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What's Inside - All 25 Questions (Q37-Q61)

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SIRS, Sepsis & Shock (Q37-41)

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Blood Coagulation (Q42-44)

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Blood Transfusion (Q45-54)

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Anaesthesia & Critical Care (Q55-61)

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MS GENERAL SURGERY EXAM - STRUCTURED ANSWERS (Q37-61)

Bailey & Love's Short Practice of Surgery, 28th Edition

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SECTION 1: SIRS, SEPSIS & SHOCK

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Q37. Criteria of SIRS (2013, 2021)

• SIRS alone = non-specific systemic response
• SIRS + confirmed/suspected infection = Sepsis
• Sepsis + organ dysfunction = Severe Sepsis
• Sepsis + refractory hypotension = Septic Shock

• Sepsis = life-threatening organ dysfunction (SOFA score increase ≥2) caused by dysregulated host response to infection
• Septic Shock = sepsis + vasopressor requirement to maintain MAP ≥65 mmHg + serum lactate >2 mmol/L despite adequate fluid resuscitation
• qSOFA (bedside screening): Altered mental status + RR ≥22/min + SBP ≤100 mmHg = 2+ points = high risk

• SIRS criteria guide early recognition of sepsis in surgical patients
• Trigger for blood cultures, lactate measurement, early antibiotics
• SOFA score used for organ dysfunction monitoring in ICU

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Q38. Pathogenesis of Sepsis-Induced Hypotension (2014)

• Gram-negative bacteria release lipopolysaccharide (LPS/endotoxin)
• Gram-positive bacteria release exotoxins and peptidoglycan
• These bind Pattern Recognition Receptors (especially TLR-4 on macrophages)

• Macrophages/monocytes release: TNF-α, IL-1β, IL-6, IL-8, IL-12
• These activate T-cells, neutrophils, complement cascade
• Positive feedback loop amplifies the inflammatory response

• Cytokines upregulate inducible NOS (iNOS) in vascular smooth muscle and endothelium
• Massive NO release → profound generalised vasodilation
• ↓ Systemic Vascular Resistance (SVR) → hypotension
• Initially: compensatory ↑ cardiac output (warm, high-flow shock)

• Cytokines and reactive oxygen species damage endothelial glycocalyx
• Increased vascular permeability → fluid leaks into interstitium
• Relative hypovolaemia compounds hypotension
• Microvascular thrombosis (platelet activation + coagulation activation)

• Tissue factor expression on damaged endothelium → extrinsic cascade activation
• Microvascular thrombosis → organ ischaemia
• Consumption of clotting factors → DIC

• TNF-α and IL-1β directly suppress myocardial contractility
• Reduced ejection fraction despite high CO state
• Later: circulatory failure with low CO, high SVR

• Cells cannot utilise O2 despite adequate delivery
• Lactic acidosis persists even after haemodynamic correction
• Hallmark of refractory septic shock

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Q39. Distributive Shock (2014)

• ↓ Systemic Vascular Resistance (SVR)
• ↑ or Normal Cardiac Output (CO)
• ↓ Mean Arterial Pressure (MAP)
• Warm peripheries (early)

• Cause: bacterial endotoxin/exotoxins → cytokine cascade → iNOS → NO → vasodilation
• Features: fever, warm skin, tachycardia, hypotension, high CO, low SVR
• Later phase: hypovolaemia + myocardial depression complicate picture

• Cause: IgE-mediated type I hypersensitivity → mast cell/basophil degranulation
• Mediators: histamine, tryptase, leukotrienes, prostaglandins → vasodilation + ↑ vascular permeability
• Features: urticaria, angioedema, bronchospasm, hypotension
• Triggers: antibiotics (penicillin), latex, contrast media, blood products, insect stings

• Cause: spinal cord injury at T6 or above → loss of sympathetic outflow
• Features: hypotension WITH bradycardia (no compensatory tachycardia - unlike other shock)
• Warm, dry skin; priapism may be present

• Noradrenaline is first-line vasopressor (restores SVR)
• Vasopressin as second agent if noradrenaline-resistant
• Monitor MAP (target ≥65 mmHg), urine output (≥0.5 mL/kg/h), lactate clearance

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Q40. Biomarkers of Sepsis (2023)

• Normal: <0.5 ng/mL
• Produced by liver, lung, and other tissues in response to bacterial infection (suppressed by interferons in viral infection)
• Rises within 6-12 hours; peaks 24-48h
• Clinical use: Antibiotic stewardship - PCT <0.25 ng/mL supports stopping antibiotics; serial PCT decline (>80%) confirms treatment response
• More specific than CRP for bacterial infection

• Normal: <2 mmol/L
• Elevated lactate = anaerobic metabolism = tissue hypoperfusion
• Lactate >2 mmol/L = part of septic shock definition
• Lactate >4 mmol/L = high mortality; requires immediate resuscitation
• Lactate clearance >10% over 2 hours = resuscitation target
• Cheap, widely available, directly guides management

• Normal: <10 mg/L
• Non-specific acute-phase reactant; produced by liver under IL-6 stimulation
• Rises slowly (peaks 48-72h); not useful for early diagnosis
• Useful for monitoring treatment response and identifying complications

• Rises very early (1-3h after insult) - earlier than CRP
• Better early predictor; useful in neonatal sepsis
• Not routinely available

• Fragment released when monocytes/macrophages phagocytose bacteria
• Normal: <314 pg/mL
• Early marker; correlates with severity and prognosis
• Better sensitivity/specificity than PCT in some studies

• Neutrophil:Lymphocyte Ratio (NLR): cheap, widely available
• Soluble urokinase plasminogen activator receptor (suPAR)
• Pentraxin-3
• Pro-ADM (proadrenomedullin)

• Early diagnosis: PCT + Lactate + CRP
• Antibiotic guidance: PCT (serial measurements)
• Severity/resuscitation: Lactate
• Monitoring response: Serial CRP + PCT

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Q41. Pathophysiology and Management of Haemorrhagic Shock

• Loss of circulating volume → ↓ O2 delivery to tissues
• Cells switch from aerobic to anaerobic metabolism
• Product: lactic acid (not CO2) → metabolic acidosis
• ATP depletion → failure of Na+/K+-ATPase pump
• Cellular swelling, lysosomal enzyme release, cell lysis
• Intracellular K+ released → hyperkalaemia

• Hypoxia + acidosis → complement activation + leukocyte priming
• Oxygen free radical generation
• Capillary endothelial injury → loss of integrity → tissue oedema
• Activation of coagulation cascade → microvascular thrombosis

• Cardiovascular: ↓ preload → baroreceptor activation → ↑ sympathetic tone → tachycardia + vasoconstriction (↑ SVR)
• Respiratory: Metabolic acidosis + sympathetic activation → ↑ RR and minute ventilation (compensatory respiratory alkalosis)
• Renal: ↓ renal perfusion → ↓ GFR → oliguria → RAAS activation → angiotensin II → vasoconstriction + aldosterone → Na+/water retention
• Endocrine: ADH release → water resorption + vasoconstriction; Cortisol release → sensitises to catecholamines; Adrenaline + noradrenaline from adrenal medulla

• Hypothermia (<35°C) - impairs enzyme activity of coagulation factors
• Acidosis (pH <7.2) - impairs coagulation cascade
• Coagulopathy - dilution + consumption of clotting factors Each worsens the others in a vicious cycle.

1. Control haemorrhage - direct pressure, tourniquet for limb bleeding, pelvic binder
2. Airway - 100% high-flow O2
3. IV access - two large-bore (≥16G) cannulae; take bloods: FBC, U&E, coagulation, G&S, lactate, ABG

• Permissive hypotension (target SBP 80-90 mmHg) until surgical haemorrhage control in penetrating trauma
• Damage Control Resuscitation (DCR):
  • Avoid crystalloid excess (worsens dilutional coagulopathy, hypothermia, acidosis)
  • Balanced transfusion: pRBC : FFP : Platelets = 1:1:1
  • Tranexamic Acid (TXA) 1g IV within 3 hours of injury (CRASH-2 trial evidence), then 1g over 8h
  • Cryoprecipitate if fibrinogen <1.5 g/L

• Damage Control Surgery if physiologically unstable
• Stop the bleed: pack, clamp, shunt; formal repair later when physiology corrected

• Warm all fluids; warming blanket (hypothermia)
• Bicarbonate only if pH <7.1 (acidosis)
• 1:1:1 balanced transfusion + TXA + cryoprecipitate (coagulopathy)

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SECTION 2: BLOOD COAGULATION

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Q42. Physiology of Blood Coagulation and Importance in Surgery (2024)

1. Vascular response
2. Primary haemostasis (platelet plug)
3. Secondary haemostasis (coagulation cascade)

• Injury → immediate vasoconstriction (reflex + endothelin release)
• Exposes subendothelial collagen and von Willebrand factor (vWF)
• Transient; buys time for platelet and coagulation responses

• Adhesion: vWF bridges subendothelial collagen to platelet glycoprotein Ib/IX receptor
• Activation: Platelets change shape; release granule contents: ADP, TXA2, serotonin, thromboxane A2
• Aggregation: ADP and TXA2 recruit more platelets; fibrinogen bridges platelets via Gp IIb/IIIa receptors
• Forms primary (unstable) platelet plug

