---

Note: Bailey & Love's Short Practice of Surgery (28th edition) is not available in the medical library. The following comprehensive account is drawn from the two most authoritative surgical texts in the library — Current Surgical Therapy, 14th edition (Sheridan & Goverman; Lee, Barie & Houng) and Sabiston Textbook of Surgery — which cover identical content and principles used in Bailey & Love.

---

Burn Management — Full Detail

1. Classification of Burns

By Cause (Sabiston Box 43.2)

By Depth

---

2. Pathophysiology

Jackson's Zones of Burn Injury

• Zone of Coagulation — central zone of irreversible cell death; protein denaturation and coagulative necrosis at the point of maximum thermal damage.
• Zone of Stasis — surrounds the coagulation zone; moderate initial insult with vascular damage and vessel leakage. This zone is salvageable if tissue perfusion is maintained; inadequate resuscitation or infection converts it to coagulation necrosis. This is the key target of early resuscitation.
• Zone of Hyperemia — outermost zone; vasodilation from inflammation; clearly viable tissue; forms the basis for healing.

Local Changes

• Burns >280°F (flame) → Maillard-type reaction → leathery, charred eschar
• Burns <280°F (scalds) → necrosis without charring → can be confused with partial-thickness burns

• Water: 0.61 W/m/°C
• Hot cooking oil: 4.2 J/g/°C (higher conductivity → deeper injury)
• Grease: 1.8 J/g/°C

Systemic Changes

• Hypodynamic state — reduced cardiac output, reduced peripheral perfusion, hypotension
• Driven by hypovolemia, hypothermia, and neurohormonal response
• NOT primarily infection

• Hyperdynamic state — tachycardia, increased cardiac output, peripheral vasodilation, elevated body temperature, muscle catabolism
• Mimics sepsis physiology — distinguishing from infection is a core daily clinical task
• Persists until wound closure
• Driven by sustained elevation of catecholamines, glucocorticoids, and glucagon → increased gluconeogenesis, glycogenolysis, proteolysis, insulin resistance, peripheral lipolysis

---

3. Initial Assessment

Primary Survey (ATLS Framework)

• Assess for inhalation injury: singed nasal hairs, carbonaceous sputum, hoarseness, stridor, facial burns, enclosed-space fire exposure
• Early intubation if any sign of airway compromise — edema develops rapidly in the first hours
• Upper airway injury: direct thermal/chemical injury
• Lower airway injury (inhalation injury below the glottis): chemical toxins in smoke → tracheobronchitis, mucosal sloughing, bronchospasm
• CO poisoning: cherry-red skin, headache, confusion; treat with 100% O₂ (reduces CO half-life from 250 min to 60 min); cyanide poisoning (combustion of synthetic materials)

• Circumferential full-thickness chest burns → restrict chest expansion → escharotomy needed
• Assess respiratory rate, oxygen saturation, ABG

• Establish two large-bore IV lines (peripheral preferred; avoid burned areas if possible)
• Assess for circumferential limb burns → compartment syndrome → escharotomy ± fasciotomy
• Insert Foley catheter (target urine output)
• Cardiac monitoring (especially electrical burns — arrhythmias)

• GCS, neurological status
• Significant neurologic deficit after electrical burns requires urgent imaging

• Remove all clothing and jewelry
• Prevent hypothermia (burn patients lose heat rapidly)

---

4. Estimating Burn Size (% TBSA)

Rule of Nines (Adults)

---

5. Fluid Resuscitation

Parkland Formula (Adults)

4 mL × kg × % TBSA burned — using Lactated Ringer's (LR)

• First 8 hours from time of injury: give half the calculated volume
• Next 16 hours: give remaining half
• Second 24 hours: colloid (albumin 0.3–0.5 mL/kg/% TBSA) + 5% dextrose for insensible losses

Target: Urine Output

• Adults: 0.5–1.0 mL/kg/hr
• Children: 1.0 mL/kg/hr
• Electrical burns with myoglobinuria/hemoglobinuria: 1–2 mL/kg/hr (maintain until urine clears)

Pediatric Formulas

Fluid Creep

• Over-resuscitation = "fluid creep" → pulmonary edema, abdominal compartment syndrome, extremity compartment syndromes, cerebral edema
• Resuscitation guided by clinical endpoints, not blind formula adherence
• Colloid supplementation (albumin) reduces total crystalloid volume needed

