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X
- •Preface to the Sixth Edition
- •Preface to the First Edition
- •Acknowledgements
- •Competencies
- •Contents
- •1. Doctor–Patient Relationship
- •2. Communication and Counselling
- •3. Ethics in General Surgery
- •6. Perioperative Care
- •7. Pain Management
- •4. Surgical Audit
- •9. Investigation and Interpretation
- •10. Asepsis, Sterilization and Disinfection
- •11. Nutrition in Surgical Patients
- •Perioperative Nutritional Support
- •Route of Administration of Nutrition
- •13. Day Case/Care Surgery
- •14. Principles of Safe General Surgery
- •15. Metabolic Response to Injury
- •17. Shock and Haemorrhage
- •Haemorrhage
- •Indicators of Fluid Responsiveness
- •18. Blood Transfusion
- •Complications of Blood Transfusion
- •Autologous Transfusion
- •Hyperbaric Oxygen
- •19. Acid–Base Balance
- •Basic Definitions
- •Regulation of Acid–Base Balance
- •Acid–Base Disorders
- •Rapid Interpretation of an ABG Report
- •20. Fluids and Electrolytes
- •Normal Physiology
- •Water Regulation (Regulation of Volume)
- •Disturbances of Volume
- •Regulation of Sodium Concentration
- •Disturbances in Concentration
- •Disturbances in Composition of Body Fluids
- •Perioperative Fluid Therapy
- •Abscess
- •Other Special Types of Pyogenic Infections
- •Surgical Site Infections (SSIs)
- •Transmissible Viral Infections
- •23. Tetanus and Gas Gangrene
- •24. Hand, Foot Infections and Tendon Transfer
- •Superficial Infections
- •Deep Infections
- •Other Hand Infections
- •Foot Infections
- •Tendon Transfer
- •25. Chronic Infectious Disease
- •Actinomycosis
- •Leprosy (Hansen’s Disease)
- •Syphilis: French Disease, Great Pox
- •AIDS and the General Surgeon
- •Clinical Examination of an Ulcer
- •Traumatic Ulcer
- •Venous Ulcer
- •Arterial/ischaemic Ulcer
- •Tropical Ulcer
- •Post-Thrombotic Ulcer
- •Rare Ulcers
- •Bazin’s Ulcer
- •Diabetic Foot
- •Pressure Sores
- •Acute Arterial Occlusion
- •Peripheral Aneurysms
- •Miscellaneous
- •Intensive Care Unit (ICU) Gangrene
- •Thoracic Outlet Syndrome
- •Axillary Vein Thrombosis
- •Vasculitis Syndromes
- •Gangrene
- •Various Types of Gangrene
- •Cancrum Oris
- •Acrocyanosis
- •Drug Abuse and Gangrene
- •Lymphoedema
- •Primary (Congenital) Lymphoedema
- •Secondary Lymphoedema (Acquired)
- •Lymphangiography
- •Hodgkin’s Lymphoma (HL)
- •Non-Hodgkin’s Lymphoma (NHL)
- •Different Sites of Lymph Nodes in NHL
- •Sézary’s Syndrome
- •Chyluria
- •Deep Vein Thrombosis (DVT)
- •More Details of Anticoagulation and DVT
- •Miscellaneous
- •31. Skin Tumours
- •Squamous Cell Carcinoma (SCC)/Epithelioma
- •Melanocytic Tumours
- •Malignant Melanoma (Melanocarcinoma)
- •Stagewise Treatment (more Details) and Recent Advances
- •Other Malignant Skin Tumours
- •32. Burns and Skin Grafting
- •Free Skin Grafting
- •Neural Tumours
- •33. Tumours and Soft Tissue Sarcoma
- •Benign Tumours
- •Malignant Tumours
- •Paraneoplastic Syndromes (PNS)
- •Soft Tissue Sarcomas (STS)
- •Cystic Swellings
- •Transilluminant Swellings in the Body
- •Swellings in Submandibular Triangle
- •Carotid Body Tumour (Chemodectoma)
- •Neck Dissections
- •Metastasis in Cervical Lymph Nodes—Various Levels
