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A scab is a beautiful thing—a coin the body has minted, with an
invisible motto: In God We Trust. Our body loves us, and, even while
the spirit drifts dreaming, works at mending the damage that we do.
1984
Wound healing is complex process to achieve anatomical and
functional integrity of disrupted tissue by various components
like neutrophils, macrophages, lymphocytes, fibroblasts,
collagen; in an organised staged pathway—haemostasis →
inflammation → proliferation → matrix synthesis (collagen and
proteoglycan ground substance) → maturation → remodelling
SRB's Manual of Surgery
Healing ulcer with healthy granulation tissue which is
ready for skin grafting.
→ epithelialisation → wound contraction (by myofibroblasts).
Wound
Primary Healing (First Intention)
It occurs in a clean incised wound or surgical wound. Wound
edges are approximated with sutures. There is more epithelial
regeneration than fibrosis. Wound heals rapidly with complete
closure. Scar will be linear, smooth, and supple.
Secondary Healing (Second Intention)
It occurs in a wound with extensive soft tissue loss like in
major trauma, burns and wound with sepsis. It heals slowly
with fibrosis. It leads into a wide scar, often hypertrophied
and contracted. It may lead into disability.
Re-epithelialisation occurs from remaining dermal elements
or wound margins.
Wound in the abdomen healing with second intention,
which requires secondary suturing once it granulates well.
Secondary suturing is done after 10–14 days, once wound
granulates well after proper control of infection. Scar in such type
is prone to form incisional hernia.
Healing by Third Intention (Tertiary Wound Healing or
Delayed Primary Closure)
After wound debridement and control of local infection, wound
is closed with sutures or covered using skin graft. Primary
contaminated or mixed tissue wounds heal by tertiary intention.
B
x Stage of haematoma and inflammation
x Stage of granulation tissue formation and organi sation. Here
due to fibroblastic activity, synthesis of of collagen and ground
substance occurs
x Stage of epithelialisation
x Stage of scar formation and resorption
x Stage of maturation
Wound
InammatoryPhase (Lag or Substrate or
Exudative Phase)
It begins immediately after formation and lasts for 72 hours.
There is initial arteriolar vasoconstriction, thrombus forma-
tion, platelet aggregation due to endothelial damage and
release of adenosine diphosphate (ADP).
Later vasodilatation and increased vascular permeability
develops.
Here haemostasis, coagulation and chemotaxis occur.
All these cause features of acute inflammation—rubor, calor,
tumour, dolor and loss of function.
Note:
Coagulation begins at wound haematoma → formation of platelet fibrin
thrombus → release of cytokines, PDGF (platelet-derived growth factor),
epidermal growth factor (EGF), transforming growth factor-β (TGF-β),
platelet activating factor and platelet factor IV, fibrin, serotonin. Chemotaxis causes initially causes initially neutrophil neutrophil migration, and
then activation of macrophages, lymphocytes leading into phagocytosis,
wound debridement, matrix activation, angiogenesis. Chemotaxis factors
are complement factors, interleukin-1, TNF-α (tumour necrosis factor-α)
TGF-β and platelet factor. Activated macrophages produce free radicals
and nitric oxide; release cytokine to activate lymphocytes which release
interferon and interleukin (called as lymphokines). These factors attract
polymorphonuclear leucocytes (PMN—polymorphonuclear cells—
neutrophills) in 48 hours secreting inflammatory mediators and bactericidal oxygen-derived free radicals. Injured tissues and platelet release
histamine, serotonin and prostaglandins which increases the vascular
permeability by vasodilatation. These actions are reduced in diabetes
mellitus, Cushing’s syndrome and immunosuppression increasing the
sepsis rate.
Proliferative Phase (Collagen/Fibroblastic Phase)
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It begins from 3rd day and lasts for 3–6 weeks. There will
be formation of granulation tissue and repair of the wound.
Granulation tissue contains fibroblasts, neocapillaries,
collagen, fibronectin and hyaluronic acid.
Note:
(1) Initial angiogenesis (growth of new blood vessels) occurs following
release of vascular endothelial cell growth factor (VEGF) by keratinocytes;
by release of TNF-α, TGF-β, PDGF, FGF by macrophages. (2)
plasia develops by fibroblast activity with formation of collagen and ground
substance/glycosaminoglycans. Type III collagen is deposited initially in a
random fashion. (3)
by migration of basal layer of the retained epidermis which proliferates,
differentiates and stratifies to form wound closure.
