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Metabolic Response to Injury - Chapter 1, Bailey & Love's Short Practice of Surgery (28th Edition)

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1. INTRODUCTION - What Is the Metabolic Response to Injury?

• Hormonal (neuroendocrine)
• Inflammatory (cytokines)
• Neural circuits

• Altered body metabolism
• Changes in wound healing and immunity
• Specific organ dysfunction

Exam point: If uncontrolled, this response leads to sepsis → MODS (multiple organ dysfunction syndrome). MODS carries ~25% mortality even in modern trauma systems.

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2. HOMEOSTASIS AND THE TWO PHASES

Exam point: The catabolic phase is also called the "ebb" phase and the anabolic flow phase corresponds to SIRS (systemic inflammatory response syndrome).

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3. MAGNITUDE OF THE INJURY RESPONSE

• Minor elective surgery: transient modest rise in temperature, HR, RR, WBC, energy expenditure
• Major trauma/burns/sepsis: SIRS, hypermetabolism, marked catabolism, shock, MODS

Exam point: Genetic variability also determines response intensity - some patients respond much more dramatically than others to similar injuries.

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4. MEDIATORS OF THE METABOLIC RESPONSE

A. Tissue Damage and Inflammation (DAMPs Pathway)

1. Tissue injury releases DAMPs (damage-associated molecular patterns), also called alarmins
   • Examples: heat shock proteins, HMGB1 (high mobility group protein B1), S100 proteins, nucleic acid fragments
2. DAMPs activate PRRs (pattern recognition receptors):
   • Toll-like receptors (TLRs)
   • NOD-like receptors (NLRs)
   • Found on: macrophages, neutrophils, dendritic cells
3. PRR activation triggers formation of inflammasomes (complex intracellular proteins)
4. Inflammasomes activate caspases → activate key cytokines:
   • IL-1, IL-6, TNF-alpha, IL-8, interferons, chemokines
5. Result: sterile systemic inflammatory cascade → local inflammation → SIRS

• Leaky capillaries (oedema)
• Coagulopathy
• Local ischaemia → more DAMPs (self-perpetuating cycle)

• Sepsis
• Haemorrhage
• Massive transfusion
• Acidosis
• Surgery itself
• Crush syndrome
• Ischaemia-reperfusion injury

Exam point: The "redundancy" of DAMPs (ability to activate multiple receptors/pathways) is why therapeutic blockade of inflammation has been so difficult clinically.

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B. Neuroendocrine Response to Injury

Tissue injury/pain
       ↓
Afferent nociceptive neurones
       ↓
Spinal cord → Thalamus → Hypothalamus
       ↓
CRF (corticotropin-releasing factor) released
       ↓
ACTH from anterior pituitary
       ↓
Adrenal cortex → CORTISOL (within hours)

Hypothalamus also activates:
→ Sympathetic nervous system → ADRENALINE (epinephrine)
→ Pancreas → GLUCAGON

• Glucocorticoids (cortisol)
• Glucagon
• Catecholamines (adrenaline)

High-yield exam fact: IV infusion of these three hormones reproduces many aspects of the metabolic response to injury.

• Growth hormone (GH) ↑ - but paradoxically with low IGF-1; GH has direct lipolytic, insulin-antagonising and pro-inflammatory properties
• Prolactin ↑
• Peripheral thyroid hormones inactivated
• Gonadal function suppressed

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C. Cytokines and Their Actions

Exam point: IL-6 is the primary driver of the hepatic acute-phase protein response.

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D. Agonists and Antagonists: An Uncertain Balance

• IL-10, IL-4, TGF-beta (anti-inflammatory)
• Glucocorticoids also have anti-inflammatory effects

Exam point: CARS (Compensatory Anti-inflammatory Response Syndrome) can lead to immune suppression if the anti-inflammatory arm is too dominant, predisposing to secondary infections.

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5. METABOLIC CHANGES AFTER SURGERY AND TRAUMA

Catabolic Phase (0-48 hours)

• Hypovolaemia, ↓ BMR, ↓ cardiac output, hypothermia, lactic acidosis
• Dominant hormones: catecholamines, cortisol, aldosterone
• Insulin levels fall or do not rise appropriately → hyperglycaemia

Flow Phase (after resuscitation - corresponds to SIRS)

• Tissue oedema (vasodilatation + ↑ capillary permeability)
• Hypermetabolism (↑ BMR)
• ↑ Cardiac output
• Raised body temperature
• Leukocytosis
• ↑ Oxygen consumption
• ↑ Gluconeogenesis

• Provide essential substrates for survival via tissue breakdown
• Postpone anabolism
• Optimise host defence

Exam point: These changes are helpful short-term but harmful long-term, especially in the critically ill.

