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// ══════════════════════════════════════════════════════════════════════════════
//  SLIDES
// ══════════════════════════════════════════════════════════════════════════════

// 1. TITLE SLIDE
titleSlide(
  "Surgical Site Infection (SSI)",
  "Pathophysiology • Classification • Prevention • Management"
);

// 2. AGENDA
contentSlide("Agenda / Overview", [
  "Definition and epidemiology of SSI",
  "Wound classification (CDC) & NNIS risk score",
  "Microbiology: key causative organisms",
  "Pathophysiology & host defence",
  "Risk factors for SSI",
  "The decisive period",
  "Classification: Superficial, Deep & Organ-Space",
  "Major vs Minor SSI",
  "Prevention strategies",
  "Surgical site preparation",
  "Antibiotic prophylaxis",
  "Management & treatment",
  "SSI, SIRS, MODS – the continuum",
]);

// 3. SECTION: DEFINITION & EPIDEMIOLOGY
sectionSlide("Definition & Epidemiology", "📋");

// 4. Definition
contentSlide("Definition of SSI", [
  "SSI = invasion of organisms into tissues after breakdown of local and systemic host defences",
  "Leads to cellulitis, lymphangitis, abscess formation, or bacteraemia",
  "One of four main hospital-acquired infections (HAIs)",
  { head: "4 Main HAI Groups:", sub: ["Respiratory infections (incl. ventilator-associated pneumonia)", "Urinary tract infections (mostly catheter-related)", "Bacteraemia (indwelling vascular catheters)", "Surgical site infections (SSIs)"] },
]);

// 5. SSI Categories
contentSlide("SSI Categories (CDC / NHSN)", [
  { head: "Superficial SSI (SSSI)", sub: ["Infection confined to skin and subcutaneous tissue of the incision", "Most common form"] },
  { head: "Deep SSI", sub: ["Infection in the deeper musculo-fascial layers of the incision"] },
  { head: "Organ / Space SSI", sub: ["Involves any part of the anatomy opened or manipulated during surgery", "Example: abdominal abscess after anastomotic leak", "Example: pelvic abscess after perforated appendicitis"] },
]);

// 6. SECTION: WOUND CLASSIFICATION
sectionSlide("Wound Classification & Risk Scoring", "🏷️");

// 7. CDC Wound Classification
tableSlide("CDC Surgical Wound Classification", [
  [
    { text: "Class", options: { bold: true, color: C.white, fill: C.darkBg, fontSize: 13 } },
    { text: "Category", options: { bold: true, color: C.white, fill: C.darkBg, fontSize: 13 } },
    { text: "Description", options: { bold: true, color: C.white, fill: C.darkBg, fontSize: 13 } },
  ],
  [
    { text: "I", options: { bold: true, color: C.accentBlue, fill: "E8F5FF" } },
    { text: "Clean", options: { fill: "E8F5FF" } },
    { text: "Uninfected wound; no inflammation; respiratory/GI/GU tracts not entered; primarily closed", options: { fill: "E8F5FF" } },
  ],
  [
    { text: "II", options: { bold: true, color: "1B8A44", fill: "E8F9EF" } },
    { text: "Clean-contaminated", options: { fill: "E8F9EF" } },
    { text: "GI/GU/respiratory tracts entered under controlled conditions without unusual contamination", options: { fill: "E8F9EF" } },
  ],
  [
    { text: "III", options: { bold: true, color: C.amber, fill: "FFFDE7" } },
    { text: "Contaminated", options: { fill: "FFFDE7" } },
    { text: "Open fresh traumatic wounds; major breaks in sterile technique; gross spillage from GI tract", options: { fill: "FFFDE7" } },
  ],
  [
    { text: "IV", options: { bold: true, color: C.red, fill: "FFEBEE" } },
    { text: "Dirty", options: { fill: "FFEBEE" } },
    { text: "Old traumatic wounds; devitalised tissue; pre-existing clinical infection or perforated viscera", options: { fill: "FFEBEE" } },
  ],
], [0.6, 1.6, 7.2]);

// 8. NNIS Risk Score
contentSlide("NNIS Risk Score for SSI Prediction", [
  "NNIS = National Nosocomial Infections Surveillance score",
  "Established to recognise effectiveness of infection surveillance in reducing SSIs",
  "Score ranges from 0 (lowest risk) to 3 (highest risk)",
  { head: "1 point allocated for each of:", sub: [
    "Contaminated or dirty wound (Class III or IV)",
    "ASA score ≥ 3",
    "Operative time > 75th percentile for the procedure",
  ]},
  "Higher NNIS score = higher probability of SSI",
]);

