§ Myelopathy (posterior compression of spinal cord – if spinal cord present at level)
§ Spinal stenosis (posterior compression of cauda equina or cervical cord)
§ Cauda equina syndrome (severe spinal stenosis)
o Pain
§ Pressure on post. intervertebral ligament – pain & stiffness fr back of neck to scapula & occiput
§ Pressure on dural envelope of nerve root – radicular pain
§ Pressure on nerve – numbness, parasthesia, muscle weakness
o Signs
§ LOOK: Listing (to relieve pain from nerve root compression), Paravertebral muscle spasm,
Protective scoliosis, loss of lumbar lordosis, may have acute torticollis
§ Feel: Midline tenderness
§ Move: Pain (& listing) worse on flexion, increase intra-abd pressure (coughing, straining,
lifting, laughing), decreased ROM due to pain
§ SLR test positive (if nerve root compression present); cross SLR positive if large central disc herniation (prodrome of CES)
• Bowstringing, Laseague’s, femoral stretch test (L4)
§ Restricted ROM
§ Segmental myotomal / dermatomal deficits (corresponding to level of lesion; sensory, power, reflexes)
• DDx: pain Hx and imaging tro DDx!
o Soft tissue sprain – neurological SnS absent.
o Neurological amyotrophy (acute brachial neuritis) – sudden, sever pain @ shoulder, back or shoulder. Multiple neurological sites
affected n might have winging of scapula. Pain followed by flaccid paralysis a few days later.
o Cervical spine infx (inc TB spine) – unrelenting n local spasm with severe pain. X-ray: erosion of bone
o Vertebral/nerve tumors – neurological signs progressive. X-ray/MRI shows bone destructn. Primary tumors rare, secondary more
common. Of primary, sarcoma n multiple myeloma most common
o Others: AS
• Investigations
o Xray (AP, lateral, oblique): decreased jt space; exclude bone disease
o MRI: for surgical planning and for cauda equina syndrome
• Management – Rest, Reduce, Remove, Rehab
o Conservative: Rest + Reduce à symptoms in 75% of patients will resolve
§ Rest: continuous bed rest (spinal corset/ collar to prevent unguarded movement), physiotherapy (& heat) and analgesia/anti-
inflammatory (NSAID; can consider epidural steroid + LA injection)
§ Reduce: traction can reduce herniation (intermittent traction applied to pelvis w hip & knees slightly flexed; 30mins @ a time up
to 8kg) + back care education
§ à Continuous bed rest & traction for 2wks decreases herniation in >90% of cases
o Surgical: Removal + Rehab
§ Indications
• Cauda equina syndrome
• Failure of conservative Rx (after 3mths) – persistent pain and neurological deterioration with frequently recurring attacks
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§ Procedure: Fenestration & discectomy OR microdiscectomy
• May fuse affected areas or maintain height using bone graft
• Alleviate symptoms of radiculopathy but not lower back pain
§ Rehabilitation (post-op); Light work after 1 month & heavy work after 3 months
Mr / Mdm XXX is a __ years old (race) gentleman / lady, shoots down the (left / right) that is associated with weakness of the lower limb
premorbid status: (ADL independent, community ambulant – w / wo aid) , and numbness over the _____.
occupation: ____________________,
with a significant PMHx of ____________________, My provisional diagnosis will be that of a ____ prolapsed intervertebral disc.
presenting complaint: currently presents with a (duration) history of acute
low back pain. PHYSICAL EXAMINATION
Regarding the low back pain, it is constantly present. On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
The pain shoots down the (anterior / lateral / posterior) aspect of the thigh and Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
the (anterior / lateral / posterior) side of the leg to the (dorsum / sole) of the ______; VAS: _____.)
foot, in a radicular pattern in the (L4 / L5 / S1) nerve root / dermatome. Heart: S1S2 were heard on auscultation.
He / she describes the pain as (nature: sharp, shooting, tingling) . Lungs: Lungs are clear.
It occurred suddenly after (activity: carrying heavy objects / bending forward / Abdo: Soft, non-tender
precipitated by sitting for long periods) and is aggravated with coughing and
straining, and relieved with lying down. Mr / Mdm XXX gait is _____________.
The current pain score is ____ and the pain can be so severe that he / she He / she has a list to the (left / right) and reduced lumbar lordosis on
cannot straighten his / her back. inspection. There were no other deformities of the spine. There are no scars, no
sinuses, no swelling and no other skin changes over the spine.
There (is / is no) associated stiffness in the back especially in the morning
that does not last more than 30 mins. There is tenderness on palpation over the lumbar vertebrae. Paravertebral
muscle spasm was noted over the (left / right) side of the lumbar spine. There
In addition, he / she experiences weakness of the (left / right) lower limb and is no step deformity noted.
associated numbness over the (site) of his / her (left / right) lower limb Lumbar excursion is _____ cm. (Schober’s test)
corresponding to (dermatome) for the past (duration) . His / her neurological Extension of the spine is _____.
symptoms are non-progressive. His / her fingers are able to reach _________ bilaterally on lateral flexion of the
spine.
Functional Status Lateral rotation of the spine was ________ bilaterally.
Currently, her symptoms have limited her daily function such as: ___________.
Straight leg raise was _____ degrees on the right and _____ degrees on the left
Systemic Review lower limb, associated with a positive Bowstring test / Lasegue sign. FABERE’s
He / she does not have any red flag symptoms such as changes in bowel or test was negative bilaterally.
urinary habits, history of night pain, fever or constitutional symptoms like loss of
weight or loss of appetite. Neurological examination of the lower limb did not reveal any wasting or
There is also no history of previous trauma to the back. deformities.
Tone in the lower limbs was normal.
Management so far (options tried) (Knee / ankle) reflex was absent over the (left / right) leg, reflexes over the
He / she was treated conservatively with ___________ for the past (duration) . other leg was normal.
Plantar reflexes were down going bilaterally.
Past Medical History Power:
Mr / Mdm XXX has a past medical history of _____________ for (duration) . ___ for hip flexion,
He / she also does not have a history of peptic ulcer disease / GI bleeding. ___ for knee flexion,
He / she had previous operations for ____________. ___ for knee extension,
He / she has NKDA and is currently on ___________ for her medical conditions. ___ for ankle dorsiflexion and
___ for plantar flexion.
Family History Sensation was decreased over the ____ dermatome in the (left / right) leg and
He / she (has / has no) family history of cancer or similar back pathologies. normal in all dermatomes in the other leg as well as both upper limbs.
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SPONDYLOLISTHESIS (LUMBOSACRAL)
• Pathology: Vertebral displacement (forward translation of upper over lower vertebral body) usually at L4/5 (more common) or L5/S1 level
due to failure of normal laminae-facet locking mechanism
• Causes: SPOTED
o Spondylolytic/ Isthmic (50%; most common) – break in pars interarticularis
§ Epidemiology: Often young patients
§ Presentation
• Intermittent back pain (worsened on movement)
• Buttocks look flat
• Step deformity felt on spine palpation
§ Effect on spinal canal size
• Initially: Unlikely to lead to spinal stenosis as only anterior portion of vertebrae translates forward (due to break)
• Late: Potential spinal stenosis if fibrosis is marked (attempted healing)
o Pathological (neoplasm) & other Destructive conditions like infx (TB)
o Operative – due to laminectomy for decompression
o Trauma
o Elderly (degenerative; 25%) – OA degeneration of facet joints (usually L4/5)
§ Mechanism:
• Degeneration of intervertebral disc (lose height, bulge)
• Arthritis of facet joints à weakening of joint and ligaments à allow sliding of one vertebrae over the other
• May have an unnoticed break in pars during adolescence, predisposing to spondylolisthesis in adulthood
§ Occurs in women >40 with facet joint arthritis
§ May cause spinal stenosis as whole vertebrae translates forward, leading to narrowing of spinal canal
o Dysplasia (20%): congenital lumbosacral facet joint dysplasia
§ Seen in children
§ May be a/w unduly protruding abdomen and associated scoliosis; usually no pain
• Presentation
o Back pain: intermittent, worse on some form of movement (due to sliding), esp w exercise or straining
o Bending backward in stepwise movements
o Step deformity of spine
o Back stiffness: for degenerative type
§ ROM usually normal in younger patients
o LOOK: buttocks flat, short lumbar spine, long sacrum, transverse loin creases
o Neurological symptoms:
§ Radiculopathy – Often both traversing and exiting root affected
§ Spinal stenosis
• Imaging
o X-ray (lateral, oblique): Forward shift of upper spinal column
o Elongation of arches / defective facets
o Gap in pars interarticularis on oblique view (Scotty dog sign) – for spondylolytic cause
o Flexion and extension views to assess stability
• Meyerding Classification
• Management
o Conservative: Bed rest and supporting corset
§ Old patient, non-disabling symptoms
o Operative: Spinal fusion (Transforaminal Lumbar Interbody Fusion – TLIF)
§ Disabling symptoms, young adult, neurological compression
SPONDYLOSIS (DEGENERATION)
• Epidemiology: >40yo, M>F, usually C5/6
o RF: smoking, drinking, excessive driving (for cervical spondylosis)
• Pathology:
o Disc Degeneration
§ Loss of proteoglycan and hence water content (reduction in shock absorptive ability)
§ Collapse, flattening and loss of disc space height
§ Disc bulging or herniation
o Facet Joint Arthritis
§ Experience increased pressure due to disc degeneration
§ Wearing away of cartilage lining facet joints
§ Rubbing of bone: Hypertrophy of facet joint + syndesmophyte formation on anterior and posterior margins of vertebral
bodies (response to abnormal stress to compensate loss of ligamentous and articular stability)
• NOTE: vertebral spurs are v common in elderly but may not be cause of S/S, thus need to exclude DDx
o Thickening of ligamentum flavum: ligamentum flavum calcification and buckling
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o Degenerative kyphoscoliosis
§ Uneven shoulders and hip asymmetry
§ Flat back (loss of lumbar lordosis)
§ Knee and hip pain because patient has to flex knee and extend hip to look straight
• Presentation
o Chronic neck or back pain (and stiffness; decreased ROM throughout w pain): gradual progression, worse in morning
§ Discogenic pain – Due to disc degeneration (annulus becomes stressed on loading as disc loses elasticity with age; mechanical
receptors on outer 1/3 of annulus stimulated causing back pain)
• Pain on loading of the disc: Worse on flexion, sitting/standing for too long, carrying weights in front, coughing/sneezing
• Extent of pain: Back and buttocks
§ Facet joint pain – Due to facet joint arthritis
• Pain on loading of facet joint: Extension, rotation, pressing on joint, getting up from chair, turning in bed
• Extent of pain: Can radiate down back of upper leg (rarely radiate below knee) for lumbosacral joints; Can radiate from
posterior neck down shoulders & upper back or up to occiput (“headache”) for cervical joints
§ à symptoms relieved by lying down
o Neurological deficits
§ Radiculopathy: Due to 1) Loss of disc height 2) syndesmophyte (posterior spurs may encroach upon the IV foramina
compressing nerve roots) 3) Facet joint hypertrophy
§ Spinal stenosis: Due to 1) Facet hypertrophy 2) Thickening/infolding of ligamentum flavum 3) Bulging of degenerate
disc 4) Spur formation 5) Listhesis (joint instability)
• Imaging (X-ray)
o AP view: vertebral tilting/ asymmetry of disc space or facet joints
o Lateral view
§ Disc space narrowing/ vacuum sign (abnormal lucency in disc space)
§ Anterior traction spurs (syndesmophyte)
§ Localised sclerosis of vertebral body adjacent to disc space
§ Spondylolisthesis/retrolisthesis
§ Osteoarthritic changes in unco-vertebral joint
o Oblique view: encroachment of IV foramina
o Flexion/extension view: assess spine stability
• Management
o Conservative: mainstay of Rx; try as long as possible as disability is rarely severe and may decrease as spine stabilizes
§ Activity modification: weight loss, stop bending, lifting, climbing
§ Physiotherapy: Exercises, gentle passive manipulation, heat treatment
§ Intermittent traction
§ Occupational therapy: Restraining collar, corset
§ Analgesics
o Surgery
§ Indications: progressive neurological deficits, multiple levels of cord compression, severe symptoms that are only relieved by
uncomfortable support
§ Anterior disc removal with fusion of most painful level
• Discectomy ± anterior fusion
• Corpectomy
• Laminoplasty
• Laminectomy ± foraminectomy
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dystrophies, spinal muscular atrophy (SMA)
• Syndromic: Ehler-danlos, marfan’s, NF, VACTERL
§ 5 patterns of idiopathic scoliosis:
• Infantile thoracic: 60%M, 90% convex L, a/w ipsilateral plagiocephaly, progressive type becomes severe
• Adolescent thoracic: 90%F, 90%R convex, rib rotation exaggerates scoliosis, 50% dvlps >70deg
• Thoracolumbar: abit F>M, convex abit R>L
• Lumbar: F>M, 80%L, 1 hip prominent but no ribs to accentuate deformity, not noticed early, backache till adult life
• Combined: 2 primary curves (1 in each direction), clinical deformity rather slight coz always well balanced though may be
radiologically severe
• Complications
o Pulmonary: Decrease total lung capacity and fixed vital capacity due to thoracic lordosis (Cobb angle >70deg)
§ Usually only affects early onset scoliosis as it affects pulmonary alveoli dvlpment
o Cardiac: Right heart disease due to pulmonary hypertension (Cobb angle >80deg)
o Early OA of the back
o Radiculopathies
o Backache
• Physical examination:
o General assessment (listing, gait, limb length discrepancy) + height
o Back examination:
§ Adam’s forward bend test: Brings apex of kyphosis into view from lateral
position (seen as thoracic hump; ddx postural and structural)
§ Scoliometer
§ Spinal balance – plumbline
o Neurological examination: esp LL neuro exam, abdominal reflexes, back sensation esp
L thoracic curves
• Important points in Hx for idiopathic scoliosis: Chronological age, menarche, family Hx, time of
Dx, severity of first XR, any previous Rx, associated symptoms (back pain, neurological
symptoms inc. clumsiness/weakness and bladder/bowel function)
• Red flags of atypical scoliosis (scolisis that is NOT idiopathic)
o Hx
§ Back pain that is well localized, constant and progressive
§ Weakness or clumsiness
§ Bladder and bowel incontinence; Ejaculation problems
o PE:
§ Foot deformity, esp unilateral
§ Abnormal curve pattern: not R thoracic and/or L lumber (rule out syringomyelia)
§ Hyperkyphosis
§ A lack of rotational deformity on Adam’s forward bending test
§ Tight hamstrings (popliteal angle >50-60deg)
§ Unequal or abnormal reflexes
o XR:
§ Widened pedicles
§ Kyphosis
§ Atypical curve pattern
§ Lack of vertebral rotation
§ Rapid curve progression (>1deg/month)
§ Absent pedicles (“winking owl”)
§ Limb length discrepancy
o MRI:
§ When to order
• Neurologic abnormalities on PE (rmber the feet)
• Structural (congenital) abnormalities on plain film
• Excessive kyphosis
• Apex L thoracic or thoracolumbar curves
• Early onset scoliosis
• Syndromic features present
§ What to look for: syringomyelia, chiari malformations, tethered cord, diastematomyelia
• Adolescent Idiopathic Scoliosis (more females)
o Epidemiology: Usually present between 10-15 (usually present before puberty, greatest progression during pubertal growth spurt,
minimal progress post-puberty)
o Pathology
§ Postulated that localized extension (straightening out) of normal dorsal kyphosis would inevitably force spine to swivel round thus
producing appearance of a lateral curvature
§ Thoracic or lumbar spine
§ Vertebrae involved are rotated arnd vertical axis so the bodies point to convexity and the spinous process point to concavity
§ In thoracic curves, ribs on convex side are carried around posteriorly and stand out as a prominent hump
§ Mobile secondary curves may dvlp above and/or below primary curve to maintain normal head and pelvic position
o Symptoms
§ Deformity
• >pronounced on flexion (vs postural curve which disappears on flexion)
• Shoulder elevated on side of convexity & hip sticks out on side of concavity
• For thoracic scoliosis: Breasts asymmetrical + rib angles protrude
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o X-ray: Full length AP spine + lateral flexion XR + pelvis
§ Cobb’s angle measured: Lines projected from uppermost and lowermost
vertebral bodies in the curve
§ Risser’s sign: Extent of ossification and fusion of iliac apophysis of pelvis;
measures progressive ossification from anterolaterally to posteromedially
(suggests skeletal maturity and provides indication for curve progression)
• Grade I: 25% ossification action of iliac apophysis
• Grade II: 50%
• Grade III: 75%
o Patient has passed peak of growth spurt, a period of rapid spinal
growth during which scoliosis curvatures can increase rapidly
• Grade IV: 100%
• Grade V: Iliac apophysis fused to iliac crest after 100% ossification
o Management
Cobb’s angle Grade 0/ premenarchal Grade 1 or 2 (pubertal) Grade 3, 4 or 5 (post-pubertal)
<20 Observation: 4 monthly f/u and full length spine XR to check for progression of scoliosis
20-40 Brace therapy (begin when Brace therapy Observation
curve is >25deg)
>40 Surgery + supports post-op to prevent recurrence Surgery (when curve >50deg): Sx indicated
coz progression is expected to be 1-2deg/year
although there is no longer growth
§ Conservative
• Exercise: Alone has no effect on curve
o Indications: approaching skeletal maturity, deformity <30deg
• Bracing
o Indications
§ Progressive curves between 20 and 40 deg (when iliac apophysis not fully ossified and fused –
usually Risser 0,1,2)
§ Apex lower than T7
§ Well balanced double curves
§ Stabiliser for younger children who need surgery (await fusion)
§ Prevent recurrence after spinal fusion
o Types: Boston brace (curves below T9), Milwaukee brace (1hr break in 24hrs)
o Prevents progression, doesn’t improve deformity
§ Surgery
• Indication: Curves > 40deg for pre-pubertal/ pubertal and >50deg for post-pubertal
• Method
o Expose entire length of curve
o Apply a distraction rod to concave side of curve to ‘jack’ curved segment out as straight as possible
§ A more robust instrumentation will have a higher risk of neurological Cx
o Entire length of curve then prepared for bone-grafting in the hope that it will fuse when back is ‘immobilised’ in
plaster jacket
• 50% correction regarded as satisfactory
KYPHOSIS
• Pathology: Excessive dorsal curvature of spine
• Classification
o Postural kyphosis: Associated with postural defects such as flat feet
o Structural kyphosis: Fixed and associated with changes in shape of vertebrae
§ Common causes: Elderly –Degenerative, Adults –AS, trauma, TB spondylitis, Adolescents -Scheurmann’s disease
• Kyphos/Gibbus: Sharp posterior angulation due to localized collapse or wedging of one or more vertebrae (due to congenital defect, fracture,
spinal TB)
• Scheuermann’s Disease (Adolescent Kyphosis) –affects boys>girls
o Pathology:
§ Developmental disorder of growing spine in which there is irregular ossification and possibly some fragmentation of vertebral
body epiphyses
