Anaesthetics

Key Facts

Regional anaesthesia provides targeted pain relief by blocking nerve transmission in specific body regions. It is increasingly used as a sole technique or in combination with GA as part of multimodal analgesia. Ultrasound guidance has transformed the practice.

Epidemiology

The use of regional anaesthesia is increasing in the UK, with approximately 30-40% of surgical cases now incorporating some form of regional technique. The NAP3 audit found a major complication rate of approximately 1 in 25,000 for neuraxial blocks. Peripheral nerve blocks have even lower complication rates.

Aetiology

Regional anaesthesia works by depositing local anaesthetic (LA) around peripheral nerves, nerve plexuses, or in the neuraxial space. The LA blocks voltage-gated sodium channels, preventing nerve impulse propagation. The order of nerve fibre blockade follows the principle that smaller, myelinated fibres are blocked first (autonomic > sensory > motor).

Pathophysiology

Mechanism of nerve blockade:

• LA in unionised form crosses the nerve membrane
• Ionised form blocks the sodium channel from the intracellular side
• Differential blockade: sympathetic (B fibres) blocked first, then pain/temperature (Aδ, C), then proprioception (Aβ), then motor (Aα)
• Onset time depends on pKa (closer to physiological pH = faster onset)
• Duration depends on protein binding and lipid solubility
• Potency correlates with lipid solubility

Upper Limb Blocks

• Interscalene: Shoulder and proximal humerus surgery; risk of phrenic nerve palsy (~100%)
• Supraclavicular: Arm and elbow surgery; risk of pneumothorax (minimal with USS)
• Infraclavicular: Elbow, forearm, hand
• Axillary: Forearm and hand - safest brachial plexus block

Lower Limb Blocks

• Femoral nerve block: Anterior thigh, knee surgery
• Fascia iliaca block: Hip fracture analgesia - blocks femoral, obturator, lateral cutaneous nerve
• Adductor canal block: Knee arthroplasty - motor-sparing
• Sciatic/popliteal block: Below-knee surgery
• Ankle block: Foot surgery

Trunk Blocks

• TAP (transversus abdominis plane) block: Abdominal wall analgesia
• Rectus sheath block: Midline incision analgesia
• Erector spinae plane (ESP) block: Thoracic/abdominal analgesia
• Paravertebral block: Unilateral thoracic/abdominal analgesia (breast surgery, rib fractures)

Red Flags

• Metallic taste, circumoral tingling, tinnitus - early LAST (stop injection immediately)
• Seizures, arrhythmia, cardiac arrest - severe LAST (Intralipid rescue)
• Progressive neurological deficit after block - suspect nerve injury or haematoma
• Respiratory distress after interscalene block - phrenic nerve palsy or pneumothorax

Bedside

• Pre-procedure assessment: Coagulation status, consent, block suitability
• Ultrasound: Standard of care for peripheral nerve blocks - real-time visualisation
• Nerve stimulation: Adjunct to USS; motor response at <0.5mA suggests intraneural needle tip
• Post-block assessment: Sensory and motor block distribution

Bloods

• Coagulation screen: Before neuraxial or deep blocks in anticoagulated patients
• Platelet count: Ensure adequate (>75 × 10⁹/L for neuraxial; >50 for peripheral)

Imaging

• Ultrasound: Pre-procedural scanning to identify anatomy, vasculature, and nerve targets
• CXR: If pneumothorax suspected after supraclavicular block

Special Tests

• Nerve conduction studies/EMG: If post-block neurological deficit persists >72 hours
• MRI: If nerve injury or haematoma suspected

Non-pharmacological

• Consent: Explain benefits, risks (nerve injury, LAST, infection), and alternatives
• Monitoring: Standard AAGBI monitoring during block performance; resuscitation equipment available
• Positioning: Appropriate for block type; aseptic technique

Pharmacological

• Bupivacaine 0.25-0.5%: Long-acting (4-8 hours); max dose 2mg/kg (150mg)
• Levobupivacaine 0.25-0.5%: S-enantiomer - less cardiotoxic; same doses as bupivacaine
• Ropivacaine 0.5-0.75%: Less motor block, less cardiotoxic; max dose 3mg/kg
• Lidocaine 1-2%: Short-acting (1-2 hours); max dose 3mg/kg (or 7mg/kg with adrenaline)
• Adjuvants: Adrenaline 1:200,000 (prolongs block, reduces LA absorption), dexamethasone 4mg perineural (prolongs block by 6-8 hours), clonidine 1mcg/kg
• Intralipid 20% rescue: 1.5mL/kg bolus for LAST → 15mL/kg/hr infusion

Surgical/Interventional

• Catheter techniques: Continuous infusions (bupivacaine 0.1-0.125% at 5-10mL/hr) for prolonged analgesia
• Combined spinal-epidural (CSE): For lower limb/pelvic surgery with extended post-operative analgesia

Referral Criteria

• Persistent neurological deficit >72 hours post-block - neurology referral
• Suspected LAST - immediate ALS and Intralipid protocol
• Infection at catheter site - remove catheter, microbiology input

• Peripheral nerve blocks: permanent nerve injury rate approximately 1 in 5,000-10,000
• Transient neuropraxia: occurs in 2-4% of blocks - resolves within days to weeks
• LAST: Incidence approximately 1 in 1,000-10,000 peripheral blocks; mortality now rare with Intralipid rescue
• Patient satisfaction with regional anaesthesia is consistently high (>90%)
• Continuous catheter techniques reduce opioid consumption by 40-60% post-operatively

Maximum Doses of Local Anaesthetics

LAST Management Algorithm

Key Facts

Local anaesthetics are the foundation of regional anaesthesia and are among the most widely used drugs in medical practice. Understanding their pharmacology is essential for safe administration.

Epidemiology

Local anaesthetic use is ubiquitous across medical specialties. LAST is rare (estimated 1 in 1,000-10,000 peripheral nerve blocks) but potentially fatal. The introduction of Intralipid rescue therapy has significantly reduced mortality from LAST.

Aetiology

LAs work by reversibly blocking voltage-gated sodium channels on the inner surface of the nerve cell membrane. This prevents depolarisation and action potential propagation. The unionised (base) form crosses the nerve membrane; the ionised form then blocks the sodium channel from the intracellular side.

Pathophysiology

Classification:

• Amides (lidocaine, bupivacaine, levobupivacaine, ropivacaine, prilocaine): Contain an amide bond; hepatic metabolism; allergic reactions rare
• Esters (cocaine, procaine, tetracaine, chloroprocaine): Contain an ester bond; hydrolysed by plasma cholinesterases; PABA metabolite can cause allergy

Differential blockade (smallest fibres blocked first):

Factors affecting LA action:

• Tissue pH: Infection (acidic pH) reduces LA efficacy - more ionised form, less crosses membrane
• Nerve fibre size: Smaller fibres blocked more readily
• Myelination: Myelinated fibres require block at 3 consecutive nodes of Ranvier

Routes of Administration

• Topical: EMLA cream, lidocaine gel, Ametop (tetracaine)
• Infiltration: Wound infiltration, field block
• Peripheral nerve block: Single injection or catheter
• Neuraxial: Spinal (intrathecal), epidural
• IV regional (Bier's block): Lidocaine 0.5% 3mg/kg for upper limb surgery under tourniquet

Systemic Toxicity (LAST) - Progression

1. Circumoral tingling, metallic taste
2. Light-headedness, tinnitus, visual disturbance
3. Slurred speech, drowsiness
4. Tremor, muscle twitching
5. Seizures (generalised tonic-clonic)
6. Loss of consciousness

Specific Toxicity Syndromes

• Bupivacaine cardiotoxicity: Resistant VF/VT - prolonged CPR needed, Intralipid essential
• Prilocaine: Methaemoglobinaemia at doses >600mg (treat with methylene blue 1-2mg/kg IV)
• Cocaine: Sympathomimetic effects - tachycardia, hypertension, arrhythmias

Red Flags

• Any CNS symptoms during or after LA administration - suspect LAST
• Cardiovascular collapse within minutes of LA injection - LAST or intravascular injection
• Cyanosis unresponsive to O2 after prilocaine - methaemoglobinaemia
• Prolonged numbness >24 hours - possible nerve injury

Bedside

• Clinical observation: Monitor for LAST symptoms during and after injection
• SpO2 monitoring: May show ~85% if methaemoglobinaemia
• ECG: Prolonged QRS, bradycardia in bupivacaine toxicity

Bloods

• ABG with co-oximetry: If methaemoglobinaemia suspected - measures metHb level directly
• Serum tryptase: If allergic reaction suspected (take at 1 hour and 24 hours)

Imaging

• Not typically required acutely

Special Tests

• Allergy testing: Skin prick and intradermal testing - if true LA allergy suspected (extremely rare with amides)
• Plasma cholinesterase levels: If prolonged ester LA effect (suxamethonium sensitivity testing as well)

Non-pharmacological

• Dose calculation: Always calculate maximum safe dose before injection
• Aspiration: Aspirate before injecting to reduce risk of intravascular injection
• Incremental injection: Inject slowly with frequent aspiration
• Monitoring: Standard monitoring during significant LA procedures

Pharmacological

• Seizure management: Midazolam 0.05mg/kg IV or propofol - small doses to avoid CVS depression
• Methaemoglobinaemia: Methylene blue 1-2mg/kg IV over 5 minutes
• Adrenaline: Added at 1:200,000 (5mcg/mL) to reduce absorption; contraindicated in end-artery regions

Surgical/Interventional

• No specific surgical management - ensure Intralipid is immediately available wherever LA is used

Referral Criteria

• Any LAST event - report to AAGBI, local incident reporting
• Suspected LA allergy - immunology/allergy clinic referral
• Persistent nerve deficit after LA procedure - neurology referral

• LAST: Historically 50% mortality from bupivacaine cardiac arrest; now significantly reduced with Intralipid rescue (>75% survival)
• Methaemoglobinaemia: Rapidly reversible with methylene blue; rarely fatal
• Nerve injury from LA: Most are neuropraxia - >95% recover fully within 6 weeks
• Allergy: True allergy to amide LAs is extremely rare (<0.01%); ester allergy more common (PABA cross-reactivity)

Pharmacological Properties of Common LAs

Physicochemical Properties and Clinical Effect

Key Facts

Spinal (subarachnoid/intrathecal) anaesthesia provides rapid, dense surgical anaesthesia for procedures below the umbilicus. It is the technique of choice for caesarean section, lower limb orthopaedic surgery, and many urological procedures.

Epidemiology

Approximately 700,000 spinal anaesthetics are performed annually in the UK. The most common indication is caesarean section (~150,000/year). NAP3 found the risk of permanent neurological injury from spinal anaesthesia to be approximately 1 in 25,000.

Aetiology

Spinal anaesthesia works by depositing LA directly into the CSF in the subarachnoid space. The LA blocks nerve roots as they traverse the CSF, producing motor, sensory, and autonomic blockade. The spread of block depends on dose, baricity (heavy/plain/light), patient position, and spinal curvature.

Pathophysiology

Autonomic effects:

• Sympathetic blockade extends 2-6 segments higher than sensory level

• Block above T4: Cardio-accelerator fibres blocked → bradycardia (Bezold-Jarisch reflex)
• Block above C3-5: Phrenic nerve involvement → respiratory arrest (total spinal)

Factors affecting block height:

• Dose and volume of LA (most important)
• Baricity: Hyperbaric settles in dependent areas; isobaric spreads less predictably
• Patient position during and immediately after injection
• Speed of injection, patient height, CSF volume (reduced in obesity, pregnancy)

Expected Effects

• Dense motor and sensory block below the level of injection
• Onset within 2-5 minutes, surgical anaesthesia within 5-10 minutes
• Duration 1.5-3 hours (bupivacaine); can be extended with intrathecal opioids

Common Side Effects

• Hypotension (30-50%) - vasodilation and reduced venous return
• Bradycardia (10-15%)
• Shivering
• Pruritus (especially with intrathecal opioids)
• Urinary retention

Complications

• Post-dural puncture headache: Postural headache, worse sitting/standing, relieved lying flat
• High/total spinal: Respiratory arrest, hypotension, loss of consciousness
• Epidural haematoma: Back pain, progressive neurological deficit (especially in anticoagulated patients)
• Epidural abscess: Fever, back pain, neurological deficit
• Cauda equina syndrome: Saddle anaesthesia, urinary retention, bilateral leg weakness
• Transient neurological symptoms (TNS): Buttock/leg pain post-spinal (more common with lidocaine)

Red Flags

• Respiratory distress/apnoea after spinal - total spinal (intubate, vasopressors)
• Severe headache worse on sitting - PDPH (epidural blood patch)
• Progressive weakness/numbness post-operatively - epidural haematoma (emergency MRI and decompression)
• Fever + back pain + neurological deficit - epidural abscess (emergency MRI)

Bedside

• Pre-procedure: Coagulation status, consent, spinal examination, IV access
• Intra-procedure: AAGBI standard monitoring - SpO2, ECG, BP every 2 min initially
• Post-procedure: Hourly motor/sensory assessment, pain score, urinary output

Bloods

• Coagulation screen: Before procedure in patients on anticoagulants
• Platelet count: >75 × 10⁹/L for neuraxial block
• FBC: Baseline

Imaging

• Urgent MRI spine: If epidural haematoma or abscess suspected (within hours)
• CT myelogram: If MRI contraindicated

Special Tests

• Assessment of block height: Cold sensation (ethyl chloride spray) to determine sensory level
• Bromage scale: Assess motor block (0=no block, 3=complete motor block)
• PDPH diagnosis: Clinical - postural headache relieved by lying flat, associated with neck stiffness, photophobia, tinnitus

Non-pharmacological

• Positioning: Left lateral or sitting for injection; supine with left tilt for caesarean section
• Pre-loading/co-loading: Crystalloid 500mL-1L or colloid to reduce hypotension
• Equipment: 25G or 27G pencil-point (Whitacre/Sprotte) needle - lower PDPH rate than cutting needles

Pharmacological

• Hyperbaric bupivacaine 0.5% (heavy): 2-3.5mL (10-17.5mg) - standard agent
• Intrathecal opioids: Fentanyl 15-25mcg (improves block quality, extends duration) or diamorphine 300mcg (for caesarean section - 12-24h analgesia)
• Hypotension management: Phenylephrine 50-100mcg IV boluses (first-line) or infusion 25-50mcg/min; ephedrine 6-12mg IV if bradycardia coexists
• PDPH treatment: Conservative (bed rest, fluids, caffeine 300mg PO, paracetamol); epidural blood patch (15-20mL autologous blood) if persistent >24-48h

Surgical/Interventional

• Epidural blood patch: Definitive treatment for PDPH - success rate >85% with first patch
• Emergency decompressive surgery: For epidural haematoma (within 6-12 hours) or abscess

Referral Criteria

• Neurological deficit post-spinal - emergency MRI and neurosurgical/orthopaedic spinal referral
• Persistent PDPH >48 hours - anaesthetic review for blood patch
• Suspected infection - microbiological and surgical input

• Permanent neurological injury: ~1 in 25,000 neuraxial blocks (NAP3)
• PDPH: 1-2% with pencil-point needles; 70% resolve within 1 week; blood patch effective in >85%
• Epidural haematoma: Neurological outcome depends on speed of decompression - >80% good outcome if operated within 6-12 hours
• Cauda equina syndrome: Permanent bladder dysfunction in up to 50% if not rapidly treated
• Overall safety: Spinal anaesthesia has lower morbidity and mortality than GA for many procedures (especially caesarean section and hip fracture surgery)

Intrathecal Drug Doses

Contraindications to Spinal Anaesthesia

Anticoagulant Timing for Neuraxial Block (AAGBI/ESRA)

Key Facts

Epidural anaesthesia/analgesia is one of the most versatile regional techniques, providing segmental blockade that can be titrated and maintained via a catheter. It is widely used in obstetrics, major surgery, and chronic pain management.

Epidemiology

Approximately 400,000 epidurals are performed annually in the UK. Labour epidural rates vary by unit (20-50%). Approximately 1% of epidurals result in accidental dural puncture (ADP). NAP3 estimated permanent harm from epidural anaesthesia at approximately 1 in 25,000.

