Here are your complete, detailed surgery notes on all 6 topics, compiled from Bailey & Love's Short Practice of Surgery (28th ed.) and Schwartz's Principles of Surgery (11th ed.):
SURGERY NOTES: WOUND, WOUND HEALING, SINUS, ULCER, FISTULA & BURNS
1. WOUND
Definition
A wound is a disruption of the normal continuity of a tissue caused by physical, chemical, or biological agents. It may involve skin, subcutaneous tissue, fascia, muscle, bone, or viscera.
Classification of Wounds
By Depth:
- Epidermal
- Dermal (superficial or deep)
- Full thickness
By Contamination (CDC Classification):
| Class | Type | Example |
|---|
| I | Clean | Elective, no GI/GU entry |
| II | Clean-contaminated | GI/GU opened under control |
| III | Contaminated | Open fracture, gross spillage |
| IV | Dirty | Pus, perforated viscus |
By Complexity:
- Simple
- Complex (significant soft-tissue loss, open fracture/joint, visceral involvement)
- Complicated (infection, necrosis, haematoma, gas gangrene, compartment syndrome)
- Chronic (vascular ulcers, pressure ulcers, diabetic ulcers)
Wound Assessment
- Assess using ATLS principles
- Note site, size, geometry, contamination, pulsatile bleeding, deformities
- Correlate with mechanism of injury (e.g., high-pressure injection injuries can track proximally and require urgent debridement)
- Assess motor and sensory function before local anaesthetic
Wound Management Principles
- Haemostasis - direct pressure, tourniquet if needed
- Analgesia - local or systemic
- Debridement - remove necrotic/foreign material; copious irrigation
- Dead space obliteration
- Closure - primary, delayed primary, or secondary intention
- Dressings - appropriate to wound type
- Tetanus prophylaxis
- Antibiotics - only if clinically indicated
Types of Wound Closure
- Primary (1st intention): Wound edges apposed directly - clean wounds <6 hours old
- Delayed primary: Closure at 3-5 days - contaminated wounds
- Secondary (2nd intention): Left open to granulate - infected/heavily contaminated
- Tertiary / healing by granulation
2. WOUND HEALING
Phases of Normal Wound Healing (Bailey & Love; Schwartz)
Classically described as three overlapping stages (with haemostasis as an immediate precursor phase):
Phase 1 - HAEMOSTASIS (Immediate: 0-10 min)
- Disruption of vascular endothelium → vasoconstriction and exposure of subendothelial extracellular matrix
- Platelets adhere, activate and aggregate → platelet plug formation
- Platelet activation releases: TXA2, ADP, serotonin, PDGF, TGF-β, EGF, VEGF
- Coagulation cascade activated → fibrin clot provides provisional wound matrix
- Fibrin clot acts as scaffold for subsequent cellular migration
Phase 2 - INFLAMMATION (Days 1-5)
- Vasodilation and increased vascular permeability
- Wound becomes red, swollen, warm, painful
- Neutrophils arrive first (0-2 days): phagocytose bacteria and debris; release proteases and reactive oxygen species
- Macrophages arrive by day 2-3: key orchestrators of wound healing
- Phagocytose debris and dead neutrophils
- Release growth factors: PDGF, TGF-β, FGF, VEGF, IL-1, TNF-α
- Macrophages are essential - macrophage-depleted wounds fail to heal
- Lymphocytes arrive later and regulate healing
Phase 3 - PROLIFERATION (Days 5-21)
Three main processes:
a) Angiogenesis (Neovascularisation)
- Stimulated by VEGF, FGF, TGF-β
- Endothelial cells sprout from existing vessels to form new capillary loops
- Essential for nutrient delivery to healing wound
- Produces the characteristic red, granular appearance of granulation tissue
b) Fibroplasia (Collagen Synthesis)
- Fibroblasts migrate into wound, stimulated by PDGF, TGF-β, FGF
- Fibroblasts synthesise collagen (primarily Type III initially, then Type I)
- Collagen synthesis requires oxygen, Vitamin C, iron, α-ketoglutarate as cofactors for hydroxylation of proline and lysine
- Initially Type III (fetal-type) collagen predominates → later replaced by Type I
- Granulation tissue = fibroblasts + new blood vessels + inflammatory cells in ground substance
c) Epithelialization
- Keratinocytes at wound margins proliferate and migrate over moist wound surface
- Epithelialization rate increases by 50% in a moist environment vs dry
- Stimulated by EGF, TGF-α, keratinocyte growth factor
d) Wound Contraction
- Myofibroblasts (modified fibroblasts with actin) generate contractile force