- •Pancoast’s Tumour
- •Oral Cancer
- •Carcinoma of Buccal Mucosa
- •Carcinoma of Tongue
- •Carcinoma of Lip
- •Carcinoma Maxillary Antrum
- •Benign Lesions in the Oral Cavity
- •Odontomes
- •Median Mental Sinus
- •Vincent’s Angina
- •Cleft Lip and Cleft Palate
- •Miscellaneous
- •Mucous Cysts
- •36. Salivary Glands
- •Surgical Anatomy of the Parotid Gland
- •Acute Parotitis
- •Chronic Submandibular Sialoadenitis
- •Salivary Gland Tumours
- •Mucoepidermoid Tumour
- •Other Tumours
- •Malignant Parotid Tumours
- •Frey’s Syndrome—Gustatory Sweating
- •Parotid Fistula
- •Minor Salivary Gland Tumour
- •Surgery for Facial Nerve Palsy
- •Peripheral Nerve Repair and Transfers
- •37. Thyroid Gland
- •Surgical Anatomy of Thyroid Gland
- •Physiology
- •Thyroid Function Tests
- •Clinical Examination of Thyroid Swelling
- •Goitre
- •Multinodular Goitre
- •Retrosternal Goitre
- •Toxic Goitre—Thyrotoxicosis
- •Graves’ Disease
- •Malignant Tumours
- •Papillary Carcinoma Thyroid (PCT)
- •Follicular Carcinoma
- •Anaplastic Carcinoma
- •Medullary Carcinoma of the Thyroid (MCT)
- •Solitary Nodule of the Thyroid Gland
- •Thyroiditis
- •Complications of Hashimoto’s Thyroiditis
- •Complications of Thyroidectomy
- •Miscellaneous
- •Ectopic Thyroid
- •38. Parathyroid and Adrenals
- •Parathyroid Glands
- •Adrenal Glands/Suprarenal Glands
- •Disorders of Adrenal Cortex
- •Incidentalomas
- •39. Breast
- •Congenital Anomalies of Breast
- •Surgical Anatomy of Breast
- •Cystic Swellings of Breast
- •Other Types of Breast Abscesses
- •Cyclical Mastalgia with Nodularity
- •Idiopathic Granulomatous Mastitis (IGM)
- •Macrocysts
- •Galactocele
- •Discharge per Nipple
- •Galactorrhoea
- •Duct Papilloma
- •Axillary Tail Hypertrophy
- •Traumatic Fat Necrosis
- •Gynaecomastia
- •Phyllodes Tumours
- •Carcinoma Breast

94
Manipal Manual of Surgery
for a longer period and hence become effective
plasma expanders.
• These are used to restore blood volume in emergency
situations, e.g.
polytrauma with severe haemorrhage,
massive GI bleed and shock.
1. Albumin
• It is available as 5 and 20%.
•
It is prepared from pooled human plasma. Since it is
pasteurised at 60°C for 10 hours, the chances of
transmission of diseases is very low. It is also tested
using nuclear acid test (NAT) to detect hepatitis B
and C viruses as well as HIV1.
•
5% albumin is used as a plasma expander. 20%
albumin can be used to replace lost albumin in severe
hypoalbuminaemia in addition to plasma expansion.
Indications
• Can be used as a plasma expander to treat shock.
• Used in severe burns—acute severe hypoalbu-
minaemia.
• Used in nephrotic syndrome.
Contraindications
• Heart failure
• Severe anaemia
2. Gelatins
• Good plasma expander.
• They are of two types: Urea-linked gelatin (Haemaccel)
and succinylated
gelatin (Gelofusine).
• Plasma expansion lasts for 4–6 hours.
• Severe reactions including anaphylaxis can occur
urea-linked gelatin but less with succinylated
with
gelatin.
3. Dextran 40
• Reduces viscosity and red cell sludging.
• Used to maintain patency of microvascular free flaps
reducing thrombosis.
by
• May affect renal function and coagulation.