Aetiology

The epidural space contains fat, lymphatics, and the internal vertebral venous plexus. LA injected into this space diffuses across the dura to block spinal nerve roots segmentally. The catheter allows continuous infusion or patient-controlled boluses.

Pathophysiology

Mechanism of action:

• LA diffuses through dural cuffs around nerve roots in the epidural space
• Also acts directly on spinal cord via transmeningeal diffusion
• Opioids act on spinal cord dorsal horn receptors (lipophilic: fentanyl - segmental; hydrophilic: morphine/diamorphine - more rostral spread)

Block characteristics:

• Onset slower than spinal (15-30 min)
• Incremental dosing allows titration of block height
• Less dense motor block than spinal (especially with dilute solutions)
• Sympathetic blockade causes vasodilation and hypotension (less than spinal)

Labour Epidural

• Effective pain relief within 15-30 minutes
• Low-dose technique maintains mobility (mobile epidural)
• PCEA with background infusion is standard practice

Surgical Epidural

• Higher concentration LA (bupivacaine 0.5%) for denser block
• Used for thoracic, abdominal, and lower limb surgery
• Thoracic epidural: T6-T10 for upper abdominal surgery; reduces respiratory complications

Post-Operative Epidural

• Continued infusion for 48-72 hours post-major surgery
• Superior analgesia to IV opioids for thoracotomy, major abdominal surgery
• Reduces respiratory complications, ileus, and opioid side effects

Complications

• Inadequate/patchy block (10-15%)
• Hypotension, nausea
• Pruritus (opioid-related)
• Urinary retention
• Accidental dural puncture → PDPH
• Epidural haematoma, abscess (rare)

Red Flags

• Sudden onset dense bilateral motor block - suspect intrathecal migration of catheter
• Unilateral block - catheter may be lateral; consider repositioning
• Severe back pain + fever + progressive weakness - epidural abscess (emergency MRI)
• High block with respiratory compromise - manage as for total spinal

Bedside

• Pre-procedure: Coagulation status, consent, IV access, monitoring
• Loss of resistance: Air or saline technique to identify epidural space
• Test dose: Lidocaine 2% 3mL with adrenaline 1:200,000 - detect intrathecal or intravascular placement
• Assessment: Bilateral cold sensation, motor power (Bromage scale)

Bloods

• Coagulation screen: Before insertion and removal in anticoagulated patients
• Platelet count: >75 × 10⁹/L required
• FBC: Baseline, especially if epidural for major surgery

Imaging

• Urgent MRI: If epidural haematoma or abscess suspected

Special Tests

• Hourly assessment: Sensory level, motor block, pain score, observations
• Daily catheter site inspection: Signs of infection (redness, swelling, discharge)
• PDPH assessment: Postural component, cranial nerve involvement (VI nerve palsy, hearing loss)

Non-pharmacological

• Positioning: Sitting or lateral for insertion; wedge/left tilt for obstetric procedures
• Aseptic technique: Full aseptic precautions including hat, mask, gown, gloves, drape
• Catheter care: Secure with adhesive dressing; daily inspection
• Nursing protocols: Hourly observations, motor block assessment, catheter site checks

Pharmacological

• Labour epidural: Bupivacaine 0.1% + fentanyl 2mcg/mL - PCEA 10mL bolus with 20min lockout ± background infusion 5-10mL/hr
• Surgical epidural: Bupivacaine 0.5% or levobupivacaine 0.5% - incremental 5mL boluses to desired level
• Post-operative infusion: Bupivacaine 0.1-0.125% + fentanyl 2mcg/mL at 5-15mL/hr
• Hypotension: Phenylephrine 50-100mcg IV or ephedrine 6-12mg IV; IV fluid co-loading
• PDPH: Paracetamol, caffeine 300mg PO TDS; epidural blood patch (15-20mL) if persistent

Surgical/Interventional

• Epidural blood patch: 15-20mL autologous blood injected into epidural space - success rate >85%
• Surgical decompression: For epidural haematoma or abscess with neurological deficit

Referral Criteria

• Failed epidural with inadequate analgesia - senior anaesthetic review
• Accidental dural puncture - anaesthetic follow-up for PDPH monitoring
• Neurological deficit post-epidural - emergency investigation and neurosurgical referral

• Labour epidural satisfaction: >85% rate effective pain relief
• Failure rate: 10-15% require re-siting or supplementation
• PDPH after ADP: Occurs in 50-80%; most resolve with conservative measures within 1-2 weeks; blood patch effective in >85%
• Permanent neurological injury: ~1 in 25,000 (NAP3) - includes epidural haematoma and abscess
• Post-operative epidural: Reduces respiratory complications by 30-50% after major abdominal/thoracic surgery (meta-analyses)

Epidural vs Spinal Anaesthesia

Labour Epidural and Obstetric Outcomes

Key Facts

Airway management is the primary responsibility of the anaesthetist. Failure to maintain the airway is the leading cause of anaesthesia-related mortality. Structured assessment, planning, and use of algorithms are essential for safe practice.

Epidemiology

NAP4 (4th National Audit Project, 2011) found that airway complications accounted for approximately 60% of anaesthesia-related deaths. CICO events occurred in approximately 1 in 50,000 anaesthetics. Poor airway management in ICU was highlighted as a significant contributor to adverse outcomes.

Aetiology

Difficult airway situations arise from:

• Anatomical factors: Obesity, short neck, receding mandible, large tongue, limited mouth opening, cervical spine immobility
• Pathological factors: Head/neck tumours, previous radiotherapy, burns, trauma, infection (Ludwig's angina, epiglottitis)
• Physiological factors: Pregnancy (oedema, reduced FRC), obesity (rapid desaturation)

Pathophysiology

The upper airway functions as a conduit for ventilation. During anaesthesia, loss of muscle tone causes posterior displacement of the tongue and epiglottis, obstructing the airway. The goal of airway management is to maintain a patent airway for oxygenation and ventilation while protecting the lungs from aspiration.

Airway Assessment (Pre-operative)

• Mallampati score (I-IV): Assess oropharyngeal view
• Thyromental distance: <6.5cm suggests difficult intubation
• Mouth opening: <3 finger-breadths concerning
• Neck mobility: Reduced extension limits intubation
• Body habitus: BMI, neck circumference
• Dental assessment: Loose teeth, prominent incisors, dental prosthetics

Signs of Airway Obstruction

• Snoring, gurgling, stridor
• See-saw (paradoxical) breathing
• Use of accessory muscles
• Desaturation
• Absent or reduced breath sounds

Airway Devices (Escalation)

1. Basic manoeuvres: Head tilt-chin lift, jaw thrust
2. Oropharyngeal (Guedel) or nasopharyngeal airway
3. Supraglottic airway device (SGA/LMA)
4. Endotracheal tube (ETT)
5. Emergency front-of-neck access (cricothyroidotomy)

Red Flags

• Rapid desaturation despite airway manoeuvres - escalate immediately
• Cannot intubate, cannot oxygenate - declare CICO, perform eFONA
• Stridor pre-operatively - suggests significant airway compromise
• Expanding neck haematoma - secure airway urgently before complete obstruction

Bedside

• Airway assessment: Mallampati, thyromental distance, mouth opening, neck extension, dentition
• Capnography (ETCO2): Gold standard for confirming ETT placement - trace confirms tracheal position
• SpO2: Continuous monitoring during airway management
• Auscultation: Bilateral chest and epigastrium after intubation

Bloods

• Not specific to airway management

Imaging

• Neck X-ray/CT: If cervical spine injury or retropharyngeal abscess suspected
• CT neck: Pre-operative planning for known difficult airway (tumour, tracheal deviation)
• CXR: Post-intubation to confirm ETT position (tip at T2-T4 level)
• Nasendoscopy: For anticipated difficult airway - ENT assessment of upper airway anatomy

Special Tests

• Fibreoptic intubation: Awake fibreoptic nasotracheal intubation for anticipated difficult airway
• Point-of-care ultrasound: Identify cricothyroid membrane, assess airway anatomy

Non-pharmacological

• Positioning: Ramped position (ear-to-sternal notch alignment) - improves laryngoscopy, essential in obese patients
• Pre-oxygenation: 100% O2 for 3 minutes (or 8 vital capacity breaths) - extends safe apnoea time
• Apnoeic oxygenation: Nasal high-flow O2 (THRIVE) during laryngoscopy - extends safe apnoea time

Pharmacological

• Induction: Propofol 2-3mg/kg or thiopental 3-5mg/kg
• Neuromuscular blockade: Rocuronium 0.6-1.2mg/kg or suxamethonium 1-1.5mg/kg (RSI)
• Sugammadex 16mg/kg: Immediate reversal of rocuronium in CICO/failed intubation scenarios
• Topical LA: 4% lidocaine spray for awake intubation
• Antisialagogue: Glycopyrrolate 200mcg IV for awake fibreoptic intubation

Surgical/Interventional

• Scalpel cricothyroidotomy (eFONA): For CICO - DAS recommends scalpel-bougie-tube technique
• Surgical tracheostomy: Planned or emergency for prolonged ventilation or known difficult airway
• Percutaneous tracheostomy: ICU - typically at 7-10 days of intubation

Referral Criteria

• Known or anticipated difficult airway - senior anaesthetist planning, ENT standby
• Failed intubation - follow DAS algorithm, consider wake-up or alternative plan
• CICO event - critical incident reporting, post-event debrief, psychological support for team

• NAP4 findings: Airway complications are responsible for ~60% of anaesthesia-related deaths
• CICO frequency: ~1 in 50,000 anaesthetics; eFONA success rate >90% when performed promptly
• Failed intubation: Occurs in ~1 in 2,000 routine anaesthetics; higher in obstetrics (~1 in 400)
• Aspiration: Mortality ~5% when it occurs; risk factors include emergency surgery, obesity, pregnancy
• Videolaryngoscopy: Reduces failed intubation rates by 50% compared with direct laryngoscopy

Mallampati Classification

DAS Failed Intubation Algorithm (Simplified)

Cormack-Lehane Grading

Key Facts

The difficult airway represents one of the most challenging scenarios in anaesthetic practice. Unanticipated difficulty accounts for significant morbidity and mortality. Structured pre-operative assessment and adherence to algorithms are the cornerstones of safe management.

Epidemiology

Difficult intubation occurs in 1-4% of anaesthetics. Failed intubation in 1 in 2,000 routine cases, rising to 1 in 400 in obstetrics. CICO events occur in approximately 1 in 50,000. NAP4 found that human factors (poor planning, failure to use algorithms) contributed to the majority of airway disasters.

Aetiology

Predictors of difficult intubation:

• Mallampati III-IV, short thyromental distance (<6.5cm), limited mouth opening (<3cm)
• Obesity (BMI >30), short thick neck, large tongue
• Previous difficult intubation (documented in notes/alert card)
• Head and neck pathology: tumours, radiotherapy, burns, infection
• Cervical spine immobility: trauma, rheumatoid arthritis, ankylosing spondylitis
• Pregnancy: Airway oedema, large breasts, weight gain

Pathophysiology

Difficult airway situations create a physiological crisis of progressive hypoxaemia. Each failed attempt at laryngoscopy worsens airway oedema and bleeding, further reducing the chances of subsequent attempts. The safe apnoea time (time to critical desaturation) varies: healthy adult ~8 minutes (after pre-oxygenation), obese patient ~3 minutes, pregnant patient ~2-3 minutes, child ~2 minutes.

Pre-Operative Assessment Findings Suggesting Difficulty

• Previous difficult intubation documented
• Mallampati III/IV
• Reduced mouth opening (<3 finger-breadths)
• Short thyromental distance (<6.5cm)
• Receding mandible, prominent upper incisors
• Limited neck extension
• Obesity, short neck, high BMI
• Head/neck pathology (radiation, tumour, abscess)

Intra-Operative Difficult Airway

• Poor laryngoscopic view (Cormack-Lehane 3 or 4)
• Multiple failed intubation attempts
• Failed SGA placement
• Inability to ventilate via facemask
• Progressive desaturation

Red Flags

• SpO2 falling below 90% - declare emergency, escalate to next plan in DAS algorithm
• Cannot ventilate despite SGA and facemask - declare CICO
• Stridor or voice change pre-operatively - suggests supraglottic pathology
• History of previous failed intubation/tracheostomy - awake technique essential

Bedside

• Structured airway assessment: LEMON, Mallampati, thyromental distance, mouth opening, neck extension, dentition
• Review previous anaesthetic records: Essential - check for documented difficulty
• Alert card/bracelet: Patient may carry difficult airway information

Bloods

• Not specifically required for airway assessment

Imaging

• CT/MRI neck: If tumour, abscess, tracheal deviation, or subglottic stenosis suspected
• Lateral cervical spine X-ray: Assess atlantoaxial subluxation (rheumatoid arthritis, Down syndrome)
• Nasendoscopy: ENT assessment of supraglottic and glottic anatomy

Special Tests

• Ultrasound of neck: Identify cricothyroid membrane (especially in obese patients or those with abnormal anatomy)
• Point-of-care airway ultrasound: Increasingly used for pre-operative planning

Non-pharmacological

• Pre-operative planning: Discuss with patient, document plan, brief theatre team
• Equipment preparation: Full difficult airway trolley available; videolaryngoscope, fibreoptic scope, cricothyroidotomy kit
• Positioning: Optimal head position (ramped in obese patients)
• Pre-oxygenation: 3 minutes tidal breathing or 8 vital capacity breaths with 100% O2

Pharmacological

• Awake fibreoptic intubation: Topical 4% lidocaine (nebulised + spray-as-you-go), sedation with remifentanil TCI 1-3ng/mL
• Neuromuscular blockade: Rocuronium (allows sugammadex reversal) preferred over suxamethonium in many anticipated difficult scenarios
• Sugammadex 16mg/kg: Immediate reversal of rocuronium - use in failed intubation before Plan D if applicable
• Dexamethasone 8mg IV: May reduce airway oedema from repeated instrumentation

Surgical/Interventional

• Emergency front-of-neck access (eFONA): Scalpel-bougie-tube technique (DAS 2015)
• Surgical tracheostomy: Under local anaesthesia for anticipated impossible intubation
• Retrograde intubation: Wire-guided technique (rarely used with availability of fibreoptic)

Referral Criteria

• Known difficult airway - senior/consultant anaesthetist involvement
• Anticipated surgical airway - ENT/maxillofacial surgery standby
• Post-CICO event - critical incident review, patient follow-up, difficult airway alert documentation

• AFOI success rate: >95% in experienced hands
• Videolaryngoscopy: Improves first-pass success rate to >95% even in difficult airways
• eFONA success rate: >90% when performed promptly using scalpel technique
• Morbidity from repeated laryngoscopy: Airway oedema, bleeding, dental damage - limits subsequent success
• Litigation: Airway management claims are among the most common in anaesthetic negligence cases

DAS 2015 Unanticipated Difficult Intubation Algorithm

Risk Factors for Difficult Mask Ventilation (MOANS)

Key Facts

RSI is performed to secure the airway rapidly while minimising the risk of regurgitation and aspiration of gastric contents. It is one of the most critical skills in anaesthetic, emergency, and intensive care practice.

Epidemiology

Aspiration during anaesthesia occurs in approximately 1 in 3,000-10,000 anaesthetics. RSI is performed in approximately 10-20% of all general anaesthetics. Mortality from aspiration is approximately 5% when it occurs. RSI is the standard induction technique for all emergency surgery in unfasted patients.

Aetiology

Indications for RSI:

• Unfasted patient / emergency surgery
• Bowel obstruction, ileus
• Pregnancy (after 16 weeks)
• Severe GORD, hiatus hernia
• Reduced consciousness (GCS <8)
• Oesophageal pathology (achalasia, stricture)
• Diabetic gastroparesis
• Recent trauma with abdominal injury

Pathophysiology

Aspiration of gastric contents (Mendelson's syndrome) causes chemical pneumonitis from acid (pH <2.5, volume >25mL), leading to acute inflammation, surfactant destruction, and ARDS. Particulate aspiration can cause mechanical airway obstruction. RSI minimises the at-risk period between loss of airway reflexes and tracheal intubation with a cuffed ETT.