- Wound edges drawn toward centre
- Important in open wounds; can cause contracture if excessive
Phase 4 - MATURATION AND REMODELLING (Day 21 onwards - up to 2 years)
- Collagen cross-linking and reorganisation
- Type III collagen gradually replaced by Type I collagen
- Wound strength increases: 30% at 3 weeks, 80% at 3 months (never reaches 100% of normal)
- Tensile strength peaks at ~80% of original skin strength
- Collagen turnover mediated by matrix metalloproteinases (MMPs) balanced by TIMPs
- Scar vascularity decreases → scar becomes pale and flat
Growth Factors in Wound Healing (Schwartz Table)
| Growth Factor | Source | Key Actions |
|---|
| PDGF | Platelets, macrophages | Chemotaxis of fibroblasts; collagen synthesis; angiogenesis |
| TGF-β1 | Platelets, T-cells, macrophages | Stimulates wound matrix; fibronectin, collagen |
| TGF-β3 | - | Inhibits scar formation |
| FGF | Fibroblasts, endothelial cells | Angiogenesis; mesoderm mitogenesis |
| EGF | Platelets, macrophages | Stimulates all epithelial cell types |
| VEGF | Macrophages, fibroblasts | Angiogenesis; proinflammatory |
| IGF-1 | Liver, platelets | Protein/ECM synthesis |
| IL-1 | Macrophages, keratinocytes | Proinflammatory; angiogenesis |
Types of Healing
- Primary intention (1st intention): Clean, apposed wound - minimal scar
- Secondary intention (2nd intention): Open wound granulates from base - more scar
- Tertiary/Delayed primary: Wound left open then closed at 3-5 days
Factors Affecting Wound Healing
Systemic Factors:
- Age: Delayed healing in elderly (decreased protein synthesis, comorbidities)
- Diabetes mellitus: Impaired neutrophil function, microvascular disease, neuropathy
- Malnutrition: Vitamin C deficiency → impaired collagen synthesis (scurvy); zinc deficiency → impaired cell proliferation
- Anaemia: Profound anaemia (<15% Hct) impairs oxygen delivery and healing
- Obesity: Adipose tissue poorly vascularised; increased tension on closure
- Immunosuppression: HIV, corticosteroids, chemotherapy
- Smoking: Vasoconstriction → tissue hypoxia; impairs neutrophil function
- Steroids: Inhibit inflammatory phase (angiogenesis, neutrophil/macrophage migration, fibroblast proliferation); inhibit collagen synthesis; effect most significant in first 3-4 days post-injury
Local Factors:
- Infection (most important local factor)
- Ischaemia/necrotic tissue
- Oedema
- Foreign bodies (sutures, implants)
- Mechanical injury and tension
- Ionising radiation
- Low oxygen tension
Hypoxia: Profoundly deleterious - collagen hydroxylation requires oxygen as cofactor. Optimal collagen synthesis needs adequate subcutaneous oxygen tension.
Abnormal Wound Healing
Hypertrophic Scars:
- Raised scar confined within the original wound margins
- More common in areas of tension (flexure surfaces)
- Occur early (within weeks), may regress spontaneously
- Treated with: topical silicone, intralesional corticosteroid injection, compression therapy, surgical excision
Keloid Scars:
- Extend beyond original wound borders - can be locally destructive
- More common in darker skin types
- Common sites: face, earlobes, deltoid, presternal region
- Arise months after injury; do not regress spontaneously
- More resistant to treatment; may require repeated excision with adjuvant radiotherapy
Wound Dehiscence:
- Failure of wound to remain closed; seen in 1-3% of abdominal wounds
- Risk factors: infection, obesity, malnutrition, poor technique, steroids
Contracture:
- Excess wound contraction causing functional limitation
- Common after burns
Healing in Specific Tissues (Schwartz)
- Bone: Haematoma → callus (woven bone) → remodelling (lamellar bone); primary bone healing requires rigid fixation
- Cartilage: Limited capacity - avascular; mainly via diffusion
- Tendon: Intrinsic (vincular blood flow, synovial diffusion) + extrinsic (fibrous adhesions) healing; early mobilisation promotes intrinsic healing
- Nerve: Wallerian degeneration distally; regeneration guided by Schwann cell bands of Büngner at 1-3 mm/day; neurotropism mediated by growth factors
- Fetal wound healing: Scarless healing - higher TGF-β3, hyaluronic acid, fewer inflammatory cells; no scar formation
3. SINUS
Definition
A sinus is a blind-ending tract connecting a cavity lined with granulation tissue (often an abscess cavity) to an epithelial surface.