---

6. Burn Wound Assessment

Wound Depth Assessment Tools

• Clinical assessment — remains primary method; accuracy ~70% for experienced surgeons
• Laser Doppler imaging — measures blood flow in dermis; helps differentiate superficial vs. deep partial-thickness burns; reduces unnecessary surgery
• Wound biopsy — histological depth assessment; not routinely used

---

7. Burn Center Referral Criteria (ABA)

1. Partial-thickness burns >10% TBSA
2. Burns involving face, hands, feet, genitalia, perineum, or crossing major joints
3. Any full-thickness burn
4. Electrical burns (including lightning)
5. Chemical burns
6. Inhalation injury
7. Preexisting medical conditions complicating management
8. Concomitant trauma where burn poses greater risk to life
9. Burned children in hospitals without pediatric-qualified personnel/equipment
10. Burns requiring specialized social, emotional, or rehabilitative intervention

---

8. Operative Management of Burn Wounds

When to Operate

• Superficial partial-thickness (<14 days expected healing): non-operative — dressings and topical agents
• Deep partial-thickness (expected healing >21 days): early excision and grafting
• Full-thickness: always requires excision and grafting
• Rule of thumb: any wound unlikely to heal within 3 weeks requires surgery

Tangential Excision

• Serial slicing of burned tissue with a Watson or Goulian knife until viable, bleeding tissue is reached
• Performed early (within 48–72 hours to 5 days of injury) — reduces infection, shortens hospital stay, improves outcomes
• Blood loss is significant — estimated 100–250 mL per 1% TBSA excised; careful hemostasis with topical thrombin, electrocautery, epinephrine-soaked dressings

Fascial Excision

• Used for very deep full-thickness or high-voltage electrical burns
• Excise down to fascia — less blood loss than tangential excision
• Results in significant cosmetic deformity (loss of subcutaneous contour); reserved for massive or life-threatening burns

Skin Grafting

• Harvested from donor sites using a dermatome (0.008–0.016 inch thickness)
• Meshing (1:1.5 to 1:4, occasionally 1:6) — expands graft coverage, allows fluid egress
• Meshing ratio affects cosmesis — unmeshed grafts for face/hands; wider mesh for trunk (cosmesis less critical)
• Graft take requires: adequate wound bed (no eschar/infection), immobilization, good hemostasis

• Heals by re-epithelialization in 10–14 days
• Covered with semi-occlusive dressings (Xeroform, Mepitel)
• Donor site pain often worse than graft site

• Biologic temporary wound coverage
• Allograft vascularizes temporarily before rejection (7–10 days)
• Used as "bridges" when autograft donor sites are insufficient in massive burns

• Patient's own keratinocytes expanded in laboratory (3–4 weeks)
• Used when donor sites are severely limited (>60–70% TBSA burns)
• Fragile — prone to shear injury and blistering

• Integra (bovine collagen + chondroitin sulfate matrix): applied first; neodermis forms over 3–6 weeks; then thin autograft applied on top
• Useful for deep burns over joints (face, hands) — improves functional and aesthetic outcomes
• Alloderm, Matriderm — similar biological scaffolds

Escharotomy

• Indicated for circumferential full-thickness burns
• Limbs: medial and lateral longitudinal incisions through the eschar down to subcutaneous fat; extend across joints; may need to include hand escharotomy (mid-axial incisions on digits)
• Chest: bilateral anterior axillary line incisions with transverse connecting incision — releases chest wall restriction, improves ventilation
• Timing: perform if compartment pressure >30 mmHg OR clinical signs (diminished/absent distal pulses, capillary refill >2 sec, pallor, paresthesias, paralysis, pain on passive stretch)
• Fasciotomy may also be needed, especially after electrical burns

---

9. Topical Agents and Wound Dressings

Traditional Antimicrobial Topicals

Modern Wound Dressings (largely replacing topicals)

• Silver-impregnated dressings (Mepilex Ag, Aquacel Ag, Acticoat): sustained silver release; fewer dressing changes; improved healing times
• Mepitel One / Biobrane: semi-occlusive; for superficial partial-thickness burns; promotes healing without daily changes
• Biological dressings (allograft/xenograft): temporary coverage for large wounds
• Negative pressure wound therapy (NPWT/VAC): over grafted wounds to immobilize graft and promote take, especially in difficult anatomical locations