• Tissue damage → Tissue Factor (TF) exposed
• TF + Factor VIIa = TF-VIIa complex
• Activates Factor X and Factor IX
• Rapidly inhibited by Tissue Factor Pathway Inhibitor (TFPI)

• Collagen contact → Factor XII activation
• XII → XI → IX
• IXa + VIIIa = tenase complex → activates Factor X

• Factor Xa + Va = prothrombinase complex → converts Prothrombin (II) to Thrombin (IIa)
• Thrombin is the central enzyme:
  • Cleaves fibrinogen → fibrin monomers
  • Fibrin monomers polymerise → fibrin mesh
  • Activates Factor XIII → cross-links fibrin → stable, insoluble clot
  • Also activates V, VIII (positive feedback) and Protein C (negative feedback)

• Antithrombin III: inhibits thrombin (IIa), Xa, IXa, XIa - potentiated by heparin
• Protein C + Protein S: inactivate Factors Va and VIIIa
• TFPI: inhibits TF-VIIa complex (limits extrinsic pathway)
• Prostacyclin (PGI2): inhibits platelet aggregation; released by intact endothelium

• Tissue plasminogen activator (tPA) converts Plasminogen → Plasmin
• Plasmin degrades cross-linked fibrin → FDPs (D-dimers)
• Regulated by PAI-1 (plasminogen activator inhibitor) and alpha-2-antiplasmin

• Preoperative assessment: PT/INR (extrinsic), APTT (intrinsic), platelet count, fibrinogen
• Identify and optimise coagulopathy before elective surgery
• Perioperative anticoagulant management (warfarin bridging, heparin reversal)
• Major haemorrhage causes dilutional + consumptive coagulopathy
• DIC recognition essential in sepsis, trauma, malignancy, major surgery
• Point-of-care testing (TEG/ROTEM) guides targeted factor replacement

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Q43. Coagulation Disorders and Management

A. Congenital Disorders:

B. Acquired Disorders:

• Vitamin K-dependent factors: II, VII, IX, X, Protein C, Protein S
• Causes: malabsorption, obstructive jaundice, warfarin, newborns (haemorrhagic disease)
• Lab: ↑PT (Factor VII shortest half-life, most sensitive), normal APTT initially
• Management: IV/oral Vitamin K; FFP for urgent surgery

• Liver synthesises all clotting factors except vWF (endothelium) and VIII (synthesised elsewhere)
• ↑PT, ↑APTT, ↓fibrinogen, thrombocytopenia (hypersplenism)
• Management: Vitamin K, FFP, platelets, cryoprecipitate; treat underlying disease

• Triggers: sepsis, trauma, obstetric complications, malignancy, major surgery
• Pathophysiology: widespread thrombin generation → consumption of all factors and platelets → paradoxical bleeding
• Lab: ↑PT, ↑APTT, ↑D-dimer, ↓fibrinogen, ↓platelets, blood film shows fragmented RBCs (schistocytes)
• Management: Treat underlying cause (most important); FFP, cryoprecipitate, platelet transfusion

• Causes: ITP, HIT (heparin-induced), drugs, hypersplenism, bone marrow suppression
• Platelet <50 x10^9/L: transfuse before surgery
• Platelet <20 x10^9/L: transfuse prophylactically
• HIT: stop heparin immediately; use alternative anticoagulant (argatroban, danaparoid)

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Q44. Coagulopathy in Trauma Patients (2021)

• Severe tissue injury + shock → systemic activation of Protein C pathway
• Activated Protein C (aPC) consumes Factors Va and VIIIa
• aPC also activates Plasminogen Activator Inhibitor-1 (PAI-1) suppression → hyperfibrinolysis
• This is the primary mechanism of TIC, present BEFORE any resuscitation

• Endothelial injury → massive release of tPA
• Plasmin dissolves clots as fast as they form
• TXA (tranexamic acid) blocks this by inhibiting plasminogen activation

• Large volume crystalloid/colloid resuscitation dilutes clotting factors and platelets
• 1.5L crystalloid reduces factor levels by ~50%

• Catecholamine surge causes endothelial glycocalyx shedding
• Exposes procoagulant surface → DIC-like consumption

• Clinical: oozing from wounds, IV sites, mucous membranes
• Lab: PT >1.5x normal; APTT >1.5x normal; Platelets <100x10^9/L; Fibrinogen <1.5 g/L
• Point-of-care: TEG (Thromboelastography) or ROTEM (Rotational Thromboelastometry) - provide real-time global assessment of clot formation, strength, and lysis

1. Stop the bleeding - surgical haemostasis is paramount
2. Tranexamic Acid (TXA) - 1g IV bolus within 3 hours (CRASH-2 trial), then 1g over 8 hours. Each hour of delay reduces benefit. No benefit after 3 hours.
3. Balanced transfusion - pRBC : FFP : Platelets = 1:1:1 (approximates whole blood)
4. Cryoprecipitate - if fibrinogen <1.5 g/L (2 adult pools; contains fibrinogen, Factor VIII, vWF, XIII)
5. Calcium replacement - 10 mL 10% CaCl2 per 4 units pRBC (citrate chelates calcium)
6. Warm all fluids - fluid warmer + warming blanket; target temperature >36°C
7. Correct acidosis - treat underlying perfusion; sodium bicarbonate only if pH <7.1
8. Avoid crystalloids where possible - worsen dilution, hypothermia, acidosis
9. TEG/ROTEM-guided factor replacement if available

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SECTION 3: BLOOD TRANSFUSION

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Q45. Blood Component Separation and Role in Surgery (2016, 2017)

• Up to 450 mL drawn per donation; maximum 3x per year (UK)
• Tested for: Hepatitis B, Hepatitis C, HIV-1, HIV-2, syphilis
• Leukodepleted (precaution against variant CJD; also reduces immunogenicity)
• ABO and Rhesus D typed; irregular red cell antibodies screened

• Restore oxygen-carrying capacity in haemorrhage
• Indications: Hb <70 g/L (symptomatic anaemia); Hb <80 g/L (cardiac patients); acute haemorrhage with haemodynamic compromise
• Each unit raises Hb by approximately 10 g/L (in adult without ongoing bleeding)
• Transfusion trigger should be based on clinical state, not Hb number alone

• Correct coagulopathy: PT/APTT >1.5x normal with active bleeding
• Massive haemorrhage protocol (1:1 ratio with pRBC)
• Reversal of warfarin effect (with Vitamin K) in urgent surgery
• Dose: 15 mL/kg

• Platelet count <50x10^9/L before elective surgery
• <100x10^9/L in massive haemorrhage or neurosurgery
• Prophylactic if <10x10^9/L (risk of spontaneous bleeding)
• Each adult therapeutic dose raises count by ~20-30x10^9/L

• Fibrinogen <1.5 g/L (commonest indication)
• Haemophilia A (Factor VIII)
• Von Willebrand disease
• DIC and massive haemorrhage (2 pools standard dose)

• Hypoalbuminaemia with oedema
• Plasma expansion in specific settings (cirrhosis, septic shock - Cochrane evidence limited)
• Not first-line for routine fluid resuscitation

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Q46. Blood Substitutes and Changes in Stored Blood (2011, 2023)

• Massive transfusion of old blood → hyperkalaemia, metabolic acidosis
• ↓ 2,3-DPG → left-shifted O2 dissociation curve → haemoglobin clings to O2 → impaired tissue delivery
• Microaggregates → pulmonary microembolism
• Reduced RBC deformability → microvascular dysfunction

• Mimic O2-carrying function of haemoglobin
• Types: polymerised human Hb, cross-linked Hb, bovine Hb (Hemopure - approved in South Africa), pegylated Hb
• Problems: free Hb scavenges NO → vasoconstriction; short intravascular half-life (12-24h); nephrotoxicity; pro-oxidant effects

• Synthetic fluorinated hydrocarbons that dissolve O2 directly
• Examples: Perftoran, Oxygent
• No cross-matching; shelf life years
• Problems: require high FiO2 to be effective; short half-life; no coagulation function; liver/spleen accumulation

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Q47. How to Assess Amount of Blood Loss in Surgical Patient (2021)

• Nature of injury/operation
• Duration of haemorrhage
• Pre-existing conditions (anaemia, anticoagulants)
• Surgeon's estimate of surgical blood loss

• Pulse pressure narrowing is an early sign (diastolic rises before systolic falls)
• Capillary refill >2 seconds
• Cold, clammy peripheries (except distributive shock)
• Urine output = most sensitive ongoing indicator of organ perfusion

• Gravimetric method: Weigh surgical swabs before and after use (1g weight gain = approximately 1 mL blood); most accurate bedside method
• Suction canister volume (subtract irrigation volume)
• Visual estimation by surgeon - commonly used but inaccurate; tendency to underestimate by 50%
• Cell salvage machines quantify blood collected in field

• Invasive arterial line (continuous BP monitoring)
• Central venous pressure
• Cardiac output monitoring (PiCCO, oesophageal Doppler)

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Q48. Classification, Indications and Complications of Allogeneic Blood Transfusion (2025)

• Cellular: pRBC, Platelet concentrate, Granulocyte transfusion (rare)
• Plasma-derived: FFP, Cryoprecipitate, Albumin, Factor concentrates (VIII, IX, VIIa)
• Whole blood (rarely used in civilian practice; being reconsidered in trauma)