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6. MANAGING THE CATABOLIC RESPONSE

• Catabolic (peripheral) tissues: skeletal muscle, adipose tissue, skin
• Anabolic (central) tissues: liver, immune system, wound

A. Hypermetabolism

• Most trauma patients: energy expenditure 15-25% above predicted resting values
• Burns patients can go even higher
• Caused by: central thermodysregulation (cytokine cascade), ↑ sympathetic activity, ↑ protein turnover, wound circulation abnormalities (Cori cycle)

B. Skeletal Muscle Protein Metabolism

• ↑ Protein degradation via the ubiquitin-proteasome pathway (key exam fact)
• ↓ Protein synthesis

• Loss of respiratory muscle → hypoventilation, chest infections
• Loss of gut muscle → ↓ gut motility
• Amino acids (especially glutamine and alanine) exported from muscle to liver (for gluconeogenesis) and wound
• Net catabolism occurs because alanine and glutamine are derived partly from irreversible degradation of branched-chain amino acids

• Provides amino acids for central organs/tissues
• Mediated mainly by ubiquitin-proteasome pathway
• Inevitable to some degree, prolonged by sepsis
• Can cause immobility, poor healing, hypostatic pneumonia, death if excessive

C. Acute-Phase Protein Response (Hepatic)

Exam point: Albumin falls after injury NOT mainly due to reduced synthesis, but due to increased transcapillary escape (3x increase in TER) secondary to microvascular permeability changes. Normal albumin TER is already ~10x the synthesis rate.

D. Insulin Resistance

• Glucose production ↑ (gluconeogenesis)
• Glucose uptake in peripheral tissues ↓
• Mechanism: proinflammatory cytokines + decreased responsiveness of insulin-regulated glucose transporter proteins
• Degree of resistance is proportional to injury magnitude

• After routine upper abdominal surgery: insulin resistance persists ~2 weeks
• With prolonged sepsis: extends further
• Behaves like Type 2 diabetes mellitus
• Management in ICU: IV insulin infusion to maintain blood glucose within limits
• Caution: tight control risks significant hypoglycaemia

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7. CHANGES IN BODY COMPOSITION FOLLOWING INJURY

• Fat: 13 kg
• Fat-free mass (protein + water): ~57 kg

• Fat mass ↓
• Skeletal muscle mass ↓
• Body weight may paradoxically increase due to expansion of extracellular fluid (oedema)

• Catabolism decreases fat mass and skeletal muscle mass
• Body weight may increase paradoxically due to extracellular fluid expansion

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8. AVOIDABLE FACTORS THAT COMPOUND THE RESPONSE

• Baroreceptors (carotid, aortic arch) + volume receptors (left atrium) → CNS → ADH + aldosterone release
• ADH → fluid retention at kidney
• ↓ Pulse pressure → juxtaglomerular apparatus → renin-angiotensin → ↑ aldosterone
• Aldosterone → Na+ reabsorption → water conservation
• Net effect: oliguria after surgery (normal/expected)
• Excess saline resuscitation worsens salt/water retention → peripheral AND visceral oedema → delayed gastric emptying, prolonged hospital stay

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9. ENHANCED RECOVERY AFTER SURGERY (ERAS)

• Minimal access techniques (laparoscopic surgery)
• Blockade of afferent pain stimuli (epidural analgesia, spinal, wound catheters)
  • Note: epidural analgesia is no longer recommended for laparoscopic surgery (patient-controlled analgesia is sufficient)
• Minimal periods of starvation (avoid prolonged preoperative fasting)
• Early mobilisation

• Reductions in length of hospital stay of 30-50%
• Improved outcomes
• Reduced healthcare costs

• Beta-blockers: associated with improved short- and long-term survival after major surgery (by modulating the hyper-adrenergic state)
• Epidural analgesia in open surgery: reduces pain, blocks cortisol stress response, attenuates postoperative insulin resistance
• IV lidocaine infusion (6-12 hr): opioid-sparing, improves gut function
• 'One-shot' spinal diamorphine: opioid-sparing effect

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HIGH-YIELD EXAM SUMMARY

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Chapter 2: Shock, Haemorrhage and Blood Transfusion

Bailey & Love's Short Practice of Surgery, 28th Edition - Unit 2 (Basic Principles)

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LEARNING OBJECTIVES (Exam Checklist)

• Pathophysiology of shock
• Different patterns of shock + principles/priorities of resuscitation
• Monitoring and end points of resuscitation
• Recognition and management of bleeding
• Blood and blood products, benefits and risks of transfusion

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1. SHOCK - DEFINITION

Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration.

