Surgical infection, SSI, sepsis and antibiotic prophylaxis

Overview

Infection, above all surgical site infection (SSI), remains one of the main complications of surgery and trauma. It delays healing, prolongs stay, can cause wound dehiscence, incisional hernia, prosthesis loss and death. Prevention rests on asepsis, antisepsis, good technique, a healthy host and correctly timed prophylactic antibiotics.

Koch's postulates (organism found in every case, grown in culture, reproduces the disease in a healthy host and recovered again) define a causal organism, but not every organism can be cultured (e.g. Mycobacterium leprae).

Common surgical pathogens

Why does a wound become infected?

Infection = organisms invading tissue after breakdown of local and systemic defences (cellulitis, lymphangitis, abscess or bacteraemia).

Sources: endogenous (patient's own flora, by far the commonest) or exogenous (theatre air, instruments, staff hands: hospital-acquired infection).

Determinants:

1. Host response
2. Virulence and size of inoculum
3. Blood supply and health of the tissue (local ischaemia, shock)
4. Dead tissue, haematoma, dead space, foreign material (sutures, drains, prostheses)
5. Whether antibiotics are present during the decisive period

Risk factors for SSI

Classification of SSI

• Superficial incisional (skin and subcutaneous tissue): the commonest.
• Deep incisional (fascia and muscle).
• Organ/space (e.g. pelvic abscess after an anastomotic leak).
• Surveillance (CDC) runs for 30 days, or 1 year after hip or knee implants. Many SSIs present after discharge.
• Major SSI: much pus, needs a procedure to drain it, or systemically unwell, delayed discharge. Grading systems: Southampton and ASEPSIS.

Wound contamination classes and SSI rates

Prevention

Before surgery

• Short preoperative stay; treat remote infection; optimise diabetes and nutrition; stop smoking.
• Hair removal: only if needed, by clipping in theatre just before surgery. Shaving the night before can double SSI in clean surgery.
• MRSA screening and decolonisation where policy requires.

In theatre

• Surgical scrub with chlorhexidine or povidone-iodine, including the nails.
• Skin preparation: one application of alcohol-based antiseptic (over 95% fall in skin bacteria). Do not let alcohol pool, as diathermy can ignite it.
• Minimal staff numbers and movement; laminar air flow for implant surgery.
• Gentle tissue handling, haemostasis, no dead space.
• Keep the patient warm and give supplemental oxygen: both reduce SSI.
• No good evidence that drains, adhesive incise drapes or wound guards reduce SSI.

Antibiotic prophylaxis

• Indicated: clean-contaminated and contaminated surgery; clean surgery with a prosthesis (joint replacement, mesh, vascular graft) because infection would be catastrophic.
• Not routinely needed: clean surgery without implants.
• Dirty wounds (or incision into an abscess): this is treatment, usually a 5-day course.
• Timing: single IV dose at induction, so tissue levels peak at incision.
• Repeat during surgery about every 4 hours in long operations, after major blood loss or unexpected contamination.
• No benefit from continuing doses after surgery; it promotes resistance and C. difficile.
• Choice: cover expected organisms, follow local policy (e.g. a cephalosporin or co-amoxiclav, plus metronidazole for bowel; a glycopeptide where MRSA risk is high).
• Patients with valve disease or prostheses may need cover for procedures causing bacteraemia, as per current guidance.

Local infections

Abscess

• Localised pus (dead neutrophils, bacteria, debris), usually S. aureus, walled off by granulation tissue.
• Classic signs: calor, rubor, dolor, tumor, loss of function; fluctuation.

• Postoperative abscesses take about 7–10 days to form; a swinging fever suggests a deep collection.
• Treatment: drainage (incision or image-guided aspiration). Leave the cavity open to heal by secondary intention; antibiotics are not needed if pus drains well, but are needed if the cavity is closed or there is cellulitis or systemic sepsis.
• Partly treated with antibiotics → antibioma (sterile, firm mass).
• Chronic abscess, sinus or fistula: think of TB, actinomycosis, foreign body, or retained loculi.

Cellulitis and lymphangitis

• Non-suppurative, poorly localised spreading infection; streptococci (commonly), staphylococci, clostridia.
• Systemic upset is common but blood cultures often negative.
• Lymphangitis: red streaks along lymphatics with tender nodes.
• Treat with antibiotics (penicillin-based, plus anti-staphylococcal cover), rest and elevation.

