The intended purpose: to prevent or reduce surgical wound/site infection. ^[2]

Every surgical incision breaches the body's primary barrier (skin or mucosa). Bacteria can inoculate the wound during surgery. The goal of prophylactic antibiotics is to have adequate drug concentrations in the tissues at the time of bacterial contamination so that bacteria are killed before they can establish infection.

You must weigh the benefit against the risks of toxic & allergic reactions, emergence of resistant bacteria & superinfection. ^[2]

This is a risk-benefit calculation: prophylaxis is NOT free — it carries risks of adverse drug reactions, Clostridioides difficile colitis, selection of resistant organisms, and superinfection. So we only use it when the infection risk or the consequences of infection justify it.

Prophylactic use of antibiotic is indicated in: ^[2]

1. Procedures associated with high risk of infection (clean-contaminated or contaminated)
2. Procedures involving implantation of prosthetic material
3. Some procedures when infections are especially serious

Why each matters:

• Clean-contaminated/contaminated procedures have baseline infection rates of 5–20%, high enough that prevention is worthwhile
• Prosthetic implants (joint replacements, mesh, vascular grafts) create a foreign body surface where even small bacterial inocula can establish biofilm — devastating consequences if infected
• Certain "clean" surgeries where infection, though rare, would be catastrophic (e.g., cardiac surgery, neurosurgery) — the consequences justify prophylaxis even at low baseline infection risk

This is a classic exam table. The classification determines whether prophylaxis is warranted and what kind:

This is the core framework the lecture builds around, summarized on slide 16 ^[2]:

1. Select a suitable agent 2. Preoperative antibiotic within 30 min of first cut 3. Intraoperative redosing for long operations (e.g., > 4h for cefazolin) 4. No more antibiotics in the postoperative period

Let's dissect each:

The dose of antibiotic should be given within 30 minutes before first surgical incision. ^[2]

That means: on induction of anesthesia. ^[2]

Don't give it on call to OT — interval to skin incision is often longer than 2h. ^[2]

Why timing matters from first principles: The antibiotic must be in the bloodstream and distributed into tissues before bacteria are introduced at the time of incision. If given too early, drug levels may have already fallen below the MIC by the time of incision. If given too late (after incision), bacteria have already inoculated the wound without any drug present.

The lecture cites the Steinberg 2009 study ^[2] showing that SSI rates are lowest when antibiotics are given 0–30 minutes before incision. Rates increase when given > 60 minutes before or after incision.

Re-dosing (i.e., 2nd dose, intra-operative) NOT necessary for most procedures, unless duration of OT is long. ^[2]

Redosing in the OT is recommended at an interval of approximately two times the half-life of the agent in patients with normal renal function. ^[2]

Re-dosing of cefazolin is recommended at 4h, if surgery longer than that. ^[2]

The logic: Cefazolin has a T½ of 2 hours. After 2 half-lives (4 hours), the blood level has dropped to ~25% of peak. For a 1g dose starting at 180 μg/mL, that's ~45 μg/mL — still above MIC for most organisms but getting marginal. So redose at 4 hours.

Additional redosing triggers ^[4]:

• Significant blood loss > 1.5L — drug is lost with blood
• The redosing interval table from clinical practice guidelines shows agent-specific intervals ^[2]

This is perhaps the most important stewardship message of the lecture:

Longer is NOT better. Not more effective. ^[2]

No prophylactic use of postoperative antibiotics. No good evidence to support their usage (although common when audited). ^[2]

There are no data to support the continuation of antimicrobial prophylaxis until all indwelling drains are removed. ^[2]

Documented that it leads to problems, such as:

• Increase risk of drug related side effects
• Increase risk of infections; including pseudomembranous colitis, line sepsis & pneumonia ^[2]

Why does continuing antibiotics INCREASE infection risk? This seems paradoxical, but:

• Prolonged antibiotics kill normal protective flora → allows overgrowth of resistant organisms
• C. difficile thrives when competing bacteria are eliminated → pseudomembranous colitis
• IV line kept in place longer for antibiotics → increased risk of line-associated bloodstream infection
• Respiratory flora disruption → increased susceptibility to pneumonia

Cardiothoracic procedures for which a prophylaxis duration of up to 48h has been accepted without evidence to support the practice. ^[2]

This is acknowledged as an accepted deviation from best practice — even the lecturer flags it as lacking evidence.