§ Resulting in irregularity of mature vertebral endplates and small central herniations of disc material into vertebral body
(Schmorl’s nodes)
§ Increasing growth and muscular activity in thoracic spine may cause vertebrae to give way slightly and become wedged,
exaggerating the normal kyphosis
o Types
§ Thoracic Scheuermann’s Disease (more common)
• Epidemiology
o Starts shortly after puberty
o More common in boys than girls
• Symptoms
o Round shouldered
o Backache
o Fatigue
• Signs: Smooth but well-marked thoracic kyphosis
• X-ray (lateral view)
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o Patchiness or irregularity of vertebral end plates
o Schmorl’s nodes
o Wedging of vertebral bodies (later on)
• Management
o Conservative: Extension brace (curves <40deg)
o Surgery: Operative correction with fusion
§ Thoracolumbar Scheuermann’s Disease
• Epidemiology
o Less common than thoracic Scheuermann’s
o Occur in adolescence or early adulthood
• Symptoms
o Usually no local deformity
o Low back pain
• X-ray (lateral view): Similar to thoracic variant but no vertebral wedging
• Management:
o Conservative: Back strengthening
o Surgery: Indicated only if there is discogenic disease
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o Complete vs Incomplete
§ Complete: No function below level of injury
§ Incomplete: Some degree of function retained à sacral sparing (perianal sensation, sphincter tone, big toe flexion)
• Treatment of SCI
o Attributed to contusion and/or compression à microvascular disruption
o Rx: methylprednisolone: bolus 30mg/kg followed by 5.4mg/kg/hr over 23 hrs. patients treated within 8hrs respond best
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§ Lateral view
• Must include all 7 cervical vertebrae and upper half of T1 (cover for cervicothoracic junction injury); swimmers view or
CT if unable to see T1
• Specific things to look out for:
o Anatomic lines: 4 parallel curves (look for deviation)
§ Down e front of vertebral bodies (ant vertebral line)
§ Down the back of the bodies (post vert line)
§ Through posterior borders of lateral masses
(spinolaminar line)
§ Along bases of spinous processes (post spinous line)
o Soft tissue outlines:
§ Look for soft tissue swelling or hematoma in
retropharyngal space: Prevertebral soft-tissue
shadow (fat stripe) should be <5-6mm in width above
trachea (@ C2) and < 1 vertebral body’s width/
<2mm below that (@ C6)
o Step deformity of >3.5mm anywhere
§ Anterior subluxation of 1 vertebra on another
indicates facet dislocation
• <50% of the width of a vertebral body implies
unifacet dislocation
• >50% implies bilateral facet dislocation
§ This is usually accompanied by widening of the
interspinous and interlaminar spaces
o Atlantodens interval (ADI): distance btw odontoid process &
post. border of arch anterior of atlas – atlantoaxial instability (AAI) present if >3mm in adults & >5mm in children
o Uniformity of shape and height (disc herniation) of IV disc (all the same except C1 & 2)
§ Fracture types: wedge compression, burst (refer below)
o Angulation 11deg greater than contiguous segments (disruption of the PLL, subluxation of C3 on C4)
o Anterior occipitoatlantal dislocation (Powers ratio)
§ SCIWORA (SCI without radiological abnormality): Normal radiographs do not exclude possibility of SCI (esp in children)
• Cervical subluxation
o Pure dislocation of the spine is commonest in the cervical region
o Mechanism of injury: Flexion injury (esp lower ½ of spine)
o Bones intact but posterior ligaments torn
o Vertebra above tilts forward on the one below, opening up interspinous space
o X-ray: Flexion extension x-rays – gap btwn spines unusually wide
o Management
§ Stable: Splintage for 6 weeks
§ Unstable: posterior spinal fusion
• Wedge Compression Fracture: anterior wedging of vertebral body or teardrop #s of antero-inferior portion of body
o Mechanism of Injury: Pure flexion injury causes compression of ant. pt of vertebral body (usually in mid and lower cervical segments)
o Stable injury
o Management: Collar for 6-8weeks
• Burst Fracture: anterior compression of >40% of normal vertebral body height (w retropulsion of fragments of the vertebral body into the
spinal canal)
o Mechanism of Injury: Axial compression of C-spine (usually in diving or athletic accidents) à Affect anterior and middle column
o Neurological involvement: Common
o Imaging
§ X-ray
• Comminuted fracture of vertebral body
• Middle column damage and posterior displacement of body fragment
§ CT/MRI: Look for retropulsion of large fragments into spinal canal
o Management
§ No neurological deficit: Halo-vest immobilisation
§ Neurological deficit: Anterior decompression + halo vest immobilisation
• Flexion Rotation Injuries
o Unilateral facet dislocation
§ Mechanism of Injury: Flexion rotation injury resulting in dislocation of one facet join
§ X-ray:
• Lateral: Vertebral body appears partially displaced (<25% its width) à stable
• AP: Alignment of spinous process disrupted
• Oblique: expected tilting of the laminae is disrupted, and the dislocated superior articulating facet of the lower vertebra
can be seen projecting within the neural foramina
§ Neurological involvement rare
§ Usually stable
§ Management
• Closed reduction: Skull traction + gentle extension and rotation maneuver
• Open reduction: Only if closed reduction fails
o Bilateral facet dislocation or Fracture dislocation
§ Mechanism of Injury:
• Severe flexion and rotation resulting in articular facets riding forwards over facets below
154
• May have facet fracture or pure dislocation
• Posterior ligaments ruptured
§ Unstable
§ Cord damage common
§ X-ray: Forwards displacement (>1.5x its width) of vertebra on one below
§ Management
• Closed reduction: Skull traction + collar / posterior fusion
• C1 ring fracture classification: Posterior arch (28%), Jefferson burst #, anterior arch “blow out”, lateral mass #, transverse process #
o Burst fracture of C1 (Jefferson’s Fracture)
§ Mechanism of Injury: Sudden severe load on head may fracture ring of atlas
§ X-ray (open mouth view): Lateral masses spread away from odontoid peg
• >6.9mm = transverse ligament avulsion
§ Neurological involvement: Usually no neurological damage (no encroachment on neural canal)
§ Management
• Undisplaced (stable; intact transverse ligament): Rigid collar or halo vest
for 10-12 weeks
• Sideways spreading of lateral masses (unstable): Skull traction
reduction or halo-body orthosis for 6 weeks + 6 weeks of semi-rigid collar
• Late instability: C1/2 fusion
§ Associated w other C-spine injury in 50% of cases (rule out odontoid and
hangman’s #)
• Fracture of Pedicle(s) of C2 (Hangman’s Fracture)
o Mechanism of Injury:
§ Commonly in RTA when forehead strikes dashboard
§ Combination of extension, compression and flexion
o Neurological damage unusual because # of posterior arch tends to decompress spinal cord
o Management
§ Undisplaced: Collar or halo vest
§ Displaced: Reduction (but not via traction as mechanism of injury often involves distraction) + halo vest
• Fracture of Odontoid Process (C2)
o Mechanism of Injury:
§ Flexion injury in young adults due to high velocity accidents or severe falls OR
§ Low energy trauma in osteoporotic patients where neck is forced into hyperextension
o Neurological Involvement: ¼ of cases
o Classification (Anderson and D’Alonzo)
§ Type 1 (Avulsion of tip): Immobilisation + Rigid collar
§ Type 2 (Fracture through the junction of the odontoid peg and body of C2)
• Unstable and prone to non-union + easily missed à WORST type
o 10% SCI due to translation
o Poor prognosis
o Associated # in 20-30%
• Undisplaced: Halo-vest
• Displaced: Traction + Screw fixation or Halo-vest
§ Type 3 (Fracture through body of C2 only): Treatment as for Type 2
• Good prognosis; heals easily
• Avulsion Injury of C7 Spinous Process
o Mechanism of Injury: Severe voluntary contraction of muscles at the back of neck
o Painful but harmless
• Sprained Neck (Whiplash injury)
o Mechanism of Injury: Hyperflexion or hyperextension of neck à soft tissue sprain of neck (acceleration-decceleration often
associated with car accidents)
o Symptoms: Pain and stiffness usually appear 12-48 hours after injury
o X-ray: Normal
o Management: Pain relief initially, then physiotherapy for return of neck movement
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THORACOLUMBAR AND LUMBAR INJURIES
• General Information
o Thoracolumbar junction particularly prone to injury because of transition btwn relatively fixed thoracic spine and relatively mobile
lumbar spine
o Minor Injuries: Fracture of vertebral processes and pars interarticularis
o Major Injuries: Compression, burst, fracture-dislocation, jack-knife injuries
• Wedge / Compression Injury
o Mechanism of Injury: Spinal flexion with posterior ligaments in tact (minimal trauma needed for osteoporotic patients) resulting in
failure of anterior column
o Usually stable
o Neurological involvement rare
o Management
§ Minimal wedging: Bed rest until pain subsides + Strengthening exercise
§ Marked wedging (anterior vertebral height reduced by 25-50%):
Thoracolumbar brace
§ Even more severe (usually indicative of damage to posterior ligaments):
Posterior spinal fusion
• Burst
o Mechanism of Injury: Failure of both anterior and middle columns (posterior
usually spared) where posterior part of vertebral body is shattered and fragments
of bone and disc may be displaced into spinal canal
§ Usually due to axial compression
§ Most common at thoracolumbar junction – T spine rigid while L spine
mobile
o Usually unstable
o May have neurological involvement
o Imaging
§ X-ray: Spreading of vertebral body with an increase of interpedicular distance
§ CT: Check for posterior displacement of bone into spinal canal
o Management:
§ Minimal retropulsion of bone, no neurological damage, minimal anterior wedging: Patient kept in bed and mobilized in
thoracolumbar brace
§ Neurological symptoms present (tingling, weakness, alteration of bladder or bowel function): Anterior decompression and
stabilisation
• Flexion-Distraction / Jack-knife injury / Chance
o Mechanism of Injury:
§ Combined hyperflexion and distraction causes mid-lumbar spine to ‘jack knife’ around an axis that is placed anterior to the
vertebral column (commonly lap belt injuries)
§ Posterior and middle columns fail in distraction (unstable in flexion)
§ Compressive failure of anterior column
o Chance Fracture (ideal example of tensile failure)
§ Split runs through spinous process, transverse process, pedicles, vertebral body
§ All 3 columns affected
§ Heals rapidly: Requires 3 months in plaster jacket / brace
§ Usually T12-L2
§ Types
• Bony Chance – Can heal with immobilization
• Ligamentous Chance – Need surgery
o Neurological damage uncommon
o Unstable
o X-ray: (CT scan can assist w diagnosis)
§ Horizontal fractures in pedicles or transverse processes
§ Increased apparent height of vertebral body (AP view)
§ Opening up of disc space posteriorly (lateral view)
§ Gap between spinous process increased
• Fracture dislocation
o Mechanism of Injury:
§ Combination of flexion, compression, rotation and shear forces may result in segmental displacement (usually high energy
injuries)
§ All 3 columns disrupted and spine unstable
§ Commonly at thoracolumbar region
o Neurological involvement common: Lowermost part of cord or cauda equina
o Imaging
§ X-ray:
• Fractures through vertebral body, pedicles, articular processes, laminae, transverse process, ribs
• Subluxation or dislocation
• Total dissociation between one part to another part of spinal column (both AP and lateral views look bad)
§ CT: Determine degree of spinal canal occlusion
o Management: Surgery
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TRAUMATIC PARAPLEGIA
• General Information
o Burst fractures and fracture dislocations most likely to have neurological involvement
o Complete vs Incomplete Transection
§ Complete: Spinal shock à Neural deficit persists after spinal shock ends
• Spinal shock: state of complete spinal areflexia
o Physiological dysfunction of spinal cord (complete paralysis and anaesthesia, with loss of anal reflex) – loss of
basal excitatory stimulus from brain to neurons
o Bulbocavenosus reflex signifies end of spinal shock (can last up to 3 days)
• Neural deficits: paraplegia (thoracic and lumbar lesions) or quadriplegia (cervical lesions)
§ Incomplete: Persistence of sensation distal to injury suggests incomplete lesion
• Neural deficits: partial sensory and motor loss below level of lesion
• Types: Central cord syndrome, anterior cord syndrome, posterior cord syndrome, Brown-Sequard
o Type of Neural Injuries
§ Neurapraxia: Neurological deficits recover within mins or hours (occurs in patients whose spinal canal have small AP diameter)
§ Cord Transection: Spinal shock à Followed by UMN signs
§ Root Transection: Neurological deficit in distribution of damaged roots (may recover and residual motor paralysis remains
flaccid)
• Management
o Incomplete transection: surgical decompression + stabilization of spine
Complete transection: overall management
o Skin: Prevent pressure sores with meticulous nursing
§ Wash, dry and powder patient’s back
§ Patient taught to relieve pressure intermittently during prolonged sitting
o Bladder and bowel:
§ Bladder: Catheterise to prevent overflow incontinence which can predispose to infections + Bladder training subsequently
§ Bowel: Trained with help of enemas, aperients and abdominal exercises
o Muscles and joints: Prevention of contractures
§ Preventing contractures: Passive exercises, standing, walking
§ Reversing contractures: Tenotomies
SPASTIC PARAPARESIS
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1. Osteoarthritis
DEFINITION
Degenerative disorder of synovial joints primarily affecting cartilage and subchondral bone.
Progressive softening & disintegration of articular cartilage + new growth of cartilage & bone at joint margins (osteophytes) + capsular fibrosis
BACKGROUND
Epidemiology • Secondary
• Frequency of OA: o Vascular
o Asians: knees > hips o Infective: Syphillis
o Caucasians: hip > knees o Site with history of Trauma (injury to articular surface):
• OA of hands and knes: F > M eg. scaphoid fracture, Kienbock’s disease
• OA of hip: M > F § Loose bodies
Morphological Changes o Autoimmune: RA
1. Cartilage degeneration o Metabolic: HyperPTH, crystal deposition dz
o Cartilage breakdown usually starts in area of excessive o Inflammatory, Iatrogenic
loading (eg. changes most marked in medial o Neoplastic
compartment in varus deformity) o Congenital
o Fissuring o Degenerative
o Pitting Types
o Eburnation as joint motion polishes surface 1. Polyarticular OA (usually primary OA): Common joints affected:
2. Bone hypertrophy à osteophyte formation 1) DIPJ of hands most common (Heberden’s nodes) 2) PIPJ of
3. Mild synovitis hands (Bouchard’s nodes) 3) 1st CMCJ, 4) 1st MTPJ, 5) knees,
4. Capsular fibrosis 6) hip 7) cervical and lumbar facet joints
X-ray Presentation (LLOSS) 2. Monoarticular OA: In weight bearing areas
1. Loss of joint space (usually only in 1 compartment; unlike 3. OA in unusual sites: If OA appears in shoulder, elbow, wrist,
panarthritis in inflammatory conditions) ankle, suspect a previous abnormality or generalized disease.
2. Loose body Grading of chondral damage (Outerbridge classification)
3. Osteophytes at margins of joint • Grade 0: Normal cartilage
4. Subchondral cyst • Grade 1: Cartilage softening and swelling due to
5. Subchondral sclerosis degeneration
6. Others: bone irregularity, signs of old injuries o water content increases from 80% to 90%
Causes • Grade II: Partial thickness defect with fissures on surface that
• Primary do not reach subchondral bone or exceed 1.5cm in diameter
o Idiopathic o Collagen fibres exposed
o Senile (degenerative) • Grade III: Fissuring to level of subchondral bone in an area
o Post-menopausal with diameter more than 1.5cm
o Joints: DIPJ and carpometacarpal joint in thumb • Grade IV: Exposed subchondral bone
o Polyarticular presentation o Cartilage completely worn off (including basal layer)
INVESTIGATIONS: 1) to confirm Dx & exclude DDx 2) to look for causes 3) to look for Cx (2 & 3 usually not applicable)
• Haematological o Culture
o FBC: raised total white for infection, Hg and platelet o Gram stain, AFB smear
for operation suitability o Crystal tests – for gout
o ESR/CRP: Inflammation o Cytology
• Biochemical • Radiological
o Renal and Liver panel: baseline renal and liver • Others (pre-op)
function, particularly if long term NSAIDs considered o Chest X-ray
• Microscopy o ECG
MANAGEMENT
• Conservative (non-surgical) • Surgical
o Non-pharmacological o General Indications
§ Lifestyle modification: weight loss, exercise, avoid § Significantly symptomatic (instability, pain, deformity,
kneeling and squatting disability)
§ Physiotherapy: strengthen muscles, preserve and § Failure of conservative management
improve joint mobility, improve symptoms § Of adequate health status to tolerate surgery and
• Knee extension or leg lifting exercises, utilize prosthesis
stationary cycling, hydrotherapy o Types of surgery
• ?Application of warmth: eg. radiant heat, § Arthroscopic debridement and washout
shock wave diathermy § Realignment osteotomy (in younger patients)
§ Occupational therapy: load reduction with walking § Arthrodesis: done only if strong contraindication to
aids, soft soled shoes arthroplasty / as a salvage procedure
o Pharmacological § Arthroplasty: Last approx 15 years
§ Analgesia: o Post-Sx: physioRx + CPM (continuous passive movment)
• Acetaminophen (paracetamol): shld be 1st line to maintain joint ROM and muscle power
drug; effective in some o Complications:
• NSAIDs (aspirin, ibuprofen, naproxen) § Intraoperative
o Must be used with special care in: • Fracture: Tibia/femur for TKR and
>60y, previous history of GI bleed, acetabulum/femur for hip replacement (HR)
concurrent warfarin/ steroid • Neurovascular injuries – peroneal nerve in
medications, renal dysfunction TKR and sciatic nerve in HR
o Prescribe with PPI/H2RA in patients • GA complications
with increased likelihood of GI bleeding • Blood loss
• COX-2 inhibitors (celecoxib, etoricoxib): Vioxx § Early
a/w increased risk of stroke & cardiac events • Infection
• Tramadol: consider if highly resistant pain • Fat embolism syndrome
§ Glucosamine (anti-inf) with chondroitin (inhibits • DVT and pulmonary embolism
cartilage breakdown and stimulate cartilage repair): o DVT prevention:
at least as effective as NSAIDS, with the added o 1) pre-operative: thromboembolic
advantage of fewer side effects deterrent (TED) stockings
§ Intra-articular injections: relieve pain, increase ROM o 2) peri-operative: TED stockings,
• H&L (triamcinolone + lignocaine): Consider in compression boots and foot pumps
patients with highly resistant pain. It is (eg. pneumatic intermittent
recommended that no more than 4 compression devices), minimize
glucocorticoid injections be administered to a length of surgery
single joint per year because of the concerns o 3) post-operative: low dose LMW
with long-term damage to cartilage heparin, early mobilization (physio)
• VIscosupplementation with hyaluronic acids • Late
(Synvisc): Marketed as ‘joint replacement’ o Heterotopic ossification
substances; expensive, no evidence to o Periprosthetic fractures
support its efficacy o Loosening of joint (septic or aseptic)
o Disruption of extensor mechanism
159
OSTEOARTHTITIS OF THE KNEES
• Risk factors § May be accompanied by cartilage regeneration
o >50yr old procedures
o Overweight • Chondrocyte transplant: Harvest condrocytes
o Hereditary from non weight-bearing sites, e.g.
