The body's response to injury is a complex, integrated physiological reaction involving neuroendocrine, inflammatory, and metabolic pathways. Its aim is to restore homeostasis, limit tissue damage, and facilitate healing. Three phases overlap — pro-inflammatory (SIRS), counter-inflammatory (CARS), and resolution — and run simultaneously rather than sequentially.
Initial trigger: Damaged cells release DAMPs (Danger-Associated Molecular Patterns), which activate pattern recognition receptors (PRRs) on immune cells. Secondary insults (sepsis, hemorrhage, massive transfusion, ischaemia–reperfusion) prolong this phase and ↑ risk of organ dysfunction.
Neuroendocrine activation: HPA axis and sympathetic nervous system activate within seconds. Counter-regulatory hormones are released — cortisol (gluconeogenesis, protein catabolism, immune modulation), adrenaline (glycogenolysis, lipolysis, ↑CO), glucagon (hepatic glucose release), and growth hormone (lipolytic, insulin-antagonising, pro-inflammatory). Net effect: ↑ glucose, ↑ free fatty acids, ↑ amino acids available for repair.
| Mediator | Source | Key Actions |
|---|---|---|
| IL-1, TNF-α | Macrophages | Fever, ↑ vascular permeability, acute-phase proteins |
| IL-6 | Macrophages, endothelium | Acute-phase protein synthesis, B-cell activation |
| IL-8 | Macrophages, neutrophils | Neutrophil chemotaxis |
| NO (iNOS) | Macrophages, endothelium | Vasodilation, antimicrobial |
| Prostaglandins (PGE₂, PGI₂) | Many cell types | Vasodilation, pain, fever |
| Bradykinin | Plasma kinin cascade | Pain, vasodilation, ↑ permeability |
| Phase | Key Mediators | Function |
|---|---|---|
| Neuroendocrine | Cortisol, adrenaline, glucagon, GH | Energy mobilisation, immune modulation |
| Inflammatory | IL-1, TNF-α, IL-6, IL-8, NO, prostaglandins, bradykinin | Vasodilation, fever, leukocyte recruitment |
| Anti-inflammatory | IL-4, IL-10, IL-13, TGF-β | Suppress inflammation, promote repair |
| Resolution | Lipoxins, resolvins, protectins, maresins | Clear debris, switch off inflammation |
| Remodelling | TGF-β, PDGF, VEGF, FGF | Angiogenesis, fibroblast activation, collagen maturation |
The cellular response to injury integrates molecular, structural, metabolic, and functional changes within cells following noxious stimuli, aiming to restore homeostasis, initiate repair, or — if injury is overwhelming — precipitate cell death.
| Category | Examples |
|---|---|
| Adaptations (reversible) | Hypertrophy, hyperplasia, atrophy, metaplasia |
| Reversible injury | Hydropic change (cellular swelling), fatty change, membrane blebs, mitochondrial swelling |
| Irreversible injury | Severe mitochondrial damage → ATP depletion; massive Ca²⁺ influx; lysosomal rupture → autolysis |
| Necrosis | Uncontrolled, pro-inflammatory cell death |
| Apoptosis | Programmed cell death, minimal inflammation |
DAMPs → TLR activation on macrophages → primary cells (macrophages, neutrophils, dendritic cells) release IL-1, TNF-α, IL-6, IL-8, NO, and prostanoids. Early neutrophilia peaks at 3 h then neutropenia at 6–12 h (sequestration and tissue migration). Myeloid-derived suppressor cells (MDSCs) prolong inflammation and suppress T cells. Neural anti-inflammatory reflex via vagus → splenic nerve → acetylcholine on macrophage α7-nAChR → inhibits NF-κB → ↓ cytokines.
Metabolic reprioritisation: Skeletal muscle breakdown via ubiquitin–proteasome pathway → amino acids for acute-phase proteins; liver ↑ fibrinogen, CRP, ↓ albumin; peripheral insulin resistance → hyperglycaemia; mitochondrial dysfunction perpetuates DAMP release.
A non-specific, generalised inflammatory state affecting the whole body, triggered by infectious or non-infectious insults. Defined by ACCP/SCCM Consensus (Bone et al., 1992) as ≥2 of 4 clinical criteria.
| Parameter | Threshold |
|---|---|
| Temperature | >38.0°C or <36.0°C |
| Heart rate | >90 /min |
| Respiratory rate | >20 /min or PaCO₂ <32 mmHg |
| WBC count | >12,000/mm³ or <4,000/mm³ or >10% bands |
Infectious: bacterial, viral, fungal, parasitic. Non-infectious: major trauma, burns, acute pancreatitis, ischaemia–reperfusion injury, massive transfusion, severe allergic reaction, autoimmune disorders.
