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Anaesthetic Management of Bronchiectasis for Right Lower Lobe Lobectomy

Based on Miller's Anesthesia, 10th Edition (9780323935920)

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1. UNDERSTANDING THE DISEASE: BRONCHIECTASIS

• Airflow obstruction
• Impaired clearance of secretions
• Accumulation of copious, often purulent secretions

1. Soiling of the contralateral (unaffected) lung by infected secretions
2. Lung isolation (essential)
3. One-lung ventilation (OLV) physiology and management
4. Hemostasis risk due to inflamed, hypervascular tissue
5. Sepsis if presenting acutely

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2. PREOPERATIVE ASSESSMENT

2.1 Pulmonary Function Evaluation

• Spirometry: FEV₁, FVC, FEV₁/FVC
• A predicted postoperative FEV₁ (ppoFEV₁) < 40% of predicted is associated with increased risk
• Diffusing capacity for carbon monoxide (DLCO) also predicts postoperative pulmonary complications

• Stair-climbing or 6-minute walk test
• A patient unable to climb 2 flights of stairs is at significantly elevated risk
• VO₂ max > 15 mL/kg/min predicts good tolerance for lobectomy

• V/Q scan: determines how much of ventilation and perfusion comes from the operative lung
• If the operative (right lower) lung is already poorly perfused/ventilated preoperatively, OLV will be better tolerated
• ABG: baseline PaO₂ and PaCO₂

2.2 Clinical Assessment

• History of hemoptysis (volume, frequency) — massive hemoptysis changes the urgency and approach
• Quantity and character of sputum — daily sputum volume, color, odor
• Current infections — active sepsis contraindicates neuraxial techniques
• Nutritional status — chronic infection leads to cachexia
• Coexisting COPD or reactive airway disease (highly prevalent in this population)
• Medications: bronchodilators, antibiotics, steroids — continue perioperatively
• Review of chest CT by the anesthesiologist personally: assess airway anatomy, extent of disease, tracheal deviation, presence of contralateral disease, mediastinal shift. CT imaging may reveal extrinsic bronchial compression or deviated anatomy that affects lung isolation

2.3 Preoperative Optimization

• Chest physiotherapy and postural drainage to reduce secretion burden
• Appropriate antibiotic therapy to reduce infection
• Bronchodilators to optimize airflow
• Correction of nutritional deficits where time allows
• Cessation of smoking (at least 8 weeks preoperatively reduces complications)

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3. LUNG ISOLATION — THE CENTRAL CHALLENGE

3.1 Why Lung Isolation is Mandatory

"Anesthetic considerations during surgery for these infective indications include the need for lung isolation to protect uninvolved lung regions from soiling by pus in the infected areas. The risk of soiling occurs if the patient is repositioned for surgery, after induction of anesthesia, before the lung is adequately isolated." — Miller's Anesthesia, Ch. 49

3.2 Choice of Isolation Device: Left-Sided Double-Lumen Tube (DLT)

• The left mainstem bronchus is longer (4–5 cm vs. 1.5–2 cm on the right)
• More margin of safety for positioning
• Right upper lobe bronchus is not at risk of obstruction by the endobronchial cuff

• Distorted left mainstem bronchial anatomy
• Left-sided pneumonectomy or sleeve resection
• Descending thoracic aortic aneurysm
• Left-sided tracheobronchial disruption

3.3 Sizing of the DLT (Table 49.7, Miller's)

3.4 Positioning and Verification

• After intubation in the supine position, confirm placement by auscultation
• Always confirm with fiberoptic bronchoscopy (FOB) — auscultation alone is unreliable
• Through the tracheal lumen: the blue endobronchial cuff should be visible 5–10 mm below the main carina in the left bronchus; identify the right upper lobe bronchus take-off
• Through the endobronchial lumen: confirm patency and visualization of left upper and lower lobe orifices
• After lateral repositioning: recheck position with FOB, as the tube can migrate (especially during turning in a bronchiectasis patient with copious secretions distorting the view)
• Photograph or note the centimeter marking at the teeth for reference

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4. INDUCTION OF ANAESTHESIA

4.1 Critical Precaution: Isolation BEFORE Repositioning

1. Induce anaesthesia in the supine position
2. Intubate with a left-sided DLT
3. Confirm position with FOB
4. Isolate and suction the right (operative) lung before repositioning
5. Only then turn the patient to the left lateral decubitus position
6. Reconfirm DLT position with FOB after repositioning

4.2 Induction Agents

• Propofol: attenuates airway reflexes, reduces bronchial reactivity — preferred first choice
• Ketamine: bronchodilator — useful if there is significant airway reactivity

• Barbiturates (thiopentone): no bronchodilating effect
• Opioids alone: no bronchodilating effect
• Drugs that release histamine (e.g., atracurium, morphine in high doses) — may worsen bronchospasm

4.3 Airway Management Philosophy

"The principles of anesthetic management are the same as for any asthmatic patient: avoid manipulation of the airway in a lightly anesthetized patient, use bronchodilating anesthetics, and avoid drugs which release histamine." — Miller's Anesthesia, Ch. 49

• Ensure deep anaesthesia before DLT insertion — the added airway manipulation of a DLT is a potent trigger for bronchoconstriction
• Pre-oxygenate thoroughly with 100% O₂
• Consider lidocaine IV or topical (4 mg/kg) to suppress cough and bronchospasm on airway instrumentation

4.4 Muscle Relaxation

• Succinylcholine for rapid sequence if full stomach/septic patient
• Rocuronium (with sugammadex reversal available) — preferred non-depolarizing agent
• Avoid atracurium/mivacurium (histamine release)

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5. INTRAOPERATIVE MONITORING

"Because surgery is usually performed in the lateral position, monitors are initially placed with the patient in the supine position and have to be rechecked and repositioned after the patient is turned. It is difficult to add additional monitoring, particularly invasive vascular monitoring, after the case is started if complications arise." — Miller's Anesthesia, Ch. 49

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6. MAINTENANCE OF ANAESTHESIA

6.1 Volatile Agents

• Sevoflurane or isoflurane — preferred volatile agents; both are bronchodilators and attenuate HPV (hypoxic pulmonary vasoconstriction) only modestly at ≤1 MAC
• Sevoflurane may be the most potent bronchodilator of the volatile anesthetics
• Keep volatile at ≤1 MAC during OLV to minimize HPV inhibition and avoid reducing cardiac output

6.2 Total Intravenous Anaesthesia (TIVA)

• Propofol infusion — does not inhibit HPV; preferred in patients where oxygenation is tenuous during OLV
• Combined propofol + remifentanil TIVA is a reliable technique for thoracic surgery

6.3 Nitrous Oxide

• Avoid N₂O in thoracic surgery — risk of enlarging blebs/bullae (though in pure bronchiectasis without bullae this is less critical)
• N₂O speeds non-operative lung collapse but its use is generally not recommended

6.4 Fluid Management

• Restrict fluids: thoracic surgery patients are particularly prone to postoperative pulmonary edema with fluid overload
• Target crystalloid infusion of 1–2 mL/kg/hr during surgery
• Blood products as needed — bronchiectasis surgery can involve significant hemorrhage due to hypervascular, inflamed tissue

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7. ONE-LUNG VENTILATION (OLV) MANAGEMENT

7.1 Initiating OLV

• Pre-oxygenate the operative lung with 100% O₂ to speed collapse (de-nitrogenation). Nitrogen in the air/O₂ mixture delays collapse significantly
• Perform a recruitment maneuver on the dependent (left) lung to eliminate atelectasis before OLV starts
• Collapse the right lung by clamping the right lumen of the DLT and confirming adequate ventilation of the left lung

7.2 Ventilation Settings During OLV

• Tidal volume: 5–6 mL/kg IBW (avoid large tidal volumes — risk of volutrauma in dependent lung)
• Respiratory rate: adjust to maintain PaCO₂ 40–45 mmHg (permissive mild hypercapnia acceptable)
• PEEP: 5–10 cmH₂O to dependent lung — titrate to maximize compliance while keeping driving pressure ≤15 cmH₂O
• FiO₂: 1.0 initially; reduce if oxygenation is satisfactory
• I:E ratio: 1:2 to 1:2.5

7.3 Prediction of Desaturation During OLV

1. High % ventilation or perfusion to the operative lung on preoperative V/Q scan
2. Poor PaO₂ during two-lung ventilation in the lateral position preoperatively
3. Right-sided thoracotomy (our case — highest risk factor)
4. Normal preoperative spirometry or restrictive disease
5. Supine position during OLV

7.4 Hypoxic Pulmonary Vasoconstriction (HPV)

• HPV is the key protective reflex — vasoconstricts pulmonary vessels in the collapsed (non-ventilated) right lung, diverting blood to the ventilated left lung
• Both volatile anesthetics and vasodilators (nitrates, dobutamine) inhibit HPV
• Maintain volatile anaesthetic at ≤1 MAC to preserve HPV

7.5 Treatment of Hypoxemia During OLV

1. Severe/precipitous desaturation: Resume two-lung ventilation immediately — reinflate operative lung, deflate bronchial cuff
2. Ensure FiO₂ = 1.0
3. Recheck DLT position with FOB — rule out lobar obstruction in ventilated lung (especially important in bronchiectasis where secretions can occlude DLT lumens)
4. Optimize cardiac output — check for IVC compression by surgeon (common during pulmonary resections); treat with inotropes/vasopressors as needed; reduce volatile to ≤1 MAC
5. Recruitment maneuver of ventilated (left) lung: inflate to 20 cmH₂O for 15–20 seconds (will cause transient hypotension and transient further desaturation)
6. Apply PEEP to ventilated lung (5–10 cmH₂O) after recruitment — titrate to maximize compliance
7. Apneic oxygen insufflation: 3 L O₂ via suction catheter into the non-ventilated (right) lumen of DLT — improves PaO₂ without surgical interference
8. CPAP 1–2 cmH₂O to the non-ventilated lung — apply after first recruiting (re-inflating) it; a commercial or improvised CPAP circuit is used. In bronchiectasis patients, CPAP to the operative lung must be used cautiously — it may impede surgical access and the surgeon must be informed
9. Partial ventilation of non-ventilated lung: intermittent IPPV, small tidal volume ventilation
10. Pharmacologic HPV augmentation: almitrine (where available)
11. Mechanical restriction of blood flow to operative lung if possible
12. Venovenous ECMO — last resort

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8. SPECIAL CONSIDERATIONS IN BRONCHIECTASIS

8.1 Secretion Management

• The DLT must be suctioned frequently throughout the case — bronchiectasis generates copious infected secretions that can obstruct the DLT lumens
• FOB should be available throughout the procedure for repeated position checks and targeted suctioning
• Secretions contaminating the tracheal lumen can cause obstruction or soiling of the left lung — vigilance is paramount

8.2 Septic Patient

• If the patient presents with active sepsis: placement of a thoracic epidural catheter is NOT recommended (risk of epidural abscess)
• Septic patients have altered pharmacodynamics and hemodynamics
• Early vasopressor support may be needed (norepinephrine infusion via central line)

8.3 Hemorrhage Risk

"Due to the inflammation, surgery is technically more difficult and there is a greater risk of massive hemorrhage." — Miller's Anesthesia, Ch. 49

• Large-bore IV access ×2 or central line with large lumen
• Type and cross-match for packed red cells
• Have vasopressors and blood products readily available
• Cell salvage may be considered (though infected field limits its use)

8.4 Hemoptysis

• If the indication is hemoptysis, the risk of contaminating the contralateral lung is highest
• Lung isolation must be secured before any patient movement
• If massive hemoptysis: the DLT also provides the ability to isolate and tamponade the bleeding lung

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9. POSITIONING

• Left lateral decubitus position (right side up for right-sided surgery)
• Recheck DLT position with FOB after final positioning
• Axillary roll under the dependent chest wall
• Dependent arm extended, upper arm supported to avoid brachial plexus injury
• Ensure all pressure points are padded
• Head in neutral position
• Lower limb in dependent position with padding between knees

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10. POSTOPERATIVE ANALGESIA

10.1 Thoracic Epidural Analgesia (TEA)

• Gold standard for post-thoracotomy pain
• Placed at T4–T6 level; local anaesthetic + opioid combination (e.g., bupivacaine 0.125% + fentanyl 2 mcg/mL or hydromorphone)
• Benefits: superior analgesia, reduced atelectasis, reduced opioid requirements, possible cardiac benefit, may reduce risk of chronic post-thoracotomy pain
• Contraindication: active sepsis/bacteremia — do NOT place epidural if patient is septic

10.2 Paravertebral Block (PVB)

• Excellent alternative to epidural when epidural is contraindicated (e.g., sepsis) or technically difficult
• Provides ipsilateral multi-dermatome analgesia
• Can be placed preoperatively or intraoperatively under direct vision by the surgeon
• Fewer side effects than epidural (no hypotension, urinary retention)

10.3 Intercostal Nerve Blocks

• Useful supplement; limited duration unless a catheter technique is used

10.4 Multimodal Analgesia

• Paracetamol (acetaminophen) IV
• NSAIDs (unless contraindicated by renal function, platelet function)
• Opioids (morphine or oxycodone PCA) as rescue

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11. EXTUBATION AND POSTOPERATIVE CARE

11.1 Extubation Criteria

"Extubation in the operating room is encouraged if the patient meets standard criteria for extubation." — Miller's Anesthesia, Ch. 49

• Awake, cooperative, following commands
• Adequate reversal of neuromuscular blockade (TOF ratio >0.9)
• Adequate respiratory effort (VC >15 mL/kg, NIF >−25 cmH₂O)
• SpO₂ ≥95% on FiO₂ ≤0.4
• Temperature and hemodynamic stability
• Controlled pain

11.2 DLT Exchange

• Convert the DLT to a standard single-lumen ETT if the patient requires postoperative ventilation — DLTs are not designed for long-term ventilation
• Use an airway exchange catheter (Cook AEC) for safe tube exchange

