REVIEW SISTEM

GERAK
Compartment Syndrome
zainuri
Review
 Definisi  Pening tekanan di dalam ruang
kompartemen fascial
 Pathophysiology
 Intracellular swelling/Hematoma
 Pressure rises and capillary perfusion drops
 Tissues vary in susceptibility to damage
○ Nerve < 4 hours
○ Muscle < 8 hours
 After 8 hours irreversible damage
 Experimentally
○ Within 10mmHg of diastolic pressure
○ Injured tissue 20 mmHg
Review
 Etiology
 Temporary vascular occlusion
○ Trauma, thrombus
 Clinical Presentation
 History of injury / energy absorbed
 Swelling, Pain
 Passive stretch
 Pallor, paresthesia, pulselessness, paralysis
 Investigation
 Compartmental pressure measurements
 Don’t delay getting measurements if diagnosis is obvious (20
mmHG less than diastolic)
Review
 Treatment
 Remove dressings
 Do not excessively elevate the foot
○ Level of the heart
 Analgesia
 Have low threshold to proceed surgically
 Emergency fascial release
 3 incisions
○ 1 medial 2 Dorsal
 Divide fascia
 Delayed closure
○ +/- skin grafting
 Prophylactic releases
komplikasi
 Early
Myonecrosis
Renal concerns
 Late
Deformities from contracture of necrotic
muscle
Nerve Injury
○ Ulcerations
osteomyelitis
zainuri
Review
Definisi  INFLAMMATORY PROCESS IN BONE & BONE
MARROW ACUTE & CHRONIC
 Pathophysiology
 Hematogenous Osteomyelitis
 Contiguous-Focus Osteomyelitis
 Peripheral Vascular Disease-associated

Bacteria escape host defenses by:

Adhering tightly to damage bone
Persisting in osteoblasts
Protective polysaccharide-rich biofilm
 PATHOPHYSIOLOGY
Microorganisms enter bone (Phagocytosis).

Phagocyte contains the infection

Release enzymes

Lyse bone
 PATHOPHYSIOLOGY
Pus spreads into vascular channels

Raising intraosseous pressure

Impairing blood flow

Chronic ischemic necrosis

Separation of large devascularized fragment

(Sequestra)

New bone formation

(involucrum)
 PATHOLOGY
Acute Infiltration of PMNs
Congested or thrombosed vessels

Chronic  Necrotic bone

Absence of living osteocyte
Mononuclear cells predominate
Granulation & fibrous tissue
 HEMATOGENOUS OSTEPMYELITIS
Rapidly growing bone
Children:
Long bone, Femur, Tibia, Humerus
Older patients: Vertebral bone

Neonate & infant < 1 year old

Septic arthritis is common.

Growth deformities is common.
Soft tissue involvement is common.
 HEMATOGENOUS OSTEOMYELITIS
Clinical manifestation
Classic presentation: Sudden onset
Usually presentation: Slow, insidious

High fever, Night sweats

Fatigue, Anorexia, Weight loss
Restriction of movement
Local edema, Erythema, & Tenderrness
HEMATOGENOUS OSTEOMYELITIS

Differentials
Cellulitis
Gas gangrene
Neoplasm
Aseptic bone infection
Clenched fist
osteomyelitis
 HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Lab study:
WBC  May be elevated, Usually normal

C-Reactive Protein (CRP)

Erythrocyte Sedimentation Rate

{ (Usually is elevated at presentation

Falls with successful therapy)

Blood culture
( Acute osteomyelitis + ve > 50% )
HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Imaging
Radiology:
Normal
Soft tissue swelling
Periosteal elevation
Lytic change
Sclerotic changew
 HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Ultrasonography
Simple & inexpensive

Demonstration anomaly 1 – 2 days after onset

Soft tissue abscess, Fluid collection, &

Periosteal elevation

It allows for aspiration

It doesn’t allow for evaluation of bone cortex.

