SEMINAR ORTHOPAEDICS &

REHABILITATION
2016/2017

SEMINAR GEN 8
Compiled by ‘Aliya & Nadhirah
 HEALING
WOUND HEALING
Definition

- It is a process of replacing missing cellular structures and tissue layers following injury to the skin.
- Involves epithelial regeneration and formation of connective tissue.

Phases of wound healing

1) Hemostasis (after injury – 2days)

• Vasoconstriction
• Platelet aggregation
• Attract inflammatory cell

2) Inflammation
• Attract more inflammatory cells
- neutrophils, macrophage and lymphocyte
• Fight infection

3) Proliferative (begin to 4d – 2w)

• Formation of granulation tissues: inflammatory cells, fibroblasts and neovascularization
• 3 sub-phases:
 Epithelialization
 Fibroplasia
 Angiogenesis

4) Remodelling &Maturation (2w – 2 years)

• continuation of cellular differentiation, scar formation and scar remodelling.
• fibroblast – major cell of tissue remodelling with deposition of collagen into an organized matrix
 i. Epithelialization
• Migration of cells at the wound edge.
• Wounds epithelize faster in moist environment – dressing to maintain moisture.
ii. Fibroplasia
• Fibroblasts produce collagen, elastin and fibronectin to increase strength.
• It starts 3-5 days after injury and lasts for about 14 days.
iii. Angiogenesis
• Macrophages release macrophage-derived angiogenic factors that act as
chemoattractant for endothelial cells.
• Epithelial cells also secrete vascular endothelial growth factor.
• It results in greater blood flow  increase perfusion.

Healing by first and second intention

Abnormal healing

Factors affecting wound healing

1. Diabetes.
 Microangiopathy  impaired tissue blood flow  poor tissue oxygen delivery
 Peripheral neuropathy predisposes to tissue trauma & increase risk of infection
2. Smoking.
 Direct toxic effect
 Vasoconstriction induced by nicotine  poor blood supply
3. Nutritional deficiency.
4. Active wound infection.

BONE HEALING

Bone fracture
= break in the structural continuity of bone cortex.
Components of bone formation

• Bone marrow
• Cortex
• Periosteum; 2 layer inner; > cellular and vascular
cambium layer
outer fibrous layer
• Soft tissue

Mechanism of bone formation

1) Cutting cones
• 1º mechanism
• Leading osteoclast removes necrotic bone
• Trailing osteoblast lay down new bone

2) Intramembranous (Periosteal)
• mechanism in which long bone grows in width
• osteoblasts differentiate directly from preosteoblast to lay down osteoid
• x cartilage precursor involved

3) Endochondral
• Mechanism in which long bone grows in length
• Osteoblast line a cartilage precursorchondrocytes hypertrophied, degenerate and calcify (produces
area of low PaO2)
• Leads to vascular invasion followed by ossification.

Bone/fracture healing
Def: a complex and sequential events to restore injured bone to pre-fracture condition

1. Primary
• Direct healing – callus formation
- occurs only with absolute stability
-new bone formation occur directly between the fragment.
-Inflammatory stage is dominated by intramembraneous ossification.
Eg: i) impacted # in cancellous bone
ii) # immobilizes by metal plate

Osteoblasts originate from endothelial and perivascular cells

↓
A cutting cone is formed that crosses the fracture site
↓
Osteoblasts lay down lamellar bone behind the osteoclast forming a secondary osteon.
↓
Gradually fracture is healed by the formation of numerous secondary osteon.

*slow process: monthsyears

 # Contact healing
-direct contact with the fracture allows heling with lamellar bone immediately.

# Gap healing
-gaps <200µm : filled by lamellar bone
-gaps 200-500µm : filled by woven bone 1st then remodeled to lamellar bone

-wider gaps indirect healing

Contact healing with osteons crossing the fracture line (left)

Healing of fracture gap (right)
Woven bone fills the gap before the osteons can bridge the fracture area.

2. Secondary
• Indirect healing + callus formation
- occurs with relative stability
(presence of motion but not enough to disrupt healing)
-Eg: i) cast treatment
ii) external fixation

STAGES of bone/fracture healing

Stage 1 : hematoma / inflammation

- lasts 1–7 days post fracture.

- bone #  injures blood vessels and soft tissue disruption.
↓
hematoma formation + inflammatory exudation
↓ ↓
local vessels thrombosis soft tissues injury and
↓ degranulation of platelets
bone necrosis of release of powerful cytokines
ends of # fragment ↓
↓ produce a inflammatory response
removed by osteoclast eg; vasodilatation and hyperaemia,
migration of PMNs, macrophages
-later, hematoma will be replaced by granulation tissue

Stage 2 : soft callus formation

• Eventually, pain and swelling decrease and soft callus is formed= when the fragments are no longer
moving freely, approximately 2–3 weeks post fracture.
• Characterized by the growth of callus.
• The progenitor cells in periosteum and endosteum are stimulated to become osteoblasts.
• Bone growth forming a cuff of woven bone periosteally, and filling the intramedullary canal
• Ingrowth of capillaries into the callus and increased vascularity follows.
Stage 3 : Hard callus formation

When the fracture ends are linked together by soft callus, the hard callus
stage starts; 3–4 months post fracture
The soft tissue within the gap ossifies and the callus is converted into rigid
calcified tissue (woven bone).

Hard callus formation starts peripherally and progressively moves towards

the centre of the fracture and the fracture gap.

The initial bony bridge is formed externally or within the medullary canal,
away from the original cortex. Then, the soft tissue in the gap is ossified
and replaced by woven bone that eventually joins the original cortex.
Stage 4 : Remodelling
• The remodelling stage begins once the fracture has solidly united with woven bone.
• Conversion of woven bonelamellar bone through surface erosion and osteonal remodeling. (takes a
few months several years)
• It lasts until the bone has completely returned to its original morphology, including restoration of the
medullary canal.
• Bone is restructured in response to stress and strain (Wolff’s law).

Factors affecting bone healing

Local Factors
• Immobilization
• Infection- debris, dead tissue in the wound
• Type of bone: Faster union in flat and cancellous bone > cortical bone
• Pattern of fracture: Spiral # > oblique # > transverse # > comminuted #
• Disturbed pathoanatomy: soft tissue interposition and ischaemic # prevent faster healing.

Systemic Factors
• Age:Fractures unite faster in children
• Nutrition- vitamin/mineral deficiency
• Smoking - decreases rate of fracture healing
- inhibits growth of new blood vessels as bone is remodeled
• Immune status
• Systemic disease
• DM
• Chronic disease
• Drugs
• NSAIDs
• Blood disorder
• Hemophilia
TENDON HEALING

Introduction
Function
◦ Transfer forces from muscle to bone to produce joint movement
Types
◦ Paratenon covered tendons
◦ Rich vascular supply
◦ Eg. Patellar, Achilles tendons
◦ Sheated tendons
◦ Less vascularized
◦ Eg. Hand flexor tendons

Structure
Groups of collagen bundles (fascicles) separated by endotenon and surrounded by epitenon
◦ microfibrils<subfibrils<fibrils<fascicles<tendon unit
Blood supply
◦ the musculotendinous junction
◦ the osseotendinous junction
◦ vessels from various surrounding connective tissue

Characteristics
Contain more collagen and are less elastic then ligaments
Strength
◦ Exercise increase, immobilisation reduce
◦ Age dependent
◦ Heat can causes tendons to shrink
Tendon injury due to
◦ traumatic event
◦ Overused and aging that cause inflammation

Tendon healing process

•Platelets initiate coagulation cascade

hemostasis •Fibrin clot and fibronectin interaction leading
to chemotaxis to stabilize torn tendon edges

•Fibroblasts produce type III collagen

inflammation •macrophages help initiate healing and
remodelling

•Tissue modelling via large amounts of

organogenesis disorganized collagen and angiogenesis

•Tissue remodelling replacing type III collagen

remodelling to type I collagen

Tendon Surgical repair

Strength following repair
◦ tendon repairs are weakest at 7-10 days
◦ most of strength by 21-28 days
◦ maximum strength at 6 months
◦ final strength only reaches 2/3 of normal strength
Early mobilization
◦ allows earlier ROM but decreased tendon repair strength
SPRAIN VS STRAIN

SPRAIN

• A sprain is an injury to a ligament

• Causes: falling, twisting, or getting hit can force a joint out of its normal position
• Common sites for sprain are ankle, knee, and wrist
• Usual signs and symptoms of a sprain are: PAIN
· Swelling
· Bruising
· Not being able to move or use the joint.
Sometimes people feel a ‘pop’ when the injury happens.
• A sprain can be mild, moderate, or severe.

Classification of sprain

• Grade 1 sprain (mild): Slight stretching and some damage to

the fibers (fibrils) of the ligament.

• Grade 2 sprain (moderate): Partial tearing of the ligament.

There is abnormal looseness (laxity) in the joint when it is
moved in certain ways.

• Grade 3 sprain (severe): Complete tear of the ligament. This

causes significant instability and makes the joint
nonfunctional.
STRAIN

• A strain is an injury to a muscle or a tendon

• Two common sites for a strain are the back and the hamstring muscle in the back of the thigh
• Strains can happen suddenly or develop over days or weeks (repetitive strain injury)
• Sports at risk of strains such as soccer, football, hockey, boxing, and wrestling
• Signs & symptoms : PAIN
· Muscle weakness
· Swelling
· Cramping
· Trouble moving the muscle.
• If a muscle or tendon is torn completely, it is often very painful and hard to move

Special test

tests

1. ANTERIOR & POSTERIOR DRAWER TEST To test for ACL and PCL tear

2. LACHMAN’S TEST To assess the integrity of ACL

3. VARUS & VALGUS STRESS TEST 30 degree = MCL & LCL rupture

4. PIVOT SHIFT TEST To assess ACL rotatory instability

5. MCMURRAY TEST To assess for lesion in the meniscus

Treatment

Conservative treatment:
1. Analgesic
2. Functional rehabilitation

SPRAIN:
Do not stop moving affected joint by doing gentle exercise
Do not play sports 3-4 weeks

STRAIN:
Immobilize the muscle
Use crutches/brace in severe case
 FRACTURES
PATHOLOGICAL FRACTURES
Definition
Fractures that occur even with normal stresses when the bone has been weakened by a change in its structure or through
a lytic lesion.

Causes

History taking

• Bones fracture spontaneously / after trivial injury must be regarded as abnormal until proven otherwise.
• Ask previous illnesses / operations
• Gastrectomy, GI disease, chronic alcoholism, prolonged corticosteroid >> METABOLIC BONE DISEASE
• Malignancy

Physical examination

• General :
– Congenital dysplasia
– Cushing syndrome
– Enlarged lymph nodes
– Mass in abdomen, breast, thyroid
– Per-rectal examination
– Age < 20 years old : benign bone tumours / cysts
– Age > 40 years old : multiple myeloma, secondary carcinoma

Investigations

1. Plain radiograph
• Cyst formation
• Cortical erosion
• Abnormal trabeculation
• Periosteal thickening
• Types of fracture

2. Full blood count

3. ESR
4. Test for metabolic bone diseases
 5. Urinalysis → blood from tumours, Bence-
Jones protein
6. Biopsy
7. Tumour markers
8. Local radionuclide imaging

Treatment
MONTEGGIA VS GALEAZZI FRACTURE
MONTEGGIA
• A fracture of the upper third shaft of the ulna
associated with dislocation of the proximal
radio-ulnar joint
• 2 types:
 Extension type  ulna fracture angulates
anteriorly, radial head dislocates anteriorly.
(most common)
 Flexion type  ulna fracture angulates
posteriorly, radial head dislocates posteriorly.
MECH. OF • A fall on an outstretched hand
INJURY • A direct blow on the back of the upper
forearm
CLASSIFICATION Bado classification
Type 1 – anterior dislocation of radial head
Type 2 – posterior dislocation of radial head
Type 3 – lateral dislocation of radial head
Type 4 – associated fracture of radius
C/F • Obvious ulnar deformity
• Pain and tenderness on the lateral side of the
elbow (dislocation of radial head)
X-ray:
Anterior posterior and lateral view of the elbow
• Radial head is dislocated
• Fracture of upper third of the ulna
GALEAZZI
• A fracture at distal third of radius and
dislocation of distal radio-ulna joint
• 2 types (based on direction of ulnar
displacement):
 Volar
 Dorsal
• Fall on an outstretched probably with a
superimposed rotation force.
Associated with :
 ulnar styloid fracture
 widening of joint
 dorsal/volar displacement of ulnar
• Tenderness over the wrist
• Instability of radio-ulna joint = balloting the
distal end of the ulna (piano key sign)
Xray (Anterior posterior and lateral view of
forearm):
• Transverse/ short oblique fracture in the lower
third of the radius with angulation or overlap
• Distal radio-ulnar joint is subluxated/
dislocated
 TREATMENT Open reduction and internal fixation with Open reduction and internal fixation with plate
plate. osteosynthesis of radius + k wiring of DRUJ

COMPLICATION 1) Nerve injury – caused by overenthusiastic 1) Mal-union - it can results in deformity and
manipulation of the radial dislocation/ limitation of supination and pronation
during surgical exposure. The usual lesion is
neurapraxia (will recover by itself)
2) Malunion – common in cases treated
conservatively.
3) Non-union – should be treated by plating
and bone grafting.
THUMB METACARPAL FRACTURES
1. Impacted fracture of the metacarpal base
2. Bennett’s fracture-dislocation of carpometacarpal joint
3. Rolando’s comminuted fracture of the base

BENNET VS ROLANDO FRACTURE

BENNET ROLANDO

• Occurs at the base of the first metatarsal carpal bone • It is an intra-articular comminuted
• Commonly due to punching fracture of the base of the first
• Oblique fracture, extending into carpometacarpal metacarpal. More unstable.
joint, unstable.
• Clinically, thumb looks short and the carpometacarpal
region swollen.

XRAY
• X-ray shows a small triangular fragment remained
in contact with the medial half of the trapezium,
while the remainder of the thumb has subluxated
proximally.
TREATMENT • Closed reduction by pulling on the thumb, abducting • Treatment is difficult. With a triple T or
and extending it. Y configuration, closed reduction and K-
• Then, held in either one of 2 ways; plaster or internal wiring or open reduction and mini
fixation screw fixation can be used.
• With more severe comminution,
external fixation is needed.
 LOWER EXTREMITY FRACTURES & DISLOCATIONS

POSTERIOR DISLOCATION OF THE HIP
MECH OF High impact energy striking the knees → travels along the
INJURY axis of femur → femoral head forced out of its socket.
o Eg : Dashboard injury (flex knee, flex hip)
FEMORAL SHAFT FRACTURE
High energy: young, high speed MVA
Low energy: elderly, fall from standing
SUPRACONDYLAR FRACTURE (DISTAL FEMUR #)
Definition: fracture from articular surface to 5cm above
metaphyseal flare
High energy: significant displacement
Low energy: osteoporotic bone with less displacement

C/F Leg, hip joint: - Swelling and deformity

- Adducted - Painful upon movement
- internally rotated - Accompanying injuries
- slightly flexed.
- Severe pain + loss of ROM
- Shortening of affected limb

CLASSIFI Winquist & Hensen Classification

CATION
IX CT scan: full extend of the associated acetabular injury. X-ray: AP and lateral view of femur, ipsilateral hip and knee  X-ray: AP, Lateral views
 CT Scan
TX 1. This is an emergency case. • Gold standard: Intramedullary nail  ORIF
2. Reduce under general anaesthesia (CMR) • External fixation  Retrograde IM Nail
Flex the patient hip and knee at 90° and pull the thigh • ORIF with plate
vertically upwards can move all direction. Apply
Allis maneuver.
3. Assess the stability of the reduced hip
4. Movement and exercise are begun as soon as the pain
allows
CX
 FEMORAL NECK INTERTROCHANTERIC SUBTROCHANTERIC
MECH OF  Commonest site in elderly  Extracapsular  From lesser trochanter to 5cm distal
INJURY  Common in elderly (osteoporotic bone)
 Other risk factors :  Unite quiet easily
- Osteomalacia  Seldom caused avascular necrosis (AVN)
- Diabetes
- Stroke  Mechanism of injury :
- Alcoholism - Fall directly onto greater trochanter
- Indirect twisting
 Mechanism of injury : - Proximal fragments tends to displace in varus.
- Elderly : simple fall
- Younger : fall from a height
(associated fracture of femoral shaft)

C/F • History of fall → pain in the hip • Old patient, unable to stand
• If displaced, limb in lateral rotation, shorten. • Leg is shorter, externally rotated

CLASSIFI Garden classification • No. of parts: head/neck, GT, LT, Shaft Russel Taylor classification
CATION - Stable
- Unstable
- Reverse obliquity

 Evan classification

IX
TX Non-operative  Stable : Dynamic hip screw (2 hole)  IM nail
 Very limited role  Unstable/reverse : IM Recon nail  Cephalomedullary IM nail
 Activity modification  ORIF
 Skeletal traction (to immobilize until surgery)
Operative
 ORIF
 Hemiarthroplasty
 Total hip replacement

CX - Avascular necrosis (AVN)

- General : Bed sore, thromboembolism
- Non-union
- Osteoarthritis
 PATELLA FRACTURE TIBIAL PLATEAU FRACTURE TIBIAL SHAFT FRACTURE
Three types of fractures :
1. Undisplaced
2. Comminuted
3. Tranverse fracture, with a gap
between fragments

MECH OF  Caused by strong bending forces combined with  Direct injury such as kick or blow with a wooden
INJURY axial loads club
 e.g. car striking a pedestrian on the side of knee  Transverse or slightly oblique fracture
(bumper fracture), fall from height, sport  Most commonly open fracture
 In children, usually caused by indirect injury

C/F  Painful, swollen knee  Swollen knee

 Hemarthrosis  Hemarthrosis
 Sometimes the gap can be felt  Tenderness
 Patient able to extend knee- intact extensor mechanism

CLASSIFI Schatzker classification

CATION
IX  Plain radiograph – AP or lateral view (usually clearly  Plane radiograph AP/ Lateral
distinguishable)  CT scan
MX 1. Non-operative – Undisplaced / minimal displaced - knee 1. Undisplaced/ minimally displaced of lateral  Non-operative
immobilized in extension by cylinder cast/brace condyle: conservatively (aspirate hemarthrosis, - Activity restriction with protected
2. Operative – ORIF with tension-band wiring compression bandage) weightbearing
2. Displaced / fractures of lateral condyle: ORIF with  Operative
lag screw and plate - Intramedullary tibial nailing
3. Fractures of medial condyle : ORIF with buttress
plate & screws
4. Bicondylar fractures : Combine internal and
external fixation.

CX - Compartment syndrome
- Joint stiffness
- Deformity
- Osteoarthritis
 TIBIAL PLAFOND FRACTURE
(PILON FRACTURE)
MECH OF  Involves distal tibia
INJURY metaphysis into the ankle
joint
 Occurs when a large force
drives the talus upwards
against the articular surface
of tibia. eg fall from high
CLASSIFI Rüedi-Allgöwer classification
CATION
ANKLA JOINT FACTURE
 Most common weight-bearing
skeletal injury
 Feature
 History of ‘twisted ankle’
 Intense pain
 Unable to stand on the leg
 Swollen ankle
Check:
- Neurovascular exam
- Obvious deformities
- Pain over the medial or lateral
malleoli
- Palpate ligaments about the
ankle
- Palpate proximal fibula, lateral
process of talus, base of 5th
MT
Weber classification
TALAR FRACTURE 5TH METATARSAL FRACTURE
 It connect leg and foot  Zone 1: hindfoot eversion
 Serious injury  Zone 2: forefoot adduction
 Vulnerable blood  Zone 3: repetitive
supply microtrauma
 Major weight bearing
structure  Symptoms
 MECH OF INJURY : - Pain over lateral border of
 Motor vehicle foot
accident  Physical examination
 Fallen from high - Resisted foot eversion
 Tenting is dangerous
sign
 Types:
 Head
 Neck (50%)
 Body
TALAR NECK Classification :
 Zone 1: Avulsion of base
 Mechanism of injury  Zone 2: Jones fracture
 A high-energy injury  Zone 3: Midshaft fracture
 Is forced dorsiflexion
with axial load
 Associated condition
 Ipsilateral lower
extremity fracture
common
 Blood supply
 Posterior tibial artery
 Anterior tibial artery
 Peroneal artery
 Hawkins classification
IX  Radiograph  X-ray
 AP and lateral view - AP, lateral & oblique
 CT scan  CT scan & MRI
 Best study to determine - Not routinely done
the degree of - Consider in setting
displacement, of delayed healing
comminution and or nonunion
articular congruity
 assess foot injuries (up to
89 % incidence)

MX  Non-operative  Non-operative  Non-operative  Protected weight bearing in

- Immobilization - Short-leg walking cast - Cast for 8-12 weeks stiff soled shoes, boot or
 Operative (4-6 weeks) (Hawkins I) bulky dressing
- Spanning external  Operative  Operative  Zone 1
fixation across ankle joint - Open reduction internal - ORIF (Hawkins II-IV)  Non weight bearing short-leg
- Open reduction internal fixation (ORIF) cast for 6-8 months or IM
fixation screw fixation
 - Intramedullary nailing  Zone 2 & 3
with percutaneous screw
fixation.

