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Obesity and Anaesthesia - Comprehensive Clinical Note

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1. DEFINITIONS AND CLASSIFICATION

• Total Body Weight (TBW) - actual measured weight
• Ideal Body Weight (IBW) - Broca index: height(cm) - 100 (males), height(cm) - 105 (females)
• Predicted Body Weight (PBW): Males = 50 + 0.91 × (height[cm] - 152.4); Females = 45.5 + 0.91 × (height[cm] - 152.4)
• Lean Body Weight (LBW): TBW minus fat mass; ~80% TBW in males, ~75% in females. In morbidly obese patients, LBW ≈ IBW + 20-30%

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2. PATHOPHYSIOLOGY

2.1 Respiratory System

• Obesity causes a reduction in FRC (Functional Residual Capacity), ERV (expiratory reserve volume), TLC, and respiratory compliance
• In the supine position, the cephalad shift of the diaphragm due to abdominal fat load drastically worsens FRC - this can fall below closing capacity (CC), causing small airway closure, V/Q mismatch, shunting, and hypoxaemia
• The obese patient's FRC may already be below CC while awake in the supine position; under anaesthesia this worsens further
• Increased chest wall load raises the work of breathing significantly
• Oxygen consumption (VO₂) and CO₂ production are both increased due to increased metabolic demands of excess tissue

• Extremely common in obese patients - soft tissue pharyngeal collapse during sleep/sedation
• STOP-BANG scoring tool is used perioperatively to screen for OSA
• OSA is characterised by repetitive episodes of complete (apnoea) or partial (hypopnoea) upper airway obstruction during sleep, causing hypoxaemia and arousal
• The obese patient with OSA is particularly vulnerable to:
  • Respiratory depression from opioids and sedatives
  • Difficult airway management
  • Postoperative apnoeic episodes

• Defined as: daytime hypercapnia (PaCO₂ >45 mmHg) + obesity (BMI ≥30 kg/m²) + exclusion of other causes of hypoventilation
• Prevalence: up to 50% of obese patients with OSA; up to 50% with BMI ≥50 kg/m²; 0.15-0.3% of the general population
• 90% of OHS patients also have OSA
• Pathophysiology of OHS:
  • Normally, severe obesity increases respiratory drive to compensate for abnormal chest wall mechanics - this maintains eucapnia
  • In OHS, this compensatory mechanism is abolished, partly explained by leptin resistance
  • Results in: reduced lung capacity, reduced vital capacity, reduced FRC, reduced ERV, reduced respiratory system compliance, reduced inspiratory muscle strength
  • Serum bicarbonate is elevated (chronic CO₂ retention with metabolic compensation)
  • Alveolar PCO₂ is elevated; CO₂ response may be blunted
  • Central fat distribution causes cranial displacement of the diaphragm in the supine position
  • Diaphragmatic myopathy may be a contributing factor
• Treatment: weight loss, non-invasive ventilation (NIV/CPAP/BiPAP)

• Obese patients who do NOT have OHS may actually hyperventilate (increased respiratory drive to compensate for increased metabolic demand and reduced compliance)
• Under anaesthesia, this drive is suppressed - a critical point
• Post-extubation hypoventilation (alveolar hypoventilation) is a major risk:
  • Residual neuromuscular blockade
  • Opioid effects on respiratory drive
  • Upper airway obstruction from OSA physiology
  • Impaired respiratory mechanics in the supine position
  • Patients with OHS are at greatest risk of postoperative respiratory failure

2.2 Cardiovascular and Haematologic Systems

• Blood volume, cardiac output, and muscle mass all increase linearly with obesity
• This manifests as increased preload and increased LV work
• Chronic pressure and volume overload leads to:
  • LV hypertrophy and dilation
  • Pulmonary hypertension (from OSA-induced hypoxic pulmonary vasoconstriction, plus increased pulmonary blood flow)
  • Biventricular failure in advanced cases
• Obese patients often appear asymptomatic from cardiovascular disease because their limited exercise tolerance prevents them from reaching the threshold where symptoms manifest
• Obese cardiomyopathy (obesity-related cardiomyopathy) can occur even without hypertension or diabetes
• Increased risk of: coronary artery disease, atrial fibrillation, DVT, PE, stroke
• Morbid obesity is a major independent risk factor for DVT and sudden death from acute postoperative pulmonary embolism
• Haematologically: polycythaemia may be present (from chronic hypoxia in OSA/OHS); increased risk of thrombosis due to immobility, venous stasis, hypercoagulability