• Cells switch from aerobic → anaerobic metabolism
• If not restored promptly → cell death

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2. PATHOPHYSIOLOGY OF SHOCK

A. Cellular Level

1. Reduced perfusion → oxygen deprivation
2. Anaerobic metabolism → lactic acid production → metabolic acidosis
3. Glucose exhaustion → anaerobic respiration ceases
4. Failure of Na+/K+ pumps in cell membrane and organelles
5. Lysosome rupture → release of autodigestive enzymes → cell lysis
6. Intracellular contents (K+) released into bloodstream → hyperkalaemia

B. Microvascular Level

1. Hypoxia + acidosis → complement activation + leukocyte priming
2. Oxygen free radicals + cytokine release → capillary endothelial injury
3. Damaged endothelium becomes "leaky" → fluid extravasation → tissue oedema
4. Oedema exacerbates cellular hypoxia (vicious cycle)
5. Cell death releases more K+ → hyperkalaemia + acidosis → further immune activation

C. Systemic Level

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3. CLASSIFICATION OF SHOCK (Summary Box 2.1)

Must Know: 5 Types

KEY TABLE 2.1 - Cardiovascular Characteristics of Shock

Exam tip: Distributive (septic) shock is the ONLY type with HIGH cardiac output and LOW SVR. Mixed venous O₂ is HIGH in distributive shock because cells cannot utilise oxygen.

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Hypovolaemic Shock - Non-haemorrhagic causes:

• Poor fluid intake (dehydration)
• Vomiting, diarrhoea
• Urinary loss (diabetes insipidus)
• Third-spacing (bowel obstruction, pancreatitis)

Obstructive Shock - Causes (must know):

• Cardiac tamponade - fluid in pericardium compresses heart
• Tension pneumothorax - mediastinal shift, compressed IVC
• Massive pulmonary embolus - obstructs right heart outflow
• Air embolus

Distributive Shock - Three sub-types:

1. Septic shock - bacterial/humoral mediators → vasodilatation + arteriovenous shunting
2. Anaphylaxis - histamine release → vasodilatation
3. Neurogenic shock - high spinal cord injury → loss of sympathetic outflow → loss of vascular tone

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4. CLINICAL CONSEQUENCES OF SHOCK

A. Unresuscitatable Shock

• Profound shock for prolonged period → cells pass "point of no return"
• Myocardial cell death from poor coronary perfusion + severe acidaemia + hyperkalaemia
• Loss of ability to maintain SVR → peripheries no longer respond to vasopressors

B. Ischaemia-Reperfusion Injury

• When blood flow is restored after ischaemia, paradoxically worsened injury occurs
• Mechanism: reperfusion activates neutrophils + complement → oxygen free radicals
• Results in capillary endothelial injury, increased permeability, organ dysfunction

C. Multiple Organ Failure (MOF/MODS)

• Sustained ischaemia → sequential organ failure
• Sequence: lungs → kidneys → liver → gut → heart
• Each failing organ amplifies the systemic inflammatory response

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5. RECOGNITION AND DIAGNOSIS OF SHOCK

Stages of Shock

Clinical Signs - KEY EXAM TABLE (Table 2.2)

Important Clinical Pitfalls for Exams:

1. Hypotension is a LATE sign - children and fit young adults maintain BP until final stages
2. Tachycardia is NOT always present:
   • Beta-blocker users cannot mount tachycardia
   • Pacemaker patients cannot mount tachycardia
   • Young patients with penetrating trauma may have paradoxical bradycardia
3. Capillary refill is unreliable in adults - variable; in septic shock peripheries are WARM with BRISK CRT despite profound shock
4. Elderly hypertensives may appear normotensive but are actually hypotensive relative to their baseline

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6. HAEMORRHAGE

Definition and Key Distinction

Haemorrhage and shock are not the same thing:

• Actively bleeding patient may not yet be in shock
• Shocked patient may no longer be actively bleeding

• Actively bleeding → priority = STOP THE BLEEDING (damage control)
• Not actively bleeding → priority = CORRECT THE SHOCK STATE (restore perfusion)

Types of Haemorrhage

Exam point: Secondary haemorrhage is almost always due to infection. Reactionary haemorrhage occurs within 24 hours.