DAMPs/PAMPs → PRR activation → cytokine storm (TNF-α, IL-1, IL-6, IL-8) → endothelial activation → ↑ permeability, leukocyte extravasation, microvascular thrombosis → ↓ SVR, ↑ venous capacitance, ↑ cardiac index (hyperdynamic phase), pulmonary oedema. Genomic storm — 3700 leukocyte genes altered after endotoxin; 80% of genome in severe trauma.
SIRS → Sepsis → Severe sepsis → Septic shock → MODS. Early mortality from SIRS; late mortality from CARS-mediated immunosuppression.
Management: (1) Treat underlying cause — source control + antibiotics or condition-specific treatment. (2) Supportive care — airway, oxygenation, fluids, vasopressors, temperature and glucose control, early enteral nutrition. (3) Prevent complications — DVT prophylaxis, stress ulcer prophylaxis, early mobilisation. (4) Experimental — anti-TNF, IL-1Ra (no proven mortality benefit).
| Feature | SIRS | Sepsis |
|---|---|---|
| Definition | ≥2 SIRS criteria | SIRS + confirmed/suspected infection |
| Cause | Infectious or non-infectious | Infectious only |
| Prognosis | Depends on cause & control | Worse if untreated; risk of MODS |
An acquired clinicopathological syndrome characterised by widespread activation of the coagulation cascade, leading to intravascular fibrin deposition and microvascular thrombosis, with subsequent consumption of platelets and clotting factors — resulting in paradoxical bleeding tendency. DIC is always secondary to an underlying disorder.
Sepsis (most common — especially Gram-negative), severe trauma, burns, malignancy (APL, adenocarcinoma), obstetric catastrophes (abruptio placentae, AFE, retained dead fetus), massive transfusion reactions, liver failure.
| Parameter | Finding in DIC |
|---|---|
| Platelet count | ↓ (thrombocytopenia) |
| PT, aPTT | Prolonged |
| Fibrinogen | ↓ |
| D-dimer, FDP | ↑ (strongly suggestive) |
| Peripheral smear | Schistocytes (MAHA) |
ISTH DIC Scoring System: score ≥5 = overt DIC. No single test is diagnostic; diagnosis is clinical + combined lab evidence.
| Step | Key Points |
|---|---|
| Treat underlying cause | Sepsis → antibiotics + source control; obstetric → deliver; trauma → surgical haemostasis |
| Supportive | Haemodynamic stability; oxygenation; organ support (RRT if needed) |
| Replace factors | Platelets <50,000 with bleeding; FFP for prolonged PT/aPTT; cryoprecipitate if fibrinogen <100 mg/dL |
| Prevent thrombosis | Low-dose heparin in predominantly thrombotic DIC (malignancy, purpura fulminans) |
| Monitor | Platelets, PT/aPTT, fibrinogen, D-dimer serially |
Severe form of acute lung injury characterised by non-cardiogenic pulmonary oedema and refractory hypoxaemia. Defined by Berlin Definition (2012): acute onset (<1 week), bilateral opacities on imaging not explained by effusion/collapse/nodules, respiratory failure not fully explained by cardiac failure, and PaO₂/FiO₂ ratio on PEEP ≥5 cmH₂O.
Direct lung injury: aspiration pneumonia, lung trauma, inhalational injury. Indirect (systemic): sepsis (most common), major trauma, acute pancreatitis, burns, massive transfusion, fat embolism.
Alveolar-capillary membrane injury → ↑ permeability → protein-rich alveolar oedema → ↓ surfactant activity → alveolar collapse (atelectasis) → ↓ lung compliance, ↓ gas exchange → refractory hypoxaemia.
| Severity | PaO₂/FiO₂ (mmHg) | PEEP |
|---|---|---|
| Mild | 200–300 | ≥5 cmH₂O |
| Moderate | 100–200 | ≥5 cmH₂O |
| Severe | <100 | ≥5 cmH₂O |
Supportive care: treat underlying cause, conservative fluid management, nutritional support, avoid high FiO₂ and barotrauma. Prognosis: mortality 30–40%; better with early detection and lung-protective ventilation.
Acute Physiology and Chronic Health Evaluation II — introduced in 1985 to quantify disease severity in ICU patients and predict hospital mortality. Uses acute physiological variables, age, and chronic health status. Widely used for ICU audit, research, and outcome prediction.