// 9. SECTION: MICROBIOLOGY
sectionSlide("Microbiology of SSI", "🦠");

// 10. Key Organisms
contentSlide("Key Causative Organisms", [
  { head: "Staphylococcus aureus (incl. MRSA)", sub: ["Most common skin commensal causing SSI", "Coagulase-positive; produces exotoxins, haemolysins, protein A", "MRSA: methicillin-resistant – treat with vancomycin / teicoplanin"] },
  { head: "Coagulase-negative Staphylococci", sub: ["Staph. epidermidis – skin commensal, infects prostheses", "Increasing resistance to antibiotics"] },
  { head: "Streptococcus pyogenes (Group A)", sub: ["Causes erysipelas, cellulitis, necrotising fasciitis", "Sensitive to penicillin"] },
], { fontSize: 14 });

// 11. Gram-negative & Anaerobes
contentSlide("Gram-Negative Bacilli & Anaerobes", [
  { head: "Aerobic Gram-negative bacilli", sub: [
    "E. coli, Klebsiella – lactose fermenting; normal large-bowel flora",
    "Act in synergy with Bacteroides → SSI after bowel ops",
    "ESBLs: increasing resistance to cephalosporins",
    "Pseudomonas – colonises burns, tracheostomy wounds; treat with aminoglycosides/quinolones",
  ]},
  { head: "Bacteroides fragilis", sub: [
    "Strict anaerobe from large bowel, vagina, oropharynx",
    "Synergistic with Gram-negatives → intra-abdominal abscesses",
    "Sensitive to metronidazole, some cephalosporins",
  ]},
  { head: "Clostridium perfringens", sub: [
    "Causes gas gangrene; produces hyaluronidase, lecithinase, haemolysin",
    "Anaerobic / necrotic conditions essential",
  ]},
], { fontSize: 13 });

// 12. SECTION: PATHOPHYSIOLOGY
sectionSlide("Pathophysiology & Host Defence", "🔬");

// 13. Host defence overview
contentSlide("Host Defence Mechanisms Against SSI", [
  "Body harbours ~10¹⁴ organisms; skin & mucosal barriers are the first line",
  { head: "Non-specific (innate) defences:", sub: [
    "Physical: intact skin, mucous membranes",
    "Chemical: lysozyme, gastric acid, bile, complement",
    "Cellular: phagocytes, macrophages, PMNs, killer lymphocytes",
  ]},
  { head: "Specific (adaptive) immunity:", sub: [
    "Humoral: antibody-mediated responses",
    "Cell-mediated: T-lymphocyte responses",
  ]},
  "ALL these mechanisms may be compromised by surgical intervention and treatment",
]);

// 14. Pathogen factors
contentSlide("Pathogen & Inoculum Factors", [
  "Chance of SSI determined by: pathogenicity of organisms + size of bacterial inoculum",
  "More virulent organism or larger bacterial contamination → higher SSI risk",
  "Even less virulent organisms cause SSI if host response is impaired",
  { head: "Poor surgical technique increases risk:", sub: [
    "Devitalised tissue",
    "Excessive dead space",
    "Haematoma formation",
    "Foreign material: sutures, drains, prostheses",
  ]},
  "Pathogens resist host defences by releasing toxins that favour spread (enhanced in anaerobic / necrotic tissue)",
]);

// 15. SECTION: RISK FACTORS
sectionSlide("Risk Factors for SSI", "⚠️");

// 16. Risk factors two-column
contentSlide("Risk Factors for Increased SSI Risk", [
  "Malnutrition (obesity or weight loss)",
  "Metabolic disease: diabetes, uraemia, jaundice",
  "Immunosuppression: cancer, AIDS, steroids, chemo, radiotherapy",
  "Poor perfusion: systemic shock or local ischaemia",
], {
  twoCol: true,
  col2: [
    "Colonisation / bacterial translocation from GI tract",
    "Foreign body material (sutures, drains, mesh)",
    "Poor surgical technique: dead space, haematoma, devitalised tissue",
    "Contaminated / dirty wound class",
  ],
  fontSize: 15,
});