2.3 Gastrointestinal System

• Obesity increases intra-abdominal pressure, which raises intragastric pressure
• There is a higher incidence of hiatus hernia and GORD (gastro-oesophageal reflux disease)
• This significantly raises the risk of aspiration at induction and extubation
• Gastric volume may not necessarily be increased, but the pressure gradient is - making aspiration more likely
• Non-alcoholic fatty liver disease (NAFLD) is common - elevated ALT is seen in many obese patients, but there is no clear correlation between liver function test abnormalities and the capacity of the liver to metabolise drugs

2.4 Renal and Endocrine Systems

• Type 2 diabetes mellitus - extremely common comorbidity; insulin resistance
• Metabolic syndrome: hypertension + dyslipidaemia + hyperglycaemia + central obesity + prothrombotic state
• Hypothyroidism - may compound respiratory depression
• PCOS (in women) - associated with perioperative complications
• Renal effects: glomerulomegaly, hyperfiltration, proteinuria, CKD risk

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3. PREOPERATIVE EVALUATION

History

• Screen for OSA using STOP-BANG:
  • Snoring, Tired, Observed apnoeas, Pressure (hypertension), BMI >35, Age >50, Neck circumference >40 cm, Gender male
  • Score 5-8 = high risk for OSA
• Assess exercise tolerance - functional capacity may underestimate cardiac disease since patients are sedentary
• Ask about CPAP/BiPAP use at home
• Ask about symptoms of OHS: daytime somnolence, morning headaches (from nocturnal hypercapnia), cor pulmonale signs

Key Physical Examination Points

• Neck circumference ≥40 cm is the single biggest predictor of difficult mask ventilation, difficult laryngoscopy, and difficult intubation
• Assess Mallampati score, mouth opening, neck mobility, jaw protrusion
• Upper body adiposity particularly increases airway difficulty
• Blood pressure: use appropriately sized large cuff; if arm is too large, use forearm cuff with standard cuff or invasive arterial monitoring may be needed
• In the supine position, forearm measurements with a standard cuff can be used when upper arm measurements are challenging

Investigations

• ECG, echocardiography (if cardiac disease suspected)
• Chest X-ray, spirometry
• ABG if OHS suspected (look for daytime hypercapnia, elevated bicarbonate)
• Full blood count (polycythaemia?), renal function, LFTs, glucose/HbA1c
• Sleep study (polysomnography) if OSA not previously diagnosed
• Chest X-ray - difficult to interpret due to body habitus

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4. PHARMACOLOGY IN OBESITY

• Total body water, plasma volume, and cardiac output (all increased)
• Protein binding (variable)
• Lipid solubility of the drug
• Hepatic and renal blood flow

Weight Descriptors for Dosing

• Larger induction doses are needed because blood volume, muscle mass, and CO all increase linearly with obesity
• Succinylcholine: pseudocholinesterase activity increases with obesity, requiring increased doses (TBW-based)
• Propofol: highly lipophilic; its volume of distribution increases substantially. Induction bolus on LBW but maintenance infusions use TBW

Sugammadex in Obesity - Special Consideration

• NMBDs (non-depolarising, e.g. rocuronium) should be dosed on IBW/LBW because they are hydrophilic and their volume of distribution is minimally affected by obesity
• Sugammadex dosing is currently recommended based on TBW (actual body weight) - this ensures complete encapsulation of all free rocuronium molecules, including those redistributing from peripheral compartments
• When dosed on lean/IBW alone, approximately 40% of morbidly obese patients have inadequate reversal
• Dosing on LBW + 40% has been shown to adequately reverse moderate rocuronium block in most patients
• Current recommendation: dose sugammadex on TBW until more data are available
• Critical importance: postoperative residual neuromuscular block in obese patients → upper airway collapse → respiratory failure
• Complete antagonism of NMB must be confirmed before extubation

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5. INTRAOPERATIVE MANAGEMENT

5.1 Equipment and Monitoring

• Operating table weight limit must be checked (most standard tables rated to 200-250 kg; bariatric tables rated to 450+ kg)
• Wide, padded table extensions may be needed
• Positioning: pressure injury risk is very high in obesity - pad bony prominences carefully
• Intravenous access: may be extremely difficult; consider ultrasound guidance or consider early central venous access
• BP cuff: size appropriately - too small a cuff gives falsely elevated readings; forearm BP measurement acceptable in supine position
• Arterial line: strongly consider for major cases, especially in OHS patients - continuous BP and ABG monitoring
• BIS/processed EEG monitoring: recommended to avoid awareness (propofol dose is complex) and to prevent excessive depth contributing to postoperative respiratory depression
• Neuromuscular monitoring (TOF/TOF-ratio): mandatory in obese patients - residual NMB must be excluded before extubation