(vs. fistula which connects two epithelium-lined surfaces)
The tract is lined by granulation tissue and may become epithelialised in chronic cases.
Classification
By Aetiology:
A. Congenital:
- Arise from remnants of persistent embryonic ducts
- Examples: branchial sinus, thyroglossal sinus, pre-auricular sinus, pilonidal sinus (disputed - may be acquired)
B. Acquired:
- Retained foreign body - ingrown hair, suture material (most common cause of post-operative sinus)
- Chronic infection - tuberculosis, osteomyelitis (most common cause in osteomyelitis), actinomycosis
- Chronic inflammation - Crohn's disease
- Malignancy - sinus may drain from an underlying tumour
- Inadequate surgical drainage of a cavity
Pathology
- The cavity from which the sinus originates maintains an ongoing source of infection/foreign material
- This prevents healing and perpetuates the tract
- Wall of sinus lined by granulation tissue
- Chronic sinuses may become epithelialised
Clinical Features
- Persistent discharge (serous, purulent, or containing flecks of material)
- History of previous infection or abscess
- Pain may be present if infection flares
- Sinogram can delineate extent and connections
Treatment
- Directed at removing the underlying cause
- Biopsy of the wall should ALWAYS be taken to exclude malignancy or specific infection
- Surgical excision of the sinus tract (sinusectomy)
- Adequate drainage
- Treat specific infection (e.g., anti-tubercular therapy for TB sinus)
- Remove foreign body if present
Important Specific Sinuses
- Pilonidal sinus: In natal cleft; caused by ingrown hair follicles; treated by excision +/- primary closure or flap
- Branchial sinus: Remnant of 2nd branchial cleft; opens along anterior border of sternocleidomastoid
- Thyroglossal sinus: Opens in midline neck following rupture of thyroglossal cyst
4. ULCER
Definition
An ulcer is a discontinuity of an epithelial surface. It is characterised by destruction of the surface epithelium and a granulating base.
Classification
A. Non-specific Ulcers (most common)
- Venous ulcer (most common leg ulcer - 70%)
- Arterial (ischaemic) ulcer
- Traumatic ulcer
- Pressure ulcer (decubitus)
- Neuropathic ulcer (diabetic foot)
B. Specific Ulcers
- Tuberculous ulcer
- Syphilitic ulcer (gumma)
- Actinomycotic ulcer
- Tropical ulcer (Meleney's synergistic gangrene)
- Marjolin's ulcer (malignant transformation in chronic scar/burn/sinus)
C. Malignant Ulcers
- Squamous cell carcinoma
- Basal cell carcinoma (rodent ulcer)
- Melanoma
Examination of an Ulcer - Clinical Features
Examine: Site, Size, Shape, Edge, Base, Floor, Depth, Discharge, Surrounding skin, Lymph nodes, Sensation
Edge Characteristics (Classic - from Figure 45.51, Bailey & Love):
| Ulcer Type | Edge |
|---|
| Non-specific (e.g., venous) | Sloping/shelving |
| Tuberculous | Undermined (overhanging) |
| Basal cell carcinoma (rodent ulcer) | Rolled edge with small vessels |
| Squamous cell carcinoma (epithelioma) | Heaped-up, everted edge |
| Syphilitic (gumma) | Punched-out edge, wash-leather slough base |
Base/Floor: Granulation tissue (healthy healing), slough (infected), bone/tendon (deep/ischaemic), carcinoma (heaped irregular)
Pathophysiology by Type
Venous Ulcer:
- Due to chronic venous hypertension → lipodermatosclerosis
- Site: Gaiter area (medial malleolus)
- Shallow, irregular edge, moist, fibrinous exudate
- Associated with varicose veins, DVT
Arterial Ulcer:
- Due to atherosclerosis → ischaemia
- Site: Toes, heel, lateral malleolus (pressure points)
- Punched-out, deep, pale/necrotic base, painful
- Associated with intermittent claudication, absent pulses, cold limb
Diabetic/Neuropathic Ulcer:
- Due to peripheral neuropathy + microvascular disease
- Site: Pressure points of foot (plantar, metatarsal heads)
- Painless despite appearance (neuropathy)
- "Punched out" surrounded by callus
Pressure Ulcer:
- Due to sustained pressure → ischaemia and tissue necrosis
- Grading: I (intact skin, redness) → II (partial thickness) → III (full thickness) → IV (bone, tendon, muscle visible)
- Prevention key: pressure-relieving mattresses, turning, skin care
Marjolin's Ulcer:
- Malignant transformation (usually SCC) in a chronic scar, burn scar, venous ulcer, or sinus
- Characteristic: slowly growing, raised, everted edge; painless (scar lacks sensation)
- Latent period: 10-25 years
Investigations
- Swab for C&S
- Ankle-Brachial Pressure Index (ABPI) - if <0.8, arterial component
- Biopsy - essential to exclude malignancy
- Blood glucose, FBC, albumin
Treatment Principles
- Treat underlying cause
- Local wound care: debridement, moist dressings
- Compression bandaging for venous ulcers (if ABPI >0.8)
- Vascular reconstruction for arterial ulcers
- Offloading for neuropathic ulcers
- Optimise nutrition (Vit C, zinc, protein), correct anaemia, prevent infection
5. FISTULA
Definition
A fistula is an abnormal communication between two epithelium-lined surfaces (Bailey & Love Fig. 45.52b).