CX  Avascular necrosis  Nonunion

 Post-traumatic arthritis  Failure of fixation
 Varus malunion
 FRACTURE COMPLICATIONS
COMPARTMENT SYNDROME

Introduction
• Osseofascial compartment pressure rises to a level that
cause decrease in perfusion.
• May cause irreversible muscle and nerve
damage.
• Common sites are the leg and forearm.
• Less common are the foot, upper arm and thigh.

Types
1) Acute
• Orthopaedic emergency.
• Caused by severe injury.
• Without treatment, lead to permanent muscle damage.

Increased volume within Compartment constriction

compartment / External compression
• Fractures (high energy) • Tight casts / bandages
• Crush injuries / • Unconscious patients
contusions (direct pressure)
• Bleeding
• Vascular injuries
• Reperfusion
• Extravasations

Vicious cycle of compartment syndrome

Clinical features – 6P
• Pain
• Pain out of proportion
• Pain on passive stretch
• Paralysis
• Paraesthesia
• Pallor late findings
• Pulselessness
 2) Chronic
• a.k.a exertional compartment syndrome.
• Usually caused by athletic exertion.
• Exercise with repetitive motions (running, biking, and swimming) → inflammation & swelling
which ↑ intracompartmental pressures → aching pain.
• Most common location;
• Anterior leg compartment (70%)
• Symptoms
• Aching or burning pain
• Paresthesia
• Symptoms reoccur by exercise & relieved by rest
• Treatment:
• Rest
• Anti-inflammatory
• Fasciotomy

Investigation
• Diagnostic – compartment pressure measurement
• Needle inserted into compartment
• Measured in mmHg
• Pressure < 30 mmHg= damage to blood vessels & nerves in compartment (HIGH RISK
for tissue necrosis)
• Compartment ischemia > 4-12 hrs can cause permanent muscle damage.
• Other findings
- FBC: ↑ WBC dt severe inflammatory response
- ESR: ↑ dt severe inflammatory response
- ↑ urine myoglobin dt muscle necrosis and protein loss
- Serum K+: ↑ dt cell damage
- Serum pH: ↓ dt acidosis

Management
• Completely remove casts, bandage, and dressings.
• Limb must be lying flat
• elevation limb cause further decrease in end capillary pressure + worsen the muscle
ischaemia
• Monitor intra-compartmental pressure: <30 mmHg = Immediate FASCIOTOMY
• Clinical ground: PAIN
• examined at 30 minutes intervals
• if no improvement within 2 hours of splitting the dressings = FASCIOTOMY
FAT EMBOLISM SYNDROME
Introduction
• A syndrome caused by an inflammatory response to embolized fat globules which is
characterized by:
– Hypoxia • Circulating of fat
– CNS depression
globules larger than
– Pulmonary edema
10um in diameter.
– Petechial rash
• Common causes: • Found in histological
– Acute long bones fracture traces of fat in lungs and
– Intramedullary instrumentation
other internal organ.
(IM nail and hip/knee arthroplasty)
• Incidence:
– 3-4% with isolated long bone trauma
– 10-15% with polytrauma
• Prognosis:
– Fatal in up to 15% of patients
• Source of fat emboli: Bone marrow

Pathogenesis

1) Mechanical theory

Trauma to the bone

Elevated intramedullary pressure

Intramedullary fat globules are released into the torn

blood vessel

Deposition of fat globules in pulmonary circulation and

may enter systemic circulation

Local ischemia, inflammation, released of inflammatory

mediators
 2) Biochemical theory

Hormonal changes following trauma, sepsis or both

Systemic release of free fatty acids (chylomicrons)

Meanwhile, acute phase reactant, C-reactive proteins

are released as well

Chylomicrons combine with C-reactive proteins

Local ischemia, inflammation, released of inflammatory

mediators

Clinical features
• Early warning signs (24h-72h):
– Tachycardia
– Pyrexia
• More pronouced cases:
– Breathlessness
– Mild mental confusion or restlessness
• Severe cases:
– Respiratory distress and coma
• Pathognomonic signs: (Clinical diagnosis)
– Petechiae on the trunk, axillae, palate and in the conjunctival folds and retinae
– Due to occlusion of dermal capillaries by fat globules  extravasation of
erythrocytes

Diagnosis criteria (Gurd’s and Wilson’s)

Diagnosis require 1 major criteria + 4 minor criteria

Investigations
1. FBC: anemia, thrombocytopenia
2. ESR: elevated
3. ABG: hypoxemia (PaO2 < 60mmHg)
4. Urinalysis: fat globule in urine
5. CHEST X-RAY: diffuse lung infiltration bilaterally (snowstorm appearance)

Management
• Supportive:
– Give high inspired oxygen concentration immediately after injury. (reduce
symptoms)
• Pharmacological:
– Corticosteroid (methylprednisolone)
– To reduce inflammation.
– S/E : GI Bleeds, Infections, Delayed healing, Cortisol issues, and CVS stability (cardiac
mostly), mortality
• Prevention (Operative):
– Early fracture stabilization (within 24 hours)
TYPES OF SHOCK AND ITS MANAGEMENT
 Shock is defined as a state of cellular and tissue hypoxia due:
• reduced oxygen delivery
• increased oxygen consumption
• inadequate oxygen utilization

 Shock is initially reversible, but must be recognized and treated immediately to prevent
progression to irreversible organ dysfunction.

Classification of shock

1) Hypovolemic shock
• Results from loss of volume within circulation
• Causes: - whole blood loss (hemorrhage)
- plasma and fluid loss (burn)
• Compensatory mechanism:
 Tachycardia
 Peripheral vasoconstriction
 Tachypnea
 Fluid shift into circulation
 Reduced urine output
• Classification of hypovolemic shock - American college of surgeon class of acute
hemorrhage
• Management of hypovolemic shock in trauma patient

• Fluid resuscitation
- Early use of blood is available
- Where blood is not available or delayed, use Hartman solution
- 0.9% of normal saline also an acceptable alternative

2) Cardiogenic shock
3) Septic shock
• Entry of toxin will activate the host defense mechanisms that cause:
• the influx of activated neutrophils and monocytes
• release of inflammatory mediators
• local vasodilation, increased endothelial permeability
• activation of coagulation pathways
• This response mechanism will result in:
• Diffuse endothelial disruption
• Thrombosis
• hypovolemia
• Toxin also can damage the myocardium, and cause capillary leakage (complicating by
presentation of cardiogenic and hypovolemic shock)

4) Neurogenic shock
• Due to high spinal cord injury
• Disrupt the sympathetic nerves controlling vasoconstriction
• Peripheral vasculature relaxes and profoundly dilated (reduced preload and afterload)
• Inadequate blood pressure and shock

5) Anaphylactic shock
DEEP VEIN THROMBOSIS
Definition
Formation of a thrombus(blood clot) within a deep vein, commonly in calf.

Risk of thrombosis:
 5 weeks after hip surgery
 2 weeks after knee surgery

Risk factors
• Restricted mobility through plaster casts, paralyses or injuries
• Lack of exercise due to restricted mobility
• Increased susceptibility to clotting after surgical interventions
• Trauma caused by accident

Aetiology
Pathophysiology

Symptoms

- Asymptomatic DVT (quite common)

Shortness of breath
Pleuritic chest pain
Coughing

Calf pain
Signs Swelling
Erythema
• General examination Warm • Chest examination (to look for signs of PE)
- Dilated neck vein
- ↑ T°, ↑ heart rate
- Central cyanosis
- Right ventricular hypertrophy
• Leg examination - Split second heart sound
- Unilateral calf/thigh swelling & tenderness - Pleural rub
- Muscle hard & tender
- Dilated superficial veins
- Warm and shiny leg
- Homan’s sign +ve
Wells’ criteria

Investigation

Treatment
Prevention
PRESSURE ULCER (BEDSORE)
Definition
• Localized injury to the skin and/or underlying tissue usually over a bony prominence, as a
result of pressure, or pressure in combination with shear.

Epidemiology
− Majority of pressure sore occur in hospital.
− 70% are in orthopaedics patient, 20-30% occur in the community.
− Commonly occur in the elderly, immobile, unconscious or paralyzed patient.

Aetiology
1. Prolonged immobility
− Paraplagia, arthritis, severe physical disease, operation and post-operative states.
2. Decreased sensation
− Coma, neurological disease, diabetes mellitus, drug-induced sleep.
3. Vascular disease
− Artherosclerosis, diabetes mellitus, scleroderma, vasculitis
4. Poor nutrition
− Anemia, hypoalbuminaemia, vitamin C or zinc deficiency

Mechanism
Two mechanism that contribute to pressure ulcer development:
1) External pressure that compresses blood vessels
− Applied over an area of bony prominence.
− Result in obstruction of blood capillaries, which deprives tissues of oxygen and
nutrients.
− Then, it will caused hypoxia, ischaemia, necrosis, and lastly ulcer formation.
2) Friction and shearing action that tear and injure blood vessels
− Friction is the mechanical force exerted when skin is dragged across a coarse
surface.
− Shear is a combination of friction and gravity.

National Pressure Ulcer Advisory Panel Classification

• Stage 1
o Most superficial, indicated by non blanchable
redness that does not subside after pressure is
relieved.
o Skin may be hotter or cooler than normal, have an
odd texture, or perhaps be painful to the patient.
• Stage 2
o Damage to the epidermis extending into, but no
deeper than, the dermis.
o In this stage, the ulcer may be referred to as a
blister or abrasion.
• Stage 3
o Damage to the epidermis extending into, but no deeper than, the dermis.
o In this stage, the ulcer may be referred to as a blister or abrasion
• Stage 4
o Deepest, extending into the muscle, tendon or even bone.
 • Unstageable Pressure Ulcer
o Are covered with dead cells, or eschar and wound exudate, so the
depth cannot be determined.
• Suspected Deep Tissue Injury
o Purple or maroon localized area of discolored intact skin or blood-
filled blister due to damage of underlying soft tissue from pressure
and/or shear. The area may be preceded by tissue that is
painful, firm, mushy, boggy, warmer or cooler as
compared to adjacent tissue.

Treatment
1. CONSERVATIVE MANAGEMENT:
• Bed rest with pillows to keep pressure off bony areas and prevent friction
• Air-filled cushions for patient in wheelchairs
• Special pressure-relieving mattresses and beds (ripple mattress)
• Regular repositioning of immobilize patient
• Ensure adequate nutrition, by increase calories and fluids intake, high-protein diet and
food rich vitamins and minerals.
• Dressing to keep wound wet and enhance granulation; regular cleansing of normal
saline.
• Systemic antibiotics for spreading infection from infected pressure sore.
• Manage the incontinence smartly (frequent diaper changes, protective lotions on
healthy skin and urinary catheters or rectal tubes).
2. OPERATIVE MANAGEMENT:
• Aims of surgery:
i. Improving the hygiene and appearance of the sore
ii. Preventing and treating infection
iii. Reducing fluid loss through the wound
iv. Lowering the risk of cancer
• The type of procedure depends mainly on the location of the wound and whether it has scar
tissue from a previous operation.
• Generally, most pressure sore are repaired using a pad of muscle, skin or other tissue to
cover the wound and cushion the affected bone (flap reconstruction).

Complications
• Sepsis, cellulitis, endocarditis, meningitis
• Fistula formation
• Osteomyelitis, septic arthritis
• Sinus tracts
• Squamous Cell Carcinoma (Marjolin’s ulcer)
• Drug resistant bacteria
• Maggot infestation
 BUMPS

GANGLION CYST

Epidemiology
 Most common hand mass (60-70%)
 Occur in young adults (15-40 years old)
 Women > men

Pathology
 Arises from leakage of synovial fluid from a joint or tendon sheath
 Contains a glairy and viscous fluid.
 Often resembles a water balloon on a stalk, no true epithelial lining.

Location
- It can develops anywhere around the carpus

 Dorsal carpal (70%)

 originate from Scapho-Lunate articulation
 Volar carpal (20%)
 originate from scapho-trapezio-trapezoid joint
 Volar retinacular (10%)
 originate from flexor tendon sheath of the finger
 Dorsal DIP joint

Imaging (not usually indicated)

 Radiographs of hand:
• Normal
 MRI:
• Not routinely indicated
• Shows well marginated mass with homogenous fluid signal
intensity.
 Ultrasound:
MRI-Wrist-Axial-T2
• Useful for differentiating cyst from vascular aneurysm
• May provide image localization for aspiration while avoiding arteries.
 Biopsy:
• Not routinely indicated
Treatment

Non-surgical
 Observation (1st line) as cyst can disappear
spontaneously
 Aspiration of the fluid (2nd line)
Surgical
 Indicated when develops severe symptoms
or neurovascular manifestations
 Requires adequate exposure to identify
origin and allow resection of stalk 
recurrence

Complication

With aspiration With excision

1. Infection (rare) 1. Infection
2. Neurovascular injury 2. Neurovascular injury (radial artery most
common)
3. Injury to scapholunate interosseous ligament
4. Stiffness
GOUT VS PSEUDOGOUT

GOUT

A Disorder of purine metabolism characterized by

1. Hyperuricaemia
2. Deposition of monosodium urate monohydrate crystals in joints and peri-articular tissues
3. Recurrent attacks of acute synovitis

Late changes :
 cartilage degeneration
 renal dysfunction
 uric acid urolithiasis.

1. Older age, male gender

2.Genetic enzyme defects, hyperparathyroidism
3. Haemolytic disorders, myeloproliferative disorders
4. Obesity, diabetes, hypertension
5. High consumption of red meat, hyperlipidaemia
6. Chronic inflammatory diseases
7. Long-term use of aspirin or diuretics
8. Alcohol abuse

Primary (95%)

- under-excretion of urate
- overproduction of urate

Secondary (5%)

- myeloproliferative diseases
- Diuretics
- renal failure

Epidemiology

1-10/1000 – race, age, sex

Caucasian > Black
MEN > WOMEN (20:1)

Pathology

Hypoxanthine  Xanthine Uric acid

Hyperuricaemia >>Urate crystals deposited in connective tissue (articular cartilage)
Clinical features

Acute gout
• Acute,self limiting monoarticular inflammatory arthritis
• Erythema,warmth,swelling
• Extreme tenderness

Chronic gout
• Polyarticular arthritis
• Tophi
• Joint erosion (chronic pain,stiffness,deformity)

Common sites :
 metatarsophalangeal joints of the big toes,
 Achilles tendons
 olecranon bursae
 pinnae of the ears.

Investigation

1. Specific investigation to confirm gout

 joint aspiration and crystal identification
 Serum urate

2.To detect presence of medical condition a/w gout

 Full blood count
 Serum creatinine/urea
 Serum urate
 Blood glucose
 Fasting lipid profile
 Urinalysis
 To detect complication
 Renal imaging
 Skeletal x-rays -punched out periarticular erosion with sclerotic overhanging border. Soft
tissue crystal deposition (tophi)
Management
 HAND & FOOT DISORDER
CARPAL TUNNEL SYNDROME
 DEFINITION: Numbness, tingling, and weakness in hand due to median nerve compression
under the flexor retinaculum of the wrist

 PATHOPHYSIOLOGY
 Soft tissue increase in bulk
− Pregnancy
− Myxoedema
− Rheumatoid arthritis (flexor tenosynovitis)
 Local obstruction
− Ganglion
− Osteophytic spur

 CLINICAL FEATURES
- Pain and paraesthesia in the distribution of the median nerve
- Night after night, the patient is woken with burning pain, tingling, numbness
- Hanging the arm over the side of the bed / shaking the arm to relieve the symptoms
- In advanced case : clumsiness and weakness
- In late case : wasting of thenar muscles, weakness of thumb abduction, sensory
dulling in the median nerve territory

 TEST
− DURKIN’S TEST: press thumbs over the carpal tunnel for 30sec
 positive: pain/paraesthesia over median nerve distribution
− TINEL’S SIGN: tap from distal index finger to the side of injury
 positive: pin and needle sensation

 INVESTIGATION
 ELECTROMYOGRAPHY: shows abnormal action
potentials in muscles that are not obviously weak or
wasted. Fibrillation in severe nerve damage
 NERVE CONDUCTION TEST : conduction is slowed
across the compressed segment

 TREATMENT
- Light splints
- Steroid injections
- Surgical decompression
DEQUERVAIN’S TENOSYNOVITIS
• Definition
• Inflammation of the synovial sheath
• Causing secondary thickening of the sheath,
• Stenosis of the compartment
• Thus compromising the involved tendon (APL & EPB).

• CAUSES
– Caused by unaccustomed overuse (relies on repetitive hand or
wrist movement):
• working in the garden
• playing golf
• lifting baby
– Idiopathic

• PATHOLOGY
– Reactive thickening of the sheath around the extensor pollicis brevis and abductor
pollicis longus tendons within the first extensor compartment

• CLINICAL FEATURES
– Pain on the radial side of the wrist
• Tenderness is most acute at the very tip of the radial
styloid
– Visible swelling over the radial styloid
– The tendon sheath feels thick and hard
• SPECIAL TEST
1. Finkelstein’s test.
– Ask the patient to fully flex the thumb.
– Places the patient’s thumb across the palm in full flexion
– Holding the patient’s hand firmly
– Adduct the wrist joint (ulnar deviation)
– In a positive test, this would be painful.
2. Hitch-hiker’s sign (resisted thumb extension)
a. Ask the patient to do:
b. Flexion of the MCP joint
c. Extension of distal IP joint of the thumb.
d. Patient complains of pain localized to 1st dorsal
compartment when asked to extend & abduct the thumb

• TREATMENT
3. Early case: corticosteroid injection into the tendon sheath.
4. Hand therapy (splintage)
5. Resistant cases (if pain persists/severe cases) need an operation (slitting the thickened
tendon sheath).
COMPLEX REGIONAL PAIN SYNDROME (CRPS)

 Reflex sympathetic dystrophy

 Sudeck’s atrophy
 Shoulder-hand syndrome
 Algodystrophy
 Causalgia

Introduction
• Definition - Sustained sympathetic activity in a reflex arch characterized by pain out of
proportion to original injury.
• Uncommon chronic pain condition that usually affects limbs.
• Precipitating cause :
- Trauma
- Surgery
- Peripheral nerve lesion
- Prolonged immobilization
• 30% of patients with fractures of the extremities develop features of this condition

Pathophysiology
• The exact mechanisms is not clearly understood
• A type of sympathetic ‘overactivity’
• Multiple mechanisms are involved :
- Abnormal cytokine release
- Neurogenic inflammation
- Sympathetic-mediated enhancement of pain responses
- Cortical reaction to noxious stimuli

Clinical Features
• Cardinal signs
− Exaggerated pain (burning)
− Swelling
− Stiffness
− Skin discolouration

Types of CRPS
CRPS TYPE 1 CRPS TYPE 2
 Most common  Causalgia
 Reflex sympathetic dystrophy  With nerve damage
 Occurs after illness or injury  Minimal positive response with
 From trauma, cast or tight bandage sympathetic blocks
 Without nerve lesions
 Budapest Criteria for CRPS

All of the following statements must be met :

• The patient has continuing pain that is disportionate to any inciting event
• The patient has at least 1 sign in 2 or more of the categories below
• The patient reports at least 1 symptom in 3 or more of the categories below
• No other diagnosis can better explain the sign and symptoms

No Category Sign/Symptom

1 Sensory - Allodynia (pain to light touch)

- Hyperalgesia (to pinprick)

2 Vasomotor • Temperature asymmetry

• Skin color changes
• Skin color asymmetry

3 Sudomotor/edema - Edema
- Sweating changes
- Sweating asymmetry

4 Motor/trophic • Decreased range of motion

• Motor dysfunction (weakness, tremor,dystonia)
• Trophic changes( hair/nail/skin)

Classification
Lankford and Evan Stages of RSD

Stage Onset Exam Imaging

Acute 0-3 months Pain, swelling, warmth, redness, Normal X-rays, positive
decreased ROM, hyperhidrosis three-phase bone scan
Subacute 3-12 months Worse pain, cyanosis, dry skin, Osteopenia on x-ray
stiffness, skin atrophy
Chronic > 12 months Diminished pain, fibrosis, glossy skin, Extreme osteopenia on
joint contractures x-ray

Treatment
• NON OPERATIVE
• Pharmacological
- NSAID
- Corticosteroids
- Calcium channel blockers
- Tricyclic antidepressant
- Sympathetic blockade
• Psychological treatment
• Physiotherapy
• OPERATIVE
 Surgical sympathectomy
 Surgical decompression
TRIGGER FINGER (STENOSING TENOSYNOVITIS)
Anatomy
• Flexor pulleys of finger
• A1 overlie the MP joints
• Muscles
• FDS
• FDP

Mechanism
• The flexor tendon irritated as it slides through the
tendon sheath tunnel → tendon may thicken &
nodules may form → more difficult.
• The tendon sheath may also thicken → smaller opening

Associated conditions
• Diabetes mellitus
• Rheumatoid arthritis

Clinical features
• Flexion: Finger clicking
• Extension: Remain bent at PIP joint and straighten cause a snap
• Tender nodule on palm
• Any digit could be affected; commonly

Imaging - No need

Classification
Green classification
Grade I Palm pain and tenderness at A-1 pulley
Grade II Catching of digit
Grade III Locking of digit, passively correctable
Grade IV Fixed, locked digit

Treatment
• Non-operative
• Injection or corticosteroid
• Operative
• A1 pulley is incised under LA
• Care should be taken to avoid injury to the digital neurovascular bundles.