4. Hydroxyethyl Starch (HES)
• Derived from starch.
• Hydroxyethyl radicals are substituted onto the
carbon atoms
of glucose molecules.
• The effects depend on the molecular weight, molar
substitution and
the C2–C6 ratio.
• HES solutions are classified as high (>450 kDa),
medium (130–200 kDa) and low (<130 kDa) molecular
Section I • Basic Principles of Surgery
weight
starches.
• The term substitution is used to represent the number
of hydroxyethyl residues per 10 glucose subunits.
Accordingly, they may be highly substituted (molar
substitution 0.62–0.75), medium (0.5–0.6) or low (<0.4).
• Thus HES 130/0.4 means the molecular weight is
130 kDa
and the molar substitution is 0.4.
• HES with a molar substitution of 0.7 is called
hetastarch,
0.6 is hexastarch, 0.5 is pentastarch, and
0.4 is tetrastarch.
Adverse Effects
• HES may interfere with coagulation.
• Incidence of severe reactions (1:16,000).
• Use in shock is associated with increased risk of renal
injury
and mortality and hence, must be avoided.
• Although initial studies showed that adverse effects
are less with lower molecular weight and lower
substitution HES 130/0.4 (tetrastarch), doubts have
been raised about the safety of tetrastarch.
Consequently, the European Medicine Agency has
recommended its withdrawal from the market.
Special Purpose Solutions
Sodium bicarbonate: It is available as 7.5% (0.9 mEq/ml
and 8.4% (1 mEq/ml) of sodium bicarbonate.
Uses:
• As an alkalinising agent
• To treat metabolic acidosis
• To treat hyperkalaemia
• Forced alkaline diuresis
Disadvantages:
• Increased sodium load
• Alkalosis with a shift of oxygen dissociation curve to
the left
(increased affinity of haemoglobin to O
reducing its unloading)
• Increased intracranial pressure and intraventricular
haemorrhages
in neonates
• Circulatory overload leading to cardiac failure
• Carbon dioxide load leading to respiratory failure
Mannitol (10 and 20%):
• It is an osmotic diuretic. Mannitol expands intra-
vascular volume initially by drawing fluid from the
interstitium. This is followed by diuresis.
• Its main use is to reduce intracranial pressure by
producing diuresis.
• It is also used to reduce intraocular pressure. It should
e used with caution in patients with cardiac failure,
b
renal failure, etc.
Hypertonic saline (1.6, 3, and 5%): These solutions are
available
to treat hyponatraemia.
)
,
2

Fluids and Electrolytes
95
1. The following electrolyte contributes most to the
osmolality of plasma:
A. Sodium B. Potassium
Magnesium D. Calcium
C.
2. The normal plasma osmolality is ________ mOsm/kg.
A. 190 B. 290
C.
160 D. 260
3. Plasma osmolality is determined in the laboratory
using:
A. Freezing point B. Boiling point
C.
Saturation point D. Isoelectric point
4. The second major intracellular cation is:
A. Sodium B. Potassium
C
Calcium D. Magnesium
.
5. In chronic hyponatraemia, the sodium concentration
should be increased at a rate not exceeding _______
mmol/Ll/h.
A. 1 B. 5
10 D. 15
C.
6. The following is one of the drugs used to treat
hyperkalaemia:
A. Digoxin B. Magnesium sulphate
C.
Atropine D. Insulin
7. Tall ‘T’ wave in the electrocardiogram is a feature
of:
A. Hypokalaemia B. Hyperkalaemia
.
Hypocalcaemia D. Hypercalcaemia
C
8. Rapid infusion of the following fluid can cause
intraventricular haemorrhage in neonates:
A. 5% dextrose
.
8.4% sodium bicarbonate
B
C. 0.9% saline
D. Ringer lactate
9. The following colloid is often used to reduce plasma
viscosity:
A. Dextran 40
Hetastarch
.