Later re-epithelialisation of the wound surface occurs
Eventual fibro-
Remodelling Phase (Maturation Phase)
Contd...
x B lymphocyte will not have any role in wound healing; T lympho-
cytes produce stimulatory cytokines like interleukin-1 supporting
the fibroblast activity.
x Collagen and glycosamines are produced by fibroblasts. Tropocol-
lagen is produced which aggregates to form collagen fibrils.
x Hydroxyproline and hydroxylysine are synthesized by specific
enzymes using iron, α ketoglutarate and vitamin C.
x Fibroblast requires vitamin C to produce collagen.
x Granulation tissue and early scar contains type III collagen.
x Final scar contains type I collagen mainly.
x Final extracellular matrix contains type I collagen and proteo-
glycans.
x Collagen production decreases after 4 weeks of wound healing
(declines in 28–42 days).
x Eighty per cent of tensile strength of normal skin will be achieved
finally but not 100%.
7
CHAPTER 1A General Surgery: Wounds and Wound Healing
It begins at 6 weeks and lasts for 6 months to 1 or 2 years.
There is maturation of collagen by cross linking and realign-
ment of collagen fibers along the line of tension, which is
responsible for tensile strength of the scar. There is reduced
wound vascularity. Fibroblast and myofibroblast activity
causes wound contraction. Type III collagen is replaced by
type I collagen causing maturation of the collagen. Ratio of
type I collagen to type III collagen becomes 4:1.
Early extracellular matrix contains fibronectin and collagen
type III; eventually it contains glycosaminoglycans and
proteoglycans; final matrix contains type I collagen.
Scar strength is 3% in 1 week; 20% in 3 weeks; 80% in 12
weeks. Final matured scar is acellular and avascular.
Note:
Initially fibrin, fibronectin, proteoglycans deposition occurs; later collagen
protein develops to form scar. Normal dermal skin contains 80% type I
(20% type III) collagen; granulation tissue contains mainly type III collagen;
scar contains both type I and III collagen, initially in equal proportion, later
becomes 4:1. Basic essential components of collagen are proline and
lysine. Hydroxylation of lysine and later glycosylation of this hydroxylysine
decides the type of collagen molecule. Hydroxylation of both proline and
lysine as essential step needs adequate concentration of vitamin C, iron
and α ketogluteric acid. Collagen deposition in the wound is assessed by
quantity of hydroxyproline excreted in urine. There is a balanced activity of
collagen production and degradation of collagen (collagenolysis). Collagen
is broken down by collagenase and MMPs (matrix metalloproteinases).
Procollagen through procollagenase → collagen fibril → cross linking →
collagen fiber → deposition. Deposited collagen → through collagenase
→ degradation and collagenolysis.
B
x PMN cells survive only for 24 hours; so after 48 hours PMNs
would not be found in the wound significantly; PMNs are not
needed for wound healing.
x Activated monocytes called macrophages predominate after 48
hours which will persist until completion of the wound healing.
Macrophages are the main cells of wound healing. Macrophages
secrete TNF-α, interleukin-1, fibroblast growth factor (FGF),
proteinases (MMPs—matrix metallo proteinases).
Contd...
Factors Affecting Wound Healing
LOCAL FACTORS
B
x Infection
x Presence of necrotic tissue and foreign body
x Poor blood supply
x Venous or lymph stasis
x Tissue tension
x Haematoma
x Large defect or poor apposition
x Recurrent trauma
x X-ray irradiated area
x Site of wound, e.g. wound over the joints and back has poor healing
x Underlying diseases like osteomyelitis and malig nancy
x Mechanism and type of wound—incised/lacerated/crush/avulsion
x Tissue hypoxia locally reduces macrophage and fibroblast activity
GENERAL FACTORS
B
x Age, obesity, smoking, alcohol, stress
x Malnutrition, zinc, copper, manganese
x Vitamin deficiency (Vit C, Vit A)
x Anaemia, hypoxia
x Malignancy
x Uraemia
x Jaundice
x Diabetes, metabolic diseases
x HIV and immunosuppressive diseases
x Steroids and cytotoxic drugs
x Neuropathies of different causes
Age: In younger age group wound healing is faster and better. In
elderly healing is delayed due to reduction in collagen synthesis,
epithelialisation, growth factors and angiogenesis. But final scar
will be excellent in old individuals.