Gas gangrene

• C. perfringens: Gram-positive, anaerobic, spore-forming; in soil and faeces.
• Risk: dirty, devitalised wounds (war, high-velocity missiles, crush), diabetics, amputation for ischaemia.
• Features: severe pain, crepitus and gas on X-ray, thin brown sweet-smelling discharge, rapid toxaemia. Toxins include alpha toxin (lecithinase), collagenase, hyaluronidase.
• Treatment: resuscitation, radical debridement (amputation if needed), high-dose IV benzylpenicillin (with broader cover); prophylaxis for amputations of dead limbs.

Necrotising fasciitis (synergistic spreading gangrene)

• Not clostridial: mixed aerobes and anaerobes in synergy (coliforms, staphylococci, Bacteroides, anaerobic streptococci); type caused by S. pyogenes alone may give toxic shock.
• Abdominal wall: Meleney's synergistic gangrene. Scrotum and perineum: Fournier's gangrene.
• Usually in diabetics or the immunocompromised; trigger may be trivial.
• Clues: pain out of proportion, oedema beyond the redness, blistering, crepitus, grey "dishwater" discharge, skin necrosis (late), shock.
• The deep spread is always wider than the skin suggests.
• Treatment: resuscitate, broad-spectrum IV antibiotics, and urgent radical debridement with repeated looks; skin grafting later.

Tetanus

• C. tetani: anaerobic, Gram-positive, terminal ("drumstick") spores in soil and manure; entry wound may be trivial.
• Exotoxin tetanospasmin travels up nerves and blocks inhibitory transmission in the spinal cord: trismus (lockjaw), risus sardonicus, opisthotonus, spasms, respiratory failure. A short incubation means a worse prognosis.
• Treatment: wound debridement, human tetanus immunoglobulin, benzylpenicillin or metronidazole, sedation and relaxants, ventilation in severe cases.
• Prevention: tetanus toxoid (active immunity). A tetanus-prone wound (late presentation, devitalised tissue, soil contamination) in a patient not fully immunised also needs immunoglobulin (passive). Follow the current national schedule.

Systemic infection

Bacteraemia

Uncommon after superficial SSI; common after deep infection such as anastomotic leak, instrumenting infected bile or urine, or infected cannulas. Dangerous if a prosthesis is present.

SIRS, sepsis and MODS

Gut failure with starvation allows Gram-negative bacteria to colonise and translocate to mesenteric nodes, releasing endotoxin (lipopolysaccharide) that drives cytokines (IL-6, TNFα).

Newer international definitions (Sepsis-3) describe sepsis as life-threatening organ dysfunction from a dysregulated response to infection, and septic shock as sepsis needing vasopressors to keep MAP at 65 mmHg or more with lactate above 2 mmol/L despite fluids. Check the current guideline in use.

Management principles: resuscitate (oxygen, fluids, vasopressors), take cultures before antibiotics where this causes no delay, start empirical broad-spectrum IV antibiotics promptly, and achieve source control (drain pus, remove dead tissue, control leaks, remove infected lines).

Blood-borne viruses and the surgeon

• Hepatitis B (vaccinate all surgeons; know your antibody status), hepatitis C, HIV.
• Universal precautions: eye protection or face shield, waterproof gowns, double gloving, boots not clogs, essential staff only, pass sharps in a dish, careful technique.
• Needle-stick: commonest on the non-dominant index finger; hollow needles carry the highest risk. Wash under running water, encourage bleeding, report, and seek occupational health for post-exposure prophylaxis and testing.

Treating established SSI

• Remove sutures to release pus, curette, leave open; send pus (not just a swab) for culture and Gram stain.
• Antibiotics for spreading cellulitis, systemic signs or bacteraemia: empirical first, then by sensitivities.
• Heavily contaminated wounds: delayed primary or secondary closure.
• Topical antiseptics only briefly; they slow epithelialisation.

Quick revision

• Most SSIs are endogenous; S. aureus is the commonest SSI organism.
• Decisive period up to 4 hours; prophylaxis IV at induction, redose about 4-hourly in long cases.
• Prophylaxis for clean-contaminated, contaminated and implant surgery; dirty wounds get treatment courses.
• SSI without prophylaxis: clean 1–2%, clean-contaminated 6–9%, contaminated 13–20%, dirty about 40%.
• Clip hair in theatre; keep warm; give oxygen; meticulous technique.
• Abscess: drain; antibiotics only if closed, cellulitis or systemic sepsis.
• Gas gangrene: C. perfringens, crepitus, sweet smell; debride plus penicillin.
• Necrotising fasciitis: polymicrobial, diabetics, pain out of proportion; urgent debridement.
• Tetanus: toxoid for prevention; immunoglobulin for tetanus-prone wounds in the non-immune.
• SIRS: 2 of temperature, pulse, RR, WCC criteria; sepsis = infection with organ dysfunction.

Written by The House Job from standard references (Bailey & Love's Short Practice of Surgery, 27th edition).

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