o Competitive contact sports (also contributed by previous patellofemoral surface, culture, reimplant
injuries like torn meniscus etc) • Microfracture of subchondral bone:
o Deformities (eg. genu valgus/varum) Subchondral penetration of bone, inducing
o Secondary OA (injury to articular surface, torn meniscus, regrowth of fibrocartilage
ligamentous instability) • Mosaicplasty: Cylindrical cartilage taken from
o NOTE: recreational running is NOT a RF non-weight bearing areas, implanted on knee
• Symptoms joint surface to form a new layer of cartilage,
o NOTE: TFOA often more significant in 1 cmpt of joint consisting of the intact original cartilage and
o Pain in knee joint the transplanted grafts
§ Medial tibiofemoral compartment OA: on walking o Realignment osteotomy:
§ Patellofemoral OA: on walking up and down stairs, § Only in certain cases (eg. unicompartmental
squatting involvement)
o Stiffness § Typically an high tibial valgus osteotomy done in
§ After inactivity (but jts feel stiff after rest and knee younger patients with medial TF compartment OA
hurts to get going after sitting for awhile) • Redistributes weight to lateral side
§ Morning stiffness <30min • Often successful in relieving symptoms,
o Swelling (mild) staving off the need for TKR
o Deformity § Contraindications:
§ Genu varum • Inflammatory arthritis
o Locking and pseudo-locking • Severe flexion deformity >15deg
§ Locking • Varus/valgus > 15deg
§ Pseudo-locking (reaction to pain) • >5mm loss of subchondral bone
o Instability/ giving way
• Lateral trust while walking
• Look
§ Mechanical axis vs Anatomical axis
o Surgical scars
• Mechanical: centre of hip to centre of ankle
o Alignment: genu varum usually (genu varum/valgus
• Anatomical: line of femur to line of tibia
predisposes to OA); externally rotated
(normally 4-6deg valgus)
o Muscle wasting of quadriceps (usually medial side)
o Arthrodesis: done only if strong contraindication against
o Gait: antalgic
arthroplasty / as a salvage procedure
o Squat: painful, cannot squat full or get up
o Arthroplasty (unicompartmental or total knee)
o Impt –ves: rheumatoid nodules, tophi, rashes, Sjogren’s
§ Indications: when symptoms are severe
• Feel
• Try to avoid doing in patients <60 as TKRs
o Joint line tenderness (for tibiofemoral OA)
usu last only 10-15y
o Patella medial or lateral facet tenderness (in PFOA)
§ Types
o Joint effusion (usually mild)
o Impt -ves: no warmth or synovial membrane thickening • Unicompartmental
• Move • Total +/- preservation of PCL; PCL
o Decreased ROM (extension lag due to quads wasting, preservation preserves proprioception function
fixed flexion deformity) but ↑ wear of prosthesis
o Crepitus (PF or TF?) § Complications
• Special tests • Intraop – GA, # of tibia or femur
o Patella grinding test (for PFOA) • Immediate – vascular injury to superficial
o Signs of ligamentous/ meniscal injuries which can initiate or femoral, popliteal and genicular vessel
accelerate OA • Early – DVT/PE, fat embolism, infx, peroneal
• Request: nerve palsy (1%)
o Examine other joints esp hip and back (exclude hip and • Infection: Management: 2 stages
back causes of knee pain à Referred pain) o Removal of implant, plus 6 weeks IV
o Neuro exam SMART: sensory, motor, autonomic, reflexes, antibiotics
trophic changes o Reimplantation after Abx completed
• Radiological (for knee): 4 views to view 3 compartments • Late – loosening, patellar instability, #,
o Weight bearing AP view: so that even small degrees of disruptn of extensor mechanism,
articular cartilage thinning can be seen periprosthetic #, Wear of polythene surfaces
o Skyline (tangential) view o For rare cases where OA confined to patellofemoral joint
§ Different patterns of PFOA: lateral, medial, global § Arthroscopy to confirm diagnosis
§ NOTE: lateral condyle is higher § Types of Sx:
o Lateral • Realignment procedures
o Long film (to see degree of varus/valgus) • Patellectomy: problems a/w it include loss of
* For knee important to view all 3 compartments: medial, lateral, normal knee power and function, quads
patellofemoral compartment weakness, and failure to resolve anterior knee
* Peripheral osteophyte formation is most specific sign pain à may eventually require TKR for knee
• Surgical Management: arthritis
o Arthroscopic debridement and washout: • Patellofemoral arthroplasty
§ For early OA or as a temporizing procedure to delay • Total knee arthroplasty
arthroplasty (up to 5 yrs) or if CI to osteotomy/ TKR • Cartilage transplantation (under research)
§ Degenerate meniscal tears, loose bodies and
osteophytes can be trimmed
160
Mr / Mdm XXX is a __ years old (race) gentleman / lady, bleeding.
premorbid status: (ADL indep, community ambulant – w/wo aid), He / she had previous operations for ____________ / TKR for the
occupation: ____________________, other knee.
with a significant PMHx of (left / right TKR in XXXX year) , He / she has NKDA and is currently on ___________ for her medical
presenting complaint: currently admitted for elective (left / right) conditions.
total knee replacement.
Social History
He / she presents with a (duration) history of bilateral progressive He / she (does not smoke / smokes / is an ex-smoker and has quit
knee pain (right > left / left > right) that has: XX years ago) , ( sticks/day x years).
1. Failed to improve with conservative management He / she (has / does not have) a habit of regular intake of alcoholic
2. Gotten progressively disabling over the years drinks.
3. Resulted in marked loss of functioning He / she has (good / poor) social support. He / she works as a
_________ and his / her condition affects her job. He /she lives with
The knee pain is associated with: his / her ________. His / her main caregiver is his / her
1. Recurrent swelling ______________.
2. Morning stiffness / stiffness after resting He / she lives in a residential (with / without) lift landing. There (is
3. Progressive deformity / is no) squatting toilet in the house.
Currently, the family (does not have any financial issues / is
The knee pain started (duration) years ago and has gotten receiving financial aid from ) .
progressively worst.
He / she describes the pain as (sharp / ) in nature. It is mechanical in In summary, Mr / Mdm XXX is a __ years old (race) gentleman /
nature, aggravated by movement when he / she does (type of lady with co-morbidities of ________________, currently presenting
activity) and relieved by rest. It is also worst at the end of the day. with bilateral mechanical knee pain for (duration) , worst on the
The pain is felt in the (site: anterior / medial) aspect of both knees (left / right) associated with recurrent swelling, stiffness and
with no radiation. progressive deformity that has severely affected her daily functioning.
His / her current pain score is ___ and the pain (severity: affects She has failed conservative management and is currently admitted
sleep / requires frequent use of painkillers) . for elective (left / right) total knee replacement.
161
The popliteal, posterior tibial and dorsalis pedis pulses were well felt
in both lower limbs.
Neurologically, power of bilateral lower limbs is full and sensation is
intact bilaterally.
162
2. Rheumatoid Conditions
RHEUMATOID ARTHRITIS
Definition: Systemic chronic inflammatory disease of unknown cause that affects the peripheral joints in a symmetrical fashion
Epidemiology
• Prevalence: 0.8% of adult population
• Risk factors
o Women (3W:1M) aged 40-50yrs old
o Genetic susceptibility
• Morbidity:
o High lvl of functional impairment
o If untreated, 20-30% will become permanently work disabled within 3yrs
• Mortality: related mainly to extra-articular manifestations
Pathophysiology
• Genetic susceptibility (HLA-DR4, HLA-DR1) à immune reaction on synovial tissueà inflammatory reaction in joints and tendon
sheathsà anti-IgG autoantibodies (rheumatoid factors) in blood and synovium à chronic synovitis and articular cartilage
destruction
o Cause unknown; postulated to be response of genetically susceptible host to an infectious agent
§ Persistent infx of articular structures/retention of microbial products in synovial tissues
§ Alterations of joint components by microorganisms/ response to microorganism
§ Molecular mimicry
Stage Pathology Signs X-Ray
Stage 1: • Synovitis of proximal joints and tendon • Pain (acute), chronic fusiform swelling (thickened • Soft tissue
Synovitis sheaths synovium), wasting, effusion, stiffness in MCPJ, swelling and
o Inflammation and thickening of PIPJ, wrists and tendon sheaths around the joints. osteoporosis
synovial membrane (Synovial cell • Gradually affects other joints: around joints
hyperplasia and proliferation) à wrists > feet > knees > shoulders
cell-rich effusion (Neutrophils and • Extensor tenosynovitis (thickening, tenderness and
aggregates of organizing fibrin) into crepitation over back of wrist or palm on passive
joints (synovial surface) and tendon movement)
sheaths • In larger joints: warmth, synovial hypertrophy,
o Increased vascularity (angiogenesis) intraarticular effusion
• Joints and tendons painful and
swollen but still intact
• Potentially reversible
Stage 2: • Joint (cartilage, subarticular bone, jt • Pain (constant ache) • Narrowing of
Destructive capsule), tendons, ligaments • Joint instability, ligamentous laxity joint spaces
destroyed • Tendon ruptures • Small
• Erosion of articular cartilage & • Restricted ROM periarticular
subarticular bone • Muscle wasting erosions
o Invasion by pannus
o Proteolytic enzymes (secreted by
neutrophils)
o Osteoclastic resorption
• Tendon sheaths: tenosynovitis,
invasion of collagen bundles à partial
or complete tendon ruptures
Stage 3: • Articular destruction (cartilage and • Pain, deformity, instability, decreased ROM, • Marked
Deformity subarticular bone), capsular stretch, disability articular
(often ligament damage & tendon rupture à o Loss of function destruction
results in progressive deformity and instability of § Class 1: normal functional activity • Joint deformity
loss of joints à loss of function § 2: normal functional ability despite discomfort and dislocation
function) o Fibrosis/ calcification of pannus § 3: can only perform a few tasks of work/ self care
o Fibrous/ bony ankylosis § 4: almost/complete incapacity
• Thumb: Z-deformity
• Fingers: ulnar deviation, subluxation or dislocation of
MCPJ, swan-neck/boutonniere deformities
• Wrist: radial and volar displacement
• Elbows: limited extension
• Shoulders: limited abduction
• Knees: swollen, held in flexion and valgus
• Toes: clawed
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o Those with a 6points or higher is classified as an RA patient, provided he has synovitis in at least one joint and given that there is
no other diagnosis better explaining the synovitis.
1) Joint involvement 1 large joint: 0 point
- Small joints: MCPJ, PIPJ, IPJ, MTPJ, wrist 2-10 larger joint: 1 point
- Large joints: shoulder, elbow, hip, knee, ankle 1-3 small joints: 2 points
4-10 small joints: 3 points
More than 10 joints (with at least 1 small joint): 5 points
2) Serological parameters Negative RF and negative ACPA: 0 points
Low positive RF or low positive ACPA: 2 points
High positive RF or high positive ACPA: 3 points
3) Acute phase reactants Elevated ESR or CRP: 1 point
4) Duration of arthritis Symptoms lasting at least 6 weeks: 1 point
Differential diagnoses
• Seronegative inflammatory polyarthritis: psoriatic arthritis, Juvenile chronic arthritis (still’s disease), SLE
• Ankylosing spondylitis: Primarily affect SIJ and intervertebral joints but may involve peripheral joints
• Reiter’s disease
o Primarily affects larger joints and lumbosacral joints
o + urethritis, colitis, conjunctivitis
• Polyarticular gout
o X-ray: erosions different from RA
o Nodules tend to be asymmetrical
• Pseudogout
• Polyarticular OA
• Polymyalgia rheumatica
o Giant-cell arteritis (vasculitis) that carries risk of temporal arteritis resulting in blindness
o Common in middle-aged or elderly women
o Signs and symptoms
§ Pain and post-inactivity stiffness around shoulders and hips
§ Muscular weakness
§ Muscles are tender, not joints
o Investigations: ESR remarkably high
o Management: corticosteroids provide rapid and dramatic relief of all symptoms (response used as diagnostic test)
Symptoms (periods of relative quiescence + periods of flare)
• Usual pattern is insidious onset (but usually more rapid onset than OA) of symmetrical polyarthritis affecting mainly hands and feet +
early morning stiffness + constitutional symptoms; sometimes may start in other joints as a chronic monoarticular synovitis
• Joints: typically PIP, MCP, wrist, elbow, shoulders, knees, ankles, feet
o Pain (insidious onset)
o Stiffness – early morning stiffness >1hour
o Swelling – symmetrical, red, warm
o Progressive deformity
§ Z-collapse (if 1 of 2 adjacent joints changes direction, then overlying long tendons will pull other joint in opposite direction)
o Decreased ROM
• Constitutional symptoms – fever, fatigue, malaise, LOW
• Associations
o Sjogren’s syndrome: dry eyes, dry mouth, recurrent chest infx
o Felty’s syndrome: splenomegaly, leg ulcers, recurrent infx, LN, weight loss
• Extraarticular manifestations: refer below
Other aspects of Hx:
• Previous Rx history
o Medications: NSAID, steroids (assess for adverse SEs)
o Intra-articular injections
o Previous operations
• Family Hx
• Social Hx: occupation, family setup, caregiver
Deformities of the hand
• Thumb:
o Z thumb deformity (flexion of IPJ and hyperextension
of MCPJ), carpometacarpal instability, ulnar collateral
instability, CMCJ swelling
• MCPJ:
o Volar subluxation or dislocation of MCPJ most
commonly over index and middle fingers – Prominent
metacarpal heads: chronic synovitisà failure of
palmar plate and collateral ligamentsà flexors drag
prox phalanx palmarwardà subluxation of joint
o Ulnar subluxation of extensor tendons
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•Fingers:
o Ulnar drift/deviation of fingers, involving the more lateral digits in the more advanced cases:
palmar grip and thumb pressure naturally tend to push fingers ulnarwardsà weakening of
collateral ligaments reduce normal resistance to this force
o Boutonniere (hyperextension of DIPJ, flexion of PIPJ): rupture of central slipà lateral slips
separate and head of prox phalanx thrusts through gap of extensor tendon
o Swan-neck (flexion of DIPJ, hyperextension of PIPJ)
1. Failure of palmar plate of PIPJ
2. Rupture of FDS
3. Dislocation/subluxation of MCPJ and tightening of intrinsic muscles
o Swelling of PIPJ
• Rheumatoid nodules: Subcutaneous, rubbery lumps (usually at pressure areas like olecranon, pulp
of fingers and radial side of index finger; also on tendons (cause triggering or rupture), viscera, eye)
o Palpate the elbows for rheumatoid nodules (present in 25% of patients): Small granulomatous
lesion consisting of central necrotic zone surrounded by histiocytes and inflammatory
granulation tissue
• Carpus: Radial tilt of and volar subluxation of carpus
• Wrist:
o Deformity
1. Prominence of DRUJ (caput ulnar syndrome): Piano key sign positive (subluxation of DRUJ causing head of ulna to pop
up on dorsum of wrist where it can be jogged up and down)
2. Radial deviation of wrist
3. Volar subluxation
4. Subluxation of extensor tendon
o Tenosynovitis related
1. Carpal tunnel compression from flexor tenosynovitis (early)
2. Swelling of tendon sheath: Dorsum of wrist on ulnar side (ECU), Volar aspect (proximal phalanges)
• Tenosynovitis (treatment to include flexor synovectomy)
o Can affect flexor and extensor tendons
o Complications
1. Joint stiffness
2. Carpal tunnel syndrome
3. Triggering
4. Tendon rupture
5. Deformity (eg. FDS synovitis contributes to swan neck)
• Tendons
o Extensor tenosynovitis and rupture
o Flexor tenosynovitis
o 2nd problems: carpal tunnel syndrome, trigger finger, tendon ruptures
Other aspects of PE:
• Look: above deformities, palmar erythema, wasting of interossei (best seen in 1st dorsal web space)
• Feel: Palpate over swollen joints to detect warmth and tenderness of acutely inflamed joints
• Move:
o Functional assessment: unbutton shirt, write w pen
§ Function
• Diminished grip strength – muscular weakness, pain, tendon malalignment / rupture, joint stiffness, nerve compression
• Loss of extension
o Joint problem – subluxation / dislocation
o Tendon – subluxation, rupture
o Hand examination: median nerve for any carpal tunnel syndrome ****
• Offer:
o Examine other joints in the body that are affected by RA
o Examine the rest of the patient for extra-articular manifestations of RA
§ Extra-articular manifestations (occurs later in course of disease)
• Opthalmic – scleritis, episcleritis, keroconjunctivitis sicca
• Pulmonary – effusion, fibrosis
• Cardiac – pericarditis
• Vacular – vasculitis (predisposes to poor healing ulcers/wounds)
• Reticuloendothelial – lymphadenopathy, splenomegaly, Felty’s syndrome
• Neurological – carpal tunnel syndrome, multifocal neuropathies, ant subluxation of C1 on C2
o Ask patient how the condition affects his/her life
Investigations
• Haemotological
o FBC –Normocytic hypochromic anaemia (abnormal erythropoiesis from chronic inflammation), thrombocytosis, WBC & D/C:
eosinophilia à exclude infx
o Inflammatory markers: raised ESR, present CRP, high mucoprotein levels
§ Indicates active disease; used for disease progression monitoring, treatment response
o RF (anti-IgG autoAb) positive (in 80%)
§ Not specific (present in healthy ppl, SBE, TB, viral infx)
§ Not required for RA diagnosis
§ Prognostic: persistently high titres herald more serious disease and poorer prognosis
o ANA present (in 30%): positive in autoimmune disease: Not specific (also in SLE, scleroderma, Sjogren’s disease, Raynaud’s dz)
165
o ACPA –anticitrullinated protein antibodies (in 67%)
§ Higher specificity (rarely positive if RA not present)
o UECr + LFT: assess renal and liver function before starting treatment
• Joint aspiration
o Analysis of synovial fluid: straw coloured, cloudy, flecks of fibrin, large numbers of WBCs esp neutrophils
o Biopsy: histological features non-specific and not diagnostic
• Imaging: X-ray à disease monitoring, treatment response
o Early (stage 1): soft tissue swelling, periarticular osteopenia
o Later (stage 2): juxta-articular erosions, narrowing of joint space (but lack of osteophytes c.f OA)
o Advanced (stage 3): articular destruction and joint deformity
o C-spine: atlanto-axial subluxation
Management
• Goals:
o Control dz activity
o Prevent/control joint damage
o Prevent loss of function
o Control pain
o Maximize QOL
• Treatment modalities
o Non-pharmacological: rest, patient education, PT, OT, splint (decrease synovitis, increase stability)
o Pharmacological: (early aggressive treatment, Esp those w poor prognostic factors)
§ NSAIDs: Indomethacin, Diclofenac, Naproxen
• Symptomatic treatment: anti-inflammatory, analgesia
• Does not alter disease progression
• ADRs: PUD
• Contraindication: Renal impairment
§ Steroids: Prednisolone
• Symptomatic treatment: anti-inflammatory
• May help slow disease progression/joint damage
§ Disease modifying anti-rheumatic drugs (DMARDs): Methotrexate, Gold, Hydroxychloroquine (See Table)
• Slow down disease progression of bone & cartilage destruction
• Take 1-6 months to be effective
• Monotherapy/Combination
§ Anti-TNF α: Etanercept, Abcliximab, Infliximab
o SURGICAL MANAGEMENT
§ Surgical Release for nerve entrapment syndromes (eg. Trigger finger, CTS, De Quervain’s)
§ Synovectomy
• For persistent synovitis > 6 mths
• Symptomatic relief of pain and swelling
• Restore ROM
§ Arthroplasty
• Mainly for knees, can also be done for hip, shoulder, elbow
• Total joint replacement advised when bone destruction is present and joint unstable
• Pain relief, correction of deformity, Stability and alignment, Preserve ROM
§ Others:
• Tendon repair
• Osteotomy (femoral or tibial osteotomy à improves function and relieves pain): genu valgum
• Arthrodesis (mainly triple arthodesis of ankle): surgical fusion of jt to give stability, pain relief, deformity correction
• Treatment by symptoms
o Synovitis: local corticosteroid injections, surgical synovectomy, splinting
o Tendon ruptures: repair, bypass by tendon transfers
o Joint instability: arthroplasty, arthrodesis
o Deformities: reconstructive surgery, splintage (eg. ulnar drift)
Onset of disease Conservative: physiotherapy, activity modifications (maintain muscle tone and joint mobility)
Pharmacological: NSAIDs (analgesics)
Early phase Conservative: physiotherapy, rest
(6-12 months) Pharmacological: NSAIDs, corticosteroids (5-7.5mg prednisolone) for up to 2 years (intra-articular
Control synovitis injections?), +/- 2nd line drugs (gold or penicillamine)
Progressive erosive Conservative: preventive splintage, orthotic devices
arthritis (1-5years) Pharmacological: already on 2nd line drugs (methotrexate, gold, penicillamine)
Operative:
• Soft tissue: synovectomy, tendon repair/replacement, joint stabilization, nerve entrapment
release (carpal tunnel, trigger finger, De Quervain’s)
• Bone: osteotomy
Late rheumatoid Occupational therapy for function
disease (5-20years) Operative:
• Indications: severe joint destruction, fixed deformity, loss of function
• Arthrodesis, osteotomy, arthroplasty
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DMARDs Pharmacology Toxicity Investigations
Methotrexate - Recommended as initial DMARD - N+V - Baseline FBCs, U/E/Cr
- Rapid onset of action (1-2mths) - Mucosal ulcers - LFTs, Hep B/C status
- Retards progression of radiological erosions - Liver cirrhosis, ↑ LFTs - CXR
- Interstitial pneumonitis
- Severe BM suppression
- Teratogenic
Hydroxy- - Rash - Eye examination (6-12 mthly)
chloroquine - Abdominal cramps
- Diarrhoea
- Retinal pigmentation
Sulfasalazine - Faster onset (1-3 mths) - N+V - FBC, LFTs
- Retard Radiographic progression - Headache
- Rash
- BM suppression
- Teratogenic
Gold - Oral: Slow onset (6mths) - Rash - FBC
- IM: Faster onset (weekly injection of 22 wks) - Ulceration, mucositis - UFEME, U/E/Cr (at every
- Nephrotic syndrome injection)
- Panctyopenia
Leflunomide - Alternative to MTX - Diarrhoea - FBC, U/E/Cr
- Slows radiographic progression - Alopecia - LFTs, Hep B/C status
- Headache
- Immunosuppression
- ↑ LFTs
- Teratogenic!