B
C. Gelatin
D. Albumin
10. Hypercalcaemia may be seen in the following
conditions except:
A. Hyperparathyroidism
. Malignant cancers of the breast and lung
B
C. Vitamin D toxicity
D. Chronic renal failure
Answers
1. A 2. B 3. A 4. D 5. A 6. D 7. B 8. B 9. A 10. D
Section I • Basic Principles of Surgery


II
General Surgery
21. Wound, Keloid and Hypertrophic Scar
22. Acute Infections, Sinuses, Fistula and Surgical Site Infections
23. Tetanus and Gas Gangrene
24. Hand, Foot Infections and Tendon Transfer
25. Chronic Infectious Disease
26. Differential Diagnosis of Leg Ulcer and Pressure Sore
27. Lower Limb Ischaemia and Popliteal Aneurysm
28. Upper Limb Ischaemia and Gangrene
29. Lymphatics, Lymph Vessels and Lymphoma
30. Varicose Veins and Deep Vein Thrombosis
31. Skin Tumours
32. Burns and Skin Grafting
33. Tumours and Soft Tissue Sarcoma
34. Cystic Swellings, Neck Swellings and Metastasis Lymph Node Neck
35. Oral Cavity, Odontomes, Lip and Palate
36. Salivary Glands
37. Thyroid Gland
38. Parathyroid and Adrenals
39. Breast


21
Wound, Keloid and Hypertrophic Scar
Types of wounds: Classification
General principles of management of open wounds
Components of wound healing
Hyperbaric oxygen
Negative pressure assisted wound closure
SU5.3: Differentiate the various types of wounds, plan
and observe management of wounds.
Definition: A discontinuity or break in the surface
epithelium.
TYPES OF WOUNDS: CLASSIFICATION
I. Simple vs Comple
• Simple wounds: Involve only skin.
• Complex wounds: Involve underlying nerves, vessels
and tendons.
II. Closed vs Open Wounds
IIa. Closed wounds
• Contusion
• Abrasion
• Haematoma
Contusions: These can be a minor soft tissue injury
without a break in the skin, or a major injury such as
when being run over by a vehicle. Generally, they
produce discolouration of the skin due to a collection
of blood underneath it.
Abrasions: In these wounds, the epidermis of the skin
is scraped away. These wounds are painful because they
expose dermal nerve endings. They require cleaning,
antibiotics, and proper dressings.
x
Factors affecting wound healing
Compartment syndrome
Hypertrophic scar and keloid
Healing of specialised tissues
Classification of surgical wounds
Haematomas: These refer to a collection of blood usually
following injury. These may occur spontaneously in
patients who have bleeding tendencies like haemophilia.
Depending on the site, they may be subcutaneous,
intramuscular, intra-articular, or even subperiosteal. A
knee joint haematoma may need to be aspirated
followed by application of a compression bandage.
Small haematomas are usually absorbed and may get
infected if they are not.
IIb. Open wounds
• Incised
• Lacerated
• Penetrating
• Crushed
Incised wounds: These are caused by sharp objects, such
as a knife, blade, or glass. They have a sharp edge and
are usually less contaminated. They are ideally treated
by primary suturing, which results in a neat and clean
scar.
Lacerated wounds: These are caused by blunt injury,
such as a fall on a stone or a road traffic accident (RTA).
The edges are jagged. The injury may either involve only
skin and subcutaneous tissue or deeper structures as
well. Due to the blunt nature of the trauma, there is
crushing of the tissue which may result in a haematoma,
bruising, or even necrosis. These wounds are treated
99

100
Manipal Manual of Surgery
by wound excision and primary suturing provided they
are performed within six hours of the injury.
Penetrating wounds: These are not uncommon. Stab
injuries of the abdomen are a very notorious example.
These may look like an innocent injury with a small
1–2 cm cut, but internal organs like the intestines, liver,
spleen, or mesenteric blood vessels might also be
damaged. All penetrating wounds of the abdomen
should be admitted and observed for at least 24 hours.
Layer by layer exploration and repair is recommended,
but may not always be possible due to the oblique track
of the injury.