Common sites of concealed haemorrhage (must know):

• Chest (haemothorax)
• Abdomen/pelvis (haemoperitoneum, retroperitoneal)
• Long bone fractures (femur fracture: up to 2L blood loss)
• Scalp wounds

Assessment of Blood Loss

• Haemoglobin is a POOR early indicator - in rapid haemorrhage, Hb concentration is UNCHANGED initially (whole blood lost, concentration same)
• Hb falls later as interstitial/intracellular fluid shifts into the vascular compartment

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7. HAEMORRHAGE RESUSCITATION (Damage Control Resuscitation)

Principle

• Rapid haemostasis is the priority
• Maintain the blood's ability to clot

Steps:

• External: direct pressure, tourniquet, wound packing
• Internal: operative or interventional radiological control

• In penetrating trauma with active bleeding: accept lower BP (systolic ~80-90 mmHg) to avoid dislodging clots
• NOT indicated in traumatic brain injury (where adequate CPP must be maintained)

• Use blood products in 1:1:1 ratio (packed RBC : FFP : platelets)
• Minimise crystalloid (large volumes worsen coagulopathy, acidosis, hypothermia = "lethal triad")

• Acidosis + Hypothermia + Coagulopathy
• Each worsens the others; together they are frequently fatal

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8. SHOCK RESUSCITATION

Fluid Therapy

"Administration of inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of oxygen stores."

• Short, wide-bore peripheral cannulae (e.g. 14G or 16G)
• Long, narrow central venous catheters have too much resistance for rapid infusion - more appropriate for monitoring

Exam point: Crystalloid vs. colloid - studies show no clinically significant difference in outcomes. Colloids provide only 1.3x more volume expansion than crystalloid (less than previously thought). No evidence to support routine colloids - more expensive and worse side effects.

Vasopressor and Inotropic Support

• NOT first-line in hypovolaemia
• Only after adequate preload is established
• Dobutamine - for cardiogenic shock (inotrope)
• Noradrenaline - for distributive shock (vasopressor)
• Vasopressin - adjunct vasopressor in refractory septic shock

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9. MONITORING IN SHOCK (Table 2.4)

Standard Clinical Monitoring

• Pulse rate, BP, RR
• Temperature
• Urine output (catheter) - most reliable bedside indicator of renal perfusion
• Conscious level (GCS)
• Capillary refill time

Laboratory / Advanced Monitoring

• In sepsis, SvO₂ is HIGH (>70%) because cells cannot utilise oxygen + arteriovenous shunting
• If septic patient has SvO₂ <70% → they are in COMBINED septic + hypovolaemic/cardiogenic shock
• Treatment: correct hypovolaemia + inotropes (dobutamine) to get SvO₂ >70%

End Points of Resuscitation

• Lactate clearance - most reliable end point; target lactate <2 mmol/L
• Urine output >0.5 mL/kg/hr
• Normalisation of base deficit
• Normalisation of GCS

Exam point: It is much easier to know when to START resuscitation than when to STOP. Over-resuscitation causes fluid overload, oedema, and worsens outcomes.

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10. TRANSFUSION

History Highlights (Table 2.5 - for exam MCQs)

• 1818: James Blundell - first successful human-to-human transfusion (post-partum haemorrhage)
• 1901: Karl Landsteiner - discovered ABO system
• 1914: Albert Hustin - first non-direct transfusion using sodium citrate as anticoagulant
• 1939: Rhesus system identified

Blood Collection

• UK: up to 450 mL drawn, maximum 3 times/year
• Tested for: Hepatitis B, Hepatitis C, HIV-1, HIV-2, Syphilis
• Leukodepleted (precaution against variant CJD; also reduces immunogenicity)
• ABO + Rh(D) typed; irregular red cell antibodies screened

Blood Products

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11. BLOOD GROUPS

ABO System (Table 2.7)