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Nutrition: Adequate vitamin, trace elements, fatty acids and
proteins are essential for wound healing. Vitamin A deficiency
affects monocyte activation, inflammatory phase, collagen
synthesis and growth factor actions. Vitamin K deficiency affects
synthesis of prothrombin (II), factors VII, IX and X. Vitamin
being an antioxidant stabilizes the cell membrane. Vitamin C
deficiency impairs collagen synthesis, fibroblast proliferation and
angiogenesis; increases the capillary fragility and susceptibility
for infection. Zinc is an essential cofactor for RNA and DNA
polymerase; magnesium is a co-factor for synthesis of proteins
and collagen; copper is a required co-factor for cytochrome
oxidase, for cytosolic antioxidant superoxide dismutase, and
for the optimal cross-linking of collagen; Iron is required for
SRB's Manual of Surgery
the hydroxylation of proline and lysine. Glutamine is the most
abundant amino acid in plasma; is a major source of energy
for rapidly proliferating cells such as fibroblasts, lymphocytes,
epithelial cells, and macrophages. The serum concentration of
glutamine is reduced after major surgery, trauma, and sepsis,
and supplementation of this amino acid improves nitrogen
balance and diminishes immunosuppression. Glutamine stimulates the inflammatory immune response in early wound healing.
Oral glutamine supplementation improves wound breaking
strength and of mature collagen. Arginine is a semi-essential
amino acid that is required in growth, severe stress, and injury.
Arginine modulates immune function, wound healing, hormone
secretion, vascular tone, and endothelial function. Arginine is a
precursor to proline; supports collagen deposition, angiogenesis,
and wound contraction. Under psychological stress situations,
the metabolic demand of arginine increases, and its supplementation hastens the wound healing. Serum albumin level less
than 2 g/d
fibroplasia, neovascularisation and cell synthesis and wound
remodeling and hence decreased wound healing. Wounds in
patients who remain in catabolic state will not heal. Collagen is
the major protein component of connective tissue; it contains
mainly glycine, proline, and hydroxyproline. Collagen synthesis
requires hydroxylation of lysine and proline, and co-factors such
as ferrous iron and vitamin C. Polyunsaturated fatty acids which
cannot be synthesized de novo by mammals, consist mainly of
omega-6 (found in soybean oil) and omega-3 [(found in fish
oil—fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)]. They affect pro-inflammatory cytokine
production, cell metabolism, gene expression and angiogenesis;
improve the systemic immune function of the host, thus reducing
infectious complications.
Wound infection Infection prolongs inflammatory phase,
releases toxins and utilizes vital nutrients thereby prevents
wound epithelialisation. The β-haemolytic streptococci more
than 10
of biofilms on the wound surface by microorganisms prevents
wound healing.
Anaemia Haemoglobin less than 8 g% causes poor oxygena-
tion of tissues preventing healing of the wounds.
Hypoxia: Hypoxia prevents fibroblast proliferation and collagen
synthesis; it also promotes bacterial invasion into the wound.
L causes prolonged inflammatory phase, decreased
5
per gram of tissue prevent wounds healing. Formation
Causes of hypoxia are—arterial diseases, cardiac failure, respiratory causes, hypotension, smoking, tobacco, infection, diabetes
mellitus and radiation.
Radiotherapy: Both external radiotherapy or ionizing radiation
E,
cause endarteritis, fibrosis and delay in wound healing. Radiation may itself cause local tissue necrosis, sepsis and hypoxia.
Systemic and metabolic causes Diabetes mellitus affects
all stages of wound healing. Cardiac, renal, hepatic, respiratory diseases prevent wound healing. Tissue oedema impairs
wound healing. HIV and immunosuppression of varying causes,
malignancy leads into poor wound healing. Jaundice interferes
with wound healing. Obesity causes hypoperfusion, reduced
microcirculation, increased wound tension and hence prevents
wound healing.
Drugs: Steroids interfere with activation of macrophages,
fibroblasts and angiogenesis in the early phase of healing
(proliferative). Nonsteroidal anti-inflammatory drugs (NSAIDs)
decrease collagen production. Chemotherapeutic agents used
in oncology inhibit cellular proliferation, protein synthesis.
Alcohol consumption decreases the phagocyte response and
pro-inflammatory cytokine release; diminishes host response
and thus increasing the infection rate.
W
Assessment of the Wound
Wound should be assessed accordingly as minor or major;
acute or chronic; number and extent; superficial or deep;
major organ injury present or not also to be assessed and
anatomical location of the wound(s). Wound is measured either
in two dimensions (length and width) or in three dimensions
(length, with and depth). Assessment includes detailed history
in relation to mode of injury and severity of pain/bleeding;
examination in relation to—loss of function, extent of injury,
involvement of deeper structures like nerves/vessels/bones/
organs; level of contamination, presence of foreign body in
the wound, presence of swelling, viability of the tissues in and
around the wound(s).