RSI Sequence

1. Preparation: Check equipment (ETCO2, suction, bougie, backup plan), preoxygenation
2. Pre-oxygenation: 3 minutes tidal breathing with tight-fitting mask and 100% O2
3. IV induction: Predetermined dose - propofol 2-3mg/kg (or thiopental/ketamine)
4. Neuromuscular blockade: Suxamethonium 1-1.5mg/kg or rocuronium 1.2mg/kg
5. Cricoid pressure: Applied by trained assistant at loss of consciousness (30N)
6. Intubation: After fasciculations cease (suxamethonium) or 60-90s (rocuronium)
7. Confirmation: ETCO2 trace - gold standard

Post-Intubation

• Inflate cuff, confirm ETT position (ETCO2, bilateral chest expansion, auscultation)
• Release cricoid pressure after cuff inflation and ETCO2 confirmed
• Secure ETT, commence anaesthesia

Red Flags

• Failed intubation after RSI - follow DAS failed intubation algorithm
• Aspiration visualised - suction, head-down tilt, continue intubation, bronchoscopy if particulate
• Desaturation during apnoea - consider modified RSI with gentle ventilation in future

Bedside

• ETCO2 (capnography): Mandatory - gold standard for confirming tracheal placement
• SpO2: Continuous monitoring
• Auscultation: Bilateral chest and epigastrium
• Pre-oxygenation assessment: EtO2 >0.87 (87%) confirms adequate denitrogenation

Bloods

• Plasma cholinesterase levels: If suxamethonium apnoea suspected (prolonged paralysis)
• Dibucaine number: Differentiates normal from atypical cholinesterase variants

Imaging

• CXR: If aspiration suspected - diffuse bilateral infiltrates
• CT chest: If severe aspiration with ARDS

Special Tests

• Bronchoscopy: If particulate aspiration suspected - therapeutic removal
• Cholinesterase phenotyping: For suxamethonium apnoea - family screening

Non-pharmacological

• Team briefing: Clear communication of roles (intubator, cricoid pressure, drug administrator)
• Equipment check: Laryngoscope, ETT (check cuff), bougie, suction, SGA as backup, eFONA kit
• Patient positioning: Head elevated 20-30°, ramped in obese patients
• Nil by mouth: 6 hours solids, 2 hours clear fluids where possible (emergency setting may preclude this)

Pharmacological

• Induction agents: Propofol 2-3mg/kg (most common), thiopental 3-5mg/kg (historical), ketamine 1-2mg/kg (haemodynamically unstable patients)
• Suxamethonium 1-1.5mg/kg: Fastest onset (45-60s), ultra-short duration (5-10 min); contraindicated in hyperkalaemia, burns >24h, denervation injuries, malignant hyperthermia susceptibility
• Rocuronium 1.2mg/kg: Alternative - onset 60-90s, longer duration but reversible with sugammadex 16mg/kg
• Opioid co-induction: Fentanyl 1-3mcg/kg or alfentanil 10-20mcg/kg - attenuates haemodynamic response to laryngoscopy
• Aspiration prophylaxis: Ranitidine 150mg PO or IV (when available), sodium citrate 30mL 0.3M PO (obstetrics)

Surgical/Interventional

• eFONA: If CICO scenario develops during RSI
• Bronchoscopy: For particulate aspiration management

Referral Criteria

• Failed RSI - senior anaesthetist involvement
• Aspiration event - ICU care for monitoring and potential ARDS management
• Suxamethonium apnoea - anaesthetic follow-up, family testing, alert card issue

• Aspiration incidence during RSI: <0.05% when properly performed
• Suxamethonium apnoea: Occurs in 1 in 2,500 (heterozygous atypical cholinesterase); 1 in 25,000 (homozygous)
• Mendelson's syndrome mortality: ~5% overall; higher if pH <2.5 and volume >25mL
• RSI first-pass intubation success: >95% in experienced hands
• Rocuronium-based RSI: Equivalent first-pass success to suxamethonium with sugammadex safety net

Suxamethonium vs Rocuronium for RSI

Contraindications to Suxamethonium

Key Facts

IV anaesthetic agents provide rapid induction of unconsciousness and are fundamental to modern anaesthetic practice. Understanding their pharmacology, indications, and side effects is essential for safe anaesthesia.

Epidemiology

Propofol is used in >90% of IV inductions in the UK. TIVA accounts for approximately 15-20% of all GAs and is increasing. PRIS is rare but fatal - reported in prolonged ICU sedation.

Aetiology

IV anaesthetic agents produce unconsciousness by enhancing inhibitory neurotransmission (GABA-A: propofol, thiopental, etomidate) or blocking excitatory transmission (NMDA: ketamine). Each agent has a distinct pharmacokinetic profile governed by redistribution (initial offset) and metabolism (terminal elimination).

Pathophysiology

Ketamine: Produces dissociative anaesthesia - eyes remain open, muscle tone preserved. Sympathomimetic effects (releases catecholamines) maintain BP and HR. Bronchodilator. Increases secretions. Emergence phenomena (hallucinations, nightmares) occur in ~10-30% of adults.

Etomidate: Minimal cardiovascular effect - ideal for shock. Inhibits 11-beta-hydroxylase → adrenocortical suppression even after single dose (24h). Not recommended for repeated/prolonged use.

Propofol

• Rapid smooth induction, antiemetic
• Pain on injection (~30-40%) - reduce with lidocaine 20-40mg IV pre-treatment
• Cardiovascular depression: hypotension (~20-30% BP drop)
• Respiratory depression: apnoea at induction
• Green discolouration of urine (harmless)

Ketamine

• Dissociative state: eyes open, nystagmus, preserved airway reflexes
• Sympathomimetic: tachycardia, hypertension, bronchodilation
• Increased salivation (give glycopyrrolate 200mcg IV)
• Emergence phenomena: nightmares, hallucinations (reduce with midazolam 1-2mg IV)
• Raises ICP (controversial - may be safe with controlled ventilation)

Etomidate

• Haemodynamic stability - minimal BP change
• Myoclonus (~30-60%) - reduce with opioid pre-treatment
• Adrenocortical suppression - avoid in sepsis, Addison's disease
• Pain on injection, nausea/vomiting

Red Flags

• Severe hypotension after propofol - consider hypovolaemia, reduce dose
• Prolonged propofol infusion >4mg/kg/hr in ICU - risk of PRIS (metabolic acidosis, rhabdomyolysis, cardiac failure)
• Emergence delirium with ketamine - treat with benzodiazepine

Bedside

• Haemodynamic monitoring: BP, HR - propofol causes significant drops
• BIS (Bispectral Index): Depth of anaesthesia monitoring for TIVA - target 40-60
• ETCO2: Ventilation monitoring

Bloods

• ABG/VBG: If PRIS suspected (metabolic acidosis, raised lactate)
• CK: Rhabdomyolysis in PRIS
• Triglycerides: Propofol emulsion contains soy bean oil - monitor in prolonged infusion
• Cortisol: If etomidate-induced adrenal suppression suspected

Imaging

• Not routinely required for IV anaesthetic agent use

Special Tests

• Processed EEG (BIS/Entropy): Monitor depth of anaesthesia during TIVA to reduce awareness risk

Non-pharmacological

• Dose adjustment: Reduce propofol dose in elderly, hypovolaemic, and ASA III-IV patients
• Pre-treatment: Lidocaine 20-40mg IV or mixed with propofol to reduce injection pain
• Fasting: Standard pre-operative fasting guidelines

Pharmacological

• Propofol induction: 1-2.5mg/kg IV (elderly 0.5-1.5mg/kg); TIVA maintenance: TCI 3-6mcg/mL (Marsh/Schnider model)
• Ketamine induction: 1-2mg/kg IV or 4-6mg/kg IM; maintenance 0.5-1mg/kg IV boluses or infusion 1-2mg/kg/hr
• Etomidate: 0.3mg/kg IV - single use for induction only
• Thiopental: 3-5mg/kg IV - declining use in UK; still used for refractory status epilepticus
• Midazolam: 1-2mg IV as co-induction agent (reduces propofol requirement by 20-30%)

Surgical/Interventional

• Not applicable

Referral Criteria

• Suspected PRIS - ICU management, stop propofol, switch to alternative sedation
• Severe emergence delirium with ketamine - anaesthetic/psychiatric support

• Propofol: Excellent safety profile; PRIS mortality >50% if not recognised early
• Ketamine: Resurgence in use for procedural sedation, analgesia, and treatment-resistant depression
• Etomidate: Adrenal suppression lasts ~24 hours after single dose - clinically significant in sepsis (CORTICUS trial context)
• Awareness under TIVA: Risk reduced to ~1:8,000 with BIS monitoring (vs 1:19,600 overall per NAP5)

Pharmacokinetic Comparison

Propofol Infusion Syndrome (PRIS)

Key Facts

Inhalational anaesthetic agents remain fundamental to anaesthetic practice for maintenance of general anaesthesia. They offer predictable pharmacokinetics, ease of administration, and built-in monitoring (end-tidal concentration correlates with brain concentration).

Epidemiology

Approximately 80-85% of general anaesthetics in the UK use volatile agents for maintenance (remainder are TIVA). Sevoflurane has largely replaced isoflurane for routine use. There is increasing awareness of the environmental impact - desflurane has a global warming potential 2,500 times that of CO2.

Aetiology

The mechanism of action of volatile agents is not fully understood. The Meyer-Overton hypothesis correlates potency with lipid solubility. Modern theory focuses on actions at specific protein targets: GABA-A receptor potentiation (enhances inhibition), NMDA receptor antagonism (reduces excitation), glycine receptor modulation, and two-pore-domain potassium channel activation.

Pathophysiology

Pharmacokinetics:

• Delivery is determined by inspired concentration, alveolar ventilation, and cardiac output
• Uptake depends on blood:gas partition coefficient (lower = faster onset)
• Blood:gas coefficients: Desflurane 0.42, sevoflurane 0.65, isoflurane 1.4
• Recovery is essentially the reverse of uptake - agents with low solubility allow faster emergence
• Metabolism is minimal for most agents; sevoflurane produces Compound A (fluoride ion) in closed circuits with soda lime

Sevoflurane

• Non-pungent - suitable for inhalational induction (especially paediatrics)
• Rapid onset and offset
• Mild cardiovascular depression
• Can cause emergence agitation in children

Desflurane

• Fastest offset of all volatiles (blood:gas 0.42)
• Pungent - NOT suitable for inhalational induction (causes coughing, laryngospasm)
• Sympathetic activation at rapid concentration increases
• Highest environmental impact (GWP)

Isoflurane

• Moderate onset/offset
• Good muscle relaxation, coronary vasodilation
• Pungent - not ideal for inhalational induction

Nitrous Oxide

• Analgesic at sub-anaesthetic concentrations (Entonox = 50% N2O + 50% O2)
• Second gas effect (accelerates uptake of co-administered volatile)
• Diffusion hypoxia on discontinuation (give 100% O2 for 5 min)
• Inhibits methionine synthase (B12 inactivation) - avoid in B12 deficiency, prolonged use

Red Flags

• Rising ETCO2 + tachycardia + rigidity + hyperthermia - malignant hyperthermia (stop volatile, dantrolene)
• Sudden hypotension with volatile - check depth, consider hypovolaemia or anaphylaxis
• Post-operative hepatitis (rare) - halothane was most common cause (now obsolete in UK)

Bedside

• End-tidal agent monitoring: Mandatory - correlates with brain concentration at steady state
• AAGBI standard monitoring: SpO2, ECG, NIBP, ETCO2, temperature
• Agent analyser: Confirms correct agent and concentration

Bloods

• LFTs: If post-operative hepatitis suspected (historical with halothane)
• Fluoride levels: Not routinely measured; relevant to sevoflurane metabolism
• CK, potassium, ABG: If malignant hyperthermia suspected

Imaging

• Not specific to volatile agent use

Special Tests

• Malignant hyperthermia susceptibility testing: In vitro contracture test (IVCT) - gold standard, performed at specialist centres (Leeds, London)
• Caffeine halothane contracture test: Muscle biopsy-based diagnostic

Non-pharmacological

• Vaporiser use: Agent-specific calibrated vaporisers (Tec 6 for desflurane - requires heating)
• Low-flow anaesthesia: Reduce fresh gas flow to 0.5-1L/min to reduce agent consumption and environmental impact
• Scavenging: Active scavenging systems mandatory in all theatres to reduce occupational exposure

Pharmacological

• Sevoflurane: MAC 2.0% in 100% O2; adjusted for age, opioids (reduce MAC by 50-70%), N2O (reduces MAC by 25-30%)
• Desflurane: MAC 6.0%; maintenance typically 3-6% in air/O2
• Isoflurane: MAC 1.15%; maintenance typically 0.5-1.5% in air/O2
• N2O: 50-70% as carrier gas with volatile; Entonox (50:50) for analgesia
• MAC reduction: Age >70 (~30% reduction), opioids, benzodiazepines, alpha-2 agonists, hypothermia

Surgical/Interventional

• Not applicable

Referral Criteria

• Suspected malignant hyperthermia - specialist centre referral for IVCT
• Environmental concerns - hospital sustainability teams promoting TIVA and low-flow techniques

• Volatile anaesthetics have an excellent safety profile with decades of clinical use
• Malignant hyperthermia mortality: <5% with early recognition and dantrolene treatment (previously >70%)
• Environmental impact: Volatile anaesthetic agents contribute approximately 5% of the NHS carbon footprint
• POCD: Some evidence of neurotoxicity in developing brains (animal models); clinical significance debated
• Sevoflurane nephrotoxicity: Compound A concerns in closed circuits have not translated to clinical harm at standard flows

MAC Values and Factors Affecting MAC

Environmental Impact of Volatile Agents

Key Facts

NMBAs are essential drugs in anaesthetic practice, enabling tracheal intubation, surgical relaxation, and ventilator synchrony. Understanding their pharmacology and the importance of neuromuscular monitoring is critical for patient safety.

Epidemiology

NMBAs are used in approximately 50-60% of all general anaesthetics. Residual neuromuscular blockade (TOF <0.9) in PACU is common (~30-40%) and is associated with a 3-fold increase in respiratory complications. Sugammadex has significantly reduced the incidence of residual paralysis.

Aetiology

Classification:

• Depolarising: Suxamethonium - mimics ACh, causing initial depolarisation (fasciculations) followed by block
• Non-depolarising: Competitive antagonists at nicotinic ACh receptors; aminosteroids (rocuronium, vecuronium, pancuronium) and benzylisoquinoliniums (atracurium, cisatracurium, mivacurium)

Pathophysiology

Depolarising block (Phase I): Suxamethonium binds receptor, causes sustained depolarisation → initial fasciculation then flaccid paralysis. Not reversed by anticholinesterases.