The tract is usually lined by granulation tissue but may become epithelialised in chronic cases.
(Key difference from sinus: sinus = blind-ending; fistula = connects two surfaces)
Classification
By Origin:
- Congenital: Tracheo-oesophageal fistula, branchial fistula
- Acquired:
- Post-inflammatory: Crohn's disease, diverticulitis, tuberculosis, actinomycosis
- Post-surgical: anastomotic leak, iatrogenic injury
- Post-radiation
- Malignant (tumour eroding into adjacent structure)
- Arteriovenous (traumatic or congenital)
By Anatomy (common surgical fistulae):
- Enterocutaneous (bowel to skin) - complicates Crohn's, bowel surgery
- Colocutaneous (colon to skin)
- Enterovesical (bowel to bladder)
- Rectovaginal / Vesicovaginal (obstetric, radiation, malignancy)
- Branchial (neck)
- Tracheo-oesophageal
- Arteriovenous
- Fistula-in-ano (anorectal)
By Output (Enterocutaneous Fistula):
- High output: >500 mL/day (small bowel)
- Low output: <200 mL/day (colon)
Causes - "FRIEND" Mnemonic (for why fistula fails to heal)
- F - Foreign body
- R - Radiation
- I - Infection / Inflammation (Crohn's)
- E - Epithelialization of the tract
- N - Neoplasm
- D - Distal obstruction
Principles of Fistula Management
Conservative (initial):
- Control sepsis
- Nutritional support (TPN if high output)
- Skin protection
- Skin barrier products, stoma bags for enterocutaneous
Spontaneous closure: Many low-output fistulae close spontaneously if:
- No distal obstruction
- No foreign body or malignancy
- No active Crohn's
- No radiation damage
Surgical:
- Address underlying cause
- Excise the fistulous tract
- Treat distal obstruction
- Bowel resection and reanastomosis for enterocutaneous fistulae
- Key principles of fistula surgery (Bailey & Love): eliminate the underlying cause, excise the tract, eliminate dead space, adequate blood supply at repair
Fistula-in-Ano
- Abnormal communication between anal canal/rectum and perianal skin
- Classified by Parks (relation to external sphincter): intersphincteric, transsphincteric, suprasphincteric, extrasphincteric
- Treatment: lay-open (fistulotomy) for low fistulae; seton for complex/high fistulae; LIFT (ligation of intersphincteric fistula tract) procedure
6. BURNS
Definition
Tissue destruction caused by thermal, chemical, electrical or radiation energy.
Epidemiology (Bailey & Love)
- UK: ~175,000 A&E visits/year; ~13,000 admissions; ~1,000 need fluid resuscitation
- Half the victims are under 16 years of age
- Children: predominantly scalds
- Adults: flame burns, contact burns
- Elderly: scalds, falls against hot objects
Non-accidental injury (NAI) must always be screened for, especially in children and elderly.
Suspicious features of NAI: delay in presentation, inconsistent history, unexpected burn pattern/depth, perceived lack of concern by caregiver.
