Peritoneal Dialysis vs. Hemodialysis

1. Basic Mechanism

2. Access

• Sabiston Textbook of Surgery notes that patients with exhausted vascular access options for HD should be considered for PD as an alternative, and vice versa.

3. Schedule and Setting

4. Contraindications and Patient Selection

• Prior intra-abdominal surgery (adhesions, scar tissue) - most common barrier
• Obesity
• Ileostomy or colostomy
• Prior renal transplant
• Advanced age, diabetes, heart failure (relative)
• Patients unable to perform exchanges at home independently

• Patients with no viable vascular access
• Those who live far from a dialysis center (especially in developing countries)
• Patients preferring home therapy

5. Advantages and Disadvantages

6. Complications

• Hypotension - most common acute complication (especially in diabetics); from excessive ultrafiltration
• Muscle cramps - from rapid volume removal
• Dialyzer reactions - Type A (IgE-mediated, anaphylactoid) or Type B (complement activation, chest/back pain)
• High-output cardiac failure from AV fistula shunting
• Vascular access infections (catheters carry highest mortality risk)

• Peritonitis - most important; can cause membrane failure; fungal peritonitis may require conversion to HD
• Catheter tunnel infections
• Mechanical issues (catheter malposition, leaks)
• Ultrafiltration failure (membrane deterioration over years)
• Encapsulating peritoneal sclerosis (rare but serious)

7. Outcomes and Survival

• No large RCT has definitively shown one modality is superior in survival - the attempted NECOSAD trial had to stop due to poor recruitment.
• Retrospective/prospective nonrandomized studies show no consistent survival advantage for either modality.
• Older evidence suggested PD may be inferior in patients with coronary heart disease or CHF long-term; more recent data suggest this may not hold.
• PD is associated with superior health-related quality of life compared to in-center HD.
• Technique failure in PD (from infection or social reasons) is associated with higher short-term mortality risk.
• In infants and pediatric patients, PD is generally preferred and widely recommended.

8. Special Situations Favoring Each

9. Key Decision Principle

• Harrison's Principles of Internal Medicine 22E, p. 535-536
• Comprehensive Clinical Nephrology 7th Ed., p. 105-135
• Sabiston Textbook of Surgery, p. 3460-3464
• Brenner and Rector's The Kidney, 2-Volume Set, p. 3633-3637

Causes of CVA (Cerebrovascular Accident / Stroke)

I. Ischemic Stroke (Infarction)

• Large vessel thrombosis - atherosclerosis of major cerebral/carotid arteries
• Small vessel (lacunar) stroke - lipohyalinosis of small penetrating arteries; associated with hypertension and diabetes

• Cardioembolic - most common sources:
  • Atrial fibrillation (most important)
  • Mural thrombus (post-MI, dilated cardiomyopathy)
  • Valvular lesions (mitral stenosis, mechanical valves, infective endocarditis)
• Artery-to-artery embolism - from carotid bifurcation plaque, aortic arch, or aortic dissection

• Systemic hypotension causing ischemia in border zones between major arterial territories

II. Hemorrhagic Stroke

• Hypertension (most common cause) - rupture of small penetrating vessels
• Cerebral amyloid angiopathy (especially in elderly)
• Arteriovenous malformations (AVMs)
• Anticoagulant/thrombolytic therapy

• Rupture of a saccular (berry) aneurysm (most common)
• AVM rupture

III. Less Common / Uncommon Causes

Quick Summary for 3 Marks

• Harrison's Principles of Internal Medicine 22E, Table 438-2
• Schwartz's Principles of Surgery 11th Ed.

Sevoflurane vs. Desflurane - Compare and Contrast

1. Physical Properties

2. Induction and Emergence

3. Cardiovascular Effects

4. Respiratory Effects

5. CNS Effects

6. Metabolism and Toxicity

7. Neuromuscular Effects

8. Contraindications (Shared and Unique)

Summary Table for 5 Marks

• Morgan & Mikhail's Clinical Anesthesiology 7e, pp. 305-313
• Barash, Cullen & Stoelting's Clinical Anesthesia 9e
• Miller's Anesthesia 10e