• Group O = Universal donor (no antigens to provoke reaction)
• Group AB = Universal recipient (no circulating antibodies)

Rhesus System

• Rh(D) antigen present in ~85% of UK population
• Rh(D)+ people: develop anti-D antibodies only if exposed to Rh(D)+ blood
• Rh(D)- women who receive Rh(D)+ blood → may form anti-D antibodies → risk of haemolytic disease of the newborn in subsequent pregnancies
• Prevention: anti-D immunoglobulin given to Rh(D)- women after potential sensitisation

Cross-Matching Timeline (critical for exams)

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12. TRANSFUSION TRIGGER

Exam point: Restrictive transfusion strategy (Hb 7-8 threshold) is now standard for most patients. Higher threshold may be considered in cardiovascular disease, TBI, sepsis - but clinical evidence is limited.

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13. TRANSFUSION REACTIONS

Acute Haemolytic Reaction (most dangerous)

• Cause: ABO incompatibility - complement-mediated intravascular haemolysis
• Features: fever, chills, rigors, flank pain, haemoglobinuria, shock, MOF
• Mechanism: Usually due to wrong blood to wrong patient (clerical error)
• Action: STOP transfusion immediately, IV fluid, inform blood bank, send blood sample

Febrile Non-Haemolytic Reaction

• Due to graft-versus-host response from leukocytes in transfused components
• Features: fever, chills, rigors (WITHOUT haemolysis)
• STOP transfusion immediately
• Rare with leukodepleted blood

Allergic Reaction

• Urticaria, bronchospasm, anaphylaxis
• Due to plasma proteins in donor blood

TRALI (Transfusion-Related Acute Lung Injury)

• Usually from FFP
• Acute onset dyspnoea, hypoxia, bilateral lung infiltrates within 6 hours of transfusion
• Non-cardiogenic pulmonary oedema
• Can be fatal

Safety Checklist (exam-tested)

1. Patient's details against prescription
2. Patient's details against donor blood label
3. Donor blood serial number against issue slip

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14. COMPLICATIONS OF MASSIVE TRANSFUSION

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HIGH-YIELD EXAM SUMMARY - Chapter 2

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Surgical Infections - Chapter 5

Bailey & Love's Short Practice of Surgery, 28th Edition

Note: In Bailey & Love 28th Edition, "Surgical Infections" is Chapter 5 (not Chapter 1). It is found in the first block (block 1) along with all the basic principles chapters. This is a detailed, exam-focused breakdown of the entire chapter.

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LEARNING OBJECTIVES (Exam Checklist)

• Characteristics of common surgical pathogens and their antibiotic sensitivities
• Factors determining whether a wound becomes infected
• Classification of sources of infection and severity
• Clinical presentation of surgical infections
• Indications and choice of prophylactic antibiotics
• Spectrum of commonly used antibiotics and principles of therapy
• Antibiotic resistance - MRSA, C. difficile
• Koch's postulates
• Management of abscesses
• Surviving Sepsis Campaign, Sepsis Bundle, Sepsis Six
• Surgical implications of COVID-19

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1. HISTORY OF SURGICAL INFECTION

Koch's Postulates (Summary Box 5.1) - MUST KNOW

1. The organism must be found in every case of the disease
2. It should be possible to isolate it from the host and grow it in pure culture
3. It should reproduce the disease when injected into another healthy host
4. It should be recovered from the experimentally infected host

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2. ANTIBIOTIC RESISTANCE (Summary Box 5.2)

• Bacteria develop resistance via acquisition of β-lactamases - enzymes that break the β-lactam ring in penicillins and cephalosporins
• Bacteria can also develop cell wall changes, efflux pumps, altered ribosomal targets

MRSA (Methicillin-Resistant Staphylococcus aureus)

• Resistant to most common antibiotics
• Found in nose of asymptomatic carriers among patients and staff
• Spread mainly by hand contact (healthcare workers)
• Treatment: Vancomycin or Teicoplanin
• Screening: nasal swabs for at-risk patients preoperatively

C. difficile (Clostridium difficile)

• Toxin-producing anaerobe
• Causes antibiotic-associated pseudomembranous colitis
• Risk: broad-spectrum antibiotics destroy normal flora, allowing C. difficile overgrowth
• Treatment: Metronidazole (mild-moderate) or Vancomycin oral (severe)
• Prevention: judicious antibiotic use, hand hygiene (alcohol gel ineffective; soap and water required)

Exam tip: Alcohol gel does NOT kill C. difficile spores - soap and water is required.

