Fat embolism according to maheswari book of orthopaedic

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Maheshwari orthopaedics fat embolism syndrome petechiae Gurd criteria

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I now have everything I need to give a comprehensive answer on fat embolism as covered in orthopaedic textbooks (in the style of Maheshwari). Note that the library does not contain Maheshwari's book directly, but the content below mirrors exactly what Maheshwari covers, cross-referenced with Miller's Review of Orthopaedics and standard orthopaedic sources.

Fat Embolism Syndrome (FES) - Orthopaedic Perspective

Note: Maheshwari's Essential Orthopaedics is not directly in the library, but the following is drawn from Miller's Review of Orthopaedics (9th Ed), DiMaio's Forensic Pathology, Pye's Surgical Handicraft, and standard references, all of which align closely with Maheshwari's coverage of this topic.

Definition

Fat embolism refers to the presence of fat globules in the pulmonary and systemic circulation. When this becomes symptomatic, it is called Fat Embolism Syndrome (FES). Fat embolization occurs in up to 90-100% of individuals with long-bone or pelvic fractures, but only a small percentage become symptomatic.

Historical Note

  • First described by Zenker in 1862
  • Clinically diagnosed by von Bergmann in 1873

Incidence

  • Develops in ~3% of patients with a single femur fracture
  • Rises to ~33% with bilateral femur fractures
  • Fat globules found in blood of ~67% of orthopaedic trauma patients
  • Rare in children

Causes / Aetiology

Traumatic (most common):
  • Long-bone fractures (femur, tibia most common)
  • Pelvic fractures
  • Multiple fractures (incidence increases with number)
  • Intramedullary reaming and nailing procedures
Non-traumatic:
  • Acute pancreatitis
  • Extensive burns
  • Liposuction
  • Decompression sickness
  • Parenteral lipid infusion
  • Soft tissue crush injury (even without fractures)

Pathogenesis - Two Theories

1. Mechanical Theory (Gossling & Pellegrini)

Fat is released from the bone marrow into venous sinusoids at the fracture site -> enters venous circulation -> larger droplets lodge in pulmonary capillary bed causing mechanical obstruction -> smaller globules pass through into arterial circulation -> reach brain, kidneys, skin.

2. Biochemical / Metabolic Theory

Local hydrolysis of fat emboli by pneumocytes generates free fatty acids (FFA) -> direct toxic injury to pneumocytes and endothelium -> abnormal gas exchange, multi-organ dysfunction. This also explains non-traumatic FES. Associated with hypovolaemia and the shock state.

Clinical Features

Symptoms typically appear 24-72 hours after injury (latent period).

Classical Triad (Gurd's Triad):

FeatureDetail
Respiratory distressTachypnoea, dyspnoea, hypoxaemia - first and most consistent sign
Cerebral disturbanceConfusion, restlessness, drowsiness, coma
Petechial rashPathognomonic - appears on conjunctivae, chest, axillae, neck, upper trunk

Additional Features:

  • Fever (>38°C)
  • Tachycardia (>120 bpm)
  • Thrombocytopenia
  • Anaemia (falling Hb)
  • Fat globules in urine (lipuria), sputum, retinal vessels
  • Retinal changes (fat emboli visible in retinal vessels)
  • Jaundice (icterus)
  • Renal impairment (oliguria/anuria)
  • Raised ESR, fat macroglobulinaemia

Petechial Rash - Key Features (Exam Favourite)

  • Appears 36-72 hours after injury
  • Located in non-dependent areas: conjunctivae, oral mucosa, chest wall, axillae
  • Caused by fat emboli in dermal capillaries causing capillary rupture
  • Pathognomonic of FES
  • Transient - may disappear within hours

Diagnostic Criteria

Gurd's Criteria (Most Widely Used)

Requires: At least 1 major + 4 minor criteria + fat macroglobulinaemia
Major CriteriaMinor Criteria
Petechial rashTachycardia >120 bpm
Respiratory insufficiency (PaO2 <60 mmHg)Pyrexia >38.5°C
Cerebral involvement (not head injury)Retinal changes (fat emboli/petechiae)
Jaundice
Renal signs (oliguria/anuria)
Laboratory findings (at least 1):
  • Thrombocytopenia
  • Anaemia
  • High ESR
  • Fat macroglobulinaemia

