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REPAIR AND WOUND
HEALING
BY DR. ABDUL AZIZ SHAIKH
HEALING BY 1ST INTENTION
INCISION (CUT) & LACERATION (TEAR):
THE LEAST COMPLICATED WOUND REPAIR IS THE HEALING OF
CLEAN, UNINFECTED SURGICAL INCISION APPROXIMATED BY
SURGICAL SUTURES. THIS IS REFERRED AS PRIMARY UNION
OR HEALING BY 1ST INTENTION.
HEALING BY 1ST INTENTION
THE INCISION CAUSES DEATH OF LIMITED NUMBER OF
EPITHELIAL AND CONNECTIVE TISSUE CELLS AS WELL
AS DISRUPTION OF EPITHELIAL BASEMENT MEMBRANE
CONTINUITY.
THE NARROW INCISIONAL SPACE IMMEDIATELY FILLS
WITH CLOTTED BLOOD CONTAINING FIBRIN AND BLOOD
CELLS.
DEHYDRATION OF THE SURFACE CLOTS FORM THE
WELL KNOWN SCAB THAT COVERS THE WOUND.
STEPS IN WOUND HEALING BY 1ST
INTENTION
• WITHIN 24 HRS, NEUTROPHILS APPEARS AT THE MARGINS OF
THE INCISION MOVING TOWARDS THE FIBRIN CLOT.
• IN 24 TO 48 HRS SPURS OF EPITHELIAL CELLS MOVE FROM
THE WOUND EDGES WITH LITTLE CELL PROLIFERATION
ALONG THE CUT MARGINS OF THE DERMIS, DEPOSITING
BASEMENT MEMBRANE COMPONENT AS THEY MOVE.
• THEY FUSE IN THE MIDLINE BENEATH THE SURFACE SCAB
PRODUCING A CONTINUOUS BUT THIN EPITHELIAL LAYER
THAT CLOSES THE WOUND.
• BY DAY 3 THE NEUTROPHILS HAVE BEEN LARGELY
REPLACED BY THE MACROPHAGES.
• GRANULATION TISSUE PROGRESSIVELY INVADES
THE INCISION SPACE.
• COLLAGEN FIBERS ARE NOW PRESENT IN THE
MARGINS OF THE INCISION, BUT AT 1ST THESE ARE
VERTICALLY ORIENTED AND DO NOT BRIDGE THE
INCISION
• EPITHELIAL CELL PROLIFERATION THICKEN THE
EPIDERMAL LAYER
• BY DAY 5, THE INCISIONAL SPACE IS FILLED WITH
GRANULATION TISSUE
• NEOVASCULARIZATION IS MAXIMUM
• COLLAGEN FIBRILS BECOME MORE ABUNDANT AND
BEGINS TO BRIDGE THE INCISION
• THE DERMIS RECOVER ITS NORMAL THICKNESS
AND DIFFERENTIATION OF SURFACE CELLS YIELD A
MATURE ARCHITECTURE WITH SURFACE
KERATINIZATION
• DURING 2ND WEEK, THERE IS CONTINUED
ACCUMULATION OF COLLAGEN AND
PROLIFERATION OF FIBROBLAST .
• THE LEUKOCYTIC INFILTRATE ,EDEMA AND
INCREASE VASCULARITY HAVE LARGELY
DISAPPEARED
• AT THIS TIME THE LONG PROCESS OF BLANCHING
BEGINS ACCOMPLISHED BY THE INCREASED
ACCUMULATION OF COLLAGEN WITHIN THE
INCISIONAL SCAR ACCOMPANIED BY REGRESSION
OF VASCULAR CHANNELS.
• BY THE END OF 1ST MONTH, SCAR IS MADE UP OF
CELLULAR CONNECTIVE TISSUE DEVOID OF
INFLAMMATORY INFILTRATE COVERED BY INTACT
EPIDERMIS.
• THE DERMAL APPENDAGES THAT HAVE BEEN
DESTROYED IN THE LINE OF INCISION ARE
PERMANENTLY LOST.
