Problem in discontinuity of tissue that makes

seperated normal continuity.

Vulnera
1. Open Wound
2. Closed Wound
Type of Vulnera
1. Open Wound
Vulnus Excoriatum
body/skin erosion, simple wound, ex: road friction
Vulnus Laceratum
body wound that cause by dull shaped object, irregular margin,
usually under skin exposed, ex: many object that cause more
massive than excoriation
Vulnus Punctum
body wound cause by long sharp object that penetrate the body,
ex: knife stab
Vulnus Scissum/Incisivum:
body wound cause by sharp object, regular margin, ex: knife
laceration
Vulnus Caesum
body wound caused by wide sharp object, ex: axe
Type of Vulnera
1. Open Wound
Vulnus Sclopetorum
shot wound, ex: gun shot wound
Vulnus Morsum
wound cause by bite, ex: human bite, animal bite
Type of Vulnera
2. Closed Wound
- Vulnus Contussum
wound that make haematom subcutan, skin
intact, ex: haematom wound at skin
- Vulnus Traumaticum
wound that not seen outside, but bleed inside,
ex: organ haematom
Type of Vulnera
Phase of Wound Healing:
1. Homeostasis and Inflamation
2. Proliferation
3. Maturation and Remodeling
Hemostasis precedes and initiates inflammation with the ensuing release
of chemotactic factors from the wound site. Wounding by definition
disrupts tissue integrity, leading to division of blood vessels and direct
exposure of extracellular matrix to platelets. Exposure of subendothelial
collagen to platelets results in platelet aggregation, degranulation, and
activation of the coagulation cascade. Platelet granules release a number
of wound-active substances, such as platelet-derived growth factor
(PDGF), transforming growth factor- (TGF-), platelet-activating factor
(PAF), fibronectin, and serotonin. In addition to achieving hemostasis, the
fibrin clot serves as scaffolding for the migration into the wound of
inflammatory cells such as polymorphonuclear leukocytes (PMNs,
neutrophils) and monocytes.

1. Homeostasis and Inflamation
The proliferative phase is the second phase of wound healing and roughly
spans days 4 through 12 It is during this phase that tissue continuity is re-
established. Fibroblasts and endothelial cells are the last cell populations
to infiltrate the healing wound, and the strongest chemotactic factor for
fibroblasts is PDGF. 11,12 Upon entering the wound environment,
recruited fibroblasts first need to proliferate, and then become activated,
to carry out their primary function of matrix synthesis remodeling. This
activation is mediated mainly by the cytokines and growth factors released
from wound macrophages.

2. Proliferation
The maturation and remodeling of the scar begins during the fibroplastic
phase, and is characterized by a reorganization of previously synthesized
collagen. Collagen is broken down by matrix metalloproteinases (MMPs),
and the net wound collagen content is the result of a balance between
collagenolysis and collagen synthesis. There is a net shift toward collagen
synthesis and eventually the re-establishment of extracellular matrix
composed of a relatively acellular collagen-rich scar.

3. Maturation and Remodeling
A. The hemostatic/inflammatory
phase.
B. Latter inflammatory phases reflecting
infiltration by mononuclear cells and
lymphocytes.
C. The proliferative phase with associated angiogenesis and collagen synthesis

Clean
Debride
Irrigate
Excise
Management of Sterile Wound
Stop the bleeding
Close one by one
Wash the area surrounding of the wound
Do desinfection surrounding the wound
Close the wound
Local anestesia
Wash the wound with H
2
O
2
/ diluted
Povidon
Do the evaluation
Wound toilet and debridement
Prevention to tetanus etc.
Disinfection surrounding the wound
Dont do infiltratif anestesia, do with
block anestesia or general anestesia
Washing by H2O2/ diluted povidone
Debridement
Dont do primary closure
Sistemic antibiotic
Prevention tetanus etc.

Antitetanus
Antibiotics if necessary
Immobilisation
Analgesics

Wound infection
Systemic infections
Chronic wounds and ulcers
Scars and contractures
Keloids
Lymphoedema
Bone complications: osteitis,
osteomyelitis
Tetanus
Pressure ulcers