1. Historical Background — ASA 1986 mandate, WHO/WFSA standards, closed-claims evidence
2. Physiologic Fundamentals — O₂ content equation, haemoglobin species, the oxydissociation curve
3. Principles of Operation — Lambert-Beer law, AC/DC signal processing, the R-ratio and calibration curve (with diagrams), transmittance vs. reflectance modes
4. Anaesthesia Applications — Mandatory monitoring, MAC sedation, endobronchial intubation detection, SpO₂ targets
5. Photoplethysmography — PVI for fluid responsiveness, Perfusion Index, goal-directed fluid therapy
6. Limitations & Errors — Full error table, dysfunctional haemoglobins in depth (COHb, MetHb, SHb), perfusion-dependent failure, accuracy at low saturations, racial bias/skin pigmentation (emerging evidence)
7. Critical Care Role — ICU monitoring, oxygenation targets, SvO₂/ScvO₂, remote monitoring (post-COVID)
8. Multi-wavelength Co-oximetry — SpCO, SpMet, SpHb; pulse spectroscopy
9. Cerebral NIRS — Cardiac surgery, carotid endarterectomy
10. Probe Selection — Site-specific advantages; forehead preference in vasoconstriction
11. Clinical Pearls — 10 high-yield practice points

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🎓 LECTURE: Pulse Oximetry — A Complete Professor-Level Teaching Session

Department of Anaesthesia & Critical Care

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Welcome. Today we are going to master pulse oximetry — not just as a gadget you clip onto a finger, but as a physiological instrument with deep physics, well-defined failure modes, and advanced hemodynamic applications. By the end of this session you will be able to explain every number and waveform it generates, predict exactly when it will lie to you, and use it at an expert level in theatre and intensive care.

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PART 1 — WHY THIS MONITOR MATTERS: A HISTORICAL PERSPECTIVE

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PART 2 — THE ESSENTIAL PHYSIOLOGY YOU MUST OWN

2.1 Oxygen Delivery — Why SaO₂ Is Everything

DO₂ = CO × CaO₂

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

• The Hüfner constant (1.34 mL/g) is the O₂-carrying capacity of haemoglobin per gram. Theoretically 1.39, but experimentally 1.31–1.37 because of small amounts of non-functional Hb species in real blood.
• The dissolved O₂ term (0.0031 × PaO₂) is negligible under normal conditions — roughly 0.3 mL/dL at a PaO₂ of 100 mmHg. It becomes relevant only during hyperbaric oxygen therapy.

• The patient is severely anaemic (low Hb — the multiplier)
• Cardiac output is critically low
• Dysfunctional Hb species are present (COHb, MetHb — which are "counted" by the oximeter but cannot carry O₂)

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2.2 Haemoglobin Species — Know All Five

= O₂Hb ÷ (O₂Hb + deO₂Hb) × 100

= O₂Hb ÷ (O₂Hb + deO₂Hb + COHb + MetHb + SHb) × 100

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2.3 The Oxyhaemoglobin Dissociation Curve — Master This

• A large fall in PaO₂ (e.g., 150 → 100 → 70 mmHg) causes only a tiny fall in SpO₂
• This protects against minor ventilation impairment
• Clinical trap: SpO₂ cannot detect hyperoxia. On 100% FiO₂, a patient might have PaO₂ of 500 mmHg — you cannot see this on the pulse oximeter. In neonates and premature infants, this is how retinopathy of prematurity develops
• The pulse oximeter will not warn you when PaO₂ rises dangerously high on supplemental oxygen

• Small falls in PaO₂ cause large falls in SaO₂ — the "cliff edge"
• At the inflection point around PaO₂ 60 mmHg → SpO₂ ≈ 90% — this is the critical threshold
• Below this, the patient falls off the cliff rapidly

• ↓pH (acidosis), ↑PaCO₂ (hypercarbia), ↑temperature, ↑2,3-DPG
• This is the Bohr effect — exercising muscle creates an acid environment that promotes O₂ unloading. Elegant physiology.

• ↑pH (alkalosis), ↓PaCO₂, ↓temperature, ↓2,3-DPG, fetal Hb, COHb
• During hypothermic bypass: the curve shifts left — haemoglobin clings to oxygen and doesn't release it to tissues easily. Metabolic rate is also reduced, so this is less of a problem — but it matters when interpreting SvO₂

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PART 3 — THE PHYSICS: HOW THE MACHINE ACTUALLY WORKS

3.1 The Beer–Lambert Law

I_trans = I_in × e^(−ε × C × D)

• I_trans = transmitted light intensity
• I_in = incident light intensity
• ε = extinction coefficient (how strongly the solute absorbs light at that wavelength — unique for each molecule)
• C = concentration of solute
• D = path length through the solution

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3.2 The Two Wavelengths — Why 660 nm and 940 nm?