• TENSILE STRENGTH F THE WOUND INCREASES
THEREAFTER BUT IT MAY TAKE MONTHS FOR THE
WOUNDED AREA TO OBTAIN ITS MAXIMAL
STRENGTH
HEALING BY 2ND INTENTION (WOUND
WITH SEPARATED EDGES)
WHEN THERE IS LARGE INJURY REGENERATION OF
PARANCHYMAL CELLS CANNOT COMPLETELY
RESTORE ORIGINAL ARCHITECTURE SO THERE IS
ABUNDANT GRANULATION TISSUE GROWS IN FROM
THE MARGINS TO COMPLETE THE REPAIR, THIS FORM
OF HEALING IS REFERRED AS 2NDRY UNION OR
HEALING BY 2ND INTENTION
STEPS INVOLVED IN
HEALING BY 2ND INTENTION
• LARGE TISSUE DEFECTS GENERATE A LARGER FIBRIN CLOT
THAT FILLS THE DEFECTS AND MORE NECROTIC DEBRIS AND
EXUDATE THAT MUST BE REMOVED .
• THE INFLAMMATORY REACTION IS MORE INTENSE.
• MUCH LARGER AMOUNT OF GRANULATION TISSUE ARE
FORMED
• WOUND CONTRACTION, THAT DECREASES THE GAP BETWEEN
THE DERMAL EDGES OF THE WOUND
• SCAR FORMATION AND THINNING OF THE EPIDERMIS
24 hrs: proliferation of fibroblasts & endothelial cells
Within 3-5 days:
Sequence of events in repair
Angiogenesis: 2 mechanisms
Summary: phases of wound healing
Wound tensile strength: 10% of normal at 7 days;
70-80% of normal at 3 months
Rabbit Ear Chamber: Direct observation of fibrous repair.
1) Exudate clots 2) Neutrophils
infiltrate
and digest clot
3) Macrophages
and
lymphocytes are
recruited
Rabbit Ear Chamber: Direct observation of fibrous repair
4) Vessels sprout,
myofibroblasts make
glycoproteins
5) Vascular network;
collagen
synthesised;
macrophages reduced
6) Maturity. Cells
much reduced; collagen
matures, contracts,
remodels
Angiogenesis
Regeneration and repair combined:
A chronic peptic ulcer
FACTORS AFFECTING WOUND HEALING
• SYSTEMIC FACTORS:
- DRUGS (STEROIDS, CYTOTOXIC DRUGS, INTENSIVE ANTIBIOTIC THERAPY)
- GENETIC DISORDERS (OSTEOGENESIS IMPERFECTA, EHLER-DANLOS
SYNDROME)
- HYPOVOLUMIA, HYPOXIA
- AGE - ANEMIA
- HORMONES - DM
- MALIGNANT DISEASES - MALNUTRITION
- INFECTIONS
- VITAMIN DEFICIENCY (VIT. C)
LOCAL FACTORS:
- BLOOD SUPPLY - DENERVATION
- INFECTIONS - FOREIGN BODY
- HEMATOMA - MECHANICAL STRESS
- NECROTIC TISSUE - PROTECTION
(DRESSINGS)
- SURGICAL TECHNIQUES - TYPE OF TISSUE
COMPLICATIONS OF WOUND HEALING
• THERE ARE THREE GENERAL CATEGORIES
1. DEFICIENT SCAR FORMATION: INADEQUATE
FORMATION OF GRANULATION TISSUE OR
ASSEMBLY OF A SCAR CAN LEAD TO 2 TYPES OF
COMPLICATIONS:
- WOUND DEHISCENCE
- ULCERATION
COMPLICATIONS OF WOUND
HEALING
WOUND DEHISCENCE: OR RUPTURE OF WOUND IS MOST
COMMON AFTER ABDOMINAL SURGERY DUE TO INCREASE
ABDOMINAL PRESSURE
ULCERATION: WOUND CAN ULCERATE BECAUSE OF
INADEQUATE VASCULARIZATION DURING HEALING E.G.
LOWER EXTREMITY WOUNDS IN PTS WITH ATHEROSCLEROTIC
PERIPHERAL VASCULAR DISEASES AND PTS WITH DIABETIC
NEUROPATHY.