Wound Cleaning
It optimizes the wound healing environment and ‘wound bed
preparation’. Ideally it should be done with all aseptic precau-
tions; wound is irrigated/washed with warm sterile isotonic
normal saline (37°C which is optimum temperature to support
cellular activity) using sterile syringe. Wash should be gentle
so that already existing wound healing process will not be
interfered. Ideal cleaning agents should be of neutral pH and
nontoxic. Delipidising agents, antiseptics and alkaline soaps
should be avoided.
‘TIME’ (Tissue; Inflammation; Moisture imbalance; Edge of
the wound) acronym by Schultz et al, 2003 (European Wound
Management Association): It is widely used now as ‘Wound Bed
Preparation’. Tissue: assessment and debridement of non-viable
or foreign material (including host necrotic tissue, adherent
dressing material, multiple organism related biofilm or slough,
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exudate and debris) on the surface of the wound. Infection/
inflammation: assessment of the aetiology of each wound,
need for topical antiseptic and/or systemic antibiotic use to
control infection and management of inappropriate inflammation
unrelated to infection. Moisture imbalance: assessment of the
aetiology and management of wound exudate. Edge of wound:
assessment of non-advancing or undermined wound edges (and
state of the surrounding skin).
Note:
Biofilm: A biofilm is a complex microbial community, consisting of bacteria
embedded in a protective matrix of sugars and proteins (glycocalyx).
Biofilms provide a protective effect for the microorganisms embedded
within them, improving their tolerance to the host’s immune system,
antimicrobials and environmental stresses. Biofilm communities interact
with host tissue resulting in stable attachment, sustainable nutrition and
a parasitic relationship. Initial reversible biofilm eventually forms mature
biofilm which shed biofilm fragments, bacteria which leads into local and
distant invasive spreading infection. Biofilm is addressed by sharp debridement and cleaning. Its reform which is common should be prevented by
rational dressings and topical antimicrobials.
SpecicTreatment
Minor wounds: Wound is cleaned with saline thoroughly; then
non-stick dressing is placed. An incised wound is treated by
primary suturing. In lacerated wound, wound edge is excised
and then apposed by primary suturing without tension.
Haematoma: Ice packs wrapped in cloth is applied and kept for
15 minutes in every 2 hours for 24 hours; compression bandage;
elevation of the part; ultrasound of the part and guided aspiration
if persists; occasionally haematoma is evacuated.
In a crushed or devitalised wound, there will be oedema and
tension; all devitalised tissue is removed (wound excision/debridement); oedema is allowed to subside for 2–6 days; then delayed
primary suturing is done. If it is a deep devitalised wound, after
wound debridement it is allowed to granulate completely. Later if
wound edges are closer, secondary suturing is done usually after
10 days using monofilament non-absorbable suture. If the wound
is wider, wound is covered with split skin grafting (SSG).
Major wounds: Airway should be maintained; Bleeding should be
controlled; intravenous fluids should be started. They need proper
management in operation theatre under general anaesthesia after
initial assessment of the patient and wound. In a wound with
tension, fasciotomy is done to prevent development of compartment syndrome. Major vessels are sutured using 6-0 nonabsorbable polypropylene sutures (round body, usually continuous
sutures). Nerve with clean cut ends is sutured primarily using
fine (6-0 or 7-0) polypropylene suture; if nerve is crushed or cut
ends are away or if there is difficulty in identifying cut ends, then
marker stitches are placed [different coloured (silk) sutures] at
the site and later secondary suturing is done.
Internal injuries are managed accordingly—laparotomy/
craniotomy/intercostal tube drainage, etc. Fracture bones are
identified and managed accordingly.
Other Management
Antibiotics, fluids, blood transfusion; electrolyte management;
tetanus toxoid injection (to deltoid muscle intramuscular);
antitetanus globulin (ATG—250–500 units); critical care—are
essential things in major injuries.
Wound debridement/wound excision/wound toilet: Liberal
excision of devitalised tissues until healthy, bleeding, vascular,
tidy wound is created. It is done at regular intervals as staged
procedures. Often it requires blood transfusions also. It may
be—surgical, sharp, autolytic, enzymatic, larval and mechanical.
B
x Primary suturing means suturing the wound immedia tely within
6 hours. It is done in clean incised wounds.
x Delayed primary suturing means suturing the wound in 48 hours
to 10 days. It is done in lacerated wounds. This time is allowed
for the oedema to subside.
x Secondary suturing means suturing the wound in 10–14 days or
later. It is done in infected wounds. After the control of infection,
once healthy granulation tissue appears, secondary suturing is done.