• At 660 nm (red): DeO₂Hb absorbs far more than O₂Hb → deoxygenated blood absorbs red light heavily → appears blue/cyanotic to the naked eye
• At 940 nm (infrared): O₂Hb absorbs more than deO₂Hb → oxygenated blood absorbs more infrared
• There is an isosbestic point around 805 nm where both species absorb equally — at this wavelength, absorption is independent of oxygen saturation

• COHb (red) and O₂Hb (blue) have very similar extinction coefficients → the oximeter cannot tell them apart → CO poisoning is invisible to a standard pulse oximeter
• MetHb (orange) has significant absorption at both 660 nm and 940 nm → it corrupts both channels equally → R approaches 1.0 → SpO₂ reads 85% regardless of true saturation

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3.3 The AC/DC Trick — How It Isolates Arterial Blood

• Skin, fat, bone, muscle (constant, non-pulsatile)
• Venous blood (constant, non-pulsatile under normal conditions)
• Capillary blood (largely constant)
• Arterial blood (pulsatile with every heartbeat)

• DC component = the constant background (all non-arterial tissue + venous blood)
• AC component = the pulsatile change caused by each arterial pulse

R = (AC₆₆₀ / DC₆₆₀) ÷ (AC₉₄₀ / DC₉₄₀)

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3.4 Hardware: What the Probe Contains

• Two LEDs (Light Emitting Diodes) at 660 nm and 940 nm
• One photodiode (photodetector) on the opposite side of the finger
• A microprocessor cycles each LED on and off in sequence. When both are off, ambient light is measured and subtracted — this is how the oximeter rejects overhead lighting artefact

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PART 4 — THE OUTPUT: WHAT THE MONITOR DISPLAYS AND WHAT IT REALLY MEANS

4.1 The SpO₂ Number

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4.2 The Plethysmographic Waveform — Your Second Data Stream

• Amplitude = pulse pressure / peripheral vascular tone. Tall waves = good perfusion. Low amplitude = vasoconstriction or low stroke volume
• Regularity = rhythm. Irregular waveform → arrhythmia
• Respiratory variation (ΔPOP) = the amplitude varies with each breath during mechanical ventilation because of cyclical changes in venous return and stroke volume. This is the plethysmography variability index (PVI).

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4.3 PVI and Fluid Responsiveness — Advanced Application

PVI (%) = [(PPG_max − PPG_min) ÷ PPG_max] × 100

1. Controlled mechanical ventilation (not spontaneous breathing — patient effort overrides the signal)
2. Sinus rhythm (arrhythmias corrupt the respiratory vs. cardiac signal separation)
3. Tidal volume ≥ 8 mL/kg (smaller tidal volumes generate smaller respiratory swings — false negatives)
4. No severe vasodilation (septic shock can produce venous pulsations that corrupt the DC component)

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4.4 Perfusion Index (PI)

• Normal PI: 1–10%
• Low PI (< 1%): peripheral vasoconstriction — shock, hypothermia, high-dose vasopressors, patient cold and clammy
• High PI (> 4%): peripheral vasodilation — warm sepsis, epidural, sympatholysis, high ambient temperature

• Predicting hypotension after spinal anaesthesia: a PI that rises after spinal block onset indicates vasodilation before blood pressure falls — gives a 1–2 minute warning
• Monitoring vasopressor effect: PI should rise as vasopressors take effect and redirect blood to periphery (actually reflects reversal of peripheral shutdown)
• Identifying poor probe signal: PI < 0.3% → SpO₂ reading unreliable

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PART 5 — LIMITS OF THE TECHNOLOGY: WHERE IT FAILS YOU

5.1 The "85% Trap" — Two Scenarios Where You Must Think

1. True SaO₂ of 85% (the patient is severely hypoxaemic)
2. Methaemoglobinaemia — MetHb absorbs equally at 660 and 940 nm → R = 1 → machine reads 85%
3. Optical shunt — probe is misplaced and direct LED light reaches the photodetector without passing through tissue → also reads 85%

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5.2 Carbon Monoxide Poisoning — The Invisible Killer

• House fires
• Enclosed space events
• Unexplained altered consciousness
• Any patient with headache, nausea and flu-like symptoms

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5.3 Venous Pulsations — An Underappreciated Error

• Severe tricuspid regurgitation — the right atrial backpressure transmits to peripheral veins, making them pulsatile
• Tight probe placement — occludes venous outflow, creating pulsatile venous pressure
• Trendelenburg position with forehead probe — dependent venous congestion produces venous pulsation
• Distributive shock — extreme vasodilation produces arteriovenous shunting where venous blood becomes pulsatile

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5.4 Motion Artefact

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5.5 Low Perfusion States

• Move to a central site: earlobe or forehead probe — the arterial supply to these areas is less catecholamine-responsive than fingers
• Earlobe: superficial temporal artery territory — relatively vasodilation-resistant
• Forehead (reflectance probe): supratrochlear and supraorbital arteries — similarly preserved in shock
• In patients on high-dose vasopressors (noradrenaline, vasopressin), finger probes often fail — switch to earlobe or forehead

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5.6 Complete Summary of Artefacts

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5.7 The Racial Bias Issue — Modern Critical Awareness