5.2 Airway Management

• Key predictors: neck circumference ≥40 cm, high Mallampati, limited neck extension, large tongue, presence of OSA
• An OSA score (STOP-BANG ≥5) combined with neck circumference >40 cm significantly increases difficult intubation risk

• The standard "sniffing position" is often inadequate in morbidly obese patients because the large occipital fat pad tilts the head forward, obscuring the view
• The ramped position: upper body elevated (usually using pillows, wedge, or operating table tilt) until the external auditory meatus is at the same horizontal level as the sternal notch
• This aligns the oral, pharyngeal, and laryngeal axes more optimally
• Improves laryngoscopic view compared to the sniffing position in obese patients
• Also improves FRC during preoxygenation

• Critical step - obese patients desaturate far more rapidly than non-obese patients due to reduced FRC and increased O₂ consumption
• Time to critical desaturation (SpO₂ <90%) is significantly shorter in obese patients
• Pre-oxygenate in the head-up position (ramped or 20-30° head elevation)
• Use tight-fitting face mask, 100% O₂ for ≥3-5 minutes (or 8 vital capacity breaths)
• Consider high-flow nasal oxygen (HFNO) during preoxygenation and apnoeic phase
• Consider CPAP/NIV pre-oxygenation in severely obese patients to recruit atelectatic alveoli and augment FRC before induction

• Strongly recommended in morbidly obese patients due to aspiration risk (raised intra-abdominal pressure, GORD)
• Succinylcholine (dose on TBW) or high-dose rocuronium (1.2 mg/kg IBW) with sugammadex reversal available
• Cricoid pressure applied (Sellick's manoeuvre)
• Avoid mask ventilation between induction and intubation if full RSI

• Video laryngoscopy is preferred when difficult airway is anticipated
• Awake fibre-optic intubation (AFOI) for the truly predicted difficult airway
• LMA (laryngeal mask airway) is generally avoided in morbidly obese patients except as a rescue device, given aspiration risk and poor seal with high airway pressures
• Have a failed intubation plan ready (wake the patient, surgical airway kit available)

5.3 Positioning

• Reverse Trendelenburg / head-up / sitting up is optimal for:
  • Preoxygenation
  • Intubation (ramped position)
  • Ventilation (improved FRC, reduced diaphragm excursion from abdominal contents)
• Avoid prolonged supine/lithotomy positions
• Lateral decubitus position improves oxygenation (non-dependent lung ventilated better)

5.4 Induction and Maintenance

• Propofol: LBW-based bolus, titrated
• Thiopentone: LBW-based
• Succinylcholine: TBW-based
• Rocuronium (non-depolarising NMB for RSI): 1.2 mg/kg IBW
• Fentanyl bolus: LBW-based

• Total intravenous anaesthesia (TIVA) with propofol: preferred by some as it avoids the risk of volatile agent sequestration in fat (though this is more relevant for prolonged cases)
• Volatile agents are acceptable - note that emergence may be slightly prolonged due to redistribution from fat stores, but this is clinically significant mainly for very long cases
• Desflurane (least lipid-soluble volatile agent): historically preferred for faster emergence; however it is being withdrawn/reduced in use due to high GWP (global warming potential)
• Remifentanil infusion: LBW-based rate; excellent for cardiovascular stability

5.5 Mechanical Ventilation Strategies

• Tidal volume: based on IBW/PBW (not TBW!) - typically 6-8 ml/kg IBW
  • Using TBW to calculate tidal volumes causes dangerous over-distension (VILI - ventilator-induced lung injury)
• PEEP (Positive End-Expiratory Pressure):
  • PEEP is the only ventilatory parameter consistently shown to improve respiratory function in obese patients
  • Prevents alveolar collapse, improves FRC, improves oxygenation
  • Typical PEEP: 8-12 cmH₂O in obese patients; titrate to oxygenation
  • Caution: PEEP decreases venous return and cardiac output - monitor haemodynamics
• Recruitment manoeuvres: used to re-open collapsed alveoli; typically a sustained inflation of 30-40 cmH₂O for 30-40 seconds, or incremental PEEP titration
  • Always reassess haemodynamics after recruitment
• Prone positioning: rarely used in obese patients intraoperatively (logistically difficult) but used in ICU for OHS/ARDS
• I:E ratio: may need adjustment for better exhalation if there is expiratory flow limitation
• Respiratory rate: adjust to achieve normocapnia (note: obese patients without OHS tolerate normocapnia; OHS patients may be used to chronic hypercapnia - permissive hypercapnia may be appropriate)
• FiO₂: start with 60-80%; titrate down with PEEP recruitment

