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Here is a complete, formatted answer for every topic on your General Surgery list.

GENERAL SURGERY - Complete Notes

Format: Definition | Types | Pathology | Clinical Features | Diagnosis & Investigation | Treatment

1. PYORRHEA (Periodontitis / Alveolar Pyorrhea)

Definition: Chronic inflammatory condition of the supporting structures of teeth (periodontium) with pus discharge from the gingival sulcus.
Types:
  • Chronic marginal periodontitis (most common)
  • Acute necrotizing ulcerative gingivitis (ANUG)
  • Juvenile periodontitis
Pathology: Bacterial plaque (Porphyromonas gingivalis, Treponema denticola) causes destruction of periodontal ligament, alveolar bone resorption, and pocket formation. PMN infiltrate followed by plasma cells and lymphocytes.
Clinical Features:
  • Bleeding gums, halitosis
  • Loose teeth, gum recession
  • Pus discharge on pressure, tooth loss in late stages
  • Pain, swelling
Diagnosis & Investigation:
  • Clinical exam: probing depth >3 mm
  • OPG/periapical X-ray: alveolar bone loss
  • Microbiology of plaque
Treatment:
  • Oral hygiene - scaling and root planing
  • Antibiotics: Metronidazole + Amoxicillin
  • Surgical: flap surgery (Widman flap), bone grafting
  • Extraction of hopeless teeth

2. MARJOLIN'S ULCER

Definition: Aggressive squamous cell carcinoma (SCC) arising in a chronic scar, burn scar, or longstanding wound/sinus. Named after Jean-Nicolas Marjolin.
Types:
  • Acute type: arises from recent injury
  • Chronic type: arises after years (average 20-30 years latency) in burn scars, osteomyelitis sinuses, pressure sores
Pathology:
  • Well-differentiated to poorly differentiated SCC
  • Malignant transformation of scar epithelium
  • Mechanism: loss of immunosurveillance in avascular scar tissue, chronic irritation
  • Low grade initially but can become aggressive
Clinical Features:
  • Painless (scar is denervated), raised everted edges
  • Slow-growing ulcer in a scar
  • Foul-smelling discharge
  • Regional lymph nodes enlarged late (lymphatics are destroyed in scar - hence late spread)
  • Hard, indurated base
Diagnosis & Investigation:
  • Biopsy (wedge biopsy) - gold standard
  • FNAC of lymph nodes
  • X-ray to assess bone involvement
  • CT scan for staging
Treatment:
  • Wide local excision with 1-2 cm margins
  • Amputation if bone involved
  • Lymph node dissection if nodes positive
  • Radiotherapy as adjunct (though relatively radio-resistant)
  • Skin grafting after excision
  • Prognosis: worse than ordinary SCC due to delayed diagnosis

3. TURBAN TUMOR (Cylindroma)

Definition: Benign eccrine/apocrine sweat gland tumor of the scalp. Multiple lesions coalesce to cover the scalp like a turban.
Types:
  • Sporadic (solitary)
  • Familial/hereditary (multiple) - due to CYLD gene mutation (also called Brooke-Spiegler syndrome)
Pathology:
  • Nests of basaloid cells surrounded by eosinophilic hyaline sheath (PAS positive)
  • "Jigsaw puzzle" pattern on histology
  • Mutation in CYLD tumor suppressor gene (chromosome 16q)
Clinical Features:
  • Pink/red nodules on scalp, coalescing to turban-like mass
  • Usually painless
  • May ulcerate or bleed
  • Malignant transformation rare but possible (malignant cylindroma)
Diagnosis & Investigation:
  • Clinical appearance
  • Biopsy and histopathology
  • Genetic testing (CYLD mutation)
Treatment:
  • Surgical excision
  • CO2 laser ablation for multiple lesions
  • Scalp excision + skin grafting for extensive disease
  • No effective medical treatment

4. UNTIDY WOUND

Definition: A wound with irregular, devitalized, contaminated edges that will not heal by primary intention. Includes lacerated, crushed, and bite wounds.
Types:
  • Incised wound - clean, neat (tidy)
  • Lacerated wound - irregular (untidy)
  • Crush wound - devitalized tissue (untidy)
  • Bite wound - heavily contaminated (untidy)
  • Avulsion wound
Pathology:
  • Devitalized and ischemic tissue at margins
  • Contaminated with bacteria, foreign bodies
  • Impaired healing due to poor blood supply
  • Risk of infection and gangrene
Clinical Features:
  • Irregular wound margins with devitalized tissue
  • Contamination visible
  • Bruising, crush injury of surrounding tissue
  • May have foreign body
Diagnosis & Investigation:
  • Clinical assessment (tissue viability, contamination level)
  • X-ray for foreign bodies/fractures
  • Wound swab for culture
Treatment (Wound Toilet/Debridement):
  • Thorough irrigation with saline/antiseptic
  • Debridement - removal of all devitalized tissue
  • Conversion to tidy wound
  • Delayed primary closure (48-72 hrs) after re-inspection
  • Antibiotics if contaminated
  • Tetanus prophylaxis
  • Split skin grafting if large defect

5. BASAL CELL CARCINOMA (BCC)

Definition: Most common malignant skin tumor arising from basal cells of the epidermis. Locally invasive but rarely metastasizes ("rodent ulcer").
Types:
  • Nodular BCC (most common)
  • Superficial BCC
  • Morphoeic (sclerosing) BCC - most aggressive
  • Pigmented BCC
  • Infiltrating BCC
  • Basosquamous carcinoma
Pathology:
  • Mutation in PTCH1 (tumor suppressor) gene on chromosome 9q, or SMO gene
  • Hedgehog signaling pathway dysregulation
  • Nests of basaloid cells with peripheral palisading and retraction artifact on histology
  • UV radiation is main carcinogen
Clinical Features:
  • Pearly/translucent nodule with rolled-out edges
  • Telangiectasia on surface
  • Central ulceration (rodent ulcer)
  • Located on sun-exposed areas (nose, cheek, periocular)
  • Painless, slow-growing
  • Local destruction of bone/cartilage in neglected cases
Diagnosis & Investigation:
  • Clinical: dermoscopy
  • Biopsy - punch/shave biopsy
  • MRI for deep invasion
  • Rare metastasis - no routine staging needed
Treatment:
  • Surgical excision: 4-5 mm margins
  • Mohs micrographic surgery (best for morphoeic/recurrent/face BCC)
  • Curettage and electrodessication (small superficial BCC)
  • Radiotherapy (elderly/inoperable)
  • Vismodegib/Sonidegib - Hedgehog pathway inhibitors (advanced/metastatic)
  • 5-FU cream / Imiquimod (superficial BCC only)