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PART 6 — PULSE OXIMETRY IN SPECIFIC CLINICAL SETTINGS

6.1 Intraoperative Anaesthesia

• Pulse oximetry detects only 50% of apnoea episodes detected by capnography
• SpO₂ drops an average of 45.6 seconds after apnoea begins (because of oxygen reserve from pre-oxygenation and supplemental O₂)
• This delay is dangerous — by the time SpO₂ falls, significant hypercapnia has already occurred
• Lesson: In sedation cases, always use capnography alongside pulse oximetry. SpO₂ is a late indicator of respiratory depression when supplemental O₂ is being given

• Pulse oximetry frequently fails to detect right mainstem intubation if the patient is pre-oxygenated on 100% FiO₂
• The non-ventilated left lung still has O₂ from pre-oxygenation — SpO₂ stays normal for several minutes
• Capnography is more sensitive (waveform unchanged in endobronchial intubation but auscultation and asymmetric chest rise are key)

• Most adult patients: SpO₂ 95–100% (avoid hyperoxia in COPD, neonates)
• Premature neonates: 91–95% (above 95% risks retinopathy of prematurity)
• Single-lung ventilation: SpO₂ ≥ 92% generally acceptable; tolerate lower if unavoidable

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6.2 Post-Anaesthesia Care Unit (PACU)

• Continuous SpO₂ monitoring is mandatory
• Shivering commonly causes motion artefact — use Masimo-technology device or earlobe probe
• Aim SpO₂ ≥ 95% before discharge to ward (or ≥ 92% in COPD)
• A persistently low SpO₂ in PACU — think: airway obstruction, residual neuromuscular block, opioid-induced respiratory depression, pneumothorax, PE, atelectasis

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6.3 ICU

SvO₂ = SaO₂ − VO₂ / (1.34 × Hb × CO)

• SvO₂ < 65% → extraction increased → shock (hypovolemic, cardiogenic, distributive) or ↑ VO₂ (sepsis, pain, shivering)
• SvO₂ > 80% → either excess delivery OR failure to extract (distributive shock with mitochondrial dysfunction, cytotoxic hypoxia, left-to-right shunt)

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6.4 Prehospital and Transport

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6.5 Neonatal Screening — Critical Congenital Heart Disease (CCHD)

• SpO₂ < 95% in either limb, OR

• 3% difference between right hand and foot (indicates right-to-left ductal shunting)

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PART 7 — ADVANCED AND EMERGING TECHNOLOGIES

7.1 Multi-Wavelength Pulse CO-Oximetry (Masimo Rainbow)

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7.2 Cerebral Near-Infrared Spectroscopy (NIRS / rSO₂)

• Cardiac surgery on CPB: detect cerebral desaturation during aortic cross-clamping, hypotension, or embolism. Intervention guided by rSO₂ ≥ 50% or not < 20% of baseline
• Carotid endarterectomy: detect cerebral ischaemia during carotid cross-clamping — guides need for shunting
• Detection of malpositioning/malfunction in ECMO
• Patients with continuous-flow ventricular assist devices (where conventional SpO₂ is impossible)

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7.3 Pulse Spectroscopy (Emerging)

• Accurate SaO₂ determination
• Reliable COHb and MetHb assessment during both normoxia and hypoxia
• Potential to fully replace ABG co-oximetry for saturation measurements in future

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PART 8 — WHAT PULSE OXIMETRY CANNOT TELL YOU

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PART 9 — THE PROFESSOR'S CLINICAL SCENARIOS

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SUMMARY FRAMEWORK — THE PROFESSOR'S ONE-PAGE MENTAL MODEL

PULSE OXIMETRY: LAYERED MENTAL MODEL

LAYER 1 — PHYSICS
  Beer-Lambert Law → Lambert-Beer extinction at 660 nm & 940 nm
  AC (pulsatile) / DC (static) separation → isolates arterial signal
  R = (AC660/DC660) ÷ (AC940/DC940) → calibration curve → SpO₂

LAYER 2 — PHYSIOLOGY
  SpO₂ estimates SaO₂ (functional, not fractional)
  CaO₂ = 1.34 × Hb × SaO₂ + 0.0031 × PaO₂
  SaO₂ is shaped by the oxyHb dissociation curve
  Curve shifts: CADET for right shift (↑CO₂, Acidosis, ↑2,3-DPG, Exercise/Temp)

LAYER 3 — WHAT IT GIVES YOU
  SpO₂ → oxygenation (not ventilation, not delivery, not tissue use)
  PPG waveform → perfusion, rhythm, PVI
  PI → vascular tone
  Heart rate → from pulsatile signal

LAYER 4 — WHEN IT LIES
  COHb → falsely HIGH (reads normal in CO poisoning)
  MetHb / SHb → locked at 85%
  Optical shunt → locked at 85%
  Methylene blue → acutely drops to ~65%
  Low perfusion → absent/low reading
  Dark skin < 80% SaO₂ → falsely HIGH (hidden hypoxaemia)
  Venous pulsation → falsely LOW

LAYER 5 — WHAT IT CANNOT DO
  Ventilation ✗    Hyperoxia ✗    Hb concentration ✗
  Tissue oxygenation ✗    CO poisoning ✗    Acid-base ✗

