Surgical site infection and sepsis

Surgical site infection

• Infection within 30 days of surgery (90 days with an implant): superficial incisional, deep incisional, or organ/space (abscess, anastomotic leak).
• *Staphylococcus aureus* is the commonest cause (including MRSA), for example after elective cholecystectomy or hernia repair; coagulase-negative staphylococci on implants; Gram-negative rods and anaerobes after bowel surgery; *Pseudomonas*, *Acinetobacter* and MRSA are the classic multiresistant wound organisms.
• Usually appears on days 5–7: pain, redness, swelling, discharge, fever.
• Wound classes and infection risk: clean (under 2%), clean-contaminated (under 10%), contaminated (15–20%), dirty (over 30%).
• Risk factors: diabetes, obesity, smoking, malnutrition, steroids, extremes of age, remote infection, long pre-operative stay, MRSA carriage; long operations, hypothermia, hypoxia, razor shaving, haematoma, dead space, foreign material, emergency surgery, mistimed prophylaxis.
• Prevention bundle and why it works:

Abscesses and wound problems

• "Where there is pus, let it out": open the wound or drain the collection, culture the pus, wash out and leave to heal by secondary intention (or negative pressure); antibiotics for cellulitis or systemic upset.
• Left shift: band forms and toxic granulation on day 5 after an anterior resection mean the marrow is releasing immature neutrophils in response to infection (steroids raise neutrophils without a left shift). Look for a leak or collection.
• Pelvic abscess (a week after perforated appendicitis or a pelvic operation): swinging fever, diarrhoea with mucus and tenesmus, a tender, boggy anterior rectal wall on rectal examination. It often drains into the rectum or is drained under imaging.
• The organism in foul pelvic or abdominal pus with pale Gram-negative rods that grow only anaerobically is *Bacteroides fragilis*; it resists aminoglycosides, which need oxygen-dependent transport to enter bacteria; metronidazole covers it.
• Burst abdomen (wound dehiscence): around day 7–10, especially in malnourished patients with peritonitis, a gush of pink serous fluid from the wound after coughing warns that the fascia has separated. Reassure, cover with moist sterile packs and return to theatre.
• Pyomyositis: a deep, hard, very tender muscle swelling (often thigh) with fever and normal overlying skin, in young men in hot climates; *S. aureus*; diagnose with ultrasound and drain.
• Liver abscess: pyogenic abscesses are mostly from biliary disease, with *E. coli* the commonest organism (*Klebsiella* in many Asian series); a single abscess with anchovy-sauce pus and negative stools is amoebic, confirmed by *E. histolytica* serology.
• Actinomyces: jaw abscesses with sinuses and yellow sulphur granules (branching Gram-positive filaments); tubo-ovarian abscess with a long-standing IUCD.
• Brodie abscess: a subacute osteomyelitis in the tibial metaphysis of a teenager: months of dull night pain, a well-defined lucency with a sclerotic rim. Sacral pressure ulcer with exposed bone and foul discharge: suspect osteomyelitis.
• Recurrent leg cellulitis: look for and treat toe-web tinea, the portal of entry. In burns, *Pseudomonas* is the classic bacterium and *Candida* the classic fungus after long antibiotics.
• Spread of infection, anatomy questions: a boil in the nasal vestibule or upper lip (the danger area) can spread through the facial and ophthalmic veins to the cavernous sinus; draining an abscess in the posterior triangle of the neck endangers the spinal accessory nerve, so the patient cannot shrug or raise the arm above the head (trapezius).
• Wound healing: macrophages are the essential coordinating cell; fibroblasts dominate the proliferative phase and lay down collagen.

Necrotising and toxin-mediated infections

• Necrotising fasciitis: infection spreading along fascia; pain out of proportion, tense oedema, bullae, necrosis, crepitus, toxicity, low sodium. Type I polymicrobial (diabetes, perineum: Fournier gangrene); type II group A streptococcus. Urgent radical debridement, broad IV antibiotics with clindamycin (stops toxin synthesis), ICU, repeat debridement.
• Progressive bacterial synergistic gangrene (Meleney): slowly spreading ulcer around a suture weeks after surgery, from microaerophilic streptococci with *S. aureus*.
• Gas gangrene (*C. perfringens*): crepitus, bronze skin; debridement, penicillin plus clindamycin.
• Toxic shock syndrome after nasal packing or tampons: fever, hypotension, sunburn-like rash, diarrhoea, multi-organ failure, negative blood cultures; peeling of palms 1–2 weeks later. TSST-1 is a superantigen: it links MHC class II on antigen-presenting cells directly to the T-cell receptor outside the antigen groove, activating up to a fifth of all T cells and causing a cytokine storm. Remove the pack, give antibiotics including clindamycin.
• Puerperal sepsis: *Streptococcus pyogenes* (group A) causes the most severe, rapidly fatal form.
• Tetanus: toxin enters motor nerve endings at the wound and travels by retrograde axonal transport to the spinal cord, where it blocks glycine and GABA release from inhibitory interneurons. Antitoxin neutralises only unbound toxin. Prophylaxis: full primary course with last dose over 10 years ago (over 5 years for a dirty, tetanus-prone wound): toxoid booster plus wound care; incomplete or unknown course: add tetanus immunoglobulin.