6. CYSTIC HYGROMA

Definition: Benign multilocular cystic lymphatic malformation arising from sequestered lymphatic tissue, most commonly in the neck. (Bailey and Love's Surgery, 28th Ed.)
Types:
  • Unilocular
  • Multilocular (most common)
  • Giant cystic hygroma
Pathology:
  • Failure of primitive lymph sacs to connect with the lymphatic system
  • Cysts filled with clear lymph fluid, lined by single layer of endothelium
  • Thin walls, no muscle coat
  • Associated with chromosomal anomalies (Turner's, Down's syndrome) when diagnosed prenatally
Clinical Features:
  • Presents at birth or early infancy
  • Soft, brilliantly transilluminant (pathognomonic)
  • Non-tender, compressible
  • Increases in size on crying/coughing
  • Location: neck (posterior triangle most common), axilla, groin, mediastinum, floor of mouth
  • May obstruct airway if large
  • May become infected
Diagnosis & Investigation:
  • Clinical: transillumination
  • Ultrasound: cystic, multilocular, no flow on Doppler
  • MRI/CT: extent of lesion
  • Prenatal: USS - associated with chromosomal anomalies
Treatment:
  • Surgical excision - complete excision is curative
  • Sclerotherapy: OK-432 (Picibanil), bleomycin, doxycycline - effective especially for macrocystic type
  • Aspiration: only temporary
  • Tracheostomy if airway compromised

7. EPITHELIOMA (Squamous Cell Carcinoma of Skin)

Definition: Malignant tumor arising from squamous (prickle) cells of epidermis. Second most common skin cancer.
Types:
  • Well-differentiated SCC
  • Moderately differentiated
  • Poorly differentiated (most aggressive)
  • Special forms: Verrucous carcinoma, Adenosquamous carcinoma
Pathology:
  • UV radiation, chronic inflammation (Marjolin's), HPV (types 16, 18), arsenic, immunosuppression
  • Irregular nests of squamous cells invading dermis
  • Keratin pearls (cell nests with central keratinization) - histological hallmark
  • Metastasis via lymphatics
Clinical Features:
  • Everted, irregular, hard edges
  • Indurated base
  • Bleeds easily
  • Central ulceration
  • Regional lymphadenopathy in metastatic disease
  • Sun-exposed areas: face, lip, ear, dorsum of hand
Diagnosis & Investigation:
  • Biopsy - histopathology
  • FNAC of lymph nodes
  • CT/MRI for staging
Treatment:
  • Wide excision with 1 cm margins
  • Mohs surgery for high-risk areas
  • Lymph node dissection if positive
  • Radiotherapy: adjuvant or primary for inoperable
  • Cemiplimab (PD-1 inhibitor) for advanced SCC

8. HEMANGIOMA

Definition: Benign vascular tumor arising from proliferation of endothelial cells, most common benign tumor of infancy.
Types:
  • Infantile hemangioma (most common) - appears at birth, proliferates then involutes
  • Capillary hemangioma (strawberry nevus)
  • Cavernous hemangioma
  • Port-wine stain (nevus flammeus) - does not involute
  • Sclerosing hemangioma
Pathology:
  • Proliferation of endothelial cells
  • Infantile type: GLUT-1 positive (key marker), involutes by age 5-7 years
  • Cavernous: large dilated vascular channels
  • Association with Sturge-Weber syndrome (port-wine stain + CNS)
Clinical Features:
  • Bright red, strawberry-like surface (capillary type)
  • Soft, bluish, compressible (cavernous type)
  • Enlarges in first year then regresses
  • Kasabach-Merritt syndrome: giant hemangioma + thrombocytopenia + coagulopathy
Diagnosis & Investigation:
  • Clinical in most cases
  • Doppler USS: confirms vascularity
  • MRI: extent of deep lesions
  • GLUT-1 staining: infantile hemangioma positive
Treatment:
  • Watchful waiting (most involute spontaneously)
  • Propranolol (systemic): first-line for problematic infantile hemangiomas
  • Timolol (topical): superficial lesions
  • Pulsed dye laser: residual lesions, port-wine stain
  • Surgical excision: persistent/complicated lesions
  • Steroids (historical - now replaced by propranolol)

9. ADENOMA

Definition: Benign epithelial tumor arising from glandular epithelium with glandular architecture.
Types (by location):
  • Colonic polyp (tubular, villous, tubulovillous)
  • Hepatic adenoma
  • Adrenal adenoma
  • Pituitary adenoma
  • Thyroid adenoma (follicular)
  • Salivary gland pleomorphic adenoma
Pathology:
  • Benign proliferation with preserved architecture
  • Tubular adenoma: lowest malignant potential (5%)
  • Villous adenoma: highest malignant potential (40%)
  • May show dysplasia - adenoma-carcinoma sequence (FAP, HNPCC)
Clinical Features:
  • Often asymptomatic
  • Colonic: PR bleeding, change in bowel habits
  • Villous: secretory diarrhea with hypokalemia
  • Pituitary: headache, visual field defects, hormonal effects
Diagnosis & Investigation:
  • Colonoscopy + biopsy (colonic)
  • CT/MRI (solid organ)
  • Hormonal assays (pituitary, adrenal)
Treatment:
  • Endoscopic polypectomy (colonic)
  • Surgical resection if large or malignant potential
  • Medical: dopamine agonists for prolactinoma
  • Surveillance colonoscopy

10. PAPILLOMA

Definition: Benign epithelial tumor with finger-like projections (fronds) of epithelium supported by vascular connective tissue core.
Types:
  • Squamous papilloma (skin tags, warts)
  • Transitional cell papilloma (urinary bladder)
  • Intraductal papilloma (breast)
  • Villous papilloma (colon)
  • Laryngeal papilloma (HPV 6, 11)
Pathology:
  • HPV-related types: koilocytes on histology
  • Branching fibrovascular cores covered by hyperplastic epithelium
  • Bladder papilloma: risk of malignant transformation
Clinical Features:
  • Skin: soft pedunculated growths
  • Breast: nipple discharge (intraductal)
  • Bladder: hematuria
  • Larynx: hoarseness of voice
Diagnosis & Investigation:
  • Clinical
  • Biopsy/histopathology
  • Cystoscopy (bladder)
  • HPV typing
Treatment:
  • Surgical excision/cauterization
  • Cryotherapy, electrocautery (skin warts)
  • Endoscopic resection (bladder)
  • Laser ablation (larynx)
  • HPV vaccine (prevention)