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• Miller's Anesthesia, 2-Volume Set, 10e — Chapter 37, pp. 5449–5473 (definitive reference)
• Morgan & Mikhail's Clinical Anaesthesiology, 7e — Chapter 6, pp. 222–225
• Barash, Cullen & Stoelting's Clinical Anaesthesia, 9e — Chapter 30, pp. 2491–2492
• Rosen's Emergency Medicine, 10e — Chapter 10 (methaemoglobinaemia)
• Gallagher JJ & Adamski JL — Accuracy of Pulse Oximetry in Non-white Patients, Crit Care Nurs Clin North Am 2025 [PMID: 40849175]
• Coutrot M et al. — Perfusion Index in Anaesthesia & Critical Care, Anaesth Crit Care Pain Med 2021 [PMID: 34687923]

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🎓 PROFESSOR'S LECTURE: Spinal & Epidural Anaesthesia

Residency Teaching Session — Anaesthesia & Critical Care

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Good morning, resident. Today we cover the two pillars of neuraxial anaesthesia — spinal and epidural. I want you to leave this session knowing not just how to perform these techniques, but why every step exists and what happens when something goes wrong. Let's begin from the ground up.

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MODULE 1 — ANATOMY: THE FOUNDATION OF EVERYTHING

1.1 The Vertebral Column and Spinal Levels

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1.2 Layers the Needle Passes Through — From Skin to CSF

SKIN
  ↓
Subcutaneous fat
  ↓
Supraspinous ligament  (connects spinous process tips — runs vertically)
  ↓
Interspinous ligament  (between spinous processes — softer, less resistance)
  ↓
Ligamentum flavum  ← STOP HERE for EPIDURAL (firm, gritty, elastic — loss of resistance)
  ↓
Epidural space  (potential space, contains fat, vessels, lymphatics)
  ↓
Dura mater  ← DANGER ZONE — perforation = PDPH
  ↓
Arachnoid mater
  ↓
Subarachnoid space (CSF)  ← ENDPOINT for SPINAL
  ↓
Pia mater (adherent to cord)

• Supraspinous ligament → firm, like penetrating dense rubber
• Interspinous ligament → softer, less distinct
• Ligamentum flavum → firm, gritty, "springy" — classic feel; when using LOR syringe, the plunger bounces back here
• Entry into epidural space → sudden loss of resistance — plunger collapses
• Entry through dura into CSF (spinal) → distinct "pop" or "give" — then free flow of CSF confirms correct placement

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1.3 Contents of the Epidural Space

• Loose fatty connective tissue — more abundant in lumbar region; absent at thoracic level (dura is closer to ligamentum flavum)
• Batson's venous plexus — an extensive network of valveless epidural veins. These are the vessels that produce bloody taps and intravascular catheter placement. They are engorged in pregnancy (by the gravid uterus compressing the IVC → blood diverts to Batson's plexus), increasing the risk of intravascular catheter placement in obstetric patients
• Lymphatics
• Spinal nerve roots in dural sleeves, exiting through the intervertebral foramina

• Lumbar: typically 4–6 cm in average adults
• Rule of thumb: 1 mm/kg body weight in children
• Ultrasound can measure this preoperatively and is increasingly used

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MODULE 2 — SPINAL ANAESTHESIA

2.1 What It Is

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2.2 Indications

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2.3 Contraindications

• Patient refusal
• Infection at injection site (local sepsis)
• Raised intracranial pressure (herniation risk from CSF pressure shift)
• Severe hypovolaemia (relative, but can precipitate catastrophic cardiovascular collapse)
• True allergy to local anaesthetic (rare but must ask)
• Coagulopathy / full anticoagulation (spinal haematoma risk)

• Anticoagulant therapy (follow ASRA timing guidelines — see later)
• Sepsis / bacteraemia (risk of haematogenous seeding of meninges)
• Fixed cardiac output states (severe aortic stenosis, hypertrophic cardiomyopathy) — cannot compensate for vasodilation
• Severe spinal deformity (scoliosis, prior spinal surgery)
• Pre-existing neurological disease (medicolegal — document carefully)
• Thrombocytopenia (platelet count < 70–80 × 10⁹/L — use judgement)
• Patient inability to cooperate

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2.4 Equipment for Spinal Anaesthesia

• Antiseptic solution (chlorhexidine or povidone iodine)
• Sterile drapes and gloves
• Introducer needle (18–19G, 2.5 cm)
• Spinal needle (see below)
• Syringe (5 mL) for local anaesthetic
• Drug, diluent
• Monitoring equipment running before you start

• Always use pencil-point (non-cutting) needles — Whitacre 25G or Sprotte 25–27G — as first choice to minimise PDPH
• A 25G Whitacre has PDPH rate < 1%; a 20G Quincke has PDPH rate 30–40%
• The bevel of a Quincke needle should be inserted parallel to dural fibres (dural fibres run longitudinally) — this minimises the hole size and PDPH risk
• An introducer (19G, 2.5 cm needle) is used to guide the fine spinal needle through skin and superficial tissues, preventing it from bending or carrying skin plugs into the subarachnoid space

