Make complete detailed notes of topic- sinus, ulcer, burns, fistula, wound and wound healing separately Subject surgery

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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):
ClassTypeExample
ICleanElective, no GI/GU entry
IIClean-contaminatedGI/GU opened under control
IIIContaminatedOpen fracture, gross spillage
IVDirtyPus, 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

  1. Haemostasis - direct pressure, tourniquet if needed
  2. Analgesia - local or systemic
  3. Debridement - remove necrotic/foreign material; copious irrigation
  4. Dead space obliteration
  5. Closure - primary, delayed primary, or secondary intention
  6. Dressings - appropriate to wound type
  7. Tetanus prophylaxis
  8. 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 FactorSourceKey Actions
PDGFPlatelets, macrophagesChemotaxis of fibroblasts; collagen synthesis; angiogenesis
TGF-β1Platelets, T-cells, macrophagesStimulates wound matrix; fibronectin, collagen
TGF-β3-Inhibits scar formation
FGFFibroblasts, endothelial cellsAngiogenesis; mesoderm mitogenesis
EGFPlatelets, macrophagesStimulates all epithelial cell types
VEGFMacrophages, fibroblastsAngiogenesis; proinflammatory
IGF-1Liver, plateletsProtein/ECM synthesis
IL-1Macrophages, keratinocytesProinflammatory; angiogenesis

Types of Healing

  1. Primary intention (1st intention): Clean, apposed wound - minimal scar
  2. Secondary intention (2nd intention): Open wound granulates from base - more scar
  3. 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:
  1. Retained foreign body - ingrown hair, suture material (most common cause of post-operative sinus)
  2. Chronic infection - tuberculosis, osteomyelitis (most common cause in osteomyelitis), actinomycosis
  3. Chronic inflammation - Crohn's disease
  4. Malignancy - sinus may drain from an underlying tumour
  5. 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 TypeEdge
Non-specific (e.g., venous)Sloping/shelving
TuberculousUndermined (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

  1. Thermal: Flame, scalds (most common in children), contact, flash
  2. Chemical: Acid/alkali (industrial, domestic)
  3. Electrical: Low voltage (<1000 V), high voltage (>1000 V), lightning
  4. Radiation: UV, ionising
  5. Cold: Frostbite

Assessment of Burns

A. Assessment of Burn AREA

1. Rule of Nines (Wallace's Rule) - for adults:
Region% TBSA
Head and neck9%
Each arm9%
Anterior trunk18%
Posterior trunk18%
Each leg18%
Perineum1%
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

DepthLayer InvolvedAppearanceSensationHealing
Superficial (epidermal)Epidermis onlyErythema, dry, no blistersPainful3-7 days, no scar
Superficial partial thickness (dermal)Superficial dermisBlistered, moist, pinkVery painful14-21 days, minimal scar
Deep partial thickness (deep dermal)Deep dermisWhite/pale, mottled, dryReduced pain>21 days, significant scar; may need grafting
Full thicknessAll layers of skinLeathery, charred, white/brownPainless (nerve destruction)Cannot heal without grafting

Pathophysiology of Burn Injury

Jackson's Zones of Thermal Injury (three concentric zones)

  1. Zone of coagulation (centre) - direct thermal damage, irreversible cell death
  2. Zone of stasis (middle) - potentially salvageable; microvascular damage, decreased perfusion; can progress to coagulation with inadequate treatment; this zone is the key therapeutic target
  3. 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:
  1. Supraglottic: Heat injury from hot gases → oropharyngeal/laryngeal oedema → airway obstruction (develops within hours); signs: singed nasal hairs, stridor, hoarse voice, soot in airway
  2. Subglottic: Chemical injury from smoke particles and toxic gases (CO, cyanide, acrolein) → chemical tracheobronchitis, bronchospasm; symptoms: dyspnoea, wheeze, carbonaceous sputum
  3. 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)

  1. Ensure rescuer safety (especially in electrical/chemical burns)
  2. Stop the burning process (Stop, Drop and Roll)
  3. Check for other injuries (ABC assessment)
  4. 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
  5. Give oxygen (anyone in enclosed space fire)
  6. Elevate burned limbs; sit patient up if airway burn
  7. 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

FeatureSinusFistulaUlcer
DefinitionBlind-ending tract from cavity to epithelial surfaceCommunication between two epithelium-lined surfacesDiscontinuity of epithelial surface with granulating base
ConnectionsOne opening (on surface)Two openingsOpen surface defect
LiningGranulation tissue (may epithelialise)Granulation tissue (may epithelialise)Granulating floor
Common causesForeign body, TB, osteomyelitisCrohn's, surgery, congenitalVenous, arterial, diabetic
TreatmentRemove underlying cause; excisionAddress cause; surgical repairTreat cause; local wound care

Sources: Bailey and Love's Short Practice of Surgery, 28th Edition; Schwartz's Principles of Surgery, 11th Edition
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