Causes of Burns
- Thermal: Flame, scalds (most common in children), contact, flash
- Chemical: Acid/alkali (industrial, domestic)
- Electrical: Low voltage (<1000 V), high voltage (>1000 V), lightning
- Radiation: UV, ionising
- Cold: Frostbite
Assessment of Burns
A. Assessment of Burn AREA
1. Rule of Nines (Wallace's Rule) - for adults:
| Region | % TBSA |
|---|
| Head and neck | 9% |
| Each arm | 9% |
| Anterior trunk | 18% |
| Posterior trunk | 18% |
| Each leg | 18% |
| Perineum | 1% |
2. Lund and Browder Chart (more accurate):
- Corrects for age-related differences in body proportions
- At birth: head = 18%, lower limb = 13.5% each
- For each year: 1% subtracted from head, 0.5% added to each lower limb
3. Patient's Hand = 1% TBSA - useful for irregular/scattered burns
Note: The Rule of Nines is only a first approximation; the Lund and Browder chart is preferred.
B. Assessment of Burn DEPTH
| Depth | Layer Involved | Appearance | Sensation | Healing |
|---|
| Superficial (epidermal) | Epidermis only | Erythema, dry, no blisters | Painful | 3-7 days, no scar |
| Superficial partial thickness (dermal) | Superficial dermis | Blistered, moist, pink | Very painful | 14-21 days, minimal scar |
| Deep partial thickness (deep dermal) | Deep dermis | White/pale, mottled, dry | Reduced pain | >21 days, significant scar; may need grafting |
| Full thickness | All layers of skin | Leathery, charred, white/brown | Painless (nerve destruction) | Cannot heal without grafting |
Pathophysiology of Burn Injury
Jackson's Zones of Thermal Injury (three concentric zones)
- Zone of coagulation (centre) - direct thermal damage, irreversible cell death
- Zone of stasis (middle) - potentially salvageable; microvascular damage, decreased perfusion; can progress to coagulation with inadequate treatment; this zone is the key therapeutic target
- Zone of hyperaemia (periphery) - vasodilation, inflammation; recovers with minimal treatment
The Burn Shock (Systemic Response)
- Burns >15-20% TBSA in adults, >10% in children cause systemic inflammatory response
- Massive release of inflammatory mediators: histamine, prostaglandins, cytokines
- Increased capillary permeability → massive fluid shift from intravascular to interstitial space
- Results in: hypovolaemic shock, hypoproteinaemia, haemoconcentration
- Maximum oedema at 8-12 hours post-burn; resolves at 48-72 hours
Pulmonary Complications (Inhalation Injury)
Three mechanisms:
- Supraglottic: Heat injury from hot gases → oropharyngeal/laryngeal oedema → airway obstruction (develops within hours); signs: singed nasal hairs, stridor, hoarse voice, soot in airway
- Subglottic: Chemical injury from smoke particles and toxic gases (CO, cyanide, acrolein) → chemical tracheobronchitis, bronchospasm; symptoms: dyspnoea, wheeze, carbonaceous sputum
- Systemic: CO poisoning; CO has 200x affinity for Hb vs. O2 → carboxyhaemoglobinaemia → tissue hypoxia; Rx: 100% oxygen
Warning signs of respiratory compromise:
- Singed nasal hairs/eyebrows
- Burns around face/mouth
- Carbonaceous sputum
- Hoarse voice/stridor
- History of fire in enclosed space
Early intubation is essential if airway burn suspected - oedema may progress rapidly.
Other Systemic Complications
- Renal: ATN from hypovolaemia; haemoglobinuria/myoglobinuria in electrical burns
- GI: Curling's ulcer (stress ulcer of duodenum); ileus; bacterial translocation; abdominal compartment syndrome from gut oedema
- Haematological: Haemolysis, thrombocytopenia, DIC in major burns
- Metabolic: Hypermetabolic state (BMR ↑ up to 200%); catabolism; hyperglycaemia
- Peripheral circulation: Circumferential full-thickness burn → coagulation of collagen fibres → loss of elasticity → tourniquet effect as limb swells → limb-threatening ischaemia; requires escharotomy
Management of Burns
Prehospital Care (First Aid)
- Ensure rescuer safety (especially in electrical/chemical burns)
- Stop the burning process (Stop, Drop and Roll)
- Check for other injuries (ABC assessment)
- Cool the burn wound:
- Cool with tepid water (~15°C) for minimum 20 minutes
- Effective up to 1 hour post-burn
- Avoid ice (worsens vasoconstriction)
- Avoid hypothermia, especially at extremes of age
- Give oxygen (anyone in enclosed space fire)
- Elevate burned limbs; sit patient up if airway burn
- Analgesia
Criteria for Admission to Burns Unit (Bailey & Love Table 46.1)
- Burns >15% TBSA (adults), >10% (children and elderly)
- Full-thickness burns >5% TBSA
- Burns of special areas: face, hands, feet, genitalia, perineum, major joints
- Circumferential burns
- Chemical/electrical burns
- Inhalation injury
- Burns at extremes of age
- Burns with significant co-morbidities
- Non-accidental injury suspected
Fluid Resuscitation
Indicated for burns >15% TBSA in adults, >10% in children.