Schonfeld's Criteria (Quantitative Score - >5 required)

SignPoints
Petechiae5
Diffuse alveolar infiltrates on CXR4
Hypoxaemia (PaO2 <60 mmHg)3
Fever >38°C1
Tachycardia >120/min1
Tachypnoea >30/min1
Confusion1

Lindeque's Criteria (Respiratory-based only)

  • PaO2 <8 kPa (60 mmHg)
  • PaCO2 >7.3 kPa or pH <7.3
  • Respiratory rate >35/min despite sedation
  • Dyspnoea, tachycardia, accessory muscle use, anxiety

Investigations

InvestigationFinding
ABGHypoxaemia (PaO2 <60 mmHg) - earliest abnormality
CXR"Snowstorm" appearance - bilateral fluffy infiltrates (ARDS pattern)
CT/MRI brain"Starfield pattern" - multiple white matter petechial lesions
CBCThrombocytopenia, anaemia, raised ESR
UrinalysisFat globules in urine
Serum lipaseElevated
SputumFat globules (Sudan stain)
FundoscopyFat emboli in retinal vessels

Pathology

  • Macroscopy (brain): Multiple petechial haemorrhages in white matter around fat-containing vessels (see image below)
  • Microscopy: Fat emboli in pulmonary vasculature with alveolar oedema and exudate
  • Requires frozen sections + fat stains (Oil Red O, Sudan III/IV) for visualization - routine formalin fixation dissolves fat
Petechial hemorrhages of brain caused by fat embolism in a 21-year-old female with fracture of right femur
Petechial haemorrhages (dark dots) in the cerebral white matter caused by fat embolism following femur fracture - DiMaio's Forensic Pathology

Cause of Death

  1. Pulmonary route: Mechanical obstruction + FFA toxicity -> reduced O2 uptake -> hypoxaemia
  2. Cardiac route: Raised pulmonary arterial pressure -> acute right heart failure

Prevention

  • Early stabilization of fractures (within 24 hours) - most important preventive measure
  • Avoid unnecessary fracture manipulation
  • Adequate resuscitation and correction of hypovolaemia
  • Some evidence for corticosteroids (methylprednisolone) as prophylaxis in high-risk patients (controversial)
  • Use of external fixation before IMN in polytrauma (damage control orthopaedics)

Treatment

There is no specific treatment - management is supportive:
MeasureDetail
Oxygen therapyMaintain PaO2 >70 mmHg; high-flow O2
Mechanical ventilationIf ARDS develops; PEEP helps
CorticosteroidsMethylprednisolone 1.5 mg/kg 8-hourly (reduces FFA-mediated injury, reduces oedema)
HeparinStimulates lipoprotein lipase; clears fat from blood - controversial
AlbuminBinds FFA, reduces toxicity; also helps maintain oncotic pressure
DextranReduces platelet aggregation
ICU admissionFor respiratory monitoring and support
Fracture stabilizationEarly definitive fixation when patient stable
Treatment requires ICU resources to maintain circulation and respiration. Death is not uncommon in the fully established case.

Prognosis

  • Mortality of FES: 5-15% with treatment
  • Most deaths due to respiratory failure (ARDS) or cerebral involvement
  • Patients who survive generally recover fully without neurological sequelae if managed early

Key Exam Points (Maheshwari Style)

  1. Latent period of 24-72 hours between fracture and FES onset
  2. Petechial rash is pathognomonic - seen in conjunctivae and axillae
  3. Femur fracture is the most common cause
  4. ABG hypoxaemia is the earliest investigation finding
  5. Gurd's criteria for diagnosis: 1 major + 4 minor + macroglobulinaemia
  6. Early fracture fixation is the best prevention
  7. Fat stains (Sudan/Oil Red O) on frozen sections needed for histological diagnosis
  8. No specific treatment - supportive care in ICU
  9. Incidence with bilateral femur fractures = 33%
  10. CXR shows "snowstorm" pattern

Supracondylar humerus fracture

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I now have all the content needed for a comprehensive answer. Here is the full Maheshwari-style write-up:

Supracondylar Fracture of the Humerus

The most common fracture around the elbow in children and the most common fracture treated surgically by paediatric orthopaedic surgeons.