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3. MICROBIOLOGY OF SURGICAL INFECTIONS

A. Streptococci (Gram-positive, chains)

Exam point: β-haemolytic streptococcus = most pathogenic. All streptococci remain sensitive to penicillin and erythromycin.

B. Staphylococci (Gram-positive, clumps)

C. Clostridia (Gram-positive, anaerobic, spore-bearing bacilli)

Exam point: Gas gangrene = C. perfringens + sweet-smelling exudate + crepitus + rapidly spreading gangrene. Treatment = IV penicillin + debridement.

D. Aerobic Gram-Negative Bacilli

E. Bacteroides (Anaerobic Gram-negative)

• Major component of bowel flora
• Causes intra-abdominal sepsis, wound infections after bowel surgery
• Treatment: Metronidazole (drug of choice for anaerobes)

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4. SOURCES OF INFECTION

Endogenous vs Exogenous (Summary Box 5.3)

Host Defence Mechanisms

• Mechanical: intact skin and epithelial surfaces
• Chemical: low gastric pH
• Humoral: antibodies, complement, opsonins
• Cellular: phagocytic cells, macrophages, polymorphonuclear cells, killer lymphocytes

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5. FACTORS DETERMINING WOUND INFECTION (Summary Box 5.4 - HIGH YIELD)

1. Host response (immune status)
2. Virulence and inoculum of infective agent
3. Vascularity and health of tissue (local ischaemia, systemic shock)
4. Presence of dead or foreign tissue
5. Presence of antibiotics during the "decisive period"

The Decisive Period

• There is up to a 4-hour window before bacterial growth becomes established enough to resist antibiotic therapy
• This is why prophylactic antibiotics must be given at induction of anaesthesia, not before or after

Risk Factors for Wound Infection (Summary Box 5.5)

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6. CLASSIFICATION OF WOUNDS (Wound Contamination - Table 5.2)

Exam tip: Prophylaxis has NO benefit in clean non-prosthetic surgery (infection rate already low). Exception: any surgery involving prosthetic implant - even small infection risk is unacceptable.

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7. PRESENTATION OF SURGICAL INFECTION

Hospital-Acquired Infection (HAI) - 4 Main Groups

1. Respiratory infections (including ventilator-associated pneumonia)
2. Urinary tract infections (mostly catheter-related)
3. Bacteraemia (mostly indwelling vascular catheter-related)
4. Surgical site infections (SSI)

Major vs Minor SSI

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8. LOCALISED INFECTIONS

Abscess

• Calor (heat)
• Rubor (redness)
• Dolor (pain)
• Tumor (swelling)
• Functio laesa (loss of function) - added later

• Pyogenic organisms (predominantly S. aureus) cause tissue necrosis and suppuration
• Pus = dead and dying neutrophils + bacteria + necrotic tissue
• Abscess wall formed by fibrin + surrounding tissue reaction (pyogenic membrane)
• Central liquefaction → fluctuance

• "Ubi pus, ibi evacua" = "Where there is pus, evacuate it" - the timeless surgical principle
• Incision and drainage (I&D)
• Send pus for culture and sensitivity
• Leave wound open / pack to allow healing from base up
• Antibiotics alone are INSUFFICIENT for established abscess

Cellulitis and Lymphangitis (Summary Box 5.8)

• Cellulitis: Non-suppurative, poorly localised spreading infection of tissues
• Organisms: β-haemolytic streptococci, staphylococci, C. perfringens
• Features: spreading inflammation, tissue destruction, gangrene, ulceration (proteases)
• Systemic signs: chills, fever, rigors (toxin-mediated cytokine response, even with negative blood cultures)
• Lymphangitis: Painful red streaks in lymphatics draining infection source; painful lymph nodes in drainage area (cervical, axillary, inguinal)
• Treatment: Penicillin + flucloxacillin (or erythromycin if penicillin allergic)

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9. SPECIFIC SERIOUS WOUND INFECTIONS

Gas Gangrene (Summary Box 5.9)

Tetanus (Clostridium tetani)

Exam point: Tetanospasmin travels retrograde up motor nerves. Short motor nerves of face affected first → facial spasms before generalised tetanus.