---

10. Inhalation Injury

Three Components

1. Supraglottic thermal injury: direct heat damage to upper airway → edema → airway obstruction (hours)
2. Subglottic chemical injury: toxic combustion products (acrolein, HCl, NO₂, aldehydes) injure tracheobronchial mucosa → bronchospasm, mucosal sloughing, ARDS
3. Systemic toxins: CO, cyanide poisoning

Management

• Early intubation if any suspicion (do not wait for stridor — edema can make intubation impossible)
• CO poisoning: 100% O₂ via non-rebreather mask (or via ETT if intubated); HBO therapy for severe cases (carboxyhemoglobin >25%, neurological symptoms, cardiac involvement)
• Bronchoscopy: diagnostic and therapeutic — remove carbonaceous plugs, assess mucosal injury
• Nebulized treatments: N-acetylcysteine, heparin (to reduce cast formation), salbutamol (bronchospasm)
• Ventilatory support: lung-protective strategy (low tidal volume 6 mL/kg IBW, permissive hypercapnia)
• Inhalation injury significantly increases fluid resuscitation requirements (add 2–4 mL/kg/% TBSA in some formulas)
• Cyanide poisoning: hydroxocobalamin (Cyanokit) — drug of choice

---

11. Special Burns

Electrical Burns

• Low-voltage (<1000 V): local tissue destruction at entry/exit points; cardiac arrhythmias (monitor 24h)
• High-voltage (>1000 V): massive deep tissue destruction (muscle, nerve, vessel) with often deceptively small skin wounds; myoglobinuria → renal failure; compartment syndrome; rhabdomyolysis; spinal cord injury; cataracts
• Management: aggressive fluid resuscitation targeting urine output 1–2 mL/kg/hr until urine clears; serial CK levels; ECG; early escharotomy/fasciotomy; amputation sometimes required

Chemical Burns

• Acid burns: coagulative necrosis — self-limiting as eschar forms barrier
• Alkali burns: liquefactive necrosis — continues to penetrate deeply (more dangerous)
• Management: immediate and prolonged water irrigation (minimum 30 minutes; DO NOT use neutralising agents — exothermic reaction); specific antidotes: HF burns → 2.5% calcium gluconate gel; white phosphorus → submerse in water, remove particles under water

Cold Burns (Frostbite)

• Rewarming in 40–42°C water bath for 15–30 minutes
• Avoid premature debridement — demarcation takes weeks
• Iloprost (prostacyclin analogue) for severe cases

Radiation Burns

• Latent period before symptoms; depth depends on radiation type
• Management: similar principles; often combined with systemic radiation toxicity

---

12. Medical Management of the Burn Patient

Analgesia and Sedation

• Burn pain is severe and often undertreated
• Multimodal analgesia: opioids (background + procedural boluses), NSAIDs, ketamine (procedural), gabapentin/pregabalin (neuropathic component)
• Procedural pain: ketamine (0.5–1 mg/kg IV) is particularly effective; inhaled methoxyflurane
• Anxiolytics and psychological support essential

Infection Control

• Burn wound sepsis is the leading cause of death in burn patients
• Signs: fever (difficult to interpret in burns — hyperdynamic state mimics sepsis), wound appearance change, conversion of partial to full-thickness, cellulitis
• Burn wound biopsy: >10⁵ organisms/gram tissue = wound infection
• Common pathogens: Staphylococcus aureus (early), Pseudomonas aeruginosa, Acinetobacter (late)
• No prophylactic systemic antibiotics — treat proven infections
• Antifungal prophylaxis: consider in patients on prolonged antibiotics, >20% TBSA, ICU >7 days

Nutrition

• Early enteral feeding (within 6 hours of admission) — reduces translocation, maintains gut barrier integrity
• Route: nasogastric or post-pyloric tube
• Energy requirements significantly elevated — use indirect calorimetry where possible; formulas (Toronto, Curreri) overestimate
• Protein requirements: 1.5–2.0 g/kg/day (higher in major burns)
• Avoid parenteral nutrition unless enteral route truly not feasible
• Insulin infusion for hyperglycemia (glucose <180 mg/dL)
• Oxandrolone (anabolic steroid): reduces catabolism and muscle wasting; improves lean body mass in children and adults
• Propranolol: reduces hypermetabolic response, heart rate, and muscle catabolism; widely used in pediatric burns