5.6 Fluid Management

• Fluid overload is poorly tolerated (impairs lung function, worsens oedema)
• Goal-directed fluid therapy is recommended
• Third-space losses are not reduced in obese patients despite excess fat (fat is poorly perfused and does not meaningfully participate in fluid shifts)
• Crystalloid choice: balanced solutions (Hartmann's/PlasmaLyte) preferred over normal saline (hyperchloraemic acidosis risk)

5.7 Regional Anaesthesia in Obesity

• Regional anaesthesia is strongly encouraged in obesity:
  • Reduces need for systemic opioids (opioid-sparing)
  • Avoids airway instrumentation in high-risk patients
  • Reduces postoperative respiratory complications
• Challenges:
  • Landmark-based techniques very difficult due to adiposity
  • Ultrasound guidance is essential
  • Spinal/epidural: shorter drug requirement because of:
    • Increased epidural fat → reduced epidural space volume → more cephalad spread of local anaesthetic
    • Position the patient carefully (lateral or sitting)
    • Use reduced doses of intrathecal local anaesthetic
  • Risk of higher/total spinal in obese patients
  • Post-spinal anaesthesia lung volumes are significantly reduced in obese and morbidly obese female patients - respiratory monitoring essential after neuraxial blocks

5.8 Emergence and Extubation

• Prompt but safe extubation reduces the likelihood that the morbidly obese patient will become ventilator dependent - especially in patients with cardiopulmonary disease
• Before extubation, ensure:
  1. Patient is fully awake and following commands
  2. Complete NMB reversal confirmed - TOF ratio ≥0.9 (ideally ≥0.95); use sugammadex dosed on TBW
  3. Patient breathing spontaneously with adequate rate, volume, and airway reflexes
  4. Patient able to open eyes, lift head for 5 seconds, grip
• Extubate in the head-up / semi-recumbent position - never supine
• Have re-intubation/video laryngoscopy equipment immediately available
• Consider CPAP at extubation (put patient back on their home CPAP mask)

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6. POSTOPERATIVE CONSIDERATIONS

6.1 Respiratory Monitoring and Management

• Obese patients face maximum respiratory risk in the first 24-72 hours postoperatively
• Key threats:
  • Opioid-induced respiratory depression (particularly in OSA/OHS patients)
  • Postoperative residual neuromuscular blockade → upper airway collapse
  • Position (supine worsens FRC)
  • Wound pain inhibiting deep breathing
• Monitoring: continuous pulse oximetry is mandatory; consider capnography in high-risk cases
• Position: nurse semi-recumbent (45°) or in lateral position rather than supine
• CPAP/NIV: if patient uses CPAP at home, resume immediately postoperatively
  • Early institution of CPAP/BiPAP is key for OHS patients
• HDU/ICU admission should be considered for:
  • BMI >50 kg/m²
  • Significant OSA/OHS
  • Cardiac or pulmonary disease
  • Major surgery or prolonged anaesthesia

6.2 Postoperative Analgesia - OSA-Aware Multimodal Approach

• Opioid-sparing multimodal analgesia is the goal
• Components:
  • NSAIDs (if no contraindications)
  • Paracetamol (acetaminophen) - IV or oral
  • Regional analgesia (epidural, TAP block, peripheral nerve blocks) - most effective opioid-sparing strategy
  • Dexamethasone - anti-inflammatory, reduces opioid requirements
  • Ketamine - low-dose adjunct; anti-hyperalgesic
  • Alpha-2 agonists (clonidine, dexmedetomidine) - analgesic + sedative-sparing
  • Gabapentin/pregabalin - use cautiously in OSA (can worsen respiratory depression)
• Opioids: if required, use minimum effective dose; avoid long-acting opioids in high-risk patients
• Delayed respiratory depression with neuraxial opioids is a specific risk - lipophilic opioids (fentanyl epidural) spread rostrally over time in obese patients