• Bacterial contamination (especially platelets stored at room temp)
• Hepatitis B (risk ~1:300,000), Hepatitis C (~1:5 million), HIV (~1:2.5 million) - current UK risk
• CMV, EBV, HTLV
• Malaria, syphilis (screened), babesiosis
• vCJD risk (mitigated by universal leukodepletion since 1999)

• Delayed haemolytic reaction (days to weeks - alloantibody to minor antigens)
• Post-transfusion purpura (day 5-10; anti-platelet antibodies)
• Transfusion-associated GvHD (TA-GvHD) - in immunocompromised patients; prevented by irradiation of blood products
• Iron overload (repeated transfusions; each unit contains ~250 mg elemental iron)
• TRIM (Transfusion-Related Immunomodulation) - immunosuppressive effect; associated with ↑ cancer recurrence and postoperative infections
• Alloimmunisation (development of antibodies to donor antigens)

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Q49. Autologous Blood Transfusion: Types and Advantages (2021, 2022)

• Patient donates 1-4 units in the weeks before scheduled surgery
• Blood stored; re-infused intraoperatively or postoperatively
• Requires: Hb >110 g/L before donation; 4-6 weeks lead time
• Uses: elective major surgery (joint replacement, cardiac, spinal), religious objectors
• Disadvantage: costly, risk of clerical error (labelling), patient may still need allogeneic blood if underestimated losses

• 1-3 units removed immediately pre-operatively; intravascular volume replaced with crystalloid/colloid
• Blood stored at bedside at room temperature; re-infused during/after surgery
• Principle: diluted blood is lost during surgery; concentrated autologous blood returned at end
• Benefit: saves quality platelets and clotting factors
• Requires: Hb ≥120 g/L; no cardiovascular disease

• Blood from surgical field suctioned into a reservoir
• Washed and centrifuged → concentrated pRBC returned to patient
• Returns only RBCs (not platelets or clotting factors)
• Uses: cardiac surgery, vascular surgery, major orthopaedic surgery, liver transplant
• Most widely used autologous technique

• Wound drainage blood collected, filtered, re-infused within 6 hours
• Used after: joint replacement, cardiac surgery
• Simple, cost-effective

• No risk of ABO/Rh incompatibility
• No risk of blood-borne infections (HIV, Hepatitis B/C, CMV)
• No febrile non-haemolytic reactions
• No TRALI, no TACO risk from own blood
• No TRIM (immunosuppressive effect)
• Preserves allogeneic blood supply
• Acceptable to some Jehovah's Witnesses (cell salvage in particular, if blood does not leave the circuit)
• Cost-effective in high-volume cases

• Active bacteraemia / gross contaminated field (relative - risk of bacteraemia)
• Malignancy (relative - risk of tumour cell reinfusion; mitigated with leukocyte depletion filters)
• Amniotic fluid in obstetrics (risk of amniotic fluid embolism - special filters used, increasingly accepted)
• Bowel content contamination

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Q50. Massive Blood Transfusion: Definition, Complications and Management (2022)

• Transfusion of >10 units pRBC in 24 hours
• Replacement of the entire blood volume within 24 hours
• Transfusion of >4 units pRBC in 1 hour with ongoing haemorrhage and haemodynamic instability

• Dilutional coagulopathy (most important) - dilution of clotting factors and platelets by large volumes; mitigated by 1:1:1 ratio
• Thrombocytopenia - platelet count falls after >10 units if not replaced

• TRALI (anti-HLA antibodies in donor FFP/platelets)
• TACO (transfusion-associated circulatory overload)

1. Activate Massive Haemorrhage Protocol - alert blood bank, senior clinician, anaesthetist, surgical team
2. Identify and control source of bleeding (surgery, interventional radiology, pelvic binder)
3. Tranexamic Acid - 1g IV over 10 minutes ASAP (within 3h of injury), then 1g over 8h
4. Ratio-based transfusion: pRBC : FFP : Platelets = 1:1:1 (avoid crystalloid/colloid)
5. Fibrinogen - Cryoprecipitate 2 pools if fibrinogen <1.5 g/L (target >2 g/L)
6. Calcium - 10 mL 10% CaCl2 IV after every 4 units pRBC
7. Warm ALL products - blood warmer device; patient warming blanket; target core temp >36°C
8. Laboratory monitoring every 30-60 minutes: FBC, PT/APTT, fibrinogen, ABG (pH, base excess, lactate), ionised Ca2+
9. Point-of-care testing (TEG/ROTEM) if available for targeted factor replacement
10. Avoid crystalloid excess; avoid synthetic colloids (starches associated with renal impairment and coagulopathy)
11. Recombinant Factor VIIa (rFVIIa) - considered as rescue therapy in refractory haemorrhage (off-label)

• Hb >70 g/L; Platelets >50x10^9/L; PT/APTT <1.5x normal; Fibrinogen >1.5 g/L; pH >7.35; Temp >36°C; Ionised Ca2+ >1.1 mmol/L

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Q51. Applications of Platelet-Rich Plasma (PRP) in Surgical Practice (2021)

1. Collect 20-60 mL autologous blood
2. First centrifugation (soft spin) - separates RBCs from plasma
3. Second centrifugation (hard spin) - concentrates platelets in small volume of plasma
4. Activated at point of use with thrombin and/or calcium chloride
5. Applied to surgical site as gel, or injected

• PDGF (Platelet-Derived Growth Factor) - fibroblast proliferation, angiogenesis
• TGF-β (Transforming Growth Factor) - collagen synthesis, tissue remodelling
• VEGF (Vascular Endothelial Growth Factor) - angiogenesis
• EGF (Epidermal Growth Factor) - epithelialisation
• IGF (Insulin-like Growth Factor) - cell proliferation
• FGF (Fibroblast Growth Factor) - wound healing

• Autologous (no infection/rejection risk)
• Concentrated growth factors at site of need
• Minimally invasive
• Relatively cheap to prepare
• Approved and safe

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Q52. Complications of Blood Transfusion

• Cause: ABO incompatibility (usually clerical error - wrong blood to wrong patient)
• Mechanism: IgM antibodies in recipient → complement activation → intravascular haemolysis
• Features: Fever, rigors, facial flushing, chest/back/loin pain, hypotension, haemoglobinuria (red/cola urine), DIC, renal failure, shock, death
• Management:
  1. STOP transfusion immediately
  2. Maintain IV access; IV fluid resuscitation
  3. Maintain urine output >100 mL/h (furosemide/mannitol)
  4. Send: blood cultures, repeat G&S, DAT, FBC, clotting, U&E, LFTs
  5. Treat DIC if present
  6. Report to blood bank; haemovigilance (SHOT in UK)

• Cause: Anti-leukocyte (HLA) antibodies reacting with donor leukocytes
• Greatly reduced by leukodepletion
• Features: Temperature rise ≥1°C, chills, malaise during transfusion
• Management: Slow/stop transfusion; paracetamol; rule out AHTR

• Cause: IgE-mediated to donor plasma proteins; risk with IgA-deficient patients (anti-IgA antibodies)
• Features: Urticaria (mild) → bronchospasm, angioedema, cardiovascular collapse (severe)
• Management: Mild - antihistamine, slow transfusion. Severe - STOP, adrenaline 0.5 mg IM, steroids, antihistamines

• Cause: Fluid overload, especially in elderly, cardiac/renal disease
• Features: Dyspnoea, ↑BP, bilateral pulmonary oedema during/after transfusion
• Management: Slow/stop transfusion; sit patient upright; furosemide IV

• Bacterial contamination (especially platelets - stored at room temperature)
• Air embolism
• Thrombophlebitis

• Delayed Haemolytic Reaction - alloantibodies to minor antigens (Kidd, Duffy, Kell); Day 3-10; mild jaundice/Hb fall
• Post-Transfusion Purpura (PTP) - Day 5-10; severe thrombocytopenia from anti-platelet antibodies; treat with IVIg
• Transfusion-Associated GvHD (TA-GvHD) - immunocompromised patients; donor lymphocytes attack host tissues; very high mortality; prevented by irradiation of cellular blood products

• Iron overload (haemosiderosis/haemochromatosis) - each unit contains ~250 mg elemental iron; treat with desferrioxamine/deferasirox
• TRIM (Transfusion-Related Immunomodulation) - immunosuppression; associated with increased rate of postoperative infection and possible cancer recurrence
• Alloimmunisation - antibody development to donor RBC/platelet/HLA antigens; complicates future transfusions

• HIV: ~1:2.5 million; Hepatitis B: ~1:300,000; Hepatitis C: ~1:5 million; CMV; Malaria; vCJD (leukodepletion)

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Q53. Blood Products, Plasma Expanders for Shock Following Polytrauma; Complications of Blood Transfusion

• Do NOT carry oxygen
• Worsen dilutional coagulopathy
• Cause hypothermia
• Should be MINIMISED; blood products preferred

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Q54. TRALI: Definition, Mechanism and Management (2021)

• Acute onset within 6h of transfusion
• PaO2/FiO2 <300 mmHg OR SpO2 <90% on room air
• Bilateral infiltrates on chest X-ray
• No evidence of circulatory overload (TACO)
• No pre-existing ALI before transfusion

• Patient's underlying condition (surgery, sepsis, trauma, haematological malignancy)
• Primes/activates neutrophils in pulmonary vasculature
• These primed neutrophils are ready to be activated by a second hit