Carbon Dioxide Transport

Three Forms of CO₂ Transport

1. Dissolved CO₂ (~7%)

• CO₂ is ~24x more soluble in blood than O₂ (solubility coefficient = 0.031 mmol/L/mmHg at 37°C)
• Venous PCO₂ = 45 mmHg → ~2.7 mL/100 mL dissolved
• Arterial PCO₂ = 40 mmHg → ~2.4 mL/100 mL dissolved
• Difference = ~0.3 mL/100 mL transported in dissolved form per circulation
• This fraction is small but important - it is the dissolved CO₂ that determines PCO₂ and drives diffusion across membranes

2. Bicarbonate (HCO₃⁻) - THE MAJOR FORM (~70%)

CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻

H⁺ + Hb⁻ → HHb

• ~70% of the HCO₃⁻ formed inside RBCs diffuses out into plasma in exchange for Cl⁻ moving in
• This exchange is mediated by Anion Exchanger 1 (AE1 / Band 3 protein) in the RBC membrane
• Occurs rapidly, essentially complete within 1 second
• Result: Cl⁻ content of venous RBCs > arterial RBCs
• Each CO₂ molecule entering the RBC adds one osmotically active particle → venous RBCs are slightly larger → venous hematocrit is ~3% greater than arterial

• The entire process reverses: Cl⁻ exits RBCs, HCO₃⁻ re-enters, carbonic anhydrase converts H₂CO₃ back to CO₂ + H₂O, and CO₂ diffuses into alveoli

3. Carbamino Compounds (~23%)

• CO₂ reacts directly with free amino (-NH₂) groups on proteins to form carbamino compounds:

R-NH₂ + CO₂ → R-NH-COO⁻ + H⁺

• The dominant carbamino compound in blood is carbaminohemoglobin (Hb-CO₂) - CO₂ binds to the globin portion, not the heme iron
• Plasma proteins contribute negligibly to carbamino transport
• Key property: Deoxygenated hemoglobin (deoxy-Hb) has 3.5 times greater affinity for CO₂ than oxyhemoglobin → venous blood (more deoxy-Hb) carries more carbamino CO₂ than arterial blood

The Haldane Effect

Binding of O₂ to Hb displaces CO₂ from blood; deoxygenation of Hb increases CO₂ uptake.

1. Carbamino: Deoxy-Hb has higher affinity for CO₂ → more carbaminohemoglobin formed in tissues; oxygenation in lungs converts Hb to a stronger acid → less CO₂ bound → CO₂ released
2. Bicarbonate: Deoxy-Hb is a weaker acid → takes up H⁺ more readily → shifts equilibrium toward HCO₃⁻ formation; oxygenation releases H⁺ from Hb → H⁺ combines with HCO₃⁻ → forms CO₂ for elimination

CO₂ Dissociation Curve

• The curve is steeper and more linear than the O₂-Hb dissociation curve (no sigmoidal shape)
• Oxygenated blood (PO₂ = 100 mmHg) has a lower CO₂ content at any given PCO₂ than deoxygenated blood (PO₂ = 40 mmHg) → this difference is the Haldane effect
• Normal venous point: PCO₂ = 45 mmHg, total CO₂ ~52 vol%
• Normal arterial point: PCO₂ = 40 mmHg, total CO₂ ~48 vol%

Summary

• Acetazolamide (carbonic anhydrase inhibitor) blocks bicarbonate formation → tissue PCO₂ can rise to 80 mmHg
• Respiratory acidosis/alkalosis reflects impaired or excessive CO₂ elimination
• The Haldane effect explains why pulmonary oxygenation is essential not just for O₂ loading but also for efficient CO₂ unloading
• Guyton & Hall Textbook of Medical Physiology, Ch. 41
• Morgan & Mikhail's Clinical Anesthesiology 7e, Ch. 23
• Ganong's Review of Medical Physiology 26e, Ch. 35

Oxygen Consumption (VO₂)

1. Definition and the Fick Principle

VO₂ = Cardiac Output (CO) × (CaO₂ - CvO₂)

• CaO₂ = arterial O₂ content (mL O₂/dL blood)
• CvO₂ = mixed venous O₂ content (mL O₂/dL blood)
• (CaO₂ - CvO₂) = arteriovenous O₂ difference (a-v DO₂ difference), normally 4-6 mL/100 mL blood

Cardiac Output = VO₂ ÷ (CaO₂ - CvO₂)