Infantile Trigger Thumb

• Often missed diagnosis as dislocation
• Spontaneous recovery often occur by age of 3 years old.
HALLUX VALGUS
- Hallux valgus is the lateral deviation & rotation of hallux with
prominence of medial side of head of first metatarsal (bunion).
- Most common foot deformity

Risk factor:
- Most in those who wearing shoes (esp high-heeled shoes)
- In elderly → loss of muscle tone at forefoot
- Common in rheumatoid arthritis → weakness of joint capsule &
ligaments
- Congenital → metatarsus primus varus
- Family history → 60% of the cases

Pathological anatomy
- Lateral deviation & rotation of hallux + bunion
- Sometimes cause overriding of adjacent toes
- Prominence of medial side of first head of metatarsal is due to subluxation of MTP joint →
inc pressure on medial side → development of overlying bursa & thickened soft tissue →
bunion
- Long standing cases, the MTP joint becomes osteoarthritic

Clinical features
- Pain over the bunion
- Difficulty in fitting shoes
- Great toe in valgus
- Bunion varies in appearance (slight prominence → red angry-looking bulge)
- Deformity at lesser toes
- Pain in the forefoot

Diagnosis
- Plain radiograph
o Intermetatarsal angle <9o
o Normal - Metatarsophalangeal angle <15o
o Any greater degree of angulation → hallux valgus

PIGGOT (1960)

TYPE 1 TYPE 2 TYPE 3

• MTP joint centred • articular surfaces not • the joint incongruent &
• articular surfaces congruent slightly subluxated
congruent but tilt to • phalangeal surfaces tilt
valgus toward valgus

stable joint & progress unstable & likely to progress unstable & almost certain to
slowly/not progress
Treatment
- Adolescents :
o Conservative —> 20-40% recurrence if do surgical correction in
this age group
o Surgical needed if incongruous deformity
- Adults :
o Surgical options are appropriate if self-care insufficient, bunion
pain & difficulty in footwear
- Elderly :
o Shoes modification / arthroplasty

1. Conservative
• Wear shoes with wide & deep toe-boxes
• Soft upper & low heels (‘trainers’ shoes)
• Bunion pads (Polo/doughnut shape) —> offload the tender bunion
• Chiropody —> take care of callosities & skin compromise
2. Operative
• Osteotomy (Aikin’s, Chevron)/ soft-tissue rebalancing
• Arthroplasty (Keller’s operation)
• Arthrodesis

Complications
• Recurrent infection & ulceration (particular problems in diabetic foot)
• Transfer metatarsalgia
• Complex regional pain syndrome
 COMMON PAEDIATRIC ORTHOPAEDIC DISORDERS
PAEDIATRIC BONE VS ADULT BONE
Bone structure in adult and children

Biomechanical properties of bone

Children Adult

Less brittle More brittle

More porous Less porous

Thick periosteum Thin periosteum

Haversian canal occupied larger space Haversian canal occupied smaller space

Less osteoid density More osteoid density

More water content Less water content

Less mineral content More mineral content

Fractures in children
1. Thicker and stronger periosteal sleeve
2. Force applied to bone
3. Incomplete fracture with periosteal intact (more stable and less displacement)
4. Closed apposition and numerous blood supply
5. Faster healing process
INJURY OF THE PHYSIS
• 10% of fractures in children involve injury to the growth
plate.
• Mechanism of injury:
• Falls or traction injuries (road accidents, sports or
playground tumbles)
• Boys > girls
• Commonly in infancy or between age 10-12 y/o.

Salter–Harris Classification
1. Salter Harris Type 1
• Transverse fracture through the
hypertrophic/calcified zone of the
plate.
• Common in infant
2. Salter Harris Type 2
• Initially similar to type 1
• But towards edge the fracture
deviates away from physis and
• Splits the metaphysial bone into
triangular fragment. (Thurston-
Holland Fragment)
• Commonest; in older children
3. Salter Harris Type 3
• Spilts the epiphysis then veers off transversely
through the hyperthrophic layer of the physis.
• May result in growth disturbance
• Need early accurate reduction to restore the joint
surface.
4. Salter Harris Type 4
• Initially same with type 3, but the fracture extends
into the metaphysis.
• Liable to displacement (need open reduction)
• Result in asymmetrical growth
5. Salter Harris Type 5
• Growth plate is crushed.
• Due to longitudinal compression injury.
• Result in growth disturbance.
Treatment
1. Salter Haris 1 & 2:
• Undisplaced: Cast splintage 2-4 weeks
• Displaced: CMR and cast splintage 3-6 weeks
2. Salter Haris 3 & 4:
• Undisplaced: Cast splintage and check x-ray after 4 days and at 10th day
• Displaced:
− CMR and cast for 4-8 weeks
− ORIF with K-wire and cast for 4-6 weeks

GREENSTICK FRACTURE
− Incomplete fracture
− Bone incompletely divided and periosteum remain in
continuity. (with plastic deformity)
− Bone is bent because child’s bone is springier than
adult’s bone.

TORUS FRACTURE (BUCKLE FRACTURE)

• Lesser force - buckling of metaphyseal cortex
• Incomplete fracture of the shaft of a long bone
• XRAY - buckle the metaphyseal cortex
• Common location – distal radius
• Treatment:
− Plaster
SUPRACONDYLAR ELBOW FRACTURE

Mechanism of injury
• Posterior angulation/displacement (95%)
• Anterior displacement

Clinical features
• Pain and swelling of elbow
• Posteriorly displaced fracture – S-deformity
• Check – pulse & capillary return
• Passive extension – pain free
• Examine hand & wrist – nerve injury

Gartland Classification
• Type I – non-displaced
• Type II – angulated with intact posterior cortex
• Type III – completely displaced fracture

X-ray – lateral view

• Fat pad sign – fat pushed forward by hematoma.
• Posteriorly displaced fracture –
o obliquely downwards and forwards
o distal fragment is tilted backwards

Treatment
• TYPE I – back slab for 3 weeks
• TYPE II: ANGULATION
1. Closed reduction
2. POP (3 weeks) – check pulse & CRT daily
3. If unstable – Kirschner wire
• TYPE III: ANGULATION & MALROTATION
1. Closed reduction
2. Percutaneous crossed Kirschner wire

Complication
• EARLY
1. Brachial artery injury
 Peripheral ischaemia
 Forearm oedema
 Compartment syndrome
2. Median nerve injury
 Resolve in 3 – 4 months
• LATE
1. Mal-union
 No visible deformities – backward/sideways
 Uncorrected angulation & malrotation – varus deformity
2. Elbow stiffness & myositis ossificans
CONGENITAL TALIPES EQUINOVARUS (CTEV)

Epidemiology
• Talipes = talus(ankle bone) + pes(foot)
• Equinovarus = equinus (flex sole) + varus
(twisted inward)
• Idiopathic club-foot; congenital
• Ratio boys to girls 2:1
• 50% bilateral, occurs in 1 per 1000 birth
• It is also seen in neuromuscular disease
patients
• Deformity usually obvious at birth

Clinical features
• Mnemonic of CAVE:
− Midfoot Cavus
− Forefoot Adductus
− Subtalar Varus
− Hindfoot Equinus
• In some of cases, the calf is abnormally thin

Radiograph
• In AP view,
o When lines are drawn through the long axis of the
tallus parallel to its medial border and calcaneum
parallel to its lateral border (Kite’s angle), they
normally cross at the angle of 20° to 40°
o In clubfoot, the two lines are almost parallel
• In lateral view,
o When lines are drawn through the midlongitudinal
axis of the tallus and the lower border of
calcaneum, they normally cross at the angle of 40°
o In clubfoot, the talocalcaneal angle < 20° either in
plantarflexion or dorsiflexion of the foot

Treatment
• First line is non-operative (repeated manipulation,
adhesive strapping, light plaster cast)
Manipulation technique:
o Forefoot is brought into rotational alignment with
the hindfoot. Increase the supination deformity of
the forefoot so it will correspond with the
relatively more supinated hindfoot.
o Both hindfoot & forefoot are together brought out of varus & supination.
Correction assisted by keeping the fulcrum on the lateral side of the talus.
o Equinus corrected by bringing the heel down & dorsiflexion the foot.
• Operative: formal open release
o Objectives
 Complete release of joint tethers. (capsular and ligamentous contractures
and fibrotic bands)
 Lengthening of tendon.
o HINDFOOT
 Lengthen Archilles tendon and tibialis posterior tendon (Z-division)
 Divide posterior capsule of ankle and subtalar joint
 Release calcaneo-fibular ligament
 Freed superficial deltoid ligament on medial side
o MIDFOOT AND FOREFOOT
 Release contracture around talonavicular and calcaneocuboid joint
 Divide the origin of intrinsic muscles and plantar fascia from calcaneum.
• Stabilization after surgery
o Plaster cast
o K-wire inserted across talonavicular and subtalar joint
• Severe relapse: lizarov fixator, calcaneal osteotomies, tendon transfer(tibialis anterior and
posterior)
• Prevent relapse: Dennis Browne boots, moulded ankle-foot orthoses
SLIPPED CAPITAL FEMORAL EPIPHYSIS (SCFE)

Epidemiology
• Uncommon (1-3 per 100 000 birth)
• Confined to children during pubertal growth spurt
o Boys (14-16 years old) more often than girls (12-14
years old)
• Left hip more commonly affected
• If one side slips, there is 25-40% risk for the other side to
slip
• Typically overweight or very tall and thin

Aetiology
1. Hormonal imbalance
− Imbalance between pituitary hormone activity
(rapid growth and physeal hypertrophy) and
gonadal hormone activity (physeal maturation and epiphyseal fusion)
− Physis unable to resist shear stress due to increase body weight
2. Perichondrial ring around the physis is thinner in this age group
3. Trauma
− 30% acute cases
− 70% slow, progressive displacement

Clinical Features
• Pain (groin, thigh or knee)
• Limping
• Examination revealed:
− Externally rotated leg
− Limitation of flexion, abduction and medial rotation
• Classic sign: tendency to increasing external rotation as hip is flexed

Imaging
1. AP view
• Widening of epiphyseal plate
• Decreased epiphyseal height
• Klein’s line not intersect the epiphysis (+ Trethowan’s sign)
• Metaphyseal blanch sign of Steel
2. Lateral frog leg view
• Femoral epiphysis tilted backwards
• Proved by measuring angle between line of epiphyseal base
and the femoral neck (normal: 90°) ; <87° = epiphysis tilted
posteriorly
Classification
1. By timing of onset (temporal)
Pre- slip Acute slip Chronic slip Acute on chronic slip

• Complains of • symptoms • symptoms lasting • long prodromal

groin and knee present <3 weeks >3 weeks history with acute,
pain • painful hip • episodes of severe
• may be a limp movements with deterioration and exacerbation
• reduced internal an external remission
rotation on rotation • loss of internal
examination • symptoms last for rotation,
• Widening or less than 3 months abduction and
irregularity of flexion of the hip
physis in x- ray

2. Loder classification (clinical)

1. STABLE
• can bear weight
• Can walk with or without aid
• 0% risk of avascular necrosis (AVN)
2. UNSTABLE
• Cannot bear weight(cannot walk)
• 47% risk of AVN

3. Radiological grading
• Percentage slip of the epiphysis in relation to femoral neck width
• Magnitude of epiphysis-femoral shaft angle
Treatment
• Aim of treatment:
− Preserve epiphyseal blood supply
− Stabilize the physis
− To correct the deformity
 Percutaneous cannulated screw fixation
− For minor and moderate slip
 Proximal femoral osteotomy
− Deformity following treatment of screw
fixation in moderate slip case
− Severe slip cases
LEGG-CALF-PERTHES DISEASE (COXA PLANA)
• A painful disorder of childhood characterized by
avascular necrosis of the femoral head.
• Uncommon, 1 in 10 000, with higher incidence in
Japanese , Inuits, and central European
• Aged 4-10 years old
• Boy: Girl is 4:1

Risk factor
− Inherited thrombophilia
− Antithrombotic factor deficiencies
− Hypofibrinolysis
− Positive family history
− Low birth weight
− Abnormal birth presentation
− Children exposed to second hand smoke

Pathogenesis
 Up to 4 months, femoral head is supply by:
 Metaphyseal vessels
 Lateral epiphyseal vessels
 Scanty vessels of ligamentum teres
 Metaphyseal vessels
 gradually declines and virtually disappeared by 4 years
old
 Vessels of ligamentum teres
 fully developed by 7 years old
 4 – 7 years old
 Depends on lateral epiphyseal vessels which situated
in the retinacular.
 Make it susceptible to stretching & pressure from
effusion (following trauma or non-specific synovitis)

Stages
1. Stage 1: Ischemia and bone death
 Bony nucleus of femoral head is dead.
 The cartilaginous part become thicker than
normal
 May also has oedema of synovium and
capsule.
2. Stage 2: Revasculation and repair
 Within weeks
 Dead marrow is replaced by granulation
tissue
 Bone is revascularised and new lamellae
are laid down on dead trabeculae
 Apperance of fragmentation of the
epiphysis on x-ray
 3. Stage 3: Distortion and remodeling
 If repair process is tardy, bony epiphysis
may collapse and growth of the femoral
head and neck will be distorted
 X –ray: mushroom head and enlarged
laterally

Clinical features
• Symptoms
− Insidious onset
− May cause painless limp or pain and start limping
− Intermittent knee, hip, groin or thigh pain
− Early - Joint irritable (movement diminish and painful)
• Physical exam
− Hip stiffness with loss of internal rotation and abduction
− Gait disturbance
 Trendelenburg gait (head collapse leads to decreased tension of abductors)
 Antalgic limp
− Limb length discrepancy is a late finding

Prognostic features
• Age: Children under 6 years has excellent
prognosis
• Gender: Poor prognosis for girls

Catteral classification
• The greater the degree of femoral head
involvement, the worse the outcome
Lateral Pillar (Herring) classification

Treatment
• Non operative
− Pain control
− Gentle exercise
− Avoid sport & strenuous activity
− Observation alone, activity restriction, and physical therapy
− Indications
 Children < 8 years of age
 Children with lateral pillar A
 Bracing and casting
− Containment:
 active step to seat femoral head as fully as possible in
acetabular socket
 Holding hips widely abducted in plaster/ removable
brace
• Operative
− Femoral and/or pelvic osteotomy
− Indication :
 Children >8 years
 Lateral pillar B and B/C
DEVELOPMENTAL DYSPLASIA OF HIP (DDH)
• A disorder of abnormal development
• Resulting in dysplasia and possible subluxation or dislocation of the hip
• Secondary to capsular laxity and mechanical factors
• A spectrum of diseases:
− Dysplasia
− Subluxation
− Dislocation
− Teratologic hip
• Most common orthopedics disorder in newborns
• Most common in left hips in females
• Bilateral in 20%

Risk factors
− Family history
− Breech presentation (pressure on hip joint)
− Oligohydramnios (less intrauterine space)
− Presence of other congenital abnormalities
− First born (less intrauterine space)
− Female (7:1 over males)

Aetiology
Genetic factors Generalized joint laxity and shallow acetabula – features predisposed to hip
instability

Hormonal factors Eg. High levels of maternal oestrogen, progestrone, relaxin in the last few
weeks of pregnancy – may aggravate ligamentous laxity in infants

Intrauterine Breech position

malposition Normal vertex presentation - unilateral dislocation usually affects the left
hip – left hip is adjacent to the mother’s sacrum, placing it in an adducted
position.

Postnatal factor Swaddle and babies with legs together, hips and knees fully extended

Physical Examination – test for instability

1. Barlow’s test - IN -> OUT
• dislocates a dislocatable hip by adduction
and depression of the flexed femur
• ‘Clunk’ felt indicate +ve findingas the
femur is dislocated from acetabulum
2. Ortolani’s test - OUT -> IN
• reduces a dislocated hip by elevation and
abduction of the flexed femur
• ‘Clunk’ felt indicate +ve findingas
dislocated femur reenter the acetabulum
 3. Late features:
• With unilateral dislocation,
− skin creases are asymmetrical
− leg is slightly short (Galeazzi’s sign) and externally rotated
• With bilateral dislocation,
− Abnormally wide perineal gap.
− Abduction is decreased.
• Galeazzi (Allis) sign
− apparent limb length discrepancy due to a
unilateral dislocated hip with hip and knee flexed
at 90 degrees
− femur appears shortened on dislocated side

Investigation
a) Ultrasound (US)
− 4 – 6 months
− For making the diagnosis in young children before ossification of the femoral head
(largely cartilagenous)
b) Plain x-ray
− > 6 months
− 3 geometric indices:
The epiphysis should lie :
- medial to Perkins’ line (a vertical line which defines
the outer edge of the acetabulum)
- below Hilgenreiner’s line (a horizontal line which
passes through the triradiate cartilages)
The acetabular roof angle should not exceed 30°

Von Rosen’s lines: with the hips abducted 45° the femoral
shafts should point into the acetabula. Left side is shown to
be abnormal.
Treatment
Age Management

First 3 – 6 months • Ultrasound – to examine

• Splintage - Von Rosen ‘s splint, Pavlik harness
Persistent dislocation: • Closed reduction
6 – 18 months • Splintage (plaster spica)
• Operation – if necessary
Persistent dislocation: • Traction
18 – 4 years • Arthrography
• Operation (osteotomy)
• Splintage (plaster spica)
> 4 years • Unilateral dislocation – non-interventions (in >8yo child often mobile
hip and little pain)
• If reduction is attempted, require open operation and acetabular
reconstruction.
• Bilateral dislocation – >6yo -- most surgeons avoid operation (because
failure of operation on one or other side turns symmetrical into an
asymmetrical deformity.

Complication
1. Failed reduction
• Acetabulum remains undeveloped, the femoral head may be deformed
2. Avascular necrosis
• Ischaemia of the immature femoral head.
• Due to vascular injury or obstruction resulting from forceful reduction and hip
splintage in abduction.
BLOUNT DISEASE (TIBIA VARA)
Definition
• A progressive bow-leg deformity associated with abnormal growth of posteromedial part of
the proximal tibia
• Disorder of the proximal medial tibial growth plate causes progressive varus alignment of
the knees
• In children or adolescents progressive and the condition worsens.

Predisposing factors
• Early walking
• Overweight
• Black
• Types

Types
Infantile/ early Adolescent/late

diagnosed at age 1-3 years Older than 10 years old

often bilateral more often unilateral

less commonly associated with obesity associated with obesity

Clinical Features
• Varus deformity of tibia
• Procurvatum (curved,bent outwards)
• Internal rotation of tibia
• Associated with a limb length discrepancy
• Abnormal gait/appearance
o non-tender bony prominence or “beak
over medial tibial condyle”
o excessive medial tibial torsion
o pronated feet
• Pain is associated in most of the adolescent cases over the medial prominence of the
proximal tibia
Pathophysiology
1. Caused by a combination of excessive compressive forces on the proximal medial
metaphysis of the tibia
2. Altered enchondral bone formation
3. Growth is selectively inhibited at the medial side of the knee due to these compressive
forces
4. A resultant varus deformity progresses.
5. The posteromedial aspect of the physis is most suppressed,
contributing to the procurvatum deformity

Diagnostic criteria
• Radiography
o The tibial shaft is in varus position
o Proximal tibial epiphysis is flattened medially
o Adjacent metaphysis is beak-shaped.
o Internal rotation of the tibia sharply angulated slope of the
medial metaphysis of the proximal tibia
• The degree of proximal tibia vara can be quantified by measuring the
metaphyseo-diaphyseal angle
o Normal = 0-11O
o Blount’s disease > 11O

Langenskiold classification

• Stage I: Medio-distal beaking of the upper proximal tibial metaphysis.