Complications
• Fixed deformities
• Muscle weakness –prevent with physiotherapy and analgesia
• Tendon rupture from nodular infiltration (mostly at wrist)
• Joint lining rupture à synovial contents spill into soft tissues
o Manage underlying synovitis: splintage and injection; synovectomy
• Infection (septic arthritis; esp those on corticosteroid therapy)
o Signs: sudden clinical deterioration, increased pain in single joint
o Management: joint aspiration
• Secondary OA due to articular damage
• RARE
o Spinal cord compression (rare complication of cervical spine instability)
o Systemic vasculitis
o Amyloidosis
This is an elderly (Chinese / Malay / Indian) lady. On inspection, I The joints are not swollen, not warm and not tender, hence disease is
note that she has a pair of rheumatoid hands as evidenced by the in the quiescent stage.
presence of bilateral symmetrical deforming polyarthropathy of the
small joints of the hands, namely the MCP joints and the PIP joints, (move joints – fingers + wrist, Tinel’s test, pronation & supination of
with sparing of the DIP joints. (I also note that she is Cushingoid in forearm)
appearance.)
She is unable to make a fist and there is severe limitation of movement
There is radial deviation of the wrist accompanied by dorsal subluxation at the wrist joint.
of the distal radioulnar joint with prominence of the radial styloid ROM of wrist flexion and extension is ____.
process. Piano key sign (is / is not) present. Ulnar deviation is ____ and radial deviation is ____.
There is also wasting of the intrinsic muscles of the hands. Supination is ____ and pronation is ____.
In addition, there is volar subluxation of the MCP joints and ulnar There are no trigger fingers or dropped fingers suggestive of tendon
deviation of the fingers. rupture or any CTS release / tendon release scars.
I note the presence of Z thumb deformity of the (left / right) thumb
and swan neck deformities over the (index / middle / ring / little) I would like to proceed to look for rheumatoid nodules at the elbow.
finger(s) as well as Boutonniere’s deformities over the (index / middle / I did not find rheumatoid nodules over the extensor surfaces of the UL
ring / little) finger(s). or over the olecranon process.
There (are / are no) swelling over the small joints of the hands. I do I would like to test for functional impairment by asking the patient to
not see any overlying skin changes or erythema. pick up coins & to hold a cup.
There (are / are no) scars seen over ___________ suggestive of Her hand function is (grossly impaired / relatively preserved) . She is
previous tendon repair or arthrodesis. able to hold a cup with both hands. She is unable to (button her shirt /
uncap a pen to write) .
I would like to proceed to palpate the joints. (ask pt for any pain first)
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SERONEGATIVE SPONDARTHRITIS
• PAIRS –psoriatic arthritis, ankylosing spondylitis, IBD, reiter’s disease, still’s disease
• Characteristic spondylitis and sacroilitis
o Grades of sacroilitis
o Sacroiliitis: causes PUB CAR: (seronegative arthropathies + Bechet’s) Psoriasis, Ulcerative colitis, Behcet's disease, Crohn's
disease, Ankylosing spondylitis, Reiter's disease
• Associated w HLA B27
• Familial aggregation
• Overlap within families
ANKYLOSING SPONDYLITIS
• Risk factors
o 4M:1F, onset at 15-25years
o Genetics: HLA-B27
§ First degree relatives at risk of psoriatic arthritis, IBD and Reiter’s syndrome
• Pathology
o Definition: chronic multi-systemic inflammatory disorder of the SIJ and axial skeleton,
w effects mainly in spine and SIJ, leading to progressive stiffening and fusion of axial skeleton
I Widening of joint Rome criteria NY criteria
II Joint erosioni Bilateral sacrolitis > grade I + any of the following: Bilat Sacroilitis > grade I OR unilat Sacroilitis > grade
III Sclerosis on both sides • LBP + stiffness > 3 mths not relieved by rest 2 AND any of the following:
IV Ankylosis • Thoracic pain or stiffness • LBP of inflammatory nature
o Pathophysiology: • ↓ lumbar spine ROM • ↓ lumbar spine movt in sagittal & frontal planes
§ 1) Synovitis of • ↓ chest expansion • ↓ chest expansion
diarthrodial joints: SIJ • Hx of uveitis
and vertebral facet
joints
§ 2) Inflammation of fibro-osseous junctions
• intervertebral discs, sacroiliac ligaments, symphysis pubis, manubrium sterni, bony insertions of large tendons
• 3 stages of Enthesitis: 1)inflammation with subchondral granulation tissue formation and erosion of adjacent bone,
2)fibrosis of granulation tissue à fibrocartilage, 3)ossification of fibrous tissue leading to ankylosis of joint (occurs in
ligamentous capsule attachment sites to bone)
o In the spine, this occurs in the junction btw vertebral bodies and annulus fibrosus of IV discs. Outer fibres of the
discs eventually undergo ossification à syndesmophyte formed à progresses to the characteristic bamboo spine
• DIAGNOSTIC CRITERIA (NEW YORK CRITERIA): (AS = radiological criterion + 1 clinical criterion)
o Low back pain > 3/12 (improved by exercise, not relieved by rest)
o Limitation of lumbar spine motion in both sagittal & frontal planes
o Limitation of chest expansion relative to normal values (< 5cm at 4th IC space)
o Radiological features of sacroilitis
• Symptoms
o Recurrent backache and stiffness
§ Worse in early morning and after inactivity; relieved w exercise
§ Insidious onset, >3months, Dull character
§ Often begins unilaterally and intermittently (recurring at intervals over number of years) à as disease persists, it becomes more
persistent (gradually becomes continuous) and bilateral and progresses more proximally
§ MAY start with symptoms in peripheral jointsà eventually backache will predominate
o Radicular pain from referred pain in buttocks and thighs
o Later symptoms: pain and swelling of joints, tenderness at tendoachillis insertion,
intercostal pain and tenderness, difficulty breathing/ chest tightness from costovertebral and
costotransverse joint involvement, jaw pain/decreased ROM from TMJ involvement
o Extraskeletal manifestations
§ Systemic: Fatigue, amyloidosis, osteoporosis
§ Ophthalmo: iritis, acute anterior uveitis à glaucoma
§ Cardio: Aortic valve disease (esp AR), carditis, cardiac conduction defects (arrhythmia)
§ Respi: apical pulmonary fibrosis
§ Archilles tendonitis, plantar fasciitis
• Signs
o Documentation of progression
§ Loss of horizontal gaze (not quantitative)
§ Finger floor distance
§ Schober’s test
§ Occipital-wall distance
§ Chest expansion (costovertebral joints)
o Early:
§ Slight flattening of lower back
§ Tenderness over spine and SIJ
§ Limited extension in lumbar spine
§ Peripheral joints: occasionally swelling and tenderness of single large joint
o Late:
§ Loss of lumbar lordosis, increased thoracic kyphosis and forward thrust of neck (loss
of cervical extension)
168
§ Upright posture maintained by flexed hips and knees
§ Limited ROM in all directions but loss of extension earliest and most severe
• Wall test: heels, buttocks, scapulae and occiput unable to touch wall simultaneously
• Decreased chest expansion (should be >7cm in young men): <5cm at 4th IC space
§ Peripheral joints (shoulders, hips, knees): inflammatory arthritis (tenderness, swelling, loss of ROM, tenderness of tendon
insertions)
§ Most advanced stages: severe deformities (eg. Hyperkyphosis)
• Complications
o Spinal fractures as spine is rigid and osteoporotic
o Myelopathy (uncommon): Due to atlanto-axial subluxation or ossification of PLL
o Lumbosacral nerve root compression à may lead to cauda equina syndrome
• DDx: primary OA, causes of LBP (esp OM, TB, mets)
• Investigations
o Bloods: Raised ESR, HLA-B27 (can be –ve in 10% of cases), Rh -ve, normochromic normocytic
anemia, MCHC from NSAIDs use
o ECG: conduction defects
o Synovial fluid complement: not depressed, decreased viscosity, leukocytosis
o X-ray
§ SIJ: Erosion and fuzziness of SIJ à may have periarticular sclerosis esp on iliac side à
ankylosis
• Whiskering: calcification of tendons attached to ischial tuberosity
§ Vertebrae: AP, lateral spine XR; AP, lateral, open mouth C-spine
1. Flattening of normal concavity (squaring) of vertebral body: (erosions at the
vertebrae occur 1st at e anterosuperior anteroinferior corners)
2. Erosion of anterior corners of vertebrae
3. Sclerosis of edges (shiny corner sign/ Romanus lesion)
4. Ossifications of ligaments around IV discs producing syndesmophytes btwn adjacent vertebrae
5. Facet joint fusion + vertebral fusion
6. Bridging at several levels + syndesmophyte formation gives
appearance of bamboo spine
7. Costovertebral joint involvement
8. Atlantoaxial dislocation
• Osteoporosis common in long-standing casesà hyperkyphosis of
thoracic spine from wedging of vertebral bodies
§ Peripheral joints: erosive arthritis or progressive bony ankylosis
o Bone scan: sacroilitis & spinal involvement
• Management
o Aims:
§ Relieve pain and stiffness Romanus
lesion
§ Maximize skeletal mobility
§ Avoid dvlpment of deformities
o Conservative
§ Education: genetic counseling (50% chance of passing to children), chronic disease, fall prevention (osteoporosis)
§ Lifestyle mod: PhysioRx (spinal extension exercises, postural trng, breathing exercises), exercise (swimming, dancing,
gymnastics), Avoid rest (increases stiffness)
§ Phamacological:
• NSAIDs (usually indomethacin): ask abt renal function, hx of GIB, coagulant Rx
• Sulphasalazine: for persistent peripheral arthritis. Not useful for axial disease
§ Radiotherapy: if drug therapy is ineffective
§ Local corticosteroid injection: for plantar fasciitis and enthesopathy
§ Systemic steroids: for acute iritis
§ Anti-TNFα
(Infliximab)
o Surgical
§ Peripheral joints: THA/ TKA + post-op indomethacin/ RT to decrease heterotrophic bone formation
§ Spine flexion deformity: lumbar or cervical osteotomy (rare)
• Anesthesia related problems (difficult to give anesthesia in AS patients):
o Stiff neck hence hard to intibuate
o Breathing problems
He / she describes the pain as (nature) and it radiates to the buttocks
Mr / Mdm XXX is a __ years old (race) gentleman / lady, and thighs. The current pain score is ___. The symptoms of pain and
premorbid status: (ADL indep, community ambulant – w/ wo aid), stiffness are worse in the mornings, lasting more than 30 min and after
occupation: ____________________, periods of inactivity. It is not aggravated by movement of the patient.
with a significant PMHx of (ankylosing spondylitis if patient offers) ,
presenting complaint: currently admitted for (THR / corrective There (is / is no) associated hip pain / knee pain for (duration) .
surgery for the spinal deformity) . There (is / is no) associated neck pain / neck stiffness for (duration)
. (from atlantoaxial subluxation)
He / she presents with a (duration) history of (progressive / non-
progressive) low back pain and back stiffness associated with an He / she also complains of pain over:
increasing inability to (extend / flex) his / her (back / neck) over 1) Sole of his / her (left / right) foot à plantar fasciitis
(duration) . 2) Posterior aspect of his / her (left / right) leg over the area of the
Archilles tendon à Archilles tendonitis
169
3) Peripheral joints à similar changes in RA, peripheral arthropathy, Social History
pauciarticular juvenile idiopathic arthritis He / she (does not smoke / smokes / is an ex-smoker and has quit XX
4) Bony prominences à iliac crest / ischial tuberosity / greater years ago) , ( sticks/day x years).
trochanter involvement He / she (has /doesnt have) a habit of regular intake of alcoholic drinks.
OR He / she has (good / poor) social support. He / she works as a
He / she has no complaints suggestive of peripheral joint involvement _________ and his / her condition affects her job. He / she lives with
or enthesopathies. his / her ________. His / her main caregiver is his / her ___________.
He / she lives in a residential (with / without) lift landing. There (is /
Functional Status is no) squatting toilet in the house.
Currently, his / her symptoms have limited his / her daily function, such Currently, the family (does not have any financial issues / is receiving
as (sitting / squatting / climbing up & down stairs / using the toilet – financial aid from ) .
having to stand to defaecate / lying down flat) .
His / her walking distance is limited to ______ from ______ previously, In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady
(with / without) a walking aid. with co-morbidities of ________________, currently presenting with
Systemic Review
He / she does not have any weakness or numbness of his / her lower PHYSICAL EXAMINATION
limbs or any red flag symptoms such as changes in bowel or urinary 1. Look:
habits, night pain, fever or constitutional symptoms like loss of weight • Loss of lumbar lordosis + fixed kyphosis
or loss of appetite. There is also no hx of previous trauma to the back. • Stooped “question-mark” posture
In addition, he / she has systemic complaints of: • Extension of C- spine to maintain horizontal visual gaze
1) Chest pain on breathing / SOB / palpitations à AR / cardiac • Protuberant abdomen
conduction defects / apical pulm fibrosis o Restricted chest expansion from a fixed spine
2) Colicky abdominal pain / bloody diarrhoea à Crohn’s disease / results in predominant diaphragmatic breathing
Ulcerative Colitis 2. Feel: tenderness
3) Blurring of vision / eye pain à acute anterior uveitis / iritis 3. Move:
4) Rash à psoriaform rashes • Examine pt’s gait
Management so far (options tried) • Limitation in range of motion
His / her symptoms have failed to improve with conservative o Lumbar flexion + Schober’s test
management such as __________________ for the past (duration) . o Lumbar extension
Past Medical History o Lumbar lateral flexion
Mr / Mdm XXX has a past medical history of _____________ for o Lumbar rotation
(duration) . (note any previous fractures) o Neck rotation
He / she also does not have a history of peptic ulcer disease / GI o Touch chest with chin
bleeding. • “Heels, hips & occiput” test to measure occiput-to-wall
He / she had previous operations for ____________. distance
He / she has NKDA & is currently on _____ for her medical conditions.