TISSUE ULCERATIONTISSUE ULCERATION
skin ulcer
ulcer
healing by second intention
2. EXCESSIVE FORMATION OF SCAR
COMPONENTS:
• HYPERTROPHIC SCAR:
THE ACCUMULATION OF EXCESSIVE AMOUNT OF
COLLAGEN GIVE RISE TO A RAISED SCAR KNOWN AS
HYPERTROPHIC SCAR.
• KELOID: IF THE SCAR TISSUE GROWS BEYOND THE
BOUNDARIES OF THE ORIGINAL WOUND AND DOESN’T
REGRESS IS CALLED KELOID.
TISSUE REPAIRTISSUE REPAIR
abnormal tissue reaction with excessive fibroplasia
collagen deposition
keloid
dense collagen
PROUD FLESH: (EXUBERANT GRANULATION)
FORMATION OF EXCESSIVE AMOUNT OF GRANULATION
TISSUE WHICH PROTRUDES ABOVE THE LEVEL OF THE
SURROUNDING SKIN AND BLOCKS RE-EPITHELIALIZATION
• DESMOIDS OR AGGRESSIVE FIBROMATOSIS:
INCISIONAL SCARS OR TRAUMATIC INJURIES MAY BE
FOLLOWED BY EXUBERANT PROLIFERATION OF
FIBROBLAST AND OTHER CONNECTIVE TISSUE
ELEMENTS AND IN FACT REOCCUR AFTER EXCISION
CALLED DESMOIDS
3.FORMATION OF CONTRACTURES :
AN EXAGGERATION OF CONTRACTION
IS CALLED CONTRACTURE AND RESULTS
IN DEFORMITIES OF THE WOUNDS AND
SURROUNDING TISSUE
PALM, SOLE AND ANTERIOR ASPECT OF
THORAX
•
•
•
•
•
•
•
•
•
•
•
•
TISSUE REPAIRTISSUE REPAIR
first intention second intentionscab
neutrophils
mitoses
new capillaries
fibrous union
wound
contraction
Granulation tissue
macrophage
fibroblast
24 hours
3 to 7 days
weeks
clot

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Repair 2

  • 1.
  • 2. REPAIR AND WOUND HEALING BY DR. ABDUL AZIZ SHAIKH
  • 3. HEALING BY 1ST INTENTION INCISION (CUT) & LACERATION (TEAR): THE LEAST COMPLICATED WOUND REPAIR IS THE HEALING OF CLEAN, UNINFECTED SURGICAL INCISION APPROXIMATED BY SURGICAL SUTURES. THIS IS REFERRED AS PRIMARY UNION OR HEALING BY 1ST INTENTION.
  • 4.
  • 5. HEALING BY 1ST INTENTION THE INCISION CAUSES DEATH OF LIMITED NUMBER OF EPITHELIAL AND CONNECTIVE TISSUE CELLS AS WELL AS DISRUPTION OF EPITHELIAL BASEMENT MEMBRANE CONTINUITY. THE NARROW INCISIONAL SPACE IMMEDIATELY FILLS WITH CLOTTED BLOOD CONTAINING FIBRIN AND BLOOD CELLS. DEHYDRATION OF THE SURFACE CLOTS FORM THE WELL KNOWN SCAB THAT COVERS THE WOUND.
  • 6. STEPS IN WOUND HEALING BY 1ST INTENTION • WITHIN 24 HRS, NEUTROPHILS APPEARS AT THE MARGINS OF THE INCISION MOVING TOWARDS THE FIBRIN CLOT. • IN 24 TO 48 HRS SPURS OF EPITHELIAL CELLS MOVE FROM THE WOUND EDGES WITH LITTLE CELL PROLIFERATION ALONG THE CUT MARGINS OF THE DERMIS, DEPOSITING BASEMENT MEMBRANE COMPONENT AS THEY MOVE. • THEY FUSE IN THE MIDLINE BENEATH THE SURFACE SCAB PRODUCING A CONTINUOUS BUT THIN EPITHELIAL LAYER THAT CLOSES THE WOUND.