• Stage II: Saucer-shaped defect of the metaphyseal beak.
• Stage III: Saucer defect deepens into step.
• Stage IV: Epiphysis bends over and fills medial beak.
• Stage V: Development of double epiphysis.
• Stage VI: Development of medial physeal bony bar.

Treatment
Non-operative Operative
• Brace treatment with KAFO (Knee Ankle • Proximal tibia/fibula valgus osteotomy
Foot Orthosis) • overcome the varus/flexion/internal
• Indications: Stage I and II in children < 3 rotation deformity
years • Indications
o Stage I and II in children > 3 years
o Stage III, IV, V, VI
o failure of brace treatment
o progressive deformity
o metaphyseal-diaphyseal angles > 20
degrees
 COMMON CHRONIC JOINT DISEASES
Synovial joint components
• Articular cartilage
- Hyaline cartilage
- Adapted to transmit load and movement
- Increase articular surface area, helps to improve adaptability and
stability
- Consisted of proteoglycan ground substance, collagen network,
chondrocytes
- High water content

OSTEOARTHRITIS (OA)
Introduction
• Chronic disorder of synovial joint in which there is:
- Progressive softening and disintegration of articular cartilage
- Accompanied by:
− New growth of cartilage
− Hyperactive new bone formation and remodeling
− Cyst formation and sclerosis in the subchondral bone
− Mild synovitis
− Capsular fibrosis
• Commonest of all joint diseases
• Asymmetrically distributed
• Often localized to only one part of a joint
• Often associated with abnormal loading rather than frictional wear (as in simple wear and
tear)
• Mnemonic – LOSS
o Loss of joint space
o Osteophytes (new growth of cartilage and bone at the joint margins)
o Subchondral cyst formation
o Subchondral sclerosis

Aetiology
1. PRIMARY
• Genetic, endocrine, metabolic
• Primary changes in cartilage matrix
− Weaken cartilage structure
− Eg: Crystal deposition disease, ochronosis
• Cartilage aging
− Diminished cellularity
− Reduced proteoglycan concentration
− Loss of elasticity
− Decrease in strength
2. SECONDARY
• previous inflammatory disorders
o Enzymes released by synovial cells and leucocytes : leaching of
proteoglycans from the matrix
o Synovial-derived interleukin-I (IL-I) : may suppress proteoglycan synthesis
o Eg: secondary OA in patients with rheumatoid diseases
 • Trauma
• Increase mechanical stress in some part of the articular surface
o Increased load and reduction of the articular contact area
o Eg: varus deformity of the knee, acetabular dysplasia

Pathogenesis
1. Collagen network degraded or disrupted
− Matrix becomes water-logged and soft
2. Loss of proteoglycans  defects appear in the cartilage
3. Secondary damage to chondrocytes  release of cell enzymes  further matrix breakdown
4. Cartilage deformation  amplifying the changes in a cycle that leads to tissue breakdown
5. Cartilage loss its integrity  loading forces are increasingly concentrated in the exposed
subchondral bone  focal trabecular degeneration and cyst formation
6. Increased vascularity and reactive sclerosis in the zone of maximal loading
7. Cartilage at the edges of the joint undergoes remodeling and endochondral ossification 
bony excrescences (osteophytes)

Pathology
Cardinal features:
1. Progressive cartilage destruction
2. Subarticular cyst formation
3. Sclerosis of the surrounding bones
4. Osteophyte formation
5. Capsular fibrosis

Risk factors
1. JOINT DYSPLASIA - Eg: Congenital acetabular dysplasia, Perthe’s disease
2. TRAUMA - Fractures involving the articular surface
3. OCCUPATION- Certain occupation which cause repetitive stress
4. OBESITY - Causes increased joint loading
5. FAMILY HISTORY

Clinical Features
• Symptoms – pain, swelling, stiffness
• Typically joints affected:
o Heberden’s nodes at DIP
o Bouchard’s nodes at PIP
o Varus deformity at knee
o Joint crepitus
Diagnosis
• OA is diagnosed clinically
• Plain radiograph – to support the diagnosis
• Laboratory investigations – to exclude other inflammatory
joint diseases

Investigations
− Laboratory investigations – CRP and ESR are likely to be
normal or only slightly elevated
− Synovial fluid analysis – normal in OA
− Imaging
o Kellgren-Lawrence Grading System (Radiological
classification)

Kellgren-Lawrence Grading System (Radiological classification)

Grade Description

Grade I Doubtful narrowing of joint space, possible osteophytic lipping

Grade II Definite osteophytes, possible narrowing of the joint space

Grade III Moderate multiple osteophytes, definite joint space narrowing, some
sclerosis, possible deformity of bone ends

Grade IV Large osteophytes, marked joint space narrowing, severe sclerosis and
definite bony end deformity
Management
1. EARLY TREATMENT
• Principles:
i. Maintain movement and muscle strength
ii. Protect the joint from overload
iii. Relieve pain
iv. Modify daily activities
• Physiotherapy - joint mobility & improve muscle strength
• Load reduction - walking stick, soft-soled shoes, weight reduction
• Analgesic medication - paracetamol, tramadol, NSAIDs & COX-2 inhibitors (celecoxib,
etoricoxib), glucosamine
• Intra-articular injection - corticosteroid for short-term pain relief in acute
exacerbation of knee OA
2. Operative treatment
• Joint debridement – by arthroscopy or open operation
• Arthroplasty / Joint replacement - reduce pain and significant improvement in daily
live activities
• Osteotomy– relieved pain and may delay OA progression
• Arthrodesis- fused the diseased joint in an optimal position. This would make the
joint stiff but stable.

RHEUMATOID ARTHRITIS
− Commonest cause of chronic inflammatory joint disease
− A systemic disease and changes can be widespread
− Women are effected 3-4x more than men
− At early stage, it will affect soft tissue and later cartilage and bone (joint subluxation,
destruction & deformity)
− Genetic susceptibility – HLA-DR4

Pathogenesis
1. External trigger sets off an autoimmune reaction
2. Production of antibodies to the own IgG
3. Infiltration of inflammatory cells into the joints lead to synovial cell proliferation → synovial
hypertrophy
4. Persistent inflammation causes joint and tendon destruction due to secretion of proteolytic
enzymes and cytokine as well as deposition of immune complex

Pathology
• Stage 1 – pre-clinical
o ↑ ESR and CRP
o presence of RF
• Stage 2 – synovitis
o Vascular congestion, infiltration of inflammatory
cells and proliferation of synovial cell
o Painful, swollen and tender
o Structures are still intact and mobile, disorder is potentially reversible
 • Stage 3 – destruction
o Articular cartilage and bone are eroded
o Tenosynovitis lead to rupture of tendon
• Stage 4 – deformity
o Progressive instability and deformity of the joint
o Mechanical and functional effects of joint and
tendon disruption are vital

Complication
1. Fixed deformity - Resulting from ignorance and neglect
2. Muscle weakness – Due to prolonged inactivity
• Prevented by control of inflammation, physiotherapy and pain control
3. Infection - RA + on corticosteroid therapy prone to infection
4. Rupture of synovial membrane - Synovial contents spill into the soft tissue
5. Spinal cord compression, systemic vasculitis - Rare

Clinical features
1. EARLY STAGE
o SYMPTOMS
 Polysynovitis : soft tissue swelling, stiffness
 Loss of mobility in proximal joints of fingers
 Morning stiffness
o SIGNS
 Symmetrical swelling & tenderness of metacarpophalangeal joints, proximal
interphalange joint & wrist
 Tenosynovitis (evidenced by thickening, tenderness and crepitation over
back of wrist or palm while passively moving the fingers)
2. LATE STAGE
o Joint deformity  caused by joint instability and rupture of tendon
o Ulnar deviation
o Valgus knee and feet
o Clawed toes
o Swan neck deformity
o Boutonniere deformity
o EXTRA-ARTICULAR
 Small subcutaneous lump
 Rubbery lumps
 Usually at back of elbow, tendon
American College of Rheumatology (ACR)/ European League against Rheumatism (EULAR)
Classification Criteria for RA

26 definite RA

Investigations
1. BLOOD
a. FBC : hypochromic normocytic anaemia
b. ESR & CRP : elevated
c. Cyclic citrullinated peptide
antibodies (anti-CCPs) : specific
d. Serology for Rheumatoid factor :
+ve in 80% of patient
2. IMAGING
a. X-RAY : Soft tissue swelling,
periarticular osteoporosis, bony
erosions, joint deformity
3. BIOPSY
a. Synovial biopsy: synovial tissue
may be obtained by needle biopsy
via arthroscope or open
operation. But histo features are
non-specific
Management
1. MEDICAL
a. Corticosteroid  to control inflammation
• Initially oral doses of 30mg of prednisolone OR 120mg IM methylprednisolone
b. Disease-modifying anti rheumatic drugs (DMARDS)
• Methotraxate 10-25 mg/week
• Can be used alone or combined with sulfasalazine or hydroxychloroquine
2. PHYSIOTHERAPY & OCCUPATIONAL THERAPY
a. Preventive splinting and orthotic devices  to delay marching of events
b. Encourage activity
3. SURGICAL
a. If pharmacological and physiotherapy fail  surgery!
b. EARLY STAGE:
• Soft tissue procedure  synovectomy, tendon repair/replacement, joint
stabilization
c. LATE STAGE:
• Severe joint destruction, fixed deformity, loss of function  indication for
reconstructive surgery
• Osteotomy, arthrodesis, arthroplasty
• Continue methotrexate in elective orthopaedics surgery
• Continue corticosteroid (low doses as possible)
GOUTY ARTHRITIS
− Disorder of purine metabolism characterized by hyperuricemia (>0.42 mmol/L, >0.36
mmol/L) ,
− deposition of monosodium urate monohydrate crystal in joints and periarticular
tissue

Classification
1. Primary (95%)
− Absence of any previous cause
− Due to constitutional under-excretion/over-production
2. Secondary (5%)
− Prolonged hyperuricemia due to acquired disease
− E.g.: myeloproliferative disease, diuretics administration, renal failure

Pathology
1. Accumulation of uric acids in the body
2. Urate crystal, minute clump deposited in connective tissue, articular cartilage -remain inert
for month to years
3. local trauma make the crystal dispersed to the joint and surrounding tissue
4. Cause acute inflammatory reaction- phagocytosed by synovial cell/polymorph or float free in
synovial fluid
5. Build up overtime in joints, peri-articular tissue, tendon, bursae .Called tophi that varied in
size
6. Ulcerate the skin, destroy cartilage and peri-articular bone

Clinical features
1. ACUTE
• Sudden onset of severe joint pain
• Erythematous skin and swelling
• Mono-articular
• Will last few days to 2-3 weeks
•
2. CHRONIC
• Formation of tophi
• Poly-articular arthritis
• Joint erosion cause chronic pain, stiffness and
deformity

Diagnostic criteria
• Two of the following criteria are required for a clinical diagnosis:
o Presence of clear history of at least two attacks of painful joint swelling with
complete resolution within 2 weeks
o A clear history or observation of podagral
o Presence of a tophus
o Rapid response to colchicine within 48 hours of starting treatment
• Definitive diagnosis: crystal of monosodium urate are seen in the synovial fluid or in the
tissue
Investigation
• Divided into 3 categories:
1. Specific investigation for confirmation of gouty arthritis
− Joint aspiration and crystal identification
− Serum urate
2. To detect the presence of medical conditions
associated with gout/hyperuricemia
− Blood test: FBC, serum creatinine/urea, blood
glucose, fasting lipid prophile.
3. To detect complication
− Renal imaging
− Skeletal x-rays

Management
 COMMON SPORT INJURIES

 KNEE INJURIES (ACL/PCL/MCL/LCL/Meniscus injuries, Patellar dislocation)

ANATOMY

Knee injuries can be due to:

• Acute knee ligament injury
• Meniscus injury
• Dislocation of patella

ACUTE KNEE LIGAMENT INJURIES

Mechanism of injury

1. MCL injury – abduction force at the knee

2. LCL injury – adduction force at the knee
3. ACL injury – forcefully twisted/hyperextended while foot in contact with ground
4. PCL injury - Anterior of tibia stricken with the knee semi-flexed

Severity of ligament injury

Clinical features

• Symptoms:
− Hx of twisting or wrenching, heard ‘pop’ sound
− Painful knee and swollen
− Abrasion
− Bruising
− Complete tear-little or no pain, abnormal movement painless or prevented by spasm
− Partial tear- painful knee, worse swelling, no abnormal movement but attempted
movement painful
• Physical examination
− Examine sideway tilting(valgus/varus)
− Anteroposterior stability
− Drawer test
− Lachman test

Investigations
• Imaging:
o Plain X-rays: show ligament has avulsed a small piece of bone
o Stress films: show whether the joint hinges open on one side
o MRI: distinguish partial from complete ligament tears.

Treatments

1. Sprains and partial tears

• Spontaneous healing
• Active exercise to prevent adhesion
• Protect knee from rotational @ angulatory strain-heavily padded bandage or f(x)
braces
• Usually return to sports training by 6-8w
2. Complete tears
• Isolated tears of MCL-stable the knee in full extension,long cast brace for 6w
• Isolated tears of LCL-same as MCL
• Isolated tears of ACL-early operative reconstruction
• Isolated tears of PCL-treat conservatively
• Combined injury-joint support&physiotherapy followed by ACL reconstruction

Complications

• Adhesions
• Ossification in the ligament
• Instability
MENISCAL TEARS

Role of menisci

1. Improve articular congruency and stability

2. Control the complex rolling and gliding actions of the joint
3. Distributing load during weight bearing

Type of tears

Clinical features

• Young patient
• Severe pain on medial side of the knee
• Knee in ‘locked’ position
• Swelling
• SPECIAL TESTS
1. McMurray’s test – classical test
2. Apley’s grinding test
3. Thessaly test – high diagnostic accuracy rate

Investigation

• Plain X-ray - NORMAL

• MRI – a diagnostic test
• Arthroscopy

Treatment

• Conservative
• ‘Locked knee’ – Unlock spontaneously (Gentle passive flexion and rotation)
• Operative
• Indication: joint cannot be unlocked, persists symptoms after conservative
treatment
• Open meniscectomy (total/partial)
• Arthroscopic meniscectomy
• Meniscus repair by suturing
PATELLAR DISLOCATION

Mechanism of injury

• Due to indirect force : sudden, severe contraction of the quadriceps muscle

while the knee is stretched in valgus and external rotation.

• Patella dislocate laterally and the medial patellofemoral ligament may be

torn.

Clinical features

• First time dislocation

− Tearing sensation & feeling that the knee has gone out of joint;
collapse & fall down when running.
• If patella remain unreduced
− Neither passive nor active movement is possible

Investigation

• X-ray : Antero-Posterior, lateral

and tangential (Skyline) views
needed

• MRI may reveal soft tissue lesion

(disruption of medial
patellofemoral ligament)

Treatment

• Most cases – Patella can be pushed back into place without much difficulty.
• Intercondylar dislocation - open reduction may be needed
• No sign of soft tissue rupture (minimal swelling, no bruising, little tenderness) - Cast
splintage
• If much bruising, swelling & tenderness medially (ligaments torn) - immediate operative
repair
  SHOULDER DISORDER

ROTATOR CUFF SYNDROME

• Impingement syndrome
• Biceps tendinitis and/or rupture
• Tears of the rotator cuff
• Adhesive capsulitis

Causes

• Sports- tennis, baseball, swimmer

• Lifting heavy weights
• Falling on your shoulder
• Using arm to break a fall

Symptoms

• Pain in shoulder and arm

• Weakness of shoulder
• Inability to sleep on the shoulder

Investigation

• MRI

Treatment

• Rest of joint, analgesics

• Surgery - arthroscopy, open tendon repair

BICEPS TENDINITIS

• Inflammation of long head of biceps tendon

• Tenderness localized to bicipital groove
• Weightlifting, tennis, wheelchair athletics

Manoeuvres

1. Speed’s test – resisted flexion with the elbow straight

and the forearm supinated
2. Yergason’s test – resisted supination of the
forearm with the elbow bent

Treatment

• Rest, local heat and deep transverse friction for relief.

• Corticosteroid injection.
• Surgical solutions in refractory cases-arthroscopic decompression, biceps tenotomy and
biceps tenodesis.
ADHESIVE CAPSULITIS (FROZEN SHOULDER)

• Pain and stiffness of shoulder – reduce

range of movement
• Unknown cause

Clinical features

• Patient aged
• 40–60
• History of trauma
• Aching in the arm and shoulder
• Pain increases in severity
• Prevents sleeping on the affected side
• Pain may subside after months, but stiffness increase
• Movement is regained, but it may not return to normal

Diagnosis

• Clinically diagnosed
• Characteristic features:
1. Painful restriction of movement in the presence of normal x rays
2. A natural progression through three successive phases (freezing, frozen, thawing)

Treatment

• Conservative
– Analgesics and anto-inflammatory drugs
• Surgical
– indication : prolonged and disabling restriction of movement which fails to respond
to conservative treatment
– Arthroscopic capsular release
SHOULDER DISLOCATION

• One that most commonly dislocates

• Accounts for up to 50% of all the dislocations in the body.
• Due to the fact that the shoulder has a great degree of
movement and that it relies on the surrounding
musculature for support.
• Occurs more commonly in adults, rare in children.

Types of dislocation
1. ANTERIOR DISLOCATION (>90%)
• Causes: Fall on an out-stretched hand with shoulder abducted and externally rotated
• Mechanism of injury:
– The head of the humerus is driven forward → tearing the capsule and
avulsing the glenoid labrum  labrum tear (also called the Bankart lesion)
→ Head of the humerus is forced out of the glenoid fossa anteriorly and
inferiorly
• Classification : depending on the position of the dislocated head :
1. PREGLENOID : The head lies in front of the glenoid
2. SUBCORACOID *most common*: The head lies below the coracoid process.
3. SUBCLAVICULAR : The head lies below the clavicle
• Clinical features:
– Shoulder abducted and the elbow is supported with opposite hand
– Severe pain and inability to move the shoulder
– History of fall on an out-stretched hand
– On examination,
• Patient loathes any kind of examination due to severe pain
• A bulge may be felt just below the clavicle
• Loss of normal round contour of shoulder joint  flattened
• The arm must always be examined for nerve and vessel injury
before reduction is attempted
• Investigation:
– AP view: the overlapping shadows of the humeral head and glenoid fossa,
with the head usually lying below and medial to the socket
– Lateral view: the humeral head out of line with the socket.
• Treeatment:
1. Closed Manipulative Reduction (CMR) under sedation or general
anaesthesia and via the following methods :
i. Hippocratic method – Gently increasing traction is applied to the
arm with the shoulder in slight abduction, while an assistant applies
firm countertraction to the body (a towel slung around the patient’s
chest, under the axilla).
ii. Stimson method – The patient is left prone with the affected limb
hanging over the edge of the bed. A 10-15lbs of weight is suspended
from the wrist. Most cases achieves reduction in 20-25 minutes
iii. Kochers method - The elbow is bent 900 and held to the body. The
arm is slowly rotated 750 laterally, the point of the elbow is lifted
forwards and finally the arm is rotated medially. This technique
carries the risk of nerve, vessel and bone injury and is not
recommended.
2. Take POST-CMR X-ray to confirm the reduction
3. When the patient is fully awake, active abduction is gently tested to exclude
an axillary nerve injury and rotator cuff tear. All neurovascular
examination should also be done.
4. Rested arm in a sling for about 3 weeks (<30 years old), or 1 week (>30 years
old).
5. Encourage movements or shoulder exercise, but combined abduction and
lateral rotation must be avoided for at least 3 weeks.
• Complications
– EARLY
1. Rotator Cuff tear
• Particularly in older people.
• May have difficulty abducting the arm after reduction
2. Nerve injury
• The axillary nerve is most commonly injured; unable to
contract the deltoid muscle.
• The nerve lesion is usually a neuropraxia which recovers
spontaneously after a few weeks
• Occasionally, radial nerve, musculocutaneous nerve, median
nerve or ulnar nerve can be injured.
3. Vascular injury – Damaged axillary artery
4. Fracture-dislocation – If there is an associated fracture of the
proximal humerus(e.g. greater tuberosity) during dislocation.
– LATE
1. Recurrent dislocation
2. Shoulder stiffness
• Prolonged immobilization may lead to stiffness of the
shoulder, especially in patients >40 years old.
• Loss of lateral rotation, which automatically limits abduction
3. Unreduced dislocation
• Undiagnosed dislocation is more likely to occur if the patient
is either unconscious or very old.
2. POSTERIOR DISLOCATION
• Rare, accounting for less than 2 per cent of all
dislocations around the shoulder.
• Cause :
– This happens most commonly during a fit
or convulsion, or with an electric shock.
– Can also follow a fall on to the flexed,
internal rotated, or a direct blow to the
front of the shoulder  driving the head
of humerus backward.
• Clinical features:
– The arm is held in internal rotation and is locked in that position.
– The front of the shoulder looks flat with a prominent coracoid, but swelling
may obscure this deformity.
• Investigation
– X-ray: Missed diagnosis in over 80% of cases
as the humeral head appears to be almost
normally aligned with the glenoid.
– AP view: The internally rotated humeral head
takes on a rounded appearance known as an
electric light bulb, and it stands away
somewhat from the glenoid fossa (the ‘empty
glenoid’ sign).
• Treatment
– CMR - Acute dislocation is reduced by pulling on the arm with the shoulder
in adduction
– A few minutes are allowed for the head of the humerus to disengage 
gently rotated laterally while the humeral head is pushed forwards.
– If reduction feels stable, the arm is immobilized in a sling;
– Otherwise the shoulder is held widely abducted and laterally rotated in an
airplane type splint for 3–6 weeks.
– Shoulder movement is regained by active exercises.
3. RECURRENT DISLOCATION
• Once a shoulder has been dislocated, this may happen repeatedly.
• With recurrent anterior dislocation, patient complains the shoulder ‘slips out’ when
the arm is lifted into abduction and lateral rotation.
• If the joint has dislocated before, a depression on the humeral head in its postero-
lateral quadrant caused by impingement by the anterior edge of the glenoid on the
head as it dislocates, known as Hill-Sachs lesion.
 4. INFERIOR DISLOCATION
• Rare.
• Caused by severe hyper-abduction force 
Subglenoid dislocation of the head of the humerus
in which the arm is in nearly full elevation and
abduction (luxatio erecta).
• Clinical features :
– Patient’s arm locked in almost full
abduction, the head of the humerus
may be felt in or below the axilla
• X-ray: humeral shaft is shown in the abducted
position with the head sitting below the glenoid.
• Treatment: Reduction is usually by applying
traction in abduction and swing the arm into
adduction the arm is rested in a sling until
pain subsides  movement is then allowed, but
avoiding abduction about 3 weeks to allow the
soft tissues to heal.