Suxamethonium Effects

• Fasciculations followed by complete paralysis
• Jaw relaxation within 45-60 seconds
• Duration 5-10 minutes (plasma cholinesterase metabolism)
• Side effects: K⁺ rise (0.5-1 mmol/L), raised IOP, raised ICP, bradycardia (especially repeat doses), masseter spasm, malignant hyperthermia trigger

Non-Depolarising Block

• Gradual onset of paralysis (60-120s for rocuronium, 2-3 min for atracurium)
• Duration 20-50 minutes depending on agent
• No fasciculations
• Histamine release with atracurium (flushing, bronchospasm, hypotension - less with cisatracurium)

Residual Neuromuscular Block

• Subjective weakness, inability to sustain head lift for 5 seconds
• Reduced tidal volume, hypoxia, inability to clear secretions
• Objective: TOF ratio <0.9

Red Flags

• Prolonged block after suxamethonium (>20 min) - plasma cholinesterase deficiency
• TOF ratio <0.9 at extubation - risk of respiratory failure in PACU
• Masseter spasm after suxamethonium - may be early sign of malignant hyperthermia
• Unexplained tachycardia with rising ETCO2 after suxamethonium - suspect MH

Bedside

• Peripheral nerve stimulator (TOF monitor): Mandatory when NMBAs used
• TOF count: Number of twitches visible (0-4); count ≥2 required before neostigmine reversal
• TOF ratio: Quantitative - ratio of 4th to 1st twitch; >0.9 required for safe extubation
• Post-tetanic count (PTC): Assess deep block when TOF count = 0

Bloods

• Plasma cholinesterase levels: If suxamethonium apnoea suspected
• Dibucaine number: Normal 80%; heterozygous atypical 40-70%; homozygous atypical <20%
• Serum tryptase: If anaphylaxis to NMBA suspected

Imaging

• Not applicable

Special Tests

• Quantitative neuromuscular monitoring (acceleromyography): Gold standard - TOFscan, TOF-Watch
• Allergy testing: Skin prick and intradermal for NMBA allergy (most common drug cause of perioperative anaphylaxis)

Non-pharmacological

• Neuromuscular monitoring: Use TOF monitor for ALL patients receiving NMBAs
• Clinical assessment: Head lift for 5s, grip strength, tongue protrusion - but objective monitoring preferred
• Ventilatory support: Continue ventilation until adequate reversal confirmed

Pharmacological

• Neostigmine 2.5mg + glycopyrrolate 0.5mg IV: Standard reversal of non-depolarising block; only effective at TOF count ≥2; glycopyrrolate prevents neostigmine-induced bradycardia
• Sugammadex: Dose depends on depth of rocuronium/vecuronium block:
  • TOF count ≥2: 2mg/kg
  • PTC ≥1 (deep block): 4mg/kg
  • Immediate reversal (CICO/failed intubation): 16mg/kg
• Suxamethonium apnoea management: Ventilate, sedate, monitor TOF, await spontaneous recovery; do NOT give neostigmine

Surgical/Interventional

• Not applicable

Referral Criteria

• Suxamethonium apnoea - anaesthetic follow-up, plasma cholinesterase testing, family screening, issue of alert card
• Suspected NMBA anaphylaxis - allergy clinic referral (6 weeks post-event)
• Myasthenia gravis - joint anaesthetic-neurological planning

• Sugammadex reversal: Complete reversal within 2-3 minutes (even from deep block)
• Residual paralysis: Incidence reduced from 30-40% to <5% with routine sugammadex use and quantitative monitoring
• Suxamethonium apnoea: Homozygous atypical cholinesterase (~1:25,000) - paralysis may last 4-8 hours; excellent prognosis with supportive care
• NMBA anaphylaxis: Rocuronium and suxamethonium are the most common causes of perioperative anaphylaxis (NAP6); mortality <5% with prompt treatment

Comparison of Common NMBAs

Sugammadex Dosing Guide

Key Facts

Pain is a subjective experience defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage (IASP definition). Effective pain management is a fundamental right and significantly impacts recovery, mobility, and patient satisfaction.

Epidemiology

Inadequate post-operative pain management affects approximately 30-40% of surgical patients. Chronic post-surgical pain develops in approximately 10-50% of patients depending on surgery type (highest after thoracotomy, mastectomy, amputation). Chronic pain affects approximately 28 million adults in the UK.

Aetiology

Pain classification:

• Nociceptive: Somatic (well-localised, sharp) or visceral (diffuse, cramping)
• Neuropathic: Nerve damage - burning, shooting, allodynia, hyperalgesia
• Nociplastic: Central sensitisation without clear tissue or nerve damage (e.g., fibromyalgia)
• Acute: <3 months, usually nociceptive, serves protective function
• Chronic: >3 months, complex biopsychosocial condition

Pathophysiology

Pain pathway:

1. Transduction: Noxious stimulus activates nociceptors (Aδ and C fibres)
2. Transmission: Via dorsal root ganglion to dorsal horn of spinal cord
3. Modulation: Gate control theory - inhibitory and facilitatory pathways in dorsal horn, descending modulation from brainstem
4. Perception: Cortical processing - thalamus, somatosensory cortex, limbic system

Peripheral sensitisation: Inflammatory mediators (prostaglandins, bradykinin, substance P) lower nociceptor threshold Central sensitisation: Wind-up phenomenon, NMDA receptor activation, increased excitability of spinal neurones

Acute Pain

• Proportional to tissue injury
• Associated autonomic responses: tachycardia, hypertension, sweating
• Functional impact: reduced mobility, impaired coughing, poor sleep
• Responds well to analgesics and resolves with healing

Chronic Pain

• Pain beyond expected healing time (>3 months)
• Often disproportionate to identifiable pathology
• Associated with depression, anxiety, sleep disturbance, disability
• Neuropathic features common: allodynia, hyperalgesia, dysaesthesia

Pain Assessment

• Self-report is the gold standard
• Use validated tools: NRS, VAS, verbal rating scale
• Special populations: FLACC (children <7), Wong-Baker faces, Abbey Pain Scale (dementia), BPS (ventilated ICU patients)

Red Flags

• Acute pain with neurological deficit - consider cord/nerve compression
• Escalating opioid requirements - consider surgical complication, tolerance, or dependence
• Pain out of proportion to expected - consider compartment syndrome, ischaemia, or infection
• New chronic pain after surgery with neuropathic features - consider post-surgical neuropathy

Bedside

• Pain scoring: NRS at rest and on movement - document regularly
• Functional assessment: Ability to cough, mobilise, sleep
• Opioid side effect monitoring: Sedation score, respiratory rate, nausea, constipation, pruritus

Bloods

• Not specific to pain assessment (guided by underlying cause)

Imaging

• Guided by suspected cause of pain - not routine for pain assessment per se

Special Tests

• Quantitative sensory testing: For neuropathic pain characterisation (specialist pain clinics)
• Nerve conduction studies/EMG: If neuropathy suspected
• Psychological assessment: PHQ-9, GAD-7 - chronic pain commonly comorbid with depression/anxiety

Non-pharmacological

• Education and reassurance: Explain expected pain levels and management plan
• Physiotherapy: Early mobilisation, exercises, TENS
• Psychology: CBT is the most evidence-based psychological intervention for chronic pain (NICE NG193)
• Ice/heat therapy: For musculoskeletal pain

Pharmacological

Acute pain (WHO ladder + multimodal approach):

• Step 1: Paracetamol 1g QDS + NSAID (ibuprofen 400mg TDS or diclofenac 50mg TDS)
• Step 2: Add codeine 30-60mg QDS or tramadol 50-100mg QDS
• Step 3: Strong opioid - morphine 5-10mg PO 4-hourly or PCA (1mg bolus, 5-min lockout)
• Regional techniques: Local anaesthetic wound infiltration, nerve blocks, epidural analgesia

Neuropathic pain (NICE CG173):

• First-line: Amitriptyline 10-75mg ON, or duloxetine 60-120mg OD, or gabapentin 300-1200mg TDS, or pregabalin 75-300mg BD
• Second-line: Combination of above, or tramadol short-term
• Topical: Capsaicin 0.075% cream or lidocaine 5% patch (for localised neuropathic pain)

Surgical/Interventional

• Nerve blocks: Diagnostic and therapeutic
• Epidural/intrathecal drug delivery: For cancer pain and refractory chronic pain
• Spinal cord stimulation: For CRPS, failed back surgery syndrome (NICE TA159)
• Radiofrequency denervation: For facet joint pain

Referral Criteria

• Acute pain not responding to standard multimodal analgesia - acute pain team
• Chronic pain >3 months affecting function - chronic pain service referral
• Neuropathic pain not responding to first-line agents - pain specialist
• Cancer pain - palliative care and pain team input

• Acute post-operative pain: Resolves within days to weeks with appropriate multimodal analgesia in the majority
• Chronic post-surgical pain: Develops in 10-50% depending on surgery type; risk factors include pre-existing pain, catastrophising, younger age
• Neuropathic pain: 50% achieve ≥50% pain reduction with first-line agents; often requires combination therapy
• Chronic pain: Complete resolution is uncommon; management focuses on function, quality of life, and self-management
• Opioid dependence: Risk with prolonged post-operative opioid use >5-7 days - prescribe with clear tapering plan

WHO Analgesic Ladder

Equianalgesic Opioid Doses (Approximate)

NICE CG173 - Neuropathic Pain Pharmacological Ladder

Key Facts

Acute pain management has evolved from reactive opioid-based regimens to proactive multimodal, procedure-specific protocols. The aim is to provide effective analgesia while minimising side effects and promoting functional recovery.

Epidemiology

Approximately 60-70% of surgical patients report moderate-to-severe pain in the first 24 hours post-operatively despite analgesic interventions. Inadequate acute pain management is associated with delayed recovery, prolonged hospital stay, increased morbidity, and development of chronic post-surgical pain.

Aetiology

Acute pain is primarily nociceptive, arising from tissue damage during surgery or illness. Inflammatory mediators (prostaglandins, cytokines, bradykinin) sensitise peripheral nociceptors. Central sensitisation can occur with severe or prolonged pain, contributing to hyperalgesia and potentially chronic pain.

Pathophysiology

Surgical tissue damage releases intracellular contents and inflammatory mediators, activating and sensitising peripheral nociceptors. Afferent impulses reach the spinal cord dorsal horn, where modulation occurs. Multimodal analgesia targets multiple points in this pathway: peripheral (NSAIDs, LA), spinal (epidural, intrathecal opioids), and supraspinal (systemic opioids, paracetamol). Pre-emptive analgesia (given before surgical stimulus) may reduce central sensitisation.

Mild Pain (NRS 1-3)

• Managed with regular non-opioid analgesics
• Patient mobile and functional

Moderate Pain (NRS 4-6)

• Requires weak opioid addition or regional technique
• May limit mobility and function

Severe Pain (NRS 7-10)

• Requires strong opioid ± regional technique
• Associated autonomic responses: tachycardia, hypertension
• Impairs coughing, deep breathing → atelectasis, pneumonia risk

Opioid Side Effects

• Nausea and vomiting (30-50%)
• Constipation, pruritus
• Sedation, respiratory depression
• Urinary retention

Red Flags

• Respiratory rate <8/min or sedation score ≥3 - opioid overdose (naloxone 400mcg IV)
• Escalating pain requirements - consider surgical complication
• Pain with numbness/weakness - consider nerve injury or compartment syndrome
• Persistent pain beyond expected duration - risk of chronic post-surgical pain

Bedside

• Pain assessment: NRS at rest and on movement - at least 4-hourly
• Sedation score: 0 (alert) to 3 (unrousable) - monitor with opioids
• Respiratory rate: <8/min indicates significant opioid-induced respiratory depression
• Functional assessment: Ability to cough, deep breathe, mobilise

Bloods

• Guided by clinical situation (not specific to pain assessment)

Imaging

• If escalating pain suggests surgical complication - appropriate imaging (CT, USS)

Special Tests

• Epidural assessment: Sensory level, motor block, catheter site inspection (if epidural in situ)
• Nerve block assessment: Sensory distribution, motor function

Non-pharmacological

• Education: Pre-operative explanation of expected pain and plan
• Positioning: Optimal comfort, elevation of surgical site where appropriate
• Ice therapy: For musculoskeletal pain, swelling
• Early mobilisation: Within ERAS protocols - reduces pain, complications, and length of stay
• TENS: Adjunctive for some patients

Pharmacological

Standard multimodal regimen:

• Paracetamol 1g QDS (PO or IV) - foundation
• NSAID: Ibuprofen 400mg TDS PO or diclofenac 50mg TDS PO (if no contraindication)
• Weak opioid: Codeine 30-60mg QDS or tramadol 50-100mg QDS for moderate pain
• Strong opioid: Morphine 5-10mg PO 4-hourly PRN, or PCA (morphine 1mg bolus, 5-min lockout, no background infusion)
• Adjuvants: Gabapentin 300mg pre-op (reduces post-op pain and opioid use), ketamine sub-anaesthetic 0.1-0.2mg/kg/hr IV (opioid-tolerant patients), clonidine, dexamethasone

Regional techniques:

• Wound infiltration with LA (bupivacaine 0.25%)
• Peripheral nerve blocks (single shot or catheter)
• Epidural analgesia (bupivacaine 0.1% + fentanyl 2mcg/mL)

Surgical/Interventional

• Regional techniques as above
• Wound catheter infusion (local anaesthetic into wound)

Referral Criteria

• Uncontrolled pain despite standard analgesia - acute pain team
• Opioid-tolerant patients - specialist input for analgesic planning
• Suspected chronic post-surgical pain developing - early pain team referral

• Adequate multimodal analgesia: Reduces post-operative complications by 20-30% and shortens hospital stay
• PCA: Patient satisfaction >85%; respiratory depression <1% with appropriate monitoring
• Chronic post-surgical pain: Risk reduced with aggressive acute pain management, regional anaesthesia, and gabapentinoids
• Opioid tapering: Most patients should be opioid-free within 1-2 weeks of surgery; prolonged use >3 months associated with dependence

Procedure-Specific Analgesia (Examples)

Opioid Side Effect Management

Key Facts

Chronic pain is a major public health issue causing significant disability, mental health comorbidity, and healthcare utilisation. It is now recognised as a disease in its own right (ICD-11). Management has shifted from a biomedical to a biopsychosocial model emphasising self-management and functional rehabilitation.

Epidemiology

Chronic pain affects approximately 28 million adults in the UK (~43% of the population). It accounts for 4.6 million GP appointments annually. Chronic pain is the leading cause of disability worldwide. The economic cost to the UK is estimated at £12 billion annually in healthcare and lost productivity.

Aetiology

ICD-11 classification:

• Chronic primary pain: No identifiable underlying condition (fibromyalgia, chronic widespread pain, chronic primary headache)
• Chronic secondary pain: Associated with an underlying condition - musculoskeletal, neuropathic, cancer, post-surgical, visceral

Risk factors for chronification: Psychological distress, catastrophising, fear-avoidance beliefs, social isolation, previous chronic pain, adverse childhood experiences, litigation/compensation

Pathophysiology

Chronic pain involves:

• Peripheral sensitisation: Ongoing inflammatory mediator release lowering nociceptor thresholds
• Central sensitisation: Wind-up, NMDA receptor activation, microglial activation in spinal cord
• Descending modulation dysfunction: Impaired inhibitory pathways (serotonergic, noradrenergic)
• Neuroplastic changes: Cortical reorganisation, grey matter changes visible on fMRI
• Psychosocial amplification: Depression, anxiety, catastrophising amplify pain experience and disability

Common Chronic Pain Conditions

• Chronic low back pain: Most common cause of chronic pain in the UK
• Fibromyalgia: Widespread pain, fatigue, cognitive dysfunction, sleep disturbance
• Complex regional pain syndrome (CRPS): Burning pain, allodynia, vasomotor changes, trophic changes
• Neuropathic pain: Post-herpetic neuralgia, diabetic neuropathy, trigeminal neuralgia
• Chronic post-surgical pain: After thoracotomy (30-50%), mastectomy (20-50%), hernia repair (10-30%)

Assessment

• Pain history: Location, character, severity, temporal pattern, aggravating/relieving factors
• Functional impact: Activities of daily living, work, sleep, relationships
• Psychological assessment: Depression (PHQ-9), anxiety (GAD-7), pain catastrophising scale
• Previous treatments and responses

Red Flags

• New neurological deficit with chronic back pain - cauda equina, cord compression
• Weight loss with chronic pain - consider malignancy
• Pain with systemic features (fever, night sweats) - consider infection, malignancy
• Escalating opioid requirements - consider opioid-induced hyperalgesia or dependence

Bedside

• Pain assessment tools: NRS, Brief Pain Inventory, DN4 (neuropathic pain screening)
• Psychological screening: PHQ-9 (depression), GAD-7 (anxiety)
• Functional assessment: Pain Disability Index, EQ-5D

Bloods

• FBC, ESR, CRP: Exclude inflammatory cause
• TFTs, calcium, vitamin D: Exclude metabolic causes of widespread pain
• HbA1c: If diabetic neuropathy suspected
• Myeloma screen: If bony pain in elderly