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2.5 Positioning the Patient — Step-by-Step

• Patient on the edge of the operating table, back parallel to you
• Knees drawn up to chest ("fetal position")
• Neck flexed (chin to chest)
• Assistant helps the patient curl and maintain position
• Advantages: Patient comfort, easy to administer sedation, useful for unilateral spinal (hyperbaric solution + keep operative side down for 10 minutes)
• Note: In females, the hips are wider than the shoulders — the spine may slope downward toward the head; compensate by adjusting table tilt

• Patient sitting upright on the table edge, feet on footstool
• Arms over a pillow in the lap or around an assistant's neck
• Head down, chin to chest, shoulders relaxed, lower back "pushed out"
• Advantages: Midline is easier to identify (especially in obese or scoliotic patients); CSF flows back readily due to gravity
• Disadvantage: Vasovagal syncope; hypotension can occur before the block is even complete; needs a good assistant
• Ideal for: Saddle block (perineal/anal procedures) — inject hyperbaric solution and keep patient sitting for 5 minutes to pool block in the saddle area

• Rarely used; reserved for when surgery is performed in this position (rectal, perineal, lumbar procedures)
• Hypobaric local anaesthetic used (spreads to non-dependent = posterior structures)

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2.6 The Midline Technique — Step by Step

This is what you will be doing. Every step has a reason.

• Establish IV access (large bore)
• Attach monitors: SpO₂, NIBP, ECG
• Pre-load or co-load with IV crystalloid (500–1000 mL)
• Position patient as above
• Open sterile trolley, don sterile gloves, clean skin with chlorhexidine (allow to dry fully — at least 30 seconds — chlorhexidine is neurotoxic if injected intrathecally while wet)

• Palpate Tuffier's line (L4–L5)
• Choose L3–L4 or L4–L5 interspace (below the spinal cord)
• Mark with your thumbnail or a pen cap
• If you cannot identify by palpation (obesity, scoliosis, oedema) → use ultrasound pre-procedure to identify midline and interspace depth

• Raise a skin wheal with 1–2 mL lidocaine 1–2% at the insertion point
• Infiltrate deeper into the interspinous ligament — this reduces procedural pain

• 19G introducer needle inserted through skin and subcutaneous tissue at slight cephalad angle (10–15°) until it engages the interspinous ligament
• The introducer acts as a guide rail for the fine spinal needle

• Insert the 25–27G pencil-point needle through the introducer
• Advance slowly, bevel oriented parallel to dural fibres (longitudinal)
• You will feel distinct changes in tissue resistance:
  • Interspinous ligament: moderate resistance
  • Ligamentum flavum: firm resistance
  • A distinct "pop" or "click" as the needle penetrates the dura-arachnoid complex
• Remove the stylet → free flow of clear CSF confirms correct placement

• Look for clear, free-flowing CSF — it should drip steadily
• If no CSF: rotate the needle 90° (bevel may be against a nerve root), advance 1–2 mm, or try the contralateral side
• Aspirate gently 0.2–0.3 mL to confirm — then replace aspirated CSF is optional

• Attach the drug syringe
• Re-aspirate gently to confirm position maintained (see blood-tinged → abort)
• Inject slowly over 15–30 seconds
• Do NOT inject rapidly — rapid injection increases turbulence, unpredictable spread, and increases the risk of TNS (transient neurological symptoms)
• Some operators aspirate a small amount midway through injection ("barbotage") — not proven to be beneficial, not recommended routinely

• Remove the needle and introducer together
• Immediately position the patient for the desired block distribution
• Apply a small sterile dressing
• Reassess block height with ice or cold spray/pinprick at 3–5 minutes

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2.7 The Paramedian Approach

• Cannot access midline (severe arthritis, calcified interspinous ligaments, prior spinal surgery, obesity)
• Thoracic level spinal (where spinous processes overlap steeply)

• Entry point is 1–1.5 cm lateral to the midline at the cephalad edge of the lower spinous process
• Needle aimed medially and cephalad at approximately 10–15°
• Bypasses supraspinous and interspinous ligaments entirely — goes directly into ligamentum flavum, then directly to dura and subarachnoid space
• Resistance feels different: less firm than midline approach since you avoid the tough interspinous ligament; ligamentum flavum still gives the characteristic resistance

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2.8 Factors Determining Block Height — Master These

A. Baricity — The Most Controllable Factor

B. Dose (Amount of Drug)

C. Volume and Concentration

D. Patient Factors

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2.9 Local Anaesthetics Used in Spinal Anaesthesia

• Caesarean section: 10–12.5 mg (some centres use 7.5–9 mg with intrathecal opioids)
• Hip fracture repair: 10–12 mg (isobaric preferred by some — more predictable for unilateral block)
• TURP / lower abdominal: 7.5–10 mg
• Knee arthroscopy: 5–7.5 mg (± unilateral technique)

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2.10 Intrathecal Additives — Why and When

Opioids

• Allows dose reduction of local anaesthetic (less hypotension, less motor block)
• Synergistic analgesia at the dorsal horn
• Fentanyl 25 mcg IT dramatically improves quality and duration of caesarean section spinal without prolonging motor block