Crushed wounds: These are caused by blunt trauma
due to RTAs, wall collapses, earthquakes or industrial
accidents. These wounds are dangerous as they may
cause severe haemorrhage, death of the tissues, and/or
crushing of blood vessels. These patients are more prone
to gas gangrene and tetanus. Adequate treatment
involves a thorough debridement to remove all dead
and necrotic tissue.
III. Tidy vs Untidy Wounds
IIIa. Tidy wounds: Incised, clean, healthy tissue, seldom
associated with tissue loss (Key Box 21.1).
Healing of the Wound
Healing by primary intention occurs in clean, incised
wounds (e.g. surgical incisions) wherein there is only a
potential space between the edges. It produces a clean,
neat, thin scar.
Healing by secondary intention occurs in infected
wounds or in those with skin loss. It produces an ugly scar.
Fig. 21.1: Wound management
COMPONENTS OF WOUND HEALING
(Table 21.1, Figs 21.2 to 21.5)
IIIb. Untidy wounds: Crushed/avulsed, contaminated,
devitalised tissues, often associated with tissue loss.
Key Box 21.1
Repair in Tidy Wound
Nerves: Fascicular repair under magnification (loupe
or microscope) using 8–0 or 10–0 monofilament nylon
Artery: To be repaired by using 6–0 prolene
Tendon repaired by monofilament nonabsorbable suture
(polypropylene 3–0 or 4–0)
Skin loss: Skin flap/skin graft
IV. Acute vs Chronic Wounds
IVa. Acute wounds: Stab wounds, RTAs, and blast
injuries.
IVb. Chronic wounds: Leg ulcers and pressure sores.
General Principles of Open Wound Management
(Fig. 21.1)
• Admission or observation in the hospital.
• Monitoring of vitals.
• Systemic antibiotics depending on the extent of
wound contamination.
• Injection tetanus toxoid for prophylaxis against
tetanus.
• Treatment of the wound by cleaning, dressing, or
Section II • General Surgery
suturing.
SU5.1: Describe normal wound healing and factors
affecting healing.
I. Inflammatory (Lag) Phase
• Injury results in the release of inflammatory
mediators, mainly histamine from platelets, mast cells
and granulocytes. This results in increased capillary
permeability.
• Later, kinins and prostaglandins play a chemotactic
role for white blood cells and fibroblasts.
• In the first 48 hours, polymorphonuclear (PMN)
leucocytes dominate and play the role of scavengers
by removing dead and necrotic tissue (Fig. 21.6).
II. Proliferative (Collagen) Phase
• Between days 3–5, PMN leukocytes diminish in
number, and monocytes, which play the role of
specialised scavengers, increase.
• By day 5 or 6, fibroblasts appear, proliferate, and
eventually give rise to a protocollagen, which is converted into collagen in the presence of protocollagen
hydroxylase. O
, ferrous ions and ascorbic acid are
2
necessary for this step.
Protocollagen Collagen
Protocollagen hydroxylase
hydroxylation
++
(Oxygen, Fe
, vitamin C)
→

Wound, Keloid and Hypertrophic Scar
Fig. 21.2: Inflammatory and proliferative phases
101
• Epithelialisation occurs mainly from the edges of the
wound through cell migration and multiplication.
This is mainly brought about by marginal basal cells.
The entire wound is re-epithelialised within 48 hours.
When there is a wound with skin loss, skin
appendages also help in epithelialisation. Slowly, the
skin surface gets keratinised.
III. Remodelling (Maturation) Phase
• It occurs between days 5 and 14.
• It is brought about by myofibroblasts (specialised fibro-
blasts with contractile elements). It is nature’s way of
reducing the size of the defect to aid in wound healing.
• Wound contraction readily occurs in areas of loose
skin like the back and gluteal region, and is greatly
reduced in wounds over the tibia (shin) or malleolar
surface. Corticosteroids, irradiation, and chemo-
therapy delay wound contraction.
• Connective tissue formation: Formation of granula-
tion tissue is the most important and fundamental
step in wound healing. (It can be compared to concrete
slab laying.)