6.3 DVT/PE Prophylaxis

• Morbid obesity is a major independent risk factor for DVT and fatal PE
• Measures:
  • LMWH (dose based on actual body weight up to maximum dose; some centres use TBW-based dosing)
  • Sequential compression devices (SCDs/TED stockings) - apply intraoperatively and postoperatively
  • Early mobilisation - difficult but critical; physiotherapy input
  • Extended prophylaxis (post-discharge LMWH) for high-risk patients

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7. OSA PERIOPERATIVE MANAGEMENT SUMMARY

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8. OHS - SPECIFIC ANAESTHETIC CONCERNS

• Aggressive over-ventilation intraoperatively may cause severe post-extubation apnoea (suppresses hypercapnic drive that was compensating)
• Maintain PaCO₂ near patient's known preoperative baseline if known; otherwise aim for normocapnia
• Pre- and postoperative NIV is essential
• Avoid all unnecessary respiratory depressants (benzodiazepines, anticholinesterases in high dose)
• ICU admission is generally warranted after major surgery

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9. AMBULATORY ANAESTHESIA IN OBESITY

• BMI alone is not a contraindication to day-case surgery
• OSA/OHS, poorly controlled comorbidities, or major procedures are contraindications
• STOP-BANG score helps risk-stratify
• Must ensure adequate pain control without heavy opioid use
• Patient must be able to maintain their airway and respiratory function independently before discharge
• Recovery monitoring must include continuous pulse oximetry

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10. CRITICAL CARE AND RESUSCITATION

• Obese patients requiring ICU admission face additional challenges:
  • Proning for respiratory failure: technically demanding, risk of pressure injuries, need for adequate staffing
  • Vasopressor doses: may need adjustment; drug distribution affected
  • Nutritional support: paradoxically, obese critically ill patients often malnourished at a cellular level - specialist dietician input
  • Difficult venous access and need for central lines/arterial lines
  • Imaging: CT scanners have weight limits; ultrasound is valuable
• Tracheostomy (if needed): technically difficult; high risk of misplacement and decannulation; longer necks are more challenging

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11. SUMMARY OF KEY POINTS (Barash, Cullen & Stoelting)

1. Obese patients may have significant cardiovascular disease and appear asymptomatic because of limited exercise tolerance
2. Elevated LFTs (mainly ALT) are common, but no clear correlation with hepatic drug metabolism capacity
3. Neck circumference ≥40 cm is the biggest predictor of difficult mask ventilation, difficult laryngoscopy, and difficult intubation
4. OSA and OHS must be assessed preoperatively - frequently associated with difficult airway and perioperative pulmonary complications
5. Blood pressure measurements can be falsely elevated with a too-small cuff; forearm BP in supine is acceptable
6. The ramped position improves laryngoscopic view compared to the standard sniffing position
7. Larger induction agent doses are required; succinylcholine dose is increased (pseudocholinesterase increase)
8. PEEP is the only ventilatory parameter consistently shown to improve respiratory function in obese patients - but decreases venous return and CO
9. Prompt but safe extubation reduces the risk of ventilator dependence
10. Opioid-sparing multimodal analgesia and regional techniques reduce the risk of opioid-related respiratory complications
11. Obese patients receiving neuraxial or parenteral opioids require careful postoperative monitoring - delayed respiratory depression is a real risk
12. Morbid obesity is a major independent risk factor for DVT and sudden fatal PE - early mobilisation is critical

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Quick Reference: Drug Dosing Weights in Obesity

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• Barash, Cullen, and Stoelting's Clinical Anesthesia, 9e - Ch. 45: Anesthesia and Obesity
• Miller's Anesthesia, 10e - Ch. 54: Obesity as a Disease; Ch. 9: Obesity Hypoventilation Syndrome
• PMID 40468902: McKechnie et al. 2025 - Society for Obesity and Bariatric Anaesthesia airway management best practice guidelines
• PMID 39366846: Carron et al. 2024 - Multimodal analgesia in obesity, systematic review/network meta-analysis

• Professionally formatted with headings, colour-coded styles, header/footer, and page numbers
• 8 sections covering definitions, pathophysiology (respiratory/CVS/GI/endocrine), preoperative evaluation, pharmacology (drug dosing weight tables), intraoperative management (airway, RSI, ramped position, ventilation, regional, extubation), postoperative care, OSA/OHS summary table, and all 12 key points from Barash
• All tables formatted with blue headers and alternating row shading for easy reading