A
B
Delayed primary suturing is done once oedema
over the wound subsides. It is done as single layer interrupted deep
sutures using monofilament polypropylene or polyethylene.
A
B
Secondary suturing is done once wound is
healthy after control of wound infection.
9
CHAPTER 1A General Surgery: Wounds and Wound Healing
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B
x Primary suturing should not be done if there is oedema/infection/
devitalised tissues/haematoma
x Always associated injuries to deeper structures like vessels/nerves
or tendons should be looked for before closure of the wound
x Wound should be widened by extending the incision whenever
needed to have proper evaluation of the deeper structures—
proper exploration
x Proper cleaning, asepsis, wound excision/debridement
x Any foreign body in the wound should be removed
x Skin closure if it is possible to be done without tension
x Skin cover by graft/flap—immediate or delayed
x Untidy wound should be made tidy and clean before suturing
SRB's Manual of Surgery
x Proper aseptic precautions should be undertaken
x Antibiotics/analgesics are needed
x Sutured wound should be inspected in 48 hours
x Sutures are removed after 7 days
B
x Wound toilet is washing the wound thoroughly using normal
saline—ideal
x Wound debridement (french-letting loose) is allowing content
to come out by release incisions or facio
debridement is used for wound excision
x Wound excision is actually correct terminology for excision of
devitalised tissues once or serially
x Radical wound excision is (pseudotumour approach) is excising
entire devitalised tissues leaving tissues with visible bleeding
from all layers
tomies. But commonly
Necrotizing fasciitis with extensive skin involvement
which requires adequate wound excision and eventual skin coverage.
hours. Progressive, persistent severe pain which is aggravated
by passive muscle stretching is the diagnostic sign. Tense tender
regional lymph node is typical. Normal pulse will be felt usually
in compartment syndrome; but may become absent if there is
associated arterial injury.
A catheter is placed in the muscle compartment connected to
a pressure monitor and compartment pressure is measured; if
it is more than 30 mm Hg, fasciotomy is indicated. Fasciotomy
includes incising skin, fat and fascia covering the muscle longitudinally with adequate length to allow the muscle to bulge out.
Leg is decompressed by two longitudinal incisions lateral to the
subcutaneous margin of the tibia allowing the decompression
of posterior, peroneal and anterior compartments.
Fasciotomy for compartment syndrome should be
longitudinal, deep and lengthy and should decompress the
compartment to expose the underlying muscle. It should be done
early.
It is common in calf and forearm. Closed injuries cause
haematoma leading to increased pressure. It is often associated
with fracture of the underlying bone which in turn compresses
the major vessel further aggravating the ischaemia causing
pallor, pulseless
ness, pain, paraesthesia, diffuse swelling
and cold limb.
If allowed to progress it may eventually lead to gangrene or
chronic ischaemic contracture with deformed, disabled limb.
Muscle necrosis releases myoglobulin which is excreted in
the urine, damages the kidneys leading into renal failure.
Compartment syndrome is a special entity; common in leg,
forearm, thigh and arm; is a syndrome due to increased intracompartmental pressure within a limited space area.
Causes are: Narrowed space due to tight dressings/plaster
cast, lying on one limb in comatous patient; increased content
within the compartment due to trauma like fractures, oedema,
ischaemic injury, haematoma, positioning after trauma, burn
injury, etc.; high pressure injection injuries like gun injury, oilbased material injury, extravasation of chemotherapeutic drugs;
snake bite.
Features are: It compromises circulation and function mainly
of muscles and nerves. It often maintains the normal colour and
temperature of the fingers and distal pulses may not be obliterated in spite of severe muscle ischaemia. Muscle ischaemia
more than 4 hours causes muscle death and myoglobinuria.
Irreversible nerve damage develops if ischaemia persists for 8
B
x Infection, septicaemia and abscess formation
x Renal failure
x Gangrene of the limb
x Chronic ischaemic contracture
x Disabled limb, Volkmann's ischaemic contracture
Note:
Affected muscle when passively stretched worsens the pain—the most
reliable clinical sign.
Compartment pressure will be persistently more than 30 mm
Hg. It can be measured by placing a fine catheter in the compart-
ment and using a pressure monitor. This is an indication for
fasciotomy. Adequate lengthy incision involving skin, fat and
deep fascia should be done until underneath muscle bulges out
properly. Multiple incisions should be made if needed. Separate
incision in each compartment should be done.
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Catheterisation.
Mannitol or diuretics to cause diuresis, so as to flush the kidney.
