Clinical Examples Of Abnormal Wound
Healing and Scaring
Dr. Syed Muhammad Ikram
MBBS(AMC), MPhil Hematology
Abnormal wound Healing and Scaring:
Arise from abnormalities in any of the basic commponents of the
process including,
 deficient
scar/granulation tissue formation (leading to
wound dehiscence and ulceration)
 excessive formation of the repair components (leading to
Hypertrophic scar, Keloid or Desmoid)
 formation of contracture
Defects in healing: chronic wounds
These are seen in numerous clinical situation as a
result of local and systemic factors.
 Venous leg ulcer
• Develop most often in elderly hypertensive people
• Fail to heal due to poor oxygen delivery
• Iron pigment deposition is common
Figure: Venous ulcers are chronic wounds, caused by
venous insufficiency and are the most common type
of leg ulcer
 Arterial
•
ulcer
atherosclerosis of peripheral arteries, especially in
diabetes
• Ischemia results in atrophy then necrosis
• Painful
• Often located on toes
• Surrounding skin is shiny and taut
• Pale and cyanotic with irregular margins
Figure 2- Ischaemic ulcers, all showing well-defined edges in peripheral parts of limbs
Pressure sore (Decubitus ulcers)
• ulceration and necrosis of underlying
tissues caused by prolonged compression of
tissue against a bone
• Bedridden, immobile patients
• Mechanical pressure and local ischemia
especially buttocks
Figure: Decubitus ulcer on the dependent part of buttocks.
 Diabetic
ulcer
•
affect the lower extremities, particularly feet
•
Ischemia, neuropathy, systemic abnormalities and secondary
infections results in necrosis and healing failure
•
Histologically, epithelial ulceration and extensive granulation
tissue in dermis
A
C
B
D
Figure 5 Healing of skin ulcers. A, Pressure ulcer of the skin, commonly found in diabetic patients. The histologic
slides show a skin ulcer with a large gap
between the edges of the lesion (B), a thin layer of epidermal reepithelialization and extensive granulation tissue
formation in the dermis (C), and continuing
reepithelialization of the epidermis and wound contraction (D). (Courtesy Z. Argenyi, MD, University of Washington,
Seattle, Wash.)
A
B
Fig. (A) Gangrenous diabetic foot (B) After surgical debridement
Excessive scarring
Excessive formation of the components of the repair process can give
rise to hypertrophic scars, keloids or desmoids.
 Hypertrophic scar
•
•
Excess accumulation of collagen resulting a raised scar
Regress over several months
develop after thermal or traumatic injury which involve deep layers of dermis

Keloid
•
Scar tissue grows beyond the boundaries of the original wound
Does not regress
African american
•
•
•
A
B
Fig. (A) and (B) shows hypertrophic scars.
A
B
Figure 3 Keloid. A, Excess collagen deposition in the skin forming a raised scar known as keloid. B, Note the thick
connective tissue deposition in the
dermis. (A, From Murphy GF, Herzberg AJ: Atlas of Dermatopathology. Philadelphia, WB Saunders, 1996, p 219; B,
Courtesy Z. Argenyi, MD, University of
Washington, Seattle, Wash.)
Fig. Shows keloid formation after surgical procedure.
 Wound
contracture
•
Exaggeration of contraction process results in contracture
•
Effects palms, soles and anterior of neck/thorax
•
Seen in severe burns
•
Compromise movement of joints
A
B
Fig. (A) Contracture wound of the palm. (B) Contracture wound of the
neck.
 Fibrosis
in parenchymal organ
•
Excessive deposition of collagen and other ECM
components in the tissues of internal organs
•
Caused by chronic infections and immunologic reactions
•
Major cytokine TGF-β
•
Myofibroblasts in lung and kidney while stellate cells in
liver cirrhosis are sources of collagen
•
Examples; Scleroderma, Pulmonary fibrosis, constrictive
pericaditis
Figure 4 Mechanisms of fibrosis. Persistent tissue injury leads to chronic inflammation and loss of tissue
architecture. Cytokines produced by macro phages and other leukocytes stimulate the migration and proliferation
of fibroblasts and myofibroblasts and the deposition of collagen and other extracellular matrix proteins. The net
result is replacement of normal tissue
Reference:
1.
Robbins and Cotran: pathologic basis of disease.
Thank you