• Anti-HLA class I/II antibodies or anti-neutrophil antigen (HNA) antibodies in donor plasma
• These antibodies bind to primed recipient neutrophils
• Neutrophil activation → degranulation → endothelial injury in pulmonary capillaries
• Increased capillary permeability → protein-rich fluid floods alveoli
• Non-cardiogenic pulmonary oedema (ARDS-like picture)

• FFP > Whole blood > Platelets > pRBC

• Fever (usually acute)
• Dyspnoea, hypoxaemia
• Bilateral crackles
• Hypotension (early)
• CXR: bilateral 'white out' (bilateral pulmonary infiltrates) without cardiomegaly
• Symptoms develop during or within 6h of transfusion

1. STOP the transfusion immediately (most important first step)
2. Supportive oxygen therapy - high-flow O2; escalate to NIV or mechanical ventilation if required
3. If mechanically ventilated: lung-protective ventilation (tidal volume 6 mL/kg, PEEP 5-10 cmH2O, plateau pressure <30 cmH2O)
4. IV fluids for hypotension (unlike TACO, these patients are volume-depleted)
5. No diuretics (non-cardiogenic mechanism; diuretics worsen hypovolaemia)
6. Corticosteroids - controversial, limited evidence
7. Report to blood bank - screen implicated donor(s) for HLA/HNA antibodies; quarantine remaining products from that donor
8. Haemovigilance reporting (SHOT in UK)

• Male-only plasma policy for FFP (UK adopted this in 2003) - dramatically reduced TRALI incidence
• Leukoreduction
• HLA antibody screening of donors, especially multiparous females

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SECTION 4: ANAESTHESIA AND CRITICAL CARE

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Q55. Pharmacological Advances in Local Anaesthetics in Surgical Practice (2015)

• Reversible blockade of voltage-gated Na+ channels on nerve axon membranes
• Prevents Na+ influx → blocks action potential propagation
• Must cross cell membrane (unionised form) then ionise intracellularly to bind channel from inside
• Work in a use-dependent manner (more active channels = better blockade)

• The S-isomer has a much safer cardiac and CNS profile than racemic bupivacaine
• Bupivacaine cardiotoxicity: severe ventricular arrhythmias, VF, very difficult to resuscitate
• Levobupivacaine provides equivalent analgesia with significantly less cardiovascular toxicity
• Preferred for epidural, brachial plexus blocks

• Pure S-enantiomer (never existed as racemate)
• Produces preferential sensory blockade (less motor block than bupivacaine at equianalgesic doses)
• Valuable in epidural analgesia (sensory-motor dissociation; patient can mobilise)
• Less cardiotoxic than bupivacaine

• Bupivacaine encapsulated in liposomes → controlled slow release
• Duration: up to 72 hours (vs 8-12h conventional bupivacaine)
• Used for wound infiltration at closure → significant reduction in postoperative opioid requirements
• Especially useful in ERAS programmes

• Combination of lignocaine 2.5% + prilocaine 2.5%
• Topical application; penetrates intact skin (eutectic formulation lowers melting point, enhances penetration)
• Application 60-90 minutes before venepuncture
• Invaluable in paediatric practice

• Added to LA solutions (typically 1:200,000 adrenaline)
• Causes local vasoconstriction → slows systemic absorption → prolongs duration by 50-100%
• Reduces peak plasma concentration (reduces toxicity risk)
• Allows higher total dose of LA to be used
• Contraindicated in end-artery regions: fingers, toes, penis, nose tip, ear lobe (risk of ischaemic necrosis)

• CNS features (first): circumoral tingling, metallic taste, tinnitus, confusion → seizures
• CVS features (second and more serious): bradycardia, QRS prolongation, VT/VF; bupivacaine most dangerous
• Treatment of LAST: Stop injection; airway; seizure control (benzodiazepines); 20% Intralipid (lipid emulsion therapy): 1.5 mL/kg IV bolus → 15 mL/kg/h infusion; CPR if needed

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Q56. Regional Anaesthesia (2006)

• Tourniquet applied; LA (prilocaine 0.5%) injected IV distally
• Used for distal limb procedures (carpal tunnel, fracture reduction)
• Risk: LA toxicity if tourniquet deflated prematurely

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Q57. Short Note on Epidural Anaesthesia

• Lies between the ligamentum flavum (posteriorly) and the dura mater (anteriorly)
• Contains: epidural fat, epidural venous plexus (Batson's plexus), lymphatics, spinal nerve roots
• Negative pressure (compared to atmosphere) - used in identification technique
• Extends from foramen magnum to sacral hiatus

1. Patient position: sitting (most common; best identification) or lateral decubitus
2. Full aseptic technique; sterile field
3. Skin infiltration with LA at chosen interspace
4. Tuohy needle (curved bevel, 16-18G) advanced through interspinous ligament
5. Stylet removed; Loss of Resistance (LOR) technique - syringe with saline (or air) attached; advance until resistance suddenly disappears (needle enters epidural space)
6. Catheter threaded 3-4 cm into space; Tuohy needle removed
7. Test dose: 3 mL of 2% lidocaine with adrenaline 1:200,000 - detects intravascular placement (tachycardia if IV) and intrathecal placement (spinal level if IT)
8. Titrated doses then given via catheter

• LA: Bupivacaine 0.1-0.25% (analgesic), 0.5% (surgical); Ropivacaine; Levobupivacaine
• Opioids added: Fentanyl 2-4 mcg/mL or Diamorphine 0.1 mg/mL (enhance quality; reduce LA dose)
• Alpha-2 agonist: Clonidine (adjunct)

• Lumbar (L2-L4): lower limb, perineal, pelvic, obstetric surgery
• Thoracic (T4-T10): thoracic, upper and lower abdominal surgery

• Excellent dynamic analgesia (pain on coughing/movement)
• Attenuates neuroendocrine stress response (reduces cortisol, catecholamines)
• Reduces postoperative insulin resistance
• Thoracic epidural significantly reduces pulmonary complications after major abdominal/thoracic surgery
• Reduces DVT/PE risk (sympatholysis → vasodilation; earlier mobilisation)
• Reduces postoperative ileus (thoracic epidural)
• No systemic opioid side effects (PONV, respiratory depression, constipation)
• Pillar of ERAS protocols

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Q58. Incentive Spirometry (2008)

• Volume-oriented (e.g. Voldyne): measures inspired volume; patient tries to reach target volume marker; more commonly used; provides better feedback
• Flow-oriented (e.g. Triflo II): measures flow by raising balls in chambers; simpler; less accurate for volume

• Normal tidal breathing: FRC maintained by periodic spontaneous deep breaths (sighs)
• After major surgery (especially abdominal/thoracic): pain inhibits deep breathing → loss of sighing → alveolar collapse → atelectasis
• Atelectasis → shunting → hypoxaemia → pneumonia
• IS encourages slow maximum inspiration → expands alveoli → maintains/restores Functional Residual Capacity (FRC)
• Prevents V/Q mismatch and atelectasis

• Post-abdominal surgery (especially upper abdominal) - highest risk of atelectasis
• Post-thoracic surgery / thoracotomy
• COPD patients in perioperative period
• Chest wall injury (rib fractures)
• Patients on prolonged bed rest
• Prevention of postoperative pneumonia in high-risk patients

1. Patient seated upright (optimises lung mechanics)
2. Breathe out normally
3. Place mouthpiece in mouth, create a seal
4. Breathe in slowly and deeply to reach target volume/raise balls
5. Hold breath for 3-5 seconds (sustained inflation most important step)
6. Exhale gently
7. Repeat 10 breaths per hour while awake
8. Begin preoperatively to establish baseline (pre-habilitation)

• Most effective for post-abdominal/thoracic surgery
• Reduces incidence of postoperative pulmonary complications (PPCs): atelectasis, pneumonia, respiratory failure
• Most beneficial when combined with:
  • Chest physiotherapy
  • Early ambulation
  • Adequate analgesia (epidural helps compliance by reducing pain with deep breathing)
  • ERAS protocols

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Q59. Management of Cardiac Arrest During Surgery (2025)

• 30 chest compressions : 2 breaths (30:2)
• If intubated: continuous chest compressions at 100-120/min without pausing for breaths
• Minimise interruptions to compressions; high-quality CPR is paramount

1. Defibrillate immediately: 200J biphasic (or maximum monophasic)
2. Resume CPR immediately for 2 minutes - do NOT check pulse/rhythm immediately
3. Reassess rhythm; if still shockable: shock again
4. After 3rd shock: Adrenaline 1 mg IV + Amiodarone 300 mg IV
5. Continue cycles: shock → CPR → reassess
6. Adrenaline 1 mg IV every 3-5 minutes (alternate cycles)
7. Amiodarone 150 mg IV after 5th shock if needed

1. Continue CPR 30:2
2. Adrenaline 1 mg IV as soon as IV access available, then every 3-5 minutes
3. Atropine no longer recommended in current guidelines
4. Find and treat reversible causes (4H + 4T)