1. Acute Physiology Score (APS) — based on worst values in first 24 hours of ICU admission. Twelve routine physiological variables, each scored 0–4 based on degree of derangement:
| Variable | Normal (Score = 0) | Score 4 (Worst) |
|---|---|---|
| Temperature (rectal °C) | 36–38.4 | <29.9 or >41 |
| Mean arterial pressure (mmHg) | 70–109 | <49 or >159 |
| Heart rate (/min) | 70–109 | <39 or >179 |
| Respiratory rate (/min) | 12–24 | <5 or >49 |
| Oxygenation (PaO₂ or A-a gradient) | PaO₂ >70 (room air); A-a <200 (FiO₂≥0.5) | PaO₂ <55 or A-a >500 = 4 |
| Arterial pH / HCO₃ | 7.33–7.49 | <7.15 or >7.7 |
| Serum Na⁺ (mmol/L) | 130–149 | <111 or >180 |
| Serum K⁺ (mmol/L) | 3.5–5.4 | <2.5 or >7 |
| Serum creatinine (mg/dL) | 0.6–1.4 | >3.5 (double if acute RF) |
| Haematocrit (%) | 30–45 | <20 or >60 |
| WBC (×10³/µL) | 3–14.9 | <1 or >40 |
| GCS | 15 = 0 points | Score = 15 – actual GCS |
2. Age Points: ≤44 = 0 pts; 45–54 = 2; 55–64 = 3; 65–74 = 5; ≥75 = 6.
3. Chronic Health Evaluation: Add 5 pts for nonoperative/emergency postoperative patients with severe organ insufficiency or immunosuppression; add 2 pts for elective postoperative. Conditions: NYHA IV, cirrhosis, dialysis, long-term immunosuppression.
APACHE II Score = APS + Age Points + Chronic Health Points (Range: 0–71)
| APACHE II Score | Predicted Mortality |
|---|---|
| 0–4 | ~4% |
| 5–9 | ~8% |
| 10–14 | ~15% |
| 15–19 | ~25% |
| 20–24 | ~40% |
| 25–29 | ~55% |
| 30–34 | ~75% |
| ≥35 | >85% |
Uses: ICU audit and benchmarking; research tool for comparing patient populations; prognostication for family counselling. Not for individual treatment decisions.
Limitations: Requires accurate data within 24 hrs; not applicable in burns, coronary care, or specific surgical populations; predicts group outcomes better than individual outcomes; does not account for subsequent clinical course.
A standardised system to grade the severity of postoperative complications based on the type of therapy required to correct them. Proposed by Clavien et al. (1992) and revised by Dindo et al. (2004). Ensures objective, reproducible, and comparable assessment of surgical outcomes.
Core Principle: Severity = intervention required to correct the complication — not the complication itself.
| Grade | Description | Example |
|---|---|---|
| I | Deviation from normal postoperative course; no pharmacological, surgical, endoscopic, or radiological intervention required. Allowed: antiemetics, antipyretics, analgesics, diuretics, electrolytes, physiotherapy. | Wound infection treated by bedside dressing; postoperative fever controlled by paracetamol |
| II | Requires pharmacological treatment beyond Grade I (e.g., antibiotics, TPN, blood transfusions) | UTI needing antibiotics; postoperative anaemia requiring transfusion |
| IIIa | Surgical, endoscopic, or radiological intervention — not under general anaesthesia | Drainage of abscess under local anaesthesia |
| IIIb | Surgical, endoscopic, or radiological intervention — under general anaesthesia | Reoperation for bleeding or anastomotic leak |
| IVa | Life-threatening complication — single-organ dysfunction requiring ICU | Dialysis for acute renal failure; ARDS |
| IVb | Life-threatening complication — multi-organ dysfunction requiring ICU | MODS on ventilator and inotropes |
| V | Death of the patient | Postoperative mortality |
Performance status scales quantify a patient's functional capacity, correlate with survival and therapy tolerance, and guide perioperative risk assessment.