SUBACROMIAL BURSITIS
• Causes
– Injury, infection (rare in the shoulder), or an underlying rheumatic condition
– Acute trauma or repetitive injury to the shoulder
– Frequent overhead work/lifting (e.g. overhead throwing sports and swimming, or
overhead work such as painting, carpentry, or plumbing)
– Frequent forceful pulling
• Clinical features:
– Typically identified by localized pain or swelling, tenderness, and pain with motion of
the tissues in the affected area.
• X-ray testing can sometimes detect calcifications in the bursa when bursitis has been chronic
or recurrent.
• Shoulder bursitis is often accompanied by tendinitis.
• Treatment:
– If there is suspected infection, do aspiration of the inflamed fluid, identify the
microbes causing the infection  antibiotic therapy
– Otherwise, apply cold therapy or ice to the shoulder, rest the shoulder, and anti-
inflammatory and pain medications.
  ELBOW

LATERAL EPICONDYLITIS
• Aka “tennis elbow,”
• In active 30-40 years old

Clinical Features
• Pain and tenderness over common extensor tendon commonly localized at extensor carpi
radialis brevis at the lateral epicondyle of the elbow.
• Pain :
– S - distal to lateral epicondyle
– O - insidious
– C - dull ache around the joint to sharp pain on
movement
– R - nil
– A - rest
– T - days-months
– E - activities that involve forceful gripping and
wrist extension
– S - pain can become severe over time and may
interfere with routine activities

Mechanism of injury:
• Forceful repetitive wrist extension (affecting extensor
muscles)muscle tearinflammation.

Special tests
1. Cozen’s test
– When the affected elbow slightly flexed and pronated,
the patient makes a fist and actively extends his/her
wrist.
– The clinician put his/her thumb over the lateral
epicondyle & attempts to flex the patient’s wrist with
the other hand.
– +ve test when there is pain felt over lateral epicondyle.
2. Mill’s test
– While palpating the lateral epicondyle, the
examiner pronates the patient’s forearm and
flexes the wrist fully and extends the elbow.
– +ve when pain is felt over lateral epicondyle.
3. Maudsley’s test
– The examiner resists the extension of the 3rd
digit, stressing the extensor digitorum ms.
– +ve when pain is felt over lateral epicondyle.

Investigation
• Imaging - Plain radiograph
– Usually normal
– Occasionally shows calcification at the tendon origin.
Management
• Conservative (90% resolves spontaneously in 6-12m)
– Rest and restrict activities
– Modification of sporty style
– Tennis elbow clasps is helpful
– Corticosteroid and LA to relieve pain
• Operative (in persistent and recurrent symptoms)
– Excision of the pathologic area of degenerated tendon.

MEDIAL EPICONDYLITIS
• Aka ‘golfer’s elbow’
• Similar but less frequent (3x < common) than lateral epicondylitis
• Caused by overused of flexor-pronator ms

Clinical features:
• Pain and tenderness over flexor-pronator origin at the medial epicondyle of the elbow.
• Pronation and wrist flexion against resistance exacerbate the pain.

Special test
• Resisted wrist flexion with clenched fist of affected arm.
– + ve when pain is felt over medial epicondyle.

Investigation
• Plain radiograph: usually normal

Treatment
− Treatment principles for the non-competitive athlete are similar to those used for lateral
epicondylitis.
 ORTHOPAEDIC SOFT TISSUE INFECTIONS INCLUDING DIABETIC FOOT
Definition
• Infection
• Invasion of the body by harmful organisms (pathogens) such as bacteria, fungi
protozoa, rickettsia or viruses.
• Soft tissues
• Tissues that connect, support or surround
other structures and organs of the body, not
being bone.
• Skin, fascia, ligament, muscle

CELLULITIS
• Definition
• Localized or diffuse inflammation of connective
tisssue due to
• Infection of deepest part of dermis of skin and
subcutaneous fat
• Aetiological agents
• S.Aeureus or S. Pyogenes :most common
• Clinical features
• Warm, erythamatous,tender, swollen, and
poorly demarcated skin lesion(different with
erysipelas)
• Can exist with pus /without pus
• Usually associted with fever, chills and rigor
• Regional lymphadenoa

ERYSIPELAS
• Intensely erythematous, indurated plaque with sharply demarcated raised margin
• Face and lower limbs are the most common site
• Risk factors
o Break in the skin, such as a cut, small puncture wound
o Post venectomy (CABG)
o Chronic leg swelling (oedema)
o A pre-existing skin infection, such as athlete’s foot or impetigo
o Immunodeficiency (Diabetics, long-term steroid therapy)
• Investigation
o History and physical examination
o Elevated white blood cell count
o Blood C&S (not routine)
o MRI (to distinguish bone and soft tissue
infection)
• Management
o Analgesics - acetaminophen/NSAIDs
o Antibiotics – IV cloxacilin, penicillin severe case
o Mild cases - Oral cloxacilin
NECROTIZING FASCIITIS
1. Uncommon soft-tissue infection, usually caused by toxin-producing, virulent bacteria, which
is characterized by widespread necrosis mainly fascia and subcutaneous tissues, but can also
extend to involve muscles and skin.
2. High mortality rate, as the disease can progress rapidly to systemic infection, sepsis and
eventually death
3. Sometimes called as ‘flesh-eating disease’
4. Referred as Fournier’s (testicular) gangrene when it occurs on the genitals

Types:
1. Type 1 – poly-microbial (MOST COMMON)
 Enterobacteriaceae &anaerobic organism
 Usually immunocompromised host, following surgery or in diabetic
2. Type 2 – monomicrobial – Group A B-haemolytic streptococcus
 Streptococcus pyogenes
 Usually immunocompetent hosts
 Extremities
3. Type 3 – marine Vibrio vulnificus
 Gas gangrene
 Clostridium bacteria
 Marine exposure
4. MRSA

Risk factors
5. Immune suppression
• Diabetes
• AIDS
• Cancer
6. Bacterial introduction
• IV drug use
• Hypodermic therapeutic injections
• Insect bites
• Skin abrasions
• Abdominal and perineal surgery
7. Other host factors
• Obesity

Pathology
• Bacteria inoculate into normal sterile area by penetrating wound or by hematogenous
spread → rapidly replicates → synthesize its own enzymes and toxins which facilitate the
spread of growth along the tissue plane + angiothrombotic microbial invasion + liquifactive
necrosis of the superficial fascia.
Clinical manifestations

Diagnosis
− Clinical diagnosis
− Blood tests and imaging, especially MRI and CT scans can be helpful but are not diagnostic
− The criterion standard for diagnosis of the disease is histology of tissue specimens obtained
during surgical exploration – facial biopsy (frozen section)
− Laboratory risk indicator for necrotizing fasciitis (LRINEC) score can help in diagnosis of the
disease and differentiate it from other
− Score of 6 and above suggests that necrotizing fasciitis should be seriously considered

Management
− Requires urgent and extensive surgical debridement and appropriate antibiotic therapy.
− Generally, treatment includes:
o Prompt diagnosis
o Immediate resuscitation
o Aggressive emergency debridement, fasciotomy, amputation if necessary
o Antibiotics – broad spectrum IV
 Start empirically with penicillin, clindamycin, metronidazole and
aminoglycoside
 Definitive antibiotic when organism known – penicilin G, imipenem,
vancomycin
− Amputation in life threatening condition.
− Treatment for complications (toxic shock, organ failure, respiratory distress)
DIABETIC FOOT ULCER

Definition
• The diabetic foot may be defined as infection, ulceration and/or destruction of deep tissues
associated with neurologic abnormalities, various degrees of peripheral vascular disease
and/or metabolic complications of diabetes in the lower limb.

Risk factors
o Long standing and uncontrolled diabetes mellitus
o Reduced joint mobility
o Smoking
o Hypertension
o Hyperlipidemia

Aetiology
1. PERIPHERAL NEUROPATHY
• Mechanism: Hyperglycemia → Increase in sorbitol and fructose → Reduce in myo-
inositol and NADPH → Ischemia and nerve dysfunction
• Sensory symptoms: Numbness, paraesthesia, hyperaesthesia, tingling and pain
beginning in the toes and soles of the feet.
• Motor nerve damage: Imbalance between flexion and extension. This causes foot
deformities that result in abnormal pressure areas that gradually cause skin breakdown
and ulceration.
• Autonomic: Poor natural lubrication and reduction in blood flow to the soles of the feet
allows the skin to become dry and cracked, form fissures and become hard

2. PERIPHERAL VASCULAR DISEASE

• Arteries in a diabetic are affected by two disease processes, namely atherosclerosis and
(Monckenberg’s) medial sclerosis.
• Peripheral vascular atherosclerosis will impact the delivery of nutrients and oxygen to
the foot, thus, lead to infections and tissue necrosis.
3. INFECTION
• Diabetic patient is not more vulnerable to infection, but is poor at fighting infections
once it developed.
• This is due to hyperglycemia state which will caused abnormal phagocytosis, altered
chemotaxis of white blood cells and poor cytotoxic environment to fight off bacteria.
• Metabolic deficiency also influence the potential of wound healing.
− Serum albumin : < 2.5 g/dL
− WBC : < 1500/mm3
4. TRAUMA
 • Acute: abrasions and burns occur often due to the absence of nociception. Poor wound
healing makes ulcerations more likely occur
• Chronic: reduced motor function results in a high arch. Together with decreased
proprioception, this creates alteration of foot shape. These result in bony prominences
which, when coupled with high mechanical pressure on the overlying skin, results in
ulceration.

Figure 1. Neuropathic ulcer Figure 2. Neuroischemic ulcer

DIFFERENCES BETWEEN ISCHEMIC AND NEUROPATHIC FOOT

NEUROPATHIC foot Characteristics ISCHEMIC foot

Warm Skin temperature Cold

Painless Pain Painful

Not altered Skin color Dependent rubor

Hard and dry at pressure Callus Usually not present

point

Usually on tips of toes & Ulcer Often on margins of foot, tips

plantar surfaces under of toes, back of heels
metatarsal head

Bounding Peripheral pulses Feeble/absent

> 0.9 Ankle-Brachial Index < 0.9

Charcot’s joints Complications Critical ischemia

 KING’S CLASSIFICATION (DESCRIBE GENERAL DFU)

1. Foot at risk (have neurovascular symptoms)

2. Pre ulcerative

3. Ulcerative

4. Infected

5. Necrotic

6. Amputation
CHARCOT ARTHROPATHY (Neuropathy Osteoarthropathy)
• A chronic, progressive, destructive process affecting bone architecture and joint alignment in
people lacking protective sensation.
• Neuropathy will caused paralysis of small muscle in the foot, which will caused clawing of
toes.
• The stages depends on the degree of warmth, swelling and erythema as the process advance
from bone resorption and fragmentation to bone formation and consolidation.

STAGES OF CHARCOT ARTHROPATHY (EICHENHOLTZ)

Stage Signs & Symptoms Radiographs

0: Pre-fragmentation Acute inflammation; confused with Regional bone demineralization

infection

1: Fragmentation Acute inflammation, swelling, Regional bone demineralization,

erythema, warmth; confused with Periarticular fragmentation, joint
infection dislocation

2: Coalescence Less inflammation, less swelling, Absorption of bone debris, early

less erythema bone healing and periosteal new
bone formation

3: Resolution Resolved erythema, swelling, and Smoothed bone edges,

warmth; consolidation of healing bony/fibrous ankylosis

Investigation
1. BIOCHEMICAL
− FBC
− FBS, RBS
− HbA1c
− RP
− Urinalysis
− Wound & Blood culture
2. FOOT IMAGING
 Plain Radiograph: Detect osteomyelitis, osteolysis, fractures, dislocations seen in
neuropathic athropathy, medial artery calcification, soft tissue gas & foreign bodies
 CT: To detect suspected bone or joint pathology not evident by on plain radiograph
 MRI: Evaluation of soft tissue & bone pathology. Aid in diagnosis of osteomyelitis or
deep abscess
 Bone scan: Useful to differentiate between soft tissue swelling, osteomyelitis and
Charcot arthropathy
3. VASCULAR EXAMINATION
 Aim:
i. evaluate extend of occlusive vascular disease
ii. assessment for healing potential
1. Doppler segmental artery pressure
2. Ankle-branchial indices (ABI)
 Easy way to determine blood flow but may be
misleading due to calcification
 Normal value = 1.1 (abnormal <0.9)
3. Toe pressure measurement
 More accurate & reliable = less calcification in digital vessels
 85%-100% of foot lesion will heal when toe pressure are >40mmhg and less than
10% will heal if <20mmHg
4. Transcutaneous oxygen tension (TcPO2)
• <10mmHg correlates with non-healing
• >30mmHg correlates with healing
4. NEUROLOGICAL EXAMINATION
 Aim : to assess peripheral sensory neuropathy  major independent risk factor for DFU
1. Monofilament test by using 5.07 Semmes-Weistein monofilament (10-g) wire
2. Vibration perception test using tuning fork 48Hz / vibration perception threshold
assessment with biothesiometer
3. 2-point discrimination

Management
o Non-operative
1. Shoe modification
− indication: potential ulcers present
− Includes deep or wide shoes, custom insoles, rocker bottom soles 
reduce plantar pressure
2. Wound care & dressing
− Absorb exudate ; act as barrier from contamination
3. Total contact casting
− Mechanical relief plantar ulceration
o Operative
1. Surgical debridement
− Indication : grade 3 or greater ulcers should undergo I&D with
antibiotic treatment before casting
2. Ostectomy +/- TAL
− Indication : bony prominent lead to internal pressure
3. Partial calcaneoctemy +/- TAL
− Indication : large heel ulcer with associated calceneal osteomyelitis
4. Syme amputation
− Indication : forefoot gangrene & a palpable post tibial artery pulse
Assessment of Diabetic Foot
1. History
• General and medical history
• Hx of foot problems
 Daily activity and current foot status
 Footwear-shoes/slippers/sandals
 Foot care- aware of foot problems/inspect foot/wash feet/proper nail
clipping/attend podiatry
 Callus formation
 Deformities and previous surgery
 Neuropathy and ischemic symptoms
 Skin and nails problem-fungal infection/blisters/sweaty feet
• Hx of foot ulcer
 Site, size, odour, any drainage, depth, margins, swelling, colour
 Precipitating event or trauma
 Recurrence of ulcer
 Associated infections
 Frequency of hospitalizations and treatment given
 Wound care/measure to reduce plantar pressure
 Patient compliance
 Previous foot trauma or surgery
 Features of charcot’s joint
• Hx of presented foot complaints and duration
• Duration of diabetes, management and control
• Cardiovascular, renal, ophthalmic evaluation and other comorbidities
• Social hx- smoking, alcohol, occupation, dietary habits
• Current medication and antibiotic use
• Allergies
• Past medical and surgical hx
• Cultural habits-walks barefoot/wets feet at work/wear socks/walks a lot
2. Physical examination(general and local examination)
• Musculoskeletal
 Attitude and posture of lower extremities and foot
 Any deformities- Hammertoes/bunions/pes planus or cavus/charcot
deformitis/amputation
 Limited joint mobility-active and passive
 Gait evaluation
 Plantar pressure assessment
• Skin and nails of the foot
 Skin appearance: colour, texture, turgor and dry skin
 Calluses, heels fissure, cracking of skin
 Nail appearance: Onychomycosis, paronychia
 Presence of hair
 Ulceration, gangrene, infection
 Tinea pedis
• Vascular status of the leg and foot
 Pulses(dorsalis pedis, posterior tibial, popliteal, femoral)
 Capillary return(normal<2 sec)
 Edema
 Temperature
 Colour changes: cyanosis, dependent rubor, erythema
 Changes of ischemia(skin atrophy, nail atrophy, abnormal wrinkling,
diminished pedal hair)
• Neurological
 Vibration
 Sensation
 SPINAL DISORDERS
SPINAL INJURY
Mechanism
1. Traction injury
• Lumbar spine: resisted muscle effort may avulse transverse processes
• Cervical spine: seventh spinous process can be avulsed (‘clayshoveller’s fracture’).
2. Direct injury
• Penetrating injuries to the spine
3. Indirect injury (most common)
• Fall from a height when the spinal column collapses in its vertical axis
• During violent free movements of the neck or trunk.

Stable and unstable fractures

• Stable fractures
o Vertebral components not displaced by normal movements
o Little risk of neuron damaged.
o Don't cause spinal deformity or neurologic (nerve) problems
o Spine can still carry and distribute your weight
• Unstable fractures
o Significant risk of displacement and damage to the neural tissues.
o Difficult for the spine to carry and distribute weight.
o May progress and causing further damage
o May also cause spinal deformity.

Denis classification: the three-column concept

1. Anterior Column:
− Front half of the vertebral body and intervertebral disc.
− Ligament – anterior longitudinal ligament
2. Middle Column:
− Key part of spinal stability.
− Back half of the vertebral body and intervertebral disc.
− Ligament – posterior longitudinal ligament
− If there's a fracture in the middle column in addition to the anterior or posterior
column, more likely to have nerve damage and spinal instability.
3. Posterior Complex:
− All the parts of the vertebra that are on the back side make up the posterior column.
− This includes the pedicles, lamina, facet joints, and spinous process.
• If fracture just in the anterior column, the spine should be able to still carry your weight well
enough.
• However, if fracture the anterior and middle column, it's more likely that your spine will be
unstable. Since the middle column connects the anterior and posterior columns, if that part
is fractured, it will be harder for the spine to function well.
Major and minor fractures
1. Minor fracture
• Fracture to posterior elements
2. Major fracture
• Fracture to the vertebral body, the pedicles, or the lamina.
• Vertebral body - carry weight and distribute the force of your movements.
• Pedicles or lamina - increased possibility of nerve damage + provide support to keep
your spine stable.