  • 7. • BY DAY 3 THE NEUTROPHILS HAVE BEEN LARGELY REPLACED BY THE MACROPHAGES. • GRANULATION TISSUE PROGRESSIVELY INVADES THE INCISION SPACE. • COLLAGEN FIBERS ARE NOW PRESENT IN THE MARGINS OF THE INCISION, BUT AT 1ST THESE ARE VERTICALLY ORIENTED AND DO NOT BRIDGE THE INCISION • EPITHELIAL CELL PROLIFERATION THICKEN THE EPIDERMAL LAYER
  • 8. • BY DAY 5, THE INCISIONAL SPACE IS FILLED WITH GRANULATION TISSUE • NEOVASCULARIZATION IS MAXIMUM • COLLAGEN FIBRILS BECOME MORE ABUNDANT AND BEGINS TO BRIDGE THE INCISION • THE DERMIS RECOVER ITS NORMAL THICKNESS AND DIFFERENTIATION OF SURFACE CELLS YIELD A MATURE ARCHITECTURE WITH SURFACE KERATINIZATION
  • 9. • DURING 2ND WEEK, THERE IS CONTINUED ACCUMULATION OF COLLAGEN AND PROLIFERATION OF FIBROBLAST . • THE LEUKOCYTIC INFILTRATE ,EDEMA AND INCREASE VASCULARITY HAVE LARGELY DISAPPEARED • AT THIS TIME THE LONG PROCESS OF BLANCHING BEGINS ACCOMPLISHED BY THE INCREASED ACCUMULATION OF COLLAGEN WITHIN THE INCISIONAL SCAR ACCOMPANIED BY REGRESSION OF VASCULAR CHANNELS.
  • 10. • BY THE END OF 1ST MONTH, SCAR IS MADE UP OF CELLULAR CONNECTIVE TISSUE DEVOID OF INFLAMMATORY INFILTRATE COVERED BY INTACT EPIDERMIS. • THE DERMAL APPENDAGES THAT HAVE BEEN DESTROYED IN THE LINE OF INCISION ARE PERMANENTLY LOST. • TENSILE STRENGTH F THE WOUND INCREASES THEREAFTER BUT IT MAY TAKE MONTHS FOR THE WOUNDED AREA TO OBTAIN ITS MAXIMAL STRENGTH
  • 11. HEALING BY 2ND INTENTION (WOUND WITH SEPARATED EDGES) WHEN THERE IS LARGE INJURY REGENERATION OF PARANCHYMAL CELLS CANNOT COMPLETELY RESTORE ORIGINAL ARCHITECTURE SO THERE IS ABUNDANT GRANULATION TISSUE GROWS IN FROM THE MARGINS TO COMPLETE THE REPAIR, THIS FORM OF HEALING IS REFERRED AS 2NDRY UNION OR HEALING BY 2ND INTENTION
  • 12. STEPS INVOLVED IN HEALING BY 2ND INTENTION • LARGE TISSUE DEFECTS GENERATE A LARGER FIBRIN CLOT THAT FILLS THE DEFECTS AND MORE NECROTIC DEBRIS AND EXUDATE THAT MUST BE REMOVED . • THE INFLAMMATORY REACTION IS MORE INTENSE. • MUCH LARGER AMOUNT OF GRANULATION TISSUE ARE FORMED • WOUND CONTRACTION, THAT DECREASES THE GAP BETWEEN THE DERMAL EDGES OF THE WOUND • SCAR FORMATION AND THINNING OF THE EPIDERMIS
  • 13.
  • 14. 24 hrs: proliferation of fibroblasts & endothelial cells Within 3-5 days: Sequence of events in repair
  • 16. Summary: phases of wound healing Wound tensile strength: 10% of normal at 7 days; 70-80% of normal at 3 months
  • 17. Rabbit Ear Chamber: Direct observation of fibrous repair. 1) Exudate clots 2) Neutrophils infiltrate and digest clot 3) Macrophages and lymphocytes are recruited
  • 18. Rabbit Ear Chamber: Direct observation of fibrous repair 4) Vessels sprout, myofibroblasts make glycoproteins 5) Vascular network; collagen synthesised; macrophages reduced 6) Maturity. Cells much reduced; collagen matures, contracts, remodels
  • 20.