DVT Prophylaxis

• High risk for VTE — immobility, hypercoagulable state, indwelling catheters
• Pharmacological prophylaxis (LMWH/UFH) as soon as hemostasis allows
• Mechanical prophylaxis (SCDs) to all unaffected limbs

Tetanus Prophylaxis

• All burn patients require tetanus prophylaxis assessment
• Toxoid ± immunoglobulin depending on immunization history

Stress Ulcer Prophylaxis (Curling's Ulcer)

• Major burns are a high-risk indication for stress ulcers
• H₂ blockers or PPI; early enteral feeding also protective

---

13. Critical Care of the Burn Patient

Unique Burn-Specific Critical Care Issues

• Hypothermia: burn patients lose heat rapidly through open wounds; keep room temperature 28–33°C (warm environment), warm IV fluids, forced air warming
• Altered pharmacokinetics: increased volume of distribution, altered protein binding, enhanced renal clearance — drug dosing is complex
• Airway management: regular reassessment — edema increases for first 48–72h; early tracheostomy in major burns (>40% TBSA or prolonged ventilation expected)
• Compartment syndrome: abdomen (monitor bladder pressures), extremities, orbit
• Renal failure: common; maintain adequate resuscitation; avoid nephrotoxins
• Anemia: blood loss from surgery, hemodilution, reduced RBC half-life; transfusion trigger ~7 g/dL in stable patients
• Coagulopathy: dilutional, consumptive; replace products as guided by TEG/ROTEM

---

14. Scar Management

Risk Factors for Hypertrophic Scar (Box 3, Current Surgical Therapy)

• Deep partial and full-thickness burns
• Burns crossing joints
• Prolonged healing (>3 weeks)
• Infection
• Pigmented skin (higher risk)
• Children and young adults
• Anatomical location (face, chest, flexor surfaces)

Management of Burn Scar

• Pressure garments: worn 23 hours/day for up to 2 years; mainstay of scar management
• Silicone gel sheets: reduce scar thickness and erythema
• Physiotherapy and splinting: prevent contractures; maintain range of motion; serial casting
• Intralesional corticosteroids (triamcinolone): for hypertrophic scars/keloids
• Laser therapy (pulsed dye laser, CO₂ fractional laser): improve texture, erythema, pliability
• Surgical scar revision: contracture release; Z-plasties; local flaps; skin grafting
• Scar maturation takes 18–24 months; surgical revision deferred until scar is mature unless function is compromised

---

15. Rehabilitation

• Positioning: splints and positioning to prevent contracture from day 1 (e.g., neck extension, anti-claw hand position, ankle dorsiflexion)
• Early mobilization: ambulation as soon as physiologically stable
• Occupational therapy: hand function, ADLs
• Psychological support: PTSD is common; body image issues; peer support groups
• Social work: return to work/school planning, financial support, home modification
• Nutritional rehabilitation: extended after discharge

---

Summary Table: Key Formulas

---

---

Management of Infective Endocarditis

Harrison's Principles of Internal Medicine, 22nd Edition (2025)

---

Overview

1. Microbiological identification
2. Antimicrobial therapy (organism- and situation-specific)
3. Management of complications
4. Surgical decision-making
5. Prevention

---

Classification

---

Etiology

---

Diagnosis — Duke Criteria

Major Criteria

1. Positive blood cultures for typical IE organisms:
   • S. aureus, viridans streptococci, S. gallolyticus, HACEK, Enterococcus (in ≥2 separate cultures)
   • Persistently positive blood cultures (≥2 drawn >12h apart; or all 3, or majority of ≥4 drawn over ≥1h)
   • Single positive for Coxiella burnetii (phase I IgG ≥1:800)
2. Imaging criteria (echocardiography or CT/nuclear imaging):
   • Vegetation on valve, supporting structures, or implanted material
   • Abscess, pseudoaneurysm, intracardiac fistula
   • New valvular regurgitation
   • New dehiscence of prosthetic valve
   • Abnormal activity around valve implant on PET-CT or radiolabelled WBC SPECT/CT (in PVE >3 months)
   • Paravalvular lesions on CT (PVE)

Minor Criteria

1. Predisposing heart condition or injection drug use
2. Fever ≥38°C
3. Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
4. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, positive rheumatoid factor
5. Microbiological evidence not meeting major criteria