DENIS CLASSIFICATION OF SPINAL TRAUMA

MAJOR INJURIES: MINOR INJURIES
1. Compression Fracture 1. Transverse process
2. Burst Fracture 2. Articular process
3. Chance Fracture 3. Par interarticularis
4. Spinous process

Specific fracture types

1. Compression Fracture:
− Very common in patients with osteoporosis, or weakened bone.
− Sudden force of a lot of pressure, the bone may not be able to
handle the stress.
− Wedge fracture: subtype of compression fracture. Part of the
vertebra—usually the anterior (front) part—collapses under
pressure and becomes wedge shaped.

2. Burst Fracture:
− Severe trauma
− Vertebra is fractured in multiple places.
− Bony fragments can spread out and cause spinal cord injury.

3. Flexion-distraction Fractures (Chance fracture,):

− Sudden forward movement that places incredible stress on
the spine
− Usually fractures in the posterior and middle column.

4. Fracture-dislocation:
− All three column are disrupted and the spine is grossly
unstable.
− Most dangerous injuries
− Associated with neurological damage to the lowermost part
of the cord or the cauda equina.
Differences between burst and compression fracture on plain radiograph
Burst fracture Compression fracture

1. Reduction of verterbral heaight of more than Reduction of vertebral height of less than 50%
50 % of its original size of its original height

2. Involve more than 1 column Usually involve the anterior column only

Clinical assessment
1. NECK
− LOOK, FEEL but do not MOVE
− Inspect head and face for bruises or grazes indicate indirect trauma
− Bruising, deformity, or penetrating injury
− Palpate bones and soft tissues for tenderness, bogginess or abnormal space
between adjacent spinous process
2. BACK
− Inspect and palpate
− 'Log-rolled' the patient
3. NEUROLOGICAL EXAMINATION
− Repeated several times in first few days
− Test each dermatome, myotome, reflexes
Investigation
• Nerve function test - reflexes and gait
• X-Ray - mandatory to examine any abnormalities (bone spurs)
• CT scan - any structural damage to spines, displacement of bone fragments
• MRI - intervertebral disc, ligamentum flavum, neural structures
• CT Myelography - spinal canal dimension, impingement by fracture fragments /
intervertebral disc and root avulsion (Done in pt who MRI is contraindicated)

Management
1. PRE-HOSPITAL
a. Immobilization - hard cervical collar (cervical spine injuries)
b. Resuscitation - airway maintenance, adequate oxygen saturation, restoring blood
pressure, preventing bradycardia. Simultaneously done to prevent any ischaemic
damage in compromised cord
2. HOSPITAL
a. Medical Management - Conservative (General/Medical)
− Epidural Steroid Injection
− Intradiscal Electrothermal Therapy(IDET)
− Nucleoplasty
− Facet Injections and/or Medial Branch Blockade
− Radio Frequency Rhizotomy or Denervation
b. Surgical Management
− Surgical Decompression
− Surgical Stabilization
− Fixation of Vertebrae
− Fixation of Spine
− Artificial disc implantation
DEGENERATIVE SPINAL DISEASES
SPONDYLOSIS
− A degenerative disorder affecting the vertebrae, facet joints, intervertebral discs and
surrounding ligaments.
− Degenerative changes occur as someone is ageing:
i. Decreased elasticity of intervetebral disc.
ii. Ligaments become less elastic and thicken.
iii. Facets over-ride and hypertrophy.
iv. Marginal osteophytes develop.

Symptoms
CERVICAL SPONDYLOSIS LUMBAR SPONDYLOSIS
Usually aged over 40 No specific age
Neck pain & stiffness Usually asymptomatic;
Radiculopathy pain develops in arms & fingers + Pain on activity/ prolonged sitting/ bending/
hyporeflexia lifting
Dermatomal sensory loss

Investigations
1. X-ray
− Narrowing of intervertebral disc
− Bony spur formation at ant. & post. edge of vertebral
body
− Osteoarthritic changes in tiny joints
− Oblique view: Bony encroachment on intervertebral
foramina
2. MRI – nerve root compression

Treatments
1. MEDICAL
a. Analgesia
b. Anti-inflammatory
c. Muscle relaxants
2. NON-OPERATIVE
a. Immobilization & brace
b. Soft cervical collar
c. Lumbosacral orthosis
d. Physiotherapy
e. Lifestyle change
3. OPERATIVE
a. Decompression
b. Fusion
SPONDYLOLISTHESIS
− Spondylo – vertebrae; listhesis – slippage
− Displacement of one vertebra on the one below.
− Slippage usually occur between L4 & L5 and L5 & sacrum.

Myerding classification
- % of slip of AP diameter of vertebrae
GRADE I II III IV V
% slip <25 25 – 50 50 – 75 75 – 100 >100

Aetiology
1. Separation/ stress fracture through pars interarticularis  allow anterior
part of vertebra to slip forward
2. Osteoarthritic degeneration of the facet joints  lose normal stability
3. Dysplasia of lumbosacral facet joints
4. Destructive conditions: fracture, TB, neoplasia

Symptoms
- Lower back pain
- Spinal claudication (leg pain + numbness after 5 min of standing
upright/walking and is relieved by sitting/ squatting)

Investigations
1. X-ray – break in the pars interarticularis
2. CT, MRI – narrowing of spinal canal

Treatment
1. Conservative – reduce sport/high impact activity
2. Operative, only if:
- Symptoms are disabling
- Upper vertebra has slipped over >50%
- Neurological compression is significant

GRADE I & II GRADE III – V

- In situ fusion / repair of the pars defect using - Extended in situ fusion
screw - Decompression
- Decompression – if there is nerve root
compression
INTERVERTEBRAL DISC PROLAPSE
- Cervical region > sacrolumbar region (mechanical environment)
- Local strain or injury (sudden unguarded flexion and rotation)

Clinical features
- Prolapsed disc → press on posterior longitudinal ligament or
dura mater → neck pain and stiffness → radiate to scapular
region → pain referred to upper limb
- Pressure on nerve roots C6 and C7 → paraesthesia and weakness of arms
- Neck is tilted forward and sideways

Imaging
- X-Ray: narrowing of disc space
- MRI: disc protrusion is pressing on adjacent nerve root

Differential diagnosis
1. Acute soft-tissue strain: pain and stiffness at neck for weeks and months
2. Neuralgic amyotrohy (acute brachial neuritis): pain over the shoulder and serratus anterior
weakness (winging of scapula)
3. Cervical spine infections: unrelenting pain and local spasm. Erosion of vertebral end-plate on
x-ray
4. Cervical tumours: progressive neurological signs and bone destruction on MRI

Treatment
1. REST: use collar to prevent unguarded movement
2. REDUCE: traction to enlarge the disc space for prolapse to subside
3. REMOVE: disc is removed and bone graft is inserted

TUBERCULOSIS SPONDYLITIS (SPINE INFECTION)

Pathology
1. Blood-borne infection settles in the vertebral body adjacent to the intervertebral disc
2. → bone destruction and caseation + spreading of the infection to the adjacent vertebrae and
disc space
3. Vertebrae collapse to each other → sharp angulation (gibbus/kyphos)
4. Major risk of cord damage due to pressure by cold abscess occasionally can cause ischemia
from spinal artery thrombosis
5. However, if there is been much angulation, spine is flares cause progressive kyphosis which
risk to cord compression

Clinical features
- Long history of ill-health and back-ache
- Cold abscess
- Paraesthesia and weakness of the legs
- Local tenderness
- Restricted spinal movements
- Late features: angular thoracic kyphosis (gibbus)
Complication
• POTT’S PARAPLEGIA (TB spine with neurological involvement)
o Clinical features : lower limb weakness , upper motor neuron signs, sensory
dysfunction
o early-onset paresis is due to pressure by the abscess or bony sequestrum
o late-onset paresis is due to increasing deformity, or reactivation of disease or
vascular insufficiency of the cord

Investigations
• Mantoux test positive
• ESR is raised
• Needle biopsy is recommended in patients with no neurological signs to confirm
the diagnosis by HPE
o If no firm diagnosis obtained, tissue biopsy should be obtained by open
operation
• IMAGING
o X-RAY
 Reduction of disc space
 Local osteoporosis of two adjacent vertebrae
 Bone destruction and collapse of adjacent vertebral bodies
(progressive disease)
 Paraspinal soft-tissue shadows (edema, or paravertebral abscess)
 Signs of healing : increase bone density, paravertebral abscess
may undergo resolution or fibrosis or calcification
o MRI and CT scan
 Investigation of hidden lesions
 To evaluate extend of compression of the cord

Treatment
• Objectives :
o To eradicate/ at least arrest the disease
o To prevent/ to correct deformity
o To treat major complication (paraplegia)
o Restore function
• Continuous bedrest (immobilization) and chemotherapy
• Antituberculous chemotherapy for 6-12 months
• Operative treatment,
o Indications :
1. Abscess formation  drained
2. Advance disease with marked bone destruction and threatened severe
kyphosis
3. Neurological deficit (paraparesis) which do not respond to drug therapy
 METABOLIC BONE DISORDER
INTRODUCTION
• Definition:
o Disorders of bone strength, usually caused by
abnormalities of minerals (such as calcium or
phosphorus), vitamin D, bone mass or bone
structure.
• Bony Composition and Structure
o Consists of collagenous matrix containing mineral
salts and populated by cells
 Osteoclasts (bone resorption)
 Osteoblasts (bone formation)
 Osteocytes (resting bone cells functioned in
communicating information about local
stress

OSTEOPOROSIS
− A clinical disorder characterized by an abnormally low bone mass and defects in bone
structure, a combination which renders the bone unusually fragile and at greater risk of
fracture

Overview
o Highest incidence in Malaysia
o Location fracture: vertebral body> hip> wrist
o FRAX score - WHO fracture risk assessment tool that calculates the 10-year risk of
hip fracture and 10-year risk of major osteoporosis-related fracture
o The risk of fracture increasing with decreasing BMD

Risk factors
Non- modifiable Modifiable

Advancing age Low calcium/vitamin intake

Ethnic group (oriental and Caucasian) Sedentary lifestyle

Female gender (Demographic-male: female Cigarette smoking

ratio is 1:4)

Premature menopause (,45years) Excessive alcohol intake or caffeine

Family history osteoporotic hip fracture in Low body weight (BMI <19kg/m2)
first degree relative

Estrogen deficiency
Clinical features
− Increasing dorsal kyphosis (Dowager’s hump)
− Low trauma fracture
− Loss of height
− Back pain
− Diagnosis: primary osteoporosis after exclude secondary causes.
− BMD using DEXA – Gold Standard
− Men > 50yo, may be diagnosed if the T score (BMD) of the lumbar spine, total hip or femoral
neck is -2.5 or less.
− WHO diagnosis for postmenopausal women:

Type of osteoporosis
• Primary osteoporosis
1. POSTMENOPAUSAL OSTEOPOROSIS
• High- turnover osteoporosis
− Early postmenopausal syndrome
− Rapid bone loss due to increased osteoclastic resorption
• Low- turnover osteoporosis
− in elderly people
− gradual slowdown in osteoblastic activities
− dietary insufficiency
− chronic ill health
2. SENILE OSTEOPOROSIS (AGE RELATED)
• Post-climacteric
− Advanced age (>75 years old)
− Causes
a. Chronic illness
b. Mild urinary insufficiency
c. Lack sunlight exposure
d. Muscular atrophy
− Treatment
a. Treat the fractures
b. Treat the causes
c. Vitamin D and Calcium
• Involutional
− Gradual depletion of androgenic hormones in men
− Usually age >60 years old
− Treatment:
a. Same as postmenopausal osteoporosis
b. Vitamin D and calcium
c. Alendronate
d. HRT – if low testosterone level
 Type 1 (POST MENOPAUSAL) Type 2 (SENILE)

Age group Post-menopausal (highest incidence in 50-70 years old) >70 years old

Bone affected Almost exclusively trabecular Trabecular > cortical

Bone Distal radius and vertebral Hip and pelvis

fractured
Effect on Net negative change in calcium levels because of Poor calcium absorption
calcium decreased intestinal absorption and increased urinary
excretion of calcium
Effect on Reduced circulating levels of total (but not free) 1,25 -
vitamin D dihydroxyvitamin D

• Secondary osteoporosis
Nutritional • Malabsorption • Scurvy
• Malnutrition
Endocrine • Gonadal insufficiency • Thyrotoxicosis
disorders • Hyperparathyroidism • Cushing’s syndrome
Inflammatory • Rheumatoid disease • Tuberculosis
disorders • Ankylosing spondylitis
Malignant • Carcinomatosis • Leukaemia
disease • Multiple myeloma
Drug induced • Corticosteroids • Anticonvulsants
• Excessive alcohol consumption • Heparin
• Immunosuppressives
Other • Smoking • Osteogenesis imperfecta
• Chronic obstructive • Chronic renal disease
• Pulmonary disease

Investigations
• Aim of investigations
1. Confirm the diagnosis of osteoporosis
2. Assess fracture risk
3. Exclude secondary causes
• Initial investigations
1. Full blood count
2. Bone profile: serum calcium, phosphate, albumin
3. Alkaline phosphatase
4. Renal function
5. Plain X-rays findings:
• compression of one or more vertebral bodies
• biconcave distortion invertebral end plates
• calcification of the aorta
6. DXA (dual-energy x-ray absorptiometry) show reduced bone mineral density in
vertebral bodies or femoral neck.
 7. Bone x-ray findings:
• Thinned cortices
• Loss of trabeculae bone
8. Screening test to rule out causes

Prevention
1. Nutrition – calcium, vitamin D
2. BMI – low BMI a/w low bone mineral status and increased fracture risk
3. Avoid smoking and alcohol
4. Exercise - Wolff’s Law
5. Prevention of falls

RICKETS & OSTEOMALACIA

RICKETS OSTEOMALACIA

Inadequate bone mineralization in CHILDREN Inadequate bone mineralization in ADULTS

affect physeal growth and ossification resulting Incompletely calcified osteoid that cause bone
in endochondral skeleton deformities become ‘softened’

Causes
− Defects in vitamin D metabolic pathway
− Nutritional lack
− Underexposure to sunlight
− Intestinal mal-absorption
− Decreased 25-hydroxylation (liver
disease,anticonvulsants)
− Reduced 1α-hydroxylation (renal disease, nephrectomy,
1α-hydroxylase deficiency).
− Calcium deficiency or hypophosphataemia.

Pathophysiology
1. Inadequate substrate for the renal hydroxylase,
2. Yields a deficiency of 1, 25(OH)2D
3. Deficient absorption of calcium and phosphorus from the gut
4. Both calcium and phosphate levels reduced
5. The hypocalcemia activates the parathyroid glands, causing mobilization of calcium and
phosphorus from bone.
6. Simultaneously, the parathyroid hormone (PTH) induces wasting of phosphate in the urine
and calcium retention.
7. Consequently, the serum calcium level may be normal or reduced, the phosphate level is
low; hence, mineralization is impaired.
Pathology
• Rickets
Inability to calcify the intercellular matrix in the deeper layers of the physis
Piling up of normally active proliferative cells in irregular order
↑ thickness of entire physeal plate
Zone of calcification is poorly mineralized, forming sparse bone.
New trabeculae are thin and weak, with joint loading the the juxtaepiphyseal, metaphysis
becames broad and cup-shaped
• Osteo-malacia
Sparse islands of bone lined by wide osteoid seams, producing un-mineralized ghost trabeculae
and thinner cortices.
If persists for a long time, there may be stress deformities of the bones:
i. indentation of the pelvis
ii. bending of the femoral neck (coxa vara)
iii. Bowing of the femora and tibiae.

Clinical features Figure 1. Coxa vara

RICKETS
− Failure to thrive, listlessness, muscular flaccidity.
− Early bone changes
o Skull deformity (craniotabes)
o Thickening of the knees, ankles and wrists (physeal overgrowth)
o Enlargement of the costochondral junctions (rickety rosary)
o Lateral indentation of the chest (Harrison’s sulcus)
− Standing
o Lower limb deformities
o Stunting of growth
− In severe rickets
o Spinal curvature
o Coxa vara
o Bending or fractures of the long bones.
OSTEOMALACIA
− Backache
− Muscle weakness
− Vertebral collapse → loss of height
− Existing deformities (mild kyphosis or knock knees)
− Unexplained pain in the hip/long bones may presage a stress fracture.

Investigation
1. Blood
a. ↓ Serum calcium
b. ↓ Serum phosphate
c. ↑Alkaline phosphatase(ALP)
2. Urine: ↓Urinary calcium excretion
3. Imaging: X-ray
a. RICKETS
• Thickening and widening of the growth plate
• Cupping of the metaphysis
• Bowing of the diaphysis.

b. OSTEOMALACIA
• Indentation of the acetabula producing the trefoil or champagne glass pelvis
 • Looser’s zones in the pubic rami and left femoral neck
• Fracture in the mid-diaphysis of a long bone following low-energy trauma
(the femoral cortices in this case are egg-shell thin).
• Biconcave vertebrae

Treatment
− Vitamin D (400–1000 IU per day)
− Calcium supplements
− Elderly people require larger doses of vitamin D (up to 2000 IU per day).
− Patient with mal-absorption(fat malabsorption), large dose of vitamin D is given (50 000
IU/day)

SCURVY
Definition
• Ascorbic acid deficiency

Pathology
• failure of collagen synthesis and osteoid formation

Clinical features
• Spontaneous bleeding
• Irritable and anemic in infants
• Spongy and bleeding gum
• Excruciating pain and tenderness near large joint
• Fractures of epiphysis separation

Investigation
• X-ray
• generalised bone rarefaction, most marked in long bone metaphysis,
• dense transverse band at juxta-epiphyseal zone and around the ossific centres of
epiphyis (ring sign)-due to calcification in growing cartilage
• Metaphysis deformed or fractured.
• Subperiosteal hematmas show as soft tissue swellings or periosseous calcification.