Imaging

• MRI: If red flags present - spinal pathology, tumour, infection
• X-ray: Chronic musculoskeletal pain with structural concern
• Not recommended routinely: Imaging findings often incidental and do not correlate with pain severity

Special Tests

• Nerve conduction studies/EMG: If neuropathy suspected
• Quantitative sensory testing: Specialist pain centres - characterise neuropathic pain
• Diagnostic nerve blocks: Identify pain generator (facet joints, sacroiliac joint, peripheral nerves)

Non-pharmacological

• Exercise: Graded activity, physiotherapy-led programmes - strongest evidence base
• Cognitive Behavioural Therapy (CBT): NICE recommends for all chronic pain (NG193)
• Acceptance and Commitment Therapy (ACT): Emerging evidence, focuses on values-based living
• Pain Management Programmes: Multidisciplinary rehabilitation (physiotherapy + psychology + OT)
• Mindfulness-based stress reduction (MBSR): Moderate evidence for chronic pain
• Self-management strategies: Pacing, goal-setting, sleep hygiene

Pharmacological

Chronic primary pain (NICE NG193):

• Do NOT start opioids, paracetamol, NSAIDs, gabapentinoids, benzodiazepines, or antidepressants for pain
• Consider: Antidepressant (amitriptyline/duloxetine) for associated mood symptoms

Chronic secondary pain with neuropathic component (NICE CG173):

• First-line: Amitriptyline 10-75mg ON, OR duloxetine 60-120mg OD, OR gabapentin 300-1200mg TDS, OR pregabalin 75-300mg BD
• Combination therapy: If monotherapy insufficient
• Topical: Capsaicin 0.075% QDS, lidocaine 5% patch (localised neuropathic pain)

Opioids in chronic non-cancer pain:

• Only if other options exhausted, clear goals set, regular review
• Avoid >120mg morphine equivalent daily dose
• Plan tapering and discontinuation

Surgical/Interventional

• Spinal cord stimulation: NICE TA159 - CRPS, failed back surgery syndrome
• Radiofrequency denervation: Facet joint pain, sacroiliac joint pain
• Intrathecal drug delivery: Severe cancer pain, selected chronic pain
• Nerve blocks: Diagnostic and short-term therapeutic
• Neuromodulation: Dorsal root ganglion stimulation, peripheral nerve stimulation

Referral Criteria

• Chronic pain affecting function and quality of life - refer to pain management service
• Complex chronic pain with psychological comorbidity - multidisciplinary pain management programme
• Neuropathic pain refractory to first-line agents - specialist pain clinic
• Consider spinal cord stimulation - if CRPS or FBSS meets NICE criteria

• Complete pain resolution is uncommon in chronic primary pain - management focuses on function and quality of life
• Pain management programmes: 50-70% of patients show clinically significant improvements in function and mood
• Neuropathic pain: ~50% achieve ≥50% pain reduction with optimised medication
• Spinal cord stimulation: ~60% achieve >50% pain relief for CRPS; cost-effective at 5 years
• Opioid tapering: Many patients report improved pain and function after opioid reduction (POINT study)
• Long-term opioids: Associated with increased mortality, endocrine dysfunction, immune suppression, and hyperalgesia

NICE NG193 Key Recommendations for Chronic Primary Pain

Budapest Criteria for CRPS

Diagnosis requires: ≥1 symptom in 3/4 categories AND ≥1 sign in 2/4 categories at examination.

Opioid Conversion Table (Oral Morphine Equivalents)

Key Facts

Opioids are the most effective analgesics for moderate-to-severe acute pain and cancer pain. However, their potential for dependence, tolerance, and serious adverse effects mandates careful prescribing. Understanding receptor pharmacology and individual drug profiles is essential.

Epidemiology

Opioid prescribing has increased significantly in the UK over the past 20 years. Approximately 5-8% of the UK adult population receive a long-term opioid prescription. Opioid-related deaths in England and Wales have doubled since 2012, reaching approximately 4,900 per year. The UK uses approximately 33 million prescriptions for opioids annually.

Aetiology

Opioids mimic endogenous peptides (endorphins, enkephalins, dynorphins) that modulate pain transmission. They act at three main receptor types:

• Mu (µ): Supraspinal and spinal analgesia, respiratory depression, euphoria, miosis, constipation
• Kappa (κ): Spinal analgesia, sedation, dysphoria
• Delta (δ): Spinal analgesia, modulation of mu receptor activity

Pathophysiology

Mechanism of action:

• Opioid receptors are G-protein coupled receptors (GPCRs)

• Pre-synaptic: Inhibits calcium channels → reduced neurotransmitter release
• Post-synaptic: Opens potassium channels → hyperpolarisation

Tolerance: Progressive reduction in response with repeated exposure - requires dose escalation for same effect. Develops fastest for euphoria and analgesia, slowest for constipation and miosis.

Physical dependence: Withdrawal symptoms (sweating, diarrhoea, tachycardia, agitation) on abrupt cessation.

Opioid-induced hyperalgesia (OIH): Paradoxical increased pain sensitivity - differs from tolerance; managed by opioid dose reduction, not increase.

Therapeutic Effects

• Analgesia (dose-dependent)
• Anxiolysis, sedation, euphoria
• Antitussive effect (codeine, dextromethorphan)

Adverse Effects

• Respiratory depression: Most dangerous - dose-dependent, CO2 response curve shifted right
• Nausea and vomiting: Stimulation of CTZ (chemoreceptor trigger zone)
• Constipation: Reduced peristalsis - does NOT develop tolerance
• Pruritus: Histamine release (morphine) or central mu receptor activation
• Urinary retention: Increased sphincter tone, reduced detrusor activity
• Miosis: Parasympathetic stimulation of Edinger-Westphal nucleus
• Rigidity: Chest wall rigidity with rapid IV bolus (especially fentanyl)

Opioid Toxicity/Overdose

• Pinpoint pupils, respiratory depression (RR <8), reduced GCS
• Cyanosis, hypotension, hypothermia

Red Flags

• Respiratory rate <8/min - administer naloxone 400mcg IV, repeat every 2-3 min
• Reduced consciousness with opioids in renal failure - M6G accumulation
• Codeine in breastfeeding - risk of neonatal toxicity in ultra-rapid CYP2D6 metabolisers
• Tramadol + SSRI - serotonin syndrome risk

Bedside

• Respiratory rate: Most important clinical monitor for opioid safety
• Sedation score: 0 (awake) to 3 (unrousable)
• Pain score: NRS to guide dosing
• Pupil size: Miosis suggests opioid effect

Bloods

• U&Es: Renal function - reduce dose and avoid morphine in severe renal impairment (use oxycodone or fentanyl)
• LFTs: Hepatic impairment reduces metabolism of most opioids
• CYP2D6 genotyping: Consider if codeine/tramadol response is unexpected (not routine)

Imaging

• Not specific to opioid pharmacology

Special Tests

• Urine drug screen: Detect opioid use/misuse
• ECG: If methadone prescribed - QT prolongation risk
• Serum opioid levels: Not routinely available or useful clinically

Non-pharmacological

• Education: Inform patients about side effects, storage, driving restrictions, and safe disposal
• Opioid stewardship: Prescribe lowest effective dose for shortest duration
• Review and taper: Regular review of ongoing need; gradual reduction (10-25% every 2-4 weeks)

Pharmacological

Acute pain prescribing:

• Morphine 5-10mg PO 4-hourly PRN (elderly: 2.5-5mg)
• Oxycodone 5mg PO 4-6 hourly PRN (renal impairment preferred)
• Fentanyl 25-100mcg IV titrated (anaesthesia/acute settings)
• PCA: Morphine 1mg bolus, 5-min lockout

Chronic pain (if opioids indicated):

• Start with lowest dose modified-release preparation
• Do not exceed 120mg oral morphine equivalent/day without specialist review
• Always co-prescribe laxative (lactulose 15mL BD + senna 15mg ON)
• Regular review with clear goals and exit strategy

Opioid reversal:

• Naloxone 400mcg IV - repeat every 2-3 min to effect (max 10mg); duration 20-90 min
• Infusion may be needed for long-acting opioids: 2mg in 500mL 0.9% saline at rate titrated to RR

Surgical/Interventional

• Not applicable (pharmacological topic)

Referral Criteria

• Chronic opioid use with dose escalation - pain specialist/addiction services
• Opioid use disorder - substance misuse team
• Cancer pain requiring dose optimisation - palliative care

• Acute use: Safe and effective when used appropriately with monitoring
• Chronic use >3 months: Associated with tolerance, dependence, hyperalgesia, endocrine dysfunction, immune suppression, increased mortality
• Opioid use disorder: Affects approximately 1-3% of chronic pain patients prescribed opioids
• Overdose mortality: Naloxone has dramatically reduced in-hospital opioid-related deaths
• Tapering: Most chronic pain patients can successfully reduce or stop opioids with appropriate support

Oral Morphine Equivalent Conversion Table

Opioid Receptor Summary

Special Populations

Key Facts

Preoperative assessment is a systematic evaluation performed before planned surgery to identify patient risk factors, optimise comorbidities, plan anaesthetic technique, and arrange appropriate post-operative care. It improves surgical outcomes and reduces cancellations.

Epidemiology

Approximately 10 million surgical procedures are performed annually in England. Same-day cancellation rates are approximately 6-8%, with medical reasons being a significant contributor. Effective preoperative assessment reduces cancellation rates by up to 50%.

Aetiology

Preoperative assessment addresses:

• Patient factors: Comorbidities, medications, allergies, functional capacity, nutritional status
• Surgical factors: Procedure complexity, estimated blood loss, position, duration
• Anaesthetic factors: Airway assessment, anaesthetic technique, post-operative care level

Pathophysiology

Surgery induces a stress response (sympathetic activation, cortisol release, catabolic state) that places demands on cardiovascular, respiratory, and metabolic systems. Patients with limited physiological reserve are at higher risk of post-operative complications. Preoperative assessment aims to identify those at risk and implement strategies to improve reserve.

Key Components of Assessment

• History: Comorbidities, previous anaesthetics (problems?), family history (MH?), functional capacity, medications, allergies, smoking/alcohol
• Examination: Airway (Mallampati, mouth opening, neck extension), cardiovascular, respiratory, BMI
• Risk stratification: ASA grade, procedure severity, estimated blood loss

Specific Conditions Requiring Attention

• Cardiovascular: Ischaemic heart disease, heart failure, valvular disease, arrhythmias, hypertension
• Respiratory: COPD, asthma, OSA, recent URTI
• Endocrine: Diabetes (HbA1c, insulin management), thyroid disease, adrenal insufficiency
• Haematological: Anticoagulants, bleeding disorders, sickle cell disease
• Renal: eGFR, electrolytes, fluid balance

Red Flags Requiring Further Investigation

• Unstable angina or recent MI (<30 days) - defer elective surgery
• Decompensated heart failure - optimise before proceeding
• Severe aortic stenosis - high-risk; cardiology input
• HbA1c >69 mmol/mol (8.5%) - optimise diabetic control
• Active respiratory infection - defer elective surgery 2-4 weeks

Bedside

• Airway assessment: Mallampati, thyromental distance, mouth opening, neck extension
• Observations: BP, HR, SpO2, BMI, NEWS2
• ECG: If cardiovascular disease, age >65 with comorbidities, ASA ≥III
• Urinalysis: Diabetes screening if indicated

Bloods

• As per NICE NG45 - targeted, not routine:
• FBC: If anaemia suspected, expected blood loss, renal/liver disease
• U&Es: If renal disease, diuretics, ACEi/ARBs, diabetes
• Coagulation: If on anticoagulants, liver disease, bleeding history
• HbA1c: Diabetic patients (target <69 mmol/mol for elective surgery)
• Group and save: If blood loss >500mL anticipated
• Sickle cell screen: At-risk populations

Imaging

• CXR: Not routine - only if acute respiratory symptoms, known cardiorespiratory disease with change in symptoms
• Echocardiography: If valvular disease, unexplained murmur, heart failure assessment
• Pulmonary function tests: Severe respiratory disease, lung resection surgery

Special Tests

• CPET: High-risk patients before major surgery (AT <11 mL/kg/min = high risk; VO2 peak <15 mL/kg/min = very high risk)
• Dobutamine stress echo or myocardial perfusion: If cardiac risk factors and poor functional capacity
• Sleep study: If suspected OSA (STOP-BANG ≥5)

Non-pharmacological

• Prehabilitation: 4-6 weeks structured exercise + nutritional optimisation + psychological preparation
• Smoking cessation: Ideally ≥8 weeks pre-operatively (reduces respiratory complications by 50%)
• Alcohol cessation: ≥4 weeks reduces post-operative complications
• Nutritional optimisation: Correct anaemia (iron supplementation), protein supplementation if malnourished
• Patient education: Explain anaesthetic plan, expected post-operative course, pain management

Pharmacological

Medication management:

• Continue: Beta-blockers, statins, anti-epileptics, Parkinson's drugs, thyroid medication, inhalers, long-term steroids (may need supplementation)
• Stop day of surgery: ACEi/ARBs (reduce intraoperative hypotension), short-acting sulfonylureas
• Stop before surgery: Warfarin (5 days, bridge with LMWH if high risk), DOACs (48-72h), clopidogrel (7 days), metformin (day of surgery for major - variable practice)
• Diabetic management: Follow JBDS perioperative guidelines - VRIII if fasting >1 meal or HbA1c poorly controlled

Surgical/Interventional

• Pre-operative anaemia correction: IV iron (ferric carboxymaltose 1g) if Hb <130 g/L and surgery in 2-6 weeks
• Blood conservation: Cell salvage, tranexamic acid, restrictive transfusion targets

Referral Criteria

• Unstable cardiac disease - cardiology optimisation before elective surgery
• Severe respiratory disease - respiratory physician input
• Complex diabetes - diabetic team involvement
• Suspected difficult airway - senior anaesthetist planning
• Morbid obesity - bariatric anaesthesia planning

• Well-assessed patients: Lower cancellation rates, shorter hospital stays, fewer complications
• Prehabilitation: Reduces post-operative complications by 20-40% (meta-analyses)
• Smoking cessation: Reduces respiratory complications by 50% if ≥8 weeks pre-operatively
• Anaemia correction: Pre-operative IV iron reduces transfusion rates by 30-60%
• CPET-directed care: Allows risk stratification and appropriate post-operative care planning (HDU/ICU vs ward)

NICE NG45 - Preoperative Tests Summary

ASA Classification Summary

Medication Management Summary

Key Facts

The ASA Physical Status Classification is the most widely used system for preoperative risk assessment worldwide. It was developed by the American Society of Anesthesiologists in 1941 and has been revised several times. Despite its simplicity, it remains a useful communication tool and predictor of perioperative outcomes.

Epidemiology

ASA classification is recorded for virtually all anaesthetics administered in the UK. Approximately 60% of patients undergoing elective surgery are ASA I-II. ASA III-IV patients account for an increasing proportion due to an ageing population with multiple comorbidities. Mortality correlates with ASA grade: ASA I ~0.1%, ASA IV ~7.8%.

Aetiology

The classification was designed to describe a patient's pre-existing physical status, independent of the planned surgical procedure. It does not account for surgical complexity, anaesthetic technique, or individual surgeon/anaesthetist expertise.

Pathophysiology

Higher ASA grades reflect diminished physiological reserve. Patients with limited cardiac, respiratory, or metabolic reserve are less able to tolerate the stress of surgery and anaesthesia. This manifests as increased rates of cardiovascular events, respiratory complications, wound infections, and mortality.