11. SKIN GRAFTING

Definition: Transfer of skin from one area (donor site) to cover a defect (recipient site) without its own blood supply (unlike a flap).
Types:
  1. Split Thickness Skin Graft (SSG/STSG): epidermis + part of dermis; donor site heals spontaneously
  2. Full Thickness Skin Graft (FTSG): epidermis + full dermis; better cosmesis, donor requires closure
  3. Free skin graft vs Pedicle graft
  4. Meshed graft: SSG expanded to cover large area
  5. Pinch graft: small circular pieces
Pathology/Mechanism of Take:
  • Phase 1 (0-48 hrs): Plasmatic imbibition - graft survives on plasma exudate
  • Phase 2 (48-72 hrs): Inoculation - capillary alignment
  • Phase 3: Neovascularization - new vessels grow into graft
  • Failure: infection, hematoma, seroma, shearing
Clinical Features/Indications:
  • Burns, traumatic wounds, ulcers, post-excision defects
  • SSG: large defects, irregular surfaces
  • FTSG: face, hands (better cosmesis)
Diagnosis & Investigation (Donor Site Selection):
  • Thigh, buttock (SSG)
  • Post-auricular, groin, upper eyelid (FTSG)
  • Assess wound bed: no active infection, good granulation
Treatment (Procedure):
  • Donor site harvested with dermatome
  • Graft secured by sutures/staples/tie-over dressing
  • Immobilization essential for 5-7 days
  • Dressing changed after 5 days

12. SCALD

Definition: Burn injury caused by hot liquids (water, steam, oil). Most common form of burn injury in children.
Types:
  • Superficial (epidermal/1st degree): erythema only
  • Superficial partial thickness (2nd degree): blisters, red, painful
  • Deep partial thickness: pale, less painful
  • Full thickness (3rd degree): leathery, insensate
  • Rule of Nines for area assessment
Pathology:
  • Protein denaturation and cell death
  • Zone of coagulation (dead), zone of stasis (potentially salvageable), zone of hyperemia (recovers)
  • Massive fluid shifts - hypovolemic shock
  • Inflammatory mediator release
Clinical Features:
  • Pain, erythema, blistering
  • Deep burns: painless, waxy appearance
  • Systemic: shock, renal failure, sepsis, ARDS
  • Airway burns: hoarseness, stridor, carbonaceous sputum
Diagnosis & Investigation:
  • Clinical assessment: depth, % surface area (Rule of Nines/Lund-Browder chart)
  • FBC, U&E, coagulation, blood group
  • Urinalysis, urine output monitoring
  • CXR (inhalation injury)
  • Wound swab
Treatment:
  • Immediate: cool with running water 10-20 mins, cover
  • Resuscitation: Parkland formula - 4 ml/kg/% BSA in 24 hrs (Hartmann's)
  • Analgesia
  • Wound care: silver sulfadiazine, Mepitel dressing
  • Surgical: escharotomy (circumferential burns), skin grafting
  • Nutritional support
  • Tetanus prophylaxis

13. INFLAMMATION

Definition: A protective vascular and cellular response of living tissue to injury (physical, chemical, biological). Classic signs: Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio laesa (loss of function) - Celsus + Virchow.
Types:
  • Acute: days to weeks; neutrophil-dominant
  • Chronic: weeks to months; lymphocyte/macrophage-dominant
  • Granulomatous: specialized chronic (TB, sarcoid, Crohn's)
  • Serous, Fibrinous, Suppurative, Hemorrhagic (by exudate)
Pathology:
  • Vascular phase: vasodilation + increased permeability (histamine, bradykinin, prostaglandins)
  • Cellular phase: margination, pavementing, diapedesis, chemotaxis of neutrophils
  • Mediators: histamine, serotonin, PGs, LTs, IL-1, TNF, C3a, C5a
  • Outcomes: resolution, fibrosis, abscess, chronic inflammation
Clinical Features:
  • Local: redness, heat, swelling, pain
  • Systemic: fever, leukocytosis, raised ESR/CRP, malaise
Diagnosis & Investigation:
  • FBC: leukocytosis
  • CRP, ESR, Procalcitonin (bacterial)
  • Blood culture, wound swab
  • Imaging as appropriate
Treatment:
  • Remove cause (drainage, debridement)
  • NSAIDs (inhibit COX, reduce PGs)
  • Corticosteroids (chronic/severe)
  • Antibiotics if infective cause
  • Rest, elevation

14. FILARIASIS

Definition: Parasitic infection by filarial nematodes causing lymphatic obstruction. (Bailey and Love's, 28th Ed.)
Types:
  • Lymphatic filariasis: Wuchereria bancrofti (most common), Brugia malayi, Brugia timori
  • Subcutaneous filariasis: Loa loa, Mansonella streptocerca
  • Serous cavity: Mansonella perstans
Pathology:
  • Adult worms lodge in lymphatics causing lymphangitis and progressive lymphatic obstruction
  • Immune response to dying worms causes fibrosis
  • Results in lymphedema, hydrocele, chyluria
  • Vector: mosquito (Culex for W. bancrofti)
Clinical Features:
  • Acute: recurrent fever, lymphangitis, orchitis, epididymitis
  • Chronic: lymphedema, elephantiasis (legs, scrotum), hydrocele
  • Tropical Pulmonary Eosinophilia (TPE): cough, wheeze, eosinophilia
Diagnosis & Investigation:
  • Nocturnal blood smear (10 pm - 2 am): microfilariae visible
  • Eosinophilia (peripheral blood)
  • Filarial antigen test (ICT card test)
  • Serology: ELISA for antibodies
  • USS: dancing filaria sign in lymphatics
  • Lymphoscintigraphy
Treatment:
  • Medical: Diethylcarbamazine (DEC) 6 mg/kg/day for 12 days - drug of choice
  • Ivermectin + Albendazole (mass drug administration)
  • Doxycycline (targets endosymbiont Wolbachia)
  • Surgical: hydrocelectomy; Charles operation/Homan's operation for elephantiasis
  • Compression bandaging, elevation
  • Supportive: hygiene, skin care