The lecture presents a simple but critical causal chain ^[2]:

Group A Streptococcus (GAS) pharyngitis → 1–3 weeks → Acute Rheumatic Fever → years → Chronic Rheumatic Heart Disease

The mechanism: GAS antigens share molecular mimicry with cardiac tissue (myosin, valve glycoproteins). The immune response against GAS cross-reacts with heart tissue, causing carditis. Each recurrent GAS infection triggers additional immune-mediated cardiac damage, progressively worsening valvular disease.

Appropriate treatment of group A streptococcal pharyngitis prevents acute rheumatic fever in most cases. ^[2]

Group A streptococcal pharyngitis is a microbiological diagnosis. ^[2]

Why is this important? Most sore throats are viral. Treating every sore throat with antibiotics is wasteful and harmful. GAS pharyngitis must be confirmed (throat culture or rapid antigen test) before treating.

Patient with confirmed GAS pharyngitis should be treated for an entire 10-day period, even though they will likely be asymptomatic after the first few days. ^[2]

Why 10 days? Shorter courses fail to eradicate GAS from the pharynx. Persistence of GAS allows the immune response to continue → risk of rheumatic fever. The 10-day course ensures bacteriological cure, not just symptom resolution.

Treatment options:

No advantage with broad-spectrum penicillins (e.g., ampicillin or amoxicillin) or cephalosporins. ^[2]

The narrowest effective agent should be used. GAS remains universally susceptible to penicillin — no resistance has ever been documented.

Macrolide (erythromycin, clarithromycin, azithromycin) resistance common among S. pyogenes in Hong Kong. ^[2]

This is a significant local caveat — macrolide resistance in HK is 40–50% ^[5], making erythromycin an imperfect alternative. This may be tested.

Post-treatment throat cultures NOT required, EXCEPT:

• With recurring symptoms
• With history of rheumatic fever ^[2]

An individual with a previous attack of rheumatic fever in whom GAS pharyngitis develops is at high risk for a recurrent attack of rheumatic fever. ^[2]

A GAS infection need NOT be SYMPTOMATIC to trigger a recurrence — hence "recognition & treatment" is insufficient. ^[2]

This is the critical rationale for continuous prophylaxis rather than episodic treatment. Asymptomatic GAS carriage or subclinical infection can trigger recurrent rheumatic fever. You cannot rely on the patient noticing symptoms.

Prevention is achieved by continuous antimicrobial prophylaxis with a narrow spectrum penicillin. ^[2]

Secondary prevention protocol:

Individualize depending on each patient situation. ^[2]

The lecture emphasizes these considerations ^[2]:

• Risk increases with multiple previous attacks
• Risk decreases as the interval since the most recent attack lengthens
• Likelihood of acquiring GAS pharyngitis — increased exposure in children, adolescents, parents of young children, teachers, physicians, nurses, military recruits
• Consequence of recurrence — rheumatic carditis

Duration guidelines (from AHA, also in Felix Lai Pediatrics notes ^[7]):

The lecture references the 2015 AHA revised Jones criteria ^[2] for diagnosing rheumatic fever. The classic mnemonic and criteria are presented (slide 25):

Major criteria: Joint (polyarthritis), ♥ (carditis), Nodules (subcutaneous), Erythema marginatum, Sydenham chorea — "JONES"

Minor criteria: Fever, arthralgia, raised ESR/CRP, prolonged PR interval

Diagnosis: Evidence of preceding GAS infection PLUS 2 major, or 1 major + 2 minor criteria.

The lecture shows a clear pathway ^[2]:

Patient with meningitis → Droplet spread to close contacts → Carriage of bacteria in nasopharynx → BLOCK with prophylaxis → Elimination of bacterial carriage

To prevent secondary cases (sporadic case, attack rate ~0.4% among close contacts). ^[2]

Spreads by respiratory droplets, not aerosols; hence close contact required for transmission. ^[2]

This distinction is important: droplet transmission requires close proximity ( < 1 meter), whereas airborne (aerosol) transmission can spread over longer distances. Meningococcal disease is droplet, so only close contacts need PEP, not everyone in the same building.