Clonidine

• α₂-agonist; intrathecal dose: 15–75 mcg
• Extends duration of both sensory and motor block
• Produces dose-dependent hypotension and sedation
• Prolongs analgesia postoperatively
• Used in ambulatory settings to extend block without prolonging discharge time (lower doses)

Epinephrine (Adrenaline)

• 0.1–0.2 mg intrathecally
• Prolongs spinal anaesthesia by causing local vasoconstriction (reduces local anaesthetic vascular uptake) and direct α₂ and β receptor-mediated spinal antinociception
• May cause TNS at higher doses
• Used less commonly now; largely superseded by intrathecal clonidine

Neostigmine

• Inhibits breakdown of acetylcholine at the spinal cord dorsal horn
• 25–100 mcg intrathecally
• Potent antinociception but significant nausea and vomiting limits routine use

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2.11 Physiological Effects of Spinal Anaesthesia — Understanding the Block

B fibres (autonomic preganglionic, myelinated) → FIRST BLOCKED
  ↓
C fibres (pain, temperature, autonomic — unmyelinated)
  ↓
Aδ fibres (pain, temperature, touch)
  ↓
Aβ fibres (touch, pressure, vibration)
  ↓
Aα fibres (motor, proprioception) → LAST BLOCKED

• A patient with sensory block to T8 may have sympathetic block to T4–T6
• The full haemodynamic consequence (hypotension, bradycardia) may exceed what the sensory level predicts
• A patient with sensory block to T10 may still have motor function preserved in the lower limbs — don't mistake residual motor power for block failure

1. Arterial vasodilation → ↓ SVR → ↓ MAP
2. Venodilation → ↓ venous return → ↓ preload → ↓ cardiac output
3. Cardiac accelerator fibres (T1–T4) blocked → bradycardia (in a high spinal)
4. Bezold-Jarisch reflex → severe bradycardia when right ventricular filling suddenly drops (empty, distended right ventricle sends parasympathetic signals → extreme bradycardia → cardiac arrest)

• Low-to-mid thoracic spinals → minor reduction in FRC, no significant respiratory compromise
• Block to T4 → intercostal muscle paralysis; patient breathes diaphragmatically, VC may fall 20%
• Total spinal (C3–C5 blocked) → diaphragm paralysed → apnoea — airway management emergency

• Sympathetic block → unopposed vagal tone → increased bowel motility, contracted bowel (good for surgeons in some cases)
• Nausea during spinal (especially with hypotension) — partially vagally mediated

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2.12 Complications of Spinal Anaesthesia

A. Hypotension (Most Common)

• Incidence: 15–33% generally; up to 80% in obstetric spinals without prophylaxis
• Mechanism: Sympathectomy → vasodilation + venodilation → ↓ preload + ↓ SVR
• Risk factors: High block level, hypovolaemia, elderly, sitting position at induction, aortic/mitral stenosis, pregnancy
• Treatment:
  • Vasopressor first line: Phenylephrine (pure α₁) is preferred in obstetrics — maintains uteroplacental perfusion without increasing HR. Dose: 50–100 mcg IV bolus; infusion 25–50 mcg/min
  • Ephedrine (α + β agonist): used if bradycardia accompanies hypotension — increases HR and BP; associated with more fetal acidosis in obstetrics
  • Noradrenaline: Increasingly used as infusion in obstetric spinal (1 mcg/mL)
  • IV fluid co-loading (not pre-loading) with crystalloid at time of spinal injection
  • Left lateral uterine displacement in pregnancy (at least 15° tilt)

B. Bradycardia and Cardiac Arrest

• High spinal blocks cardiac accelerator fibres (T1–T4) → vagally unopposed → severe bradycardia
• Bezold-Jarisch reflex: sudden reduction in venous return → reflex bradycardia
• Treatment: Atropine 0.3–0.6 mg IV; Ephedrine IV; Adrenaline (epinephrine) if arrest
• Rule of 5s for spinal cardiac arrest: Give Adrenaline 1 mg every 5 minutes, perform CPR (Trendelenburg position to increase venous return)

C. High/Total Spinal

• Definition: Block extending to cervical levels → respiratory paralysis, hypotension, loss of consciousness
• Causes: Excessive dose, accidental intrathecal injection of epidural dose, patient positioning error with hyperbaric solution
• Signs: Rapidly ascending block, dyspnoea, inability to speak, bilateral arm weakness, then unconsciousness and apnoea
• Management:
  1. Call for help immediately
  2. 100% O₂ by face mask
  3. Prepare to intubate (RSI if necessary)
  4. Aggressive vasopressor therapy (ephedrine/epinephrine)
  5. IV fluid bolus
  6. Keep calm — this is a temporary, self-limiting situation as local anaesthetic redistributes