// 17. Reduced resistance detail
contentSlide("Factors That Impair Host Resistance", [
  { head: "Malnutrition", sub: ["Low or high BMI weakens host response", "Impairs inflammatory response"] },
  { head: "Metabolic diseases", sub: ["Diabetes mellitus, uraemia, jaundice", "Disseminated malignancy, AIDS"] },
  { head: "Iatrogenic immunosuppression", sub: ["Radiotherapy, chemotherapy", "Drugs: steroids, methotrexate"] },
  { head: "GI colonisation & translocation", sub: [
    "Suspension of enteral feeding → aerobic Gram-negative bacilli colonise upper GI",
    "Especially with cancer, immunosuppression, shock or sepsis",
  ]},
], { fontSize: 14 });

// 18. SECTION: THE DECISIVE PERIOD
sectionSlide("The Decisive Period", "⏱️");

// 19. Decisive period
contentSlide("The Decisive Period – Key Concept", [
  "Up to 4-hour interval before bacterial growth becomes established enough to cause infection",
  "Starts from the moment of tissue breach (trauma or surgery)",
  "Strategies aimed at preventing infection become INEFFECTIVE after this window",
  "Prophylactic antibiotics must be given to COVER this period",
  { head: "Antibiotic tissue levels during contamination should be:", sub: [
    "Above the MIC90 (minimum inhibitory concentration) for expected pathogens",
    "Timing: ideally at induction of anaesthesia",
    "Re-dosing required for prolonged operations",
  ]},
  "Understanding the decisive period guides all infection prevention strategy",
]);

// 20. SECTION: PRESENTATION
sectionSlide("Clinical Presentation of SSI", "🩺");

// 21. Major vs Minor SSI
contentSlide("Major vs Minor SSI", [
  { head: "Major SSI", sub: [
    "Discharges significant quantities of pus spontaneously OR",
    "Requires secondary procedure to drain it",
    "Systemic signs: tachycardia, pyrexia, raised WCC",
    "Delayed return home / prolonged hospital stay",
  ]},
  { head: "Minor SSI", sub: [
    "May discharge pus or infected serous fluid",
    "Not associated with excessive discomfort",
    "No significant systemic signs",
    "No delay in return home",
    "Often settles spontaneously without antibiotics",
  ]},
], { fontSize: 14 });

// 22. Localised SSI forms
contentSlide("Localised Wound Infection – Abscess", [
  "Celsus' cardinal signs: calor (heat), rubor (redness), dolor (pain), tumor (swelling)",
  "Plus: functio laesa – loss of function",
  "Usually follows puncture wound or surgery; can be metastatic after bacteraemia",
  "Pyogenic organisms (predominantly S. aureus) → tissue necrosis and suppuration",
  "Pus = dead and dying WBCs (predominantly neutrophils) killed by bacterial toxins",
  "Abscess wall = fibrinous exudate + oedema + cells of acute inflammation",
  "Later: granulation tissue (macrophages, fibroblasts, new vessels) surrounds the process",
]);

// 23. Cellulitis & lymphangitis
contentSlide("Cellulitis & Lymphangitis", [
  "Non-suppurative, poorly localised infection of skin and soft tissue",
  "Commonly caused by streptococci, staphylococci or clostridia",
  "Systemic signs (toxaemia): chills, fever, rigors – from toxin-mediated cytokine release",
  "Blood cultures often NEGATIVE despite systemic signs",
  { head: "Lymphangitis:", sub: [
    "Painful red streaks in affected lymphatics draining the source of infection",
    "Accompanied by painful regional lymph nodes (cervical / axillary / inguinal)",
  ]},
]);

// 24. Specific infections
contentSlide("Specific Local Wound Infections", [
  { head: "Gas Gangrene (Clostridium perfringens)", sub: [
    "Gram-positive anaerobic spore-bearing bacilli from soil and faeces",
    "Risk: immunocompromised, diabetic, malignant disease, necrotic/foreign-material wounds",
    "Military wounds: high-velocity missiles create devascularised tissue",
    "Presentation: severe wound pain, crepitus, thin brown sweet-smelling exudate",
    "Spreading oedema and gangrene; circulatory collapse if untreated",
    "Treatment: large-dose IV penicillin + aggressive debridement; consider hyperbaric O₂",
  ]},
], { fontSize: 14 });

// 25. SECTION: SSI → SIRS → MODS
sectionSlide("SSI → SIRS → MODS Continuum", "📈");