Definite IE: 2 major, or 1 major + 3 minor, or 5 minor

Possible IE: 1 major + 1 minor, or 3 minor

---

Investigations

• Blood cultures: 3 sets from 3 separate venepuncture sites over ≥1 hour before starting antibiotics
• Echocardiography:
  • Transthoracic echocardiogram (TTE): first-line; sensitivity ~60–75% for NVE, lower for PVE
  • Transoesophageal echocardiogram (TEE): sensitivity 85–95%; preferred when TTE non-diagnostic, in PVE, intracardiac devices, and when complications suspected
  • Repeat TEE at 7–10 days if initial negative but IE still suspected
• CT cardiac: excellent for perivalvular extension, abscesses, fistulae; recommended in all cases pre-surgery
• PET-CT (¹⁸F-FDG): for PVE and CIED-IE; detects metabolic activity around prosthetic material
• FBC: anaemia, leukocytosis
• ESR, CRP: elevated; track response
• Renal function, urinalysis: renal emboli, immune complex GN
• Chest X-ray: pulmonary emboli (right-sided IE), heart failure
• 12-lead ECG: new PR prolongation = aortic root abscess until proven otherwise
• MRI brain: in neurological complications (emboli, abscesses)
• Dental evaluation: source of bacteraemia; concurrent dental disease common

---

Antimicrobial Therapy

General Principles

• Bactericidal agents in high doses for prolonged courses — minimum 4–6 weeks for most cases
• IV route preferred (ensures adequate serum bactericidal levels)
• Time from diagnosis to antibiotic initiation: take 3 blood culture sets first, then start antibiotics immediately (do not delay >1–2 hours in unstable patients)
• Serum trough/peak levels for vancomycin (target AUC/MIC 400–600) and aminoglycosides
• Daily reassessment: fever curve, blood cultures, echo findings, embolic events

---

Empirical Therapy (Before Culture Results)

---

Definitive Antibiotic Regimens (Harrison's Table 133-A)

Penicillin-Susceptible Streptococci (MIC ≤0.12 μg/mL)

PVE: use 6-week regimens. Avoid 2-week regimen in PVE, complicated IE, or when aminoglycoside toxicity risk is high.

---

Relatively Penicillin-Resistant Streptococci (MIC 0.12–0.5 μg/mL)

---

Fully Penicillin-Resistant Streptococci + Nutritionally Variant Streptococci (Granulicatella, Abiotrophia, Gemella) (MIC ≥0.5 μg/mL)

---

Enterococci (Enterococcus faecalis and E. faecium)

---

Staphylococci — Native Valves

Do NOT use rifampicin for NVE staphylococcal disease — no benefit and risk of resistance. Daptomycin is inactivated by pulmonary surfactant — avoid if pulmonary involvement (right-sided IE with septic emboli).

---

Staphylococci — Prosthetic Valves (PVE)

Rifampicin is essential in PVE — penetrates biofilm on prosthetic material; only start after blood cultures are negative (to prevent emergence of rifampicin resistance).

---

HACEK Organisms

---

Culture-Negative IE

---

Fungal IE

Fungal IE almost universally requires surgical valve replacement — antifungal therapy alone rarely curative.

---

Oral / Outpatient Therapy

• Amoxicillin (viridans strep, E. faecalis susceptible to ampicillin)
• Ciprofloxacin or levofloxacin (HACEK)
• The POET trial supports oral step-down after initial stabilization in left-sided IE caused by streptococci, S. aureus, enterococci, or HACEK

---

Management of Complications

1. Heart Failure (Most Common Indication for Surgery)

• Mechanism: valvular destruction → acute severe regurgitation; valve obstruction by large vegetation; perivalvular abscess
• Urgent/emergency surgery indicated for:
  • Acute severe aortic or mitral regurgitation causing pulmonary oedema or cardiogenic shock
  • Valve obstruction causing heart failure
  • Fistula into cardiac chamber or pericardium
• Moderate HF from valvular regurgitation: surgery within days (urgent)
• Mild HF responsive to medical treatment: may defer surgery to elective timing during antibiotic course

2. Perivalvular Extension (Abscess, Pseudoaneurysm, Fistula)

• Complicates 10–40% of cases; more common in aortic IE and PVE
• Signs: new PR interval prolongation on ECG (aortic root abscess eroding into conduction system), persistent bacteraemia despite appropriate therapy
• Detected by TEE (best) or CT
• Surgery almost always required
• High risk of recurrence if treated medically alone