15. MALNUTRITION

Definition: Deficiency, excess, or imbalance of energy, protein, and/or other nutrients causing measurable adverse effects on body function.
Types:
  • Protein-energy malnutrition (PEM):
    • Marasmus: deficiency of calories AND protein; wasted appearance
    • Kwashiorkor: protein deficiency with adequate calories; edema, pot belly
    • Marasmic-kwashiorkor: combined
  • Micronutrient deficiency (vitamins, minerals)
  • Overnutrition/Obesity
Pathology:
  • Protein catabolism, negative nitrogen balance
  • Impaired immune function, poor wound healing
  • Fatty liver (kwashiorkor), muscle wasting
  • Electrolyte imbalances, hypoalbuminemia
Clinical Features:
  • Marasmus: severe muscle wasting, monkey-face, irritable
  • Kwashiorkor: edema, hair changes (flag sign), dermatitis, hepatomegaly, apathy
  • Poor wound healing, pressure sores, increased infection risk
  • In surgical patients: increased complications, anastomotic leak
Diagnosis & Investigation:
  • BMI <18.5 (underweight)
  • Serum albumin <3.5 g/dL (chronic); prealbumin (acute)
  • Transferrin, total lymphocyte count
  • Anthropometry: MUAC, skinfold thickness
  • MUST score / NRS-2002 (surgical nutrition screening)
Treatment:
  • Gradual refeeding (avoid refeeding syndrome - hypophosphatemia)
  • High protein, high calorie diet
  • Micronutrient supplementation
  • Enteral nutrition (NG tube) > parenteral (TPN if gut non-functional)
  • F75 (stabilization) then F100 (rehabilitation) formulas (WHO)
  • Treat underlying cause

16. HYPOKALEMIA

Definition: Serum potassium < 3.5 mEq/L.
Types:
  • Mild: 3.0-3.5 mEq/L
  • Moderate: 2.5-3.0 mEq/L
  • Severe: < 2.5 mEq/L
Pathology:
  • Causes: GI loss (vomiting, diarrhea), renal loss (diuretics, hyperaldosteronism), intracellular shift (alkalosis, insulin, beta-agonists), inadequate intake
  • Hyperpolarization of cell membranes - muscle/cardiac dysfunction
Clinical Features:
  • Muscle weakness, cramps, ileus, constipation
  • Polyuria (nephrogenic DI)
  • ECG: flattened T-waves, prominent U-waves, prolonged QU interval, ST depression
  • Ventricular arrhythmias in severe cases
  • Metabolic alkalosis (H+ enters cell as K+ exits)
Diagnosis & Investigation:
  • Serum K+ < 3.5 mEq/L
  • ECG changes
  • ABG (metabolic alkalosis)
  • Urine K+ (>20 mEq/day = renal loss; <20 = GI loss)
  • Serum Mg (hypomagnesemia worsens and perpetuates hypokalemia)
Treatment:
  • Mild-moderate: oral KCl (Slow-K)
  • Severe/symptomatic: IV KCl - max 40 mEq/hr (never IV bolus, causes cardiac arrest)
  • Correct magnesium deficiency (otherwise K replacement ineffective)
  • Treat underlying cause
  • Dietary: banana, orange, potato

17. HYPERKALEMIA

Definition: Serum potassium > 5.5 mEq/L.
Types:
  • Mild: 5.5-6.0 mEq/L
  • Moderate: 6.0-6.5 mEq/L
  • Severe (life-threatening): > 6.5 mEq/L or ECG changes
Pathology:
  • Causes: renal failure (most common), acidosis (shift out of cells), Addison's disease, rhabdomyolysis, hemolysis, ACE inhibitors, K-sparing diuretics, massive transfusion
  • Partial depolarization of cell membranes - cardiac conduction defects
Clinical Features:
  • Muscle weakness, paralysis
  • Palpitations, syncope
  • ECG (in order of severity): peaked T-waves -> widened QRS -> sine wave pattern -> VF -> asystole
Diagnosis & Investigation:
  • Serum K+ > 5.5 mEq/L
  • ECG - mandatory in all cases
  • ABG (metabolic acidosis)
  • Renal function tests
  • Rule out pseudohyperkalemia (hemolyzed sample)
Treatment (Mnemonic: C-BIG-K-Drop):
  • Calcium gluconate IV (10 ml of 10%) - membrane stabilization (first and most urgent)
  • Bicarbonate IV - shifts K into cells (if acidotic)
  • Insulin + Glucose (10 units regular insulin + 50 ml 50% dextrose) - shifts K into cells
  • Glucose alone
  • Kayexalate (sodium polystyrene sulfonate) - oral/rectal - removes K from body
  • Diuretics (furosemide)
  • Dialysis (severe/refractory)

18. HYPONATREMIA

Definition: Serum sodium < 135 mEq/L.
Types:
  • By volume status: Hypovolemic, Euvolemic, Hypervolemic
  • By onset: Acute (<48 hrs), Chronic (>48 hrs)
  • By severity: Mild (130-135), Moderate (125-129), Severe (<125)
Pathology:
  • Hypovolemic: GI loss, burns, diuretics (Na + water lost, water replaced)
  • Euvolemic: SIADH (commonest cause in hospital), hypothyroidism, psychogenic polydipsia
  • Hypervolemic: heart failure, cirrhosis, nephrotic syndrome
Clinical Features:
  • Nausea, vomiting, headache
  • Confusion, seizures, coma (cerebral edema)
  • Severity depends on rate of fall (acute is more dangerous)
Diagnosis & Investigation:
  • Serum Na < 135 mEq/L
  • Plasma osmolality (usually low; if normal - pseudohyponatremia)
  • Urine sodium, urine osmolality
  • Serum K, urea, creatinine, TFTs
  • SIADH criteria: urine osmolality >100 mOsm/kg, urine Na >40 mEq/L, euvolemia
Treatment:
  • Hypovolemic: 0.9% normal saline
  • SIADH/Euvolemic: fluid restriction (first line); demeclocycline, Tolvaptan (V2 antagonist)
  • Hypervolemic: fluid restriction + diuretics
  • Severe/symptomatic: 3% hypertonic saline (ICU setting)
  • CRITICAL: Correction rate max 8-10 mEq/L per 24 hrs - faster correction causes osmotic demyelination syndrome (central pontine myelinolysis)

19. PYAEMIC vs. PYOGENIC ABSCESS

FeaturePyogenic AbscessPyaemic Abscess
DefinitionSingle abscess from direct local infectionMultiple abscesses from bacteremia (septic emboli)
CauseE.coli, Staph, Strep, KlebsiellaStaph aureus most common; from septic thrombophlebitis, infective endocarditis
SiteSingle, localizedMultiple, bilateral, different organs (liver, lung, brain)
OnsetGradualSudden, hectic
FeverModerate with local signsHigh swinging fever with rigors (Charcot's intermittent fever)
PusThick, foul smellingThin, odorless
ToxemiaModerateSevere
Blood cultureMay be negativeUsually positive
TreatmentDrainage + antibioticsIV antibiotics (prolonged) + drainage of accessible collections
PrognosisGoodPoor/guarded