• VO₂ = 250 mL O₂/min
• CaO₂ = 0.20 mL O₂/mL blood
• CvO₂ = 0.15 mL O₂/mL blood
• CO = 250 ÷ (0.20 - 0.15) = 5000 mL/min = 5 L/min ✓

2. Oxygen Delivery (DO₂) - The Supply Side

DO₂ = CO × CaO₂ × 10

CaO₂ = (Hb × 1.34 × SaO₂) + (PaO₂ × 0.0031)

• Normal CaO₂ = 16-22 mL O₂/dL
• Normal DO₂ = 700-1400 mL/min
• Under normal conditions, DO₂ exceeds VO₂ by ~75% (delivery far exceeds demand)

3. Relationship of DO₂ to VO₂ - The Critical Threshold

• Above the critical DO₂ threshold: VO₂ is independent of DO₂ - tissues extract more O₂ as needed (increased O₂ extraction ratio), keeping VO₂ constant over a wide range of delivery
• Below the critical DO₂ threshold: VO₂ becomes supply-dependent - tissues cannot extract enough O₂ to meet metabolic needs → anaerobic metabolism begins → lactic acidosis

O₂ER = (CaO₂ - CvO₂) / CaO₂ (normal ~25%)

4. Normal Resting Values

5. Regional O₂ Consumption

6. Myocardial O₂ Consumption - Special Case

1. Wall tension (pressure work) - dominant determinant; explains why aortic stenosis causes massive ↑ in myocardial O₂ consumption
2. Heart rate - more contractions per minute = more O₂ used
3. Contractility - increased inotropy increases O₂ consumption
4. Volume work (less costly than pressure work)

• Aortic stenosis → greatly ↑ myocardial VO₂ (high pressure work even with low CO)
• Exercise → ↑ VO₂ but less than pressure overload states
• Left ventricle wall is thicker than right ventricle → compensates for higher pressure work (aortic pressure 100 mmHg vs. pulmonary 15 mmHg) via the Law of Laplace (P = 2HT/r)

7. VO₂max (Maximal Oxygen Consumption)

8. Clinical Relevance

Summary

VO₂ = CO × (CaO₂ - CvO₂) Normal ~250 mL/min at rest; increases up to 20x during maximal exercise VO₂ is normally independent of DO₂ (supply-independent zone) Below critical DO₂, VO₂ falls and lactic acidosis ensues Myocardial VO₂ is dominated by pressure work, not volume

• Costanzo Physiology 7e, Ch. on Cardiac Output
• Ganong's Review of Medical Physiology 26e, Ch. 30, 33, 37
• Miller's Anesthesia 10e, Ch. on Shock
• Barash's Clinical Anesthesia 9e, Ch. 38

Buffer Systems of the Body

1. Chemical buffer systems (immediate, seconds)
2. Respiratory regulation (minutes)
3. Renal regulation (hours to days)

Key Concept: Henderson-Hasselbalch Equation

pH = pKa + log ([A⁻] / [HA])

pH = 6.1 + log (HCO₃⁻ / 0.03 × PCO₂)

• Normal: pH = 6.1 + log (24 / 1.2) = 6.1 + log 20 = 6.1 + 1.3 = 7.4
• HCO₃⁻ regulated by kidneys; PCO₂ regulated by lungs

LINE 1: Chemical Buffer Systems

1. Bicarbonate-Carbonic Acid Buffer System - THE PRIMARY EXTRACELLULAR BUFFER (~70%)

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

H⁺ + HCO₃⁻ → H₂CO₃ → CO₂ + H₂O (CO₂ exhaled by lungs)

OH⁻ + H₂CO₃ → HCO₃⁻ + H₂O

• Present in large quantities in ECF (HCO₃⁻ ~24 mEq/L)
• The "acid" component (CO₂) is continuously produced by metabolism - inexhaustible supply
• CO₂ is a volatile acid that can be rapidly blown off by the lungs - the system is "open" and continuously regenerated
• HCO₃⁻ is regulated by the kidneys

2. Phosphate Buffer System

• Buffering an acid:

HCl + Na₂HPO₄ → NaH₂PO₄ + NaCl (strong acid HCl replaced by weak acid NaH₂PO₄)

• Buffering a base:

NaOH + NaH₂PO₄ → Na₂HPO₄ + H₂O (strong base NaOH replaced by weak base Na₂HPO₄)

3. Protein Buffer System - THE LARGEST INTRACELLULAR BUFFER

Protein-NH₂ + H⁺ ⇌ Protein-NH₃⁺ (acts as base) Protein-COOH ⇌ Protein-COO⁻ + H⁺ (acts as acid)

H⁺ = K₁ × [HA₁]/[A₁⁻] = K₂ × [HA₂]/[A₂⁻] = K₃ × [HA₃]/[A₃⁻]

4. Hemoglobin Buffer System - MOST IMPORTANT BLOOD BUFFER

• Present in very high concentration inside RBCs
• Rich in histidine residues (imidazole groups)
• Deoxyhemoglobin is a weaker acid than oxyhemoglobin → accepts H⁺ more readily in tissues

H⁺ + Hb⁻ ⇌ HHb

CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ H⁺ + Hb⁻ → HHb (prevents pH from falling sharply)

5. Bone Buffer System

• More than half of total body alkaline buffer content is outside the ECF, largely in bone
• Bone mineral (calcium carbonate and calcium phosphate) can release HCO₃⁻ and phosphate to buffer chronic acidosis
• Important in chronic metabolic acidosis (e.g., renal failure) - explains why chronic acidosis causes demineralization of bone

LINE 2: Respiratory Regulation (Second Line of Defense - Minutes)

↑ H⁺ (acidosis) → ↑ respiratory rate → ↓ PCO₂ → pH rises ↓ H⁺ (alkalosis) → ↓ respiratory rate → ↑ PCO₂ → pH falls

LINE 3: Renal Regulation (Third Line - Slowest but Most Powerful)

1. Excreting H⁺ into tubular urine
2. Regenerating HCO₃⁻ (reabsorbing filtered bicarbonate or generating new HCO₃⁻)
3. Excreting titratable acid (H₂PO₄⁻ via the phosphate buffer)
4. Excreting NH₄⁺ (ammonium) - ammonia combines with secreted H⁺ → NH₄⁺

Summary Table: Buffer Systems

Acid-Base Disorders and Compensation

• Guyton & Hall Textbook of Medical Physiology, Ch. 31
• Basic Medical Biochemistry: A Clinical Approach 6e, Ch. 4
• Lippincott's Illustrated Reviews: Biochemistry 8e, Ch. 1
• Mulholland & Greenfield's Surgery 7e, Ch. 11

Calculating Predicted Decrease in Lung Capacity After Pneumonectomy

Why It Matters

• A ppoFEV₁ ≤40% is associated with significantly increased risk of postoperative dependence on supplemental oxygen and/or mechanical ventilation
• Both ppoFEV₁% and ppoDLCO% <50% are associated with increased perioperative complications
• Risk increases in a stepwise fashion for every 10% decline

Step 1: Establish Baseline Pulmonary Function

• FEV₁ - Forced Expiratory Volume in 1 second (most important)
• FVC - Forced Vital Capacity
• DLCO - Diffusing capacity for carbon monoxide (reflects alveolar-capillary surface area)
• TLC - Total Lung Capacity

If preoperative FEV₁ and DLCO are both ≥80% predicted and the patient has no dyspnea on exertion, the patient is cleared for pneumonectomy with no further testing needed.

Step 2: Calculate PPO Values

METHOD A: Segment Counting Method (for lobectomy; used when perfusion scan unavailable)

ppoFEV₁ = preopFEV₁ × (1 - y/z)

• y = number of functional segments to be removed
• z = total number of functional segments (obstructed/non-functional segments excluded)

• Planned right lobectomy removing 3 segments, total 20 functional segments
• Patient retains (20 - 3) = 17 segments → 85% of original lung capacity remains
• If baseline FEV₁% = 30%: ppoFEV₁ = 30% × 0.85 = 25% (high risk)
• If baseline FEV₁% = 59%: ppoFEV₁ = 59% × 0.85 = 50% (acceptable)

METHOD B: Quantitative Perfusion (Q) Scan - PREFERRED FOR PNEUMONECTOMY

ppoFEV₁ = preopFEV₁ × (1 - fraction of total perfusion going to the resected lung)

ppoDLCO = preopDLCO × (1 - fraction of total perfusion going to the resected lung)