D. Post-Dural Puncture Headache (PDPH)

• Classic presentation: Positional headache — worse when upright, relieved when supine — onset 24–48 hours after dural puncture, lasting days to weeks
• Mechanism: Persistent CSF leak through dural hole → low CSF pressure → traction on pain-sensitive intracranial structures when upright
• Risk factors: Young age, female sex, pregnancy, large needle gauge, cutting (Quincke) needle, multiple attempts, perpendicular bevel orientation
• Prevention: Use 25–27G pencil-point (Whitacre/Sprotte) needles — the single most important intervention

E. Transient Neurological Symptoms (TNS)

• Description: Severe aching or shooting pain in buttocks and legs radiating to feet; onset 6–24 hours after resolution of spinal block
• Incidence: Lidocaine (highest — up to 40%), prilocaine (low), bupivacaine (very low < 1%)
• Risk factors: Lithotomy position, ambulatory patients, concentrated lidocaine (5%)
• Treatment: NSAIDs; self-limiting, resolves within days
• Lesson: This is why 5% hyperbaric lidocaine has been largely abandoned in favour of bupivacaine and prilocaine for spinal

F. Spinal Haematoma

• Rare but catastrophic — spinal cord compression → permanent paralysis
• Risk factors: Anticoagulation, thrombocytopenia, traumatic insertion
• Presentation: Back pain after resolution of block, followed by return of motor weakness (permanent, not the normal wearing off)
• Diagnosis: Urgent MRI
• Treatment: Immediate neurosurgical decompression within 6–12 hours (outcomes worsen dramatically with delay)
• ASRA Guidelines (key anticoagulant timings for neuraxial):

G. Meningitis and Infection

• Septic meningitis: Haematogenous seeding or contamination — Streptococcus or Staphylococcus; strict aseptic technique prevents this
• Chemical (aseptic) meningitis: Contamination from antiseptics (chlorhexidine — must be dry before injection), detergents, preservatives in drugs
• Cauda equina syndrome: Neurotoxicity from maldistribution of concentrated local anaesthetic (continuous microcatheter spinals with concentrated lidocaine) — irreversible bowel/bladder dysfunction

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MODULE 3 — EPIDURAL ANAESTHESIA

3.1 What It Is and Why It Differs from Spinal

• Larger volume of drug needed (10–20 mL vs. 2–3 mL for spinal)
• Slower onset (10–20 minutes vs. 3–5 minutes)
• More controllable — catheter allows titration, top-ups, and prolonged use
• Can be segmental — a thoracic epidural blocks only thoracic levels, leaving cervical and lumbar roots intact
• Motor block is titrable — dilute solutions produce sensory-only (differential) block, useful for labour analgesia
• Septa in the epidural space can cause patchy or unilateral blocks (explains some failures)

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3.2 Equipment

• Blunt, curved (Hustead) tip — does not cut the dura easily if it inadvertently touches it
• Huber point — the tip curves cephalad, directing the catheter cephalad when inserted
• Markings at 1 cm intervals from the tip to guide depth

• 10 mL syringe filled with saline (or air) — used to detect loss of resistance as needle enters epidural space
• Glass syringes have lower friction and give better tactile feedback

• Standard catheter is soft, radio-opaque, graduated in cm
• Multi-orifice (3 holes at tip) > single-orifice for drug distribution and less chance of complete vascular cannulation
• Inserted 3–5 cm into the epidural space — no more than 5 cm (risk of lateralisation, coiling, vascular/intrathecal migration)

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3.3 Patient Positioning

• Spinal cord moves anteriorly in lateral position with flexion → away from the ligamentum flavum → larger epidural space at the posterior aspect
• Better patient cooperation

• Better midline identification in obese patients
• Higher risk of vasovagal episode

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3.4 Standard Lumbar Epidural Technique — Step by Step

• Large bore IV access established and running
• Monitoring in place (NIBP every 2–3 minutes, SpO₂, ECG)
• Vasopressors drawn up and ready (ephedrine 6 mg/mL, phenylephrine 100 mcg/mL)
• Resuscitation equipment immediately available (airway, drugs, defibrillator)
• Patient positioned (lateral decubitus or sitting)
• Sterile preparation and draping

• 3–5 mL lidocaine 1% into skin and subcutaneous tissue down to interspinous ligament
• Generous infiltration makes the procedure significantly more comfortable and reduces patient movement

• Insert needle in midline at slight cephalad angle (10–15° at lumbar level)
• Advance through skin, subcutaneous tissue, supraspinous ligament
• Attach LOR syringe filled with 2–3 mL saline (with or without a small air bubble)
• Feel the firm, gritty resistance of the ligamentum flavum
• Advance millimetre by millimetre with continuous or intermittent thumb pressure on the syringe plunger
• At the ligamentum flavum, the plunger bounces back (resists injection)

• As the needle tip exits the ligamentum flavum into the epidural space:
  • Plunger suddenly collapses (with continuous pressure technique)
  • Plunger freely compresses without bounce-back (intermittent technique)
• Stop advancing immediately — over-advancement perforates the dura

• Saline: More popular; does not compress into the space (no compressible bubble artifact on ultrasound if needed); associated with slightly fewer PDPHs in some studies
• Air: Simpler, makes accidental dural puncture immediately visible (bubbles in CSF return if dura punctured); but: > 2–3 mL of epidural air can cause incomplete blocks, pneumocephalus if intrathecal, and subcutaneous emphysema