11.3 Postoperative Care

• HDU or ICU admission for at least 24 hours
• Aggressive chest physiotherapy and airway suctioning — bronchiectasis patients have persistent secretion burden
• Early mobilization
• Regular chest X-ray to detect atelectasis, pneumothorax, haemothorax
• Monitor drain output (chest drain placed by surgeon intraoperatively)
• Incentive spirometry
• Watch for bronchopleural fistula (persistent air leak, purulent drainage)

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12. COMPLICATIONS SPECIFIC TO THIS CASE

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SUMMARY ALGORITHM

PREOP: PFTs + V/Q scan + CT airway review + optimize secretions
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INDUCTION: Supine → Propofol/Ketamine → Left-sided DLT
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CONFIRM: FOB verification of DLT → Suction right lung → Isolate
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POSITION: Left lateral decubitus → Re-confirm DLT with FOB
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OLV: 100% O₂ pre-denitrogenation → Tidal vol 5-6 mL/kg → PEEP 5–10 cmH₂O
     Volatile ≤1 MAC → Frequent DLT suctioning
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HYPOXIA: Box 49.12 stepwise → CPAP to non-ventilated / PEEP to ventilated
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EXTUBATION: OT extubation if criteria met → TEA or PVB analgesia
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POSTOP: ICU/HDU → Chest physiotherapy → Monitor for BPF

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• Miller's Anesthesia, 2-Volume Set, 10th Edition — Chapter 49: Anesthesia for Thoracic Surgery
  • Section: Bronchiectasis/Lung Abscess/Empyema (p. 7282–7285)
  • Section: Anesthetic Management (p. 7285)
  • Section: Double-Lumen Tubes and Positioning (pp. 7148–7155)
  • Section: One-Lung Ventilation — Management, Prediction of Desaturation, Treatment of Hypoxemia (pp. 7121–7217)
  • Box 49.7: Risk Factors for Desaturation During OLV
  • Box 49.8: Indications for Right-Sided DLT
  • Box 49.12: Therapies for Desaturation During OLV
  • Table 49.7: DLT Size Selection

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Pulmonary Edema — Anaesthetic Considerations and Intraoperative Management

Based on Miller's Anesthesia, 10th Edition (9780323935920)

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1. DEFINITION AND PATHOPHYSIOLOGY

1.1 The Starling Equation — Governing Principle

Qf = Kf [(Pmv − Ppmv) − σ(πmv − πpmv)]

• Qf = net fluid filtration
• Kf = filtration coefficient (capillary permeability × surface area)
• Pmv = microvascular (capillary) hydrostatic pressure
• Ppmv = perimicrovascular (interstitial) hydrostatic pressure
• σ = reflection coefficient (protein permeability of membrane)
• πmv = plasma oncotic pressure
• πpmv = interstitial oncotic pressure

"Pulmonary edema is a hallmark of lung injury. It can result from increased hydrostatic pressure in the pulmonary capillaries (cardiogenic), increased permeability of the alveolar capillary membrane (noncardiogenic), and reduced lymphatic drainage from the lungs." — Miller's Anesthesia, Ch. 37 (Lung Water)

1.2 Stages of Pulmonary Edema (Anatomic Progression)

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2. CLASSIFICATION OF PULMONARY EDEMA — TYPES RELEVANT TO ANAESTHESIA

2.1 Cardiogenic (Hydrostatic) Pulmonary Edema

• Acute left ventricular failure (myocardial ischaemia/infarction intraoperatively)
• Volume overload from aggressive IV fluid administration
• Hypertensive crisis intraoperatively
• Acute valvular dysfunction (papillary muscle rupture, valve disease)
• Post-cardiac surgery low-output states
• Myocardial depression from volatile anaesthetics

"Pulmonary edema in the immediate postoperative period is often cardiogenic in nature, secondary to intravascular volume overload or congestive heart failure." — Miller's Anesthesia, Ch. 76 (PACU)

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2.2 Noncardiogenic (Increased Permeability) Pulmonary Edema

A. Acute Respiratory Distress Syndrome (ARDS)

• The most severe form of noncardiogenic pulmonary edema
• Diagnostic criteria (Berlin Definition):
  • Onset within 7 days of inciting event
  • Bilateral lung infiltrates NOT fully explained by cardiogenic edema, effusions, or collapse
  • PaO₂/FiO₂ <300 (mild), <200 (moderate), <100 (severe)
  • Not fully explained by cardiac failure
• Causes: sepsis, aspiration, trauma, pneumonia, pancreatitis, transfusion
• Managed with lung-protective ventilation (see below)

B. Transfusion-Related Acute Lung Injury (TRALI)

• Develops within 6 hours of transfusion of plasma-containing blood products (pRBC, FFP, platelets)
• Mechanism: Donor antibodies (anti-HLA, anti-HNA) or biological response modifiers activate recipient neutrophils → release of inflammatory mediators → increased capillary permeability → noncardiogenic pulmonary edema
• Features: acute hypoxemic respiratory failure, fever, bilateral infiltrates on CXR without cardiomegaly, cyanosis, systemic hypotension, leukopenia (granulocyte sequestration in lungs)
• Diagnostic criteria (American–European Consensus):
  1. Acute onset of signs/symptoms
  2. Hypoxemia: PaO₂/FiO₂ <300, OR SpO₂ <90% on room air
  3. Bilateral infiltrates on CXR without cardiomegaly
  4. No clinical evidence of left atrial hypertension
  5. No pre-existing ALI before transfusion
  6. Onset within 6 hours of transfusion
  7. No temporal association with alternative ALI causes
• Treatment: Supplemental O₂, supportive ventilation; ~80% recover within 48–96 hours; vasopressors for refractory hypotension; diuretics are not indicated (PCWP is normal)

C. Transfusion-Associated Circulatory Overload (TACO)

• Occurs in patients with pre-existing impaired cardiac/renal function following rapid, large-volume blood product transfusion
• Mechanism: volume overload → elevated PCWP → cardiogenic pulmonary edema
• Features: respiratory distress, hypoxemia, hypertension (contrasting with TRALI's hypotension), signs of right and left heart failure, cardiomegaly on CXR, elevated BNP
• Treatment: O₂, diuresis (furosemide), PPV if needed
• TACO and TRALI can coexist

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2.3 Postobstructive (Negative Pressure) Pulmonary Edema (NPPE)

"Postobstructive pulmonary edema (also referred to as negative pressure pulmonary edema, NPPE) is a rare but significant consequence of laryngospasm and other upper airway obstruction that may follow tracheal extubation." — Miller's Anesthesia, Ch. 76

1. Müller maneuver: Forced inspiration against a closed glottis generates exaggerated negative intrathoracic pressure (−50 to −100 cmH₂O)
2. Negative intrathoracic pressure → augments venous return to the right heart → RV dilation → elevated pulmonary hydrostatic pressure → fluid transudates into interstitium and alveoli
3. Simultaneously, negative intrathoracic pressure → increases LV afterload → reduces LV ejection fraction → elevated LVEDP → elevated left atrial pressure → elevated pulmonary venous pressure → worsens pulmonary edema
4. The two mechanisms are additive

• Muscularly fit, young adults — able to generate enormous negative inspiratory pressures (greatest risk)
• Laryngospasm (most common cause in PACU)
• Biting on the endotracheal tube peri-extubation
• Foreign body in the airway
• Epiglottitis, croup, upper airway tumors
• Obesity — predisposes to post-extubation obstruction
• Head and neck surgery

• Develops within 90 minutes of airway obstruction
• Dyspnoea, tachypnoea, tachycardia
• Pink frothy sputum (hallmark)
• SpO₂ fall, hypoxemia
• Bilateral fluffy infiltrates on CXR
• Occasionally: pulmonary hemorrhage, hemoptysis

• Resolve the obstruction immediately (release laryngospasm — succinylcholine 0.1–0.2 mg/kg if needed; jaw thrust, CPAP mask)
• Supplemental high-flow oxygen
• Diuresis (furosemide)
• Positive-pressure ventilation (non-invasive CPAP/BiPAP or invasive mechanical ventilation in severe cases)
• Monitor in PACU/HDU for 2–12 hours
• Resolution typically occurs within 12–48 hours when treated promptly
• If delayed treatment: mortality can reach 40%

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2.4 Neurogenic Pulmonary Edema (NPE)

• Rapid onset after the CNS insult
• Bilateral infiltrates, pink frothy secretions
• May occur intraoperatively during neurosurgery for aneurysm clipping, tumour resection, or trauma

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2.5 Re-expansion Pulmonary Edema

• Occurs after thoracic surgery involving prolonged lung collapse (OLV)
• After drainage of large effusions (thoracocentesis)
• Risk higher if lung has been collapsed for >3 days

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2.6 High-Altitude Pulmonary Edema (HAPE)

"Pulmonary vascular pressures that are elevated due to immersion increase even further during exercise, particularly in cold water... Blood centralization then raises pulmonary vascular pressures, which can be sufficiently elevated in susceptible individuals to induce acute pulmonary edema." — Miller's Anesthesia, Ch. 71

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3. PREOPERATIVE ANAESTHETIC ASSESSMENT IN A PATIENT WITH PULMONARY EDEMA

3.1 History

• Establish type of pulmonary edema (cardiogenic vs. noncardiogenic)
• Cardiac history: prior LV dysfunction, valvular disease, ischaemic heart disease
• Fluid balance: recent fluid administration, urine output
• Drug history: diuretics, ACE inhibitors, beta-blockers, digoxin
• Baseline exercise tolerance and functional capacity (METs)
• Pulmonary history: prior episodes of edema, ARDS, aspiration

3.2 Clinical Examination

• Vital signs: HR, BP, SpO₂ on air
• Respiratory: air entry, bilateral crackles (basal > diffuse), work of breathing
• Cardiovascular: S₃/S₄, elevated JVP, peripheral edema, murmurs
• Fluid status assessment

3.3 Investigations

"Pulmonary edema is a hallmark of lung injury… assessment of pulmonary edema is made with imaging techniques (e.g., chest radiography, ultrasonography, and computed tomography), thermodilution, bioimpedance, bioreactance, and remote dielectric sensing." — Miller's Anesthesia, Ch. 37

3.4 Optimisation Before Elective Surgery

• Diuresis: furosemide IV/oral — target euvolaemia; monitor urine output and electrolytes
• Vasodilators: nitrates (GTN infusion) reduce preload and afterload
• ACE inhibitors/ARBs: for chronic LV dysfunction
• Beta-blockers: for rate control in tachycardia-driven LV dysfunction
• Inotropes: if acute cardiogenic edema with reduced EF (dobutamine, milrinone)
• Treat precipitating cause: ACS → revascularization; AF → rate/rhythm control
• Correct hypoalbuminaemia (reduces oncotic pressure — worsens edema)
• Withhold surgery until euvolaemia is achieved in elective cases

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4. INTRAOPERATIVE ANAESTHETIC MANAGEMENT

4.1 Monitoring

"The PVPI… can be used to differentiate between cardiogenic and noncardiogenic pulmonary edema." — Miller's Anesthesia, Ch. 37

4.2 Choice of Anaesthetic Technique

Volatile Anaesthetics

• Isoflurane and sevoflurane: moderate cardiac depressants — use with caution in cardiogenic pulmonary edema with reduced EF
• However, volatile agents have cardioprotective (preconditioning) effects
• At ≤1 MAC they are generally tolerated; titrate carefully

TIVA (Total Intravenous Anaesthesia)

• Propofol: vasodilates (reduces preload and afterload) — may worsen hypotension in cardiogenic shock but improves hemodynamics if primarily afterload-dependent
• Ketamine: sympathomimetic → increases HR and SVR — may worsen cardiogenic pulmonary edema; avoid in cardiogenic edema unless patient is in shock (then use ketamine to maintain pressure)
• Dexmedetomidine: reduces sympathetic tone, useful as an adjunct in hypertension-precipitated pulmonary edema

Regional Anaesthesia

• Thoracic epidural or spinal anaesthesia provides sympathetic blockade → reduces preload and afterload → can improve cardiogenic pulmonary edema
• Useful adjunct in thoracic and abdominal surgery where fluid shifts are expected
• Contraindicated if patient is on anticoagulants or haemodynamically unstable

4.3 Airway and Ventilation Management

Non-invasive Ventilation (NIV) — Peri-induction

• In a patient arriving to the operating theatre with acute cardiogenic pulmonary edema who has not been intubated: CPAP/BiPAP may stabilize the patient before induction

Intubation

• Use rapid sequence induction (RSI) if there is a risk of aspiration (frothy secretions, full stomach)
• Pre-oxygenate thoroughly — patient has reduced FRC and increased O₂ consumption
• Expect reduced apnoea time before desaturation
• Suctioning of airways may be needed after intubation to clear frothy secretions

Lung-Protective Mechanical Ventilation — Cornerstone

The Role of PEEP in Pulmonary Edema — Crucial

"The application of external PEEP can improve lung ventilation, preventing alveolar and airway collapse… In patients with cardiogenic pulmonary edema… decreasing venous return will have a dual beneficial effect: the LV may be overdistended and also be working at a less-than-optimal point of the Frank–Starling curve. Decreasing preload, the left ventricle will work on a more optimal point of the Frank–Starling curve, increasing cardiac output and improving pulmonary edema. At the same time, decreased venous return means less blood pumped by the right ventricle and less pulmonary edema being generated." — Miller's Anesthesia, Ch. 12

1. Recruits collapsed alveoli → improves V/Q matching → improves oxygenation
2. Reduces shunt fraction (blood perfusing non-ventilated, atelectatic alveoli)
3. Increases FRC above closing capacity → prevents cyclic collapse-reopening (atelectrauma)
4. Reduces preload (via increased intrathoracic pressure) → directly beneficial in cardiogenic edema
5. Reduces LV afterload by increasing intrathoracic pressure around the LV

• High PEEP → increases RV afterload → may cause RV failure (especially in ARDS)
• Reduces cardiac output if patient is volume-depleted
• Worsens oxygenation in patients with significant auto-PEEP (COPD)
• Monitor driving pressure: if driving pressure increases with PEEP, PEEP is over-distending rather than recruiting