ASA I - Healthy

• No comorbidities
• Non-smoker, no/minimal alcohol use
• Normal BMI

ASA II - Mild Systemic Disease

• Controlled hypertension, mild asthma
• Current smoker, social alcohol use
• BMI 30-39, pregnancy
• Well-controlled diabetes

ASA III - Severe Systemic Disease

• Poorly controlled hypertension or diabetes (HbA1c >64)
• COPD, moderate reduction in exercise tolerance
• Morbid obesity (BMI ≥40)
• Stable angina, previous MI (>3 months)
• Chronic hepatitis, moderate renal impairment
• Regular dialysis, implantable defibrillator

ASA IV - Severe Life-Threatening Disease

• Recent MI (<3 months) or CVA (<3 months)
• Ongoing cardiac ischaemia or valve disease causing symptoms at rest
• Severe heart failure (EF <25%)
• Sepsis, DIC, ARDS
• ESRD not undergoing regularly scheduled dialysis

ASA V - Moribund

• Ruptured abdominal or thoracic aortic aneurysm
• Massive trauma, intracranial haemorrhage with mass effect
• Not expected to survive 24 hours without surgery

Red Flags

• ASA grade alone does not capture all risk - consider surgical complexity and institutional factors
• Disagreement on ASA grading between clinicians is common - document rationale

Bedside

• Clinical assessment: History, examination, functional capacity
• Observations: BP, HR, SpO2, BMI

Bloods

• As guided by NICE NG45 based on ASA grade and procedure severity
• Higher ASA grades require more extensive investigation

Imaging

• Guided by clinical findings and comorbidities
• ECG recommended for ASA ≥III or cardiovascular disease

Special Tests

• CPET: Consider for ASA III-IV patients before major surgery
• Echocardiography: If valvular disease or heart failure

Non-pharmacological

• Risk communication: Use ASA grade as part of informed consent discussion
• Prehabilitation: Optimise modifiable risk factors before elective surgery
• MDT discussion: High-risk patients (ASA IV+) should be discussed at pre-operative MDT

Pharmacological

• Comorbidity optimisation guided by ASA-related conditions
• Medication management per preoperative assessment protocols

Surgical/Interventional

• Post-operative care level should match ASA grade and procedure complexity
• ASA IV-V patients typically require HDU/ICU post-operatively

Referral Criteria

• ASA III with complex comorbidities - consultant anaesthetist pre-operative review
• ASA IV-V - senior anaesthetist involvement, ICU bed planning
• ASA III-IV with poor functional capacity - consider CPET

• ASA grade is an independent predictor of perioperative morbidity and mortality
• ASA I-II: Low risk, majority suitable for day case surgery
• ASA III: Moderate risk - requires careful perioperative planning
• ASA IV: High risk - surgery only if benefits clearly outweigh risks
• ASA V: Very high risk - emergency surgery is life-saving but with high mortality
• ASA classification is used in national databases (e.g., NELA, NHFD) to benchmark outcomes

ASA Classification with Examples

Limitations of ASA Classification

Key Facts

Emergency anaesthesia is one of the most challenging aspects of anaesthetic practice. Time pressure, limited information, physiological instability, and the need for RSI create a high-risk environment. Structured assessment and team communication are critical.

Epidemiology

Approximately 30,000 emergency laparotomies are performed annually in England and Wales. NELA data shows 30-day mortality of ~9.6% and 1-year mortality of ~25%. Higher mortality is associated with increasing age, ASA grade, and delay to surgery. Emergency surgery accounts for approximately 11% of surgical procedures but 80% of surgical deaths.

Aetiology

Common emergency surgical conditions requiring anaesthesia:

• Abdominal: Bowel obstruction, perforation, appendicitis, ischaemic bowel, haemorrhage
• Trauma: Laparotomy, thoracotomy, orthopaedic fixation, neurosurgery
• Vascular: Ruptured AAA, acute limb ischaemia
• Obstetric: Emergency caesarean section, ectopic pregnancy
• Other: Necrotising fasciitis, testicular torsion, acute compartment syndrome

Pathophysiology

Emergency patients are often physiologically deranged: hypovolaemic, septic, acidotic, coagulopathic, or hypothermic. The stress response to both the disease process and surgery places extreme demands on the cardiovascular and respiratory systems. Anaesthetic agents cause further cardiovascular depression in already compromised patients.

Pre-Operative Assessment (Rapid)

• ABCDE approach: Simultaneous assessment and resuscitation
• Key information: Working diagnosis, allergies, medications, last meal, events leading to admission
• Risk stratification: NELA risk calculator, P-POSSUM, SORT
• Airway assessment: Often limited time - assume full stomach

Physiological Derangement

• Sepsis: Tachycardia, hypotension, fever/hypothermia, raised lactate
• Haemorrhage: Tachycardia, hypotension, pallor, falling Hb
• Obstruction: Dehydration, electrolyte imbalance, distension, aspiration risk
• Trauma: Multi-system injury, C-spine immobilisation, blood loss

Red Flags

• Lactate >4 mmol/L - tissue hypoperfusion, high mortality
• Predicted mortality >5% - trigger for consultant involvement and ICU booking
• Hypothermia <35°C + acidosis + coagulopathy - lethal triad
• Deteriorating consciousness - may indicate raised ICP, septic encephalopathy, or haemorrhage

Bedside

• ABG/VBG: pH, lactate, Hb, K⁺ - immediate results
• Point-of-care coagulation: TEG/ROTEM in major haemorrhage
• Blood glucose: Capillary
• ECG: Arrhythmia, ischaemia
• Urine output: Catheterise - assess perfusion

Bloods

• FBC: Hb, WCC, platelets
• U&Es: Renal function, K⁺ (hyperkalaemia risk with renal failure, massive transfusion)
• Coagulation: PT, APTT, fibrinogen
• Group and save / crossmatch: At least 2 units; activate major haemorrhage protocol if needed
• Lactate: Prognostic marker - serial monitoring

Imaging

• CT (trauma series): CT head, C-spine, chest, abdomen, pelvis
• CXR: Pneumoperitoneum, pleural pathology
• FAST scan: Focused Assessment with Sonography for Trauma - free fluid

Special Tests

• NELA risk calculator: Predicts 30-day mortality for emergency laparotomy
• P-POSSUM: Physiological and operative severity score
• SORT (Surgical Outcome Risk Tool): Predicts 30-day mortality

Non-pharmacological

• Team briefing: WHO checklist adapted for emergency; clear communication of plan
• Resuscitation before/during induction: IV access, fluid resuscitation, blood products
• Temperature management: Active warming from the outset - warm fluids, forced-air warmer, warm theatre
• Cell salvage: Consider for major blood loss cases

Pharmacological

• RSI: Standard for unfasted patients - propofol (reduced dose in shock) or ketamine (1-2mg/kg for haemodynamic stability) + rocuronium 1.2mg/kg
• Ketamine: Preferred induction agent in haemodynamically unstable patients
• Vasopressors: Phenylephrine 50-100mcg boluses; noradrenaline infusion if persistent hypotension; metaraminol 0.5-1mg boluses
• Major haemorrhage protocol: O-negative blood → crossmatch blood; 1:1:1 ratio of RBC:FFP:platelets; tranexamic acid 1g IV (within 3 hours - CRASH-2)
• Antibiotics: As per surgical team - administer before incision where possible

Surgical/Interventional

• Damage control surgery: Abbreviated surgery (control haemorrhage and contamination), then ICU resuscitation, planned return to theatre
• Interventional radiology: Embolisation for haemorrhage (pelvic fractures, GI bleeding)

Referral Criteria

• NELA mortality >5% - consultant surgeon and anaesthetist must be present
• NELA mortality >10% - ICU bed booked pre-operatively
• All emergency laparotomies - anaesthetic and surgical consultant notification

• NELA 30-day mortality: ~9.6% overall; ranges from 3% (low-risk) to >30% (highest risk)
• NELA 1-year mortality: ~25%
• Consultant involvement: Associated with lower mortality - NELA standards require consultant presence for high-risk cases
• Delay to surgery: Each hour delay beyond indicated time increases mortality
• Damage control approach: Improves survival in severely physiologically deranged patients

NELA Standards of Care

Induction Agent Selection in Emergency

Key Facts

Anaesthesia in pregnancy presents unique challenges due to the physiological changes of pregnancy, the presence of a second patient (foetus), and the potential for rapid deterioration. Obstetric anaesthesia accounts for approximately 25% of all anaesthetic workload.

Epidemiology

Approximately 700,000 births occur annually in the UK. Caesarean section rate is approximately 30% (elective 13%, emergency 17%). Maternal mortality rate is approximately 9-10 per 100,000 maternities (MBRRACE-UK). Anaesthetic-related deaths have declined significantly but remain a focus of the confidential enquiry.

Aetiology

Physiological changes in pregnancy affecting anaesthesia:

• CVS: CO increased 40%, HR increased 15-20 bpm, SVR decreased, aortocaval compression from 20 weeks
• Respiratory: Minute ventilation increased 50% (progesterone), FRC decreased 20%, O2 consumption increased 20% → rapid desaturation
• GI: Delayed gastric emptying, reduced LOS tone → aspiration risk
• Haematological: Dilutional anaemia (Hb ~110g/L), hypercoagulable, increased fibrinogen
• Pharmacological: Increased sensitivity to inhalational agents (MAC reduced 30-40%), increased sensitivity to LA (reduced epidural dose requirement)

Pathophysiology

The pregnant patient at term has minimal respiratory reserve - the combination of decreased FRC and increased O2 consumption means that desaturation occurs approximately twice as fast as in a non-pregnant patient during apnoea. Aortocaval compression by the gravid uterus can reduce cardiac output by up to 40% in the supine position.

Indications for Obstetric Anaesthesia

• Labour analgesia: Epidural (gold standard), remifentanil PCA, Entonox
• Caesarean section: Spinal (elective/Cat 2-4), epidural top-up (Cat 2-3), GA (Cat 1 if no epidural in situ)
• Instrumental delivery: Epidural top-up or spinal
• Non-obstetric surgery in pregnancy: Any trimester - minimise teratogenic risk

Urgency Classification (Caesarean Section)

• Category 1: Immediate threat - decision-to-delivery interval <30 min (aim <15 min)
• Category 2: Maternal or foetal compromise but not immediately life-threatening - <75 min
• Category 3: No compromise but early delivery needed - within hours
• Category 4: Elective - at a time to suit mother and team

Obstetric Emergencies Requiring Anaesthetic Input

• Massive obstetric haemorrhage
• Eclampsia (magnesium sulphate 4g IV loading)
• Maternal cardiac arrest (perimortem caesarean within 5 min)
• Placental abruption, uterine rupture
• Cord prolapse

Red Flags

• Maternal tachycardia >100 bpm or hypotension - suspect haemorrhage or aortocaval compression
• Difficulty with intubation - higher failed intubation rate in pregnancy
• Desaturation during pre-oxygenation - decreased FRC, consider head-up positioning
• Post-partum collapse - consider haemorrhage, amniotic fluid embolism, PE

Bedside

• Airway assessment: Mallampati may worsen during pregnancy (oedema)
• Observations: BP, HR, SpO2 - left lateral position
• CTG: Foetal heart rate monitoring
• Estimated blood loss: Weigh swabs, measure suction volume

Bloods

• FBC: Hb (physiological anaemia of pregnancy; Hb <105g/L in 3rd trimester is abnormal)
• Group and save/crossmatch: For all caesarean sections and high-risk deliveries
• Coagulation: If pre-eclampsia, haemorrhage, or liver disease
• U&Es, LFTs, urate: Pre-eclampsia assessment
• Fibrinogen: <2g/L in obstetric haemorrhage predicts severe PPH

Imaging

• USS: Placental localisation, foetal assessment

Special Tests

• Point-of-care coagulation (ROTEM/TEG): Guide blood product replacement in massive haemorrhage
• Acid-base (cord gases): Post-delivery to assess neonatal condition

Non-pharmacological

• Left lateral tilt (15°): From 20 weeks gestation - mandatory during all procedures
• Pre-oxygenation: Essential - ramped position, 100% O2 for 3 minutes
• Antacid prophylaxis: Ranitidine 150mg PO (night before + morning of CS) + sodium citrate 0.3M 30mL PO immediately pre-operatively
• WHO checklist: Adapted for obstetric theatre

Pharmacological

Spinal for caesarean section:

• Hyperbaric bupivacaine 0.5% 2.2-2.8mL + fentanyl 15mcg + diamorphine 300mcg
• Phenylephrine infusion 25-50mcg/min or boluses to maintain BP

GA for emergency caesarean:

• Avoid excessive volatile concentration before delivery (uterine relaxation)

Labour epidural:

• Bupivacaine 0.1% + fentanyl 2mcg/mL via PCEA
• For Cat 1 CS top-up: Lidocaine 2% 15-20mL or 3% 2-chloroprocaine

Obstetric haemorrhage:

• Uterotonic: Oxytocin 5 IU slow IV → infusion 40 IU in 500mL over 4h
• Ergometrine 500mcg IM (not in hypertension/pre-eclampsia)
• Carboprost 250mcg IM (not in asthma)
• Tranexamic acid 1g IV (WOMAN trial)
• Major haemorrhage protocol: O-neg blood, 1:1:1 ratio

Surgical/Interventional

• Perimortem caesarean section: Within 5 minutes of maternal cardiac arrest - improves both maternal and foetal survival
• Intrauterine balloon tamponade (Bakri balloon): For post-partum haemorrhage
• Interventional radiology: Uterine artery embolisation
• B-Lynch suture: Surgical compression of uterus

Referral Criteria

• High-risk pregnancy - antenatal anaesthetic assessment (obesity, cardiac disease, difficult airway, anticoagulants)
• Category 1 CS - immediate senior anaesthetic and obstetric team activation
• Massive obstetric haemorrhage - major haemorrhage protocol activation

• Maternal mortality (UK): ~9-10 per 100,000 maternities (MBRRACE-UK)
• Anaesthesia-related maternal deaths: Now very rare (<1 per year in UK) - mostly GA-related
• Regional vs GA for CS: Regional anaesthesia associated with significantly lower maternal mortality
• Perimortem CS: Improves maternal survival (autotransfusion from uterus, improved venous return)
• Massive PPH: Accounts for ~10% of direct maternal deaths; multidisciplinary management saves lives

Caesarean Section Categories

Drugs to Avoid in Pregnancy

Key Facts

Paediatric anaesthesia is a subspecialty requiring specific training and expertise. Children have higher metabolic rates, different airway anatomy, and age-dependent pharmacokinetics that influence drug dosing and monitoring.

Epidemiology

Approximately 500,000 paediatric anaesthetics are administered annually in the UK. Perioperative cardiac arrest in children occurs in approximately 1 in 10,000 anaesthetics (higher than adults). The highest risk is in neonates and infants under 1 year.

Aetiology

Key anatomical differences in children:

• Airway: Large head/occiput, large tongue, high anterior larynx (C3 vs C5), epiglottis long and floppy, narrow subglottis (narrowest part in children vs glottis in adults)
• Respiratory: Fewer alveoli, compliant chest wall, horizontal ribs, diaphragmatic breathing, higher closing volume
• Cardiovascular: Heart rate-dependent cardiac output, limited contractile reserve
• Thermoregulation: High surface area:volume ratio → rapid heat loss
• Pharmacological: Larger volume of distribution, immature hepatic/renal function in neonates, higher MAC requirement

Pathophysiology

Neonates and infants are particularly vulnerable to hypoxia, hypothermia, and hypoglycaemia. Their limited respiratory reserve (FRC close to closing volume) means rapid desaturation during apnoea. Cardiac output is heart rate-dependent with limited stroke volume reserve. Immature hepatic metabolism prolongs the action of many drugs in neonates.