• FABERE test (SI joint involvement)
Family History
• Tests for Achilles tendonitis and plantar fasciitis
He / she (has / has no) family history of cancer or similar back
4. Complete the examination by:
pathologies.
• Shoulder and knee involvement
• Look for extra-articular involvement / complications
• Abdominal examination to look for signs of inflammatory
bowel disease
PSORIATIC ARTHRITIS
• Epidemiology: Affects men and women equally
• Signs/ distinguishing features
1. Assymetrical polyarthritis
2. Affects mainly IPJ of fingers and toes (may become completely flail and deformed (arthritis mutilans))
3. ¼ have sacroilitis and spondylitis like ankylosing spondylitis
4. Absence of rheumatoid nodules
5. Psoriasis of skin or nails usually precedes arthritis (hidden lesions in natal cleft or umbilicus
overlooked)
REITER’S DISEASE AND REACTIVE ARTHRITIS
• Pathology: aseptic inflammatory arthritis triggered by non-specific urogenital or bowel infection
o Shigella, Campylobacter, Yersinia, lymphogranuloma venereum, chlamydia trachomatis
• Epidemiology: Affects men more than women (10:1)
• Signs
o Clinical triad: polyarthritis, conjunctivitis, non-specific urethritis (+/- colitis)
o Mainly affects large joints like knee and ankle
JUVENILE CHRONIC ARTHRITIS (STILL’S DISEASE)
• Pathology: non-infective inflammatory joint disease for more than 3 months in children under 16years
• Epidemiology: 1 per 1000children; Affects boys and girls equally
• Types
o Pauciarticular JCA (commonest): pain and swelling of medium-sized joints –knees, ankles, elbows, wrists
o Polyarticular seropositive JCA: multiple small-joint involvement
§ Positive for RF
§ Juvenile RA
o Seronegative spondarthritis: sacroiliitis and spondylitis
§ Juvenile AS
o Systemic JCA (classic Still’s disease): fever, rashes, malaise, lymphadenopathy, splenomegaly, hepatomegaly, joint swelling
• Prognosis: most children recover from arthritis; left with only moderate deformity and limitation of function
170
SYSTEMIC CONNECTIVE TISSUE DISEASE
SLE
• Symptoms
o Systemic symptoms: malaise, anorexia, weight loss, fever
o Butterfly rashes, Raynaud’s phenomenon, peripheral vasculitis, splenomegaly, disorders of kidney, heart, lung, eye and CNS
o Joint pain (often overshadowed by above)
• Investigations
o Haematology: anaemia, leucopenia, elevation of ESR
o Anti-nuclear factor always positive
• Complications: AVN of femoral head (predisposed by disease and steroid medication)
171
Chronic gout:
§
• Tophi: excavations at joint/ rat bitten lytic areas/ punched-out ‘cysts’ or deep erosions (occupied by crystalline tophi) in
para-articular bone ends (larger than rheumatoid erosions) w overhanging edges à usually only found after 1 yr of dz
• Erosion w joint space preservation is typical
• But may have secondary OA (thus joint space narrowing)
o Joint aspiration & Polarizing microscopy (diagnostic)
§ Turbid fluid
§ Needle-shaped strongly negatively birefringent
urate cyrstals in synovial fluid (vs rhomboid
shaped crystals in pseudogout)
§ Crystals appear bright on dark background
§ If compensator added, background appears
purple, birefringent crystals yellow or blue
depending on spatial orientation a)urate
crystals
b)
pyrophosphate
crystals
§ Synovial fluid WBC count usually elevated
• Management: to relieve pain, prevent dz progression and prevent tissue deposition of uric acid
o NOTE: avoid aspirin (increases urate absorption)
o During acute attack
§ Rest and protect foot
§ Phamacological: NSAIDs +/- colchicine
• NSAID (e.g. naproxen 500mg twice daily or indomethacin 50mg three times daily) at full dosage (2-5 days), reduce to1/2
or 1/4 once attack controlled
• Low dose NSAIDs for the 1st 6-18 mnts Mx of underlying hyperuricemia - ppt gouts in up to 50% of patients
• Oral colchicine (anti-inflammatory) frequently causes unpleasant side-effects
§ For tense joint effusion: aspiration and local injection of hydrocortisone
o Between attacks: Treatment of underlying hyperuricemia – most untreated pts with gout will experience a recurrent episode in 2 yrs
§ Lifestyle modifications: weight loss, stop alcohol and diuretics, dietary modifications
• Dietary: caloric restriction (↑ protein – low fat dairy not meat/fish, replace refined with complex carbos, ↓saturated fat)
§ Pharmacological (AVOID during acute attack, cover by NSAIDs or colchicine)
• Xanthine oxidase inhibitor: allopurinol
o Allopurinol (antihyperuricaemic) – once daily
§ Frequent and disabling attacks,Signs of chronic gouty joint disease, Tophi, Renal insufficiency, Recurrent
nephrolithiasis, or Urinary uric acid excretion > 1100 mg/day
• Uricosuric drugs: probenecid, sulfinpyrazone
o Probenicid, Sulphinpyrazone (urocosuric) – multiple times daily
§ Initial therapy < 60 who excrete <800 mg of uricacid perday, no renal insufficiency, hx of urolithiasis or tophi
• Colchicine: Low dose prophylaxis during the initiation of anti hyperuricemic therapy. NSAIDs if cannot tolerate colchicine
• **Normalising uric acid level (<0.4mmol/l)à tophi may dissolve à ulcerating tophi that fail to heal evacuated by curettage
§ Surgical: treat complications (infection, nerve compression, joint deformities, intractable pain, cosmesis)
This is an elderly (Chinese / Malay / Indian) gentleman. On Some of the swellings have ulcerated and are extruding a chalky white
inspection, there are multiple swellings located at the extensor surface substance onto the surface of the skin.
of the hands involving the _____________ joints. These swellings
range from ___ cm to ___ cm. I would like to move on to palpate the swellings. (ask patient for any
There are no overlying skin changes or erythema or scars noted. pain first)
OR
172
The swelling is firm, non-tender and not warm. The overlying skin is not • Bony lesion like enchondroma
attached to the swelling but it is attached to the underlying structure.
The joints are non tender and not warm to touch. I would like to test the ROM of the joints. There is limitation of the
________________.
The above findings are consistent with that of gouty tophi, my
differentials will be: I would like to look for gouty tophi over the pinna, olecranon bursa,
• Multiple exostosis (if at knee) prepatellar bursa and Achilles tendon.
• Pigmented villionodular synovitis (PVNS) I would like to complete my examination by performing a functional
• Ganglion assessment (ask pt to hold a cup and to pick up coins).
173
CALCIUM HYDROXYAPATITE DEPOSITION DISORDERS
• Risk factors: Local tissue damage: torn ligaments, tendon attrition, cartilage damage or degeneration
• Pathology
o HA crystals deposited around chondrocytes in cartilage and damaged parts of tendons and ligaments (esp shoulder and knee)à
crystal accretion
o Crystals may be inert; in symptomatic cases surrounded by acute vascular reaction and inflammation
o Crystals shedding into joints can cause synovitis
• Signs and symptoms
o Acute or subacute periarthritis
§ Pain close to larger joints (shoulder or knee)
§ Swelling, warm, tenderness of tissues around joint (tendon or ligament rather than the joint)
§ Symptoms may subside after weeks or months or require removal or decompression
o Chronic destructive arthritis
§ Rapidly destructive OA of joint
• Investigations
o X-ray
§ Periarthritis: calcification in tendons or ligaments close to joint esp rotator cuff
§ Destructive arthritis: loss of joint space, no sclerosis, no ostepophytes
• Management
o Periarthritis:
§ Rest
§ Pharmacological: NSAIDs
§ Local injection of steroids for resistant cases
§ Operative: removal of calcific deposit or decompression of affected tendon or ligament
o Erosive arthritis
§ Treatment as for OA
• Shoulder: synovectomy and soft tissue repair
• Hip: THA
4.
Metabolic
Conditions
1. General Information
• Bone Types
o Woven – immature bone where collagen fibers are arranged haphazardly
o Lamellar – mature bone where collagen fibers arranged parallel to each other
§ Compact (Cortical): Found where support matters most: outer walls of all bones (esp shaft of tubular bones), subchondral
plates supporting articular cartilage
§ Cancellous (Trabecular): Interior meshwork of all bones and ends of tubular bones and vertebral bodies
• Role of Vitamin D and Parathyroid hormone
o Vitamin D
§ Sources
• Diet
• Action of UV light on 7-dihydrocholesterol in skin à 25 hydroxylation in liver à 1 hydroyxlation in kidney
§ Action
• Small Intestine: Increase absorption of calcium and phosphate
• Bone: Promote osteoclastic resorption (release calcium and phosphate into blood)
o Parathyroid hormone
§ Kidney:
• Increase phosphate excretion (restrict absorption) and conserve calcium (increase reabsorption)
• Controls 1 hydroxylation of vit D metabolite
§ Bone: Promote osteoclastic resorption (release calcium and phosphate into blood)
§ Small Intestine: Indirect effect via vit D (refer to 2nd point of ‘kidney’)
2. Osteoporosis
Background
• Definition:
o Normal mineralization (qualitatively normal)
o Decrease bone mass per unit volume (quantitatively deficient)
o Weakening of microarchitectural structure of bone
o WHO Definition (1994): Bone mineral density > 2.5 SD below the mean seen in peak bone mass of young (25-30) normal subjects
(T-score ≤ -2.5SD)
• Pathogenesis of osteoporosis
o Loss of balance between bone resorption and bone formation
§ Bone matrix manufactured by osteoblasts. Bone resorption by osteoclasts.
o Each cyle of remodelling takes abt 4-6 mnths. Annual rate of turnover is abt 4% for cortical and 25% for trabecular bone.
§ Bone loss occurs within 2weeks; bone formation takes 3 months
174
o Normal physiology:
§ Between puberty and 30 years: Bone density increases (haversian canals and intertrabecular spaces filled in and cortices
increase in overall thickness) at about 3% per year
and peaks during 3rd decade
§ From 30 years onwards: Slow loss (haversian spaces
enlarge, trabeculae thin, endosteal surface resorbed,
medullary space expands
• 0.3% per year in men
• 0.5% per year in women till menopause
o From onset of menopause (and for next
10 years): bone loss of 3%/yr due to
decrease is oestrogen.
§ Age 65-70: Rate of bone loss tails off to approx 0.5%
per year
§ Wolff’s law - Bone is deposited and resorbed in
accordance with the stresses placed upon it.
o Estimated that half of all women and 1/3 of men will sustain
a fragility fracture in their lifetimes
• Scoring
o BMD T Score
§ Number of sds below means of peak bone mass of young healthy adults (based on BMD of 25yo Caucasian females)
• Normal: > -1
• Osteopenia: between -1 and -2.5
• Osteoporosis: <-2.5
• Severe osteoporosis: <-2.5 + fragility #
o Z Score: Number of standard deviations below average person of the same age
o Normal Z score, abnormal T score à Primary osteoporosis
o Abnormal Z and T scores à Secondary osteoporosis
• Classification
o Site: Generalised vs Localised
o Pathology: Primary vs Secondary
o Congenital
§ Osteogenesis imperfecta
§ Neuromuscular diseases and dystrophies Osteoporosis
§ Gonadal dysgenesis
§ Trisomy 18, 13-15
§ Ehlers Danlos Syndrome
§ Inborn errors of metabolism
o Acquired Primary
Secondary
§ Endocrine
• Hypogonadism
• Adrenal cortical (Adrenal cortical
hyperplasia or neoplasm, Addison’s
dz) Postmenopausal
Senile
Congenital
Acquired
• Pituitary (Cushing’s syndrome,
acromegaly)
• Thyroid (hyperthyroidism)
• Hyperparathyroidism
§ Pancreatic (Diabetes mellitus)
§ Disuse atrophy
§ Nutritional deficiency (Vit C, protein, calcium deficiency, malnutrition)
§ Liver disease
§ Iatrogenic (Steroid therapy, heparin)
• Risk Factors
o Non-modifiable
§ Race: Caucasoid / Asiatic
§ Family history of osteoporosis/ fragility fracture
§ History of anorexia nervosa and amenorrhea
§ Low peak bone mass in early adulthood
§ Estrogen exposure related
• Early onset of menopause (<45yo)
• Early oophorectomy
§ Previous adult # history
o Modifiable
§ Dietary insufficiency
§ Alcohol abuse and Cigarette smoking: both assoc w nutritional deficits
§ Chronic lack of exercise/ immobilisation
§ Drugs: Corticosteroids, thyroxine, anticonvulsants
§ Lifelong low calcium intake (<500mg/day)
§ Comorbidities: hyperthyroidism, hyperPTHism, cushings syndrome, liver disease, COPD, CRF, RA, organ transplant etc
§ Weight: lean ppl predisposed to osteoporosis
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• Clinical Features
o Mostly asymptomatic
o Fragility fractures:
§ Vertebral compression #
• Compression # of vertebrae
• Back pain
• Increased thoracolumbar kyphosis (Dowager hump)
• Diminished height
§ Hip #: Neck, intertrochanteric, subtrochanteric #s
§ Forearm # (esp distal radius -Colles)
§ Pubic rami
§ Humeral head
• Screening
o Indications
§ Individuals with prior fragility fractures during adulthood
§ Radiological evidence of osteopenia or vertebral deformity
§ Patients w strong RF
§ High risk postmenopausal women as categorized by OSTA
§ Women who are considering prevention therapy for osteoporosis
§ Monitoring of Rx
o US National Osteoporosis Foundation (NOF) guidelines (Uses age as the criterion)
§ Recommends BMD testing in all women over the age of 65 years
§ Recommends BMD testing in postmenopausal women under 65 yrs of age with risk factors for hip fracture:
• History of previous fractures as an adult
• Family history of fragility fracture
• Body weight < 57kg
• Cigarette smoking
o Osteoporosis Self Assessment Tool for Asians (OSTA):
§ Use weight and age to stratify risk: age – weight = x
• If x>20: measure BMD
• If x 0-20, measure if other RF present
• If x<-20: low risk, don’t need to measure unless +ve hx of fragility fracture
o Frequency of screening
§ Women with osteoporosis: Yearly (monitor
progression or treatment outcome)
§ Women with osteopenia: Every 2 years
§ Normal BMD: Every 2-5 years (for peri/post
menopausal women)
o Method: Dual Energy X-ray Absorptiometry
o Criteria
• Investigations
o BMD
§ Indications
§ Methods
• Dual Energy X-ray Absorptiometry; DEXA (Gold standard)
o Rationale for dual energy: to take XR of soft tissues and of bone at different penetrance lvls
o DEXA of hip for diagnosis, spine for monitoring of treatment
§ DEXA of lumbar spine preferred site for monitoring therapeutic response as largest chances in BMD with
treatment occur at this site
• Other rarely done investigations: quantitative U/S heel/ tibia, quantitative CT scan, Single-energy x-ray absorptiometry
§ Criteria
o X-rays
§ Picture frame vertebrae–accentuation of cortical outline
§ Increased concavity of endplates
§ Vertical trabeculae bears the most weight of stress hence disappears last
• Osteoporosis got prominent vertical trabeculae but no horizontal.