Recruitment Maneuvers

• Sustained inflation at 30–40 cmH₂O for 30–40 seconds or incremental PEEP titration
• Open collapsed alveoli, then maintain with PEEP
• Monitor: transient hypotension and desaturation during recruitment are expected

4.4 Fluid Management — The Cornerstone of Intraoperative Management

• Restrictive fluid strategy: crystalloid at 1–2 mL/kg/hr
• Avoid hypotonic fluids (worsen hyponatraemia and increase interstitial edema)
• Colloids (albumin): may help in hypoalbuminaemic patients by restoring oncotic pressure, but evidence for outcome improvement is limited
• Balanced crystalloids (Lactated Ringer's, PlasmaLyte) preferred over 0.9% saline (reduces hyperchloraemic acidosis)
• Goal-directed fluid therapy: use cardiac output monitoring (PAC, PiCCO, oesophageal Doppler, TEE) to guide fluid boluses — target stroke volume optimisation
• Intraoperative diuresis: furosemide IV (20–40 mg boluses; 0.1–0.2 mg/kg) if evidence of volume overload or worsening pulmonary edema intraoperatively

4.5 Pharmacological Management Intraoperatively

4.6 Positioning

• Head-up (reverse Trendelenburg) position — reduces preload, reduces work of breathing, improves FRC
• Avoid steep Trendelenburg intraoperatively in at-risk patients — dramatically increases preload and can precipitate acute pulmonary edema
• Lateral decubitus during thoracic surgery: dependent lung ventilated, non-dependent collapsed — see OLV precautions

4.7 Intraoperative Recognition of Acute Pulmonary Edema

• Rising peak airway pressures with unchanged tidal volume
• Falling SpO₂ / deteriorating PaO₂/FiO₂
• Pink frothy fluid in the ETT/circuit
• Increasing ETCO₂ (from reduced lung compliance)
• Bilateral crackles on auscultation (if conscious of checking)
• Rising CVP or PCWP
• Increasing B-lines on lung ultrasound

1. Increase FiO₂ to 1.0
2. Increase PEEP (5 → 10 → 15 cmH₂O titrated)
3. Reduce tidal volume to 5–6 mL/kg IBW (switch to lung-protective strategy)
4. Furosemide IV 20–40 mg if CVP/PCWP elevated
5. GTN infusion if cardiogenic (hypertensive) component
6. Dobutamine if LV dysfunction with low output
7. Norepinephrine if hypotension
8. Suction airway to clear frothy secretions
9. TEE assessment to identify cause (LV failure vs. volume overload vs. permeability)
10. Inform surgeon — consider shortening the procedure or staging it
11. If refractory: lung recruitment maneuver; consider veno-venous ECMO (last resort)

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5. SPECIFIC PERIOPERATIVE SCENARIOS

5.1 Patient with Pre-existing LV Dysfunction Undergoing Major Surgery

• Optimise cardiac function preoperatively (ACE inhibitor, beta-blocker, diuretics, revascularisation)
• Use intraoperative TOE/TTE
• Avoid excessive fluid loading — restrict to goal-directed strategy
• Avoid volatile anaesthetics at >1 MAC
• Prefer epidural analgesia to reduce sympathetic stress response
• Aggressive postoperative monitoring in HDU/ICU

5.2 Intraoperative Volume Overload (e.g., TURP, Major Abdominal Surgery)

• Common during prolonged procedures with rapid crystalloid infusion
• Maintain strict fluid balance — urine output, CVP trends
• Furosemide as needed
• Early CPAP/NIV post-extubation if signs develop

5.3 Aspiration-Induced Pulmonary Edema

• Gastric acid damages the alveolar-capillary membrane → chemical pneumonitis → noncardiogenic edema (Mendelson syndrome)
• Management: lung-protective ventilation, bronchoscopy for large particulate matter, antibiotics if secondary infection, no benefit from prophylactic steroids

5.4 Postoperative Pulmonary Edema in PACU

• Cardiogenic: volume overload, LV failure → diuresis, vasodilators, oxygen
• NPPE: treat airway obstruction → CPAP → diuresis if needed
• TRALI: supportive — O₂, PPV; no diuretics if PCWP normal
• TACO: diuresis, O₂, PPV
• All require monitoring for 2–12 hours minimum; intubation if SpO₂ <90% on maximal O₂

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6. EXTRAVASCULAR LUNG WATER (EVLW) — MONITORING TOOL

"EVLW may be a predictor of mortality in patients with severe sepsis and ARDS. It is a diagnostic tool in detecting early pulmonary edema… The PVPI can be used to differentiate between cardiogenic and noncardiogenic pulmonary edema." — Miller's Anesthesia, Ch. 37

• Normal EVLW: 3–7 mL/kg
• EVLW >10 mL/kg: significant pulmonary edema
• Measured by transpulmonary thermodilution (PiCCO device)
• PVPI (pulmonary vascular permeability index):
  • PVPI <3: cardiogenic edema
  • PVPI >3: permeability edema (ARDS/TRALI)
• Guides ventilator settings, fluid therapy, and diuretic use

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7. SUMMARY TABLE — DIFFERENTIAL DIAGNOSIS OF INTRAOPERATIVE/PERIOPERATIVE PULMONARY EDEMA

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• Chapter 76: Post-Anaesthesia Care Unit — Pulmonary Edema, NPPE, TRALI, TACO (pp. 11582–11586)
• Chapter 37: Respiratory Monitoring — Lung Water, EVLW, PVPI (pp. 5585–5588)
• Chapter 12: Respiratory Physiology During Anaesthesia — Physiologic Effect of PEEP (pp. 1311–1312)
• Chapter 71: Environmental, Wilderness, and Immersion Medicine — Immersion Pulmonary Edema, HAPE (pp. 10455–10458)
• Chapter 49: Anaesthesia for Thoracic Surgery — Re-expansion Pulmonary Edema
• Chapter 81: ECMO — ARDS and Cardiogenic Pulmonary Edema (p. 11869)The above is a comprehensive discussion sourced directly from Miller's Anesthesia, 10th Edition. Here is a quick orientation to the structure:

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1. Pathophysiology — Starling equation, stages of pulmonary edema (interstitial → alveolar), mechanisms (hydrostatic vs. permeability vs. lymphatic)
2. Classification — All 6 types relevant to anaesthesia:
   • Cardiogenic (volume overload, LV failure)
   • ARDS (noncardiogenic permeability)
   • TRALI (transfusion-related, with full diagnostic criteria)
   • TACO (transfusion-associated circulatory overload — distinguished from TRALI)
   • Postobstructive/Negative Pressure Pulmonary Edema (NPPE) — particularly important perioperatively after laryngospasm
   • Re-expansion and neurogenic types
3. Preoperative assessment — History, examination, investigations (CXR, echo, BNP, ABG, lung ultrasound, EVLW)
4. Intraoperative management — Monitoring (PAC, PiCCO, TEE, lung USS), anaesthetic agent selection, lung-protective ventilation strategy with PEEP physiology, fluid restriction, pharmacotherapy (furosemide, GTN, dobutamine, norepinephrine), stepwise response to acute intraoperative onset
5. Differential diagnosis table — Quick bedside comparison of all perioperative forms

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Six Core Respiratory Topics — Miller's Anesthesia, 10th Edition

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1. HYPOXIA

1.1 Definition

1.2 Classification — The Four Types

1.3 Causes of Hypoxic Hypoxia (Five Mechanisms)

• Reduced alveolar ventilation → CO₂ retention → PAO₂ falls (governed by alveolar gas equation)
• PAO₂ = FiO₂(PB − 47) − PaCO₂/0.8
• Causes: opioids, residual anaesthetics, neuromuscular blockade, obesity, pain splinting
• Anaesthetic relevance: the most common cause of hypoxia in the PACU

• Most common cause of intraoperative hypoxia
• Low V/Q areas act as shunt equivalents — blood leaves without being oxygenated
• High V/Q areas act as dead space — wasted ventilation
• Causes: atelectasis (universal in anaesthesia), pneumonia, pulmonary embolism, bronchospasm, one-lung ventilation

"Mild to moderate hypoxemia (SaO₂ 85%–90%) is common [during anaesthesia] and lasts from seconds to minutes; sometimes it is severe, and approximately 20% of patients may suffer from SaO₂ less than 81% for up to 5 minutes. Indeed, greater than 50% of claims in anaesthesia-related deaths relate to hypoxemia during anesthesia." — Miller's Anesthesia, Ch. 12

• Blood bypasses ventilated alveoli completely
• Does not respond to supplemental O₂ (unlike V/Q mismatch which does)
• Causes: atelectasis, consolidation, pulmonary oedema, ARDS, intracardiac shunt (PFO)

• Thickened alveolar-capillary membrane limits O₂ transfer
• Occurs with exercise (reduced transit time) or disease (fibrosis, interstitial lung disease)
• Usually mild at rest; significant exercise hypoxaemia

• Equipment failure, pipeline hypoxia, high altitude

1.4 Diffusion Hypoxia (Fink Effect) — Anaesthetic-Specific

"Diffusion hypoxia is a sequela of rapid outgassing from the tissues of patients anesthetized with N₂O. During the initial 5–10 minutes after discontinuation of anaesthesia, the flow of N₂O from blood into the alveoli can be several litres per minute, resulting in dilution of alveolar oxygen." — Miller's Anesthesia, Ch. 18

• N₂O also reduces alveolar PCO₂ → blunts respiratory drive
• Combined with respiratory depression from residual anaesthetic → hypoxaemia
• Prevention: 100% O₂ for 5–10 minutes after discontinuing N₂O

1.5 Signs and Symptoms of Hypoxia

"Initially, hypoxemia may not result in any EEG changes because the brain can increase cerebral blood flow to compensate. When the hypoxemia becomes severe enough… 'Slowing' of the EEG during hypoxia is a nonspecific global effect. Fast frequencies are lost, and low frequencies dominate. Eventually, the EEG is abolished as the brain shuts down electric activity and diverts all oxygen delivered to maintenance of cellular integrity." — Miller's Anesthesia, Ch. 39

1.6 Physiological Responses to Hypoxia

From Ch. 70 (High Altitude Medicine), acclimatization responses apply to hypoxia in general:

• Peripheral chemoreceptors (carotid/aortic bodies) stimulated → hyperventilation (hypoxic ventilatory response — HVR)
• Sympathetic activation → tachycardia, ↑ cardiac output, vasoconstriction
• Erythropoietin (EPO) release → ↑ RBC production, ↑ haemoglobin
• Hypoxic pulmonary vasoconstriction (HPV) → diverts blood from poorly ventilated lung areas
• 2,3-DPG increases → right-shifts ODC → facilitates O₂ unloading at tissues

1.7 Treatment of Hypoxia

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2. OXYGEN–HAEMOGLOBIN DISSOCIATION CURVE (ODC)

2.1 The Curve — Shape and Significance

2.2 The Upper (Flat) Part of the Curve

• Between PaO₂ 60–100 mmHg
• Hb remains near-fully saturated despite large changes in PaO₂
• Protective plateau: even if PaO₂ falls from 100 → 60 mmHg, SaO₂ only falls from 97.5% → 90%
• Ensures O₂ loading in the lungs remains adequate across a range of PAO₂

2.3 The Lower (Steep) Part of the Curve

• Below PaO₂ 60 mmHg
• Small further falls in PaO₂ produce large falls in SaO₂
• Facilitates O₂ unloading at the tissues: tissues consuming O₂ drop PO₂ from 40 → 20 mmHg → large amount of O₂ released per mmHg change

2.4 The P₅₀

• Increased P₅₀ = right shift = lower O₂ affinity = more O₂ released to tissues (beneficial at tissues)
• Decreased P₅₀ = left shift = higher O₂ affinity = less O₂ released to tissues (beneficial for loading in hypoxic lungs)

2.5 Factors Shifting the ODC

RIGHT SHIFT (↑ P₅₀ → ↓ Hb-O₂ affinity → facilitates O₂ UNLOADING)

LEFT SHIFT (↓ P₅₀ → ↑ Hb-O₂ affinity → facilitates O₂ LOADING)

2.6 The Bohr Effect

The Bohr effect describes the rightward shift of the ODC in the presence of CO₂ and acidosis (↑ H⁺). At the tissues, metabolically active cells produce CO₂ and lactic acid → local acidosis → Hb affinity for O₂ decreases → O₂ released more readily. In the lungs, CO₂ is eliminated → local alkalosis → Hb affinity increases → O₂ loaded more readily.