• Massive haemorrhage - most common surgical cause; aggressive transfusion
• Anaesthetic drug toxicity - propofol infusion syndrome, suxamethonium apnoea, volatile agents
• Local anaesthetic toxicity (LAST) - give 20% Intralipid
• Air/CO2 embolism (laparoscopy) - left lateral head-down position; aspirate from CVP line
• Vagal cardiac arrest during peritoneal traction, rectal stimulation, oculocardiac reflex
• Anaphylaxis (antibiotics, muscle relaxants, latex, blood products) - adrenaline
• Tension pneumothorax (during mechanical ventilation, central line insertion) - immediate needle decompression
• Pulmonary embolism - consider thrombolysis

• Target SpO2 94-98% (avoid hyperoxia)
• Target PaCO2 35-45 mmHg (normocapnia; avoid hypocapnia)
• Target MAP ≥65 mmHg (vasopressors if needed)
• 12-lead ECG - identify STEMI → immediate PCI
• Avoid hyperthermia; consider Targeted Temperature Management (TTM) 36°C if comatose
• Transfer to ICU
• Treat the precipitating cause

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Q60. Pain Relief in Surgery / Postoperative Pain Management (2009, 2011)

• Uncontrolled pain → ↑ stress hormones (cortisol, catecholamines) → catabolism, immunosuppression
• Pain → splinting of abdomen/chest → reduced respiratory effort → atelectasis, pneumonia
• Pain → immobility → ↑DVT/PE risk
• Pain → delayed gastric emptying, ileus
• Chronic pain development (if acute pain poorly managed → central sensitisation)
• Better pain control → earlier mobilisation → ERAS compliance

• Step 1 (mild pain): Non-opioids - Paracetamol + NSAIDs
• Step 2 (moderate): Weak opioids - Codeine, Tramadol
• Step 3 (severe): Strong opioids - Morphine, Fentanyl, Oxycodone
• Adjuvants at all steps: Gabapentinoids, Ketamine, α2-agonists

• IV opioid (morphine 1 mg bolus standard), lockout period (5 minutes)
• Patient self-administers within preset parameters
• Advantages: rapid titration to individual needs; patient empowerment; no nursing delay; good patient satisfaction scores
• Disadvantages: requires IV access, alert patient; not suitable for confused/sedated patients

• Thoracic epidural: best evidence for thoracic and abdominal surgery; attenuates stress response
• TAP (Transversus Abdominis Plane) block: anterior abdominal wall surgery; sonar-guided
• Rectus sheath block: midline incisions (umbilical, laparotomy)
• PECS block (I and II): breast surgery
• Intrathecal morphine (0.1-0.3 mg): hip and knee arthroplasty, Caesarean section
• Wound infiltration catheter (soaker catheter): continuous LA infusion at wound site

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Q61. Invasive and Non-Invasive Techniques of Postoperative Analgesia (2021)

Non-Invasive Techniques:

Invasive Techniques:

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QUICK REFERENCE SUMMARY TABLE (Q37-Q61)

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MS GENERAL SURGERY EXAM - STRUCTURED ANSWERS (Q90-Q98)

SECTION: WOUND & BURNS

Bailey & Love's Short Practice of Surgery, 28th Edition

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SECTION 1: WOUND

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Q90. Define and Classify Wound. Physiology of Wound Healing. Molecular/Cellular Events. Factors Affecting Wound Healing. Biological Problems. Phases of Wound Healing. Untidy Wounds. Facilitating and Interfering Factors. Scar Prevention and Management (2023, 2027)

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PART A: Definition and Classification of Wounds

• Superficial (epidermis only)
• Partial thickness (epidermis + dermis)
• Full thickness (epidermis + dermis + subcutaneous tissue; may involve muscle/bone)

• Acute: heals in orderly, timely manner
• Chronic: fails to proceed through normal healing stages (>4-6 weeks)

• Primary intention: wound edges directly apposed
• Secondary intention: wound left open; granulation, contraction, re-epithelialisation
• Tertiary (delayed primary) intention: open initially; closed surgically once clean

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PART B: Physiology / Phases of Wound Healing

• Vascular disruption → immediate vasoconstriction
• Exposure of subendothelial collagen → platelet adhesion via vWF-GpIb
• Platelet activation → release of alpha-granule contents: TGF-β, PDGF, FGF, EGF, VEGF
• Platelet aggregation → primary plug
• Tissue Factor activates coagulation cascade → fibrin clot forms (scaffold for healing cells)
• Fibrin + fibronectin = provisional extracellular matrix

• Platelet activation → histamine and serotonin release → vasodilation + increased vascular permeability
• PMN leukocytes (neutrophils) dominate - phagocytose bacteria and debris
• Neutrophils release proteases and reactive oxygen species (ROS)

• Monocytes migrate from blood → differentiate into macrophages
• Macrophages: most important cells in wound healing
  • Phagocytose bacteria, apoptotic neutrophils, debris
  • Release cytokines: IL-1, TNF-α, TGF-β, PDGF → recruit fibroblasts
  • Coordinate transition to proliferative phase
• Classical signs: rubor (redness), tumor (swelling), calor (heat), dolor (pain)

1. Fibroplasia: fibroblasts migrate into wound → proliferate → produce collagen (initially Type III) and glycosaminoglycans (ground substance)
2. Angiogenesis: VEGF drives new capillary formation → formation of granulation tissue (pink, granular, highly vascular)
3. Re-epithelialisation: keratinocytes at wound margins and hair follicles proliferate and migrate across wound surface; driven by EGF and TGF-α
4. Wound contraction: myofibroblasts (specialised fibroblasts with actin cytoskeleton) contract the wound; reduces wound size; important in secondary healing

• Immature collagen (Type III) replaced by mature Type I collagen
• Collagen fibres reorganise along lines of tension (parallel pattern)
• Fibroblasts and blood vessels reduce → almost acellular scar
• Tensile strength increases progressively but never exceeds 80% of normal skin
• Scar: initially pink, raised, itchy → becomes pale, soft, flat over 1-2 years
• This phase produces abnormal scars if dysregulated

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PART C: Molecular and Cellular Events

• Proteases that degrade extracellular matrix components
• Essential for cell migration and tissue remodelling
• Regulated by TIMPs (tissue inhibitors of metalloproteinases)
• In chronic wounds: MMP activity is excessive, degrading growth factors and impeding healing

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PART D: Factors Affecting Wound Healing

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PART E: Biological Problems of Wound Healing (Abnormal Healing)

• Fail to progress through normal healing stages
• Characterised by prolonged inflammation, biofilm, excess MMPs, low growth factors
• Causes: ischaemia, infection, pressure, metabolic disease

• Excessive collagen deposition within wound boundaries
• Parallel collagen pattern
• Raised, red, itchy
• Does NOT extend beyond wound margins
• Eventually regresses spontaneously (months to years)
• More common in: high-tension areas, wounds crossing skin tension lines, deep dermal burns, wounds healing by secondary intention >3 weeks

• Extends beyond original wound margins (pathognomonic)
• Disorganised collagen (nodular pattern)
• Does NOT spontaneously regress
• Hard to treat; high recurrence after surgery alone
• Predisposing factors: dark skin pigmentation, genetic predisposition, ear lobe/deltoid/sternum sites, even minor trauma
• Mechanism: unknown but fibroblasts resistant to apoptosis; TGF-β1 overactivity

• Separation of wound edges
• Causes: infection, haematoma, poor technique, malnutrition, steroids
• Burst abdomen (fascial dehiscence) = surgical emergency

• Excessive contraction across a joint → restricted movement
• Common after burns across flexion surfaces

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PART F: Untidy Wounds - Management

• T - Tissue debridement (remove non-viable tissue)
• I - Infection/Inflammation control
• M - Moisture balance (appropriate dressing)
• E - Epithelial edge advancement (facilitate re-epithelialisation)

1. Stop haemorrhage - direct pressure
2. Clean the wound - thorough irrigation with saline; remove foreign bodies, debris
3. Debridement - excise all devitalised tissue; methods:
   • Surgical (most rapid, complete)
   • Sharp (bedside, selective)
   • Autolytic (moist dressings; body's own enzymes)
   • Biological (maggot therapy - Lucilia sericata larvae)
   • Enzymatic (collagenase preparations)
4. Assess wound - depth, contamination, tissue viability, vascularity
5. Tetanus prophylaxis - assess tetanus status; administer toxoid ± immunoglobulin
6. Antibiotics - only if infected or high-risk
7. Wound closure options (Reconstructive Ladder):
   • Healing by secondary intention
   • Delayed primary closure (tertiary)
   • Split-thickness skin graft
   • Full-thickness skin graft
   • NPWT as bridge to definitive reconstruction
   • Local/regional/free flap

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PART G: Facilitating and Interfering Factors; Adverse Scar Prevention and Management (2023)

• Adequate oxygenation and perfusion
• Good nutritional status (protein, Vitamin C, Zinc)
• Blood glucose control in diabetics
• Tension-free wound closure along relaxed skin tension lines (Langer's lines)
• Meticulous surgical technique (atraumatic)
• Early debridement and wound closure
• Appropriate moist wound dressings
• NPWT to promote granulation
• Smoking cessation preoperatively

• Infection (>10^5 organisms/gram impairs healing; biofilm formation)
• Ischaemia, hypoxia
• Haematoma, seroma (dead space = ideal culture medium)
• Poor technique (excess tension, devascularisation)
• Radiation damage
• Metabolic disease (diabetes, uraemia, liver failure)
• Drugs (steroids, chemotherapy, anticoagulants)
• Immunodeficiency
• Malnutrition