§ Codfish appearnace of vertebrae due to concave end-plates
§ Pathological fractures – vertebral compression fracture (ant height of
vertebrae is 80% or less of the posterior height)
• If multiple of spine -> Dowager’s hump
§ Singh’s index for trabeculae at hip jnt/ femoral neck fractures: radiographic
measurement of osteoposis (grade I only one present to grade VI all
present)
• Grade 1: principal compressive trabeculae are markedly reduced in
number and are no longer prominent
• Grade 2: only principal compressive trabeculae stand out
prominently, remaining trabeculae have been absorbed
• Grade 3: a break in the continuity of the principal tensile trabeculae opp e greater trochanter à definite osteoporosis
• Grade 4: principal tensile trabeculae are markedly â but can still be traced from lat cortex to upp pt of the femoral neck
• Grade 5: principal tensile & principal compressive trabeculae is accentuated
• Grade 6: all normal trabecular groups are visible, upper end of femur completely occupied by cancellous bone
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o Bloods:
§ Calcium and phosphate levels NORMAL in osteoporosis, low in osteomalacia
§ FBC, ESR, UECr, VitD
§ Others if susepect underlying assoc disease: TFT; LFT; Tumor markers and myeloma screen (FBC, ESR, bone marrow
aspiration, urine electrophoresis, skull X-ray)
• Management
Management
Underlying
Cause:
Osteoporosis
For
Secondary
Fractures
Osteoporosis
Non-‐
Pharmacological
pharmacological
BMD T-score Action
>+1 Re-BMD in 5y
1 to -1 Re-BMD in 2y
-1 to -2.5 Medical prevention, F/U BMD @ >1yr
Prophylactic
Definitive
< -2.5 + fragility fracture Medical treatment, F/U BMD @ >1yr
PRIMARY OSTEOPOROSIS
Post-Menopausal
• Pathology:
o Increased bone resorption due to withdrawal of estrogen which restricts osteoclastic activity
o Accelerated rate of bone loss (about 3% per year) compared to 0.3% during preceding decade
• Distinctive Clinical Features
o Only affects women
o Onset around menopause
Senile Osteoporosis
• Pathology: Gradual slowdown in osteoblastic activity
• Increased risk factors:
o For osteoporosis: Dietary insufficiency, lack of sunlight exposure, muscular atrophy
o For fractures: Preceding post-menopausal osteoporosis, predisposition to falls, concomitant osteomalacia
SECONDARY OSTEOPOROSIS
Hypercotisonism
• Pathology: Endogenous Cushing’s disease or glucocorticoid overload
• Mechanism: Suppress osteoblast function, reduce calcium absorption, increase calcium excretion
Gonadal Hormone Insufficiency
• Conditions: Oophrectomy, Turner’s syndrome, ovarian agenesis, amenorroeic femal athletes, anorexia nervosa
• Mechanism: Decreased estrogen to limit osteoclast activity
Hyperthyroidismà Mechanism: Increase rate of formation and resorption; but extent of resorption increase greater
Multiple myeloma and carcinomatosis à Mechanism: Overproduction of local osteoclast-activating factors
Alcohol abuse à Mechanism: Decreased calcium absorption, liver failure, toxic effect on osteoblast function
178
Clinical Varieties
• Vitamin D Deficiency
o Dietary lack
o Under-exposure to sunlight
o Malabsorption
• Vitamin D Metabolites Deficiency
o Reduced conversion to active metabolite (liver and kidney disease)
o Increased breakdown of active metabolite
• Hypophosphataemic Rickets and Osteomalacia (impaired renal tubular reabsorption of phosphate where calcium levels normal but
bone mineralization defective) – managed with phosphate and vit D
o Familial Hypophosphatemic Rickets / Vit D Resistant Rickets
§ Excessive urinary excretion of phosphate
§ Postulated mutation that results in failure to inactivate normally synthesized phosphatonin which then exerts
unrestrained action on kidney tubules à excessive phosphate loss
§ Symptoms: Growth lag, knee deformities
o Adult-onset Hypophosphatemia
§ Cause of unexplained bone loss in adults
o Osteogenic Osteomalacia
§ Induced by tumours: Vascular tumours, fibrohistiocytic lesions (GCT, PVNS)
4. Hyperparathyroidism
Pathology
• Biochemical Changes
o Hypercalcemia: Increased tubular absorption, intestinal absorption, bone resorption
o Hypercalciuria: Increased glomerular filtration (despite increased tubular reabsorption)
o Hyperphosphaturia: Suppressed tubular reabsorption
• Clinical features:
o Kidney: Calcinosis, stone formation, recurrent infection, impaired function
o Soft tissue: Calcification
o Bone
§ Osteoporosis
§ Osteitis fibrosa cystica: Replacement of marrow spaces by vascular granulations and fibrous tissue
§ Brown tumour:
• Arises due to excessive osteoclast activity
• Contents: Fibrous tissue, woven bone, supporting vasculature
Primary Hyperparathyroidism
• Cause: Solitary adenoma
• Clinical features
o Hypercalcemia: Anorexia, nausea, abdominal pain, fatigue, muscle weakness, polyuria, kidney stones, nephrocalcinosis
o Joint symptoms: Chondrocalcinosis
o Bone: Minority; and even so it is usually osteoporosis ONLY
• X-ray
o Pathognomonic feature: Subperiosteal cortical resorption of middle phalanges
o Osteoporosis (may have vertebral collapse and cortical erosion)
o Brown tumours
• Biochemical
o Hypercalcaemia
o Hypophosphatemia
o Raised PTH (other causes of hypercalcemia like multiple myeloma, metastasis usually have lowered PTH)
• Management
o Conservative (Usual): Hydration, decreased calcium intake
o Surgery: Parathyroidectomy
Secondary Hyperparathyroidism
• Cause: Parathyroid oversecretion in response to chronic hypocalcemia
• Etiology
o Kidney failure
o Calcium deficiency
o Impaired phosphate breakdown
o Vit D disorders
• Biochemical
o Phosphate
§ High – Kidney failure
§ Low – Absorption problems
Tertiary Hyperparathyroidism
• Cause: Secondary hyperplasia leading to autonomous activity
179
5. Renal Osteodystrophy
• Pathology: Combination of rickets/osteomalacia, secondary hyperparathyroidism, osteoporosis
• Mechanism (due to renal failure)
o Phosphate retention: Phosphate complexes with calcium to form insoluble calcium phosphate, reducing calcium levels
o Decreased 1 hydroxylation of Vit D: Decreased vit D activity
• X-ray
o Widened, irregular or even displaced epiphyseal plates
o Osteosclerosis (mainly in axial skeleton) – may produce ‘rugger jersey’ appearance of alternating bands of increased and
decreased bone density
• Biochemical
o Low serum calcium
o High serum phosphate
o High alkaline phosphatase
o Decreased urinary calcium and phosphate
5. Genetic Disorders
1. General Information
• Classification
o Disorders of cartilage and bone growth
§ Physeal and Metaphyseal: Hereditary multiple exostosis, Dyschondroplasia
§ Epiphyseal
§ Metaphyseal and diaphyseal
§ Mixed
o Connective tissue disorders
§ Marfan’s
§ Ehlers-Danlos Syndrome
§ Osteogenesis Imperfecta
o Storage disorders and other metabolic defects
o Chromosome Disorders
180
2. Hereditary Multiple Exostosis (Diaphyseal Aclasis/ Osteochondromatosis) – refer to bone tumour
3. Dyschondroplasia (Enchondromatosis/Ollier’s Disease)
• Pathology
o Defective transformation of physeal cartilage columns into bone
o Embryonal disorder ( not inherited)
• Clinical features
o Usually unilateral
o Signs and Symptoms
§ Deformities (Bone grows bent): femur or tibia bowing, valgus/varus knee or ankle etc
§ Multiple enchondromata at fingers or toes – may undergo malignant change
• X-Ray
o Radiolucent streaking extending from physis into metaphysis
o Multiple enchondromata at fingers or toes
• Maffucci’s Syndrome: Multiple enchondromas + haemangiomas of skin and viscera
o Associated with higher risk of malignant change
4. Marfan’s Syndrome
• Pathology
o Generalised disorder affecting skeleton, ligaments, eyes, CVS structures
o Due to cross linkage defect in collagen and elastin
o Autosomal dominant inheritance
• Clinical Features
o Appearance: Tall, disproportionately long legs and arms, pectus excavatum, arachnodactyly
o Spine: Scoliosis, spondylolisthesis
o Joint laxity: flat feet, dislocation of patella or shoulder
o Eyes: Lens dislocation, retinal detachment
o CVS: Aortic aneurysm, mitral or aortic incompetence
o Others: SCFE, High arched palate, hernias
5. Ehlers Danlos Syndrome
• Pathology
o Abnormality of elastin and collagen formation
o Manifestation: Skin laxity, joint hypermobility, vascular fragility
• Clinical Features
o Hypotonia
o Joint laxity: Recurrent dislocation
o Skin: Soft, hyperextensible and easily damaged
o Vascular fragility: Spontaneous bruising
o Scoliosis
6. Osteogenesis Imperfecta (Brittle bones)
• Pathology
o Heritable connective tissue disorder (Abnormal synthesis and structural defects of type I collagen)
o 2-3 new cases per yr in Sg (25% sporadic mutations, 75% inherited)
o Affects: Bones, teeth, ligaments, sclera, skin
• Clinical Features
o Bone fragility, osteopenia, recurrent #s
§ Fractures heal with florid callus producing lumps and deformities
o Ligament laxity
o Dentinogenesis imperfecta (crumbling teeth)
Type I Most common, mildest (structure of collagen normal, but low quantity)
Little or no bone deformity, but fragile (prone to #s, cracked teeth / cavities)
Blue sclera
Type II Most severe (collagen structure defect)
Bones break while fetus is in the womb à many infants don’t survive
Type III Improperly formed collagen
Infant often born with #s
+ / - Blue sclera
Shorter than average
Spinal deformities, respi complications, brittle teeth
Type IV Moderately severe, improperly formed collagen
No blue sclera
Bone deformities mild to moderate
• X-Ray
o Generalised osteopenia: Thinning of long bones, fractures in various stages of healing, vertebral compression, spinal deformity
7. Neurofibromatosis
• NF1 (aka Recklinghausen’s Disease)
o Inheritance: Autosomal dominant – NF1 genes on Ch17 and 22
o Clinical Features:
§ Neurofibromata (Schwann cell tumours)
§ Café-au-lait spots
181
§ Single large plexiform neurofibroma
§ Spine
• Scoliosis – very sharp, short curve
• Localised vertebral abnormalities: Scalloping of posterior aspects of vertebral bodies, erosion of pedicles, intervertebral
foraminal enlargment
• Dystrophic spinal deformities: Deformities of cervical spine
• Dumbell lesions of spine
§ Eye: Lisch nodules (pigmented spots on iris)
§ Tibia: Dysplasia and pseudoarthrosis
§ Malignant change
• NF2: Associated with intracranial lesions like acoustic neuromas and meningiomas
6. Osteochondritis
Definition: Group of conditions in which there is compression, fragmentation or separation of small segment of articular cartilage and bone
Features
• Pathology
o Ischemic necrosis
o Reactive vascularity
o Osteogenesis in surrounding bone
• Symptoms
o Pain
o Limit ROM
o Swelling
o Joint locking (esp for splitting osteochondritis)
Note: No signs of inflammation
Risk Factors
• Adolescents and young adults
• Trauma: Physical activity, repetitive stress
• Vascular coagulopathy
Types
• Crushing: Impact injuries cause bleeding/edema in subarticular bone, resulting in capillary compression, thrombosis and localized ischemia
o Freiberg’s disease (metatarsal)
o Kohler’s disease (navicular)
o Kienbock’s disease (lunate)
o Panner’s disease (capitulum)
o Scheuermann’s disease (vertebra)
• Splitting (Osteochondritis dissecans): Osteoarticular fractures can cause severance of local blood supply and separation of a necrotic
osteochondral fragment
o Lateral surface of medial femoral condyle in knee
o Anteromedial corner of talus in ankle
o Superomedial part of femoral head
o Capitulum
o First metatarsal head
• Pulling (Traction apophysistis): Traction injuries may damage blood supply to apophysis
o Osgood Schlatter’s disease (tibial tuberosity)
o Sever’s disease (calcaneal apophysis)
182
7.
Bone
Tumours
FACTORS IN ASSESSMENT
1. Age of patient – Young (<30) vs Old (>30)
a. Malignancy commoner in adults (except osteosarcoma
and Ewing’s sarcoma in young)
b. ***NOTE: Osteosarcoma has bimodal distribution; occurs in elderly because of Paget’s disease
c. NOTE MCQ: child w cystic lesion at epiphysis of long bone, most likely diagnosis is osteoblastoma
2. Location in long bones
a. Epiphysis
i. Young: Chondroblastoma, infection
ii. Over 20: GCT
iii. Older: Geode
b. Metaphysis: Osteosarcoma (esp knee and proximal humerus), non-ossifying fibroma (cortex), SBC, ABC, GCT (proximal tibia, distal
radius, distal femur), osteochondroma, chondromyxoid fibroma, chondrosarcoma, infections
c. Diaphysis: Ewing’s sarcoma, fibrous dysplasia, osteoblastoma
d. Non-specific: enchondroma, osteoid osteoma, metastatic
3. Location of lesion in skeleton
a. Finger: Enchondroma
b. Calcaneum: GCT
c. Spine: ABC, GCT, Multiple myeloma, mets (note that disc space not eroded in spinal mets)
d. Pelvis: Mets
e. Flat bones: Chondrosarcoma, Ewing’s sarcoma
f. Skull: Multiple myeloma
g. Red marrow populated areas: multiple myeloma, metastatic
h. Cartilage cap of osteochondroma OR central medullary: chondrosarcoma
4. Morphology – Malignant looking vs Benign looking
a. Transition zone: Applies only to osteolytic lesions
i. Narrow zone: Benign
ii. Broad zone: Malignant
b. Periosteal reaction: Left to right à Solid, lamellated, spiculated (sunburst), Codman’s
183
c. Soft tissue mass
d. Cortical destruction
5. Single vs Multiple
a. Commonly mutiple: Metastasis, multiple myeloma, osteochondromatosis (multiple exostosis), enchondromas (Maffucci syndrome)
CLASSIFICATION
Epiphysis Metaphysis Diaphysis
Young Benign Malignant Benign Malignant Benign Malignant
(<20) Chondroblastoma SBC (simple bone cyst) Osteosarcoma Osteoid osteoma Ewing’s
Infection Non-ossifying fibroma sarcoma
Enchondroma (arise at puberty,
presents ~30yo)
Osteochondroma
Osteoid osteoma
Adult (20- Benign Malignant Benign Malignant Benign Malignant
40) GCT ABC (aneurysmal bone cyst) Osteoid osteoma
GCT (to epiphysis)
Enchondroma
Osteoid osteoma (<30)
Middle/ Benign Malignant Benign Malignant Benign Malignant
elderly Geode Osteosarcoma (~50yo)
(>40) (degen cyst) Chondrosarcoma
Multiple myeloma (solitary
type/non-specific)
NOTE: consider 1)infections, 2)metastasis from primary sites esp in older age groups
• Head and neck: thyroid, NPC
• Thorax: breast, lung
• Abdomen: kidneys, GIT (except rectum), prostate, testes
*Midline & paired structures
*Most are osteolytic except prostatic CA (blastic) & breast (blastic & lytic
Malignant bone tumours by frequency: 1) metastatic 2) multiple myeloma 3) osteosarcoma 4) chondrosarcoma 5) ewing’s sarcoma
184
TREATMENT
Intra-compartmental Extra-compartmental
Low grade Wide excision (w/o exposing tumour) Radical incision +/- bone graft or prosthetic replacement
High grade Radical incision and prosthetic replacement or
amputation +/- chemo to reduce risk of mets
1. Osteosarcoma: neoadjuvant chemotherapy given before surgical resection
2. Mets (ELDERLY)
a. Wheelchair and admit patient (avoid weight bearing) – even if not yet fractured; fracture risk
b. Possible differential infection
Fibrous Dysplasia
• Pathology
o Developmental disorder in which trabecular bone is replaced by fibrous tissue containing flecks of osteoid and woven bone
• Clinical Features (mono or polyostotic)
o Pathological Fractures
o Deformities
o Albright’s syndrome: Café-au-lait spots, precocious sexual development in girls
o Malignant transformation: 5-10% in patients with polyostotic lesions
• X-Ray
o ‘Ground glass’ cystic lesions in metaphysis or shaft
o Shepherd’s crook deformity of proximal femur
Osteosarcoma risk factors PRIMARY: Paget's, Radiation, Infaction of bone, Male, Alcohol, poor diet, sedentary lifestyle [adults only]
Retinoblastoma, Li-Fraumeni syndrome, Young [10-20 yrs].
Osteosarcoma is the most common primary malignant tumor of bone.
185
Osteochondroma
Pathophysiology
• Lump that sticks out of bone, mainly cancellous bone with a covering of cortical bone and a cartilaginous cap
• Derived from small pieces of metaphyseal cartilage which were not remodelled during growth of bone and have become separated from the
main cartilaginous epiphyseal plate
• Continue to grow and ossify and produce a bony knob just above the epiphyseal line, sometimes have an adventitious bursa over their cap
• Usually single, may be congenital and multiple
On inspection, I note a ___ by ___ cm spherical lump over the medial aspect of the (left / right) knee. There are no overlying skin changes or
scars noted in the surrounding skin. The surface is smooth, edges are distinct and the lump feels bony hard (can be masked by soft, fluctuant bursa
overlying cap). It is non-tender and not warmth to touch. The overlying skin is not attached to the lump; it is attached to the deep structures and is
not freely mobile. (move joint and feel)
• Excise if symptomatic, recent á in size + pain (malignant • Remove if troublesome + start to grow after parent bone
change) stops growing
Management
• Risk of malignant change: esp with pelvic exostoses (may • Risk of malignant change: 6% for multiple lesions
go unnoticed for long periods even with enlargement); 1%
for solitary lesions
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187
188
8.
Diabetic
Foot
Epidemiology
• Prevalence of 12% (no sex prevalence; malays>Indians>chinese)
• 5% develop foot ulcers
o Mortality: 10% at amputation, 30% within 1 year, 70% within 5 years
Pathogenesis
• Neuropathy (20-40% of all diabetics)
o Sensory: Glove and stocking sensory distribution (hands and feet)
o Motor – Clawing of toes
o Autonomic – Dryness of skin
• Vasculopathy
o Macrovascular (Peripheral Vascular Disease)
§ Atherosclerosis: Involve large/medium sized arteries (eg. dorsalis pedis,
posterior tibial)
o Microvascular (Microangiopathy)
§ Thickening of basement membrane of terminal arteriole endothelium
§ Pulses can be normal but gangrene taking place because of microangiopathy
• Immunopathy
o Susceptibility to infection due to defective leukocyte function and renal failure
o Exact mechanism unknown but postulated decrease in leukocyte phagocytosis and chemotaxis
o Pathogens involved (commonest 2 are staph aureus and pseudomonas aeruginosa)
§ Predominantly GPC: Staph aureus, Group A strep pyogenes, Group B strep agalactiae, MRSA, coagulase –ve staph like
epidermidis, enterococci, corynebacterium
• Staph a/w increased risk of mortality!
§ Followed by gram negative rods and anaerobes
• GNR: Pseudomonas aeruginosa, E. coli, Proteus vulagris
• Anaerobes: Bacteroides fragilis, peptostreptococcus
§ à prior use of ABx predisposes to MRSA and Pseudomonas
o Mild (monomicrobial) infections and severe (polymicrobial; a/w osteomyelitis) infections dominated by gram positive cocci
o Diabetics covered with Augmentin (amoxicillin + clavulanate)
Presentations of Diabetic Foot
• Ulcer (neuropathic, vascular, decubitus –pressure ulcer): commonest complaint
• Cellulitis: IMPT TO DIFFERENTIATE FROM NECROTISING FASCIITIS
• Gangrene: Dry, Wet
• Infection
o Osteomyelitis: Metatarsals, Phalanges
o Septic Arthritis: MTPJ, PIPJ
o Abscess: supf or deep
• Charcot Joint Disease
o Pathology: Degeneration of foot joints due to damage sustained from loss of proprioception
o Increased size of foot
o Rocker bottom deformity (severe)
o Often unilateral but can be bilateral
• Necrotising Fasciitis
History
• Biodata
o Age: Mainly in 5th to 6th decades of life
o Race: Malays and Indians have higher incidence than Chinese
o Socio-economic status: DM foot affects lower socioeconomic group (Malays, education up to secondary school, average monthly
household income <2000SGD)
o Occupation: high risk jobs like housewife, taxi driver, manual labourer, factory workers wearing safety boots
• Presenting complaint: ulcer/ abscess/ gangrene, pain/ swollen/ infection
o General questions about CPC
§ Lesion: when, how, what he was doing
§ Precipitating injuries: trauma (when, how, what you were doing), foreign body penetration (eg. rusty nails), pressure
§ Discovery of lesion: when and how
• If not discovered at point of injury, why? Numbness (check for neuropathic conditions if no pain), weakness?
§ Type of wound: open/closed, bleeding
§ Progression of injury: grew bigger, more painful, discharge, gangrene
§ 1st episode? Any previous injuries of similar nature? Ask for poor wound healing
§ Footwear (ill-fitting shoes, slippers, barefeet)
§ Functional impairment
o Ulcer
§ Site
• Ischemic: Dorsum foot, 1st web space, heel, toes
• Neuropathic: Sole of foot, pulp of toe
• Decubitus: Heel, lateral aspect base of 5th metatarsal
§ Size
§ Pain
• Painful: Infective, Ischemic
• No pain: Neuropathic
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§ Presence of Pus (Note colour and odour)
§ Differentiating between vascular and
neurogenic Organism Colour Smell Abx
• Vascular: Punched out, Gangrene, Staph aureus Brownish Little smell Cloxacillin
Ischemic limb symptoms Bacteroides fragilis Feacal smell
• Neurogenic: Painless, Deformed joints, P. aeruginosa Greenish Rotten fruit smell Ciprofloxacin
Loss of sensation (vibration, proprioception)
o Gangrene
§ Site: Toes, forefoot, heel
§ Type: dry or wet
§ Other symptoms of ischemia: claudication, rest pain, cold extremities, discolouration
o Swelling
§ Abscess: Acute onset, painful, red, warm
§ Septic arthritis: must rule out deep osteomyelitis!