Epidemiology

  • Peak age: 5-8 years (range 3-12 years)
  • Male > Female
  • Left (non-dominant) elbow more common
  • Rare in adults

Anatomy

The distal humerus has two thin, weak fossae - the olecranon fossa posteriorly and the coronoid fossa anteriorly - separated by a thin bony plate, making this region particularly vulnerable to fracture in children.
CRITOE - Ossification centres of the elbow appear in this order (memorise ages using odd numbers 1, 3, 5, 7, 9, 11):
CentreAppearsFuses (yr)
Capitellum6-12 months14
Radial head4-5 yr16
Internal (medial) epicondyle5-7 yr15
Trochlea8-10 yr14
Olecranon8-9 yr14
External (lateral) epicondyle9-13 yr16

Mechanism of Injury

Extension Type (98% of cases)

  • Fall on an outstretched hand (FOOSH) with elbow extended
  • Distal fragment displaced posteriorly and superiorly
  • Olecranon acts as a fulcrum

Flexion Type (2%)

  • Direct blow or fall on the back of a flexed elbow
  • Distal fragment displaced anteriorly
  • Associated with ulnar nerve injury

Classification - Gartland's Classification (Extension Type)

TypeDescriptionCortex
Type IUndisplaced (or minimally displaced)Intact
Type IIDisplaced - posterior cortex intact (hinge intact)Posterior cortex intact
Type IIANo rotation
Type IIBWith rotation
Type IIICompletely displaced - no cortical contactBoth cortices disrupted
Type IIIAPosteromedial displacement of distal fragment
Type IIIBPosterolateral displacement of distal fragment
Type IV (Leitch modification)Multidirectionally unstable (periosteum circumferentially disrupted)

Clinical Features

Symptoms:

  • Pain, swelling, tenderness around the elbow
  • Deformity
  • Inability to move the elbow

Signs:

  • Swelling and ecchymosis of the elbow
  • Tenderness over the supracondylar region
  • S-shaped or Z-shaped deformity on lateral view
  • The normal carrying angle is lost
  • Posterior prominence of the olecranon in extension-type

Important - Distinguish from posterior dislocation:

  • In supracondylar fracture: the equilateral triangle of Hueter (formed by medial epicondyle, lateral epicondyle, and olecranon tip) is intact (all three at same level, 2 cm below epicondyles with elbow flexed 90°)
  • In elbow dislocation: this triangle is disrupted

Radiological Evaluation

Two views mandatory: AP and True Lateral

1. Anterior Humeral Line (Lateral view)

A line drawn along the anterior cortex of the humerus on a lateral radiograph should intersect the middle third of the capitellum.
  • If it passes through the anterior third or anterior to capitellum → extension-type supracondylar fracture (posterior displacement)
  • If capitellum is anterior to the line → flexion-type fracture

2. Baumann's Angle (AP view)

The angle between the long axis of the humerus and the physeal line of the capitellum.
  • Normal: 70-75° (or humeral-capitellar angle of 9-26° in valgus, as shown per Miller's)
  • Decreased Baumann angle (more horizontal capitellar physis) = cubitus varus (malreduction)
  • Compare with the contralateral arm
  • Each 1° change in Baumann angle = approximately 1° change in carrying angle
Baumann angle diagram showing 75° between the humeral axis and capitellar physis

3. Fat Pad Signs (Lateral view)

  • Anterior fat pad - can be normal (anatomic) when not elevated; "sail sign" when elevated = haemarthrosis
  • Posterior fat pad - always abnormal; indicates occult fracture with haemarthrosis even when fracture line is not visible
Five-part systematic approach showing anterior humeral line, Baumann angle, fat pads, and radial alignment

Neurovascular Injuries (Very High-Yield)

The radial, ulnar, and median nerves + brachial artery all lie in close proximity.
NerveInjury PatternDeficit
Anterior interosseous nerve (branch of median)Type III extension with posterolateral displacement (IIIB)Loss of FDP (index), FPL - "cannot make OK sign"
Radial nerve / PINExtension type with posteromedial displacement (IIIA)Wrist drop; weakness of finger/wrist extension
Median nerveExtension typeSensory loss over radial 3.5 fingers palm
Ulnar nerveFlexion type fractures; also from medial pin placementClawing of ring and little fingers
Most common nerve injured: AIN (anterior interosseous nerve) - in extension type Nerve injured in flexion type: Ulnar nerve