• Place incisions along relaxed skin tension lines (Langer's lines)
• Avoid straight-line incisions across flexion creases (Z-plasty principle)
• Minimise tissue handling; atraumatic technique
• Early debridement to prevent infection
• Proper initial wound scrubbing (prevents tattooed scars)
• Close dead space (reduce haematoma/seroma)
• Early scar management (begin after epithelialisation)

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Q91. Describe the Role of Biofilms in Wound Management (2014)

1. Reversible attachment - planktonic bacteria attach to wound surface
2. Irreversible attachment - adhesins anchor bacteria firmly to surface
3. Early biofilm development - bacteria begin producing EPS matrix
4. Biofilm maturation - 3D community develops; microcolonies with water channels; phenotypic changes
5. Dispersal - planktonic cells released → seed new sites

• EPS matrix acts as a physical barrier to antibiotics and host immune cells
• Slow metabolic state of biofilm bacteria (persister cells) makes them insensitive to antibiotics that target active metabolism
• Biofilm bacteria are 1000-fold more resistant to antibiotics than planktonic forms
• Conventional antibiotic swabs often show no growth despite biofilm presence

• EPS prevents phagocytosis by neutrophils and macrophages
• Biofilm triggers a chronic, ineffective inflammatory response
• Sustained inflammation → sustained MMP production → degradation of growth factors → impaired healing

• Estimated that >80% of chronic wounds contain biofilm
• Biofilm shifts wound from healing to chronic inflammatory state
• Chronic wounds with biofilm: high MMP activity, low growth factors, low TIMP activity

• Most wound biofilms are polymicrobial (Staph. aureus, Pseudomonas aeruginosa, anaerobes)
• Species synergistically enhance virulence and resistance

• Clinical suspicion (non-healing wound despite treatment, recurrent infection)
• Wound appearance: dull, viscous exudate; failure to granulate
• Fluorescence imaging (MolecuLight i:X device) detects bacterial load in real time
• Confocal microscopy (research/specialist)
• Standard cultures often falsely negative (biofilm bacteria grow poorly on standard media)

• Sharp debridement (most effective) - physically disrupts and removes biofilm
• Must be repeated regularly as biofilm reforms within 24-72 hours
• Wound irrigation under pressure (≥8 psi) dislodges biofilm

• Topical antiseptics (not antibiotics): iodine (Povidone-iodine, Cadexomer iodine), silver (nanocrystalline silver, silver sulfadiazine), PHMB (Polyhexamethylene biguanide), chlorhexidine
• These penetrate biofilm better than systemic antibiotics
• Cadexomer iodine: slow-release iodine from starch microspheres; excellent biofilm disruption

• Dialkylcarbamoylchloride (DACC) - hydrophobic dressings bind and remove bacteria
• Honey (medical-grade manuka honey) - osmotic + H2O2 + methylglyoxal; disrupts biofilm
• Surfactant-containing dressings (e.g. benzyl benzoate) - disrupt EPS hydrophobic bonds

• Reduces bacterial load; mechanical removal of exudate and biofilm
• Changes wound environment unfavourable for biofilm

• Bacteriophage therapy (lytic phages specific to biofilm species)
• DNase (degrades extracellular DNA in EPS)
• Quorum sensing inhibitors (block biofilm communication signals)

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Q92. VAC (Vacuum-Assisted Closure) / NPWT: Indications, Contraindications and Complications of Negative Pressure Wound Therapy (2024)

1. Macro-deformation: Negative pressure draws wound edges together (reduces wound size)
2. Micro-deformation: Mechanical stretch of cells at foam-tissue interface → cell proliferation and angiogenesis (mechanotransduction via integrins)
3. Fluid removal: Removes excess exudate → reduces oedema → improves local blood flow
4. Bacterial clearance: Continuous removal of wound fluid reduces bacterial load and disrupts biofilm
5. Promotes granulation tissue: Creates a warm, moist, mechanically stimulated environment optimal for granulation
6. Reduces wound volume: Progressive filling of wound cavity

• Continuous mode: standard (-125 mmHg); good for heavily exudating wounds
• Intermittent/variable mode: better for granulation tissue formation (cycling between -125 and 0 mmHg)
• Instillation NPWT (NPWTi): adds periodic instillation of saline or antiseptic solution; better for infected wounds

• Malignancy in the wound bed (promotes tumour growth)
• Exposed/unanastomosed blood vessels or organs
• Non-enteric and unexplored fistulae
• Necrotic tissue with eschar (must debride first)

• Acute/active bleeding (risk of haemorrhage from suction)
• Infected wounds (can be used but with caution; NPWTi preferred)
• Anticoagulated patients (risk of haemorrhage)
• Proximity to exposed nerves
• Patients on anticoagulation

• Less frequent dressing changes (every 48-72h vs daily)
• Better granulation tissue formation
• Reduced wound volume faster
• Better skin graft take rates
• Reduced nursing time and cost in high-exudate wounds

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Q93. Enumerate Causes of Non-Healing Ulcers of Leg and Foot

1. Vascular Causes (most common overall):

• Chronic venous hypertension (CVI) → ambulatory venous hypertension
• Venous reflux (varicose veins, deep venous incompetence) or outflow obstruction (DVT)
• Mechanism: ↑ venous pressure → capillary leakage → fibrin cuffs form around capillaries → impair O2 diffusion + leucocyte trapping → local ischaemia → ulceration
• Location: gaiter area (medial lower leg, above medial malleolus) - "champagne bottle" leg
• Appearance: shallow, irregular margins; exudative; granulating base; surrounding lipodermatosclerosis and haemosiderin pigmentation

• Peripheral arterial disease (atherosclerosis) → ischaemia → tissue death
• Risk factors: smoking, DM, hypertension, hypercholesterolaemia
• Location: pressure points - toes, lateral foot/ankle, heel, dorsum of foot
• Appearance: deep, punched-out, pale necrotic base; minimal exudate; very painful; no granulation tissue
• Associated: absent/weak peripheral pulses, ABPI <0.5, pallor on elevation, Buerger's angle <20°

• Combined features; important to assess ABPI before compression therapy

2. Diabetic/Neuropathic Ulcers:

• Peripheral neuropathy → loss of protective sensation → repetitive trauma unnoticed
• Peripheral vascular disease often coexists
• Location: plantar aspect of foot, pressure areas (metatarsal heads, heel)
• Appearance: punched-out; surrounding callus; painless (neuropathic); warm or cold depending on vascular component
• Wagner Classification of diabetic foot ulcers (0-5)

3. Pressure Ulcers (Decubitus Ulcers):

• Prolonged pressure over bony prominence → ischaemic necrosis
• Sites: sacrum, heel, lateral malleolus, greater trochanter, occiput
• Risk factors: immobility, malnutrition, incontinence, sensory impairment
• NPIAP Staging (I-IV + unstageable):
  • Stage I: non-blanchable redness of intact skin
  • Stage II: partial thickness dermis loss; shallow open ulcer
  • Stage III: full thickness skin loss; subcutaneous fat exposed; bone/tendon not visible
  • Stage IV: full thickness tissue loss; bone, tendon, muscle exposed
  • Unstageable: depth unknown due to slough/eschar coverage

4. Infective Causes:

• Bacterial: Streptococcal cellulitis → ulceration; Ecthyma (deep Streptococcal); Buruli ulcer (Mycobacterium ulcerans - tropical)
• Fungal: Chronic fungal infections
• Tropical/parasitic: Leishmaniasis, Yaws
• Sexually transmitted: Syphilitic gumma, Chancre

5. Neoplastic:

• Marjolin's ulcer - squamous cell carcinoma arising in chronic wound/scar (Marjolin described in burn scars); important to biopsy any chronic ulcer not responding to treatment
• Basal cell carcinoma
• Lymphoma cutis
• Kaposi's sarcoma

6. Metabolic/Haematological:

• Diabetes mellitus (as above)
• Gout (tophaceous deposits)
• Calciphylaxis (calcium deposits in vessel walls; renal failure patients)
• Sickle cell disease (sickling crises → vascular occlusion → ulceration; medial malleolus)
• Thalassaemia

7. Autoimmune/Inflammatory:

• Pyoderma gangrenosum - rapidly progressive, painful ulcer with violaceous/undermined edges; associated with IBD, rheumatoid arthritis, haematological malignancy; responds to steroids NOT surgery
• Vasculitis (SLE, rheumatoid arthritis, polyarteritis nodosa)
• Systemic sclerosis
• Antiphospholipid syndrome

8. Lymphatic:

• Lymphoedema → ulceration
• Chronic oedema → repeated infection → fibrosis → ulceration

9. Traumatic/Factitial:

• Self-inflicted wounds
• Burns-related chronic wounds
• Radiation ulcers

• ABPI (Ankle Brachial Pressure Index): normal 0.9-1.2; 0.5-0.9 = arterial disease; <0.5 = critical ischaemia
• Duplex Doppler ultrasound (venous/arterial assessment)
• FBC, ESR, blood glucose, HbA1c, autoimmune screen
• Wound swab (culture and sensitivity)
• Biopsy if no healing after 12 weeks (exclude Marjolin's)

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Q94. Recent Advances in Management of Open Wounds - NPWT, Ultrasound Therapy and Hydrotherapy (2021)