• Fibroplasia and capillary budding give rise to
granulation tissue.
• Ground substance and mucopolysaccharides
(proteoglycans) are secreted by fibroblasts, and help
in the binding of collagen fibres. Thus, a wound is
composed of Fibre + Gel + Fluid system (resembles
Iron rods + Cement + Water used for a concrete slab).
Table 21.1 Wound healing
Day 0–1 0–2 days 48–96 hours 5–7 days
• Tissue loss • Polymorphonuclear cells Macrophages Fibroblast
↓
• Exposure of extracellular Bridge the transition of inflammatory
matrix to platelet
• Platelet aggregation • Remove dead and necrotic Phagocytosis • Role of T-lymphocytes is not clear
• Inflammatory mediators • Epithelialisation • Wound contraction takes place
↓
↓
s to proliferative phase
(PMN) Granulation tissue
↓
tissue
↓
IV. Phase of Scar Formation
• Fibroplasia and laying of collagen increases
• Vascularity reduces (devascularisation)
• Epithelialisation continues
• Ingrowth of lymphatics and nerve fibres takes place
• Remodelling of collagen takes place with cicatrisa-
tion, resulting in a scar.
s appear
↓
↓
Fig. 21.3: Platelets
Fig. 21.4: Polymorph Fig. 21.5: Macrophage Fig. 21.6: L
ymphocytes
Section II • General Surgery

102
Manipal Manual of Surgery
Complications of Wound Healing
1. Infection: It is the most important complication
and results in delayed wound healing. Majority of
bacteria are endogenous. Depending upon pus/
culture-sensitivity report, appropriate antibiotics are
given.
Ugly scar: It is the result of infections.
2.
. Keloid and hypertrophic scar (see page 106)
3
4. Incisional hernia and wound dehiscence
5. Pigmentation of the skin
6. Marjolin’s ulcer (see page 242).
WOUND CLOSURE OR WOUND SUTURING
1.
Primary suturing: Wound suturing within a few
(ideally 6) hours following an injury.
Primary suturing can be done provided:
• The wound was incised or cut with a sharp object,
such as a knife or razor blade.
• There is minimal injury to surrounding structures.
• There is no wound infection. If a wound is sutured
in the presence of infection, the suture material is
eaten away (digested) by organisms, which results
in wound gaping.
Precautions to be taken:
• If any foreign body is present, it should be
removed.
• Any associated injuries to blood vessels, nerves,
or tendons should be recognised and repaired.
• Wounds over the abdomen may have associated
visceral injuries—look for and treat them, if
present.
• Tetanus toxoid 0.5 ml should be administered
intramuscularly to prevent tetanus.
2. Wound excision and primary suturing of skin
This is indicated when:
• Wound edges are jagged.
• The wound is contaminated.
• Tissues are crushed and devitalised.
In such situations, the wound is explored and the
devitalised tissues and/or foreign body, if present,
are removed. The wound is irrigated with antiseptic
agents. Thus, lacerated wound is converted into an
incised wound and then sutured.
Precautions to be taken are:
• It should be done within 6 hours.
• Prophylaxis should be given for tetanus and gas
gangrene.
• Repair of tendons and nerves may be done at a
Section II • General Surgery
later date if there is excessive contamination.
3. Wound excision and delayed primary suturing
This is indicated in lacerated wounds with major
crush injuries. Primary suturing within 6 hours is not
performed in these wounds because of:
• Gross oedema
• Increased tissue tension
• Haematoma
• Contamination with bacteria
Compartment syndrome may result if primary
suturing is performed in such situations.
• All dead tissues should be excised
• Wound should be irrigated with saline and left
open without suturing. A dressing should be
applied.
• Wound should re-examined 4–6 days later. If there
is no infection or non-viable tissues, the wound is
sutured. This two-stage procedure is called delayed
primary suturing.
Saline is increasingly being used to wash wounds as H2O2 and
betadine may cause more damage.
Wound with skin loss (Fig. 21.7): It may occur after
surgical procedures or accidents, etc.
