KULIAH BEDAH DASAR

Dr. Jufri Latief, Sp.B., Sp.OT

BONE HEALING
 I. Stage of Inflamation
Hematoma
Disruption of blood vessels
Intraosseous
Periosteal & surrounding
Bone at edges of fracture dies
Leucocytes
Macrophages Infiltrate clot & begin to
Mast cells remove dead bone

Fibroblast
 II. Stage of soft callus formation
Clot organized by collagen fiber & vascular
elements
New vessels grawn in
PO2 , PH (acidic)
Osteoprogenitor cells, preosteocytes & osteoblast of
periosteum & endosteum proliferasi
Osteoblast & chondroblast from mesenchymal
appear in clot
Soft callus farms as : osteoid, cartilage & collagen
 III. Stage of hard callus formation

Osteoid, cartilage of external, periosteal &

medullary soft callus mineralized
converted to fiber bone (hard callus)
 IV. Stage of bone remodelling
Osteoblastic & osteoclastic activity converts
fiber bone to lamellar bone with true
haversian system
Restored normal bone contours
PO2 retern to normal
 Stage of bone healing
Inflammation stage hemapoetic cells,
osteoprogeniter cells
Repair stage callus formation (soft or
hard) waven bone formation (enchondral)
Remodelling stage lamellar bone
replaces waven, bone assumes normal shape
& repopulation of the marrow
NERVE HEALING
 Pathology of nerve injury
Ischaemia
Compression
Traction / distraction
Laceration
Burning
 Compression / transient ischaemia

15 minutes Numbness & tingling

30 minutes loss of pain sensibility
45 minutes muscle weakness
Classification of nerve injury
 I. Seddon classification
Neuropraxia (good) : transient disorder / ischaemia &
conduction block.
EMG distally normal
- Recovery in days to weeks
Axonotmesis (Fair) : loss of axon continuity but endoneural
tube intack
- Conduction block wallerian degeneration & regeneration
1 mm/day
Neurotmesis (poor) : nerve trunk rupture include endoneural
tube
Recovery requires surgical repair
 II. Sunderland classification
1. Loss of axonal conduction
2. Loss of continuity of axon, endoneuron intack
3. Transection of nerve fibers (axon & sheat),
perineurium & epineurium intack
4. Loss of perineurium & fascicular continuity
epineuron intack
5. Loss of continuity of entire nerve trunk epi, peri,
endoneurium rupture
 Principle of nerve treatment
1. Nerve exploration exploration release & identified
2. Primary repair clean cut non absorsible suture 10-0 to epineurium
3. Delayed repair weeks month (6 month) before 18 month / 2 years (mator
& plate damaged)
1. Closed injury
2. Missed diagnosis or patient present late
3. Primary repair has failed
4. Nerve grafting
5. Nerve transfer
6. Care of paralysed part dynamic splint move the joint etc.
7. Tendon transfer after 18 24 months still not recovery
Nerve conduction myelium axons conduct action potentials
Nerve blood supply
Extrinsic connective tissue surrounding the nerve trunk
Intrinsic flexus epi & endoneurium
TENDON HEALING
 TENDON
Dense, regulary arranged tissue that attack
muscle to the bone
Composed of fascicle (group of collagen
bundles)
Separated by endotenon & surrounded by
epitenon
 Two types tendon exist (hidup)
1. Paratenon cavered tendon supplying a
rich capillary system
2. Sheathed tendon mesotenon vessel
supplies only one tendon segment
avascular area receive nutrition via
diffusion from vascularised segment
 Tendon healing after injury
1. Initiated by fibroblast from epitenon and macrophage initiated
healing & remodeling
2. Treatment affects the repair process. Tendon healing occurs in large
part through intrinsic capabilities
3. Tendon repair are weakest at 7 10 day. Regain
most of their original strength at 21 28 days. Acive maximum
strength at 6 months
4. Early mobilization allows increased ROM but decreased tendon
repair strength
5. Immobilization lead to increased tendon substance strength
6. Bony avulsion of tendon insertion heal more rapidly than
midsubstance tears
 Ligament
70% collagen type I
More variable fibersa higher elastin
content
Recives blood supply from insertion site