20. CEREBRAL CONCUSSION vs. CONTUSION

FeatureConcussionContusion
DefinitionTransient neurological dysfunction after head injury with no structural brain damageStructural brain damage - bruising/hemorrhage of brain parenchyma
MechanismDiffuse axonal shearing forcesDirect impact with bruising, hemorrhage
LOCBrief (<30 min) or noneProlonged or absent recovery
GCSReturns to 15 quicklyMay remain depressed
Post-traumatic amnesia<24 hours>24 hours
PathologyReversible neuronal dysfunction; no structural changePetechial hemorrhages, edema, necrosis of brain tissue
CT ScanNormalHeterogeneous hyperdense areas ("salt-and-pepper"), edema
Focal deficitNoneMay have focal neurological deficits
Headache/VomitingMild, transientSevere, persistent
TreatmentObservation, rest, analgesia; return to play protocolICU, ICP monitoring, surgical evacuation if indicated, mannitol, hyperventilation

21. BLOOD TRANSFUSION

Definition: Transfer of whole blood or blood components from a donor to a recipient.
Types:
  • Whole blood
  • Packed red blood cells (pRBC)
  • Fresh Frozen Plasma (FFP)
  • Platelets concentrate
  • Cryoprecipitate (for fibrinogen/Factor VIII)
  • Single donor plasma (SDP)
Pathology (Indications):
  • Anemia (Hb <7 g/dL or <10 in cardiac disease)
  • Hemorrhage (acute blood loss)
  • Coagulopathy, thrombocytopenia
Clinical Features (Transfusion Reactions):
  • Febrile non-hemolytic (most common): fever, chills (anti-WBC antibodies)
  • Hemolytic (ABO incompatibility - most dangerous): fever, loin pain, hemoglobinuria, shock, DIC
  • Allergic/Anaphylactic: urticaria, bronchospasm
  • TRALI (Transfusion-Related Acute Lung Injury): non-cardiogenic pulmonary edema within 6 hrs
  • Delayed hemolytic: jaundice 5-14 days later
  • Infective: if improperly stored/cross-checked
Diagnosis & Investigation:
  • Blood grouping and cross-matching (ABO + Rh)
  • Coombs test (direct and indirect)
  • FBC, coagulation screen
Treatment:
  • Stop transfusion immediately if reaction suspected
  • Maintain IV access, fluids
  • For hemolytic reaction: IV fluids, furosemide, mannitol (maintain urine output)
  • Antihistamines for allergic reactions
  • Corticosteroids for severe reactions
  • Report all adverse reactions

22. HAEMORRHAGE

Definition: Escape of blood from the blood vessel.
Types:
  • By time:
    • Primary: at time of injury
    • Reactionary: within 24 hrs (clot dislodgement as BP rises)
    • Secondary: 7-14 days (infection erodes vessel)
  • By source: Arterial (bright red, spurting), Venous (dark red, oozing), Capillary (slow ooze)
  • Class I-IV (American College of Surgeons):
    • Class I: <15% blood volume (750 ml) - minimal signs
    • Class II: 15-30% (750-1500 ml) - tachycardia, anxiety
    • Class III: 30-40% (1500-2000 ml) - hypotension, confusion
    • Class IV: >40% (>2000 ml) - lethal without intervention
Pathology:
  • Compensatory mechanisms: tachycardia, vasoconstriction, ADH, RAAS activation
  • Failure of compensation: distributive shock, organ failure
Clinical Features:
  • Tachycardia, hypotension, pallor
  • Cold clammy skin, restlessness, altered consciousness
  • Decreased urine output
Diagnosis & Investigation:
  • Clinical: ABCDE assessment
  • FBC, coagulation, cross-match
  • Arterial blood gas (metabolic acidosis = poor tissue perfusion)
  • Imaging: FAST ultrasound, CT angiography
Treatment:
  • Two large-bore IV cannulae, IV fluid (Hartmann's)
  • Massive transfusion protocol: pRBC:FFP:platelets = 1:1:1
  • Surgical hemostasis: ligation, suturing
  • Endovascular: coiling, embolization
  • Damage control surgery
  • Tranexamic acid (within 3 hrs of trauma - CRASH-2 trial)

23. TUBERCULOSIS (TB) & MDR-TB

Definition: Infectious disease caused by Mycobacterium tuberculosis (acid-fast bacillus).
Types:
  • Pulmonary TB (most common)
  • Extrapulmonary: lymph node (most common extra-pulmonary), pleural, skeletal (Pott's disease), renal, meningeal, miliary (hematogenous spread)
  • MDR-TB: resistant to Isoniazid AND Rifampicin
  • XDR-TB: MDR + resistant to fluoroquinolones + injectable second-line agents
Pathology:
  • Inhaled droplet nuclei infect alveolar macrophages
  • Caseating granuloma: central caseous necrosis + Langhan's giant cells + epithelioid cells + lymphocytes
  • Ghon focus: primary lesion in lung. Ghon complex = Ghon focus + lymph node involvement
  • Ghon complex + lymph node calcification = Ranke complex
Clinical Features:
  • Chronic cough (>2 weeks), hemoptysis, weight loss, night sweats, evening fever
  • Lymphadenopathy (matted, non-tender, "collar stud" abscess in neck)
  • Spine: kyphosis, paraplegia (Pott's disease)
Diagnosis & Investigation:
  • Sputum AFB smear (ZN staining)
  • CBNAAT (GeneXpert MTB/RIF) - rapid, detects rifampicin resistance
  • Sputum culture: LJ medium (gold standard, 6-8 weeks)
  • Tuberculin skin test (Mantoux): >10 mm = positive
  • IGRA (Interferon Gamma Release Assay): more specific
  • CXR: upper lobe consolidation, cavitation, hilar lymphadenopathy
  • Drug Sensitivity Test (DST) - mandatory for MDR-TB
Treatment:
  • 2HRZE + 4HR (standard regimen)
    • H = Isoniazid, R = Rifampicin, Z = Pyrazinamide, E = Ethambutol
  • MDR-TB (18-24 months): Bedaquiline + Pretomanid + Linezolid (BPaL regimen)
  • Directly Observed Therapy (DOTS) - WHO
  • Pyridoxine (Vit B6) with Isoniazid (prevents peripheral neuropathy)
  • BCG vaccine (prevention)