Principles of debridement
• Ideally done under general anaesthesia
• Assess the extent of injury/tissue loss
• Control bleeding
• Excision of devitalised tissue, ideally using scissors
• Good saline wash/irrigation is better than
betadine/hydrogen peroxide wash.
Fig. 21.7: Wound with skin loss

Wound, Keloid and Hypertrophic Scar
Aim is to convert an untidy wound into a tidy wound.
Complications of skin loss
• Secondary wound infection.
• The underlying structures like tendons and nerves
are in danger.
• Diabetic patients may develop septicaemia.
• Deformity and disability may occur at a later date.
Hence, skin grafting should be done as soon as
possible.
4. Secondary suturing
Postoperatively, sutures may give way due to persistent
discharge of pus caused by severe infections. In such
cases, 7–14 days later (after controlling infection), the
skin is freed from the edge of the wound and the
granulation tissue and skin are approximated. This type
of suturing is called secondary suturing.
CHARACTERISTICS OF AN IDEAL WOUND DRESSING
• Creates a moist environment
• Removes excess exudates
• Prevents desiccation
• Allows gaseous exchange
• Impermeable to microorganisms
• Thermally insulating
• Prevents particulate contamination
• Provides mechanical protection
• Non-toxic
• Non-traumatic
• Easy to use and cost-effective
Types of dressings:
• Non-adherent fabrics
• Absorptive: Gauze, foams
• Occlusive:
– Nonbiologic: Films, hydrocolloids, alginates,
hydrogels
Biological: Homografts, xenografts
–
• Creams and ointments: Antibacterial, enzymatic
HYPERBARIC OXYGEN (HBO)
• HBO uses oxygen as a drug and a hyperbaric
chamber as a tool for elevating oxygen concentration
to the target area.
• Transcutaneous oxygen pressure (TcPO
) is used to
2
assess wound oxygenation (<35 mmHg is significant).
• The rationale for HBO treatment is that tissue hypoxia
or ischaemia results in impaired wound healing.
103
• Patients who benefit from HBO are those with
marked hypoxic wounds.
• HBO therapy involves inhalation of 100% oxygen at
a pressure 1.9–2.5 times the atmospheric pressure for
90–120 min. Oxygenation may be up to 10 times
higher than usual.
• Treatment is given once daily, 5–6 times/week.
• Complications include middle ear barotrauma, pneumo-
thorax, seizures, and respiratory distress syndrome.
• Contraindications for HBO include pneumothorax,
and treatment with doxorubicin, bleomycin or
disulfiram.
NEGATIVE PRESSURE ASSISTED WOUND CLOSURE
• This technique can be used to treat acute and chronic
wounds (see page 171).
• It may lead to a reduction in oedema, an increase in
local blood flow, and stimulation of granulation tissue.
• Its exact mechanism is unknown. However, it is
believed that this technique leads to wound healing
by removing exudates while keeping the wound moist.
• It stimulates endothelial proliferation and angio-
genesis and causes increased cellular proliferation
and a higher microvessel density.
• It also alters wound fluid composition by removing
proteinases and inflammatory cytokines, and
increases the speed of healing.
• It causes significant improvements in cost-effective-
ness and a decreased length of hospital stay.
• It is particularly beneficial for large wounds.
FACTORS AFFECTING WOUND HEALING
General Factors
SU5.1: Describe normal wound healing and factors
affecting healing.
1. Age: Wounds heal faster in children. In old age,
wound healing is delayed because dermal collagen
content decreases with aging. In addition, collagen
fibres in elderly patients show distorted architecture
and organisation.
2. Debilitation results in malnutrition. Wound healing
is delayed probably because of vitamin C deficiency.
Following injury, vitamin C deficiency can occur after
3–4 weeks. Vitamin C is necessary for the synthesis
and maintenance of collagen. Zinc deficiency is
known to delay the healing of pilonidal sinus. Zinc
deficiency is rare—it occurs in large burns, severe
polytrauma, and hepatic cirrhosis.
Section II • General Surgery
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