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1. NPWT (Negative Pressure Wound Therapy)

• NPWTi (NPWT with instillation): periodic instillation of normal saline or antiseptics (e.g. PHMB, dilute hypochlorous acid) directly into wound; dwell time 10-20 min before suction resumes; significantly better for infected/biofilm-containing wounds
• Single-use NPWT devices (sNPWT): portable, disposable (e.g. PICO, Prevena); patient can be ambulatory; useful for closed incision NPWT to reduce SSI in high-risk wounds
• NPWT + skin grafts: foam placed over meshed split-skin graft → significantly improves graft take by maintaining contact and removing fluid that would cause graft-bed separation

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2. Ultrasound (US) Therapy in Wound Management

• Therapeutic (low-intensity) ultrasound: 0.5-3 MHz; thermal and non-thermal effects
• Low-frequency ultrasound (LFUS/MIST therapy): 20-40 kHz; non-contact delivery via mist of saline; better tissue penetration; most evidence in wound healing

• Thermal effects (high-frequency): ↑ local temperature → ↑ cellular metabolism; ↑ blood flow; ↑ collagen extensibility
• Non-thermal/cavitation effects (low-frequency):
  • Stable cavitation: microstreaming around gas bubbles → ↑ cell membrane permeability → ↑ uptake of nutrients and growth factors
  • Acoustic streaming: fluid movement → mechanical stimulation of fibroblasts → ↑ collagen synthesis
  • Disrupts biofilm EPS mechanically
• Biological effects:
  • ↑ Fibroblast activity and proliferation
  • ↑ Collagen synthesis and organisation
  • ↑ Angiogenesis (VEGF upregulation)
  • Bactericidal effect (cavitation disrupts bacterial cell walls)
  • Anti-inflammatory (reduces chronic oedema)

• Venous leg ulcers (significantly improves healing rate)
• Diabetic foot ulcers (MIST therapy - Level I evidence from RCTs)
• Pressure ulcers
• Chronic wounds with biofilm

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3. Hydrotherapy / Wound Irrigation / Water-Based Therapies

• Pulsed lavage with suction (PLwS): mechanical irrigation using pulsed pressure (8-15 psi) with simultaneous suction
• Removes biofilm, necrotic tissue, surface bacteria
• Used in heavily contaminated traumatic wounds and chronic wounds

• Patient limb or whole body placed in whirlpool tank
• Warm water turbulence loosens and removes wound debris
• Less used now due to infection control concerns (cross-contamination risk)

• Normal saline wound irrigation: most widely used; reduces bacterial load; removes loose necrotic tissue
• Pressure matters: >8 psi removes significant biofilm; <4 psi insufficient

• Maggot therapy (Lucilia sericata larvae): secrete proteolytic enzymes → selective debridement; produce antimicrobial compounds; stimulate granulation
• PRP (Platelet-Rich Plasma): concentrated growth factors; promotes wound healing (see Q51)

• Acellular dermal matrices (e.g. Integra, MatriDerm): scaffold for fibroblast ingrowth; used for full-thickness wounds, burns
• Cellular bioengineered substitutes (e.g. Apligraf, Dermagraft): contain living fibroblasts ± keratinocytes; release growth factors; close chronic venous ulcers
• Indication: chronic ulcers unresponsive to 4+ weeks of standard care

• Electrical current applied to wound → stimulates fibroblasts and keratinocytes; reduces oedema; antimicrobial
• Evidence in pressure ulcers and diabetic ulcers

• Red and near-infrared light → ↑ cellular ATP production; ↑ fibroblast activity; anti-inflammatory; angiogenesis
• Evidence emerging for chronic wounds

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Q95. Methods of Promoting Soft Tissue Healing (2018)

• Nutritional support: ensure adequate protein (1.2-1.5 g/kg/day), Vitamin C (cofactor for collagen hydroxylation), Zinc (cofactor for cell proliferation and DNA synthesis), Vitamin A (epithelialisation); enteral nutrition preferred
• Blood glucose control (target HbA1c <7%; perioperative glucose <10 mmol/L)
• Smoking cessation (8 weeks before elective surgery optimises healing)
• Treat anaemia (ensure adequate O2 delivery)
• Medication review (wean steroids if possible; withhold chemotherapy if possible perioperatively)
• Treat underlying disease (venous HTN, arterial insufficiency, immune deficiencies)

• T - Tissue debridement: remove necrotic tissue, slough, eschar, biofilm; shifts chronic wound to acute wound status
• I - Infection/Inflammation control: topical antiseptics (cadexomer iodine, silver, PHMB); systemic antibiotics only for cellulitis/spreading infection
• M - Moisture balance: optimal moisture accelerates healing; too dry = cell death; too wet = maceration; moist wound dressings maintain optimal level
• E - Epithelial edge: remove wound edge fibrous margin if wound stalling; growth factors at edge

• See Q92; promotes granulation by macro/micro-deformation; reduces oedema; removes exudate; reduces bacterial load

• Becaplermin (recombinant PDGF) - FDA-approved gel for neuropathic diabetic foot ulcers; stimulates fibroblast chemotaxis and proliferation
• PRP - autologous growth factor delivery (see Q51)

• 100% O2 at 2-2.5 atmospheres; increases dissolved O2 in plasma 10-15x
• Overcomes local tissue hypoxia; essential cofactor for collagen hydroxylation
• Stimulates angiogenesis (VEGF upregulation)
• Bactericidal (anaerobic organisms; potentiates antibiotics)
• Indications: diabetic foot ulcers (Wagner Grade III+), radiation wounds, osteomyelitis, problem wounds
• Evidence: moderate; Level I evidence for diabetic foot ulcers

• Provides cellular coverage; immediately stops wound from contracting and desiccating
• Split-thickness skin graft (STSG): donor site heals spontaneously; meshed to cover large areas
• Full-thickness skin graft (FTSG): better cosmesis; donor site requires closure; used for face/hand

• Provides vascularised tissue coverage
• Essential when bare bone, tendon, or implant exposed (avascular surfaces)
• Local, pedicled or free flap depending on wound size and location

• Scaffold for tissue ingrowth; growth factor delivery
• Integra (acellular dermal matrix) - bilayer; inner collagen-glycosaminoglycan layer + outer silicone layer
• Used in burns; complex wounds

• Ultrasound therapy (see Q94)
• Electrostimulation
• Photobiomodulation (LLLT)

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Q96. Role of NPWT in Management of Surgical Wounds (2020)

• Damage control surgery: abdomen left open to prevent abdominal compartment syndrome; correct lethal triad
• NPWT (Bogota bag or commercial NPWT systems, e.g. ABThera): covers viscera; removes peritoneal fluid; maintains fascial tension; prevents fascial retraction; facilitates delayed primary closure
• Sequential NPWT changes every 24-48h with progressive fascial closure attempts
• Primary fascial closure rate improved from 30% to >80% with NPWT protocols

• Mediastinitis with sternal dehiscence: high mortality if untreated
• NPWT: continuous negative pressure stabilises sternum; removes infected material; promotes granulation before definitive reconstruction (pectoralis/omentum flap)
• Bridges to reconstruction; reduces mortality

• Applied prophylactically over closed incisions in high-risk patients
• Evidence: reduces incisional SSI in obese patients, joint replacements, abdominal surgery
• Devices: PICO (single-use, 7-day), Prevena
• Mechanism: ↓ haematoma/seroma; ↓ dead space; maintains wound edge apposition; removes serous exudate; ↑ local perfusion

• NPWT applied over meshed split-skin graft
• Maintains uniform graft-bed contact; removes fluid that would cause graft lift; reduces shear forces
• Significantly improves graft take rates compared to conventional tie-over dressings

• Post-laparotomy wound dehiscence; abdominal wound breakdown
• NPWT promotes granulation tissue formation before secondary closure or skin grafting

• Wound opened and debrided; NPWT applied
• Removes infected fluid; reduces bacterial load; promotes granulation
• NPWTi (with antiseptic instillation) especially useful

• After excision; NPWT accelerates healing by secondary intention
• Reduces healing time compared to conventional dressings

• Strong evidence (Level I/II): open abdomen, skin graft take
• Moderate evidence: diabetic foot, pressure ulcers, sternal wounds
• Emerging evidence: ciNPWT for SSI prevention

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SECTION 2: BURNS

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Q97. Burn Injuries Result in Both Local and Systemic Responses - Explain

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LOCAL RESPONSE - Zones of Injury (Jackson's Model, 1947):

• Maximum tissue damage; cells irreversibly destroyed by heat
• Protein denaturation and coagulative necrosis
• No viable tissue; this becomes the eschar (slough)

• Potentially salvageable tissue
• Cells initially viable but at risk from ischaemia, oedema, and vasoconstriction
• Microvascular injury → delayed capillary thrombosis over 24-48h
• Clinical goal: prevent zone of stasis from converting to zone of coagulation
• Prevention: adequate fluid resuscitation; cooling (tepid water for 20 min within 1h); avoid vasoconstrictors; avoid hypothermia; avoid wound desiccation

• Increased blood flow; minimal cell damage
• Heals spontaneously unless infection or ischaemia occurs

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LOCAL RESPONSE - Effects on Skin and Adjacent Structures:

• Heat → mast cell degranulation → histamine release → local vasodilation + ↑ capillary permeability
• Protein-rich plasma leaks → local oedema (blistering)
• In deep burns: haemostatic plugging of microvessels → progressive ischaemia over 24-48h

• Burn eschar = devitalised protein-rich medium = ideal bacterial culture
• Colonisation begins within hours
• Invasive infection → sepsis (most common cause of death in major burns)
• Common organisms: Pseudomonas aeruginosa, Staph. aureus, Streptococcus, Candida

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SYSTEMIC RESPONSE:

• Burn injury → massive release of vasoactive mediators (histamine, serotonin, bradykinin, prostaglandins, TNF-α)
• Generalised increase in capillary permeability (not just local) in burns >20% TBSA
• Burn shock: fluid shifts from intravascular → interstitial space
  • Protein-rich oedema forms throughout body
  • Intravascular volume depletion → reduced cardiac output → circulatory shock
  • Haemoconcentration (initially): Hb and haematocrit rise as plasma volume falls
• Fluid loss is directly proportional to TBSA burned
• Fluid resuscitation required for burns >15% TBSA (adult) or >10% TBSA (extremes of age)

• Hartmann's solution (Ringer's lactate): 4 mL x TBSA% x weight (kg) in first 24h
• Half in first 8 hours from time of burn; half in next 16 hours
• Monitor: urine output target 0.5 mL/kg/h (adult); 1 mL/kg/h (child)

• Direct thermal injury to mouth, pharynx, larynx, supraglottic structures
• Heat dissipated above glottis (glottis is effective heat barrier)
• Oedema → progressive airway obstruction → rapidly fatal
• Warning signs: hoarse voice, stridor, singed nasal hairs/eyebrows, soot in nares/oropharynx, facial burns
• Management: early elective intubation (before oedema makes intubation impossible); delay is dangerous

• Smoke contains toxic products: carbon monoxide, hydrogen cyanide, acrolein, aldehydes, nitrogen oxides
• Direct chemical burn to bronchial mucosa → mucosal oedema, bronchospasm, exudate, cast formation
• Tracheobronchitis → pseudomembrane/fibrin cast formation → small airway obstruction
• Pulmonary oedema (chemical) → ARDS-like injury (can develop over 24h to 5 days)
• Clinical features: progressive dyspnoea, rising respiratory rate, rising pulse, anxiety, confusion, falling SpO2
• Management: 100% O2; physiotherapy; nebulised bronchodilators (albuterol); nebulised heparin + N-acetylcysteine (prevent cast formation); PPV/intubation if deteriorating

• Carbon monoxide (CO) poisoning: CO binds haemoglobin with 250x affinity of O2 → carboxyhaemoglobin (COHb) → impairs O2 delivery and utilisation; COHb >10% = significant poisoning; cherry-red skin; headache; confusion; coma; seizures; SpO2 falsely normal on standard pulse oximetry
  • Treatment: 100% O2 for ≥24h (displaces CO from Hb; half-life of COHb reduces from 5h on air to 90min on 100% O2)
  • Hyperbaric O2 for COHb >25%, neurological symptoms, pregnancy
• Cyanide poisoning: from burning plastics, synthetic materials; inhibits cytochrome oxidase → cellular asphyxia despite O2 delivery; lactic acidosis; high anion gap
  • Treatment: IV hydroxocobalamin (Cyanokit) 5g IV; binds cyanide → forms harmless cyanocobalamin; excreted in urine

• Cell-mediated immunity significantly impaired in large burns (>20% TBSA)
• Depressed T-cell activity, macrophage dysfunction, ↓ NK cell activity
• Leaves patient vulnerable to bacterial and fungal infections
• Systemic inflammatory response → SIRS (see Q37) and potential sepsis
• Burn wound = portal of entry; most common cause of death in major burns = sepsis

• Burns trigger the most severe hypermetabolic state known in medicine
• Resting metabolic rate can increase to 200% of normal in major burns
• Catecholamine and cortisol surge (persistent for weeks to months)
• Protein catabolism → negative nitrogen balance → massive muscle wasting
• Glucose intolerance (insulin resistance)
• Management: aggressive early enteral nutrition within 6 hours of burn; target: 25-30 kcal/kg/day total; 1.5-2g/kg/day protein; oxandrolone (anabolic steroid) in major burns; insulin infusion for glucose control

• Burns shock → reduced renal perfusion → acute kidney injury (AKI)
• Haemoglobinuria and myoglobinuria (electrical burns and deep muscle injury) → tubular obstruction → acute tubular necrosis
• Management: maintain urine output >0.5 mL/kg/h; forced diuresis with mannitol if myoglobinuria; alkalinise urine

• Splanchnic ischaemia → gut mucosal injury → loss of mucosal barrier → bacterial translocation → endotoxaemia → sepsis
• Ileus; Curling's ulcer (stress ulcer in duodenum of burn patients) → GI haemorrhage; prevented by early enteral feeding + proton pump inhibitors
• Abdominal compartment syndrome in massive oedema states

• Haemoconcentration initially (plasma loss)
• Haemolysis of red cells in burn zone → release of haemoglobin → haemoglobinuria
• Anaemia develops after 2-3 days as fluid resuscitation dilutes
• Thrombocytopenia possible (consumption in large burns)
• Coagulopathy (DIC in very large burns)

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Q98. 60kg Male with Second Degree Burns to Head, Neck, Front and Back of Chest + Smoke Inhalation 8 Hours Ago - Management and Complications (2022)

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IMMEDIATE MANAGEMENT:

• History of smoke inhalation 8 hours ago + burns to head/neck = HIGH RISK of evolving airway obstruction
• Look for: hoarse voice, stridor, soot in nose/oropharynx, singed nasal hairs/eyebrows, facial oedema
• Early elective intubation is life-saving - if any doubt, intubate NOW before oedema progresses (oropharyngeal oedema peaks at 24-48h)
• RSI with experienced anaesthetist; have surgical airway (cricothyrotomy/tracheostomy) prepared as backup
• Post-intubation: CXR; ventilate with lung-protective strategy (TV 6 mL/kg, PEEP 5 cmH2O)

• 100% high-flow O2 via NRB mask (pre-intubation) or via ETT post-intubation
• Carbon monoxide poisoning suspected (enclosed space fire, smoke inhalation): 100% O2 for ≥24h
  • Check ABG including COHb (standard SpO2 falsely reassuring in CO poisoning)
  • COHb >25% → consider hyperbaric O2
• Assess chest for respiratory effort; circumferential chest burns may cause mechanical restriction → escharotomy if needed
• Bronchoscopy: diagnostic and therapeutic; visualise airway injury; remove casts; obtain BAL cultures

• Large bore IV access x2 (through unburnt skin if possible; through burn if necessary)
• Fluid resuscitation - Parkland Formula:
  • Hartmann's (Ringer's Lactate): 4 mL x 27 x 60 = 6480 mL in first 24h from time of burn
  • Patient was burned 8 hours ago, so 24h deadline is already running
  • First 8 hours from burn time = 3240 mL (give remaining balance of this in remaining time to 8h mark, i.e. immediately)
  • Next 16 hours = 3240 mL
  • Urine output target: 0.5 mL/kg/h = 30 mL/h (strict hourly monitoring via IDC)
  • Adjust rate based on urine output response

• GCS; pupil response
• Confusion/agitation may indicate CO poisoning, hypoxia, or pain

• Full assessment; keep warm (risk of hypothermia especially with wet dressings and large burns)
• Remove all clothing and jewellery

• IV morphine titrated (NB: inhalation injury patients need ICU monitoring for opioid respiratory depression)
• Consider IV ketamine (analgesic + sedative; bronchodilator - useful in burns)

• Cool wound only if <1 hour since burn (tepid 15°C water for 20 min) - at 8 hours, cooling is no longer beneficial
• Cover wounds with sterile non-adherent dressings (cling film initially; avoids hypothermia; reduces pain; allows assessment)
• Do NOT burst blisters (protective barrier)
• Formal wound assessment and dressings in burns unit

• Early enteral nutrition within 6 hours (reduces hypermetabolism; preserves gut barrier; prevents Curling's ulcer)
• Target: 25-30 kcal/kg/day, 1.5-2g/kg/day protein

• Hourly urine output monitoring essential

• ABG (O2, CO2, COHb, MetHb, pH, base excess, lactate)
• FBC, U&E, Cr, coagulation, LFTs, group and save
• Blood glucose
• Blood cultures if febrile

• Continuous: ECG, SpO2, non-invasive (or invasive) BP, temperature
• Hourly: urine output, respiratory rate, GCS
• 4-hourly: blood glucose, pain score

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SPECIFIC MANAGEMENT OF INHALATION INJURY:

1. Secure airway (as above; intubate early)
2. 100% O2 for ≥24h (CO displacement)
3. Bronchoscopy (fiberoptic): assess airway injury; remove casts; obtain cultures
4. Nebulised bronchodilators (salbutamol/albuterol): treat bronchospasm
5. Nebulised heparin (5000 units 4-hourly alternating with N-acetylcysteine): prevents fibrin cast formation; N-acetylcysteine acts as mucolytic
6. Chest physiotherapy: mobilise secretions; prevent atelectasis
7. Ventilatory support: lung-protective strategy; prone ventilation for ARDS if needed

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COMPLICATIONS:

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QUICK REFERENCE SUMMARY (Q90-Q98)

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