 TREATMENT
Initial treatment shoud be aggressive.
Inadequate therapy  Chronic disease
Antibiotic use:
Parenteral
High doses
Good penetration in bone
Full course
Empiric therapy

Surgery
Diagnostic
Hip joint involvement
Neurologic complication
Poor or no response to IV therapy
Sequestration
Contiguous-focus Osteomyelitis
Clinical setting:
Postoperative infection
Contamination of bone
Contiguous soft tissue infection
Puncture wounds
Microbiologic features
Staphylococci  Aureus, Epidermidis
Gram-negative bacteria
Anaerobic infection
Unusual organisms Clostridia, Nocardia
 Contiguous-focus Osteomyelitis
Diagnosis
Leukocyte count
Blood culture (infrequently positive)
ESR & CRP
Radiologic evaluation
Technetium bone scan
Open bone biopsy
Culture of wound & draining sinuses??

Treatment
Surgery is essential.

Antibiotics  Specific
Duration
Arthritis
zainuri
review

Types of arthritis

Symptoms of arthritis

Signs of arthritis

Treatment of arthritis
Types of Arthritis

Rheumatoid arthritis (RA)

Osteoarthritis (OA)


Sero-negative arthritis

Ankylosing spondylitis

Reiter’s disease

Crystal arthropathies
Rheumatoid Arthritis
Pathology

Synovitis
chronic infl, synovial hypertrophy,
effusion

Destruction
proteolytic enzymes, pannus

Deformity
articular destruction, capsular stretching,
tendon rupture
Rheumatoid Arthritis
extra-articular


nodules

tendon sheath

vasculitis

myopathy and neuropathy

reticulo-endothelial system

visceral - lungs, heart, kidneys, brain, GI
Rheumatoid Arthritis
early symptoms

myopathy, tiredness, weight loss, malaise

proximal finger joints

wrists, feet, knees, shoulders

start up pain

tendon crepitus

late symptoms

joint destruction

pain

deformity

instability
Rheumatoid Arthritis
advanced joint changes
Rheumatoid Arthritis
X-ray findings

joint space narrowing

peri-articular osteopenia

erosions
Rheumatoid Arthritis
treatment

stop synovitis

prevent deformity

reconstruct

Rehabilitate
Prognosis

10% improve

60% intermittent, slowly worsening

20% severe joint erosion, multiple surgery

10% completely disabled
Osteoarthritis

A chronic joint disorder in which there is

progressive softening and disintegration
of articular cartilage accompanied by
new growth of cartilage and bone at the
joint margins (osteophytes) and capsular
fibrosis
Osteoarthritis
classification

Primary or idiopathic


Secondary - infection
- dysplasia
- Perthes’
- SUFE
- trauma
- AVN
Osteoarthritis
aetiology


Genetic

metabolic

hormonal

mechanical

ageing
Osteoarthritis
mechanism 1

Disparity between:-

stress applied to articular cartilage

and
strength of articular cartilage
Osteoarthritis
mechanism 2
Increased stress (F/A)


increased load eg BW or activity

decreased area eg varus knee or
dysplastic hip
Osteoarthritis
mechanism 3
Weak cartilage


age

stiff eg ochronosis

soft eg inflammation

abnormal bony support eg AVN
Osteoarthritis
X-ray changes


joint space narrowing

subchondral sclerosis

osteophytes

cysts
Osteoarthritis
X-ray changes
Arthritis
symptoms


pain

swelling

stiffness

deformity

instability

loss of function
Arthritis
non-surgical treatment


analgesia

disease modifying drugs (RA)

altered activity

walking aids

physiotherapy
Arthritis
surgical treatment


arthroscopy

osteotomy

arthrodesis

excision arthroplasty

replacement arthroplasty
Arthritis
knee arthroplasty
Joint Replacement
indications

Disabling pain

Functional limitations

History

pain

function

medical

expectations
Joint Replacement
investigation

X-ray - alignment
- deformity
- previous fractures and implants
- AVN
- osteophytes
- bone loss