2.7 Anaesthetic Implications

• Hypothermia during CPB: left-shifts ODC → Hb holds on to O₂ → less O₂ delivered. Must target adequate PaO₂ to compensate.
• Alkalosis from hyperventilation (during controlled ventilation): left shift → potential tissue hypoxia despite adequate SaO₂
• Stored blood (low 2,3-DPG after 2 weeks storage): left shift → transfused blood initially has ↑ Hb-O₂ affinity, reduced O₂ delivery. Returns to normal within 24 hours
• CO poisoning: SpO₂ by pulse oximetry is falsely normal — carboxyhaemoglobin is read as oxyhaemoglobin. PaO₂ may be normal but CaO₂ is drastically reduced. Use CO-oximetry.
• MetHb: also falsely elevates SpO₂ readings

2.8 Oxygen Content Equation

• Hb 15 g/dL, SaO₂ 98%, PaO₂ 100: CaO₂ ≈ 19.7 + 0.3 = 20 mL/dL
• The dissolved component (×0.003) is minimal at atmospheric pressure but significant at hyperbaric pressures

• Normal DO₂ ≈ 1000 mL/min
• Normal VO₂ ≈ 250 mL/min
• O₂ extraction ratio = VO₂/DO₂ ≈ 25%

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3. FLOW–VOLUME LOOPS

3.1 What They Are

"Spirometry can display flow–volume loops… The characteristic shape of some respiratory flow–volume loops can help diagnose various respiratory diseases." — Miller's Anesthesia, Ch. 67

3.2 Components of a Normal Flow–Volume Loop

• Begins at TLC with a sharp peak expiratory flow rate (PEFR)
• Rapidly rises to PEFR then gradually declines as lung volume decreases toward RV
• The declining portion is effort-independent — determined by elastic recoil and airway resistance, not patient effort
• Ends at RV

• From RV to TLC
• Rounded curve; lower peak flow than expiration
• Effort-dependent throughout — determined by patient effort
• Peak inspiratory flow (PIF) < peak expiratory flow in normal subjects

3.3 Patterns of Abnormal Flow–Volume Loops

A. Obstructive Pattern (e.g., COPD, Asthma)

• FEV₁/FVC <70%
• Characteristic "scooped-out" (concave) expiratory limb — airway collapse during forced expiration reduces flow disproportionately at lower lung volumes
• TLC normal or increased (air trapping)
• PEFR may be preserved but mid-expiratory flow (FEF 25–75%) is markedly reduced
• Auto-PEEP visible on ventilator FVL as a persistent end-expiratory flow that does not return to zero

"There is a classic scooped-out appearance to the exhalation portion of a flow–volume curve with obstructive lung disease." — Miller's Anesthesia, Ch. 67

B. Restrictive Pattern (e.g., Pulmonary Fibrosis, Neuromuscular Disease)

• FEV₁/FVC preserved (>70%) but FVC reduced
• Both inspiratory and expiratory flows reduced proportionally
• Loop is narrow but normally shaped — a "small normal loop"
• TLC and RV both reduced

C. Variable Intrathoracic Obstruction (e.g., Tracheomalacia, Intrathoracic Tumour)

• Expiratory limb flattened (plateau) — during forced expiration, positive pleural pressure compresses the intrathoracic trachea at the site of lesion
• Inspiratory limb normal — negative intrathoracic pressure during inspiration stents the airway open
• Classic pattern: expiratory plateau with normal inspiratory curve

D. Variable Extrathoracic Obstruction (e.g., Vocal Cord Paralysis, Subglottic Stenosis)

• Inspiratory limb flattened — during forced inspiration, negative pressure in the trachea below the glottis collapses a flaccid extrathoracic trachea
• Expiratory limb normal — positive subglottic pressure during expiration stents airway open

E. Fixed Obstruction (e.g., Tracheal Stenosis, Rigid Goitre)

• Both inspiratory AND expiratory limbs are flattened — the lesion is rigid and unyielding regardless of transmural pressure
• Classic box-shaped loop (plateau on both sides)
• Seen with bilateral vocal cord paralysis, rigid tracheal stenosis

"Spirometry can also help identify variable intrathoracic or fixed (intra- or extrathoracic) airway obstruction from the shape of the forced expired flow–volume curve (Fig. 12.22)." — Miller's Anesthesia, Ch. 12

3.4 Anaesthetic Implications of Flow–Volume Loops

• Mediastinal masses: FVL should be performed preoperatively; exacerbation of a variable intrathoracic obstructive pattern (expiratory plateau) on supine FVL is a warning of dynamic airway compression under GA

"Children with tracheobronchial compression greater than 50% on CT scan cannot be safely given general anaesthesia. Flow–volume loops, specifically the exacerbation of a variable intrathoracic obstructive pattern (expiratory plateau), confirm the risk." — Miller's Anesthesia, Ch. 49

• Intraoperative FVL monitoring (continuous spirometry during OLV):
  • Persistent end-expiratory flow on FVL = auto-PEEP development
  • Sudden loss of tidal volume on FVL = DLT migration or circuit disconnection
  • Air leak quantified by difference between inspiratory and expiratory VT

3.5 FVL vs Pressure–Volume Loops

• PV loops during mechanical ventilation: identify lower inflection point (begin PEEP above this), upper inflection point (reduce tidal volume to avoid overdistension — "bird's beak" appearance)
• Used to optimize PEEP and tidal volume in ARDS

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4. WORK OF BREATHING

4.1 Definition and Formula

"The work of breathing (W) represents the energy required to inflate or deflate the lungs, or chest wall, or both, by a specified volume." — Miller's Anesthesia, Ch. 37

4.2 Components of Work of Breathing

• Work done against the elastic recoil of the lungs and chest wall
• Represented by the triangular area under the static pressure-volume relationship
• Stored during inspiration; recovered during passive expiration (does not contribute to total WOB in passive expiration)
• Increased in: pulmonary fibrosis (↑ elastic recoil), pulmonary oedema, ARDS, obesity, abdominal distension

• Work done to overcome airway resistance (turbulent and laminar flow) and lung tissue viscoelasticity
• Dissipated as heat — cannot be recovered
• Represented by the area between the actual P-V curve and the static compliance line
• Increased in: COPD, asthma, bronchospasm, secretions, narrow airway devices (small ETT)

"Respiratory work is further divided into elastic work (required to overcome the recoil of the lung) and resistive work (required to overcome airway flow resistance and viscoelastic resistance of pulmonary tissues). The work of breathing is usually derived from transpulmonary pressure–volume curves." — Miller's Anesthesia, Ch. 19

4.3 Mechanical Power

"Mechanical power, as an index of the rate of energy dissipation, can be used to assess the risk of developing ventilator-induced lung injury (VILI), particularly with changes in transpulmonary pressure during ventilation." — Miller's Anesthesia, Ch. 37

• High mechanical power → excessive energy transfer to the lung per unit time → risk of VILI
• Relevant to ventilator settings in ARDS — high respiratory rate, high driving pressure, and high PEEP all contribute to mechanical power

4.4 Energetically Optimal Breathing Frequency

"For a given VT, W varies as a function of respiratory rate and, in most cases, achieves a minimum at a specified frequency. This frequency is termed the energetically optimum breathing frequency, as this is the rate at which energy expenditure is minimised."

• Normal individuals: ~15 breaths/min
• Emphysema: decreased elastic recoil → lower optimal frequency (breathe slowly and deeply)
• Restrictive disease: increased elastic recoil → higher optimal frequency (breathe fast and shallowly)
• Neonates: high RR is energetically optimal due to compliant chest wall

4.5 Factors Increasing Work of Breathing

4.6 Anaesthetic Effects on Work of Breathing

"In general, volatile anesthetics decrease the work of breathing in adults and children… Sevoflurane reduces pulmonary compliance at the lung periphery rather than at the airway level, thereby increasing viscoelastic and elastic pressures in the lung. In a murine model of chronic asthma, sevoflurane significantly decreased resistance in central and distal airways and lowered resistance in the lung periphery." — Miller's Anesthesia, Ch. 19

• All volatile agents (except desflurane at standard doses) reduce respiratory system resistance by ~15% at 1 MAC, reducing WOB
• Desflurane: does NOT reduce bronchomotor tone; can actually increase WOB via airway irritation
• Mechanical ventilation takes over WOB from the patient entirely — WOB from the patient = 0 during controlled ventilation

4.7 Reduction of Work of Breathing (Clinical Strategies)

From Miller's Ch. 9 (reduction of WOB section):

• Positive pressure ventilation (PPV): takes over resistive and elastic WOB
• CPAP/PEEP: reduces WOB by preventing cyclic alveolar collapse and re-recruitment; shifts PV curve to more compliant region
• Bronchodilators: reduce resistive WOB
• Positioning (head-up/semi-recumbent): reduces abdominal splinting of diaphragm
• Extubation to CPAP/NIV: bridges the transition to independent breathing
• Adequate analgesia: prevents splinting from pain (especially after thoracic/upper abdominal surgery)

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5. INCENTIVE SPIROMETRY

5.1 Definition and Rationale

• Prevent and treat postoperative atelectasis
• Restore functional residual capacity (FRC) after surgery
• Improve mucociliary clearance
• Strengthen respiratory muscles

5.2 Physiological Basis

• Pain causes splinting → shallow breathing → low VT → atelectasis
• Residual anaesthetics/opioids → reduced respiratory effort
• Supine position → ↓ FRC, diaphragm elevation → dependent atelectasis
• Neuromuscular weakness → ↓ inspiratory force

"The atelectasis that develops intraoperatively may last for some days after surgery and may be a cause of postoperative pulmonary complications." — Miller's Anesthesia, Ch. 12

5.3 Types of Incentive Spirometers

5.4 Technique of Incentive Spirometry

1. Patient assumes upright or semi-upright position (maximises FRC, diaphragm excursion)
2. Exhale normally to FRC
3. Place mouthpiece in mouth — seal lips
4. Inhale slowly and deeply to achieve target volume (TLC)
5. Hold breath for 3–5 seconds — allows recruited alveoli to stabilise (like a sustained sigh)
6. Exhale passively
7. Repeat 10 times per hour while awake

5.5 Clinical Indications

• Post-thoracotomy / lobectomy / pneumonectomy
• Post-upper abdominal surgery (gastrectomy, hepatectomy, oesophagectomy)
• COPD patients perioperatively
• Neuromuscular disease (Myasthenia Gravis, Guillain-Barré)
• Obesity — reduced FRC
• ICU ventilator weaning

5.6 Goals and Monitoring

• Target volume should be set at ≥80% of predicted inspiratory capacity or above pre-illness baseline
• Monitor SpO₂ during sessions
• Combine with chest physiotherapy, airway clearance techniques, early mobilisation, and adequate analgesia for best effect
• Can be used from POD 0 if patient is awake and cooperative

5.7 Limitations

• Requires patient cooperation and understanding — not useful in confused or sedated patients
• Does not address secretion clearance directly (combine with coughing, huffing, nebulisation)
• Evidence for routine universal use is mixed — most benefit in high-risk patients (COPD, obesity, thoracic/upper abdominal surgery)

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6. THE OXYGEN CASCADE

6.1 Concept

6.2 The Steps of the Oxygen Cascade

ATMOSPHERE → TRACHEA → ALVEOLUS → ARTERIAL BLOOD → CAPILLARY BLOOD → TISSUE CELL → MITOCHONDRIA

6.3 Key Equations Along the Cascade

• A-a gradient = PAO₂ − PaO₂
• Normal = 5–15 mmHg (increases with age: approx. age/4)
• Causes of raised A-a gradient:
  • V/Q mismatch (most common)
  • Intrapulmonary shunt
  • Diffusion impairment
  • Hypoventilation does NOT raise the A-a gradient (both PAO₂ and PaO₂ fall equally)

• Mixed venous PO₂ (PvO₂) reflects DO₂ / VO₂ balance
• Normal PvO₂ = 40 mmHg, SvO₂ = 75%
• SvO₂ <60% indicates increased O₂ extraction (↑ metabolic demand or ↓ DO₂)
• SvO₂ >80% in sepsis = distributive defect — cells cannot extract O₂

6.4 The Cascade Under Anaesthesia

"Anesthesia impairs pulmonary function, whether the patient is breathing spontaneously or is receiving mechanical ventilation. Impaired oxygenation of blood occurs in most subjects who are anaesthetized, and this is why supplemental O₂ (FiO₂ usually 0.3–0.5) is almost invariably used." — Miller's Anesthesia, Ch. 12

6.5 The A-a Gradient in Clinical Practice

• A patient breathing 100% O₂ with PaO₂ of 400 mmHg has a different clinical situation than one with PaO₂ of 400 mmHg breathing 40% O₂
• PaO₂/FiO₂ ratio (P:F ratio) is a practical bedside index:
  • Normal: >400–500
  • Mild ARDS: 200–300
  • Moderate ARDS: 100–200
  • Severe ARDS: <100

• Normal <0.4

• 1.0 indicates severe respiratory failure

6.6 Hyperbaric Oxygen and the Cascade

"At an elevated PaO₂ in the range of 1000–2000 mmHg, significant quantities of O₂ may exist in dissolved form… Increased PaO₂ has at least five pharmacologic effects: increased blood O₂ content, vasoconstriction, antibacterial action, inhibition of endothelial neutrophil adhesion, and anti-inflammatory effect." — Miller's Anesthesia, Ch. 71

• PaO₂ ~2100 mmHg
• Dissolved O₂ alone (×0.003) = 6.3 mL/dL — sufficient for resting metabolic needs without haemoglobin
• Cascade is "widened" but tissue PO₂ increases dramatically

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SUMMARY TABLE — Key Numbers to Remember

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• Chapter 12: Respiratory Physiology During Anaesthesia — Spirometry, FVL, Atelectasis, A-a gradient (pp. 1295–1322)
• Chapter 18: Inhaled Anaesthetics — Diffusion Hypoxia (p. 1977)
• Chapter 19: Inhaled Anaesthetics on Airway — Work of Breathing, bronchomotor effects (pp. 2074–2076)
• Chapter 28/70: High Altitude Medicine — Physiological Responses to Hypoxia (pp. 10262–10265)
• Chapter 37: Respiratory Monitoring — Work of Breathing and Mechanical Power (pp. 5535–5540)
• Chapter 39: Neurophysiological Monitoring — EEG changes in Hypoxia (pp. 5297–5298)
• Chapter 49: Thoracic Anaesthesia — FVL during OLV, Continuous Spirometry (pp. 7130–7132)
• Chapter 67/71: Pediatric/Hyperbaric — FVL in respiratory monitoring; O₂ cascade at pressure (pp. 11319–11321)

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Asthma, Status Asthmaticus, and Perioperative Management

Based on Miller's Anesthesia, 10th Edition (9780323935920)

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PART 1: ASTHMA — DISEASE OVERVIEW AND ANAESTHETIC MANAGEMENT FOR LAPAROSCOPIC HERNIA REPAIR

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1.1 Definition and Epidemiology

"The Global Initiative for Asthma defines asthma as a 'heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness, and cough that vary over time and in intensity, together with variable expiratory airflow limitation.'" — Miller's Anesthesia, Ch. 29

• Worldwide prevalence: >300 million people
• Responsible for 1 in every 250 deaths globally
• Bronchospasm occurs in approximately 9% of asthmatics in the perioperative period
• 25% of asthmatics may present with wheezing after induction of anaesthesia
• 1.7% sustain a poor respiratory outcome
• ASA Closed Claims data: 40 cases of bronchospasm resulted in malpractice claims; 88% involved brain damage or death; only 50% had pre-existing asthma

1.2 Pathophysiology

• Infiltration of submucosal airways with mast cells, eosinophils, and CD4+ T lymphocytes
• Mast cell degranulation → release of leukotrienes, histamine, prostaglandins → oedema, mucus hypersecretion, chemotaxis of WBCs
• Airway hyperresponsiveness — exaggerated bronchoconstrictor response to stimuli