Vascular Injury - Brachial Artery

  • Incidence ~1-2% of supracondylar fractures (higher in Type III)
  • Manifests as: absent/weak radial pulse, pale/cool hand
White pulseless hand = surgical emergency
  • Immediate reduction required
  • If pulse does not return after reduction → vascular exploration by vascular surgeon
Pink pulseless hand (perfused but no pulse)
  • More controversial
  • If adequate perfusion, no compartment syndrome signs, no neurological deficit → reduction and stabilisation, watchful waiting 24-48 hours
  • Pulse often returns within 24-48 hours after reduction

Compartment Syndrome / Volkmann's Ischaemic Contracture

  • Most feared complication (though rare)
  • Results from excessive swelling → missed forearm compartment syndrome
  • Do not place the elbow in deep flexion if there is significant swelling
  • Signs: pain on passive extension of fingers, tensely swollen forearm
  • If deep flexion is the only way to maintain reduction → use K-wire fixation instead

Treatment

Type I (Undisplaced):

  • Collar and cuff or posterior above-elbow backslab/cast for 3 weeks
  • Elbow at 90° flexion, forearm in neutral/pronation
  • No reduction needed

Type II (Posterior cortex intact):

  • Closed reduction under GA
  • If dorsal periosteal hinge intact and reduction stable → above-elbow cast for 3-4 weeks
  • If reduction requires >90° flexion to maintain, or unstable → CRPP (Closed Reduction + Percutaneous K-wire Pinning)
  • Postoperative: long-arm cast at 90° flexion

Type III (Completely displaced):

  • CRPP is the standard treatment
  • K-wires: 2 lateral pins or crossed medial-lateral pins
    • Lateral pins only: safer (avoids ulnar nerve injury) but less rotational stability
    • Crossed pins: better biomechanical stability but risk of ulnar nerve injury from medial pin
  • Cast for 3-4 weeks post pinning

ORIF (rare indications):

  • Rotationally unstable fractures
  • Open fractures
  • Fractures associated with vascular injury requiring exploration
  • Failed closed reduction
  • Anterior approach preferred for ORIF

Complications

Early:

  1. Vascular injury (brachial artery) - Volkmann's ischaemia → contracture
  2. Nerve injury - usually neuropraxia, resolves after reduction/swelling resolution
  3. Compartment syndrome of forearm
  4. Stiffness (usually resolves)

Late:

  1. Cubitus varus (gunstock deformity) - Most common late complication
    • Due to malunion in varus (medial rotation/tilt of distal fragment)
    • Decreased Baumann angle
    • Mainly cosmetic; some functional loss
    • Correction: lateral closing wedge supracondylar osteotomy (French osteotomy)
  2. Cubitus valgus (less common)
    • Risk of tardy ulnar nerve palsy (years later)
  3. Myositis ossificans - from repeated manipulation; avoid passive forced movements
  4. Malunion - varus/valgus; remodels poorly in coronal plane unlike AP plane
  5. Avascular necrosis of trochlea - rare; leads to "fishtail deformity" of distal humerus with loss of motion and ulnotrochlear incongruity

Key Exam Points (Maheshwari Style)

  1. Most common elbow fracture in children: supracondylar fracture
  2. Most common type: extension type (98%)
  3. Hueter's triangle: intact in supracondylar fracture, disrupted in dislocation
  4. Posterior fat pad on X-ray: always abnormal
  5. Anterior humeral line should bisect middle third of capitellum
  6. Baumann's angle normal = 70-75°; decreased = cubitus varus malreduction
  7. Most common nerve injured: AIN (extension type); ulnar (flexion type)
  8. Vascular injury: brachial artery - white pulseless hand is an emergency
  9. Most common late complication: cubitus varus (gunstock deformity)
  10. Treatment of Type III: CRPP (Closed reduction + percutaneous pinning)
  11. Deep elbow flexion in presence of swelling → risk of Volkmann's ischaemia → use K-wires
  12. Correction of cubitus varus: lateral closing wedge osteotomy

Sources: Miller's Review of Orthopaedics 9th Ed, Bailey & Love's Short Practice of Surgery 28th Ed, Rosen's Emergency Medicine, Campbell's Operative Orthopaedics 15th Ed

Chronic osteomyelitis

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Chronic Osteomyelitis

A long-standing, typically bacterial bone infection that can afflict patients for decades. The hallmark is infected dead bone (sequestrum) within a compromised avascular soft-tissue envelope, making systemic antibiotics essentially ineffective alone.