  • 21.
  • 22.
  • 23. Regeneration and repair combined: A chronic peptic ulcer
  • 24.
  • 25.
  • 26. FACTORS AFFECTING WOUND HEALING • SYSTEMIC FACTORS: - DRUGS (STEROIDS, CYTOTOXIC DRUGS, INTENSIVE ANTIBIOTIC THERAPY) - GENETIC DISORDERS (OSTEOGENESIS IMPERFECTA, EHLER-DANLOS SYNDROME) - HYPOVOLUMIA, HYPOXIA - AGE - ANEMIA - HORMONES - DM - MALIGNANT DISEASES - MALNUTRITION - INFECTIONS - VITAMIN DEFICIENCY (VIT. C)
  • 27. LOCAL FACTORS: - BLOOD SUPPLY - DENERVATION - INFECTIONS - FOREIGN BODY - HEMATOMA - MECHANICAL STRESS - NECROTIC TISSUE - PROTECTION (DRESSINGS) - SURGICAL TECHNIQUES - TYPE OF TISSUE
  • 28. COMPLICATIONS OF WOUND HEALING • THERE ARE THREE GENERAL CATEGORIES 1. DEFICIENT SCAR FORMATION: INADEQUATE FORMATION OF GRANULATION TISSUE OR ASSEMBLY OF A SCAR CAN LEAD TO 2 TYPES OF COMPLICATIONS: - WOUND DEHISCENCE - ULCERATION
  • 29. COMPLICATIONS OF WOUND HEALING WOUND DEHISCENCE: OR RUPTURE OF WOUND IS MOST COMMON AFTER ABDOMINAL SURGERY DUE TO INCREASE ABDOMINAL PRESSURE ULCERATION: WOUND CAN ULCERATE BECAUSE OF INADEQUATE VASCULARIZATION DURING HEALING E.G. LOWER EXTREMITY WOUNDS IN PTS WITH ATHEROSCLEROTIC PERIPHERAL VASCULAR DISEASES AND PTS WITH DIABETIC NEUROPATHY.
  • 30. TISSUE ULCERATIONTISSUE ULCERATION skin ulcer ulcer healing by second intention
  • 31. 2. EXCESSIVE FORMATION OF SCAR COMPONENTS: • HYPERTROPHIC SCAR: THE ACCUMULATION OF EXCESSIVE AMOUNT OF COLLAGEN GIVE RISE TO A RAISED SCAR KNOWN AS HYPERTROPHIC SCAR. • KELOID: IF THE SCAR TISSUE GROWS BEYOND THE BOUNDARIES OF THE ORIGINAL WOUND AND DOESN’T REGRESS IS CALLED KELOID.
  • 32. TISSUE REPAIRTISSUE REPAIR abnormal tissue reaction with excessive fibroplasia collagen deposition keloid dense collagen
  • 33. PROUD FLESH: (EXUBERANT GRANULATION) FORMATION OF EXCESSIVE AMOUNT OF GRANULATION TISSUE WHICH PROTRUDES ABOVE THE LEVEL OF THE SURROUNDING SKIN AND BLOCKS RE-EPITHELIALIZATION • DESMOIDS OR AGGRESSIVE FIBROMATOSIS: INCISIONAL SCARS OR TRAUMATIC INJURIES MAY BE FOLLOWED BY EXUBERANT PROLIFERATION OF FIBROBLAST AND OTHER CONNECTIVE TISSUE ELEMENTS AND IN FACT REOCCUR AFTER EXCISION CALLED DESMOIDS
  • 34. 3.FORMATION OF CONTRACTURES : AN EXAGGERATION OF CONTRACTION IS CALLED CONTRACTURE AND RESULTS IN DEFORMITIES OF THE WOUNDS AND SURROUNDING TISSUE PALM, SOLE AND ANTERIOR ASPECT OF THORAX
  • 35.
  • 37.
  • 39.
  • 40.
  • 41. TISSUE REPAIRTISSUE REPAIR first intention second intentionscab neutrophils mitoses new capillaries fibrous union wound contraction Granulation tissue macrophage fibroblast 24 hours 3 to 7 days weeks clot