Age-Related Considerations

• Neonate (0-28 days): Highest risk; transitional circulation, immature systems
• Infant (1-12 months): Rapid growth, high metabolic rate
• Pre-school (1-5 years): Separation anxiety, uncooperative
• School age (5-12 years): Generally cooperative, can understand explanations
• Adolescent (12-18 years): Approaching adult physiology

Common Paediatric Procedures

• Myringotomy/grommets, tonsillectomy/adenoidectomy
• Circumcision, inguinal hernia repair
• Orthopaedic (fracture reduction)
• Dental extractions
• Neonatal surgery (NEC, TOF, CDH)

Red Flags

• Stridor in a child - potential airway emergency (croup, epiglottitis, foreign body)
• Active URTI with fever, productive cough - postpone elective surgery 2-4 weeks (increased airway reactivity)
• Ex-premature infant <60 weeks post-conceptual age - risk of post-operative apnoea
• Difficult IV access in a dehydrated/shocked child - use intraosseous (IO) access

Bedside

• Weight: Essential for drug dosing (estimated by age-based formulae if unable to weigh: APLS weight = (age+4) × 2 for 1-5yr)
• Airway assessment: Age-appropriate assessment
• Observations: HR, RR, SpO2, BP (age-appropriate cuff)
• Blood glucose: Especially neonates and infants

Bloods

• FBC: If anaemia suspected or blood loss expected
• Group and save: If blood loss anticipated
• U&Es: If renal disease, dehydration, or IV fluid therapy needed
• Sickle cell screen: In at-risk populations
• Blood glucose: Neonates, infants, diabetic children

Imaging

• CXR: Not routine; only if respiratory symptoms or neonatal pathology

Special Tests

• Echocardiography: If congenital heart disease suspected
• Sleep study: If OSA suspected (tonsillectomy patients)

Non-pharmacological

• Parental presence: At induction - reduces anxiety
• Play specialist: Preparation and distraction
• EMLA/Ametop cream: Applied 45-60 minutes before for painless cannulation
• Fasting: 6h solids, 4h breast milk, 1h clear fluids (1-4-6 rule)
• Temperature management: Warm theatre (26°C for neonates), warming mattress, hat, forced-air warmer, warm fluids

Pharmacological

• Inhalational induction: Sevoflurane 8% in O2 (standard paediatric induction)
• IV induction: Propofol 3-4mg/kg (higher dose than adults)
• Maintenance: Sevoflurane 2-3% in O2/air; or TIVA
• Analgesia: Paracetamol 15mg/kg PO/IV QDS + ibuprofen 5mg/kg TDS + morphine 0.1mg/kg IV PRN; caudal block (bupivacaine 0.25% 0.5-1mL/kg) for sub-umbilical surgery
• Suxamethonium: 2mg/kg IV in children (higher dose due to larger Vd); 4mg/kg IM if no IV access
• Atropine 20mcg/kg: Pre-treat before suxamethonium in children (vagal response more common)
• Emergence agitation prophylaxis: Fentanyl 1mcg/kg or dexmedetomidine 0.5mcg/kg

Surgical/Interventional

• Caudal epidural: Most common regional technique in paediatric anaesthesia (sacral approach)
• Peripheral nerve blocks: USS-guided, similar to adults but weight-based dosing

Referral Criteria

• Neonatal surgery - specialist paediatric anaesthetic centre
• Congenital heart disease - specialist paediatric cardiac centre
• Ex-premature infants <60 weeks post-conceptual age - specialist centre with apnoea monitoring
• Suspected malignant hyperthermia - TIVA, specialist centre

• Perioperative cardiac arrest: ~1 in 10,000 paediatric anaesthetics (higher in neonates)
• Laryngospasm: Occurs in ~1-3% of paediatric anaesthetics - usually managed with basic manoeuvres
• Post-operative apnoea: Risk in ex-premature infants - monitor for 12-24h post-operatively
• Neurotoxicity concerns: Animal evidence of volatile/propofol neurotoxicity in developing brain; GAS and PANDA trials showed no significant neurodevelopmental difference after single brief anaesthetic in infants
• Long-term outcomes: Paediatric anaesthesia is very safe with appropriate training and equipment

Paediatric Equipment Sizing

Paediatric Fluid Management

Common Drug Doses (Paediatric)

Key Facts

Intensive care medicine is a multidisciplinary specialty providing advanced organ support and monitoring for the most critically ill patients. Early recognition of deterioration, protocolised care, and multidisciplinary teamwork are fundamental to good outcomes.

Epidemiology

Approximately 250,000 patients are admitted to ICU annually in the UK. ICU bed provision is approximately 6.6 per 100,000 population (lower than many comparable countries). Overall ICU mortality is approximately 20%, varying from <5% for elective post-surgical to >50% for multi-organ failure.

Aetiology

Common reasons for ICU admission:

• Sepsis/septic shock (most common medical)
• Acute respiratory failure/ARDS
• Post-operative monitoring (complex surgery, complications)
• Cardiovascular failure (MI, cardiogenic shock, arrhythmia)
• Neurological (stroke, status epilepticus, traumatic brain injury)
• Trauma (polytrauma, burns)
• Post-cardiac arrest

Pathophysiology

Critical illness is characterised by the failure or threatened failure of one or more organ systems. The systemic inflammatory response syndrome (SIRS) and its progression to multi-organ dysfunction syndrome (MODS) represents a common final pathway in many critically ill patients, driven by dysregulated inflammation, endothelial dysfunction, microcirculatory failure, and mitochondrial dysfunction.

Levels of Care

• Level 0: Ward care - can be met through normal ward care
• Level 1: Acute ward care with additional advice from critical care (step-down)
• Level 2 (HDU): Single-organ support (excluding advanced respiratory)
• Level 3 (ICU): Advanced respiratory support or ≥2 organ support

Assessment of the Critically Ill Patient

• ABCDE approach: Systematic assessment
• Monitoring: Continuous ECG, SpO2, invasive arterial BP, CVP, urine output, temperature
• Organ support: Ventilation, vasopressors/inotropes, renal replacement therapy, blood products

Common ICU Interventions

• Endotracheal intubation and mechanical ventilation
• Central venous catheter (internal jugular, subclavian, femoral)
• Arterial line (radial most common)
• Vasopressor/inotrope infusions
• Renal replacement therapy (CVVHDF most common in ICU)
• Enteral/parenteral nutrition
• Sedation and analgesia

Red Flags

• Rising NEWS2 score on the ward - early warning of deterioration
• Lactate >4 mmol/L - tissue hypoperfusion, high mortality
• Acute deterioration in ventilator parameters - consider pneumothorax, blocked ETT, PE
• New onset organ failure - reassess for sepsis, haemorrhage, or drug reaction

Bedside

• ABG: pH, PaO2, PaCO2, lactate, Hb, glucose, electrolytes
• Echocardiography (point-of-care): Assess cardiac function, fluid status, tamponade
• Lung USS: Pleural effusion, pneumothorax, consolidation
• Urine output: Hourly monitoring - target >0.5 mL/kg/hr

Bloods

• FBC, U&Es, LFTs, CRP, lactate: Baseline and serial monitoring
• Coagulation, fibrinogen: DIC screening
• Blood cultures: Before antibiotics in sepsis
• Procalcitonin: Guide antibiotic duration
• Troponin: If cardiac ischaemia suspected

Imaging

• CXR (daily or as indicated): ETT position, line position, lung pathology
• CT: Guided by clinical question (CT head, CTPA, CT abdomen)

Special Tests

• Cardiac output monitoring: PiCCO, LiDCO, PA catheter, echocardiography
• EEG: Status epilepticus, prognostication post-cardiac arrest
• Bronchoscopy: Persistent collapse, suspected VAP, bronchoalveolar lavage

Non-pharmacological

• Early mobilisation: Reduces ICU-acquired weakness, delirium, and duration of ventilation
• Nutrition: Enteral feeding within 48 hours of admission (nasogastric)
• DVT prophylaxis: LMWH + mechanical (IPC/TEDS)
• Stress ulcer prophylaxis: PPI or ranitidine (for mechanically ventilated patients)
• Glycaemic control: Target glucose 6-10 mmol/L (NICE-SUGAR trial)
• ABCDEF bundle: Assess/manage pain, Both SATs and SBTs, Choice of sedation, Delirium management, Early mobilisation, Family engagement

Pharmacological

• Sepsis: IV antibiotics within 1 hour of recognition; noradrenaline 0.05-1mcg/kg/min to target MAP ≥65mmHg; hydrocortisone 200mg/day if vasopressor-refractory (ADRENAL trial)
• Sedation: Propofol 0.3-4mg/kg/hr or midazolam 0.03-0.2mg/kg/hr; target RASS 0 to -2
• Analgesia: Morphine 1-5mg/hr IV or fentanyl 25-200mcg/hr
• Delirium: Non-pharmacological first; haloperidol 0.5-2mg IV if agitated delirium; dexmedetomidine 0.2-1.4mcg/kg/hr
• Vasopressors: Noradrenaline (first-line), vasopressin 0.03 units/min (adjunct), dobutamine 2.5-20mcg/kg/min (inotrope)

Surgical/Interventional

• Renal replacement therapy: CVVHDF for AKI with refractory hyperkalaemia, acidosis, fluid overload, or uraemia
• Percutaneous tracheostomy: Consider at day 7-10 of mechanical ventilation
• Source control: Drainage of abscesses, debridement of infected tissue

Referral Criteria

• Any patient with acute organ failure or threatened failure - ICU outreach/referral
• NEWS2 ≥7 or single parameter score of 3 - urgent senior review and ICU referral
• Post-cardiac arrest - ICU for targeted temperature management and neuroprognostication

• Overall ICU mortality (UK): ~20%; hospital mortality ~25%
• Septic shock: Mortality 30-40% despite best care
• ARDS: Mortality 35-45% depending on severity (Berlin classification)
• Post-ICU outcomes: 25-50% of ICU survivors have significant physical, psychological, or cognitive impairment at 1 year (post-intensive care syndrome - PICS)
• ICU-acquired weakness: Affects 25-50% of patients ventilated >7 days

Sequential Organ Failure Assessment (SOFA) Score

Key ICU Trials

Key Facts

Mechanical ventilation is the most common organ support provided in the ICU. Understanding ventilator physiology, modes, and settings is essential for all ICU practitioners. The shift to lung-protective strategies has significantly reduced mortality in ARDS.

Epidemiology

Approximately 50-60% of ICU patients require mechanical ventilation. Average duration of ventilation is 5-7 days. Prolonged ventilation (>21 days) affects approximately 5-10% of ventilated patients. VAP incidence is approximately 5-15 per 1,000 ventilator-days.

Aetiology

Indications for mechanical ventilation:

• Acute respiratory failure (type 1 or type 2)
• Airway protection (GCS <8)
• Post-operative (major surgery, failed extubation)
• Neuromuscular disease (Guillain-Barré, myasthenia crisis)
• ARDS, pneumonia, COPD exacerbation (failing NIV)
• Shock (reduce respiratory work, redirect O2 to vital organs)

Pathophysiology

Normal spontaneous breathing: Negative intrathoracic pressure (diaphragmatic contraction) draws air into lungs. Venous return enhanced by negative pressure.

Positive pressure ventilation: Reverses normal physiology - positive pressure inflates lungs. This reduces venous return (may cause hypotension), increases intrathoracic pressure, and can cause barotrauma. Ventilator-induced lung injury (VILI) results from volutrauma (overdistension), atelectrauma (cyclic collapse and recruitment), and biotrauma (inflammatory mediator release).

Ventilator Modes

• CMV (Controlled Mandatory Ventilation): Full ventilator support; patient passive (used with paralysis)
• SIMV (Synchronised Intermittent Mandatory Ventilation): Set rate + patient-triggered breaths between; supports weaning
• Pressure Support (PS): Patient triggers all breaths; ventilator augments with set pressure; used for weaning
• BIPAP/APRV: Airway pressure release ventilation - maintains high CPAP with brief releases for CO2 clearance
• High-Frequency Oscillatory Ventilation (HFOV): Rescue in refractory ARDS (OSCAR/OSCILLATE trials - no benefit)

Non-Invasive Ventilation

• CPAP: Continuous positive airway pressure - cardiogenic pulmonary oedema, OSA
• BiPAP: Bilevel - COPD exacerbation with respiratory acidosis (pH 7.25-7.35)
• High-flow nasal oxygen (HFNO): Optiflow at 30-60 L/min - hypoxic respiratory failure, pre-oxygenation

Red Flags

• High airway pressures (>30 cmH2O) - risk of barotrauma; check for obstruction, bronchospasm, pneumothorax
• Sudden desaturation on ventilator - use DOPE mnemonic: Displacement, Obstruction, Pneumothorax, Equipment failure
• Rising CO2 despite adequate minute ventilation - consider increased dead space (PE), metabolic acidosis, or shunt
• Fighting the ventilator - assess sedation, pain, tube position, trigger sensitivity

Bedside

• ABG: PaO2, PaCO2, pH, lactate - guide ventilator adjustments
• P/F ratio: PaO2/FiO2 - classifies ARDS severity and guides prone positioning
• Ventilator graphics: Pressure-volume and flow-time waveforms - detect auto-PEEP, patient-ventilator asynchrony
• Peak vs plateau pressure: Difference indicates airway resistance (bronchospasm, secretions)

Bloods

• ABG/VBG: Serial for monitoring ventilation and oxygenation
• FBC, CRP, procalcitonin: If VAP suspected
• Sputum culture: Before starting antibiotics for suspected VAP

Imaging

• CXR: ETT position, pulmonary pathology, pneumothorax, line positions
• CT chest: ARDS characterisation, abscess, empyema
• Lung USS: Increasingly replacing CXR - pleural effusion, consolidation, pneumothorax, B-lines

Special Tests

• Recruitment manoeuvres: Sustained inflation or stepwise PEEP increases to recruit collapsed alveoli
• Transpulmonary pressure monitoring: Oesophageal manometry - optimise PEEP in severe ARDS
• SBT (Spontaneous Breathing Trial): T-piece or low PS (5-8 cmH2O) for 30-120 min to assess readiness for extubation

Non-pharmacological

• Lung-protective ventilation: VT 6mL/kg IBW, Pplat <30, PEEP 5-15, FiO2 titrated to SpO2 88-95%
• Prone positioning: 16+ hrs/day for moderate-severe ARDS (P/F <150) - PROSEVA trial showed 50% mortality reduction
• Conservative fluid strategy: After initial resuscitation - reduces ventilator days (FACTT trial)
• VAP prevention bundle: Head-up 30-45°, daily sedation hold, oral care with chlorhexidine, peptic ulcer prophylaxis, DVT prophylaxis, assess readiness for extubation daily

Pharmacological

• Sedation: Propofol 0.3-4mg/kg/hr or midazolam 0.03-0.2mg/kg/hr; target light sedation (RASS 0 to -2) - DahLIA and SPICE III trials
• Analgesia: Fentanyl 25-200mcg/hr or morphine 1-5mg/hr - analgesia-first approach
• Neuromuscular blockade: Cisatracurium 0.15mg/kg/hr for early severe ARDS (ACURASYS trial - benefit; ROSE trial - no benefit with current light sedation practice)
• Inhaled nitric oxide: Rescue therapy for refractory hypoxaemia - improves oxygenation, no mortality benefit
• Corticosteroids: Dexamethasone 6mg OD for COVID-19 ARDS (RECOVERY trial); role debated in non-COVID ARDS

Surgical/Interventional

• Tracheostomy: Consider day 7-10 for patients expected to require prolonged ventilation (TracMan trial - no mortality difference early vs late)
• ECMO: Extracorporeal membrane oxygenation for refractory respiratory failure (CESAR trial - refer to ECMO centre)
• Chest drain: For pneumothorax, empyema, significant pleural effusion

Referral Criteria

• Refractory hypoxaemia (P/F <80) despite optimal ventilation and prone positioning - consider ECMO referral
• Failed extubation ×2 - consider tracheostomy
• Difficult to wean - consider weaning centre referral for prolonged ventilation

• ARDS mortality: Mild 27%, Moderate 32%, Severe 45% (Berlin classification)
• Prone positioning: Reduces mortality from ~33% to ~16% in moderate-severe ARDS (PROSEVA)
• Duration of ventilation: Median 5-7 days; lung-protective ventilation and protocolised weaning reduce duration
• Ventilator-free days: Key outcome measure - more clinically meaningful than raw duration
• Post-ICU: ICU-acquired weakness, PTSD, cognitive impairment affect 25-50% of survivors

Berlin Criteria for ARDS

Key Ventilation Trials

Key Facts

Shock is a life-threatening condition requiring rapid identification and targeted treatment. Haemodynamic monitoring guides resuscitation to achieve adequate tissue perfusion while avoiding fluid overload.

Epidemiology

Shock affects approximately 30-40% of ICU patients. Septic shock is the most common form in ICU (62%), followed by cardiogenic (16%), hypovolaemic (16%), and obstructive (2%). In-hospital mortality for septic shock is approximately 30-40%.