Worked Example (from Sabiston Textbook of Surgery)

• Preoperative FEV₁ = 2.83 L predicted; measured = 2.23 L (79% predicted)
• Quantitative perfusion scan: left lung contributes 46% of total perfusion

ppoFEV₁ = 2.83 L × (1 - 0.46) = 2.83 × 0.54 = 1.53 L

ppoFEV₁% = 79% × 0.54 = ~43% predicted

• Perfusion scan: right lung = 21% of total perfusion (tumor-obstructed)
• Baseline FEV₁% = 60%
• ppoFEV₁% = 60% × (1 - 0.21) = 60% × 0.79 = 47% → tolerable
• If right lung = 55% normal perfusion: ppoFEV₁% = 60% × 0.45 = 27% → high risk

Step 3: Risk Stratification Based on PPO Values

Step 4: Functional Exercise Testing (if ppo values borderline)

Summary: The Complete Calculation Formula

ppoFEV₁ = preop FEV₁ × [1 - fraction of perfusion to resected lung]

ppoDLCO = preop DLCO × [1 - fraction of perfusion to resected lung]

ppoFEV₁ = preop FEV₁ × [1 - (segments removed ÷ total functional segments)]

• ppoFEV₁ or ppoDLCO >60% = low risk, cleared
• ppoFEV₁ or ppoDLCO 40-60% = acceptable with exercise testing
• ppoFEV₁ or ppoDLCO <30% = high risk, consider alternatives

• Sabiston Textbook of Surgery, Ch. 110
• Schwartz's Principles of Surgery 11e, Ch. 19
• Morgan & Mikhail's Clinical Anesthesiology 7e, Ch. 25
• Fishman's Pulmonary Diseases and Disorders, Ch. 102
• Mulholland & Greenfield's Surgery 7e, Ch. 14

Rapid Shallow Breathing Index (RSBI)

Definition

Formula

RSBI = Respiratory Rate (f) ÷ Tidal Volume (VT in litres)

RSBI = f (breaths/min) / VT (L)

• RR = 20 breaths/min, VT = 500 mL (0.5 L)
• RSBI = 20 / 0.5 = 40 → low, favourable for extubation

• RR = 35 breaths/min, VT = 250 mL (0.25 L)
• RSBI = 35 / 0.25 = 140 → high, predicts weaning failure

Physiological Basis

• Healthy, comfortable breathing: Patient breathes slowly with large tidal volumes → low RSBI
• Respiratory distress / muscle fatigue: Patient breathes rapidly with small tidal volumes (rapid and shallow) → high RSBI

How to Measure RSBI

1. Patient is placed on minimal ventilator support: either
   • T-piece (disconnected from ventilator, breathing room air/O₂ through the ETT)
   • CPAP 5 cm H₂O with minimal or no pressure support
   • Low PSV (e.g., PSV 7 / PEEP 5) - essentially only compensating for ETT resistance
2. Observe for 1-2 minutes of spontaneous breathing
3. Measure respiratory rate (f) and tidal volume (VT in litres)
4. Calculate RSBI = f / VT

Threshold Values and Interpretation

"RSBI >105 accurately predicts weaning failure, but RSBI ≤105 is less accurate at predicting weaning success"

RSBI in Context: Other Weaning Criteria

Prerequisites Before Measuring RSBI

• Reversal or control of the precipitating illness
• Treatment of bronchospasm, infection, heart failure
• Correction of acid-base disorders, anaemia
• Adequate nutrition (malnutrition → respiratory muscle wasting)
• Adequate analgesia and sedation interruption
• Intact airway reflexes (cough, gag) and ability to handle secretions

Limitations of RSBI

1. Moderate sensitivity, poor specificity - a recent meta-analysis (cited in Sabiston) found only moderate sensitivity and poor specificity across a variety of cutoff values
2. Affected by sedation - sedation reduces respiratory drive and artificially lowers RSBI
3. Does not assess airway protection - a patient can have a low RSBI but still fail extubation due to inability to clear secretions, aspiration risk, or stridor from laryngeal oedema
4. ETT size matters - smaller ETTs impose more resistance; low-level PSV used to compensate may affect the measured VT
5. Not superior to clinical judgement - newer aids (lung ultrasound, diaphragm thickening fraction, age, maximal inspiratory pressure) have been studied but none is clearly better than RSBI