| Grade | Description |
|---|---|
| 0 | Fully active; able to carry out all pre-disease activities without restriction |
| 1 | Restricted in physically strenuous activity but ambulatory; able to do light/sedentary work |
| 2 | Ambulatory and capable of self-care but unable to carry out work; up >50% of waking hours |
| 3 | Capable of only limited self-care; confined to bed/chair >50% of waking hours |
| 4 | Completely disabled; cannot carry on any self-care; totally confined to bed/chair |
| 5 | Dead |
| Score | Description |
|---|---|
| 100 | Normal; no complaints; no evidence of disease |
| 90 | Able to carry on normal activity; minor symptoms |
| 80 | Normal activity with effort; some symptoms |
| 70 | Cares for self; unable to carry on normal activity/work |
| 60 | Requires occasional assistance but can care for most needs |
| 50 | Requires considerable assistance and frequent medical care |
| 40 | Disabled; requires special care and assistance |
| 30 | Severely disabled; hospitalisation indicated; death not imminent |
| 20 | Very sick; hospital care necessary; active supportive treatment required |
| 10 | Moribund; fatal processes progressing rapidly |
| 0 | Dead |
| Feature | ECOG | Karnofsky |
|---|---|---|
| Range | 0–5 | 0–100 (10-point increments) |
| Simplicity | Very simple; practical for routine use | More detailed |
| Common use | Oncology trials, treatment eligibility | Palliative care, prognostication |
| Focus | Ambulatory status & self-care | Detailed functional capacity & assistance needed |
Both correlate with survival, tolerance to chemo/targeted/immunotherapy, and perioperative risk.
Definitions (Sepsis-3, 2016): Sepsis = suspected/confirmed infection + acute organ dysfunction (↑ SOFA score ≥2). Septic shock = sepsis + persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg + serum lactate >2 mmol/L after adequate fluid resuscitation.
| Domain | Recommendation |
|---|---|
| Antibiotics | ≤1 hr for septic shock; avoid unnecessary antibiotics if alternate diagnosis clear |
| Fluids | Balanced crystalloids over 0.9% NS (weak recommendation); dynamic measures preferred over static CVP |
| Vasopressors | Norepinephrine first; add vasopressin rather than escalating NE; epinephrine as next option |
| Lactate | Recheck every 2–4 hrs during resuscitation; decreasing lactate = improved perfusion |
| Corticosteroids | IV hydrocortisone only if vasopressor-dependent despite adequate fluids |
| Transfusion | Hb <7 g/dL (unless active ischaemia) |
| Monitoring targets | MAP ≥65 mmHg; urine output ≥0.5 mL/kg/hr |
A structured tool introduced by WHO (2008) as part of the Safe Surgery Saves Lives campaign. Designed to improve patient safety by ensuring adherence to essential perioperative safety practices and reducing surgical morbidity and mortality.
| Phase | When | Team | Key Checks |
|---|---|---|---|
| Sign In | Before induction of anaesthesia | Anaesthetist, Surgeon, Nurse | Patient identity, procedure, site, consent; anaesthesia machine & medications; allergy; airway risk; blood loss risk & availability of blood products |
| Time Out | Before skin incision | Entire surgical team | Team introductions; reconfirm patient/procedure/site; antibiotic prophylaxis within 60 min; anticipate critical events (surgeon: blood loss/duration; anaesthetist: patient concerns; nursing: equipment/sterility); verify imaging available |
| Sign Out | Before patient leaves OT | Surgeon, Anaesthetist, Nurse | Confirm procedure name; instrument/sponge/needle counts; specimen labelling; equipment problems; key postoperative concerns |
Defined as temperature >38.5°C on ≥2 occasions at least 4 hours apart after surgery. Temporal pattern of onset guides the differential.
| Timing | Cause | Mnemonic |
|---|---|---|
| 0–24 h (immediate) | Streptococcal/clostridial wound infection; pre-existing infection; transfusion reaction; malignant hyperthermia; drug reaction | — |
| Within 48 h | Atelectasis (most common); inflammatory response — usually non-infective | Wind |
| 3–5 days | UTI (catheter-associated) | Water |
| 5–7 days | Wound infection (cellulitis 3–4 days; suppuration 7–10 days) | Wound |
| 7–10 days | DVT/PE | Walk (thrombosis) |
| Any time | Drug fever; intra-abdominal abscess; anastomotic leak | Wonder drugs |
CBC, blood cultures (at fever peak), urine MC&S, wound swab, CXR, Doppler USG of lower limbs if DVT suspected, CT abdomen if abscess suspected.
Identify and treat underlying cause. Supportive: antipyretics, hydration, oxygenation. Specific: atelectasis → chest physiotherapy + incentive spirometry + early ambulation; UTI → remove/replace catheter + antibiotics; wound infection → drain pus + antibiotics; DVT/PE → anticoagulation + LMWH prophylaxis; drug fever → withdraw offending agent.
Temporary impairment of bowel motility after abdominal or other major surgery, in the absence of mechanical obstruction. Characterised by abdominal distension, delayed passage of flatus/stool, nausea, and intolerance to oral intake.
| Segment | Recovery |
|---|---|
| Small intestine | 12–24 h |
| Stomach | 24–48 h |
| Colon | 48–72 h |
Persistence of impaired motility beyond this timeline = pathological ileus.