Household & other intimate (e.g., close contact > 4h in the week before onset, kissing) contacts of patients with documented meningococcal disease. ^[2]

Medical personnel with unprotected, direct contact with oral secretions (e.g., mouth-to-mouth resuscitation, intubation). ^[2]

NOT indicated for:

• Casual contacts (brief encounters, same classroom but not close contact)
• Medical personnel who used appropriate PPE during patient contact

Start prophylaxis as soon as possible, < 24h (interval between exposure & onset of disease can be very brief). ^[2]

One dose: either oral ciprofloxacin or intramuscular ceftriaxone. ^[2]

Risk of infection: ^[2]

• Human: > 70%
• Cat bite: 50%
• Dog: < 10%
• Rodent: 2%

Why are human and cat bites higher risk than dog bites?

• Human bites involve the most virulent oral flora, often deep puncture wounds over metacarpophalangeal joints ("fight bites")
• Cat bites involve narrow, deep puncture wounds from thin sharp teeth → inoculate bacteria deep into tissues where irrigation is difficult; Pasteurella multocida is common in cat oral flora and causes rapidly progressive cellulitis
• Dog bites tend to be crush/tear injuries (broader, more accessible to irrigation) rather than deep punctures

Clean & copiously irrigate with normal saline or povidone-iodine solution with a syringe. ^[2]

Using a syringe provides pressurized irrigation to flush bacteria from deep tissues. Soaking alone is NOT adequate ^[2].

Explore for possible tendon or bone involvement, possible foreign bodies. ^[2]

May be closed if cosmetically desirable. ^[2]

Historically, bite wounds were left open due to infection risk. Current practice allows primary closure for cosmetically important areas (face) provided adequate irrigation and prophylaxis are given.

Immunization – tetanus, rabies. ^[2]

The lecture includes a tetanus prophylaxis guide ^[2]:

"Tetanus-prone" wounds include those contaminated with dirt, faeces, or saliva; punctures; burns; crush injuries; or injuries with necrotic tissue. ^[2]

Bite wounds are tetanus-prone by definition (contaminated with saliva). Management depends on immunization history:

• Fully immunized ( ≥ 3 doses, last dose < 5 years): no treatment needed
• Last dose 5–10 years: booster Td
• Incomplete or unknown: Td + tetanus immunoglobulin (TIG) for tetanus-prone wounds

The lecture shows global rabies epidemiology ^[2] and emphasizes risk assessment by WHO categories:

Key geographic knowledge ^[2]: China (especially southern provinces — Guangdong, Guangxi, Guizhou, Hunan), India, Myanmar, Philippines, Sri Lanka, Vietnam, Ethiopia, Kenya are endemic for dog-transmitted rabies.

Always a mixed infection by aerobes and anaerobes. ^[2]

Capnocytophaga canimorsus (part of oral flora in cats & dogs) — can cause rapidly fatal infections in patients without spleen (or immunosuppressed patients). ^[2]

This organism is a classic exam association: asplenic patient + dog/cat bite = Capnocytophaga canimorsus → fulminant sepsis → death. This is part of the Overwhelming Post-Splenectomy Infection (OPSI) spectrum ^[6].

Antibiotic prophylaxis, consider if: ^[2]

• Moderate to severe injury
• Involve bone or joint
• Hand or face bite
• Wound near a prosthetic joint
• Underlying disease (e.g., splenectomy)
• Present > 8 hr (Cat; human/dog ±)

Why these specific risk factors?