Parkland Formula (crystalloid - most widely used):
4 mL × weight (kg) × %TBSA burned = total fluid in 24 hours
- Half given in first 8 hours (from time of burn, not time of admission)
- Half given in next 16 hours
- Fluid of choice: Hartmann's (Ringer's lactate)
- Urine output target: 0.5-1.0 mL/kg/hour
Muir and Barclay Formula (colloid-based):
TBSA% × weight (kg) × 0.5 = one portion
- Six portions given over 36 hours:
- 3 portions given 4-hourly for 12 hours
- 2 portions given 6-hourly for 12 hours
- 1 portion given over 12 hours
- Colloid: albumin or fresh-frozen plasma
Monitoring: Urine output is the key monitoring parameter. Also monitor: HR, BP, CVP, base deficit, lactate.
Children: Additional maintenance fluid required (dextrose-saline):
- 100 mL/kg for first 10 kg
- 50 mL/kg for next 10 kg
- 20 mL/kg for each kg >20 kg
Wound Care
- Superficial burns: Simple non-adherent dressings; silver sulfadiazine cream or moist wound dressings; healing in 2-3 weeks
- Deep partial-thickness burns: Silver-based dressings (Mepilex Ag, Aquacel Ag); review at 5-7 days; if not healing by 21 days → skin grafting
- Full-thickness burns: Require skin grafting (split-thickness skin graft)
- Escharotomy: Required for circumferential full-thickness burns to limbs or chest; longitudinal incisions through eschar to release constriction
Surgical Management
- Tangential excision and grafting (early, within 48-72 hours of injury)
- Split-thickness skin graft (STSG): From unburned donor sites; 0.2-0.5 mm thick
- Meshing allows graft to cover larger area (up to 3:1 ratio)
- Biological dressings: Cadaver skin, amnion - temporary cover
- Dermal substitutes: Integra, Matriderm - for full-thickness burns
- Full-thickness grafts: For small areas of cosmetically/functionally important sites (face, hands)
Special Burns
Electrical Burns:
- Entry and exit wounds often small but deep tissue damage (arc effect; current travels along vessels/nerves)
- Risk of cardiac arrhythmia - ECG monitoring essential
- Myoglobinuria risk → renal failure; forced alkaline diuresis
- High-voltage (>1000 V): explosive soft tissue injury, fractures, nerve/vessel injury
Chemical Burns:
- Remove contaminated clothing immediately (with protection)
- Copious water irrigation for minimum 20 minutes
- Alkali burns typically deeper than acid (saponification of fat vs. protein precipitation)
- Do NOT attempt neutralisation (exothermic reaction)
Inhalation Injury Management:
- 100% O2 via non-rebreather mask
- Early intubation if airway compromise
- CO poisoning: 100% O2 (reduces CO half-life from 5 hours to 90 minutes)
Nutritional Support
- Hypermetabolic state requires aggressive nutritional support
- Early enteral feeding is preferred (within 6 hours)
- High protein, high calorie diet
- Nasogastric tube if needed
Complications
- Infection: Most common cause of death in burns patients; wound, pneumonia, catheter sepsis, bacteraemia
- Scar formation: Hypertrophic scars; treated with compression garments, silicone sheets, intralesional steroids
- Contracture: Joint contracture; requires physiotherapy and early splinting; may need surgical release
- Psychological: Depression, PTSD, body image issues
COMPARISON TABLE: SINUS vs FISTULA vs ULCER
| Feature | Sinus | Fistula | Ulcer |
|---|
| Definition | Blind-ending tract from cavity to epithelial surface | Communication between two epithelium-lined surfaces | Discontinuity of epithelial surface with granulating base |
| Connections | One opening (on surface) | Two openings | Open surface defect |
| Lining | Granulation tissue (may epithelialise) | Granulation tissue (may epithelialise) | Granulating floor |
| Common causes | Foreign body, TB, osteomyelitis | Crohn's, surgery, congenital | Venous, arterial, diabetic |
| Treatment | Remove underlying cause; excision | Address cause; surgical repair | Treat cause; local wound care |
Sources: Bailey and Love's Short Practice of Surgery, 28th Edition; Schwartz's Principles of Surgery, 11th Edition