Multifactorial: (1) Neurogenic inhibition — activation of inhibitory spinal reflexes from peritoneal handling. (2) Inflammatory response — macrophage activation in intestinal muscularis releases NO, prostaglandins, cytokines → suppresses smooth muscle. (3) Pharmacological suppression — opioids decrease acetylcholine release at the enteric nervous system.
Surgical: bowel handling, extensive laparotomy (vs laparoscopic), peritoneal contamination. Patient: hypokalaemia, hyponatraemia, hypomagnesaemia, severe illness, sepsis, advanced age, malnutrition. Pharmacological: opioids, anticholinergics, calcium channel blockers. Secondary causes: anastomotic leak, intra-abdominal abscess, peritonitis, acute pancreatitis, mesenteric ischaemia.
Enhanced Recovery After Surgery (ERAS) is a multimodal, evidence-based perioperative care pathway designed to minimise surgical stress response, accelerate recovery, and reduce hospital stay without increasing readmission rates.
| Phase | Key Elements |
|---|---|
| Preoperative | Patient education; carbohydrate loading (solids till 6 h, clear fluids till 2 h before anaesthesia); avoid routine bowel prep; optimise comorbidities; prehabilitation |
| Intraoperative | Short-acting anaesthetics; regional/epidural/multimodal analgesia; normothermia; goal-directed fluid therapy; laparoscopic approach preferred; no routine NG tubes or peritoneal drains; single-dose antibiotic prophylaxis; VTE prophylaxis |
| Postoperative | Early oral intake (clear liquids within 24 h); early mobilisation (POD 0–1); catheter removal within 24–48 h; multimodal opioid-sparing analgesia; glycaemic control; thromboprophylaxis; early discharge |
| Aspect | Conventional | ERAS |
|---|---|---|
| Fasting | Midnight NPO | Solids till 6 h, fluids till 2 h |
| Bowel prep | Routine | Selective only |
| NG tube/drains | Routine | Avoid unless indicated |
| Analgesia | Opioid-based | Multimodal, opioid-sparing |
| Mobilisation | Delayed | Early (POD 0–1) |
| Feeding | Delayed till bowel sounds/flatus | Early enteral within 24 h |
| Fluid therapy | Liberal | Goal-directed, restrictive |
↓ Postoperative complications (esp. ileus, infections, pulmonary complications); ↓ length of hospital stay by 2–4 days; no increase in readmission rates; cost-effective; improves patient satisfaction. ERAS Society Guidelines (2022 update, colorectal surgery) — over 20 evidence-based recommendations.
Limitations: requires multidisciplinary team adherence; variable compliance in low-resource settings; contraindicated in emergency surgery, haemodynamic instability, high-risk patients; patient compliance (especially elderly, frail). Recent Advances
Artificial assistance in maintaining adequate oxygenation and ventilation in critically ill patients unable to do so independently. May be non-invasive (mask interfaces) or invasive (endotracheal intubation with mechanical ventilation).
| Type | Modes | Indications | Contraindications |
|---|---|---|---|
| Non-invasive ventilation (NIV) | CPAP, BiPAP | COPD exacerbation, cardiogenic pulmonary oedema, mild hypoxaemic RF, post-extubation support | Cardiac/respiratory arrest, inability to protect airway, facial trauma, uncooperative patient |
| Invasive mechanical ventilation | Volume control, pressure control, SIMV, pressure support | All indications above where NIV is inadequate or contraindicated; GCS <8; post-operative ventilation for major surgery | — |
| Parameter | Standard Setting | Notes |
|---|---|---|
| Tidal volume | 6–8 mL/kg IBW (6 mL/kg in ARDS) | Low tidal volume = lung protection |
| PEEP | 5–10 cmH₂O (higher in ARDS) | Prevents alveolar collapse; improves FRC |
| Plateau pressure | ≤30 cmH₂O | Marker of static lung compliance |
| FiO₂ | Titrate to SpO₂ 92–96% | Avoid prolonged high FiO₂ (O₂ toxicity) |
| Respiratory rate | 12–20 /min | Adjust PaCO₂ accordingly |
Haemodynamic stability; FiO₂ ≤0.4 with SpO₂ ≥92%; PaO₂/FiO₂ >150–200; PEEP ≤5–8 cmH₂O; neurological recovery; able to generate inspiratory effort. Perform Spontaneous Breathing Trial (SBT) for 30–120 min. Extubate if successful.