3. Uncontrolled Infection

• Persisting positive blood cultures or fever after 5–7 days of appropriate antibiotic therapy
• Infection by fungi, or highly resistant organisms (VRE, MRSA with suboptimal response)
• Persistent bacteraemia with S. aureus, MRSA
• Culture-negative PVE (suspect fungal or unusual organisms)
• Enlarging vegetation on serial echocardiography

4. Systemic Emboli

• Occur in 22–50% of IE cases; cerebral most clinically significant
• Risk is highest in first 2 weeks; drops dramatically after 2 weeks of antibiotics
• Large vegetations (>10 mm) on anterior mitral leaflet = highest embolic risk
• Mitral valve IE embolic risk > aortic valve IE
• Surgery to prevent embolism is indicated when: vegetation >10 mm + ≥1 embolic event despite antibiotics; or vegetation >15 mm (even without prior embolism) in cases with low operative risk

5. Neurological Complications

• Embolic stroke, TIA, cerebral abscess, mycotic aneurysm, meningitis, encephalopathy
• MRI brain in all patients with neurological symptoms
• Mycotic aneurysm: cerebral angiography (CT or conventional); treat medically (antibiotics), intervene if enlarging or ruptured
• After ischaemic stroke: cardiac surgery not contraindicated if stroke is non-haemorrhagic and neurological deficit is not severe; defer ≥72h; defer ≥4 weeks after haemorrhagic stroke
• Anticoagulation: discontinue in IE patients with haemorrhagic stroke; continue with care in those with mechanical valves and ischaemic stroke

6. Mycotic Aneurysms

• Form where septic emboli seed arterial walls
• Most common in intracranial arteries; also mesenteric, splenic, iliac
• Detected by CT/MR or conventional angiography
• Non-haemorrhagic: continue antibiotics; repeat imaging in 6–8 weeks — if enlarging, treat surgically/endovascularly
• Ruptured: neurosurgical/endovascular emergency

7. Renal Failure

• Multiple mechanisms: immune-complex GN, septic renal emboli, drug nephrotoxicity (aminoglycosides, vancomycin), haemodynamic compromise
• Adjust antibiotic dosing to renal function
• Avoid aminoglycosides if creatinine clearance <30 mL/min (or use once-daily dosing with careful drug level monitoring)

8. Splenic Abscess

• Complicates ~5% of IE
• CT-guided aspiration or laparoscopic splenectomy
• Should be treated before cardiac surgery if possible

---

Surgical Management

General Indications for Surgery During Active IE (Harrison's Table 133-3)

• Acute AR or MR with haemodynamic compromise (cardiogenic shock, pulmonary oedema not responsive to medical therapy)
• Rupture of sinus of Valsalva into right heart
• Fistula into cardiac chamber or pericardium

• Valve dysfunction causing persistent heart failure or haemodynamic compromise
• Uncontrolled local infection: perivalvular extension, abscess, false aneurysm, fistula
• PVE caused by S. aureus, fungi, or highly resistant organisms
• Recurrent embolism or enlarging vegetation despite antibiotics
• Vegetation >10 mm + embolic event, or >15 mm (even without embolism)

• Progressive aortic or mitral regurgitation (moderate–severe) without haemodynamic compromise
• PVE caused by streptococci or enterococci that respond to antibiotics
• Vegetation >10 mm on mitral valve (high embolic risk)

Key Surgical Principles

• Infected tissue must be fully debrided — bactericidal concentrations do not penetrate vegetation adequately
• Duration of antibiotics before surgery: patients may proceed to surgery after as little as 24–72 hours of antibiotics if indication is urgent — do not delay life-saving surgery to "complete" antibiotic course
• Post-operatively: antibiotics restarted using the same IV regimen; total post-operative duration:
  • Blood cultures negative at time of surgery → complete pre-operative course (count from first negative culture)
  • Blood cultures positive at time of surgery → restart full treatment course post-op (6 weeks from date of surgery)
• Valve selection: biological vs. mechanical prosthesis — similar reinfection rates; decision based on standard cardiac surgical principles

---

Right-Sided IE (IVDU)