Fresh blood transfusion.
Hyperbaric oxygen.
done in forearm anterior compartment is a specific
method. Carpal tunnel should be released by cutting flexor
retinaculum. Incision begins at the junction of the thenar and
hypothenar area; extends proximally initially transverse across
flexion crease of the wrist at the ulnar border; then across
forearm towards radial side of forearm; then in proximal forearm
towards medial side creating convex flap towards lateral side. In
the elbow it crosses along the medial border to reach the arm
where it runs in arm along the medial part of the anterior arm.
Injury to major nerves, palmar cutaneous branch of median
nerve should be avoided while placing the incision. Incision
should be deepened by cutting the deep fascia along the entire
length of the incision. Dorsal fasciotomy should be added by
placing longitudinal lengthy incision in the midline. Two longitudinal incisions on the dorsum of the hand also should be made.
It is due to crushing of muscles causing extravasation of
blood and release of myohaemoglobin into the circulation
leading to acute tubular necrosis and acute renal failure.
Causes: Earthquakes, road traffic accidents; Mining and
industrial accidents; Air crash; Tourniquet.
Initially tension increases in the muscle compart ment
commonly in the limb, which itself impedes the circulation and
increases the ischaemic damage. In 3 days, urine becomes
discoloured and scanty, patient becomes restless, apathy and
delirious with onset of uraemia. Crush syndrome is often life-
threatening. Injury is much worser than initial look.
B
x Renal failure
x Toxaemia
x Septicaemia
x Disability with extensive tissue loss
x Gas gangrene
11
CHAPTER 1A General Surgery: Wounds and Wound Healing
Incision for fasciotomy in upper limb begins at flexor
retinaculum extending into the forearm with a convex flap towards radial
side eventually leading towards medial epicondyle of the elbow joint.
Crush injury is one where a part of the body is being squeezed/
compressed between two high force or pressure systems. It
causes extensive lacerations, bruising, compartment syndrome,
crush syndrome, fractures, haemorrhage, etc. with extensive
tissue destruction and devitalisation. Renal failure, hypovolaemic
shock and sepsis are the most dreaded problems in crush injuries.
Tension in the muscle compartment is relieved by placing
multiple parallel deep incisions in the limb so as to prevent
further damage—Fasciotomy.
Rheomacrodex, or mannitol is given to improve the urine
output by improving the renal function.
Alkalisation of urine is done by giving sodium citrate or sodium
bicarbonate. It increases the solubility of acid haematin in the
urine and so promotes its excretion. Urinary pH should be
above 6.5 until urine does not show any myoglobin. Mannitol-
alkaline diuresis should be 8 litre/day.
Initial aggressive volume load using saline about 1-1.5 litres/
hour is ideal in these patients.
Haemodialysis is done sometimes as a life-saving procedure.
Other measures:
Blood transfusion; Correction of severe hyperkalaemia.
Catheterization; Oxygen therapy; Antibiotics;
A B
Traumatic crush injury pelvis exposing testis and iliac vessels. Patient underwent hemipelvectomy.
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Note:
Doing fasciotomy several days after crush injury may not be safe as it
may lead to sudden release of myoglobulin causing myoglobulinuria and
renal failure.
DEGLOVING INJURIES
It occurs due to shearing force between tissue planes as
traction—avulsion injury. It usually occurs between subcutaneous tissue and deep fascia or between muscle and bone.
It can be localised or circumferential.
Avulsion injury strips off the superficial tissues exposing
the neurovascular bundle, muscles, tendons, and bone.
SRB's Manual of Surgery
Degloving injury can be open or closed.
B
x A mature scar is paler, acellular, softer, flat, with reduced blood
vessels and fibroblasts, without itching (diminishes).
x An atrophic scar is pale, flat and stretched.
x A hypertrophic scar is excess scar but will not extend beyond
the margin of the scar of the original wound; there is prolonged
inflammatory phase of wound healing. It develops in 1 to 3
months after trauma. It improves spontaneously.
x Keloid is persistent excessive growth of the scar beyond its margin
into the adjacent skin; occurs in a triangular area between two
shoulder points and xiphisternum. It develops 3 months to years
after the trauma; progressive. Presternal area is the commonest site.
Note:
x A linear scar is supple, thin, soft occurs after healing by primary
intention.
x A wide, irregular firm scar occurs after healing by secondary
intention or when there is infection.
Degloving injury—finger; note the avulsed skin.
It can be in one plane or multiple planes.
It is commonly observed in machinery injuries or major road
traffic accidents. It is much more extensive than of on initial
presentation.