CT, MRI, bone scan - rarely
Ankylosing Spondylitis


0.2% of population

mainly affects spine and SI joints

male > female

HLA B27 in 90%

synovitis

enthesopathy
Ankylosing Spondylitis
hips and knees


flexion deformities

arthritis with large osteophytes

ankylosis
Ankylosing Spondylitis
X-ray changes


joint space narrowing

large osteophytes

heterotopic bone

ankylosis
Tumor Musculoskeletal
zainuri
Introduction
 Primary Musculoskeletal
tumors arise from tissue
of mesenchymal origin
(ie. bone, muscle,
connective tissue,
adipose.)
 These primary tumors
may spread to other
sites, usually other
bones or lung.
 Secondary bone tumors
arise from a host of other
tissues and in the
appropriate age category
must be looked for.
Introduction
 The work-up of any tumor must be
thought of in terms of Local disease
and Systemic disease.
 By doing so you will have a sensible
approach to determining the ultimate
pathologic diagnosis and the extent of
the disease in the body.
Local Investigations
 X-ray….the most helpful
in focusing our
differential and further
investigations.

 Cat scan….. Bone

architecture,
neocorticalization, ?
fracture.

 MRI….marrow extent,
soft tissue extent,
neurovascular
involvement, skip
lesions.
Radiographic Features of the
Various Tumors
 Benign: well circumscribed, narrow transition,
no reaction, sclerotic border, ‘does one thing’.
 Benign Aggressive: neocorticalization,
expansion, thinning of cortex, usually lytic, +/-
reaction, +/- narrow zone of transition.
 Malignant: ++++reaction, large, permeative,
moth eaten, ‘does more than one thing’.
 Conditions/Mets: more than one bone,
symmetry.
Invasive Investigation
 Biopsy…..the goal is to obtain a piece of
tissue adequate to make a pathologic
diagnosis.
 Should be done after all other
investigations are complete
 Needle, Tru-cut, incisional.
 CT/US guided.
Primary Bone Tumors
 Osteogenic
 Fibrous
 Chondroid
 Lipomatous
 Other

 *****These are the

broad
categories******
Osteogenic
 Benign: Osteoma,
Osteoid Osteoma,
Bone Islands

 Benign Aggressive:
Osteoblastoma

 Malignant:
Osteogenic Sarcoma
Fibrous Tumours
 Benign: Fibrous Cortical
Defect, Non-Ossifying
Fibroma, Fibroma of Bone.
 Benign Aggressive:
Fibromatosis(desmoid),
Ossifying Fibroma of bone,
Fibrous Dysplasia.

 Malignant: Malignant
Fibrous Histiocytoma of
bone, Fibrosarcoma.
Chondroid
 Benign:
Enchondroma, Peri-
osteal Chondroma,
Osteochondroma.

 Benign Aggressive:
Chondromyxoid
Fibroma,
Chondroblastoma.

 Malignant:
Chondrosarcoma.
Other Bone Tumors
 Benign: Bone Cyst,
Ganglion,
Hemangioma.

 Benign Aggressive:
Giant Cell Tumor,
Aneurysmal Bone
Cyst, EOG.

 Malignant:
Adamantinoma,
Chordoma, Ewings.
Sites of Tumors
 Diaphyseal: Ewings, Osteoid Osteoma,
Mets, Adamantinoma, Fibrous Dysplasia

 Epiphyseal: Chondroblastoma, Clear

Cell Chondrosarcoma, GCT, Ganglion of
Bone.

 Metaphyseal: Everything!!!!!!
Age of Tumors
 20>…..Osteogenic Sarcoma, Ewings.

 40……GCT, Chondrosarcoma, MFH,

Lymphoma, Mets.

 60……Mets, Myeloma,
Chondrosarcoma, late Osteogenic,
MFH, Fibrosarcoma.