HBOT is the intermittent inhalation of 100% oxygen at a pressure >1 atmosphere absolute (ATA), usually 2–3 ATA, inside a pressurised chamber. Results in supraphysiological oxygen delivery by increasing dissolved O₂ in plasma (Henry's law).
| Mechanism | Effect |
|---|---|
| Hyperoxygenation | PaO₂ may rise >1500 mmHg; O₂ delivery to ischaemic tissues independent of Hb |
| Neovascularisation | Promotes fibroblast proliferation, collagen synthesis, angiogenesis |
| Enhanced leukocyte killing | Oxygen-dependent phagocytosis improved |
| Oedema reduction | Vasoconstriction without compromising oxygenation |
| Toxin inhibition | Inhibits anaerobes (e.g., Clostridium perfringens), reduces α-toxin production |
| Antibiotic synergy | Synergistic with aminoglycosides, quinolones |
Protocol: 2–3 ATA; 60–120 min/session; 1–3 sessions/day; 20–40 sessions for chronic conditions. Evidence: Meta-analyses show improved healing and reduced amputation in refractory diabetic foot ulcers.
A modern operation theatre complex is a scientifically planned, functionally efficient, and aseptically safe area designed for performing surgical procedures under sterile conditions, with provisions for patient safety, infection control, and efficient workflow.
| Zone | Description | Examples |
|---|---|---|
| 1. Protective Zone | Entry zone for staff and patients; prevents outside contamination | Changing rooms, pre-op rooms, admin office, record room, sterile store |
| 2. Clean Zone | Transition zone for personnel in OT attire | Pre-operative holding area, scrub rooms, sterile store, corridors |
| 3. Aseptic Zone | Where actual operations are performed under strict asepsis | Operating theatre itself, instrument trolley area |
| 4. Disposal Zone | Removal of soiled instruments, linen, waste | Dirty utility room, soiled linen hold, waste disposal area |
Mechanical and/or pharmacological measures undertaken preoperatively to cleanse the colon of faecal content, aiming to reduce bacterial load and decrease infectious and anastomotic complications in colorectal surgery.
| Type | Agents | Aim |
|---|---|---|
| Mechanical Bowel Preparation (MBP) | Polyethylene glycol (PEG) 4 L; sodium picosulfate; lactulose. Sodium phosphate now avoided (renal/cardiac risk) | Physically empty bowel of faeces |
| Oral Antibiotic Bowel Prep (OABP) | Neomycin + Metronidazole (or Erythromycin + Neomycin) in divided doses the day before surgery. Always added to systemic IV prophylaxis. | Reduce intraluminal bacterial load (aerobic + anaerobic) |
| Combined MBP + OABP | Both regimens together | Strongest evidence; recommended by ACS and ERAS Society |
Normal arterial blood gas: pH 7.35–7.45; PaCO₂ 35–45 mmHg; HCO₃⁻ 22–26 mmol/L; Base Excess ±2 mmol/L. Four primary disorders, each with a predictable compensatory response. Compensation never fully normalises pH.
| Disorder | Primary Change | Compensation | Common Surgical Causes |
|---|---|---|---|
| Metabolic Acidosis | ↓ HCO₃⁻ (primary) | Hyperventilation → ↓ PaCO₂ (Winter's formula: PaCO₂ = 1.5×HCO₃ + 8 ± 2) | Shock, sepsis, DKA, renal failure, large-volume NS (hyperchloraemic), lactic acidosis, fistulae |
| Metabolic Alkalosis | ↑ HCO₃⁻ (primary) | Hypoventilation → ↑ PaCO₂ (expected PaCO₂ = 0.7×HCO₃ + 21 ± 2) | Prolonged vomiting (gastric outlet obstruction), nasogastric suction, diuretic excess, hypokalaemia, hyperaldosteronism |
| Respiratory Acidosis | ↑ PaCO₂ (primary) | Kidneys retain HCO₃⁻ (acute: HCO₃⁺1 per 10 ↑ PaCO₂; chronic: HCO₃⁺3.5 per 10 ↑ PaCO₂) | Post-op hypoventilation, opioid sedation, airway obstruction, COPD, pneumothorax, flail chest |
| Respiratory Alkalosis | ↓ PaCO₂ (primary) | Kidneys excrete HCO₃⁻ (acute: HCO₃⁻2 per 10 ↓ PaCO₂; chronic: HCO₃⁻5 per 10 ↓ PaCO₂) | Pain, anxiety, fever, early sepsis, pulmonary embolism, over-ventilation on MV |
Anion Gap (AG) = Na⁺ − (Cl⁻ + HCO₃⁻). Normal = 8–12 mEq/L.
| High AG Metabolic Acidosis (MUDPILES) | Normal AG Metabolic Acidosis (HARD-UP) |
|---|---|
| Methanol, Uraemia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates | Hyperchloraemia (excess NS), Addison's disease, Renal tubular acidosis, Diarrhoea, Ureteroenteric diversion, Pancreatic fistula |
Infections that develop ≥48 hours after hospital admission, not incubating at time of admission, or within 30 days of an operative procedure. (Bailey & Love, 28th ed.)