Aetiology

• Hypovolaemic: Haemorrhage, burns, dehydration, third-space losses
• Cardiogenic: MI, arrhythmia, valvular disease, cardiomyopathy
• Distributive: Sepsis (most common), anaphylaxis, neurogenic
• Obstructive: PE, cardiac tamponade, tension pneumothorax

Pathophysiology

Tissue hypoxia is the final common pathway in all forms of shock. Compensatory mechanisms (tachycardia, vasoconstriction, ADH/aldosterone release) initially maintain vital organ perfusion. Decompensation leads to lactic acidosis, cellular dysfunction, and multi-organ failure. The type of shock determines the primary circulatory abnormality: reduced preload (hypovolaemic), reduced contractility (cardiogenic), reduced SVR (distributive), or mechanical obstruction to flow (obstructive).

General Features of Shock

• Tachycardia, hypotension (MAP <65 mmHg)
• Tachypnoea, altered mental status
• Oliguria (<0.5 mL/kg/hr)
• Cool, clammy peripheries (except distributive - warm peripheries early)
• Raised lactate (>2 mmol/L)

Differentiating Features

• Hypovolaemic: Dry mucous membranes, flat neck veins, clear lungs
• Cardiogenic: Raised JVP, pulmonary crackles, S3 gallop
• Septic: Fever/hypothermia, warm peripheries, suspected source of infection
• Obstructive: Distended neck veins, muffled heart sounds (tamponade), absent breath sounds (tension pneumothorax)

Red Flags

• MAP <65 mmHg despite fluid resuscitation - start vasopressors
• Lactate >4 mmol/L - high mortality, aggressive resuscitation needed
• Rising lactate despite treatment - reassess diagnosis and adequacy of resuscitation
• New onset AF with hypotension - consider cardioversion if haemodynamically unstable

Bedside

• ABG with lactate: Immediate - assess oxygenation, ventilation, acid-base, tissue perfusion
• ECG: Arrhythmia, MI, PE (right heart strain)
• POCUS/echocardiography: Cardiac function, fluid status, pericardial effusion, RV dilatation
• Urine output: Catheterise - target >0.5 mL/kg/hr
• CVP monitoring: Useful trend; absolute value less informative

Bloods

• FBC, U&Es, LFTs: Organ function
• Lactate (serial): Guide resuscitation; clearance rate is prognostic
• Troponin: If cardiogenic shock suspected
• Blood cultures (×2): Before antibiotics in sepsis
• Coagulation, fibrinogen: DIC screening
• Procalcitonin: Differentiate septic from non-septic causes

Imaging

• CXR: Pulmonary oedema, pneumothorax, mediastinal widening
• CTPA: If PE suspected
• CT abdomen: If intra-abdominal source of sepsis suspected
• Focused echocardiography: Rapid assessment (FATE/FICE protocol)

Special Tests

• Cardiac output monitoring: PiCCO (transpulmonary thermodilution), LiDCO, oesophageal Doppler, PA catheter (now rarely used)
• Fluid responsiveness assessment: PLR test, SVV/PPV on arterial waveform, IVC variability on USS
• Mixed/central venous oxygen saturation (ScvO2): <70% suggests inadequate oxygen delivery

Non-pharmacological

• ABCDE assessment: Simultaneous assessment and resuscitation
• IV access: Two large-bore cannulae; central venous access for vasopressors
• Position: Supine with legs raised (if hypovolaemic); sit up (if cardiogenic pulmonary oedema)

Pharmacological

Fluid resuscitation:

• Crystalloid (Hartmann's or 0.9% NaCl) 250-500mL boluses, reassess after each
• Blood products for haemorrhagic shock (O-neg → crossmatched; 1:1:1 ratio in massive haemorrhage)

Vasopressors and inotropes:

• Noradrenaline: First-line vasopressor for septic/distributive shock - 0.05-1mcg/kg/min
• Vasopressin: 0.03 units/min - adjunct to noradrenaline in septic shock
• Dobutamine: 2.5-20mcg/kg/min - inotrope for cardiogenic shock with low CO
• Adrenaline: 0.05-0.5mcg/kg/min - combined inotrope/vasopressor; anaphylactic shock first-line (500mcg IM)
• Milrinone: PDE3 inhibitor - inodilator for acute heart failure (not first-line)

Sepsis-specific:

• IV antibiotics within 1 hour (Surviving Sepsis Campaign hour-1 bundle)
• Hydrocortisone 200mg/day if vasopressor-dependent >4 hours despite adequate fluid resuscitation

Surgical/Interventional

• Chest drain: Tension pneumothorax
• Pericardiocentesis: Cardiac tamponade
• Thrombolysis/embolectomy: Massive PE
• Source control: Drainage of abscess, debridement, laparotomy for peritonitis
• IABP/Impella/ECMO: Cardiogenic shock refractory to medical therapy

Referral Criteria

• Any shock not responding to initial resuscitation - ICU referral
• Cardiogenic shock - cardiology/cardiac surgery
• Massive PE - interventional radiology or cardiothoracic surgery
• Septic shock - ICU admission

• Septic shock: 30-40% mortality despite best care; early antibiotics and fluids improve outcomes
• Cardiogenic shock (MI-related): ~50% mortality; PCI/CABG improve outcomes
• Haemorrhagic shock: Outcome depends on rapidity of haemorrhage control and transfusion
• Lactate clearance: >10% decrease in lactate at 6 hours is associated with improved survival
• Obstructive shock: Rapidly fatal if cause not identified and treated; excellent recovery if treated promptly

Haemodynamic Monitoring Devices

Classification of Haemorrhagic Shock (ATLS)

Key Facts

Malignant hyperthermia is a rare but life-threatening anaesthetic emergency. It results from uncontrolled intracellular calcium release in skeletal muscle, leading to hypermetabolism, rhabdomyolysis, and multi-organ failure if not treated promptly.

Epidemiology

Incidence is approximately 1 in 10,000-15,000 paediatric anaesthetics and 1 in 50,000-100,000 adult anaesthetics. MH susceptibility follows an autosomal dominant pattern with variable penetrance. Approximately 1 in 3,000-5,000 individuals carry a susceptibility gene.

Aetiology

Genetic basis:

• RYR1 gene mutations (chromosome 19q13.1) - most common (~70%)
• CACNA1S gene mutations (L-type calcium channel) - less common
• Autosomal dominant with incomplete penetrance - a patient may have had previous uneventful anaesthetics before triggering an episode

Triggering agents:

• All volatile anaesthetic agents (halothane, sevoflurane, desflurane, isoflurane)
• Suxamethonium
• NOT triggered by: Propofol, ketamine, midazolam, non-depolarising NMBAs, local anaesthetics, N2O, opioids

Pathophysiology

Early Signs

• Rising ETCO2 (earliest sign - often before other manifestations)
• Tachycardia (unexplained)
• Masseter spasm after suxamethonium (may be isolated or herald full MH)

Established MH

• Hyperthermia (temperature rise 1-2°C every 5 min - may exceed 43°C)
• Generalised muscle rigidity
• Tachycardia, arrhythmias (VT, VF)
• Metabolic acidosis (mixed respiratory and metabolic)
• Hyperkalaemia
• Myoglobinuria (dark/cola-coloured urine)
• DIC (late)

Late Complications

• Rhabdomyolysis → acute renal failure
• DIC → haemorrhage
• Multi-organ failure
• Cerebral oedema

Red Flags

• Unexplained rising ETCO2 during anaesthesia - always consider MH
• Masseter spasm after suxamethonium - may proceed to full MH in ~15-30% (abandon volatile, continue TIVA, observe)
• Core temperature rising rapidly (>2°C/hr) - strongly suspicious
• Family history of anaesthetic death - must investigate for MH susceptibility

Bedside

• ETCO2 monitoring: Rising trend is the earliest sign
• Core temperature: Oesophageal, bladder, or rectal probe - rising rapidly
• ECG: Tachycardia, arrhythmias, hyperkalaemic changes

Bloods

• ABG: Mixed metabolic and respiratory acidosis, hyperkalaemia, raised lactate
• CK (creatine kinase): Massively elevated - may exceed >10,000 U/L; peaks at 12-24 hours
• Potassium: Dangerously elevated - treat urgently
• Myoglobin (serum and urine): Elevated - myoglobinuria causes renal damage
• Coagulation: DIC screen (PT, APTT, fibrinogen, D-dimer)
• Renal function: Rising creatinine from rhabdomyolysis

Imaging

• Not acutely required

Special Tests

• In vitro contracture test (IVCT): Gold standard - performed on fresh muscle biopsy (vastus lateralis) at specialist centres; tests muscle response to halothane and caffeine
• Genetic testing: RYR1 and CACNA1S mutations - can confirm susceptibility but cannot exclude it (some mutations unknown)
• Family screening: All first-degree relatives of confirmed MH patients should be tested

Non-pharmacological

• Stop all trigger agents immediately: Turn off vaporiser, disconnect from anaesthesia machine
• Call for help: Declare MH emergency, assign roles
• Hyperventilate with 100% O2: High fresh gas flow (>10 L/min) to wash out volatile
• Active cooling: IV cold saline (40mL/kg), ice packs to groins/axillae, cold gastric/bladder lavage; target temp <38.5°C then stop cooling (avoid overshoot)
• Change to TIVA: Propofol, opioids, non-depolarising NMBAs are all safe

Pharmacological

• Dantrolene sodium 2.5mg/kg IV: Given as rapidly as possible; repeat every 5-10 minutes until ETCO2 falling, temperature decreasing, and rigidity resolving (max 10mg/kg initially; may need more)
• Hyperkalaemia treatment: Calcium gluconate 10% 0.2mL/kg IV, insulin/dextrose, salbutamol nebuliser
• Treat arrhythmias: Amiodarone 5mg/kg IV (NOT calcium channel blockers - dangerous interaction with dantrolene)
• Sodium bicarbonate 8.4%: 1-2 mmol/kg if severe acidosis (pH <7.1)
• IV fluids: Aggressive crystalloid (target UO >2 mL/kg/hr to protect kidneys from myoglobin)
• Continue dantrolene: 1mg/kg IV 6-hourly for 24-48 hours post-event

Surgical/Interventional

• Not applicable acutely; muscle biopsy for IVCT is a later elective procedure

Referral Criteria

• All suspected MH episodes - report to MH Investigation Unit (Leeds)
• All first-degree relatives - screening referral
• Issuing of MH alert card/bracelet
• Register with UK MH hotline for advice

• Mortality: Reduced from >70% (historical) to <5% with early recognition and dantrolene
• Key prognostic factor: Time to dantrolene administration - survival correlates inversely with delay
• Recrudescence: MH can recur in 25% within 24-36 hours - continued monitoring and dantrolene maintenance essential
• Long-term: MH susceptibility is lifelong; all future anaesthetics must use trigger-free techniques (TIVA)
• Undiagnosed MH susceptibility: Estimated prevalence ~1 in 3,000-5,000 individuals

MH Emergency Treatment Algorithm

Triggering vs Non-Triggering Agents

Key Facts

Perioperative anaphylaxis is one of the most feared anaesthetic emergencies. Multiple drugs and substances are administered simultaneously during anaesthesia, making identification of the causative agent challenging. Immediate adrenaline administration is life-saving.

Epidemiology

NAP6 (2018) found the incidence of perioperative anaphylaxis to be approximately 1 in 10,000 anaesthetics. Mortality was approximately 3.8% (1 in 260,000 anaesthetics). Female patients are more commonly affected (2:1 ratio). NMBAs cause the majority of reactions.

Aetiology

Common triggers (NAP6 data):

• NMBAs: 56% (rocuronium and suxamethonium most common)
• Antibiotics: 22% (teicoplanin, co-amoxiclav most common)
• Chlorhexidine: 9%
• Patent blue dye: Used in sentinel lymph node biopsy
• Latex: Declining due to latex-free environments
• Colloids: Gelatins (Gelofusine) more than starches
• Other: Opioids, propofol (egg/soy allergy - rare), bone cement

Pathophysiology

Clinical Features (may present with any combination)

• Cardiovascular: Hypotension (most common feature under GA), tachycardia, cardiovascular collapse, cardiac arrest
• Respiratory: Bronchospasm (wheeze, increased airway pressures), laryngeal oedema, desaturation
• Cutaneous: Urticaria, erythema, angioedema - may be absent or late under drapes
• Gastrointestinal: Abdominal cramps, vomiting (if awake)

Grading (Ring and Messmer)

• Grade 1: Cutaneous signs only (urticaria, erythema)
• Grade 2: Moderate multisystem (hypotension, bronchospasm, cutaneous)
• Grade 3: Severe life-threatening (severe hypotension, severe bronchospasm, arrhythmia)
• Grade 4: Cardiac and/or respiratory arrest

Red Flags

• Sudden unexplained cardiovascular collapse at induction - anaphylaxis until proven otherwise
• Severe bronchospasm unresponsive to bronchodilators - consider anaphylaxis
• Hypotension refractory to fluids - adrenaline required
• Any reaction to chlorhexidine or latex exposure - remove all sources immediately

Bedside

• AAGBI standard monitoring: Continuous during event - note timing of drug administration relative to reaction onset
• Document: All drugs given with times, exact nature and timing of clinical features

Bloods

• Serum tryptase: Sample 1 - as soon as possible after initial treatment; Sample 2 - at 1-2 hours; Sample 3 - at >24 hours (baseline). Elevated tryptase confirms mast cell degranulation.
• ABG: Assess oxygenation, ventilation, lactate

Imaging

• CXR: If bronchospasm or laryngeal oedema - exclude pneumothorax

Special Tests

• Allergy testing at 6 weeks: Skin prick testing and intradermal testing for all potential triggers - performed at specialist allergy centres
• Specific IgE: For NMBAs, latex, chlorhexidine, antibiotics
• Component testing: Morphine quaternary ammonium IgE as surrogate for NMBA allergy
• Drug provocation test: In selected cases where skin tests are equivocal

Non-pharmacological

• Stop suspected trigger: Discontinue most recently administered drug
• Call for help: Declare anaphylaxis, assign roles
• Remove latex: If latex suspected, change gloves and equipment
• Position: Supine with legs raised (improves venous return)

Pharmacological

• Adrenaline (FIRST-LINE): 50mcg IV boluses (0.5mL of 1:10,000); titrate to response; up to 100-300mcg for severe reactions; infusion 0.05-1mcg/kg/min if refractory
• IV fluids: Aggressive crystalloid resuscitation - 20mL/kg bolus, repeat as needed (massive capillary leak may require >4L)
• Chlorphenamine: 10mg IV (antihistamine - second-line)
• Hydrocortisone: 200mg IV (prevents late-phase reaction - given after adrenaline)
• Bronchospasm: Salbutamol 250mcg IV or nebulised 5mg; aminophylline 5mg/kg IV over 20 min if refractory
• If cardiac arrest: ALS algorithm with adrenaline 1mg IV every 3-5 min; prolonged CPR may be needed

Surgical/Interventional

• Abandon or abbreviate surgery if possible during active anaphylaxis
• ICU transfer for observation (biphasic reaction may occur in 5-20% at 4-12 hours)

Referral Criteria

• ALL suspected perioperative anaphylaxis - refer to specialist allergy clinic at 6 weeks
• Complete AAGBI anaphylaxis reaction form
• Report to MHRA (Yellow Card Scheme)
• Issue patient with interim letter documenting suspected triggers and advising future avoidance

• Mortality: ~3.8% overall (NAP6); higher in grade 4-5 reactions
• Early adrenaline: Key determinant of survival - delayed adrenaline is the most common factor in fatal anaphylaxis
• Biphasic reaction: Occurs in 5-20% at 4-12 hours - observe in ICU/HDU for minimum 12-24 hours
• Future anaesthesia: Safe with avoidance of identified triggers - specialist allergy testing provides a 'safe drug list'
• Recurrence: Avoidable with appropriate investigation and planning

Perioperative Anaphylaxis Management Algorithm

NAP6 - Causes of Perioperative Anaphylaxis