24. SYPHILIS

Definition: Sexually transmitted infection caused by Treponema pallidum (spirochete).
Types/Stages:
  • Primary: Chancre (painless ulcer + painless inguinal lymphadenopathy)
  • Secondary: Disseminated (rash on palms/soles, condylomata lata, snail track ulcers)
  • Latent: No clinical signs
  • Tertiary: Gumma formation, cardiovascular (aortitis), neurosyphilis
  • Congenital syphilis
Pathology:
  • Treponema invades through mucous membranes
  • Primary: endarteritis obliterans + perivascular plasma cell infiltrate
  • Gumma: granulomatous lesion with central necrosis, abundant plasma cells
  • Aortic aneurysm (ascending aorta): endarteritis of vasa vasorum -> ischemia of tunica media -> weakening
Clinical Features:
  • Primary: single painless chancre on genitalia (10-90 days after exposure), heals spontaneously
  • Secondary (6-8 weeks): generalized maculopapular rash including palms/soles, alopecia, hepatitis, nephritis
  • Tertiary: gumma (skin, bone, liver), Argyll Robertson pupil, Charcot's joint, tabes dorsalis, general paralysis of insane (GPI), aortic regurgitation, aortic aneurysm
Diagnosis & Investigation:
  • Darkfield microscopy of chancre (primary)
  • Non-treponemal: VDRL, RPR (screening; titres indicate disease activity)
  • Treponemal: TPHA, FTA-ABS (confirmatory; remain positive for life)
  • CSF: VDRL (neurosyphilis)
Treatment:
  • Benzathine Penicillin G 2.4 MU IM single dose (primary/secondary/early latent)
  • Late latent/tertiary: Benzathine Pen G 2.4 MU IM weekly x 3 doses
  • Neurosyphilis: IV Aqueous Penicillin G 18-24 MU/day x 10-14 days
  • Penicillin allergy: Doxycycline or Ceftriaxone
  • Jarisch-Herxheimer reaction: fever/rigors 2-8 hrs after first dose (treat with paracetamol, not stop antibiotics)

25. AIDS / HIV

Definition: Acquired Immunodeficiency Syndrome caused by Human Immunodeficiency Virus (HIV-1/HIV-2), a retrovirus.
Types:
  • HIV-1 (predominant worldwide)
  • HIV-2 (West Africa, less virulent)
  • Stages: Acute HIV, Clinical latency, AIDS (CD4 <200/µL or AIDS-defining illness)
Pathology:
  • HIV binds CD4+ T-cells via gp120 (CD4 receptor) and CCR5/CXCR4 (co-receptor)
  • Reverse transcriptase converts RNA to DNA; integrates into host genome
  • Progressive depletion of CD4 T-helper cells
  • AIDS: opportunistic infections and malignancies due to profound immunodeficiency
Clinical Features:
  • Acute HIV (2-4 weeks): flu-like illness, lymphadenopathy, rash
  • Latent: PGL (Persistent Generalized Lymphadenopathy)
  • AIDS: Pneumocystis jirovecii pneumonia (PCP), CMV retinitis, Toxoplasmosis, Cryptococcal meningitis, Kaposi's sarcoma, NHL, MAC infection, Candidiasis
Diagnosis & Investigation:
  • ELISA: screening (4th generation p24 antigen + antibody)
  • Western Blot: confirmatory
  • CD4 count: monitoring (AIDS <200/µL)
  • HIV viral load: RNA PCR (guides treatment, monitoring)
  • NACO protocol: 3 different rapid tests
Treatment (ART - Antiretroviral Therapy):
  • Initiate in ALL HIV+ patients regardless of CD4 count
  • First-line (WHO 2023): TDF + 3TC + DTG (Tenofovir + Lamivudine + Dolutegravir)
  • Prophylaxis: Co-trimoxazole (CD4 <200) for PCP
  • PEP (Post-Exposure Prophylaxis): within 72 hrs
  • PrEP (Pre-Exposure Prophylaxis): TDF/FTC daily
  • Opportunistic infection treatment as appropriate

26. ACTINOMYCOSIS

Definition: Chronic suppurative granulomatous infection caused by Actinomyces israelii (Gram-positive, anaerobic, filamentous bacterium - NOT a fungus).
Types:
  • Cervicofacial (most common - 50%): "lumpy jaw"
  • Thoracic
  • Abdominal/pelvic
Pathology:
  • Actinomyces is normal oral flora; invades after trauma/dental extraction
  • Forms chronic abscess with interconnecting sinuses
  • Characteristic: sulfur granules (yellow, gritty) in pus - aggregates of bacteria
  • Histology: sulfur granules with peripheral "clubs" (Splendore-Hoeppli phenomenon)
  • Does NOT respect anatomical planes (crosses fascial planes)
Clinical Features:
  • Cervicofacial: firm, woody, indurated swelling of jaw; multiple discharging sinuses; yellowish sulfur granules in discharge; trismus
  • Thoracic: chest pain, productive cough, sinus through chest wall
  • Abdominal: right iliac fossa mass mimicking appendix/Crohn's, sinuses through abdominal wall
Diagnosis & Investigation:
  • Pus examination: sulfur granules (macroscopic and microscopic)
  • Culture: anaerobic, slow-growing (2-4 weeks)
  • Biopsy: granuloma with sulfur granules
  • CT scan: multiloculated mass
  • Gram stain: Gram-positive filamentous organisms
Treatment:
  • High-dose IV Penicillin G (first choice): 18-24 MU/day for 2-6 weeks
  • Then oral Amoxicillin for 6-12 months
  • Alternative: Tetracycline, Clindamycin
  • Surgical: drainage of abscess, excision of sinus tracts
  • Long treatment required - DO NOT stop early