• Bronchial smooth muscle spasm — narrows airway lumen
• Mucosal oedema — thickens airway wall
• Mucus plugging — obstructs distal airways
• Airway remodelling — chronic thickening with fibrosis in severe disease

• ↑ Airway resistance (for laminar flow: resistance ∝ 1/r⁴; for turbulent flow ∝ 1/r⁵)
• Air trapping → ↑ RV, ↑ TLC (hyperinflation)
• V/Q mismatch → hypoxaemia
• ↓ FEV₁/FVC ratio (<0.7)
• Initially: ↓ PaCO₂ (hyperventilation compensates)
• Late/severe: normal or ↑ PaCO₂ = respiratory fatigue, impending failure

"A normal or elevated PaCO₂ may identify respiratory fatigue or impending failure." — Miller's Anesthesia, Ch. 75

• Allergens, smoke, cold air, exercise
• Airway instrumentation (intubation, laryngoscopy — major anaesthetic trigger)
• Medications (NSAIDs, β-blockers, ACE inhibitors, aspirin)
• Viral infections
• Emotions, stress

1.3 Classification of Severity

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1.4 Preoperative Assessment

History — Key Questions

"In a patient with known asthma, the anesthesiologist should enquire about dyspnea, chest tightness, cough (especially nocturnal), recent exacerbations (with associated triggers), therapy (especially corticosteroids), prior hospitalizations, prior emergency department visits, prior critical care unit admissions, prior need for endotracheal intubation, and recent upper respiratory tract infections." — Miller's Anesthesia, Ch. 29

• Current control status — compare to patient's "normal" or "best" based on symptoms, exercise tolerance, and medication requirements
• Severity of most recent exacerbation — was ICU/intubation required?
• Triggers — identify and plan to avoid intraoperatively
• Current medications: bronchodilators (SABAs, LABAs), inhaled corticosteroids, oral corticosteroids, theophylline, leukotriene antagonists
• History of NSAID/aspirin sensitivity (Samter's triad — aspirin-exacerbated respiratory disease)
• GERD — common trigger; especially relevant for laparoscopic surgery (head-down positioning)
• Recent URTIs — double the risk of perioperative bronchospasm

Physical Examination

• Quality of breath sounds, degree of wheeze, air entry
• Accessory muscle use, prolonged expiratory phase
• SpO₂ on room air
• Note: degree of wheeze does NOT always correlate with severity — severe obstruction may cause a "silent chest" (no air movement to generate sound)

Investigations

• Spirometry (PFTs): FEV₁, FVC, FEV₁/FVC — establishes baseline and severity; confirm reversibility (≥12% improvement after bronchodilator)
• Note: Normal PFTs do NOT exclude asthma in a currently asymptomatic patient; PFTs generally have no perioperative prognostic value in well-controlled asthma
• ABG: only if severe acute exacerbation
• CXR: only if infection or pneumothorax suspected
• Blood glucose: if on oral corticosteroids
• ECG: if theophylline toxicity suspected (tachyarrhythmias)

Preoperative Optimisation

"Bronchodilators, corticosteroids (inhaled and oral), and any antibiotics must be continued on the day of surgery. β-Adrenergic agonists are a useful prophylactic intervention to lower the risk of bronchospasm after induction of anesthesia. This therapy can be supplemented with a short preoperative course of oral corticosteroids (prednisone 20 mg to 60 mg daily for 3 to 5 days) in any newly diagnosed or poorly controlled asthmatic patient." — Miller's Anesthesia, Ch. 29

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1.5 Anaesthetic Management — Laparoscopic Hernia Repair

Effect of CO₂ Pneumoperitoneum on Respiratory Physiology

"Laparoscopic operations are usually performed by insufflation of CO₂ into the abdominal cavity. The effects are twofold. First, the consequences of hypercapnic acidosis include depressed cardiac contractility, sensitization of the myocardium to the arrhythmogenic effects of catecholamines, pulmonary vasoconstriction, and systemic vasodilation… the physical effects of pneumoperitoneum include decreased FRC and vital capacity (VC), formation of atelectasis, reduced respiratory compliance, and increased peak airway pressure." — Miller's Anesthesia, Ch. 12

Choice of Airway Device

• Preferred in well-controlled, mild-moderate asthma for laparoscopic hernia repair
• Avoids tracheal intubation — the most potent trigger for bronchospasm
• Bypasses the subglottic cough reflex
• Proseal/Supreme LMA (second-generation): provides a seal adequate for laparoscopy (up to 20–25 cmH₂O), allows gastric venting
• Limitations: cannot be used if airway pressures will exceed seal pressure (severe asthma with high resistance may preclude LMA use)

• Required if LMA seal is inadequate for laparoscopic pressures
• Required in severe or uncontrolled asthma with risk of bronchospasm requiring deep suctioning
• Must be performed under deep anaesthesia to prevent bronchospasm on intubation

Premedication

• Anxiolytics: benzodiazepines (midazolam) — reduce anxiety-triggered bronchospasm
• Antisialagogues (glycopyrrolate 0.2 mg) — dry secretions, reduce mucus, mild bronchodilation
• H₂ receptor blocker + PPI — particularly relevant as GERD is an asthma trigger and GA + Trendelenburg position ↑ aspiration risk
• Avoid antihistamines (H₁ antagonists) — may dry secretions → mucus plugging

Induction of Anaesthesia

"Ketamine is a bronchial smooth muscle relaxant. When it is given to patients with reactive airway disease and bronchospasm, pulmonary compliance is improved. Ketamine is as effective as halothane or enflurane in preventing experimentally induced bronchospasm." — Miller's Anesthesia, Ch. 22

• Fentanyl (1–2 mcg/kg) or remifentanil — suppress laryngeal reflexes before intubation
• Lidocaine IV (1.5 mg/kg) 2–3 minutes before laryngoscopy — blunts the reflex bronchoconstriction

• Rocuronium — preferred; no histamine release
• Succinylcholine — use with caution; histamine release is minimal at clinical doses; acceptable for RSI
• Avoid atracurium — significant histamine release → may precipitate bronchospasm
• Avoid mivacurium — histamine release

Maintenance of Anaesthesia

"At 1 MAC, sevoflurane reduced respiratory system resistance by 15% in patients undergoing elective surgery, whereas desflurane had no effect. All volatile agents, except for desflurane, significantly reduced respiratory resistance." — Miller's Anesthesia, Ch. 19

• Direct inhibition of voltage-dependent Ca²⁺ channels (VDC) in bronchial smooth muscle
• ↑ cAMP → Ca²⁺ efflux → smooth muscle relaxation
• Inhibition of Rho-kinase signalling
• Indirect suppression of reflex neural bronchoconstriction

"Therefore, volatile anesthetics, except desflurane, may be an effective therapeutic modality in status asthmaticus when conventional therapy has failed." — Miller's Anesthesia, Ch. 19

• Propofol infusion + remifentanil — no bronchospasm; attenuates airway reflexes; excellent for asthma
• Avoids volatile agents entirely — useful when sevoflurane is unavailable or in severe cases

Ventilation Strategy During Laparoscopic Hernia Repair in Asthma

• Incomplete exhalation during each breath → gas trapping → dynamic hyperinflation
• Detected as: persistent end-expiratory flow on spirometry; rising peak/plateau pressures; haemodynamic compromise
• Treatment: reduce RR, prolong expiration, disconnect from ventilator briefly to allow passive decompression

Intraoperative Monitoring

• Continuous SpO₂, ETCO₂, peak and plateau airway pressures
• ABG if clinical deterioration
• Capnography: rising ETCO₂ with ↑ airway pressures = bronchospasm vs. equipment obstruction
• Note: during pneumoperitoneum, ETCO₂ rises due to CO₂ absorption — must increase MV to compensate

Drug Avoidance in Asthma

Reversal and Extubation

• Reverse NMB with sugammadex (for rocuronium) — preferred; avoids neostigmine's cholinergic bronchoconstriction
• If neostigmine is used: always co-administer glycopyrrolate to counteract muscarinic effects
• Extubate under deep anaesthesia (if LMA used — remove when awake but avoid coughing on ETT)
• If ETT used: extubate under deep anaesthesia OR under full consciousness (not at the "bucking" stage — this triggers bronchospasm)
• Apply salbutamol nebulisation immediately prior to extubation if at high risk

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PART 2: STATUS ASTHMATICUS

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2.1 Definition

2.2 Pathophysiology

• Intense bronchospasm + mucus plugging → severe ↑ airway resistance
• Patient hyperventilates → ↓ PaCO₂ (respiratory alkalosis)
• SpO₂ may be maintained through hyperventilation
• V/Q mismatch → hypoxaemia despite ↑ minute ventilation

• Respiratory muscles fatigue (prolonged high WOB)
• PaCO₂ normalises → eucapnia in context of hyperventilation = warning sign
• PaO₂ falls despite supplemental O₂
• Worsening V/Q mismatch and shunt

• PaCO₂ rises above normal (hypercapnia) = respiratory muscle fatigue and failure
• Severe hypoxaemia
• Metabolic acidosis from lactic acid (respiratory muscle fatigue, hypoxia)
• Combined respiratory and metabolic acidosis = impending arrest

"A normal or elevated PaCO₂ may identify respiratory fatigue or impending failure." — Miller's Anesthesia, Ch. 75

• Extreme hyperinflation → ↑ pulmonary vascular resistance → RV strain
• Pulsus paradoxus (>10 mmHg drop in systolic BP during inspiration) — sign of severe asthma
• ↑ intrathoracic pressure → ↓ venous return → hypotension

2.3 Clinical Assessment of Severity

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PART 3: PERIOPERATIVE MANAGEMENT OF STATUS ASTHMATICUS

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3.1 Initial Emergency Management

• Supplemental O₂: target SpO₂ ≥94%
  • Nasal cannula (up to 28% FiO₂)
  • Face mask (up to 50% FiO₂)
  • Non-rebreather mask (FiO₂ ~100%)
  • High-flow nasal cannula (HFNC): near-complete humidification, FiO₂ → 1.0; reduces effort of breathing; improves delivery of nebulised medications

3.2 Pharmacological Management

"Continuous albuterol is preferred for initial therapy in the ICU, and the usual dose is 0.15 to 0.5 mg/kg/h or 10 to 20 mg/h. After improvement in air movement with decreased respiratory distress, intermittent doses can be given every 1 to 2 hours." — Miller's Anesthesia, Ch. 75

• Salbutamol (Albuterol):
  • Continuous nebulisation: 0.15–0.5 mg/kg/hr (or 10–20 mg/hr in adults)
  • MDI with spacer: 4–8 puffs every 20 min × 3 doses
  • Mechanism: β₂-agonist → ↑ cAMP → bronchial smooth muscle relaxation
  • Side effects: tachycardia, arrhythmias (usually PVCs), hypokalaemia (K⁺ driven intracellularly), diastolic hypotension, tremor, agitation
• Ipratropium bromide: inhaled anticholinergic; combined with albuterol in initial treatment; promotes bronchodilation without decreasing mucociliary clearance

"Steroids should be given early as the effect will take some time." — Miller's Anesthesia, Ch. 75

• IV methylprednisolone: preferred in ICU (oral absorption unreliable in distressed patient)
  • Initial dose: 2 mg/kg IV
  • Maintenance: 0.5 mg/kg q6h (or 1 mg/kg q6h in severe cases)
• Mechanism: ↓ airway inflammation, ↓ eosinophil infiltration, ↓ mucus production, ↑ β-receptor expression
• Effect onset: 4–6 hours
• IV vs. oral: no difference in outcome if oral is absorbed; IV preferred in ICU

"Mixtures of helium and oxygen (heliox) can be used to improve laminar gas flow. This occurs due to the decreased density of helium compared to nitrogen (approximately one-seventh). For helium to be beneficial in small airways, it must occur in a high ratio with oxygen. The greatest benefits may be seen with an 80:20 or 70:30 ratio of helium:oxygen." — Miller's Anesthesia, Ch. 75

• Reduces turbulent flow through narrowed airways → decreases WOB
• Limitation: requires high ratio of He:O₂ → hypoxaemic patients cannot use 80:20 mix
• Role: severe critical asthma refractory to standard therapy; also used as carrier gas for nebulised β-agonists

3.3 Non-Invasive Ventilation (NIV)

"NIV may allow time for therapies to become effective (steroids) and prevent intubation. This should not be used when the level of alertness or ability to protect the airway is diminished." — Miller's Anesthesia, Ch. 75

• BiPAP: positive pressure on inspiration and expiration
  • May improve medication delivery
  • Reduces WOB
  • Buys time for steroids to work
  • Contraindicated: altered consciousness, inability to protect airway, combative/uncooperative patients, haemodynamic instability

3.4 Ketamine — The Anaesthetist's Special Drug

"Owing to its bronchodilating effect, administration of ketamine can treat status asthmaticus unresponsive to conventional therapy." — Miller's Anesthesia, Ch. 22

"For patients with asthma who are intubated and mechanically ventilated, ketamine may be a good choice for sedation, along with a benzodiazepine. There was one pediatric study showing an improvement in the PaO₂/FiO₂ ratio and dynamic compliance in mechanically ventilated children with refractory bronchospasm who were receiving a continuous infusion of ketamine." — Miller's Anesthesia, Ch. 75

• Mechanism of bronchodilation:
  • Direct antagonism of spasmogenic effects of carbachol and histamine at bronchial smooth muscle
  • Sympathomimetic effect → ↑ endogenous catecholamines → β₂ stimulation
  • NMDA receptor antagonism
• Dosing:
  • Bolus: 1 mg/kg IV (for intubation or procedural sedation)
  • Infusion: 5–30 mcg/kg/min titrated to effect (for ongoing sedation in mechanically ventilated patients)
• Side effects: excessive secretions (give atropine/glycopyrrolate concurrently), dysphoria/emergence reactions (give midazolam concurrently), ↑ HR and BP (caution in hypertensive/tachycardic patients)