Under anaesthesia fluoroscein is injected intravenously and
viable skin is visible as fluorescent yellowish—green colour
under ultraviolet light. As injection of fluoroscein is not fully
safer, serial excision is better to look for dermal punctate
bleeding.
It needs examination under general anaesthesia, wound exci-
sion/radical excision, flap coverage, microflap surgeries, skin
grafting, with proper asepsis, and blood transfusion as there
is significant blood loss in these injuries.
SCAR
Scar is defined as formation of final relaxed, randomly arrayed
collagen bundles (Type I) with formation of matured scar.
Initially immature scar is formed during remodeling phase;
this scar is disorganized and contains type III collagen. Such
scar is raised, itchy, hard and pink in colour. Over the span
of 12 months scar gets matured fully wherein disorganised
collagen gets aligned along the stress lines and there is formation of more type I collagen. This matured scar is soft, supple,
pale and flat without any itch. Hypertrophic scar and keloid
persists to have more type III collagen than type I collagen
unlike the matured scar.
Diagrammatic representation of linear,
hypertrophic and keloid scar.
’
Keloid is the excessive abnormally stretched (type III thick)
collagen tissue bundles arranged with aligning in the same plane
as the epidermis but extends beyond the original scar margin
which continues to grow for long period.
Keloid is common in blacks. Common in females.
Genetically predisposed. Often familial. Very rare in Caucasians.
There is defect in maturation and stabilization of collagen
fibrils. Normal collagen bundles are absent.
Keloid continues to grow even after 6 months, may be for many
years. It extends into adjacent normal skin. It is brownish black/
pinkish black (due to vascularity) in colour, painful, tender and
sometimes hyperaesthetic; spreads and causes itching.
Keloid may be associated with Ehlers-Danlos syndrome or
scleroderma.
When keloid occurs following an unnoticed trauma without
scar formation is called as spontaneous keloid, commonly
seen in dark skinned people.
Some keloids occasionally become non-progressive after
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initial growth.
Pathologically keloid contains proliferating immature fibro-
blasts, proliferating immature blood vessels and type III thick
collagen stroma.
Common over the sternum. Other sites are upper arm,
chest wall, lower neck in front.
Hypertrophic scar.
Controversial.
Steroid injection—intrakeloidal triamcinolone, is injected at
regular intervals, may be once in 7–10 days, of 6–8 injections.
Triamcinolone reduces the fibroblast proliferation and collagen
synthesis; it is first line of therapy for keloid.
Steroid injection—excision—steroid injection.
Methotrexate, vitamin A and C therapy into the keloid.
Silicone gel sheeting; topical retinoids.
Laser therapy—Nd-YAG laser.
Vitamin E/palm oil massage.
Intralesional excision retaining the scar margin may prevent
recurrence. It is ideal and better than just excision.
Excision and irradiation or irradiation alone.
Excision and skin grafting may be done.
Note:
Excision and primary suturing has got high recurrence rate; hence it is not
usually practiced.
Recurrence rate is very high—more than 50%.
A
B
Keloid over the sternum (butterfly shaped;
commonest site) and upper part of the arm near shoulder—common
sites of occurrence.
13
CHAPTER 1A General Surgery: Wounds and Wound Healing
Keloid at laparoscopic port (cholecystectomy) sites.
Hypertrophic scar is excessive formation of abnormal scar tissue
containing type III collagen (thin) which is raised, often vascular
but confined within the margin of the original wound; usually its
growth stops in 6 months and often regresses spontaneously.
Occurs anywhere in the body.
Not genetically predisposed. Not familial.
Growth usually limits up to 6 months.
It is limited to the scar tissue only. It will not extend to
normal skin.
Spontaneous improvement with time occurs commonly.
It is pale brown in colour, not painful, nontender.
Often self-limiting also. It responds very well for injection.
Recurrence is uncommon.
It is common in wounds crossing tension lines, deep dermal
burns, wounds healed by secondary intention.
Often this scar breaks repeatedly and causes infection, pain.
After repeated breakdown it may turn into Marjolin’s ulcer.
A B
Keloid in the ear lobule and chest
It is controlled by pressure garments or often revision exci-
sion of scar and closure, if required with skin graft.
Triamcinolone injection is the 2nd line of therapy for hyper-
trophic scar.
A
wall near shoulder.
It is not how much we have, but how we enjoy, that makes us happy.