Occur in 5–10% of hospitalised patients; up to 30% in ICU patients. Major cause of morbidity, mortality, prolonged stay, and increased cost. Most common sites: urinary tract > surgical wound > respiratory tract > bloodstream.
| Site | Common Organisms |
|---|---|
| Urinary tract (CAUTI) | E. coli, Klebsiella, Enterococcus, Pseudomonas |
| Surgical wound (SSI) | S. aureus (esp. MRSA), Enterococcus, Gram-negative bacilli |
| Respiratory (VAP/HAP) | Pseudomonas, Acinetobacter, Klebsiella, S. aureus |
| Bloodstream (CRBSI) | S. epidermidis, S. aureus, Candida |
| GI (C. difficile colitis) | Clostridioides difficile |
| Letter | Principle |
|---|---|
| S | Sterilisation of instruments |
| H | Hand hygiene (single most effective measure) |
| E | Environmental cleaning |
| I | Isolation of cases |
| S | Surveillance and reporting |
| C | Catheter care |
| L | Line care |
| E | Education of staff |
| A | Antibiotic stewardship |
| N | Normothermia (perioperative) |
Identify and remove source (infected catheters, drains, debride necrotic tissue). Empirical broad-spectrum antibiotics then modify per culture sensitivity. Supportive care: fluids, nutrition, organ support. Infection control team involvement for outbreak management.
Recent Advances: Antimicrobial stewardship programs (ASP); infection control committees with surveillance; bundles (VAP bundle: head elevation, sedation holiday, oral hygiene; CAUTI bundle: aseptic insertion, early removal; SSI bundle: prophylactic antibiotics, normothermia, glucose control); alcohol-based hand rubs; chlorhexidine bathing; UV disinfection systems.
A strain of S. aureus resistant to all β-lactam antibiotics due to acquisition of the mecA gene, encoding penicillin-binding protein 2a (PBP2a) with low affinity for β-lactams.
HA-MRSA (Hospital-Acquired) — multidrug resistant; ICU, burns, postoperative, catheterised patients. CA-MRSA (Community-Acquired) — often more virulent, less resistant; "spider-bite" skin lesions characteristic.
| Site | Manifestation |
|---|---|
| Skin/Soft tissue | Abscesses, furuncles, cellulitis |
| Wounds/SSI | Purulent discharge, delayed healing |
| Lungs | Necrotising pneumonia |
| Bloodstream | Sepsis, endocarditis |
| Bone/Joint | Osteomyelitis, septic arthritis |
| Catheter-related | Bacteraemia, line sepsis |
| Infection Type | First-Line | Alternatives |
|---|---|---|
| Mild (skin/soft tissue) | Clindamycin, Doxycycline, TMP-SMX (CA-MRSA) | Linezolid (oral) |
| Severe/systemic | Vancomycin (IV) | Linezolid, Daptomycin, Teicoplanin, Ceftaroline |
| Pneumonia | Linezolid preferred | Vancomycin |
| Decolonisation | Mupirocin 2% nasal ointment BD × 5 days + Chlorhexidine body wash × 5 days | — |
Recent Advances: Ceftaroline, ceftobiprole (anti-MRSA β-lactams); dalbavancin, oritavancin (long-acting lipoglycopeptides); rapid PCR for mecA gene (gold standard) — same-day detection.
Infection occurring at or near a surgical incision within 30 days (or within 1 year if implant used) that appears related to the surgery.
Classification: Superficial (skin/subcutis); Deep (fascia/muscle); Organ-space (cavity or organ operated upon). SSIs account for 20–30% of all HAIs and ↑ hospital stay, morbidity, cost, and mortality.
| Type | Description | SSI Rate (no prophylaxis) | With Prophylaxis |
|---|---|---|---|
| Clean | No viscus opened | 1–2% | 1–2% |
| Clean-contaminated | Viscus opened, minimal spillage | 6–9% | 3% |
| Contaminated | Gross spillage; inflamed viscus | 13–20% | 6% |
| Dirty | Pus; perforation; abscess | 40% | 7% |
Preoperative: alcohol-based hand hygiene (soap for C. diff); chlorhexidine bath (night before); hair removal with clippers immediately before surgery; glycaemic control <180 mg/dL; smoking cessation ≥4 weeks; short hospital stay (↓ MRSA risk).