3.5 Indications for Intubation and Mechanical Ventilation

"By the time patients with asthma require intubation and mechanical ventilation, they are hypoxemic, acidotic, fatigued, and have limited reserve. It is suggested that the most experienced person available perform the intubation." — Miller's Anesthesia, Ch. 75

• Deteriorating mental status / confusion / coma
• Respiratory arrest or impending arrest
• SpO₂ <90% despite maximal O₂
• PaCO₂ ≥45 mmHg with clinical deterioration (hypercapnic failure)
• Silent chest
• Haemodynamic collapse
• Patient fatigue with worsening ABGs

1. Pre-oxygenate: 100% O₂ for 3–5 minutes
2. Position: ramped/semi-upright to maximise FRC
3. Fluid bolus: 10–20 mL/kg if haemodynamically compromised (intubation + IPPV → ↑ intrathoracic pressure → ↓ venous return → cardiovascular collapse)
4. Induction: Ketamine 1–2 mg/kg IV (bronchodilates + maintains haemodynamics) + Midazolam 0.05–0.1 mg/kg (prevents dysphoria, amnesia)
5. Glycopyrrolate 0.2 mg IV (ketamine-induced secretions)
6. Muscle relaxant: Rocuronium 1.2 mg/kg IV (for RSI; sugammadex 16 mg/kg reversal available)
7. Intubation: use large ETT (8.0 if possible — reduces resistance)
8. Post-intubation: immediately hand-ventilate at slow rate to prevent overdistension

3.6 Mechanical Ventilation Strategy in Status Asthmaticus

• Perform an expiratory pause manoeuvre — auto-PEEP measured as airway pressure at end-expiration when expiratory valve is closed
• Auto-PEEP >10–15 cmH₂O = significant air trapping

• Pneumothorax (tension) — most feared; ↑ airway pressure + ruptured bulla
• Cardiovascular collapse at intubation — ↑ intrathoracic pressure → ↓ venous return
• Hypotension post-intubation: disconnect from circuit briefly → passive decompression
• ICU-acquired weakness from prolonged NMB

3.7 Sedation in Mechanically Ventilated Asthma

"Neuromuscular blocking drugs (NMBDs) may be used for… elimination of unwanted movement in patients with status asthmaticus." — Miller's Anesthesia, Ch. 9

• Sedation regimen: Ketamine infusion (5–30 mcg/kg/min) + midazolam or propofol — preferred combination
• NMBDs (e.g., rocuronium, vecuronium infusion): for ventilator dyssynchrony, dangerous air trapping, or when sedation alone is inadequate
  • Use continuous peripheral nerve monitoring to avoid prolonged blockade (especially if on corticosteroids — risk of steroid myopathy + NMBD → prolonged weakness)
• Avoid: aminosteroidal NMBDs in combination with steroids (steroid myopathy risk); atracurium (histamine release)

3.8 Volatile Anaesthetics for Refractory Status Asthmaticus (ICU Use)

"Therefore, volatile anesthetics, except desflurane, may be an effective therapeutic modality in status asthmaticus when conventional therapy has failed. However, formal guidelines on this application remain unavailable." — Miller's Anesthesia, Ch. 19

• Isoflurane or sevoflurane inhaled via the AnaConDa device (anaesthetic conserving device for ICU ventilators) or portable vaporiser
• Reserved for refractory status asthmaticus not responding to standard therapy
• Mechanism: direct bronchial smooth muscle relaxation via Ca²⁺ channel inhibition
• Isoflurane 0.5–2% or sevoflurane 0.5–3% delivered via ICU ventilator
• Requires scavenging system in ICU
• Halothane previously used for status asthmaticus in children but largely abandoned (arrhythmia risk, halothane hepatitis)

3.9 ECMO in Refractory Status Asthmaticus

"Box 81.1 Indications for VV ECMO includes: Status asthmaticus." — Miller's Anesthesia, Ch. 81

• Veno-venous ECMO (VV ECMO): indicated when conventional mechanical ventilation fails
• Provides oxygenation and CO₂ removal while allowing the lungs to rest
• Bridge to recovery — asthma is reversible → ECMO can sustain life while bronchospasm resolves with aggressive medical therapy
• Survival with ECMO for status asthmaticus: generally favourable when deployed early

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PART 4: PERIOPERATIVE MANAGEMENT OF STATUS ASTHMATICUS — SPECIAL INTRAOPERATIVE SCENARIOS

4.1 Intraoperative Bronchospasm — Recognition and Stepwise Management

• Sudden ↑ peak airway pressure with ↓ tidal volume delivered
• Rising ETCO₂ (reduced alveolar ventilation) or ↓ ETCO₂ (severe obstruction)
• Bilateral expiratory wheeze on auscultation
• Silent chest = severe obstruction (no gas movement)
• SpO₂ falling
• Haemodynamic deterioration (obstructive physiology → ↓ cardiac output)

• D — Displacement (ETT malposition, endobronchial intubation)
• O — Obstruction (kinked ETT, mucus plug, bronchospasm, biting on tube)
• P — Pneumothorax
• E — Equipment failure (circuit obstruction, expiratory valve failure)

1. Increase FiO₂ to 1.0 — immediately
2. Check and confirm ETT position — rule out endobronchial intubation, kinked tube
3. Deepen anaesthesia — increase sevoflurane to 1.5–2.5 MAC (profound bronchodilation)
4. Switch to TIVA if desflurane being used — desflurane worsens bronchospasm; switch to propofol infusion
5. Administer nebulised salbutamol — 2.5–5 mg via ETT inline nebuliser; or MDI with adapter (4–8 puffs)
6. Ipratropium bromide — nebulised 0.5 mg
7. Ketamine IV bolus — 0.5–1 mg/kg (if not already in use)
8. IV methylprednisolone — 125 mg (anti-inflammatory; onset 4–6 hours)
9. IV magnesium sulphate — 2 g over 20 minutes
10. Epinephrine (adrenaline) SC or IV — 0.3–0.5 mg SC (1:1000); or 50–100 mcg IV boluses in extremis
11. Manual ventilation at slow rate — allows auto-PEEP to decrease; confirm bilateral breath sounds
12. If tension pneumothorax suspected — emergency decompression

"According to the ASA Closed Claims Project, 40 cases of bronchospasm resulted in settled malpractice claims, with 88% involving brain damage or death." — Miller's Anesthesia, Ch. 19

4.2 Postoperative Care

• ICU or HDU admission in all patients with history of severe/ICU-requiring asthma
• Continue all bronchodilators (nebulised salbutamol, ipratropium) throughout
• Oral/IV corticosteroids continued until clinical resolution
• Stress-dose steroids in patients on chronic steroids (hydrocortisone 50–100 mg q8h)
• Pain management without NSAIDs — paracetamol ± opioids ± regional blocks
• Incentive spirometry post-extubation — prevent atelectasis
• CPAP/NIV if desaturation post-extubation
• Monitor for pneumomediastinum, pneumothorax post-severe attack
• Electrolyte monitoring: correct hypokalaemia from β-agonists
• Avoid early discharge in unstable patients

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SUMMARY ALGORITHM

PREOP: Identify severity → continue all medications → SABA pre-op
→ Oral steroids if poorly controlled → Avoid triggers
        ↓
INDUCTION: Propofol or Ketamine → Deep anaesthesia before airway manipulation
→ LMA preferred if possible → Rocuronium (avoid atracurium)
→ Fentanyl + Lidocaine IV before ETT if required
        ↓
MAINTENANCE: Sevoflurane (bronchodilator) ≤1-2 MAC
→ TIVA if desflurane previously used → Avoid desflurane
→ Slow RR, prolonged I:E (1:3 to 1:4), low PEEP → Monitor for auto-PEEP
→ ↑ MV by 10-20% during pneumoperitoneum
        ↓
BRONCHOSPASM: FiO₂ 1.0 → Deep sevoflurane → Salbutamol nebuliser
→ Ketamine → Magnesium → Adrenaline → Consider DOPE
        ↓
STATUS: O₂ → Continuous albuterol → IV steroids → IV MgSO₄
→ Ketamine → NIV → Intubation (Ketamine + Midazolam + Rocuronium)
→ Permissive hypercapnia, slow RR, I:E 1:4, low PEEP
→ Volatile if refractory → ECMO as last resort
        ↓
POSTOP: ICU/HDU → Continue bronchodilators + steroids → No NSAIDs
→ Incentive spirometry → Monitor K⁺

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• Chapter 29: Perioperative Management of Coexisting Conditions — Asthma (pp. 3945–3947)
• Chapter 19: Inhaled Anaesthetics on Airway — Volatile agents in asthma/bronchospasm, status asthmaticus (pp. 2073–2083)
• Chapter 22: Ketamine — Bronchodilation, status asthmaticus (pp. 2557–2559)
• Chapter 75: Paediatric Critical Care — Asthma, status asthmaticus, therapy, intubation, mechanical ventilation (pp. 11367–11376)
• Chapter 12: Respiratory Physiology — Pneumoperitoneum effects, atelectasis (pp. 1323–1327)
• Chapter 9: NMBDs in ICU — NMBDs in status asthmaticus (p. 2376)
• Chapter 81: ECMO — VV ECMO indications including status asthmaticusThe answer covers all three requested topics in detail. Here is a quick orientation:

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• GINA definition, epidemiology, cellular pathophysiology (mast cells, eosinophils, leukotrienes)
• Severity classification, physiological consequences
• Preoperative history (the "9-question Miller's checklist"), examination, investigations
• Optimisation — continue all medications, SABA pre-op, stress-dose steroids
• Laparoscopic-specific: CO₂ pneumoperitoneum effects on FRC, airway pressures, compliance, atelectasis
• Airway device choice (LMA vs. ETT), premedication
• Induction: Propofol or Ketamine (not thiopentone)
• Maintenance: Sevoflurane (most potent bronchodilator); avoid Desflurane
• Ventilation: slow RR, prolonged I:E ratio (1:3–1:4), low PEEP, monitor auto-PEEP
• Drug avoidance table (NSAIDs, atracurium, desflurane, β-blockers, morphine, neostigmine alone)
• Extubation under deep anaesthesia

• Definition, 3-stage pathophysiology, clinical severity scoring table
• The critical sign: normal PaCO₂ during hyperventilation = impending failure

• Stepwise drug therapy: O₂ → continuous albuterol → IV steroids → IV MgSO₄ → heliox → ketamine
• Ketamine: the anaesthetist's pivotal drug — doses for both sedation and RSI
• RSI protocol (Ketamine + Midazolam + Rocuronium + Glycopyrrolate)
• Mechanical ventilation: permissive hypercapnia, slow RR (6–10/min), I:E 1:4, low PEEP
• Volatile anaesthetics (sevoflurane/isoflurane) for refractory cases
• VV-ECMO as last resort

• Recognition, DOPE differential diagnosis, 12-step treatment ladder
• Postoperative care checklist

• Pro vs. free plan differences
• Whether credits are required
• What features are unlocked at each tier

• The platform's official website or FAQ
• Their pricing/plans page
• Reaching out to their support team directly

Five Topics in Abdominal and Hepatobiliary Anaesthesia

Based on Miller's Anesthesia, 10th Edition (9780323935920)

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TOPIC 1: ANAESTHETIC MANAGEMENT IN LAPAROSCOPIC SURGERY

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1.1 Introduction and Advantages

"The advantages of laparoscopic surgery over conventional open surgery, including decreased hospital stay, improved visualization, decreased blood loss, expedited recovery time, reduced postoperative pain, and improved cosmetic outcomes, have been well described." — Miller's Anesthesia, Ch. 55

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1.2 Physiology of CO₂ Pneumoperitoneum

"Laparoscopic operations are usually performed by insufflation of CO₂ into the abdominal cavity. The effects are twofold. First, the consequences of hypercapnic acidosis include depressed cardiac contractility, sensitization of the myocardium to the arrhythmogenic effects of catecholamines, pulmonary vasoconstriction, and systemic vasodilation… In addition, the physical effects of pneumoperitoneum include decreased FRC and vital capacity (VC), formation of atelectasis, reduced respiratory compliance, and increased peak airway pressure." — Miller's Anesthesia, Ch. 12

A. Respiratory Effects

"Shunt is reduced and arterial oxygenation is mostly improved during CO₂ pneumoperitoneum… efficient redistribution of blood flow away from collapsed lung regions is attributable to hypercapnic acidosis CO₂ potentiating hypoxic pulmonary vasoconstriction." — Miller's Anesthesia, Ch. 12

B. Cardiovascular Effects (Box 55.6, Miller's)

• On insufflation: abrupt ↑ SVR; possible vagally mediated bradycardia/asystole
• Established pneumoperitoneum: ↑ SVR, ↑ MAP, variable CO

C. Renal Effects

"Despite adequate intravascular hydration, intraoperative oliguria may occur… Increased perirenal pressure exerted by insufflated gas causes an increase in renal vascular resistance with direct compression of the renal parenchyma and renal vein. This causes release of renin and aldosterone, along with antidiuretic hormone, which temporarily decreases renal blood flow, renal function, and urinary output." — Miller's Anesthesia, Ch. 55

• Transient intraoperative oliguria is common and usually reversible post-desufflation
• Transient ↑ serum creatinine may occur
• Fluid restriction is practised but avoid excessive oliguria in patients with pre-existing renal disease

D. Endocrine/Hormonal Effects

• ↑ Vasopressin (ADH), ↑ cortisol, ↑ catecholamines
• Renin–angiotensin–aldosterone activation
• Insulin resistance intraoperatively

E. Other System Effects

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1.3 Preoperative Assessment

• Standard anaesthetic assessment PLUS specific laparoscopic concerns:
  • Cardiac function: patients with poor LV function may not tolerate ↑ afterload and ↓ CO
  • Pulmonary function: pre-existing lung disease → compromised by ↓ FRC + ↑ airway pressures
  • Obesity: exaggerates all effects of pneumoperitoneum; ↓ FRC; ↑ atelectasis; ↑ airway pressures
  • GERD: pneumoperitoneum + head-down position → ↑ aspiration risk
  • Raised ICP: relative contraindication to laparoscopy
  • Coagulopathy: ↑ DVT risk from venous stasis