Newer Adjuncts to RSBI

• Diaphragm thickening fraction (DTF) on ultrasound combined with RSBI improves weaning prediction accuracy
• Lung ultrasound - aeration score before and after SBT helps identify patients at risk for post-extubation respiratory failure
• Cuff leak test - absence of cuff leak after ETT cuff deflation suggests laryngeal oedema; preclude extubation and treat with IV corticosteroids for 12-24 hours

Summary (5 Marks)

• Morgan & Mikhail's Clinical Anesthesiology 7e, Ch. 58
• Miller's Anesthesia 10e, Ch. on Weaning
• Sabiston Textbook of Surgery, Ch. on Critical Care
• Washington Manual of Medical Therapeutics
• Fischer's Mastery of Surgery 8e
• Mulholland & Greenfield's Surgery 7e

Neurally Adjusted Ventilatory Assist (NAVA)

Definition

The Core Problem NAVA Solves: Patient-Ventilator Dyssynchrony

• The ventilator is triggered by pressure or flow changes in the circuit
• This creates a time lag between neural inspiration and ventilator response
• The delivered pressure/volume is independent of patient effort - too much support during weak effort, too little during strong effort
• This mismatch is called patient-ventilator dyssynchrony and occurs during all three phases: triggering, flow delivery, and breath cycling
• Dyssynchrony causes discomfort, increases sedation requirements, and may contribute to ventilator-induced lung injury (VILI) and diaphragm injury

How NAVA Works - The Mechanism

Step 1: The Edi Catheter

• A specially modified nasogastric tube is placed into the oesophagus (positioned near the gastro-oesophageal junction)
• It contains miniaturised EMG electrodes that detect the electrical activation of the diaphragmatic crura (the neural signal travelling from the brainstem via the phrenic nerve to the diaphragm)
• This signal is the Edi (electrical activity of the diaphragm)

Step 2: Signal Processing

• The raw EMG signal is filtered, amplified, and processed by the ventilator
• The Edi signal waveform is continuous - it rises with each inspiratory effort and falls at end-inspiration

Step 3: Pressure Delivery

Paw (airway pressure) = NAVA Level × Edi (μV) + PEEP

• The ventilator triggers as soon as the Edi signal rises above a threshold (neural trigger)
• It delivers pressure proportional to the magnitude of the Edi signal throughout inspiration
• It cycles off when the Edi signal falls (typically to 70% of peak Edi)
• The clinician sets the NAVA Level (cmH₂O/μV) - the proportionality gain between Edi and delivered pressure

Key Features and Terminology

Advantages of NAVA Over Conventional Modes

Comparison: NAVA vs. Pressure Support Ventilation (PSV)

Limitations and Concerns

1. Signal instability: The Edi catheter can move within the oesophagus, causing artefactual changes in signal amplitude - all NAVA patients need careful monitoring and a backup ventilation mode must always be active
2. Low respiratory drive: Since NAVA provides no minimum flow/pressure, it cannot support patients with absent or very weak respiratory drive (e.g., heavy sedation, neuromuscular disease, brainstem injury) - PAV has the same limitation
3. NAVA Level titration: There is no established consensus on the optimal NAVA level for different clinical scenarios - titration remains partly empirical
4. Limited RCT evidence: The single major randomized controlled trial published (Kacmarek et al., 2020, Intensive Care Med) found no benefit from NAVA compared to PSV in acute respiratory failure patients, despite improved synchrony metrics
5. Availability: Not available on all ventilators; requires specific Edi catheter equipment
6. Cardiac EMG interference: Cardiac electrical activity can occasionally auto-trigger NAVA (reported in case reports)

Clinical Applications

Edi as a Monitoring Tool (Separate from NAVA)

• Edi peak rising over time → increasing respiratory load/distress → early warning of impending failure
• Edi min elevated → auto-PEEP present → guide PEEP titration
• Edi absent during weaning → patient may be over-supported → reduce support
• Neuro-ventilatory efficiency (NVE) = VT/Edi - assesses how much volume is generated per unit of neural effort

Summary

• Murray & Nadel's Textbook of Respiratory Medicine 2-Vol Set, Ch. 135
• Goldman-Cecil Medicine International Edition, Ch. on Mechanical Ventilation
• Miller's Anesthesia 10e