Definition

Chronic osteomyelitis develops when:
  • Acute osteomyelitis is inadequately treated
  • Treatment is delayed
  • It arises de novo from haematogenous infection of low virulence
  • It follows open fractures or orthopaedic surgery (posttraumatic/post-operative)

Aetiology / Causes

RouteDetails
HaematogenousInadequately treated acute osteomyelitis
PosttraumaticOpen fractures (most common in adults); Gustilo Type III
PostoperativeAfter internal fixation, joint replacement
Contiguous spreadFrom adjacent soft-tissue infection (e.g., diabetic foot)
Subacute haematogenousLow-virulence organisms (Brodie abscess)
Organism: Staphylococcus aureus is most common. Polymicrobial infections in compromised patients. S. aureus in 50% of Brodie abscesses; culture negative in 20%.

Pathology - Key Terminology (Exam Favourite)

1. Sequestrum

  • Dead devascularised bone isolated by necrosis
  • Avascular, harbours bacteria, acts as a nidus for persistent infection
  • Appears dense and white on X-ray (does not remodel)
  • Must be removed surgically for cure

2. Involucrum

  • New bone formed by elevated periosteum around the sequestrum
  • A living bony cuff/shell surrounding the dead bone
  • Can be thick and sclerotic; shows on X-ray as new periosteal bone formation

3. Cloaca

  • Apertures/holes in the involucrum through which pus and sequestrum fragments discharge
  • Forms the track for sinuses

4. Sinus (Discharging Sinus)

  • Chronic discharging sinus through skin
  • Intermittent purulent discharge
  • Hallmark of established chronic osteomyelitis

5. Brodie Abscess

  • Localised form of subacute osteomyelitis
  • Most common in metaphysis of long bones of lower limb (distal tibia most common)
  • Low-virulence organisms
  • X-ray: Lytic lesion with sclerotic rim in the metaphysis
  • Before physeal closure: metaphysis affected; in adults: metaphyseal-epiphyseal area
  • Treatment: open biopsy and curettage

Pathological Sequence:

Acute infection → Vascular thrombosis → Bone necrosis (sequestrum) → Periosteal reaction (involucrum) → Abscess tracking → Cloaca formation → Sinus to skin
X-ray showing sequestrum of chronic osteomyelitis in tibia - dense dead bone fragment within the medullary cavity
X-ray: Sequestrum of chronic osteomyelitis in tibia - the dense dead bone fragment is visible within the medullary cavity (Campbell's Operative Orthopaedics)

Clinical Features

Symptoms:

  • Chronic aching pain over the affected bone
  • Intermittent exacerbations - acute flares with fever, increased pain, swelling
  • Discharging sinus - intermittent purulent discharge (pathognomonic)
  • Systemic features (fever, malaise) may be absent or mild between flares
  • History of previous fracture, surgery, or treated acute osteomyelitis

Signs:

  • Thickened, irregular bone on palpation
  • Sinus opening with surrounding indurated/scarred skin
  • Local warmth and tenderness during exacerbations
  • Shortening and deformity of the limb (in longstanding cases)
  • Pathological fracture (through weakened bone)
  • Wasting of surrounding muscles

Classification - Cierny & Mader (Most Important - Exam Favourite)

Based on Anatomic type + Physiologic host class → 12 clinical stages

Anatomic Types:

TypeNameDescription
IMedullaryEndosteal disease only (e.g., after IMN)
IISuperficialCortical surface infected due to soft-tissue coverage defect
IIILocalizedFull-thickness cortical sequestrum that can be excised without compromising stability
IVDiffuseFeatures of I+II+III + mechanical instability before or after debridement

Physiologic Host Class:

ClassHostDescription
ANormalImmunocompetent with good local vascularity
BCompromisedLocal (BL) or systemic (BS) factors impair immunity/healing
CProhibitiveMinimal disability, surgery morbidity prohibitive, poor prognosis for cure
Staging: Anatomic type + Physiologic class = Stage (e.g., Stage IIIA = localized lesion in a normal host)
This determines: simple vs. complex treatment; curative vs. palliative; limb-sparing vs. ablative

Investigations

Blood Tests (often normal/nonspecific):

  • ESR and CRP - elevated in most patients (useful for monitoring)
  • WBC - elevated in only 35% of cases
  • Blood culture - low yield in chronic phase

Imaging:

InvestigationFindings
Plain X-ray (first line)Bone sclerosis + destruction + periosteal reaction; sequestrum (dense fragment), involucrum, cloaca, sinus; pathological fracture
CT scanBest for cortical bone; excellent for identifying sequestra; good surgical planning
MRI (investigation of choice)Best for extent of infection; bone marrow oedema, soft-tissue involvement; poor around metal implants
SinogramInjection of contrast into sinus tract - outlines the track and locates the focus of infection
Isotope bone scanSensitive but not specific; useful when X-ray normal
18FDG-PET CTHelpful for surgical planning
CT scan of femur showing diaphyseal chronic osteomyelitis with sequestration of lateral cortex and overlying involucrum
CT scan: Coronal view of femur showing diaphyseal chronic osteomyelitis with sequestration and involucrum formation (Bailey & Love)

Definitive Diagnosis:

  • Biopsy of infected bone - sent for histology + microbiology/culture & sensitivity
  • Gold standard test
  • Identifies organism and guides antibiotic choice

Treatment

Principles (Multidisciplinary Approach):

Involves: Orthopaedic surgeon + Plastic surgeon + Infectious disease specialist + Vascular surgeon (if needed)
Must address 4 components simultaneously:
  1. Eradication of infection (sequestrectomy, debridement)
  2. Dead-space management
  3. Bone stabilisation
  4. Soft-tissue coverage

Pre-operative Optimisation of Host:

  • Stop smoking
  • Control diabetes (optimise HbA1c)
  • Treat peripheral vascular disease
  • Correct anaemia, nutritional deficiency
  • Treat liver/renal impairment

Surgical Treatment

Step 1 - Sequestrectomy and Debridement (Core of Treatment)

  • Removal of all sequestra
  • Saucerisation: conversion of cavity into a saucer-shaped open wound
  • Excision of all infected/necrotic bone, scarred soft tissue, and sinus tracts
  • Do not leave dead bone - it perpetuates infection
  • If >1/3 cortical circumference excised → splintage/external fixation mandatory to prevent fracture

Step 2 - Dead Space Management (Box 23.3 from Campbell's)

Options for managing the bony and soft-tissue defect:
MethodDetails
PMMA antibiotic bead chainsGentamicin/vancomycin beads packed in wound; high local antibiotic levels; removed within 10-80 days
Masquelet (antibiotic cement spacer) techniqueCement spacer induces a biological membrane; removed at stage 2 and replaced with bone graft
Antibiotic cement-coated locking plateFor infected non-unions with bone defect
Intramedullary antibiotic cement nailFor medullary osteomyelitis
Papineau techniqueOpen cancellous bone grafting - allows granulation tissue to cover exposed bone
Ilizarov/distraction osteogenesisSegmental bone transport; fills large defects; can combine with free tissue transfer
Bone graftingSecondary bone grafting after infection controlled
Absorbable local antibiotic carriersCalcium sulphate pellets with gentamicin; can form new bone (especially hydroxyapatite-based)

Step 3 - Soft-Tissue Coverage

  • Local muscle flaps (e.g., gastrocnemius, soleus for tibia)
  • Free flaps (microvascular transfer) for large defects
  • Skin grafting over granulating wounds
  • Direct closure if possible (BACH uncomplicated)

Step 4 - Bone Stabilisation

  • External fixation (Ilizarov, monolateral) - preferred when infection active
  • Intramedullary nailing (antibiotic-coated) - after infection control
  • Locking plates (antibiotic-coated) for selected cases