// 26. SIRS Table
tableSlide("SIRS, Sepsis & MODS – Definitions (Bailey & Love)", [
  [
    { text: "Condition", options: { bold: true, color: C.white, fill: C.darkBg } },
    { text: "Definition / Criteria", options: { bold: true, color: C.white, fill: C.darkBg } },
  ],
  [
    { text: "SIRS", options: { bold: true, color: C.red, fill: "FFEBEE" } },
    { text: "≥2 of: Temp >38°C or <36°C; HR >90/min or RR >20/min; WCC >12 or <4 ×10⁹/L", options: { fill: "FFEBEE" } },
  ],
  [
    { text: "Sepsis", options: { bold: true, color: C.amber, fill: "FFFDE7" } },
    { text: "SIRS + documented source of infection", options: { fill: "FFFDE7" } },
  ],
  [
    { text: "Severe Sepsis", options: { bold: true, color: "E65100", fill: "FFF3E0" } },
    { text: "Sepsis + evidence of failure of ≥1 organ (ARDS, septic shock, ARF, hepatic failure, coagulopathy, encephalopathy)", options: { fill: "FFF3E0" } },
  ],
  [
    { text: "MODS", options: { bold: true, color: C.red, fill: "FFEBEE" } },
    { text: "Multiple organ dysfunction – the systemic effect of SIRS; mediated by IL-1, TNF-α; may progress to MSOF", options: { fill: "FFEBEE" } },
  ],
  [
    { text: "Quick definition", options: { bold: true, color: C.accentBlue, fill: "EDF2F7" } },
    { text: "SSI = infected wound/organ space | SIRS = body's systemic response | MODS = systemic effect of SIRS", options: { fill: "EDF2F7" } },
  ],
], [1.8, 7.6]);

// 27. SIRS Pathophysiology
contentSlide("SIRS Pathophysiology", [
  "Lipopolysaccharide endotoxin from dying Gram-negative bacilli stimulates macrophage cytokine release",
  "Pro-inflammatory cytokines: IL-1 and TNF-α drive the inflammatory cascade",
  "Activated neutrophils adhere to endothelium → chemotaxis → respiratory burst",
  "Respiratory burst releases lysosomal enzymes, oxidants and free radicals → kills bacteria BUT damages adjacent cells",
  "If excessive: activated neutrophils damage vascular endothelium in remote organs",
  "Increased vascular permeability → cellular damage → organ dysfunction (MODS)",
  "Progression: MODS → MSOF (multiple system organ failure) – respiratory, cardiac, renal, liver, bowel, circulatory",
  "Vicious cycle: more organs fail → further immunosuppression → death despite ICU support",
], { fontSize: 14 });

// 28. SECTION: PREVENTION
sectionSlide("Prevention of SSI", "🛡️");

// 29. Surgical site preparation
contentSlide("Surgical Site Preparation", [
  { head: "Removal of metals & foreign bodies", sub: [
    "Piercings, rings → nidus for infection",
    "Metallic objects → thermal injury with diathermy",
    "Rings → digital vascular compromise if postop oedema",
  ]},
  { head: "Hair removal", sub: [
    "Only when hair interferes with the operation",
    "Hair removal causes microabrasions → risk of cellulitis and SSI",
    "Ideal timing: on the operating table AFTER prophylactic antibiotic given",
    "Preoperative removal outside the OR is discouraged",
    "Method: skin clippers with disposable blades preferred (fewest SSIs); razor blades discouraged",
  ]},
], { fontSize: 13 });

// 30. Skin antisepsis
contentSlide("Skin Antisepsis & Draping", [
  "Skin antisepsis removes transient organisms and dirt → prevents SSI",
  "WHO recommends: chlorhexidine-alcohol solution",
  "Clinical difference between povidone-iodine and chlorhexidine is marginal",
  "Any alcohol-based antiseptic solution is acceptable",
  "Apply antiseptic to extension incisions, additional incision sites and drain placement areas",
  { head: "Draping:", sub: [
    "Sterile drapes isolate the operative field",
    "Plastic adhesive (iodophor-impregnated) drapes may be used over skin",
  ]},
  "Avoid shaving; clipping immediately preop is the safest approach",
]);