14
T
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Keloid Hypertrophic scar
a. Genetic predisposition Yes No
b. Site of occurrence Chest wall, upper arm, lower neck, ear Anywhere in the body, common in flexor surfaces
c. Growth Continues to grow without time limit Growth limits for 6 months
Extends to normal skin Limited to scar tissue only
d. Treatment Poor response Good response to steroids
e. Recurrence Very high Is uncommon
f. Collagen synthesis 20 times more than normal skin (Type III thick) 3-6 times more than normal skin (Type III fine collagen)
g. Relation of size of injury
SRB's Manual of Surgery
and lesion
h. Age Adolescents, middle age Children
i. Sex Common in females Equal in both
j. Race More in blacks (15 times) No racial relation
k. Structure Thick collagen with increased epidermal
l. Features Vascular, tender, itching Not vascular, nontender, no itching
m. Natural history Progressive Shows regression
n. Problems Hyperaesthesia, ulceration Not much
No relation. Small healed scar can form large
keloid
hyaluronic acid
Related to size of injury and duration of healing
Fine collagen with increased alpha actin
B
Different contractures in hypertrophic scars
over forearm, finger and neck—in old burns patients.
Hypertrophied scar in the abdominal healed wound.
Wound infection is common in devitalized deep difficult
wounds. Diabetes, immunosuppression, cytotoxic drugs,
‘Z’ plasty is very useful method to release small contractures.
anaemia, malnutrition, malignancy increases the chances of
wound infection.
Wound dehiscence is common in all above said adverse
factors. Wound suddenly gives away with pain causing
copious serosanguineous discharge. After laparotomy when
done specially as an emergency in trauma, acute abdomen
and also in malignancy, abdominal closed wound may burst
in 5–7 days. Usually all layers of abdomen give away causing
discharge, occasionally bowel will also extrude out. It needs
emergency closure of the abdominal wound using specialized
sutures or retention sutures.
Hypertrophic scar or keloid formation due to altered collagen
synthesis in the wound healing process. Collagen synthesis is
increased by 3–6 times in hypertrophic scar and 20 times in
keloid.
Deeper wounds will cause specified problems like paraes-
thesia, ischaemia, paralysis, etc.
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C hapter Outline
·
Ulcer
·
Granulation Tissue
·
Investigations for an
Ulcer
·
Management of an Ulcer
·
Traumatic Ulcer
·
Trophic Ulcer
·
Ulcer due to Chilblains
·
Ulcer due to Frostbite
·
Martorell’s Ulcer
·
Arterial/Ischaemic Ulcer
·
Bairnsdale Ulcer
·
Carcinomatous Ulcer
·
Rodent Ulcer
Ulcer
·
Melanotic Ulcer
·
Diabetic Ulcer
·
Meleney’s Ulcer
·
Lupus Vulgaris
·
Tuberculous Ulcer
·
Bazin’s Disease
·
Tropical Ulcer
·
Venous Ulcer
·
Syphilitic Ulcer
·
Soft Chancre/Soft Sore/
Ducrey’s Ulcer/
Chancroid/Bubo
·
Climatic Bubo/Tropical
Bubo
Sloping edge. It is seen in a healing ulcer.
Its inner part is red because of red, healthy granulation
tissue.
Its outer part is white due to scar/fibrous tissue.
Its middle part is blue due to epithelial prolife ration.
Undermined edge is seen in a tuberculous ulcer. Disease
process advances in deeper plane (in subcutaneous tissue)
whereas (skin) epidermis proliferates inwards.
Punched out edge is seen in a gummatous (syphilitic) ulcer
and trophic ulcer. It is due to endarteritis.
Raised and beaded edge (pearly white) is seen in a rodent
ulcer (BCC). Beads are due to proliferating active cells.
Everted edge (rolled out edge): It is seen in a carcino matous
ulcer due to spill of the proliferating malignant tissues over
the normal skin.
Floor: It is the one which is seen. Floor may contain discharge,
c.
granulation tissue or slough.
d. Base: Base is the one on which ulcer rests. It may be bone
or soft tissue.
An ulcer is a break in the continuity of the covering epithelium,
either skin or mucous membrane due to molecular death.
A B
(A) Nonhealing ulcer foot;
(B) Malignant (SCC) ulcer leg.
Parts of an Ulcer
a. Margin: It may be regular or irregular. It may be rounded or
oval.
b. Edge: Edge is the one which connects floor of the ulcer to the
margin. Different edges are:
Parts of an ulcer.
Ulcer edges.
Induration is a clinical palpatory sign which means there is a
specific type of hardness in the diseased tissue. It is obvious in
well-differentiated carcinomas. It is better felt in squamous cell
Happiness is never found until we have the grace to stop looking for it.
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