• Predominantly tricuspid valve; S. aureus commonest pathogen
• Septic pulmonary emboli, pneumonia, pleuritic chest pain, haemoptysis, multifocal pulmonary infiltrates
• Prognosis generally better than left-sided IE
• Medical therapy preferred where possible:
  • MSSA tricuspid IE: Nafcillin × 2 weeks (uncomplicated; no left-sided involvement, no metastatic infection, no renal failure, vegetation <20 mm)
• Surgery reserved for: large tricuspid vegetations causing recurrent septic emboli, right heart failure from severe TR, failure of medical therapy, fungal IE
• Valve repair preferred over replacement in IVDU (risk of reinfection of new prosthesis from ongoing drug use)

---

Prosthetic Valve Endocarditis (PVE)

• Early PVE (<60 days): hospital-acquired, S. epidermidis, S. aureus, GNRs, fungi; very high mortality
• Intermediate PVE (60 days–1 year): similar to early PVE
• Late PVE (>1 year): community-acquired; microbiology similar to NVE
• TEE essential — TTE insensitive for paravalvular complications
• Surgery more often required than for NVE — perivalvular extension, valve dysfunction, persistent infection
• All PVE caused by S. aureus, fungi, or resistant organisms → surgery strongly recommended
• Rifampicin added for all staphylococcal PVE (after cultures negative to prevent resistance)

---

Cardiovascular Device-Related IE (CIED-IE)

• Pacemakers, ICDs, CRT devices
• Diagnosis: TEE + nuclear imaging (PET-CT or SPECT)
• Management:
  • Complete device removal (all leads + generator) is required for definitive cure — even if only generator pocket infection initially
  • Percutaneous lead extraction preferred if leads in place <1 year; surgery for leads >1 year or large vegetations on leads (>2 cm)
  • Prolonged antibiotics (4–6 weeks) following device removal
  • Reimplantation: delay until blood cultures have been negative for ≥72 hours (ideally ≥14 days)
  • Contralateral site preferred for new device

---

Monitoring Response to Therapy

• Blood cultures every 24–48 hours until negative
• Daily temperature, clinical assessment
• Repeat TEE at week 1–2 (assess vegetations, new complications), and if clinical deterioration
• Weekly CBC, CMP, drug levels (vancomycin AUC/MIC, aminoglycoside peaks/troughs)
• PR interval on daily ECG — monitor for aortic root abscess
• Target: clinical improvement + blood culture clearance by 5–7 days

---

Outpatient Parenteral Antibiotic Therapy (OPAT)

• Most appropriate for streptococcal NVE (once-daily ceftriaxone)
• Requires: reliable PICC/Hickman, weekly labs, daily nursing contact, clear instructions for when to return
• NOT appropriate for: S. aureus IE (first 2 weeks minimum), active HF, renal impairment requiring dose adjustment, high-risk features

---

Prophylaxis

AHA/ESC Current Guidance

• Prosthetic heart valves (including TAVR/TAVI)
• Previous IE
• Congenital heart disease:
  • Unrepaired cyanotic CHD (including palliative shunts/conduits)
  • Repaired CHD with prosthetic material or device within 6 months of repair
  • Repaired CHD with residual defects at or adjacent to site of prosthetic patch/device
• Cardiac transplant recipients who develop valvulopathy

• Dental procedures involving manipulation of gingival tissue, periapical region of teeth, or perforation of oral mucosa
• (NOT routine dental cleaning, anaesthetic injections through non-infected tissue, X-rays)
• Non-dental: gastrointestinal/genitourinary procedures only if established infection present (not routine procedures)

---

IE in Special Populations

Injection Drug Users (IVDU)

• Right-sided predominance (S. aureus)
• Polymicrobial, Pseudomonas, fungi possible
• High recurrence risk with ongoing drug use
• Addiction medicine consultation, harm reduction, and opioid use disorder (OUD) treatment integral to care
• Ethical controversies around surgical reoperation in active IVDU — multidisciplinary ethical + clinical discussion

Pregnancy

• IE in pregnancy is rare but carries high maternal and fetal mortality
• Avoid aminoglycosides (fetal ototoxicity) — use alternative regimens
• Penicillins and cephalosporins generally safe
• Surgery (if required) in second trimester preferred

Elderly

• Degenerative valve disease is the leading predisposition
• Higher rates of enterococcal and S. aureus IE
• Increased drug toxicity risk (aminoglycosides, vancomycin) — careful dose adjustment

---

Prognosis

---