Treatment
• Large doses of vitamin C
RADIOLOGY SEMINAR
METABOLIC BONE DISEASES
1. OSTEOPOROSIS
• The commonest metabolic bone disease characterize by a decrease in bone mass/density.
• Occur when bone resorption > bone formation
• Decrease bone mass → defect in bone structure → high risk of fracture
• Clinical Feature:
o Asymptomatic
 Having weaker bones does not in itself give you any symptoms.
 Silent disease
 Symptoms presented when complication occur
o Bone fracture
 Occurring after a trivial fall
 Neck of femur, Colle’s fracture (wrist), spine
o Vertebral fracture
 Back pain
 Stooping of posture
 Loss of height
• Diagnosis
o Dual Energy X-ray Absorptiometry scan (DEXA scan) measures the bone density
o It is the most common used and most reliable in diagnosing osteoporosis.
o Look for features of osteoporosis in CT scan or X ray of spine.
o It is calculated as a standard deviation (SD) score.It measures the difference
between the patient’s bone density and the expected value in healthy population.
o Translates as bone density score:
 T-score: compares with a healthy/younger population score
• Above -1 is normal
• Between -1 and -2.5 is abnormal ( indicate a reduced bone mass)
• Less than -2.5 ( osteoporotic)
 Z-score: compare with the same population (age and gender)
• Below -2 (lower bone density than those in same population)
• Features of osteoporosis in CT Scan or
X ray of spine.
o Loss of vertebral height due to
collapse
o Cod’s fish appearance: when
disc bulges into adjacent
vertebral bodies. Disc look
concave.
o Ground glass appearance of
bone
2. RICKETS AND OSTEOMALACIA
• Inadequate bone mineralization → Defect anywhere along the metabolic pathway for
Vitamin D
• Rickets: Inability to calcify intercellular matrix in deeper layer of physis → Cells in
proliferative zone piled up irregularly → Increase thickness in entire physeal plate
• Sparse islands of bones are lined by osteoid seams → Producing unmineralized ghost
trabeculae (not very strong) → Cortices are thinner than normal
• Caused by :
o Nutritional lack
o Underexposure to sunlight
o Intestinal malabsorption
o Decreased 25-hydroxylation
o Reduced 1α-hydroxylation
• Clinical Features:

RICKETS OSTEOMALACIA

Presents with tetany and convulsion Bone pain

Failure to thrive Backache
Listlessness Muscle weakness
Muscular flaccidity Loss of height
Kyphosis / knock knees

Bowing diaphysis widening of physis cupping of metaphysis

Looser’s zone

Champagne glass pelvis (indentation of

acetabula)
 Biconcave vertebrae Fracture in mid-diaphysis of
long bone (low-energy
trauma)

3. HYPERPARATHYROIDISM
• Overproduction of PTH enhances Ca conservation → Tubular
absorption, intestinal absorption, bone resorption → Increased
osteoclastic activity causing subperiosteal erosions

BONE INFECTION
1. OSTEOMYELITIS Subperiosteal cortical
resorption of middle phalanx
− Infection of bone characterized by progressive inflammatory
destruction.
− Mechanism of spread by:-
• Hematogenous (most common in children)
• Penetrating injury or any surgical contamination
• Adjacent soft tissue infection
− Acute: Classical: Pain, fever, malaise, bone tenderness, restricted movements. Non-
classical: neonates / infants: fever, generally unwell, shock.
− Chronic: Non-resolving acute OM
− Most common organism is S aureus (up to 70%), Group B haemolytic streptococci esp in
infants, H. influenza (younger than 3 years old)
− Pathophysiology
1. INFLAMMATION
− Increase intraosseous pressure  pain and obstructive the blood flow
2. SUPPURATION (2nd to 3rd days)
− Pus appear and form subperioestal abscess  spread along the shaft 
re-enter the bone/ burst out into other soft tissue.
3. NECROSIS (one week)
 − Further increase of intraosseous pressure and vascular stasis  more
compromise the blood supply  necrosis  sequestra
4. NEW BONE FORMATION (end of second week)
− New bone from the deep layer of periostreum forming the involucrum
enclosing the sequestra if pus and sequestra start to discharge
through involucrum( cloaca) and through sinus to the skin chronic
osteomyelitis.
5. RESOLUTION
− Infection is controlled and intraosseous pressure releasedbone will
heal by fibrosis formation and periosteal reaction(sclerosis and
thickening of bone)

Diagnostic Imaging
1. Plain radiograph
− Normal for the 1st 10 days, only soft tissue swelling
− By the end of second week;
i. the faint extra cortical outline due to periosteal bone formation (classic x-ray
sign of pyogenic osteomyelitis) ,
ii. sign of periosteal reaction , the periosteal thickening become obvious
iii. Occasionally, shows necrotic bone (sequestrum) - radiodense area within
lytic lesion
iv. patchy rarefaction of metaphysis
Chronic Osteomyelitis
− AP and Lateral of Distal femur shows mixed of bone lysis
and sclerosis
− Extensive , thick and mature new bone formation
surround femoral shaft

2. Ultrasound
− Detect the subperiosteal collection of fluid
− Early stage osteomyelitis
− Cannot distinguish hematoma and pus
3. MRI
− More sensitive
− Help to differentiate between soft tissue infection and
osteomyelitis
− Limitation: time-consuming, patient cooperation
(paeds: sedation), claustrophobia
4. CT SCAN
− Better defining of periosteal new-bone formation &
sequestrum or involucrum.
− Limitation: ionizing radiation
5. Acute osteomyelitis – bone scan
− More sensitive than MRI but not specific
− Dye will accumulate at the affected side BONE SCAN
2. SPONDYLODISCITIS
− Infection of the intervertebral disc along with infection of the vertebrae
− Start at end plate extend to adjacent verterbra and disc
− Most common occur at lumbar levels.
− Investigation:
• Plain radiograph
− Normal up to 2-4 weeks.
− Narrowing of disc space.
− Bone sclerosis may appear 10-12 weeks.

• MRI
− More sensitive and specific
− Useful for differentiation between pyogenic infection, TB or neoplastic
process.
3. TB SPONDYLITIS
− Common site- upper lumbar and lower thoracic spine
− From anterior part of the vertebral body - spreads to involve the adjoining disk spaces 
manifests as collapse of the intervertebral disk space
− Progressive vertebral collapse with anterior wedging  angulation and gibbus formation

• Narrowing of the disk space. MRI and CT scan is to evaluate extend of

• Osteoporosis two adjacent vertebrae compression
• Destruction of the adjacent vertebra Of the cord and any hidden lesion
bodies.

ARTHRITIS
1. RHEUMATOID ARTHRITIS
− Chronic systemic autoimmune disease with genetic predisposition
− Affect soft tissue early, and later cartilage and bone (joint subluxation, destruction &
deformity)
− Women 3x more often than men
− Minimal criteria for diagnosing RA:
• bilateral, symmetrical polyarthritis
• Involving proximal joint of hand or feet
• Present at least 6 weeks
− Imaging
• X-rays
− Early - features of synovitis (soft tissue swelling and periarticular
osteoporosis)
− Later (± 2 years) - marginal bony erosion + narrowing of articular surface
− Advanced – articular destruction and joint deformity are obvious
• Ultrasound scanning and MRI
− Soft tissues changes, early erosion within joints.
 juxta-articular erosions juxta-articular erosions Joints became unstable and
appeared → appeared → deformed.

2. OSTEOARTHRITIS
− Chronic irreversible disease of articular cartilage
− 2 mechanism of disintegration of cartilage:
o Weakening of articular cartilage
o Increased mechanical stress at articular
surface
− Radiological findings:

Joint narrowing, osteophyte formation &

subchondral sclerosis Subchondral cyst
3. NEUROPATHIC ARTHRITIS (CHARCOAT’S DISEASE)
− A chronic, progressive, destructive process affecting bone
architecture and joint alignment in people lacking protective
pain sensation.
• Peripheral neuropathy (especially in diabetic)
• Tabes dorsalis
• Cauda equina lesion
− Lack of normal protective reflex against abnormal stress or
injury  repetitive trauma  articular surface and bone
destruction  deformity
− Characterized by pathological fracture, joint dislocation &
fragmentation of articular cartilage
− Radiological findings:
1. Increased Density (subchondral sclerosis)
2. Destruction of articular surface
3. Debris in the joint
4. Dislocation of the bone
5. Deformity
6. Disorganization of the joint

4. GOUT
− Pathogenesis
o Deposition of sodium urate monohydrate crystals in synovial membranes, articular
cartilage, ligaments, bursae leading to destruction of cartilage
− Imaging
o X-ray
 Acute attack - soft tissue swelling
 Chronic – joint space narrowing, secondary OA
 Tophi – punched out ‘cysts’ or deep erosion on the para articular bone ends
(excavation are larger and slightly further from the joint margin than the
typical rheumatoid erosions)
 Occasionally, destruction more marked and may resemble neoplastic
disease
5. PSORIATIC ARTHRITIS
− Almost always accompanies skin disease, especially nail changes
− Mostly involves DIP joints of hands > feet
− There is often resorption of terminal phalanges
− There is usually no osteoporosis
− Most are HLA-B27 positive, RA factor negative
− Imaging
o X-ray
 Tends to involve smaller joints of hand and foot more than larger joints
 Asymmetrical joint involvement
 Affects both the juxta-articular and articular margins of joint
 Severe destruction of interphalangeal joint of the hands and feet
 Classical deformity is called “cup-and-pencil deformity”
• Erosion of one end of bone with expansion of the base of the
contiguous metacarpal
 In large joint – similar to RA
 Sacroiliac erosion – fairly common
 If in spine – identical to ankylosing spondylitis
o Ultrasound scanning and MRI
 Greater definition of the extent and activity of synovitis

Cup-and-pencil deformities of both thumbs and erosion of

DIP joint of left middle finger

Large, asymmetric osteophytes

(white arrow). They are thicker
than the syndesmophytes of
ankylosing spondylitis
 ORTHOPAEDIC MEDICATIONS

ANTIBIOTICS PROPHYLAXIS

Antimicrobial
therapy

Prophylactic Empirical

• Give to the patients who are not yet infected or have not yet developed the disease.
• Goals :
- To prevent infection in some patients.
- To prevent development of a potentially dangerous disease in those who already have evidence of
infection.

Antibacteria

• Penicillin
• Cephalosporin
• Aminoglycosides
• Macrolides
• Glycopeptides
• Nitroimidazole

Suggested treatment

Preferred Alternatif Comment

THROMBOEMBOLIC PROPHYLAXIS

Introduction

• Venous thromboembolism (VTE) is the commonest complication of lower limb surgery.

• Comprises 3 associated disorders :
1) Deep Vein Thrombosis
2) Pulmonary Embolism
3) Chronic Venous Insufficiency
• 5% risk of symptomatic DVT/PE after joint replacement surgery
• 0.25-0.5% risk of Fatal Pulmonary Embolism (FPE)
• 1% risk of FPE in elderly with hip fx and major trauma

Methods

MECHANICAL PHARMACOLOGICAL

1) ANTI EMBOLISM STOCKING / TED STOCKING
• Graduated compression and produce a calf
pressure of 14 -15 mmhg
• Encourage patients to wear day and night
until they no longer have significantly
reduced mobility
• Remove stockings daily for hygiene
purposes and to inspect skin
2) FOOT IMPULSES DEVICE
• Encourage patient to use foot devices both
in bed and when sitting in a chair
3) INTERMITTENT PNEUMATIC COMPRESSION
DEVICE
• Encourage patient to use IPC devices for as
much time as possible both in bed and
when sitting in a chair
1) LOW MOLECULAR WEIGHT HEPARIN (LMWH)
• Preferred by most surgeons.
• SC route
a) ENOXAPARIN : Enoxaparin 40 mg daily or
20 mg daily (for moderate renal impairment)
b) TINZAPARIN : 3500 units daily (lower VTE risk or
moderate renal impairment) or 4500 units daily
(higher VTE risk e.g. hip or knee surgery or during
pregnancy)
2) FONDAPARINUX SODIUM
• Starting dose at 2.5 mg (6 hours after surgery)
followed by2.5 mg daily
• Contraindicated in severe renal impairment
• SC route

3) RIVAROXABAN

• Starting dose at 10 mg (6 10 hours after surgery)

followed by 10 mg daily.
• No dose adjustment in renal impairment with
prophylactic dose
• PO
• Superior to enoxaparin in VTE prevention studies
during hip and knee replacement surgeries.
 4) DABIGATRAN ETEXILATE

• Alternative to LMWH and fondaprinux.

• Starting dose at 110 mg (1-4 hours after surgery)
followed by 220 mg daily.
• For elderly >75 years, moderate renal
impairment: 75 mg starting dose, followed by
150 mg daily.
• PO

5) UNFRACTIONATED HEPARIN

• For patients with severe renal impairment

• UFH dose is 5000 units bd
• SC route

Orthopaedic surgery

• Offer combined VTE prophylaxis with mechanical and pharmacological methods for lower limb
surgery.
• Do not routinely offer VTE prophylaxis to patients undergoing upper limb surgery.
PAIN MANAGEMENT

PAIN : An unpleasant sensory and emotional experiences associated with actual and potential tissue damage

Acute vs chronic pain

Pain management
Opioid overdose

Benzodiazepine overdose
ORTHOPAEDIC PROCEDURES & INSTRUMENTS
1) Splinting & Casting
2) Bandaging
3) Taping
4) Close Manipulative Reduction (CMR)
5) POP
6) Traction
7) Wound Dressing
8) Tourniquet
9) Ankle-brachial systolic index (ABSI)
10) Implants
11) Bone graft
12) Types of lower limb amputation
 SPLINTING & CASTING

• SPLINT – half cast used temporarily immobilise and

protect body parts
• CAST – hard circular dressing with soft padding inside of
it used to immobilises and protects until healing occurs
• selection either cast or splint being used is made by
injury assessment (skin, neuromuscular status, soft
tissue, bony structure)
• by qualified physician / health care professional

SPLINTING CASTING

CONSTRUCTION uncircumferential circumferential

soft tissue injuries (sprains, tendons) severe, non-acute soft tissue injuries
INDICATION acute management of injuries awaiting unable to be managed with splinting
intervention

allow for acute swelling more effective mobilization

decreases risk of complications
ADVANTAGES faster & easier application
commercial splints available &
appropriate for selected injuries

lack of compliance higher risk of complications

increase range of motion at injury site more technically difficult to apply
DISADVANTAGES
not useful for definitive care of unstable
/potentially unstable fractures

Complications of cast or splint immobilization

1. Compartment syndrome
2. Ischemia
3. Heat injury
4. Pressure sores and skin breakdown
5. Infection
6. Dermatitis
7. Joint stiffness
8. Neurologic injury

Materials
Plaster Fiberglass

• Preferred material for splints • Produces less mess

• More pliable
• Slower setting time  allowing more time to
apply and mold the material before it sets;
produce less heat  reducing patient
discomfort and the risk of burns.
• Lighter than plaster.
• Commonly used for non-displaced fractures
and severe soft-tissue injuries.
Upper limb splint & cast
Type of Indications
splint/cast
Ulnar gutter 4th and 5th proximal/ middle phalangeal shaft
splint/cast fractures and metacarpal fractures

Radial gutter 2nd and 3rd proximal/middle phalangeal shaft

splint/cast fractures and metacarpal fractures

Thumb spica Injuries to scaphoid/trapezium

splint/cast Non displaced, non angulated, extra-articular
first metacarpal fractures
Stable thumb fractures

Buddy taping Non displaced proximal/middle phalangeal

shaft fracture and sprains

Aluminum U- Distal phalangeal fracture

shaped splint

Dorsal extension- Middle phalangeal volar plate avulsions and

block splint stable reduced PIP joint dislocations

Mallet finger Extensor tendon avulsion from the base of the

splint distal phalanx

Volar/dorsal Soft tissue injuries to hand and wrist

forearm splint Acute carpal bone fractures (excluding
scaphoid/trapezium)
Childhood buckle fractures of the distal radius
Short arm cast Non displaced, minimally displaced, or buckle
fractures of the distal radius
Carpal bone fractures other than
scaphoid/trapezium

Forearm Single sugar-tong splint

Elbow, proximal Long arm posterior splint, long arm cast

forearm, and
skeletally
immature wrist
injuries Double sugar-tong splint

Lower limb splint & cast

Type of Indications
splint/cast
Posterior ankle Severe sprains
splint (“post- Isolated, nondisplaced malleolar fractures
mold”) Acute foot fractures

Stirrup splint Ankle sprains

Isolated, nondisplaced malleolar fractures

Short leg cast Isolated, nondisplaced malleolar fractures

Foot fractures—tarsals and metatarsals

Posterior knee Acute soft tissue and bony injuries of the

splint lower extremity

Short leg cast Distal metatarsal and phalangeal fractures

with toe plate
extension
 BANDAGING
• Bandage is a strip of material used mainly to support and immobilize part of the body

Functions
1. To prevent contamination of wound by holding dressings in position
2. To provide support to the part that is injured, sprained or dislocated joint
3. To provide rest to the part that is injured
4. To create pressure over a bleeding prevent and control hemorrhage
5. To immobilize a fracture or dislocation

Types of Materials
1. Roller gauze bandages
− Used to hold dressings in place in any body parts
2. Triangular bandages
− Used to secure dressings on the forehead or scalp and as sling of arm
3. Elastic bandages
− Used to provide compression to an injured body part
− Helps control swelling and ease pain

Methods of wrapping bandages

− Several techniques used
− Depends on the body part involved
− Loosen bandages immediately if any signs of impaired circulation are noted:
1. Swelling or edema
2. Pale or cyanotic color
3. Coldness to touch
4. Numbness or tingling
5. Poor or slow return to pink color after nailbeds are
blanched

Types of Bandage
1. Circular Bandages
- Frequently used to hold dressings on body parts such as
arms, legs, chest or abdomen
- Provides thick support in one area

2. Spiral wrap bandage

- Used to hold dressings in place on arm or leg or used to
provide support to a limb

3. Spiral Reverse Wrap

- To bandage parts of the body that are not uniform in circumference :
- Lower leg
- Forearm
- Used to hold bandages or provide support to joints such as ankle or
wrist
- Permits flexibility of the elbow, knee and ankle without disturbing the
dressing – Elastic bandage is used
4. Figure Eight Wrap
- Used to hold bandages or provide support to joints
such as ankle or wrist
- Permits flexibility of the elbow, knee and ankle
without disturbing the dressing – Elastic bandage is
used

5. Cervical Arm Sling

- Provides support for forearm, wrist and hand injuries
- Use Triangular bandage
 TAPING

Adhesive plaster
1. Elastic  To compress and support joints and muscle
2. Non-elastic type  To restrict joint movement

Function
1. Provide additional support, stability, and compression for an affected body part without
affecting circulation and range of motion
2. Act as a preventive measure or as protection for new healing injury

Taping materials
1) Elastic
- An elastic tape that is highly ‘twistable’, offers added flexibility when applied on skin,
muscles and soft tissues.
- Useful for taping around muscles expand during exercise and the tape will allow
this to some extent.
2) Non-elastic
- White/tan/brown in color, non-elastic and sticky.
- Limit the ROM of a joint or protect the skin against blisters.
- Should never be used to surround or enclose muscles expand during exercises
thus restrict blood flow to the area.

Indications
• PREVENTIVE
• Use during match, sports training
• To stabilize joints
• To support muscles and ligaments
• THERAPEUTIC
• With acute or chronic injury
• To prevent the worsening of an injury

Contraindications
- Allergy to taping materials
- Open wounds, active infection or irritation of area of skin to be taped
- History of hypersensitive skin or preexisting skin conditions e.g.; psoriasis, eczema,
dermatitis
- Circulation compromised in area
- Sensation compromised in area
- No one available at home to remove tape if it causes irritation or discomfort
Types of Taping
1. Ankle Taping 2. Achilles Tendon 3. Turf Toe Taping
Taping

Help stabilize the MPJ of the

big toe by keeping it from
Taping is an effective way to
hyper-extending.
relieve strain
4. Shin Splint Taping 5. Wrist Taping 6. Elbow Taping

Circumferential elastic taping Wrist taping adds support to Prevents hyperextension and
is a common method for the wrist. prevents hyper mobility, a
providing gentle compression body part from moving beyond
its normal range of motion.
CLOSE MANIPULATIVE REDUCTION (CMR)
Definition
• Reduction: repositioning a bone/bones to their normal or near normal position after a
fracture or dislocation
• Close reduction: a non-operative external manipulation to achieve reduction

Aim
− To restore position of:
o Alignment
o Rotation
o Length of bones and joints after injury
− To promote normal function after the fractured bone or dislocated joint
− To support tissue healing

Indication
• All minimally displaced fractures
• Most fractures in children

Contraindication
• Undisplaced fractures
• Reduction is impossible eg severely comminuted fracture
• Reduction which cannot be maintained

CMR
1. Fracture
• Apply traction at or across the fracture to relax and lengthen the
muscles
• Manipulate the bone fragments back into position
• Hold the new position with a cast or splint
2. Dislocation
• Apply traction to overcome muscle spasm and regain muscle
length
• Apply pressure to guide the bones into correct position
(manipulative reduction).

Common Closed Manipulative Reduction

1. Elbow Dislocation – traction, flexion, and direct manual push
2. Shoulder Dislocation – relaxation, traction, gentle rotation if necessary
3. Hip Dislocation – relaxation, flexion, traction, adduction and internal
rotation
 PLASTER OF PARIS (POP)
History
• In 1666, a fire raged across London, destroying many parts of it.
• In its aftermath, the king of France ordered that all walls made of wood in Paris be immediately
covered with plaster, as a protection against such fires.
• This resulted in large-scale mining of gypsum which was available around Paris in huge quantities.
• Thus, during the early 18th century, Paris became the centre of plaster production, and hence the
name, plaster of Paris.