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1.4 Choice of Anaesthetic Technique

• Regional anaesthesia alone (spinal/epidural) can be used for shorter procedures (e.g., gynaecological laparoscopy in experienced centres) but diaphragmatic irritation from CO₂ and the discomfort of pneumoperitoneum make it less ideal
• TIVA vs. volatile maintenance: both acceptable; TIVA with propofol-remifentanil provides excellent haemodynamic stability and reduced PONV; volatile anaesthetics (especially sevoflurane) have anti-inflammatory effects on the peritoneal cavity

• Endotracheal intubation with cuffed ETT: standard; allows positive pressure ventilation against ↑ airway pressures from pneumoperitoneum
• Laryngeal Mask Airway (LMA): second-generation LMAs (ProSeal, Supreme) provide adequate seal pressures (25–30 cmH₂O) for many laparoscopic procedures; reduces pharyngolaryngeal complications; allows gastric suctioning via drain tube; appropriate in well-selected patients with low aspiration risk for elective laparoscopic hernia, cholecystectomy

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1.5 Induction of Anaesthesia

• Rapid Sequence Induction (RSI) if:
  • Symptomatic GERD, hiatus hernia
  • Obesity with significant GERD risk
  • Bowel obstruction
  • Any full stomach condition
• Routine cases: standard IV induction (propofol 1.5–2.5 mg/kg + opioid + muscle relaxant)
• Muscle relaxation: complete neuromuscular blockade facilitates laparoscopic surgery by enabling lower IAP to achieve the same surgical exposure; deep NMB (post-tetanic count level) allows reduction of IAP from 15 → 10 mmHg with equivalent surgical conditions — reduces haemodynamic and respiratory consequences
• Suggest monitoring: NMT (neuromuscular transmission) throughout to ensure optimal relaxation

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1.6 Positioning-Specific Considerations

Trendelenburg (Head-Down) Position — for pelvic laparoscopy, RARP, gynaecological

"Respiratory effects of SHDT including decreased compliance, reduced vital capacity and functional residual capacity, 20% decrease in lung volumes, and ventilation-perfusion mismatch compound the effects of pneumoperitoneum. Pulmonary congestion and edema have been reported in susceptible patients. Facial, pharyngeal, and laryngeal edema may also occur." — Miller's Anesthesia, Ch. 55

• ↑ Risk of aspiration, endobronchial intubation (ETT migrates distally), laryngeal oedema, raised ICP/IOP, brachial plexus stretch
• Check ETT position after final positioning
• Venous congestion of head and neck → do not extubate until oedema assessed

Reverse Trendelenburg (Head-Up) — for upper abdominal laparoscopic surgery

• ↓ Venous return → hypotension
• Improves diaphragm excursion → better respiratory mechanics

Lateral Decubitus — for laparoscopic nephrectomy

"Anesthetic concerns for urologic minimally invasive surgeries surround the physiologic effects of pneumoperitoneum, the use of lateral decubitus, and steep head-down tilt positions." — Miller's Anesthesia, Ch. 55

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1.7 Ventilation Strategy

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1.8 Complications of Laparoscopic Surgery — Anaesthetic Recognition

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1.9 Fluid Management

• Restrictive fluid strategy preferred for abdominal laparoscopic procedures
• Excessive fluid worsens bowel oedema and delays recovery
• Balanced crystalloids (Lactated Ringer's, PlasmaLyte): 1–2 mL/kg/hr maintenance
• Goal-directed fluid therapy for longer procedures: oesophageal Doppler, pleth variability index

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1.10 Analgesic Strategy (ERAS Principles)

• Multimodal analgesia: reduces opioid requirements → faster recovery
• Paracetamol 1g IV scheduled
• Ketorolac/NSAIDs (if no contraindications)
• Local anaesthetic wound infiltration at port sites
• Intraperitoneal local anaesthetic (bupivacaine instilled into peritoneum) — reduces diaphragmatic irritation pain
• TAP block / quadratus lumborum block for abdominal cases
• Dexamethasone 8 mg IV — anti-emetic + anti-inflammatory
• Ondansetron 4 mg IV — PONV prophylaxis (PONV risk is high in laparoscopic surgery: female sex, non-smoker, PONV history, opioid use)

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1.11 Postoperative Care

• Pain: shoulder-tip pain from diaphragmatic irritation by residual CO₂ — multimodal analgesia; self-resolves in 24–48 hours
• PONV: very common; prophylaxis essential
• Urine output: brief oliguria expected; ensure adequate hydration; monitor creatinine
• Subcutaneous emphysema: can cause post-op CO₂ retention; watch SpO₂

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TOPIC 2: ANAESTHESIA CONSIDERATIONS IN INFECTIVE HEPATITIS

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2.1 Types and Overview

• Hepatitis A (HAV): faecal-oral; self-limiting; rarely fulminant; no chronic disease
• Hepatitis B (HBV): parenteral/sexual; can become chronic; cirrhosis and HCC risk
• Hepatitis C (HCV): parenteral; most common cause of post-transfusion hepatitis (90%)
• Hepatitis D (HDV): requires HBV co-infection; parenterally transmitted
• Hepatitis E (HEV): faecal-oral; self-limiting; high maternal mortality in pregnancy
• Hepatitis G: parenteral; not clearly pathogenic

"The hepatitis C virus causes 90% of posttransfusion hepatitis. Fewer than a third of these patients develop jaundice. Chronic active hepatitis (51%), chronic hepatitis (23%), and hepatocellular carcinoma (11%)." — Miller's Anesthesia, Ch. 46

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2.2 Impact of Liver Disease on Pharmacology and Physiology

• Drug metabolism (Phase I: CYP450 oxidation/reduction; Phase II: conjugation)
• Protein synthesis (albumin, clotting factors)
• Coagulation factor production (II, V, VII, IX, X, fibrinogen)
• Gluconeogenesis and glycogenolysis
• Detoxification of ammonia, bilirubin, drugs

Altered Drug Pharmacokinetics in Hepatitis/Liver Disease:

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2.3 Anaesthetic Concerns in Active/Infective Hepatitis

• Acute hepatitis (any cause) — markedly elevated perioperative mortality
• Fulminant hepatic failure
• Acute liver injury (AST/ALT >3× normal with symptoms)

• Elective surgery mortality: up to 10% in acute hepatitis
• Emergency surgery: mortality as high as 50%

1. Hepatotoxicity of anaesthetic agents:
   • Halothane: causes immune-mediated fulminant hepatitis ("halothane hepatitis") — strictly avoid; incidence 1:10,000 with first exposure, 1:1000 with repeat exposure
   • Enflurane/Isoflurane: very rare hepatotoxicity — avoid in active liver disease where possible
   • Sevoflurane, Desflurane: minimal hepatic metabolism; safest volatile agents; preferred
   • Propofol, Ketamine: generally safe
   • Nitrous oxide: inhibits methionine synthase → disrupts folate/methionine metabolism; avoid in prolonged cases; contraindicated in bowel obstruction
2. Reduced hepatic blood flow during anaesthesia:
   • All anaesthetic agents reduce portal blood flow
   • N₂O and positive pressure ventilation further reduce hepatic blood flow
   • Hypotension → hepatic ischaemia → worsens hepatitis
   • Maintain haemodynamic stability and adequate perfusion pressure
3. Coagulopathy:
   • Hepatocellular damage → ↓ clotting factor synthesis (II, V, VII, IX, X)
   • Check PT/INR, APTT, fibrinogen pre-operatively
   • Correct with FFP (if surgery essential), Vitamin K (for obstructive component), cryoprecipitate (if fibrinogen <1.5 g/L)
4. Hypoalbuminaemia:
   • ↓ Drug protein binding → ↑ free drug fraction → exaggerated drug effects
   • ↑ Third-space oedema
   • ↓ Oncotic pressure → ascites, peripheral oedema
5. Hypoglycaemia:
   • Impaired gluconeogenesis → monitor blood glucose intraoperatively; infuse dextrose
6. Encephalopathy risk:
   • Avoid benzodiazepines and opioids if possible
   • Avoid constipation, hypovolaemia, sepsis (precipitants of hepatic encephalopathy)
7. Renal function:
   • Hepatorenal syndrome risk in advanced liver disease
   • Avoid nephrotoxic drugs (NSAIDs, aminoglycosides)
   • Maintain adequate renal perfusion
8. Universal precautions:
   • HBV and HCV are major occupational hazards for theatre staff
   • All staff: appropriate PPE, double-glove technique
   • Minimise needlestick risk; follow hospital infection control protocols
   • HBV vaccination for all theatre and anaesthetic staff

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2.4 Child-Pugh Score — Stratifying Perioperative Risk

• Class A (5–6): good function; perioperative mortality ~10%
• Class B (7–9): moderate risk; mortality ~30%
• Class C (10–15): poor function; mortality >70–80%

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2.5 MELD Score

• MELD = 9.6 × ln(creatinine) + 3.8 × ln(bilirubin) + 11.2 × ln(INR) + 6.4
• MELD >15 → perioperative mortality significantly elevated
• MELD >20 → mortality for major abdominal surgery >20%

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TOPIC 3: ANAESTHETIC MANAGEMENT IN A PATIENT WITH JAUNDICE

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3.1 Types of Jaundice Relevant to Anaesthesia

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3.2 Systemic Consequences of Jaundice — Anaesthetic Implications

• Bradycardia — bile salts in circulation sensitise the SA node
• ↓ Response to catecholamines
• Risk of intraoperative hypotension
• Cardiomyopathy in chronic hepatic failure

• Vitamin K malabsorption in obstructive jaundice → ↓ fat-soluble vitamin K → ↓ factors II, VII, IX, X (Vitamin K-dependent)
• Liver cell damage → ↓ all clotting factors (not K-dependent ones)
• Thrombocytopenia in portal hypertension (hypersplenism)
• DIC in fulminant hepatic failure
• Check INR, PT, APTT, fibrinogen, platelet count
• Give IV Vitamin K 10 mg daily × 3 days preoperatively — corrects coagulopathy of obstructive jaundice if hepatocytes are intact (PT should normalise)
• If PT does not correct → hepatocellular damage likely

• Hepatorenal syndrome (HRS) — functional renal failure
• Bile nephropathy — tubular damage from bilirubin
• ↑ Risk of acute tubular necrosis perioperatively
• Prevention: Maintain intravascular volume; use mannitol (0.5 g/kg) perioperatively in obstructive jaundice to protect renal tubules; avoid NSAIDs and contrast agents; measure urine output hourly

• ↓ Fat absorption (bile salt deficiency) → nutritional deficiencies
• ↑ Bacterial translocation from gut → sepsis risk
• Ascites in hepatic failure → ↑ aspiration risk; ↑ IAP

• ↓ Reticuloendothelial function → ↑ infection risk
• Endotoxaemia from gram-negative bacteria → systemic inflammatory response

• Hepatopulmonary syndrome (intrapulmonary shunts in cirrhosis)
• Portopulmonary hypertension
• Ascites → ↓ FRC → atelectasis and hypoxaemia

• Hepatic encephalopathy (↑ ammonia)
• Enhanced sensitivity to CNS depressants (sedatives, opioids)

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3.3 Preoperative Assessment and Optimisation

• IV Vitamin K 10 mg daily × 3 days; check response in INR
• FFP if surgery cannot be delayed and INR >1.5
• Correct anaemia (target Hb >10 g/dL)
• Treat sepsis (biliary sepsis common in obstructive jaundice)
• Nutritional support (TPN if severe malnutrition)
• Drain ascites if causing respiratory compromise
• Endoscopic biliary drainage (ERCP stenting) preoperatively for obstructive jaundice → reduces post-operative liver failure

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3.4 Intraoperative Management in Jaundice

• Induction: Propofol — safe; attenuates response; titrate dose (↑ free fraction due to ↓ albumin)
• Maintenance: Sevoflurane or isoflurane (avoid halothane); TIVA with propofol acceptable
• Opioids: Use cautiously; fentanyl preferred (no active metabolites); avoid morphine (6-glucuronide accumulation); remifentanil ideal (non-hepatic metabolism)
• NMBDs: Cisatracurium preferred (Hofmann degradation — independent of liver and kidney function); vecuronium/rocuronium have prolonged action in severe liver disease
• Reversal: Sugammadex (for rocuronium) preferred; neostigmine metabolised by liver but generally safe
• Local anaesthetics: reduce doses (↓ protein binding → ↑ toxicity risk)

• Arterial line (invasive BP + serial ABGs + glucose monitoring)
• Central venous catheter
• Urine output (hourly) — target >0.5 mL/kg/hr; oliguria = early sign of renal compromise
• Temperature monitoring — jaundiced patients have impaired thermoregulation

• Avoid hepatotoxic colloids (some starches are harmful in liver disease)
• Balanced crystalloids (lactate-containing solutions used with caution in severe hepatic failure — impaired lactate metabolism)
• Albumin infusion (20–25%) — if albumin <25 g/L; maintains oncotic pressure; reduces hepatorenal syndrome risk

• Maintain adequate MAP (≥65–70 mmHg) for renal perfusion
• Mannitol 0.5 g/kg IV (osmotic diuretic) before biliary decompression in obstructive jaundice — reduces risk of acute tubular necrosis
• Monitor hourly urine output throughout

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TOPIC 4: ANAESTHETIC MANAGEMENT OF WHIPPLE SURGERY (PANCREATICODUODENECTOMY)

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4.1 Overview of the Whipple Procedure

• Head of pancreas
• Duodenum
• Common bile duct
• Gallbladder
• +/− Pylorus (classic Whipple vs. pylorus-preserving)

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4.2 Preoperative Assessment

• Obstructive jaundice (head of pancreas compressing CBD)
• Weight loss / malnutrition (cancer cachexia)
• Diabetes mellitus (exocrine + endocrine pancreatic insufficiency)
• Anaemia (chronic disease, nutritional deficiency)
• Coagulopathy (Vitamin K malabsorption, ↓ clotting factors)
• Derangements of renal and hepatic function