27. LEPROSY (Hansen's Disease)

Definition: Chronic granulomatous disease caused by Mycobacterium leprae, primarily affecting skin and peripheral nerves.
Types (Ridley-Jopling Classification):
  • TT (Tuberculoid): high immunity, few lesions, nerve involvement
  • BT (Borderline Tuberculoid)
  • BB (Mid-borderline)
  • BL (Borderline Lepromatous)
  • LL (Lepromatous): low immunity, many lesions, bilateral involvement
  • WHO Classification: Paucibacillary (PB: <5 lesions) and Multibacillary (MB: ≥5 lesions)
Pathology:
  • M. leprae: obligate intracellular parasite; grows at 27-30°C; cannot be cultured in vitro
  • TT: well-formed granuloma, few bacilli, strong cell-mediated immunity
  • LL: diffuse macrophage infiltrate (foam cells/Virchow cells), massive bacilli load, poor cell-mediated immunity
Clinical Features:
  • Hypopigmented or erythematous skin patches with LOSS OF SENSATION (pathognomonic)
  • Thickened peripheral nerves: ulnar, radial, common peroneal, facial, great auricular
  • Lagophthalmos (facial nerve), claw hand (ulnar nerve), foot drop (peroneal nerve), wrist drop
  • Leonine facies, loss of eyebrows (madarosis), saddle nose - LL type
  • Lepra reactions: Type 1 (reversal), Type 2 (ENL - Erythema Nodosum Leprosum)
Diagnosis & Investigation:
  • Clinical: anesthetic skin patch + thickened nerve
  • Slit skin smear: AFB (Leprosy bacilli) from earlobe/lesion - Bacteriological Index (BI)
  • Histopathology (Fite-Faraco stain for AFB)
  • Lepromin test: positive = TT (NOT diagnostic, only indicates immunity)
Treatment - WHO Multi-Drug Therapy (MDT):
  • PB (Paucibacillary): Rifampicin 600 mg once/month + Dapsone 100 mg daily x 6 months
  • MB (Multibacillary): Rifampicin 600 mg once/month + Clofazimine 300 mg once/month + Dapsone 100 mg daily x 12 months
  • Lepra Reactions: Prednisolone (Type 1); Thalidomide/Prednisolone (Type 2)
  • Reconstructive surgery for deformities

28. TETANUS

Definition: Acute spastic illness caused by Clostridium tetani toxin (tetanospasmin) - a Gram-positive, anaerobic, spore-forming bacillus. (Pye's Surgical Handicraft, 22nd Ed.)
Types:
  • Generalized (most common)
  • Local
  • Cephalic (after head/neck injuries)
  • Neonatal (through umbilical stump)
Pathology:
  • C. tetani produces tetanospasmin (a zinc metalloprotease)
  • Toxin travels retrogradely along peripheral nerves to spinal cord
  • Blocks release of inhibitory neurotransmitters (GABA, glycine) at Renshaw cells
  • Result: unopposed motor neuron firing - sustained muscle spasm
Clinical Features:
  • Incubation: 4-21 days (shorter = worse prognosis)
  • Trismus (lockjaw) - first symptom
  • Risus sardonicus (sardonic grin)
  • Opisthotonus (extreme back arching)
  • Tonic spasms triggered by stimuli (light, sound, touch)
  • Autonomic instability: tachycardia, hypertension, sweating
  • Apnea during spasms
Diagnosis & Investigation:
  • Clinical diagnosis (no reliable lab test)
  • Wound culture (C. tetani) - unreliable
  • Low tetanus antibody levels
  • "Spatula test" positive: touching posterior pharynx causes jaw spasm
Treatment:
  • Secure airway (tracheostomy if needed)
  • Human Tetanus Immunoglobulin (HTIG) 3000-6000 IU IM (neutralize unbound toxin)
  • Wound debridement
  • Metronidazole (500 mg IV 8-hourly) - preferred over Penicillin
  • Diazepam (IV) for spasm control; Magnesium sulphate
  • ICU care, sedation, muscle relaxants + ventilation
  • Tetanus toxoid (start active immunization - disease does not confer immunity)
  • Prophylaxis: Tetanus toxoid 3-dose primary series

29. INFECTIVE GANGRENE

Definition: Necrosis of tissue (usually skin, soft tissue, or a limb) caused by infective (bacterial) agents, associated with toxemia.
Types:
  • Gas gangrene (Clostridial myonecrosis): C. perfringens; rapid, life-threatening
  • Fournier's gangrene: necrotizing fasciitis of perineum and genitalia; polymicrobial
  • Synergistic gangrene (Meleney's): slow, peripheral; S. aureus + microaerophilic Strep
  • Streptococcal gangrene: Group A Strep
  • Diabetic gangrene (with infection)
Pathology:
  • Anaerobic/mixed organisms produce proteolytic enzymes, toxins, gas (CO2 + H2)
  • Tissue necrosis, thrombosis of vessels, edema
  • Alpha toxin (C. perfringens): lecithinase - destroys cell membranes
  • Rapid spread along fascial planes
Clinical Features:
  • Gas gangrene: severe wound pain (disproportionate), bronze/black discoloration, crepitus (gas in tissue), foul smell, sweet-sour odor, toxemia, rapid deterioration
  • Fournier's: pain in perineum, skin discoloration, crepitus, septic shock
  • Systemic: high fever, tachycardia, hypotension, DIC
Diagnosis & Investigation:
  • Clinical
  • X-ray: gas in soft tissues
  • CT scan: extent, gas tracking along fascial planes
  • Blood culture, wound culture
  • FBC (leukocytosis), coagulation, LFT, ABG
Treatment:
  • EMERGENCY - surgical debridement is priority
  • Aggressive radical surgical debridement/necrosectomy
  • Amputation if limb involved
  • High-dose IV Penicillin G + Metronidazole + Gentamicin
  • Hyperbaric Oxygen Therapy (HBO) - adjunct for gas gangrene
  • ICU resuscitation, vasopressors
  • Wound management, repeated re-look surgeries every 24-48 hrs

30. TUMOR (General Principles)

Definition: Abnormal new growth of cells (neoplasm) that lacks normal regulatory controls.
Types:
  • Benign: well-differentiated, encapsulated, non-invasive, does not metastasize
  • Malignant (Cancer): invasive, de-differentiated, metastasizes
  • By cell of origin: Epithelial (carcinoma), Mesenchymal (sarcoma), Lymphoid (lymphoma), Neural, Germ cell
Pathology:
  • Cell cycle dysregulation; mutations in proto-oncogenes (gain of function) and tumor suppressor genes (loss of function)
  • Hallmarks of cancer: uncontrolled proliferation, evade apoptosis, angiogenesis, invasion, metastasis, immune evasion
  • Metastasis routes: lymphatic (carcinomas), hematogenous (sarcomas), transcoelomic (peritoneal), direct spread
Clinical Features:
  • Local: mass, ulceration, obstruction, bleeding
  • Systemic: weight loss, anorexia, cachexia, fever, paraneoplastic syndromes
  • Metastatic: site-specific (bone pain, jaundice, breathlessness)
Diagnosis & Investigation:
  • Biopsy (gold standard): FNAC, core biopsy, excisional biopsy
  • Imaging: USS, CT, MRI, PET-CT (staging)
  • Tumor markers: PSA, CEA, AFP, CA-125, CA 19-9 (NOT diagnostic alone)
  • Endoscopy, bone marrow biopsy as appropriate
  • TNM staging (T = tumor, N = node, M = metastasis)
Treatment:
  • Surgery: curative (wide excision, lymph node dissection) or palliative
  • Radiotherapy: adjuvant/primary/palliative
  • Chemotherapy: adjuvant, neoadjuvant, palliative
  • Targeted therapy: Imatinib (GIST), Trastuzumab (HER2+), Vemurafenib (BRAF)
  • Immunotherapy: Checkpoint inhibitors (PD-1/PD-L1, CTLA-4)
  • Hormonal therapy: Tamoxifen (breast), LHRH analogues (prostate)