Sepsis and septic shock

• Sepsis: life-threatening organ dysfunction from a dysregulated response to infection (SOFA rise of 2 or more). Septic shock: vasopressors needed to keep MAP at 65 mmHg or more and lactate over 2 mmol/L despite fluids.
• How Gram-negative shock starts: LPS (lipid A) binds LBP and CD14, then TLR4 on macrophages, activating NF-κB: TNF-α and IL-1 (the early mediators), IL-6, and inducible nitric oxide synthase.
• Why the peripheries are warm: nitric oxide from iNOS relaxes vascular smooth muscle, causing profound vasodilatation and low systemic vascular resistance; cardiac output initially rises (warm or distributive shock). Warm peripheries do not mean adequate perfusion. Late shock adds myocardial depression and capillary leak.
• Sites: lungs are the commonest source overall, then abdomen and urinary tract; the urinary tract is the commonest source of Gram-negative bacteraemia, with *E. coli* the leading organism.
• Screening: qSOFA (RR 22 or more, altered mentation, systolic BP 100 or less), NEWS2 5 or more.
• Sepsis Six within one hour: oxygen, blood cultures before antibiotics, IV antibiotics, IV fluid bolus, lactate and Hb, urine output monitoring.
• Source control: drain abscesses, remove infected lines, debride, laparotomy for leaks, decompress obstructed bile ducts (ERCP) or kidneys (nephrostomy). Noradrenaline for persistent hypotension; hydrocortisone in refractory shock.
• Neutropenic patients: pus and consolidation need neutrophils, so signs are blunted; treat fever as infection.

Post-operative fever by day

Sterilisation and asepsis in theatre

• Asepsis keeps organisms out (sterile field); antisepsis kills them on living tissue; sterilisation kills everything including spores.
• Moist heat (autoclave) kills by coagulating and denaturing proteins: 121 °C at 15 psi for 15 minutes, or 134 °C for 3 minutes. Dry heat (hot air oven, 160 °C for 2 hours) kills by oxidation of cell components and needs higher temperatures and longer times.
• Boiling is not sterilisation: 100 °C for 20 minutes kills vegetative bacteria but spores survive, because their calcium dipicolinate core resists heat. Instruments must also be cleaned of blood first.
• Ethylene oxide for heat-sensitive plastics (then aeration), gamma irradiation for single-use items, hydrogen peroxide plasma, and glutaraldehyde or peracetic acid for high-level disinfection of endoscopes. Theatre floors and walls after any case, including HIV or hepatitis, are cleaned with hypochlorite.
• Checks: *Geobacillus stearothermophilus* spores (biological), Bowie–Dick test (air removal), autoclave tape (exposure only). Prions need disposal or extended cycles.
• Universal precautions: all blood is potentially infectious; double gloving, eye protection, neutral-zone passing of sharps, staff hepatitis B vaccination, prompt post-exposure care.

Remember Pus needs drainage, dead tissue needs debridement, and septic shock needs antibiotics and source control within the hour.

Exam trap Boiling is disinfection, not sterilisation: spores survive.

Exam trap Warm peripheries in septic shock come from nitric oxide vasodilatation; they do not mean good perfusion.

How FCPS asks about this

• Commonest wound infection organism: *S. aureus*; wound infection appears on days 5–7.
• Gram-negative septic shock: LPS binds TLR4 on macrophages; vasodilatation from iNOS nitric oxide.
• Toxic shock after nasal packing: superantigen linking MHC II to the T-cell receptor.
• Pelvic abscess after appendicectomy: mucus diarrhoea, boggy anterior rectal wall; *Bacteroides fragilis* resists aminoglycosides.
• Pink serous discharge on day 7: impending burst abdomen.
• Sterilisation: dry heat kills by oxidation, moist heat by protein coagulation; boiling leaves spores alive.
• Tetanus: toxin reaches the cord by retrograde axonal transport; booster for a full course with last dose over 10 years ago (over 5 years for a dirty wound).