• Hand bites — complex anatomy with tendons, joints, tendon sheaths in close proximity; limited blood supply; infection can rapidly destroy function
• Face bites — cosmetically critical; deep structures at risk
• Near prosthetic joints — biofilm formation on prosthesis = catastrophic
• Splenectomy — lack of splenic clearance of encapsulated organisms + Capnocytophaga
• > 8 hours for cat bites — Pasteurella causes rapid cellulitis, so delayed presentation means bacteria have had time to establish

Usually either amoxicillin-clavulanate or ampicillin-sulbactam. ^[2]

Why amoxicillin-clavulanate (Augmentin)? The lecture provides an antimicrobial susceptibility table ^[2] that shows amoxicillin-clavulanate is the ONLY agent that covers ALL major bite wound pathogens:

The lecture ties bite wound management to OPSI [2, 6]. Post-splenectomy patients are at risk of fulminant infection from encapsulated organisms AND Capnocytophaga:

OPSI prevention bundle ^[6]:

1. Pre-operative vaccination: Pneumococcus, H. influenzae type b, Meningococcus, Influenza (ideally 2 weeks before elective splenectomy; within 2 weeks after emergency splenectomy)
2. Post-operative antibiotic prophylaxis: "Pill in the pocket" — standby Augmentin/amoxicillin for immediate self-treatment upon febrile illness
3. Patient education: Seek medical attention immediately for any febrile illness
4. Vaccination: Annual influenza vaccine

The lecture slide lists this as a non-surgical prophylaxis indication ^[2]. Options include [7, 8]:

• Continuous prophylaxis — cotrimoxazole or nitrofurantoin
• Post-coital prophylaxis — single dose after intercourse (for UTIs temporally related to sexual intercourse)
• Intermittent self-treatment — patient-initiated therapy for women who prefer minimal antibiotic use

While not a major focus of this lecture, the IE prophylaxis framework is frequently tested alongside this material [9, 10]:

High-risk patients requiring IE prophylaxis:

• Prosthetic heart valves / repair with prosthetic material
• Previous IE
• Unrepaired cyanotic CHD
• Repaired CHD with residual defects
• Completely repaired CHD within first 6 months after procedure

Procedures requiring IE prophylaxis:

• Dental procedures involving gingival manipulation or perforation of oral mucosa
• NOT for GI or GU procedures (solely to prevent IE)

Regimen:

• Amoxicillin 2g PO (or ampicillin IV) 30–60 min before procedure
• Clindamycin 600mg PO/IV if penicillin allergic

Related context from GI lectures [11, 12]:

• After GI bleeding in cirrhosis: IV ceftriaxone × 7 days OR PO norfloxacin BD × 7 days
• After first episode of SBP: long-term norfloxacin or ciprofloxacin (levofloxacin)
• Primary SBP prophylaxis: if ascitic fluid protein < 1.5 g/dL with impaired RFT or liver failure

1. A 55-year-old man undergoes elective total hip replacement. What is the most appropriate surgical antibiotic prophylaxis?

   • Answer: IV cefazolin 1–2g, given within 30 minutes of incision (at induction of anesthesia). Single dose unless surgery > 4 hours.

2. A 4-year-old child's classmate is diagnosed with meningococcal meningitis. The child sat next to the patient for 6 hours daily. What prophylaxis is indicated?

   • Answer: Single dose oral ciprofloxacin (adult) or IM ceftriaxone (child/pregnant). Start within 24 hours.

3. A 30-year-old woman presents 4 hours after a cat bite to her hand. Describe your management.

   • Answer: Irrigate wound with saline/povidone-iodine using syringe; explore for tendon/bone/FB; check tetanus immunization status; start amoxicillin-clavulanate prophylaxis (hand + cat bite = high-risk); consider rabies risk based on geography.

4. A 12-year-old boy had acute rheumatic fever with carditis 2 years ago. His echo now shows mitral regurgitation. How long should secondary prophylaxis continue?

   • Answer: 10 years from last attack OR until age 40 (whichever is longer); consider lifelong.

5. List the 4 classes of surgical wound classification with their infection rates and give one example of each.

6. Explain why prophylactic antibiotics should NOT be continued postoperatively. Give 3 specific complications of prolonged prophylaxis.

7. A surgeon asks you to continue IV cefazolin until the surgical drain is removed on postoperative day 3. What is your response, with evidence?

   • Markscheme: No evidence supports continuing prophylaxis until drain removal. Prolonged prophylaxis increases risk of C. difficile colitis, line sepsis, pneumonia, and antibiotic resistance. A single preoperative dose is sufficient. ^[2]

8. Distinguish between primary and secondary prevention of rheumatic fever.