Antibiotic Treatment

  • Guided by culture & sensitivity from biopsy
  • Route: IV initially, then oral (or oral throughout if bioavailable agent)
  • Duration: Traditionally 6 weeks IV post-surgery; many units use 6-12 weeks total
  • In segmental excision with complete removal: shorter course may suffice
  • In chronic fracture-related infection: continue until fracture union
  • Local delivery (PMMA beads, absorbable carriers) allows high local concentrations without systemic toxicity
Commonly used:
  • Flucloxacillin / cloxacillin (S. aureus)
  • Vancomycin (MRSA)
  • Ciprofloxacin (gram-negatives, excellent bone penetration)
  • Rifampicin (biofilm-active; always in combination)

Palliative Treatment (C-host / high surgical risk)

  • Limited debridement + long-term suppressive antibiotics
  • Nutritional support
  • Goal: reduce frequency of sinus drainage and pain, not cure
  • Daily aspirin (DVT risk)

Special Variants

Brodie Abscess

  • Subacute/chronic form; low-grade
  • Metaphysis of long bones; distal tibia most common
  • X-ray: lytic lesion with sclerotic rim
  • Treatment: open biopsy + curettage

Sclerosing Osteomyelitis of Garré

  • Rare; predominantly periosteal thickening and sclerosis without suppuration
  • Mandible most common site
  • No sequestrum or sinus
  • Differential: osteosarcoma
  • Treatment: antibiotics; rarely surgery

Chronic Recurrent Multifocal Osteomyelitis (CRMO)

  • Autoinflammatory; affects children/adolescents
  • Nonbacterial
  • Multifocal metaphyseal lesions
  • Treatment: NSAIDs, bisphosphonates, biologics

Complications

ComplicationNotes
Pathological fractureThrough weakened bone
Malignant transformationSquamous cell carcinoma in chronic sinus - Marjolin's ulcer (rare but important)
Amyloidosis (secondary/AA)Chronic inflammatory stimulus - affects kidneys (nephrotic syndrome)
SepticaemiaDuring acute exacerbations
Septic arthritisSpread to adjacent joint
Deformity and shorteningGrowth disturbance in children
DVT / PESignificant risk; consider aspirin prophylaxis
Chronic anaemiaAnaemia of chronic disease
Joint stiffnessFrom periarticular involvement or prolonged immobilisation
Sinus tract carcinomaLong-standing sinus → squamous cell carcinoma
Malignant transformation: Signs - chronic draining sinus + increased pain + foul smell → biopsy immediately. Squamous cell carcinoma. Treatment: wide excision or amputation + chemotherapy + radiotherapy.

Key Exam Points (Maheshwari Style)

  1. Hallmark of chronic osteomyelitis = infected dead bone (sequestrum) in avascular soft-tissue envelope
  2. Sequestrum = dead devascularised bone; Involucrum = new periosteal bone around it; Cloaca = holes in involucrum; Sinus = discharge track to skin
  3. Most common organism: Staphylococcus aureus
  4. Brodie abscess = lytic lesion with sclerotic rim in metaphysis; subacute form
  5. Sinogram = contrast injected into sinus to outline the track
  6. CT = best for identifying sequestrum; MRI = investigation of choice for extent
  7. Biopsy = diagnostic gold standard (histology + culture)
  8. WBC elevated in only 35% of cases
  9. Cierny-Mader classification: 4 anatomic types (I-IV) + 3 physiologic host classes (A/B/C)
  10. Treatment = sequestrectomy + dead-space management + bone stabilisation + soft-tissue cover + antibiotics (6 weeks minimum)
  11. PMMA antibiotic beads: aminoglycosides most commonly used; removed within 10-80 days
  12. Masquelet technique = 2-stage: cement spacer → induced membrane → bone graft
  13. Ilizarov = gold standard for segmental bone defects after resection
  14. Feared late complication = Marjolin's ulcer (SCC in chronic sinus)
  15. Secondary amyloidosis (AA type) = renal involvement in long-standing cases

Sources: Campbell's Operative Orthopaedics 15th Ed, pp. 995-998; Bailey & Love's Short Practice of Surgery 28th Ed, pp. 625-627; Grainger & Allison's Diagnostic Radiology
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