// 31. Prevention summary
contentSlide("SSI Prevention – Core Strategies", [
  "Correct wound class identification and appropriate prophylaxis",
  "Antibiotic prophylaxis timed to the decisive period (at induction)",
  "Re-dosing for prolonged operations (>3–4 h)",
  "Optimise modifiable host factors: glycaemic control, nutritional support, stop smoking",
  "Meticulous surgical technique: avoid dead space, haematoma, devitalised tissue",
  "Minimise use of drains and foreign material",
  "Maintain normothermia and oxygenation intraoperatively",
  "Surveillance of SSI rates to drive quality improvement (NNIS methodology)",
], { fontSize: 14 });

// 32. Antibiotic prophylaxis
contentSlide("Antibiotic Prophylaxis Principles", [
  "Aim: achieve tissue antibiotic levels above MIC90 during the decisive period",
  "Give at induction of anaesthesia (not hours before, not after incision)",
  { head: "Choice based on expected organisms:", sub: [
    "Clean procedures: cover Gram-positive cocci (e.g. co-amoxiclav, cefazolin)",
    "Colorectal: cover Gram-negatives + anaerobes (e.g. metronidazole + cephalosporin)",
    "MRSA-risk patients: consider vancomycin / teicoplanin",
  ]},
  "Single dose is usually sufficient for most elective surgery",
  "Prolonged prophylaxis → antibiotic resistance and Clostridioides difficile risk",
  "Bowel preparation: mechanical cleansing + purgatives/enemas reduces contamination risk",
]);

// 33. SECTION: MANAGEMENT
sectionSlide("Management of Established SSI", "💊");

// 34. Management
contentSlide("Management of Established SSI", [
  { head: "Minor SSI:", sub: [
    "Often settles spontaneously without antibiotics",
    "Wound opening / drainage if localised pus",
    "Regular dressings",
  ]},
  { head: "Major SSI:", sub: [
    "Secondary procedure to drain pus (incision and drainage)",
    "Wound swab for culture and sensitivity",
    "Systemic antibiotics once pus/spreading infection identified",
    "Wound infection needs antibiotics only when progressive/spreading with systemic signs",
  ]},
  { head: "Specific organisms:", sub: [
    "MRSA: vancomycin or teicoplanin",
    "Gram-negative (Pseudomonas): aminoglycosides, quinolones, carbapenems (e.g. meropenem)",
    "Anaerobes: metronidazole",
    "Gas gangrene: high-dose IV penicillin + aggressive debridement ± hyperbaric O₂",
  ]},
], { fontSize: 13 });

// 35. Negative pressure wound therapy
contentSlide("Adjuncts: Negative Pressure Wound Therapy", [
  "Negative pressure wound therapy (NPWT) / vacuum-assisted closure (VAC)",
  "Single-use negative pressure dressing (SUNPD) studied in emergency laparotomy (RCT evidence)",
  "May reduce SSI rates after high-risk and emergency laparotomy",
  { head: "Wound edge protection devices:", sub: [
    "ROSSINI Trial: multicentre RCT – wound edge protectors evaluated after laparotomy",
    "Evidence base continues to evolve",
  ]},
  "Mechanical bowel preparation + oral antibiotics (colorectal): reduce intraoperative contamination and SSI risk",
]);

// 36. SECTION: KEY SUMMARY
sectionSlide("Key Summary Points", "📝");

// 37. Summary
contentSlide("Key Take-Home Points", [
  "SSI is classified as superficial, deep, or organ-space – each with distinct management",
  "Wound class (I–IV) and NNIS score guide prophylaxis and risk stratification",
  "The decisive period (≤4 hours) is the window in which prophylaxis is effective",
  "Host factors (nutrition, metabolic disease, immunosuppression) determine SSI susceptibility",
  "Antibiotic prophylaxis must be given at induction, tailored to expected organisms",
  "Surgical technique is the single most modifiable intraoperative risk factor",
  "Major SSI requires active drainage ± systemic antibiotics; minor often resolves conservatively",
  "Untreated / progressive SSI → SIRS → MODS → MSOF – a potentially fatal cascade",
  "Surveillance (NNIS methodology) is fundamental to SSI reduction programmes",
]);

// 38. THANK YOU
titleSlide(
  "Thank You",
  "Based on Bailey & Love's Short Practice of Surgery, 28th Edition – Chapter 5 & Related Sections"
);

// ── WRITE FILE ───────────────────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/ssi-presentation/SSI_Bailey_Love_28e.pptx" })
  .then(() => console.log("✅  Presentation saved."))
  .catch(err => { console.error("❌ Error:", err); process.exit(1); });