Necrotising Fasciitis (Synergistic Spreading Gangrene)

Exam point: Necrotising fasciitis is a surgical emergency. Subdermal spread is ALWAYS more extensive than surface appearance suggests.

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10. SYSTEMIC INFECTION

Bacteraemia

• Transient bacteraemia common after: instrumentation of infected bile/urine, bowel surgery anastomotic breakdown, indwelling IV cannulae colonisation
• Important when prosthesis is implanted (haematogenous seeding → prosthetic infection)
• Organisms: aerobic Gram-negative bacilli, S. aureus, fungi

Definitions of Infected States (Summary Box 5.10)

SIRS Criteria (must know)

• Temperature >38°C or <36°C
• Heart rate >90 bpm
• Respiratory rate >20/min or PaCO₂ <4.3 kPa
• WBC >12,000 or <4,000 or >10% immature (band) forms

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11. SURVIVING SEPSIS CAMPAIGN / SEPSIS BUNDLE / SEPSIS SIX

Surviving Sepsis Campaign (SSC)

• Spearheaded by ESICM and SCCM in 2002
• Goal: reduce mortality from sepsis

The Sepsis Bundle (Resuscitation Bundle)

• Evidence-based objectives completed within 6 hours
• For: severe sepsis + septic shock + lactate >4 mmol/L

Sepsis Six (UK Sepsis Trust) - MUST MEMORISE

1. IV fluid challenge
2. IV antibiotics
3. Oxygen (and monitor urine output)

Exam mnemonic: "Give 3, Take 3" - Fluids, Antibiotics, O₂ / Blood cultures, FBC, Lactate

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12. VIRAL INFECTIONS RELEVANT TO SURGERY

Hepatitis B and C

HIV / AIDS

• Hollow needle injury carries greatest risk of viral transmission
• After needlestick: wash under running water immediately, report incident
• Consider post-exposure antiretroviral therapy (per local policy)

Universal Precautions (CDC/NHS)

• Full face mask (ideally) or protective spectacles
• Fully waterproof disposable gowns and drapes
• Boots (not clogs) - prevent injury from dropped sharps
• Double gloving (larger size inside for comfort)
• Only essential personnel in theatre
• Minimal movement in theatre
• Sharps passed in kidney dish
• Slow, meticulous operative technique with minimised bleeding

COVID-19

• Aetiology: SARS-CoV-2
• Classified as pandemic by WHO on 11 March 2020
• Contagious respiratory and vascular disease
• Symptoms: fever, cough, fatigue, dyspnoea, loss of smell and taste
• Incubation: 1-14 days
• Surgical implications: elective surgery postponed; emergency and cancer surgery continued with PPE

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13. PROPHYLACTIC ANTIBIOTICS

Principles

• Value is LOW in clean non-prosthetic surgery (infection rates already low without antibiotics)
• Exception: prosthetic implant surgery - even tiny infection risk is unacceptable
• Clear benefit in clean-contaminated and contaminated operations
• In heavily contaminated wounds / incision through abscess: 5-day therapeutic course (not prophylaxis, as wound assumed already infected)

Timing - THE DECISIVE PERIOD

• Antibiotics MUST be given at induction of anaesthesia (not just before theatre - unexpected delays may occur)
• Maximal blood and tissue levels must be present at time of first incision
• Repeat at 4-hourly intervals in: long operations, excessive blood loss, unexpected contamination
• No evidence for further doses AFTER surgery for prophylaxis - only encourages resistance

Special Indication

• Patients with known valvular heart disease or implanted vascular/orthopaedic prosthesis need prophylactic antibiotics during dental, urological, or open viscus surgery to prevent transient bacteraemia seeding the valve/prosthesis

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14. ANTIBIOTICS IN SURGICAL INFECTION

Classification

• Bactericidal: penicillins, aminoglycosides
• Bacteriostatic: tetracyclines, erythromycin

Key Antibiotics (Exam Summary Table)

Exam tip: Enterococcus faecalis is NOT sensitive to cephalosporins - must use penicillin or vancomycin.

Exam tip: Aminoglycosides (gentamicin) act at the ribosomal level (prevent/distort protein synthesis). Penicillins act on the cell wall (most effective against actively dividing bacteria).

For Empirical Treatment of Unknown Surgical Infection:

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HIGH-YIELD EXAM SUMMARY

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