• Joints: MTP, PIP
• Symptoms of inflamm (red, hot, swollen, pain, loss of function) + Severe limitation in joint ROM
• Difficulty in walking
§ Associated fever, chills, rigors (absent in 80% of elderly; and likely to be immunopathic too)
o Charcot’s arthropathy: Weakness, difficulty walking, deformity
o Pain: SOCRATES
§ Infection
§ Ischemia – In gangrene, pain felt at junction of living and dead tissue
• Vascular claudication
o Pain in calf (usu described as a cramp)
o Brought on by exercising (claudication distance) and relieved by rest – especially rest while standing because
column of blood above site of compromised supply exerts pressure and facilitates perfusion
o Not common in diabetic foot
• Rest pain
o Continuous severe aching pain due to severe ischemia
o Usually at most distal part of limb (toes and forefoot)
o Difficulty in walking
o Night pain affecting sleep à Hangs leg over side of bed (below level of heart); Prefer to sleep in sitting position
o Begs for amputation
• Medical History
o Medication/Treatment
§ Self Treatment: Cutting callosity (w unsterile scissors, rusty blades), digging of nails
§ TCM: Malays – Coffee powder, Indians – Turmeric, Chinese – Sinseh powder (skin burns à ulceration à sepsis)
§ Foot reflexology, massage chairs
o Medical Conditions
§ Type II DM > Type 1
• Diagnosis: when, how, how long
• Treatment: diet, OHGA, insulin, combinations + dosage/med changes
• Control:
o Follow-ups, past hospitalisations for DM, any Sx done (DKA, HHNK, abscess, ulcer, gangrene etc?
o Medicine compliance
o Symptoms of poor control: Polyuria, Polydypsia, Polyphagia
o Monitoring of DM: Hypocount, HbA1C usual values? How often f/u? doctor say good control?
• Complications (usually approx 20 years): Ask for symptoms and screening, and duration of Cx
o Macrovascular
§ Coronary artery disease: IHD (chest pain, SOB), AMI, cardiomyopathy
§ Cerebrovascular accident: Transient ischemia attack, stroke
§ PVD: parasthesia, intermitten claudication, pallor, poor wound healing
o Microvascular
§ Retinopathy: blurring, cataract, previous laser PRP
§ Nephropathy à Chronic renal failure (bubbly urine, sallow appearance), 24hr urine test CCT, UTP
§ Neuropathy – Glove and stocking disturbance (numbeness, parasthesia, loss of proprioception), motor
(weakness), autonomic (postural hypotension, gastroparesis, diarrhea, impotence)
*Note: CRF + DM: Worst combination
§ Other Co-Morbidities: Hypertension (worsen atherosclerosis; increased risk of major amputation), Hyperlipidemia, IHD, CVA
• Family History: DM in parents/siblings as well as their life span
• Social History
o Footwear
§ 70% wear slippers or sandals for outdoor use
§ Appropriate footwear must cover all toes, foot and heel
o Smoking
o Functional status (ADL): important for prognosis
§ Walking ability: Community walker, Housebound, Unable to walk
§ Able to do household chores (esp cooking)
§ How does the current orthopedic problem affect the patient’s function in general?
§ Occupation: High risk jobs: Cook, housewife, taxi driver, factory worker wearing safety boots
o Care-giver Profile: Spouse, sibling, domestic help
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Examination of the Diabetic Foot
The preliminaries: Introduce yourself to patient, ask for permission to examine. Ensure adequate exposure (at least til mid thigh) but consider
patient modesty also. Ensure good lighting, and good positioning of bed.
The examination of a diabetic patient is to elicit signs in the following 4 aspects: 1) Neuropathy 2) Vasculopathy 3) Immunopathy 4) Dermopathy
GENERAL EXAMINATION -- Start with GE before moving to local examination of the foot:
General Inspection
- Well or toxic looking (RR, comfortable?), Kussmaul breathing (ketoacidosis)?
- Mental state – alert, oriented or drowsy (hypoglycemia)
- Dehydration – furrowed tongue, dry mucosa, sunken eyes
- Skin: scars, sinuses, healed wounds, sallow (RF)
- Eyes: conjunctival pallor, cataract, sunken (dehydration), Fundoscopy for diabetic retinopathy
Volunteer to check vitals
- Temperature – fever suggests sepsis
- BP – both sides, postural hypotension
- Hypocount
- PR
- RR
Quick general examination
- Locate apex beat (exclude cardiomegaly, which may point to CVS problem for the feet)
- CVS, respiratory (infx), abdomen (hepatic abscess, AAA) screen
LOCAL EXAMINATION
General examination
- Generally: scars, sinus, healed wounds, muscle wasting (motor neuropathy)
- Deformity:
Ø Charcot’s joint – other causes include leprosy, syphilis:
§ Enlargement of the affected joint (usually unilat)
§ Hypermobility of the joint
§ Warm and swollen initially, followed by crepitus in the later stages
§ Mid-tarsal joints are the most commonly affected followed by the metatarsophalangeal and ankle joint
§ Can have rocker-bottom deformity from collapse of the midfoot
Ø Mallet toes – can occur in RA as well:
§ Flexion deformity at the DIPJ of involved toes, usually the 2nd toe with no PIPJ or MTPJ involvement; caused by imbalance
btw intrinsic (lumbricals and interossei) and extrinsic (long flexors and extensors) muscles
Ø Claw toes – other causes include RA, polio, stroke:
§ Flexion deformity at the PIPJ and DIPJ which usually affect the lesser toes; due to imbalance btw intrinsic and extrinsic
muscles
Ø Others: High arch foot, Hammer toe, hallux valgus, jt subluxations
- Ulcer – must describe:
Ø 5Ss – Site (interdigital web space, dorsum, sole, heel), Size, Shape, Surrounding tissue condition (erythematous, gangrenous, necrotic,
warm, tender), Smell
Ø Inside the ulcer – Depth, Edge (vascular is punched out; irregular? Everted? Gangrenous?), Floor (pus, exudate, slough, necrotic tissue,
granulation tissue, exposed bone/ joint capsule/ tendons), foreign body
Ø Palpation – Tenderness, Discharge (squeeze surrounding skin and note qty, colour and odor of dc), Bogginess around ulcer
Ø Ask for PAIN! Painless ulcers/sores=> neuropathy
- Trophic changes (dermopathy, signs of ischemia & signs of neuropathy)
Ø Signs of PVD: Shiny, loss of hair, dusky discolouration/pale, trophic nail changes, hyperpigmentation, NO varicose veins
Ø Signs of autonomic neuropathy: dry skin/ scaling, fissuring, callosity (tips of toes, sole)
- Swelling – cellulitis, abscess à note site and size/extent
- Gangrene – wet vs dry; dusky looking? à note site and extent
- Any amputations – eg AKA, BKA
Assess for immunopathy – to exclude abscess, septic arthritis, osteomyelitis, necrotizing fasciitis
- Ulcers + discharge
- Warmth – Compare with other foot
- Tenderness – palpate foot ray by ray for osteomyelitis (MT, phalanx) from tip of toe over MT, tip of toe to Ankle joint, one Ray at a time à
dorsal surface + deep palpation of sole (pus tends to be dependent)
o Probe test: If a sterile metal probe or the gloved finger on palpation reaches bone = Osteomyelitis of Bone is present
- Move all joints – PIPJ, DIPJ, MTPJ for septic arthritis
- Look for cellulitis and document extent: impt to differentiate from necrotising fasciitis; wrinkle sign indicates subsiding cellulitis
- Gas Gangrene – Crepitus under skin
- Common DM foot infections
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- 4. Palpate all pulses: (report as palpaple/not palpable)
Ø Carotids –feel for thrill and listen for bruit
Ø Upper limb – axillary, brachial, radial, ulnar
Ø LL – dorsalis pedis (absent in 10% of population à try anterior tibial), posterior tibial, popliteal, femoral
Note: Pulses can be preserved till late in the disease due to calcification of the walls.
Vasculopathy assessment (prognostic significance for distal amputation)
- 2 pulses palpable: v good chance (80-90%) of success
- 1 pulse: fairly good (60-70%)
- 0 pulse: POOR chance à do BKA
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Investigations
• Biochemical
o Markers of Infection
§ FBC: TWC w differential count for infx (Leukocytosis, Increase in polymorphic neutrophils), Anemia
§ Acute phase reactants: ESR, CRP
o Renal panel: Assess renal function
o HbA1C (Glycosylated haemoglobin)
§ Normal: 4-7%
§ Indicator of diabetes control over last 3 months
o Hypocount monitoring 4 times daily: normal 4-8mmol/l
o Urinanalysis: Glycosuria, ketonuria (DKA), proteinuria (nephropathy)
o Hb: nutritional status (affects ulcer healing)
o For medical case: include urine dipstix, lipid profile
• Culture (blood/ ulcer swab): blood culture done for all cases even w/o fever (often no systemic response due to immopathy or old age)
o Taken before starting antibiotics
o Take pus and swab from deepest portion of ulcer to increase yield
o Gram stain + c/s (aerobic and anaerobic organisms)
• Imaging
o ECG, CXR (anaesthesia fitness)
o X-ray of foot / ankle
§ AP, lateral views
§ Osteomyelitis –osteopaenic/ rarefaction, erosions, periosteal reaction(early), cortical sclerosis(chronic)
§ Septic arthritis –widened joint space, perarticular osteoporosis(early), joint space narrowing +/- erosions (late)
§ Gas gangrene (clostridium, strep. microaerophiles) –exclude necrotizing fasciitis if gas present
§ Bony destruction (Charcot’s foot) and other neuropathic changes
§ Calcification of vessels
§ Foreign body
§
Management
• Classifications
o Wagner classification of DM foot ulcers: determines Mx à generally lower grades respond to Abx + debridement while higher grades
(2-5) require amputation
King’s College Classification Wagner’s classification
Stage Features Grade Description Treatment
Stage 1: Normal No risk factors present: 0 No ulcer in a high risk Conservative:
Foot foot education, footwear,
• Neuropathy
regular clinical and
• Ischemia
podiatry exams
• Deformity (eg. dystrophic nails)
1 Superficial ulcer Conservative:
• Callus
involving the full skin Total contact cast for
• Swelling thickness but not offloading, walking
Stage 2: High Risk One or more of 5 aforementioned risk factors present underlying tissues; no brace, special
Foot infection) footwear
Stage 3: Ulcerated • Skin breakdown and ulceration 2 Deep ulcer, penetrating Surgical debridement
Foot • Infective, ischemic or neuropathic down to ligaments and Wound care
Stage 4: Cellulitic muscle, but no bone Offloading
Foot involvement or abscess Culture specific Abx
formation
3 Deep ulcer with inf of Surgical debridement
deep tissue w pus; or partial amputation
cellulitis, deep abscess Offloading
tendinitis, osteomyelitis Culture specific Abx
Stage 5: Necrotic Gangrene (dry or wet)
Foot 4 Forefoot gangrene Lower extremity
amputation
Stage 6: Major Indications for Amputation
Vascular consultation
Amputation • Agonising pain
5 Whole foot gangrene Major extremity
• Overwhelming infection in foot
amputation
• Extensive necrosis in foot Vascular consultation
• General measures
o Hydration status:
§ IV line at least 1.5L a day to prevent dehydration
§ Intake/output charts –urine output monitoring
o Diabetic chart –hypocount TDS including 10pm (watch out for hypoglycemia)
o IV antibiotics: Broad spectrum Augmentin (GPC, GNR, anaerobes) OR Clindamycin (gram positive, anaerobes, esp for
necrotizing fasciitis) + Ciprofloxacin (gram negatives) à change to culture-specific antibiotics
o Topical antibiotics
§ BNP (bacitracin, neomycin, polymycin) powder for pseudomonas
§ Bactroban cream for MRSA
o Daily wound dressing –Chlorhexidine, flush with H2O2 and saline, then chlorhexidine dressing
o Elevate leg if swollen
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• Surgery
o Abscess: I&D
o Ulcer: radical debridement
§ All slough and exposed tendons excised else become necrotic (in heel whole part of tendoarchilles exposed excised)
§ Heel ulcer/ gangrene unless successfully resurfacedà Below Knee Amputation
o If vascular cause, consider whether amenable to bypass or not
o Dry gangrene
§ Pulses usually very bad
§ Toe may auto-amputate
§ Management: clean with ethanol, splint, dressing, prophylactic antibiotics (sides usu get infected), consider ray amputation
in young patient (better to leave it alone in older patients as it is quite easy to care for dry gangrene) +/- hyperbaric oxygen
therapy (HBOT)
o Wet gangrene à AMPUTATE
§ Types of amputation
Amputation Site
Disarticulation at jt PIP, DIP
Ray (open or closed) Through metartarsal
Open ray: for adequate drainage of pus involving 1 ray, upon
healing w healthy granulation tissue, split skin graft is used
Closed ray: if after debridement all infectious tissue has been
removed, close wound by tagging
Forefoot
Lisfranc Tarsometatarsal
Chopart’s Mid-tarsal
Syme’s (rare) Through ankle (requires good post tibial pulse)
Below knee (requires 30% more energy to walk; bilateral BKA 40%; Able to
fit patella tendon bearing prosthesis)
Stokes-Gritti Through knee
Above knee (Requires 40% more energy to walk)
Hip disarticulation
Hindquarter Hemipelvectomy
• Multidisciplinary
o Case manager manages clinical pathway for DFP
§ Surgeons: orthopaedic surgeon, vascular surgeon
§ Medical: endocrinologist, Infectious diseases specialist
§ Others: podiatrist, dietitian, physiotherapist, occupational therapists, MSW
§ Nurses: diabetic nurses, wound-care nurses
§ Amputation support group
Charcot Joints
• Pathology: Progressive degeneration of a weight bearing joint resulting in deformity
• Pathophysiology
o Neurovascular theory (German): Neuropathy à loss of autonomic tone à vasodilation à increased blood supply à increased
osteoclast load to site à brittling and osteopenia à collapse
o Neurotrauma theory (French): Sensory loss à abnormal movementsà repetitive trauma à inflammatory resorption of traumatized
bone à further damage (vicious cycle) à collapse
• Clinical Features
o Inflammation: erythema, pain, warmth
o Loss of protective sensation
o Rocker bottom deformity
§ Bone arches collapse + soft tissue contracture
§ Complications: callositiesà fissuresà infection
• X-ray
o Atrophic: Osteolysis
o Hypertrophic (more common)
§ Distended joint
§ Density increase
§ Debris
§ Dislocation
§ Disorganisation
§ Destruction
• Classification
o Brodsky Classification
§ Type 1: Tarsometatarsal and naviculocuneiform joints
§ Type 2: Subtalar joint
§ Type 3A: Ankle joint
§ Type 3B: Posterior calcaneal tuberosity
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o Eichenholtz Classification and management: classification, characteristics and Rx strategies for charcot foot
Grade Characteristics Treatment*
0 Clinical stage Erythema, edema, increased Limited weight bearing (possibly TCC or PPWB; prefabricated
temperature to foot; but radiographs pneumatic walking brace), close observation, Pharmacological
negative (Bisphosphonate)
1 Fragmentation stage Periarticular #s, joint dislocation, TCC (total contact cast), limited weight bearing
instability, deformed foot
2 Coalescence stage Reabsorption of bone debris TCC followed by CROW (Charcot restraint orthotic walker)
3 Reparative stage Remodelling and reorganisation Possible surgical intervention (osteotomy) for removal of bony
Stable foot prominences associated with ulceration: esp if young
Charcot’s joint song The ulcer is non tender and the surrounding skin does not feel warm.
On inspection, I note the presence of a grossly deformed ankle joint There is no discharge expressed from the ulcer.
which (is / is not) swollen, associated with a rocker bottom foot.
There is a previous amputation of the _____________________. (move the joint)
The skin around the joint is not erythematous / there are skin changes There is instability of the joint as evidenced by abnormal movements
suggestive of diabetic dermopathy. and hypermobility.
There are no scars noted. There is wasting of the intrinsic muscles of
the foot. The above findings are consistent with that of a Charcot’s joint which is
likely complicated by a neuropathic ulcer.
In addition, there is a ___ by ___ cm irregularly shaped ulcer located on
the sole. The ulcer has a regular edge, the floor consists of I would like to complete the examination by performing a neurological
_____________. The surrounding skin around the ulcer looks normal / examination of the affected limb to look for loss of sensation and joint
does not appear erythematous. There are callosities located over ____. position sense.
I would also like to palpate the pulses in the LL to determine if there is
I would like to move on to palpate the joint. (ask pt for any pain first) concurrent arterial insufficiency.
The joint is non tender and does not feel warm. There is creptius felt on I would also like to perform a urine dipstick to look for glycosuria.
passive movement of the joint. The normal contours of the joint are lost
and the joint may be subluxed or dislocated.
195
Doctors have told him / her from blood tests The (femoral / popliteal / posterior tibial / dorsalis pedis) pulse(s) is /
that kidney function is poor. are well felt on the (left / right) limb.
His / her DM is complicated by ESRF, However the (left / right) (femoral / popliteal / posterior tibial /
currently on (haemodialysis / peritoneal dorsalis pedis) pulse(s) is / are diminished.
dialysis) .
There are no significant foot deformities or signs suggestive or previous
3. Neuropathy He / she c/o (weakness of his foot / difficulty amputations of toes OR
walking / decrease in sensation / frequent There is a BKA of the (left / right) leg and there is Charcot’s foot
falls / postural hypotension / bladder or bowel deformity over the (left / right) foot, as evidenced by joint swelling,
dysfunction) since (duration) ago. rocker bottom deformity and loss of plantar arch. There is also wasting
4. PVD He c/o (claudication pain / rest pain) . of intrinsic muscles over the dorsum of foot, clawing of the (left / right)
He has previous (amputations / surgeries) toe, and overriding of the ___ toe over the ___ toe.
done in __________________.
ULCER
5. Previous CVA/ AMI Mr / Mdm XXX has a ____ x ____ cm, (shape) ulcer over the (site:
medial malleolus / heel / underneath the metatarsal heads / webspace),
6. Previous DM-related hospital admissions (sepsis (DKA), AMS
with a clean, punched-out edge.
(HHNK), hypoglycaemia)
The floor of the ulcer is (clean / dirty) and has (slough / pink
granulation tissue / exposed tendon & bone) .