Stellate Ganglion Block (SGB)

1. Anatomy of the Stellate Ganglion

• Lies anterior to the longus colli muscle
• Posterior to the origin of the vertebral artery from the subclavian artery
• Anterior to the first rib and the transverse process of C7
• Anteromedial to the scalene muscles
• Medial to the carotid sheath
• At the level of the C7 vertebral body (though injection is typically performed at C6 for safety)

• Ipsilateral head and neck
• Ipsilateral upper extremity (including T1 contribution)
• Upper thoracic viscera (heart, great vessels, lungs)
• Note: T2-T3 sympathetic fibres to the arm may travel via Kuntz nerves joining the brachial plexus in the axilla - these can be missed by a stellate block but not by an axillary block

2. Anatomy Diagram

3. Indications

• Complex Regional Pain Syndrome (CRPS) Type I and II affecting the head, neck, and upper extremities - primary indication; may even reverse early-stage CRPS I
• Acute herpes zoster (shingles) involving head, neck, upper limb - pain relief and possibly reduces risk of postherpetic neuralgia
• Postherpetic neuralgia
• Cancer pain of head, neck, and upper extremity

• Peripheral vascular disease and vasospastic disorders of the upper extremity (Raynaud's phenomenon, obliterative arterial disease)
• Vascular insufficiency of the arm - improves blood flow by blocking vasoconstrictor tone

• Refractory ventricular tachycardia (VT) / ventricular arrhythmias - particularly left stellate ganglion block for long-QT syndrome-associated VT (left SGB reduces cardiac sympathetic drive)
• Electrical storm (recurrent refractory VT)

• Post-traumatic stress disorder (PTSD) - emerging indication; reduces sympathetic nervous system hyperactivity
• Severe vasomotor symptoms associated with menopause (hot flushes)
• Hyperhidrosis of the face, head, neck

4. Contraindications

5. Technique

Patient Positioning

• Supine, neck hyperextended, head turned slightly to contralateral side
• IV access mandatory; resuscitation equipment available

Landmark (Paratracheal) Technique - C6 Level (Traditional)

1. Identify Chassaignac's tubercle - the anterior tubercle of the C6 transverse process (at level of cricoid cartilage, ~3 cm above clavicle)
2. Retract the sternocleidomastoid muscle and carotid sheath laterally with the non-operative hand to displace carotid artery away from midline
3. Insert a 22-gauge, 4-5 cm needle at the medial edge of SCM, perpendicular to skin, advancing to the transverse process of C6
4. Withdraw needle 2-3 mm (to come off the transverse process/longus colli) before injection
5. Aspirate in two planes to exclude intravascular placement
6. Inject 1 mL test dose first - observe for intravascular signs (tachycardia, metallic taste, dizziness)
7. Inject 5-10 mL of local anaesthetic (e.g., 0.25-0.5% bupivacaine or 1-1.5% lignocaine)

• At C7, the vertebral artery has already entered the transverse foramen - risk of vertebral artery puncture is higher
• At C6, the vertebral artery is still lateral and protected in the foramen

Ultrasound-Guided Technique (Preferred)

1. Linear probe placed transversely over cricoid cartilage, moved laterally until C6 transverse process (Chassaignac tubercle) is visualised
2. Identify: carotid artery, internal jugular vein, longus colli muscle, and the tubercle
3. In-plane needle approach from lateral to medial
4. Target: medial to Chassaignac tubercle, anterior to the prevertebral fascia (on the longus colli muscle surface)
5. Test dose 1 mL after negative aspiration, then 4-5 mL total
6. Ultrasound visualises local anaesthetic spread in the correct fascial plane

6. Signs of Successful Block - Horner's Syndrome

Horner's syndrome confirms cervical sympathetic block but does not guarantee adequate thoracic sympathetic block of the upper extremity.

7. Complications

8. Agents Used

• For neurolytic (permanent) blocks: phenol or alcohol (rarely used)
• For cardiac arrhythmia emergencies: faster-onset agents (lignocaine) preferred

9. Summary Table

• Morgan & Mikhail's Clinical Anesthesiology 7e, Ch. 47
• Miller's Anesthesia 10e, Ch. 74
• Bradley & Daroff's Neurology in Clinical Practice, Ch. 52