Antibiotic prophylaxis: indicated for clean with implant, clean-contaminated, contaminated; single IV dose at induction; repeat if >4 h duration or heavy blood loss; stop after skin closure (no postoperative doses); choice based on site and local flora (e.g., cefazolin ± metronidazole).
Intraoperative: alcohol-based chlorhexidine/povidone-iodine skin prep; minimise traffic; maintain normothermia, oxygenation, tissue perfusion; avoid dead space, haematoma, tissue trauma, unnecessary drains.
Postoperative: keep dressing clean for 24–48 hrs; hand hygiene before wound handling; early recognition (cellulitis 3–4 days; suppuration 7–10 days); audit and surveillance post-discharge.
Golden rule: Pus = Drain it.
| Step | Description |
|---|---|
| 1. Source control | Remove sutures/clips → drain pus → debride necrotic tissue |
| 2. Antibiotics | Start empirically → modify per culture/sensitivity |
| 3. Closure | Delayed primary (3–5 days) or secondary intention; dirty wounds — leave open until clean and granulating |
| 4. Supportive | Dressings, NPWT for large wounds, nutritional support |
Pneumonia occurring ≥48 hours after endotracheal intubation. Most common HAI in ICU, associated with ↑ mortality (30–50%), prolonged ventilation, and ICU stay.
Aspiration of oropharyngeal secretions around the cuff → inoculation of lower respiratory tract. Common organisms: Pseudomonas aeruginosa, Acinetobacter baumannii, Klebsiella pneumoniae, MRSA.
Fever >38°C + purulent sputum + new/progressive infiltrate on CXR + ↑ FiO₂ requirement. Confirmation: quantitative BAL culture ≥10⁴ CFU/mL (or tracheal aspirate ≥10⁵ CFU/mL).
Treatment: Empirical broad-spectrum antibiotics (carbapenem or piperacillin-tazobactam + MRSA cover if risk factors); de-escalate per BAL culture; 7–8 day course typically adequate.
Both systems aim to break the chain of infection and protect healthcare workers and patients from transmission of blood-borne and other pathogens.
| Feature | Universal Precautions | Standard Precautions (Current Standard) |
|---|---|---|
| Scope | Blood, semen, vaginal secretions, CSF, pleural/pericardial/peritoneal/synovial/amniotic fluid | All body fluids, secretions and excretions except sweat, whether or not they contain visible blood |
| Key components | Hand hygiene, PPE (gloves, gowns, masks), safe sharps handling, waste disposal, PEP after exposure | All Universal Precautions + respiratory hygiene/cough etiquette, safe injection practices, environmental cleaning, proper linen management |
| Status | Precursor system (replaced) | Current WHO-recommended infection control standard |
| Goal | Protect HCWs from blood-borne diseases | Protect both HCWs and patients from all infections |
HIV (Human Immunodeficiency Virus) — retrovirus causing progressive immunosuppression (AIDS), increasing susceptibility to opportunistic infections and malignancies. For surgeons, HIV poses a dual concern: occupational exposure risk and perioperative management of HIV-positive patients.
| Exposure Type | Estimated HIV Transmission Risk |
|---|---|
| Needle-stick injury (hollow-bore needle) | ~0.3% |
| Mucocutaneous exposure (splash to eye/mucosa) | ~0.09% |
| Intact skin exposure | Negligible |
| Scalpel injury during surgery | Variable; up to 0.3–0.5% if deep |
Risk increases with: deep injury, visible blood on device, device used in vein/artery, high viral load in source patient. For comparison: HBV ~6–30% (without vaccination); HCV ~1.8%.
Preoperative: assess opportunistic infections; check CD4 count and viral load; continue ART perioperatively; prophylactic antibiotics (higher SSI risk); optimise nutrition.
Intraoperative: full barrier precautions; minimise blood loss; avoid deep sharps injury — use blunt dissection, electrocautery, staplers.
Postoperative: meticulous wound care; higher SSI and delayed healing risk; avoid unnecessary drains or catheters.
| Aspect | Surgeon's Responsibility |
|---|---|
| Confidentiality | Patient's HIV status must remain confidential |
| Informed consent | Discuss higher infection risk and wound complications preoperatively |
| Testing | Routine HIV testing of patients is unethical without consent |
| HIV-positive surgeon | May continue non–exposure-prone procedures; must seek occupational health guidance for EPPs |