Introduction
• POP cast bandage – consist of a tough open-weave fabric coated with hemihydrated calcium sulphate
powder
• Book muslin or crinoline were originally used as the fabric
• Dipped in water – becomes hard with crystalline hydrated CaSO4
• The reaction is exothermic - becomes heat as it sets

Uses
• Immobilization of the fracture site
- Prevent displacement, promote healing
- Reduce pain
• Postoperative immobilization of limbs and joints until healing occur
• Stabilise and rest joints in ligamentous injuries
• Correct a deformity

Forms of POP
INCOMPLETE COMPLETE
- Slab : covers only part of the circumference of a - Cast : covers the whole circumference of limb
limb (back slab, U slab) - Spica

Types of pop cast

ARM
LEG

HIP-LEG

Application of POP

1) Padding : apply padding of wool bandage (othoban)/ stockinnette especially at the bony prominence.
This is done to avoid sore pressure
2) Dipping : dip the plaster into water and hold in the water until air bubble stop.
3) Application : wet POP is rolled around the limb. Mould the plaster evenly.
4) Once the plaster is set up:
- check the edge and circulation (colour, temperature, pulse, capillary refill)
*POP does not gain its full strength until completely dry
* Complete dry : about 24 hours for a small arm cast to 96 hours for a total
Advantages vs Disadvantages
Advantage Disadvantage
• Sufficiently rigid • Joints encased in plaster cannot move and
• Easy to mould are liable to stiffness
• Cost-effective • Heavy
• Easily breaks when come in contact with
water
• Burns due to exothermic reaction

Complications

• Tight cast
- put on tightly or d/t limb swelling
- vascular compression
• Pressure sores
- pressure over bony prominence
- prevent by padding
• Skin abrasions or laceration
• Loose cast
- once swelling has subsided, cast no longer hold the fracture securely
 TRACTION
• Applied to limb distal from fracture
• The intact muscle of the limb act as splint to protect the fracture

The Aim of Traction

− Relieve pain due to spasm
− Restore and maintain alignment of bone following fracture and dislocation
− Allow movement of joint during fracture healing
− Rest injured or inflamed joints and maintain them in functional position

Continuous Traction
− Hold : Can pull a long bone straight and hold it out to length
− Move : Can move joint and exercise the muscles
− Safe : Care need to be taken during insertion of pin
− Speed : Lower limb traction keep patient in hospital

Type of Traction
1. Traction by Gravity
• Only to Upper Limb injuries
• Using a wrist sling, weight of arm provide continuous
traction to humerus
2. Skin Traction
• Sustain pull of ≤ 4 to 5 kg
• Holland strapping is stuck to shaved skin and held on
with bandage
• Malleoli protected by Gamgee tissue
3. Skeletal Traction
• Stiff wire or pin is inserted and cords tie to them for
applying traction
• Behind Tibial Turbecle: Hip, Thigh and Knee Injuries
• Through the Calcaneum: Tibial Fractures

Method of Traction
Fixed Traction Balanced Traction Combined Traction

Pull is exerted against fixed Traction cord are guided over Thomas splint is used, and
point pulley and loaded with weight entire splint is suspended

Using Thomas Splint Counteract provided by weight

of body when foot of bed is
raised

Complication
1. Circulatory Embarrassment
• In children: Traction tapes and Circular bandage may constrict circulation
• Gallows traction not used in child >12kg
2. Nerve Injury - In older people: peroneal injury can cause drop foot
3. Pin Site Infection
 WOUND DRESSING
Purpose of dressing
• To promote rapid wound healing
• To protect from mechanical trauma
• To prevent infection
• To absorb exudate
• To reduce pain

Types
1. Alginate
- Alginates are made from seaweed
- The dressing is highly absorbent
- Some of the alginate dressings have haemostatic properties and are ideal for
bleeding wounds
- Used in:
• Good for exudating wounds and helps in debridement of sloughing wounds
• Eg: bleeding wounds, dehiscence wound

Advantages Disadvantages

Provides a moist environment Can’t be used on dry wounds

Keeps nerve endings moist and Dressings can sometimes adhere

can reduce pain to the wound

May be used in sinuses and cavities (if

able to see the base of the wound bed)

Moderately to highly absorbent

Suitable for bleeding wounds

2. Hydrocolloid
- Containing gel-forming agents, such as sodium
carboxymethylcellulose (NaCMC), gelatine pectin,
elastomers and adhesives that turn into a gel
when exudate is absorbed.
- Impermeable to water allow the patient to bathe or
shower
- Depending on the hydrocolloid dressing chosen can be used in wounds with light to
heavy exudate, sloughing or granulating wounds
- Wounds producing low to high levels of exudate
- Eg: Pressure injuries, Leg ulcers, Surgical incisions
Advantages Disadvantages

Waterproof which allows patients to Care should be taken when using

shower hydrocolloids as they can encourage the
growth of anaerobic bacteria

Absorbs exudate Use with caution on fragile or

compromised skin as the adhesive may
cause trauma

Gel that forms from the wound fluid May be difficult to keep in place
provides a moist wound environment

Reduces pain Sometimes have a distinctive malodour

that is mistaken for pus

The moist environment promotes the

formation of new tissue

3. Hydrogel
- Hydrogels have a high water content and contain insoluble polymers
- They are designed to hydrate the wound and promote autolytic debridement
- Used in:
o Necrotic or sloughy wound beds to rehydrate and remove dead tissue.
o Eg: Pressure injuries

Advantages Disadvantages

Provides a moist wound environment Cannot be used if you cannot visualise

for cell migration all of the wound base

Rehydrates necrotic tissue which Some of the dressings may require a

helps in its removal without harming secondary dressing
good cell growth

Reduces pain by keeping nerve Some people experience sensitivity

endings moist to the preservatives

4. Hydrofiber
- Soft non-woven pad or ribbon dressing made from
sodium carboxymethylcellulose fibres
- Interact with wound drainage to form a soft gel
- Silver-impregnated hydrofiber ( commonly used)- anti
microbial function
- Used in:
o Absorb exudate in highly exudating wound
 5. Foam
- Foam dressings are made from a variety of different materials
- Foam dressings are hydrophilic which means that they attract
fluid which aids in absorption
- Foams are used for exudate absorption, padding and to
maintain thermal temperature in the wound
- Used in:
• Low to heavily exuding wounds
• Granulating and epithelialising wounds
• Eg: Pressure sores, Leg ulcers

Advantages Disadvantages

Available in many different shapes and sizes, Not use in dry wound
non-occlusive and semi occlusive/water repellent
dressings

attract fluid which aids in absorption

Provides protection

6. Collagen
- Animal sources : bovine, equine (horse) or porcine
- Promote the deposit of newly formed collagen in the
wound bed
- Absorb exudate and provide a moist environment
- Used in:
• wounds with minimal to heavy exudate
• Eg: skin grafts and skin donation sites, second-degree burns,
granulating or necrotic wounds

7. Semi permeable Membrane or film

- Synthetic adhesive film dressing
- Promote moist wound healing
- Promote autolytic debridement
- Occlusive barrier against wound contamination from external
- Should not be used in infected & draining wound

8. Impregnated gauze
- To prevent infection, unnecessary dressing adherence (
sticking) to the wound bed, and maintain a healthy and
moist wound environtment
- Recommended for light exudative wounds
- Absorb exudates in lightly exudating wounds
- Promote moist wound healing
- Permit gaseous exchange
- Antimicrobial effect
- Prevent dryness of affected area
 TOURNIQUETS
Definition
- Constricting or compressing device used to control venous and arterial circulation to the
upper or lower extremity for a period of time

Functions
- Promote optimum surgical conditions (create a bloodless field)
- To engorge vessels for venipuncture
- To control bleeding in life or limb threatening situations
o Uses an air-inflated cuff to constrict blood flow.
o A regulating device on the Tourniquet machine can control the amount of cuff
pressure exerted on the limb.
o The cuff pressure and inflation time are displayed on a monitor that can be easily
read by clinical staff
Types
1. Pneumatic Tourniquets
- Uses an air-inflated cuff to constrict blood flow.
- A regulating device on the Tourniquet machine can control
the amount of cuff pressure exerted on the limb.
- The cuff pressure and inflation time are displayed on a
monitor that can be easily read by clinical staff
2. Non-pneumatic Tourniquets
- A type of rubber band that was wrapped around the extremity to
exsanguinate the blood and tied it at the proximal end so as to
facilitate relatively bloodless surgery in the distal extremity.

Tourniquet time
- Absolute maximum time : 3 hours
- Advisable : 2 hours
- More than 3 hours  ransient nerve related symptoms may occur– full recovery in 5th day
- How to minimize time?
o Ensure limb is shaved, prepared, draped and marked before inflating the cuff
o Record the time of application of the tourniquet
o Inform the surgeon of the elapsed time at regular interval, particularly as the 2-hour
period is approached.

Tourniquet pressure
- Lower Limb : 150 mmHg above systolic
- Upper Limb : 80 – 100 mmHg above systolic
* May need to be increased in muscular, obese and hypertensive patients
* Higher pressure – unnecessary, & will increase risk of damage to underlying muscles and nerves

Complication
1. Nerve injury (dt mechanical compression/duration of neural ischemia)
2. Skin burns from leakage of alcoholic antiseptic solutions beneath the tourniquet cuff
3. Post-tourniquet syndrome  swelling, weakness, stiffness and numbness of the affected
limb (tends to recover 3 weeks postoperatively)
 ANKLE-BRACHIAL SYSTOLIC INDEX

• Also known as the ankle-brachial index (ABI), ankle-brachial pressure index (ABPI)
= noninvasive vascular screening test to identify peripheral arterial disease by comparing systolic
blood pressures in the ankle to the brachial systolic blood pressures, which is the best estimate of
central systolic blood pressure.
= the ratio of the blood pressure at the ankle to the blood pressure in the upper arm (brachium).
• Used to detect the presence of lower extremity peripheral arterial disease (PAD).
• Lower blood pressure in the leg is an indication of blocked arteries due to peripheral artery disease
(PAD).

Advantages
– Simple
– Non-invasive
– Relatively cheap

Interpretation of ABSI

*HOSP AMPANG : NORMAL (0.9 – 1.2)

Preparation

• Equipment
 A sphygmomanometer with appropriate cuff size for the upper and lower extremities
 A Doppler device with transmission gel
 Documentation
• Patient Preparation
 Supine position
How do I do it?

1. Place the patient in the supine position

– The arms and legs at the same level as the heart
– 10 minutes before measurement
2. Palpate for arterial pulses
– Brachial artery
– Dorsalis pedis artery (DPA)
– Posterior tibialis artery (PTA)
3. Obtain the brachial systolic pressures of both arms
– Use Doppler to locate the brachial artery and determine the systolic pressure
– the higher of the 2 values represents the brachial systolic pressure
4. Obtain the ankle systolic pressures
– The cuff placed on the affected leg between the malleolus and the calf
– Use Doppler to locate the anterior tibial and posterior tibial arteries and determine the
respective systolic pressures
– the higher of the 2 values represents the ankle systolic pressure
5. Divide the ankle pressure by the brachial artery pressure;
 COMMON ORTHOPAEDIC IMPLANTS, ITS USES AND BIOMECHANICS.

1. KIRSCHNER WIRE (K-WIRE)

• Indication: small fragments fracture
• Wrist fracture
• Metatarsal, metacarpal, phalangeal fracture
• Patella fracture

• Olecranon fracture
• Clavicle fracture
• Other uses: guide wire for implant insertion
• Types of K-wire:
• Threaded end
• Trocar end

2. SCREWS
- Use to compress fracture fragment
- Use to hold plates on bone
1. Cortical Screw
• Threaded at whole length
• Function as positional screw
• Indication: Cortical bone fracture /diaphysis fracture
2. Cancellous Screw
• Partially threaded
• Wider and deeper thread
• Indication: Cancellous bone fracture/ metaphyseal fracture
3. Cannulated cancellous Screw
• Modified cancellous hollow screws
• Better hold compare to cancellous screw
• Use: Metaphyseal fracture , Femoral neck fracture
• Easy insertion by guided wire

3. PLATES
• Screw provide compression and stability
• Plate bridges the fracture, protecting screw from bending
1. Dynamic compression plate (DCP)
− Fixation of fractures of shaft of femur, humerus, ulnar,
radius
− Dynamic pressure is created by the oval shape hole.
− Screw slides down the inclined hole, forcing the bone to
move creating compression.
− Types of DCP
i. Broad DCP - Fracture of humerus, femur
ii. Narrow DCP - Fracture of tibia
iii. Small DCP - Fracture of ulnar and radius
 2. Locking compression plate
− Combination hole concept
− Two types of hole for two types of screw,
conventional and locking head screws.
− Conventional
i. Create compression at fracture site
− Locking
i. Plate-bone gap
ii. No compression
− Benefits of LCP
i. Less damage to periosteum and blood supply
ii. Better fixation in osteoporotic bone
3. Buttress plate
− Use: to prevent displacement of fracture fragment
− Indication: condylar fracture of femur, tibia) Tibial
plateu fracture
− Condylar, T-shape, Clover shape, L-shape
4. Reconstruction (Recon) plate
− Notched edges allows bending.
− Indication: complex anatomy sites fractures: pelvic,
distal humerus, clavicle

4. INTRAMEDULLARY FIXATION
• Fixation of long bone fracture
1. Standard intramedullary nail
• Kuntscher nail
• Indication: long bone shaft fracture (femur,
tibia, humerus)
• Clover-shaped
• Square nail & Rush nail - Ulnar and radius fracture
2. Interlocking Nail
• Indication: simple or complex fracture ( comminuted, segmental)
• Type:
• Dynamic: locked at one end
• Stable: locked at both ends
• Site:
• Femoral interlocking nail
• Shaft fracture
• Subtrochanteric fracture
• Humeral Interlocking Nail
• Shaft of humerus fracture
• Tibia Interlocking Nail
• Tibia shaft fracture
3. Flexible medullary nail
• Indication: Paediatric long bone fracture
5. OTHER SPECIAL IMPLANTS
1. Angle blade plate
• Indication: supracondylar fracture of femur & humerus
• Advantage: stronger fixation, restoration of the correct
biomechanical axis
2. Dynamic condylar screw
• Indication: supracondylar femur fracture
3. Dynamic hip screw (DHS)
• Screw + plate
• Indication: Intertrochanteric femur fracture, neck of femur
fracture.

6. JOINT REPLACEMENT
1. Hemiarthroplasty
• Indication: neck of femur fracture ( home ambulatory
elderly )
• Types:
• Unipolar
• Thompson – no fenestrations
• Austin Moore – fenestrations for bone to
grow through and help in fixation
• Bipolar
• Acetabular component, head component.
• Movement at acetabular component with
acetabulum and head component
• Bipolar vs unipolar: less pain, more motion, lower
dislocation rate.

2. Total hip replacement (THR)

• Replacement of severely damage hip with an artificial joint.
• Indication:
• Neck of femur fracture (active elderly, acetabulum changes)
• Severe osteoarthritis, rheumatoid arthritis
• Failure of previous reconstructive surgery
• Neck of femur fracture complication (AVN, non-union)
• Malignant bone tumors
3. Total knee replacement (TKR)
• Aim: reduce pain, improve knee function, correcting deformity.
• Indication:
• Irreversibly damaged joints (Osteoarthritis, Rheumatoid
arthritis)
• Daily knee pain (fail to manage conservatively)
• Restriction of ordinary activities
7. EXTERNAL FIXATOR
• Method of fixing a fracture by cluster of pins connected with bars.
• Supportive/definitive treatment
• Provide stability of fracture before reconstructive surgery.
• Indication:
• Acute (control damage) : multiple injuries, extensive soft tissue injury, multi
segmental fracture
• Chornic ( treatment ): mal/non union, infected fracture
• Basic components
• Rods/bars
• Schanz Pin
• Clamp
• Types
• Type 1: Unilateral Uniplanar
• Type 2: Bilateral Uniplanar
• Type 3: Unilateral Biplanar, Bilateral Biplanar

• Illiazarov External Fixator

• Multiplanar external fixator
• Use: treatment of non-union fracture, osteomyelitis,
limb lengthning, complex fracture, limb deformity
 BONE GRAFT
Osteogenesis
= formation of bone
• Requirement of osteogenesis
- Osteoprogenitor cells
- Growth factor
- Bone matrix

Indication
• Assist in healing of fracture, delayed union or non-union
• Assist in arthrodesis and spinal fusion
• Replace bone defect

Types of bone graft

1) Autograft
• Transferring bone graft from one site to another in same individual
• Most common
• Osteogenic, Osteoconductive and Osteoinductive
• Types of Autografts:
I. Cancellous and Cortical Autografts (iliac crest)
II. Vascularised Grafts (fibula and ribs)
III. Bone Marrow Aspirate (iliac crest and vertebral body)
IV. Platelet Derived Activators

2) Allograft
• Bone from one individual to another of the same species
• Osteoconductive only
• Antigenicity:
– Allograft has many potential antigens that can induce immune response causing rejection
– Reduce Antigenicity:
 Frozen or freeze dried
 Demineralisation

3) Demineralised bone matrix

• Acidic extraction of bone matrix from allograft
• Removes mineral and leaves collagenous and non collagenous structure and protein
• Osteoconductive without structural support
• Minimal osteoinductive

4) Synthetic
• Alternative to autografts and allografts
• Calcium phosphate, Calcium sulphate, Hydroxyapatite
• Made in powder, pellet or putty form
• Osteoconductive only
• Allow bone defect filling, early rehabilitation, and prevention of articular subsidence in distal radius
and tibial fracture
 5) Bone Morphogenic Proteins
• Osteoinductive
• Stimulate undifferentiated perivascular mesenchymal cells to differentiate into osteoblast
• rhBMP-2 and rhBMP-7

Graft healing

Complications
• Disease Transmission
 Hepatitis B
 Hepatitis C
 HIV
 Allografts are tested for HIV, HBV, HCV, HTLV-1 and syphillis
• Serous Wound Drainage
 Calcium Sulphate bone graft substitute associated with increased wound drainage
TYPES OF LOWER LIMB AMPUTATIONS
− Definition: Amputation is a procedure where a part of the limb is removed through one or more
bones.
− INDICATIONS (3D):
o Dead (or dying)
 Peripheral vascular disease (90%)
 Severe trauma
 Burns
 Frostbite
o Dangerous
 Malignant tumors
 Potentially lethal sepsis
 Crush injury
o Damned nuisance
 Retaining the limb may be worse than having no limb at all because of :
 Pain
 Severe loss of function
 Gross malformation
Hip Amputation
1. HINDQUARTER AMPUTATION/HEMIPELVECTOMY/TRANS-PELVIC OR TRANS-ILIAC AMPUTATION – rare
− the removal of the entire limb and the partial removal of the pelvis
− This operation is performed only for malignant disease
2. HIP DISARTICULATION
− The removal of the entire limb up to and including the femur.
− A variation leaves the upper femur and hip joint for better shape/profile when sitting
− Rarely indicated and prosthetic fitting is difficult

Amputations about the knee

1. TRANSFEMORAL AMPUTATION (ABOVE KNEE AMPUTATION)

− Amputation of the leg above the knee joint
− Maintain as much length as possible, ideally 12 cm above the knee
joint
− Use the Adductor Myodesis technique; 5-10 degrees of adduction is
ideal for improved prosthesis function
− Improves clinical outcome
− Creates dynamic muscle balance
− Provide soft tissue envelope that enhances prosthethic fitting
2. THROUGH-KNEE AMPUTATION
− Removal of the lower leg and knee joint. The remaining stump is still able to bear weight as the
whole femur is retained.
− Rarely performed because bone may not unite securely; end-bearing stump is not satisfactory; no
space for knee mechanism
− Main indication is in children because lower femoral physis is preserved
− Outcomes
• Poorer functional and psychological outcomes to AKA
• Troublesome fitting a modern knee mechanism
• Sitting position reveals the knees to grossly unequal in level
3. TRANSTIBIAL AMPUTATION (BELOW KNEE AMPUTATION)
− Amputation of the leg below the knee that retains the use of the knee joint.
− Best results : long posterior musculocutaneous flap (12-15 cm below knee joint is ideal), well
cushioned mobile muscle mass, full thickness skin, very anterior scar
− Use osteomyoplastic transtibial amputation (Ertl) technique to create a strut from the tibia to
fibula
− Advantages over AKA
• Longer lever arm
• Good Healing : > 90% in DM with BKA
• Higher prosthesis wearing rates : 74% vs 26% for AKA
• Reduced energy required for walking : 74% BKA < 45 year old walk > 1 mile
• Reduced mortality : 10% vs 30%

AMPUTATIONS OF FOOT

1. SYME AMPUTATION
− Amputation of the foot through the ankle joint, leaving a person still able to move around without a
prosthesis over short distances
− Patent tibialis posterior artery is require
− Excellent function in children (preserve distal physis)
− Stump is designed to be end-bearing, the fibrofatty heel pad must be viable.
− can still fit ankle prosthesis
− Common complication is heel pad migration.
2) CHOPART AMPUTATION
− A partial foot amputation through the talonavicular and calcaneocuboid joints (through midfoot
leaving only talus and calcaneum)
− Primary complication is equinus deformity  avoid by lengthening of the Achilles tendon and transfer
or reattachment of the tibialis anterior to the talar neck
3) LISFRANC AMPUTATION
− Through tarsometatarsal joints
− Tendon achilles lengthening and muscle reattachment especially Peroneus brevis at base of fifth MT
may be required to avoid later equinus deformity
4) TRANSMETATARSAL AMPUTATION
− When trauma, gangrene, or other pathology is confined to the toes, a transmetatarsal amputation is
suitable
5) RAY AMPUTATION
 − A particular form of minor amputation where a toe and part of the corresponding metatarsal bone is
removed.
− A forefoot amputation can sometimes be helpful in patients with more than one toe involved by
gangrene.

COMPLICATIONS OF AMPUTATIONS
• Early
o Secondary hemorrhage
o Breakdown of skin flaps
o Gas gangrene
• Late
o Ulceration of stump
o Painful neuroma
o Spur formation on the bone
o Phantom limb

Aftercare
− Evacuate hematoma (if present)
− Use gradual compression stump socks (after satisfactory wound healing)
− Exercise the limb
− Educate patient about prosthesis