(Drug History & Diabetic Drug History) The ulcer is adherent or invading deep structures such as (tendon /
He / she has NKDA and is on (insulin / OHGA) for DM control (+ periosteum / bone) .
name of drug & frequency). A (quantity) of (odour: foul smelling) , (colour: serous /
Mr / Mdm XXX (is / is not) compliant with his / her medications and serosanguinous / purulent) discharge was noted.
has no SE of medications / complications of treatment such as
(hypoglycaemia / lipodystrophy / infection at injection site / weight gain) GANGRENE
. Mr / Mdm XXX has (dry / wet) gangrene noted over (site) .There is
There (has been no / has been) recent adjustment to his medication. a clear line of demarcation at the (site) .
He / she is also on (other drugs) for (other comorbidities) . It is a/w a (quantity) of (odour: foul smelling) , (colour: serous /
serosanguinous / purulent) discharge.
(Follow-up, Control and Lifestyle Management) There (is / is no) associated erythema and / or (generalised /
He / she is on regular ___-monthly follow-up at the (polyclinic / GP) discrete) swelling in the surrounding skin over the foot extending up to
and his recent HbA1c is _____. the _____________.
He / she was told by his / her doctor that his / her control is (sub- However / in addition, I note that there are scars suggesting the
optimal / good) . presence of previous ulcers.
He / she (does not perform / performs) self monitoring of blood The skin appears (pale / normal / dusky) and has signs of chronic
glucose levels at home. ischaemia such as (shininess of skin / loss of hair / trophic nail
He / she has adjusted his / her diet to ______, and he usually eats changes) . There (is no / are) signs of diabetic dermopathy as
(outside / hawker food / home-cooked food) . evidenced by the increased skin pigmentation as well as dry skin
He / she (is / is not) compliant to foot wear advice and visits the suggestive of autonomic neuropathy.
podiatrist (frequency) . There is presence of callosities over the (sole / tip of the toes / side of
the foot) .
Family History
He / she has a significant family history of Type 2 Diabetes Mellitus. PALPATION
His / her _____________ has DM diagnosed at (age) and has The foot is non-tender and does not feel warm. The capillary refill is less
passed away because of (cause of death) . than 2 seconds. OR
There is tenderness in his / her foot over the (site: 1st / 2nd / 3rd / 4th /
Social History 5th ray – distal phalanx / middle phalanx / proximal phalanx / metatarsal
He / she (does not smoke / smokes / is an ex-smoker and has quit XX bone / up to the ankle; between the rays) on superficial and deep
years ago) , ( sticks/day x years). palpation.
He / she (has / does not have) a habit of regular intake of alcoholic
drinks. MOVEMENT
He / she has (good / poor) social support. He / she works as a There is pain on movement of the (PIPj / DIPj / MTPj) .
_________ and lives with his / her ________. The ankle joint is subluxed / dislocated, with creptius (in Charcot’s foot).
His / her main caregiver is his / her ______________. There is hypermobility and instability noted on the (left / right) ankle.
He / she lives in a residential (with / without) lift landing.
Currently, the family (does not have any financial issues / is receiving NEUROLOGICAL EXAMINATION
financial aid from ) . There is glove & stocking sensory loss over the (left / right) foot. The
Semmes Weinsein Monofilament test revealed an inability to perceive
PHYSICAL EXAMINATION sensation over (1st toe / 3rd toe / 5th toe / forefoot below 1st toe /
forefoot below 3rd toe / forefoot below 5th toe / medial mid foot / lateral
On physical examination, Mr / Mdm XXX is alert n comfortable at rest. mid foot / heel / dorsum of foot between 1st & 2nd toe) , indicating loss
Appearance: He / she does not appear to be sallow, pale or of protective sensation with less than 7 sites felt by patient. There is
dehydrated. loss of vibration and proprioception over the (left / right) foot and the
Vitals: Her PR is _______, RR is _______ and BP is ankle jerk is absent.
_______. (SpO2: ______; VAS: _____.)
Heart: S1S2 were heard on auscultation. Buerger’s test is positive at ____ degrees.
Lungs: Lungs are clear. In summary, Mr / Mdm XXX has diabetic foot (ulcer) with / without signs
Abdo: (look for lipodystrophy at insulin injection sites & of infection such as erythema, warmth and tenderness on palpation and
comment on absence / presence) movement over ___________. There are also signs of vasculopathy as
evidenced by pallor, coldness, prolonged capillary refill time and
Pulses: diminished ____________ pulses, associated with a positive / negative
The axillary, brachial, radial and ulnar pulses are well felt bilaterally. Buerger’s test. In addition, he / she has peripheral neuropathy as
196
evidenced by loss of pain, vibration and proprioception over _______,
with an inability to perceive ___ out of 10 pts in the monofilament test.
OR
9. Paediatric Conditions
197
TIBIAL BOWING (& PSEUDOARTHROSIS)
• Posteromedial bowing: physiological
o Clinical problem: limb-length discrepancy (treat if >/=5cm difference)
• Anteromedial bowing: deformity
o Missing cruciates
o Ankle valgus
o Tarsal coalition
o Limb-length discrepancy
• Congenital pseudoarthrosis of tibia
o Associated w NF-1
o Crawford’s classification
§ Type I – medullary canal is preserved, cortical thickening
§ Type II – thinned medullary canal, cortical thickening
§ Type III – cystic lesion, may be fractured
§ Type IV – pseudoarthrosis (tibial & fibular non-union)
o Management: circumferential brace to protect leg from fracture
o Definitive Rx: excision and reconstruction (bone transplantation using fibular graft)
CEREBRAL PALSY
• Definition
o Non-progressive insult on a dvlping brain
o The brain lesion is permanent and non-progressive, but the natural history of CP is not static
o If non-progressive insult on a dvlped brain = stroke
• Aetiology:
o Abt 10-15% of patients documental perinatal hypoxia
o CP is not solely the result of prematurity coz 60-65% of afflicted children were born at full term
o Although only abt 10% of CP patients weigh <1500g at birth, in this low birth ewight grp, the risk of having CP is 90 per 1000, compared
w 3 per 1000 if weighing >2500g and appropriate for gestational age
o Low birth weight for gestational age and prematurity are commonly a/w dvlpment of spastic diplegia
• Types
o Neuropathic types:
§ Spastic: overactive Golgi apparatus; the only one in which the ortho team can intervene
§ Other types: ataxic, athetoid, hypotonic, mixed
o Anatomic patterns: hemiplegic, diplegic, quadriplegic, total body, triplegic, monoplegic
• Management: dependent on functional assessment of child
Type Functional aim
Hemiplegic Efficient walking: supple hamstrings & TA
UL is the best position for function
Diplegic Walker
- Efficient walking
§ No crouch/ jump gait
§ No tiptoeing
§ Feet in neutral position
§ No scissoring
- Consider need for assistance if power
and control poor
- Dietary control (optimal BMI: patient
cannot bear weight if too heavy)
- All should walk!!! (if not, could be due to
poor parental support, laziness; rehab
into society would be even more difficult)
Non-walker
- Investigate reason
- If reason for inability to walk is
neurological then aims same as
quadriplegic sitter
Quadriplegic - Painless seating: seating clinic
- Spine fairly straight and stable
- Hips painless and reduced
- No pelvic tilt
- Adequate abduction for hygiene care
- Adequate knee flexion
o Areas to address
§ UL
§ Spine: paralytic scoliosis
§ Hip: paralytic subluxation/ dislocations
§ Knee: contractures, gait problems
§ Foot/ ankle: equinus, varus/valgus
o Methods
§ Conservative:
• Early intervention for stimulation
• Seating for poor trunk control
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• PhysioRx
• Orthotics
• Botulinum A toxin
o Intramuscular injection of neurotoxin produced by Clostridia bacteria
o MOA:
§ Delivered into or near sites of nerve arborisation, and blocks the release of Ach from presynaptic vesicles at
myoneural junction
§ Recovery of tone results form the sprouting of new nerve terminals, which peaks at abt 60days
o Technique:
§ To reach muscles that are deep/difficult to localize,
electromyographic guidance & electrical stimulation
can be used
§ BTX diffuses readily, so the injection shld be placed
in the muscle belly
§ Surgical: Single event multi-level surgery
• Soft tissue Sx: Post-op casting required! --------------------------à
o Only done when deformity progresses to contracture and is
not dynamic (passive ROM still possible) anymore
o CI in joints w correctable deformity
o Purpose: Sx done w functional aim in view; cosmesis only
a consideration in UL
o Tendo-archilles lengthening (done percutaneously in v young): indicated when ankle cannot be dorsiflexed to
neutral in walker
o Hamstring release: In those w v severe crouch gait and popliteal angles usually >45deg
§ Release of semitendinosus and fractional lengthening of semimembranosus and biceps femoris
o Adductor release:
§ Done for significant scissoring in walker
§ Uncorrectable tight adductor in non-walker such that perineal hygiene is compromised
§ Painful subluxed hips
• Bony Sx: Usually in older children
o When soft tissue Sx has failed w recurrence of deformity (ie. once joints are stuck/immoible)
o In areas where soft tissue Sx alone is inadequate:
§ Spine
• Paralytic scoliosis due to muscle imbalance
• Not treatable w bracing
• Seating is difficult for quadriplegics if uncorrected
§ Unstable hips
• Hips need to be reduced due to 1) pain 2) severe pelvic tilt causing secondary scoliosis 3) pressure
sores due to unequal pressure when sitting
• Not the same as DDH!
• Usualy needs open reduction +/- femoral and/or acetabular osteotomy
§ Feet: Severly deformed due to uncorrected muscle imbalance
• Usually done in the older age grp
• Many methods; principle is to correct the foot alignment
• Indicated in walkers w passively uncorrectable deformities
• Valgus feet: calcaneal shift, grice extra-articular fusion
• Tendon transfers: split posterior tibialis tendon transfer
• Bony fusion à Triple arthrodesis: salvage procedure
Paediatric Fractures
BASIC PRINCIPLES
• Presence of growth plate which gets injured before ligaments (à avulsion #s)
• Presence of secondary ossification centre – CRITOE
o Ossification starts at
§ Capitalium (1yo)
§ Internal/medial epicondyle (3yo)
§ Trochlea (5yo)
§ Olecranon (7yo)
§ External/lateral epicondyle (9yo)
• Potential for remodeling in <10yo
o Remodelling occurs 75% at physis, 25% at fracture site
o Physeal remodeling
§ Once physis is aligned, it resumes symmetrical growth
o Diaphyseal remodeling
§ Follows Wolff’s law – “form follows function”
o The closer the fracture to an active physis, the greater the
remodeling potential
• Greenstick fractures
o Definition: Break at one cortex with bending at opposite cortex
(no disruption)
o For reduction, need to complete break of other cortex
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• Buckle fractures: due to buckling of the periosteum
o Definition: Incomplete fracture resulting in
buckling/bulging of cortex
o Often due to axial compression
• Plastic deformation
• Pathological #s
• Non-accidental #s
o Specificity of skeletal trauma for abuse
§ High specificity: classic metaphyseal lesions,
posterior rib #, scapular #, spinous process #,
sternal #
§ Moderate specificity: multiple #s esp bilateral,
#s in various stages of healing, epiphyseal
separation, vertebral body # or subluxation,
digitial #, clavicular #, long-bone shaft #, linear
skull #
§ Low specificity: complex skull #
SALTER-HARRIS CLASSIFICATION
• Classification for physeal injuries: Salter Harris Classification uses visualizing long bone distal portion w diaphysis superiorly placed and
epiphysis inferiorly placed
• 5 Types (SALTR)
o Type 3-5 may result in growth disturbance due to involvement of reproductive layers of physis
o Type 2 most common
Type Description Example Basic Mx principles of physeal #s
I Straight across - Transverse # of cartilage in physis 11yo w ankle inversion injury Extra articular #s usually treated
(presents as widened epiphyseal plate) Distal fibula # w M&R; # crosses hypertrophic
II Above physis- Type 1 + triangular metaphyseal fragment Distal radius fracture zone thus wont affect growth
III Lower than physis in epiphysis - # splits through 13yo w ankle injury
epiphysis and veers off transversely to one side through Tillaux fracture Intra-articular extension
hypertrophic layer Requires anatomical reduction
IV Through metaphysis, physis and epiphysis - Type 3 + 5yo w elbow injury Usualy involves ORIF
metaphyseal involvement Lateral condylar # of humerus
V Rammed, as in a compression injury – physis crushed
PRINCIPLES OF MANAGEMENT
• All dislocation must be stably reduced ASAP
• Aim for acceptable alignment based on
o Age
o Potential for remodeling
o Plane of motion
o Fractured bone
o Fracture site: epiphysis, metaphysis, diaphysis
o Fracture personality: spiral, oblique, transverse, buckle, greenstick,
Bayonet and Salter Harris
• Reduction maintained w plaster as children less likely to get joint stiffness
• Rx usually non-surgical
o If Sx is required
§ Minimal dissection to ensure no damage to growth plate
§ Usually smooth pins used instead of plate & screws as smooth
pins produce minimal damage to growth plate & periosteum
§ Usually combined w casting postoperatively for added stability
to fixation
§ Pins inserted percutaneously where possible
FRACTURES IN ADOLESCENTS
• Tibial spine #s
o In older children/adults, more likely ACL tear (ligament < bone); but since
ligament is stronger than bone, more likely avulsion # of tibial spine (site of
attachment still has cartilaginous contact, not bone)
o Classification: Meyers & McKeever
§ Type I: minimal or no displacement
§ Type II: angular elevation of anterior portion w intact posterior hinge
§ Type III: complete displacement w or w/o rotation
• Tillaux #s
o Fracture of anterolateral distal tibial epiphysis
§ Tibal fragment avulsed fr its epiphyseal attachment due to strong anterior
tibiofibular ligament (growth plate not completely closed yet & ligament >
bone) in an external rotation injury of the foot in relation to the leg
o More unfused physeal parts = more # parts (eg. triplane # in a 12yo): surgical Rx,
w partially threaded cancellous screws
§ Multiplanar # (SH type 3 on AP, SH type 1 on lat), extends thru transverse (growth
plate), sagittal (epiphysis), and coronal (distal tibial metaphysis) anatomic planes
• Imbalance of muscle and bone growth cause tension in unfused apophysis à Tension can convert
to # during sporting activity esp in those who are heavy for their age
o Eg.
§ Tibial tuberosity (OSD)
§ Inferior pole of patella (Sindig Johanssen Larsen)
§ Apophysis of calcaneum (Sever’s syndrome)
TRAUMATIC BIRTH INJURIES
• Osteogenesis imperfect: LIFE THREATENING CONDITION à refer early
• Humerus fracture: mechanism of injury ------------------------à
• Obstetric Brachial plexus injuries (REFER to hand injuries)
• Clavicle fracture
o No intervention
o Reassure family
o Ensure no pressure on # site
o Exclude brachial plexus injury
o In the infant initially demonstrates discomfort w the fracture, the long arm sleeve of the infant’s shirt can be pinned to the shirt for 7-10
days to provide adequate immobilization
• Femur fracture: treat w pavlik harness
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10.
Bone
and
Joint
Infections
• Types:
o Acute haematogenous osteomyelitis
o Subacute haematogenous osteomyelitis
o Post-traumatic/operative osteomyelitis
o Chronic osteomyelitis
o Acute suppurative arthritis
o TB infxns of bone & joints
• Waldvagel Classification
o A – haematological spread
o B – a/w wound
o C – contiguous spread from local infection
• 3 things to consider:
o 1) type of organism
o 2) site of infection
o 3) host response (immunocompromised?)
• Principles of Rx:
o Rest affected part
o Provide analgesia and general supportive measures
o Initiate Abx Rx
o Surgical debridement (of pus and necrotic tissue)
• Osteomyelitis complications FIBRES: Fractures, Intraosseous (broidie) abscesses, Bacteremi/ Brodie abscess, Reactive amyloidosis,
Endocarditis, Sinus tracts/ Squamous cell CA
TUBERCULOSIS (uncommon)
• Common sites (wt bearing joints): Spine (50%; usually settles in vertebral body adjacent to intervertebral disc), Hip, Knees
• Main TB entities in orthopaedics: TB spondylitis, TB osteomyelitis, TB arthritis, TB tenosynovitis, TB myositis
• Pathology
o Starts as osteitis, rarely diagnosed til arthritis supervenes
o Spreads to skeleton by haematogenous seeding
o May spread to articular surfaces causing jt destruction and fibrosing ankylosis
o May spread to soft tissue to form subacute abscess, which may form a chronic discharging sinus
• Clinical features
o TB S/S: fever, wt loss, night sweats, enlarged lymph nodes etc
o Joint symptoms: chronic course (months), constant pain & stiffness, swelling, wasting, synovial thickening, ↓ROM, deformity, diffuse
warmth and tenderness
o Spine:
§ May have kyphos
§ Long history of ill health and backache
§ Local tenderness, restricted ROM
§ Pott’s Paraplegia
• Pathology: Compression of spinal cord by soft inflammatory material (abscess, caseous mass, granulation tissue) or by
hard solid material (bony sequestrum, ridge of bone at kyphos); vertebrae may collapse causing a Pott’s gibbus (usu.
thoracic)
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• S/S: Paraplegia (motor and sensory neurological signs) + aforementioned spine TB signs and symptoms
• Types
o Early onset paresis:
§ Due to pressure by abscess or bony sequestrum
§ Treatment: anterior decompression + debridement + spinal fusion
o Late onset paresis:
§ Due to increasing deformity or reactivation of disease or vascular insufficiency of cord
§ Treatment: Operative removal of necrotic tissue (if MRI shows block)
• Investigations:
o X-ray:
§ Early: soft tissue swelling, generalized rarefraction of bone, joint space narrowing & irregularities w bone erosion of jt surfaces
§ Late stages: may have cystic destruction of the joint, periarticular osteoporosis
§ Spine:
• Local osteoporosis of 2 adjacent vertebrae
• Narrowing of intervertebral space
• Fuzziness of end plates
• Collapse of adjacent vertebrae onto each other (produce angular deformity of spine)
• Paraspinal soft tissue shadows: edema, abscess
o Synovial biopsy
o Spine: Diagnosed with needle biopsy
o ESR ↑
o Mantoux test +
• Management:
o Anti-TB drugs – as for pulmonary TB (isoniazid, rifampicin, pyrazinamide - RHZ)
o Rest (rest the joint until acute symptoms settle), traction, splintage, operation
o If articular surfaces are destroyed – Immobilize joint
o Long term – Joint arthrodesis or replacement
§ Indications: repeated flares, articular surfaces extensively destroyed
o Surgical indications for spinal TB
§ Abscess formation – drainage
§ Marked bone destruction and progressive deformity – spinal fusion
§ Threatened paraplegia that does not respond to conservative treatment
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