• FBC, U&E, LFTs, coagulation screen (PT, APTT, fibrinogen)
• Blood glucose + HbA1c
• Serum albumin, prealbumin (nutritional markers)
• Tumour markers (CA 19-9, CEA)
• CT pancreas protocol (surgical planning)
• MRCP (biliary anatomy)
• Pulmonary function tests if poor respiratory reserve
• Echocardiogram (assess cardiac function; elderly patients with significant CAD)

• Biliary drainage (ERCP + stenting): controversial but may be indicated for cholangitis, severe jaundice, or planned neoadjuvant chemotherapy delay
• IV Vitamin K 10 mg × 3 days; correct INR with FFP if needed
• Nutritional support (TPN or enteral feeding via nasojejunal tube for 5–7 days preoperatively if severely malnourished)
• Blood glucose control (target HbA1c <8.5% perioperatively)
• Anaemia correction (IV iron, transfusion threshold Hb <8 g/dL in elective setting)
• Smoking cessation (at least 4–8 weeks preoperatively)
• ERAS Whipple protocol (Enhanced Recovery After Surgery): carbohydrate loading night before; avoid prolonged fasting; bowel preparation not recommended; DVT prophylaxis

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4.3 Intraoperative Anaesthetic Management

• Arterial line — right radial (early placement; continuous BP; serial ABGs/glucose)
• Central venous catheter — large-bore; multiple lumens for drug infusions, CVP, vasopressors
• Oesophageal Doppler or PiCCO — goal-directed fluid therapy; stroke volume optimisation
• Urinary catheter — hourly urine output
• Temperature monitoring (oesophageal or rectal) — forced-air warming blanket essential
• Neuraxial/epidural catheter monitoring if thoracic epidural placed
• Neuromuscular monitoring — TOF

• Rapid Sequence Induction (not fasting well, ascites, ↑ aspiration risk) OR standard induction with video laryngoscopy
• Large-bore ETT; throat pack if surgeon requests
• Confirm ETT position before draping

• Placed at T6–T8 level preoperatively
• Bupivacaine 0.25% + fentanyl (or hydromorphone) infusion intraoperatively and continued 48–72 hours postoperatively
• Benefits:
  • Superior postoperative pain control (enables deep breathing → ↓ pulmonary complications)
  • ↓ Perioperative opioid use → earlier bowel return → faster ERAS recovery
  • Sympathectomy → ↓ stress response → better glycaemic control
  • Possible reduction in cancer recurrence (anti-inflammatory effects)
• Contraindications to epidural: severe coagulopathy (INR >1.4), thrombocytopenia (<80×10⁹/L), patient refusal, local sepsis

• Bilateral TAP blocks (Transversus Abdominis Plane) — single shot or catheters
• Wound infiltration catheters placed by surgeon
• Paravertebral blocks bilaterally
• IV lidocaine infusion (1–1.5 mg/kg/hr — anti-inflammatory, reduces ileus, reduces opioid use)

• Propofol 1.5–2.5 mg/kg IV (reduce if hypovolaemic, hypoalbuminaemic — ↑ free fraction)
• Fentanyl 2 mcg/kg (or remifentanil infusion)
• Cisatracurium (0.15 mg/kg) — preferred NMB due to Hofmann elimination (independent of liver function — likely impaired from obstructive jaundice)
• RSI with modified cricoid pressure if aspiration risk

• Sevoflurane 1–1.5 MAC (bronchodilator; volatile anaesthetics have ischaemic preconditioning properties for the liver — relevant as hepatic blood flow is significantly reduced during the dissection phase)
• Or TIVA: propofol + remifentanil infusions
• Epidural supplement started 30 min before skin closure

• Point-of-care coagulation (TEG/ROTEM) — guides targeted factor replacement
• FFP for INR >1.5 with active bleeding
• Cryoprecipitate for fibrinogen <1.5 g/L
• Platelet transfusion for count <50×10⁹/L with bleeding
• Tranexamic acid (TXA) 1 g IV at incision — reduces blood loss in major hepato-pancreatic surgery

• Restrictive fluid strategy — target 1–2 mL/kg/hr crystalloid
• Avoid excess fluid → exacerbates bowel oedema, delays anastomotic healing, increases complications
• Goal-directed therapy: titrate fluid to stroke volume; oesophageal Doppler or pulse pressure variation (PPV) as dynamic indices
• Blood transfusion threshold: Hb <7 g/dL (or <9 g/dL if cardiac disease)
• Mannitol (0.5 g/kg) before hepatic resection phase — renal and hepatic protection

• Blood glucose monitoring every 30–60 minutes intraoperatively
• Target: 6–10 mmol/L
• Insulin infusion if >10 mmol/L; dextrose if <4 mmol/L

• Forced-air warming blanket
• Warm IV fluids
• Warm irrigation fluid by surgeon
• Target: maintain core temperature >36°C (hypothermia → coagulopathy)

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4.4 Postoperative Care

• ICU/HDU for 24–48 hours minimum
• Thoracic epidural infusion continued 48–72 hours
• Glycaemic control (insulin infusion or subcutaneous insulin regime)
• Hepatic monitoring: daily LFTs; monitor for post-pancreatectomy hepatic failure
• Renal monitoring: hourly urine output; creatinine daily
• Drain amylase on day 1–3 (detects pancreatic fistula — most feared complication)
• DVT prophylaxis: LMWH from POD 1 (ERAS); TED stockings + pneumatic compression
• Early enteral nutrition (nasojejunal tube placed intraoperatively by surgeon) — preferred over TPN
• Incentive spirometry and respiratory physiotherapy

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TOPIC 5: ANAESTHETIC IMPLICATIONS AND CONSIDERATIONS IN OBSTRUCTIVE JAUNDICE

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5.1 Pathophysiology of Obstructive Jaundice

• Intrinsic biliary obstruction: choledocholithiasis (stones), cholangiocarcinoma, primary sclerosing cholangitis
• Extrinsic compression: carcinoma of the head of pancreas (most common surgical cause), periampullary tumours, lymphadenopathy

• ↑ Conjugated (direct) bilirubin
• ↑ ALP, GGT (biliary enzymes)
• ↑ Bile acids in blood (pruritis)
• Normal or mildly ↑ ALT/AST (unless secondary hepatocellular damage)

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5.2 Systemic Consequences Specific to Obstructive Jaundice

A. Coagulation Defect (Vitamin K Malabsorption)

• Bile is required for micelle formation → absorption of fat-soluble vitamins (A, D, E, K)
• Vitamin K deficiency → ↓ carboxylation of clotting factors II, VII, IX, X → ↑ PT/INR
• IV Vitamin K 10 mg/day × 3 days → corrects INR if hepatocellular function is intact
• Failure of INR to correct → hepatocellular damage + obstructive component → FFP needed

B. Renal Dysfunction — The Critical Risk

1. Bile cast nephropathy: conjugated bilirubin is directly toxic to renal tubular cells
2. Endotoxaemia: impaired Kupffer cell function → gut-derived endotoxins reach systemic circulation → renal vasospasm
3. Reduced intrinsic renal prostaglandin synthesis → ↓ renal vasodilation
4. Hypovolaemia (poor oral intake, bile losses)
5. Sepsis (cholangitis) → renal ischaemia

• Pre-operative hydration (IV normal saline or balanced crystalloids — ensure euvolaemia)
• Mannitol 0.5 g/kg IV before biliary decompression surgery → osmotic diuresis → tubular flushing
• Oral lactulose preoperatively → reduces gut endotoxaemia by acidifying colon
• Bile salts (sodium deoxycholate) oral preoperatively — experimental; may reduce endotoxaemia
• Avoid NSAIDs (inhibit renal prostaglandins — catastrophic in obstructive jaundice)
• Avoid aminoglycosides (nephrotoxic)
• Maintain MAP ≥65 mmHg throughout
• Target urine output ≥0.5 mL/kg/hr — monitor hourly

C. Cardiovascular Effects

• Bradycardia: bile salts absorbed systemically stimulate vagal tone → bradycardia, impaired chronotropy
• ↓ Response to vasopressors and catecholamines
• ↑ Risk of intraoperative hypotension on induction
• Premedication with atropine (0.6 mg IV) at induction if bradycardic

D. Sepsis — Cholangitis

• Common in choledocholithiasis
• Organisms: E. coli, Klebsiella, Enterococcus, Pseudomonas
• Charcot's triad: fever + RUQ pain + jaundice
• Reynold's pentad (severe): Charcot's triad + hypotension + altered consciousness = emergency ERCP
• Must treat cholangitis BEFORE elective surgery
• Intraoperatively: if biliary sepsis present → blood cultures + broad-spectrum antibiotics (Piperacillin-tazobactam or carbapenem) + source control

E. Impaired Drug Metabolism

• Obstructive jaundice alone (without hepatocellular failure) — synthetic function usually preserved initially
• As biliary obstruction persists → secondary biliary cirrhosis → hepatocellular dysfunction
• Phase I and Phase II metabolism progressively impaired
• ↓ Plasma albumin → ↑ free drug fractions

F. Nutritional Deficiency

• Fat malabsorption → ↓ vitamins A, D, E, K
• Cachexia in malignant obstruction
• Impaired immune function

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5.3 Preoperative Endoscopic Biliary Drainage (EBD)

• ERCP + plastic stent or metallic stent can decompress biliary tree before surgery
• Benefits: ↓ bilirubin → ↑ hepatic function preoperatively; ↓ coagulopathy; ↓ renal risk; treat cholangitis
• Indication in obstructive jaundice: bilirubin >200 μmol/L; cholangitis; delayed surgery (chemotherapy); patient unfit for immediate surgery
• Anaesthetic considerations for ERCP: usually moderate sedation (propofol + midazolam + fentanyl); lateral position; risk of pancreatitis post-procedure

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5.4 Anaesthetic Management of Surgery for Obstructive Jaundice

• Correct coagulopathy: IV Vitamin K × 3 days → check response → FFP if INR >1.5
• Treat cholangitis: antibiotics + biliary drainage
• Ensure euvolaemia: IV crystalloid overnight
• Strict NBM with IV fluids
• Renal protection: mannitol plan, strict urine output targets

• Aspiration risk is HIGH: distended duodenum, poor gastric motility, ↑ abdominal distension
• RSI with modified cricoid pressure: Propofol (1.5–2 mg/kg) + Succinylcholine (1.5 mg/kg) or Rocuronium (1.2 mg/kg with sugammadex available)
• Avoid: morphine (histamine release + ↑ sphincter of Oddi tone → worsen biliary obstruction), atracurium (histamine)
• Atropine available: bradycardia risk on induction

• Sevoflurane or isoflurane (avoid halothane/enflurane — hepatotoxic)
• Cisatracurium for NMB — Hofmann degradation
• Avoid N₂O if bowel distension
• Consider TIVA if liver function severely compromised

• Meticulous haemostasis (coagulopathy present)
• Strict fluid balance: balance between adequate renal perfusion and avoidance of fluid overload
• Mannitol 0.5 g/kg before opening biliary system
• Monitor urine output hourly — target ≥0.5 mL/kg/hr
• Blood glucose monitoring if pancreatic involvement
• Vasopressors (norepinephrine) if hypotensive despite adequate filling
• Avoid hypothermia → worsens coagulopathy

• HDU monitoring minimum 24 hours
• Hepatic function monitoring: LFTs daily
• Renal function: creatinine daily; urine output hourly
• Continue IV Vitamin K until oral feeds established
• Watch for: bile leak, cholangitis recurrence, hepatorenal syndrome, DIC

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SUMMARY TABLE

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• Chapter 55: Urology and Laparoscopic Surgery — Physiological effects of pneumoperitoneum, SHDT position, robotic surgery (pp. 8499–8507)
• Chapter 12: Respiratory Physiology — Pneumoperitoneum effects, CO₂, atelectasis (pp. 1323–1326)
• Chapter 46: Transfusion Medicine — Posttransfusion hepatitis (HBV, HCV) (pp. 6567–6569)
• Chapter 29: Perioperative Management of Coexisting Conditions — Liver disease, Child-Pugh, MELD, jaundice, coagulopathy, hepatic pharmacology
• Chapter 22 / 7: Ketamine, Propofol pharmacology in liver disease
• Chapter 9: NMBDs — Cisatracurium and Hofmann elimination in liver diseaseAll five topics are covered comprehensively. Here's a quick orientation to help you navigate the answer:

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• Physiology of CO₂ pneumoperitoneum (respiratory, cardiovascular, renal, endocrine effects) with the important paradox of less shunt despite more atelectasis
• Positioning-specific concerns: Trendelenburg (laryngeal oedema, ICP/IOP rise), Reverse Trendelenburg, lateral decubitus
• Deep NMB to reduce IAP from 15 → 10 mmHg
• LMA vs. ETT selection, ventilation strategy (↑ MV by 10-25%), PONV prophylaxis
• Recognition and management of intraoperative emergencies (vagal arrest, CO₂ embolism, subcutaneous emphysema, pneumothorax)

• All 5 hepatitis types; HCV causing 90% of post-transfusion hepatitis
• Elective surgery mortality in acute hepatitis: up to 10% (emergency: 50%)
• Drug pharmacokinetics in liver disease; halothane hepatitis; cisatracurium preference
• Child-Pugh scoring and MELD score for perioperative risk stratification

• All three types; systemic consequences across all organ systems
• IV Vitamin K response testing as the pivotal preoperative test
• Cisatracurium, fentanyl/remifentanil, sevoflurane as preferred drugs
• Mannitol for renal protection

• Thoracic epidural as cornerstone (T6–T8; bupivacaine + fentanyl)
• Cisatracurium; restrictive + goal-directed fluids; TEG/ROTEM-guided coagulation
• Glycaemic control (monitoring every 30–60 min); temperature management; ERAS protocol
• ICU post-op; drain amylase day 1–3 for pancreatic fistula

• Highest perioperative AKI risk of any hepatobiliary condition — detailed multifactorial mechanism
• Mannitol + oral lactulose + hydration for renal protection
• Bradycardia from bile salts (atropine at induction); RSI; avoid NSAIDs/morphine/atracurium
• EBD (ERCP stenting) indications preoperatively