31. HIDRADENITIS SUPPURATIVA

Definition: Chronic, recurrent, inflammatory skin disease of apocrine gland-bearing areas characterized by painful nodules, abscesses, and sinus tracts.
Types (Hurley Staging):
  • Stage I: Abscess formation, single or multiple, no sinus tracts or scarring
  • Stage II: Recurrent abscesses with sinus tracts and scarring, single or multiple, widely separated lesions
  • Stage III: Diffuse/near-diffuse involvement with multiple interconnected sinus tracts and abscesses
Pathology:
  • Follicular occlusion is the primary pathology (NOT sweat gland infection)
  • Follicular hyperkeratosis -> plugging -> rupture -> inflammation
  • Secondary bacterial colonization (S. aureus, anaerobes)
  • Chronic inflammation -> fibrosis, sinus tract formation
  • TNF-alpha plays key role
Clinical Features:
  • Affects: axillae, groin, perianal/perineal, inframammary, inner thighs
  • Tender, fluctuant nodules/abscesses
  • "Double-headed" or "bridged" comedones (pathognomonic)
  • Chronic discharge (sero-purulent) from sinus tracts
  • Scarring, rope-like fibrosis
  • Strongly associated with: obesity, smoking, diabetes, metabolic syndrome
Diagnosis & Investigation:
  • Clinical diagnosis
  • Culture: polymicrobial (not diagnostic; no single causative organism)
  • Biopsy (if atypical)
  • Hurley staging for management guidance
Treatment:
  • Stage I: Clindamycin topical + Tetracycline/Doxycycline oral; antiseptic washes; weight loss, smoking cessation
  • Stage II: Oral clindamycin + rifampicin (combination), hormonal therapy (females), intralesional triamcinolone
  • Biologics: Adalimumab (anti-TNF) - FDA-approved first-line biologic; Secukinumab (anti-IL-17A) - second approved biologic
  • Stage III / Surgical: Wide local excision with primary closure or skin grafting; deroofing of sinus tracts; laser (Nd:YAG)
  • No cure - management is long-term

32. FLUID, ELECTROLYTES & ACID-BASE BALANCE

Fluid Balance

Compartments: Total body water = 60% body weight
  • ICF (intracellular): 40% BW
  • ECF (extracellular): 20% BW (interstitial 15% + plasma 5%)
Daily Requirements: 30-35 ml/kg/day water; Na+ 1-2 mEq/kg/day; K+ 0.5-1 mEq/kg/day
IV Fluids:
  • 0.9% Normal Saline: isotonic, expands ECF (but hyperchloremic acidosis with excess)
  • Ringer's Lactate (Hartmann's): closest to plasma; preferred for resuscitation
  • 5% Dextrose: distributes throughout TBW, used for free water replacement
  • Colloids: Albumin, gelatin (expand plasma volume)

Acid-Base Balance

Normal Values: pH 7.35-7.45 | PaCO2 35-45 mmHg | HCO3 22-26 mEq/L | BE ±2
DisorderpHPaCO2HCO3Compensation
Metabolic acidosis↓↓ (compensation)↓ (primary)Hyperventilation (Kussmaul)
Metabolic alkalosis↑↑ (compensation)↑ (primary)Hypoventilation
Respiratory acidosis↓↑ (primary)↑ (compensation)Renal HCO3 retention
Respiratory alkalosis↑↓ (primary)↓ (compensation)Renal HCO3 excretion
Anion Gap = Na - (Cl + HCO3); Normal = 12 ± 2 mEq/L
  • High AG metabolic acidosis: MUDPILES (Methanol, Uraemia, DKA, Propylene glycol, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates)
  • Normal AG (hyperchloremic): diarrhea, RTA, excess saline

33. SCOPE & LIMITATIONS OF SURGERY

Scope:
  • Diagnosis (biopsy, diagnostic laparoscopy)
  • Curative (excision of tumor, repair of hernia, trauma)
  • Palliative (debulking, bypass, colostomy)
  • Reconstructive (post-cancer, burns)
  • Transplantation
  • Elective vs Emergency surgery
Limitations:
  • High-risk patients: poor cardiac/pulmonary reserve
  • Advanced malignancy: not resectable
  • Patient refusal
  • Anesthetic risk
  • Complications: bleeding, infection, wound dehiscence, DVT, PE, anastomotic leak

34. PRE-OPERATIVE & POST-OPERATIVE CARE

Pre-operative:
  • History and examination, risk stratification (ASA grade)
  • Investigations: FBC, coagulation, U&E, LFT, ECG, CXR, group and save
  • Optimization: control diabetes (HbA1c <8%), BP control, stop anticoagulants
  • NBM (nil by mouth): 6 hrs for food, 2 hrs for clear fluids
  • Consent, marking, VTE prophylaxis (LMWH + TED stockings)
  • Antibiotics prophylaxis (30-60 mins before incision)
Post-operative:
  • Monitoring: pulse, BP, SpO2, urine output, drain output
  • Pain management (multimodal: paracetamol, NSAIDs, opioids, regional)
  • DVT prophylaxis: LMWH, early mobilization
  • Fluid management: IV fluids until oral intake established
  • Wound care
  • Complications to watch: bleeding, infection, PE, ileus, anastomotic leak, pressure sores
  • Early nutrition, physiotherapy, discharge planning (ERAS - Enhanced Recovery After Surgery)
Sources: Bailey and Love's Short Practice of Surgery (28th Ed.), Fitzpatrick's Dermatology, Pye's Surgical Handicraft (22nd Ed.), Sabiston Textbook of Surgery
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