• Place a drop of saline at the needle hub
• As the needle enters the thoracic epidural space, the negative intrapleural pressure is transmitted → drop is sucked in
• More reliable at thoracic level (where epidural pressure is more negative) than lumbar level
• Not a standalone technique — always confirm with LOR as well

• Thread epidural catheter through the Tuohy needle
• Insert 3–5 cm beyond the needle tip (if needle is at 5 cm depth and catheter enters at 5 cm marker on catheter = tip is at the needle tip; advance to 8–10 cm on the catheter to leave 3–5 cm in the epidural space)
• Never withdraw the catheter through the needle — the Huber tip can shear off the catheter
• If catheter won't advance: rotate needle 90°, slightly withdraw the needle, try again
• Withdraw the needle over the catheter carefully
• Confirm no blood or CSF aspirates from catheter — if blood, withdraw 1 cm and recheck; if CSF aspirates throughout, you are intrathecal

• Tape securely to the back (loop the catheter under the patient's arm around to the front)
• Place a yellow epidural label on the catheter and connection
• Never connect to IV tubing (wrong route error prevention)

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3.5 Identifying the Epidural Space — The LOR in Detail

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3.6 The Epidural Test Dose

• The adrenaline (15 mcg in 3 mL) causes an increase in heart rate of ≥ 20 bpm within 30–60 seconds if injected intravascularly
• Also: tinnitus, metallic taste, circumoral numbness from the lidocaine component
• Limitation: In laboring women under β-blockade, tachycardia may be blunted — use clinical judgment; watch for subjective symptoms too

• 3 mL of 1.5% lidocaine = 45 mg lidocaine intrathecally → produces a dense motor block at the lower limbs within 3–5 minutes
• Ask the patient: "Can you feel/move your legs?" — sudden inability indicates inadvertent intrathecal placement
• If intrathecal: you have effectively performed a spinal — manage accordingly (convert to spinal technique or use as labour analgesia dose)

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3.7 Thoracic Epidural — Special Considerations

• Spinous processes at T5–T9 are steeply angled caudad → they overlap like roof tiles → the interlaminar window is much smaller and the needle must be angled 30–50° cephalad
• The epidural space is narrower at the thoracic level (< 3–4 mm)
• The dura is immediately behind the ligamentum flavum with minimal epidural fat → accidental dural puncture is easier
• The cord (not just cauda equina) is present at thoracic levels → dural puncture carries spinal cord injury risk

• Major thoracic surgery (thoracotomy, oesophagectomy)
• Major upper abdominal surgery (open hepatectomy, Whipple, aortic surgery)
• Rib fractures / chest trauma (superior to systemic opioids for respiratory function)
• Postoperative pain management where a high dermatomal band of analgesia is needed

• The catheter tip should be at the midpoint of the surgical incision's dermatomes
• For thoracotomy at T6–T7 incision → catheter at T6
• For upper laparotomy (T6–T10 incision) → catheter at T7–T8
• The paramedian approach is often preferred at the thoracic level — the steep spinous processes make midline access very difficult at T5–T9

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3.8 Epidural Drugs and Dosing

Local Anaesthetics

• Lumbar (surgical): 15–25 mL of 0.5% bupivacaine or 0.75% ropivacaine
• Labour analgesia: 10–15 mL of 0.1% bupivacaine + fentanyl 2 mcg/mL
• Thoracic epidural infusion: 5–10 mL/h of 0.1–0.2% ropivacaine ± fentanyl

Epidural Opioids

• Improve block quality
• Reduce local anaesthetic dose (reduce motor block and hypotension)
• Extend duration of postoperative analgesia

Additives to Epidural Solutions

• Adrenaline 1:200,000 (5 mcg/mL): Added to reduce vascular absorption, prolong block, and serve as a marker for intravascular injection. Improves block quality.
• Clonidine 1–2 mcg/mL: Prolongs epidural analgesia; may cause hypotension and sedation at higher doses
• Sodium bicarbonate: Alkalinises solution, ↑ proportion of un-ionised drug → faster onset (particularly useful with lidocaine)

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3.9 Complications of Epidural Anaesthesia

A. Dural Puncture ("Wet Tap")

• Incidence with Tuohy needle: ~0.5–1.5% in experienced hands
• Recognition: CSF flowing freely from the needle hub; LOR syringe fills with clear fluid
• Consequence: Near-certain severe PDPH (Tuohy needle is 17–18G — very large hole in dura)
• Options:
  1. Re-site epidural at adjacent level and insert catheter carefully
  2. Deliberate intrathecal catheter placement — place the epidural catheter intrathecally as a continuous spinal catheter (use with very small doses, clearly label, intensive monitoring, manage PDPH with EBP when catheter removed)
  3. Prophylactic epidural blood patch (controversial; some evidence supports it)

B. Intravascular Injection / Catheter Migration

• Batson's venous plexus is rich — epidural catheters can enter vessels even after initially correct placement
• Prevention: Aspirate before every bolus, fractionate doses, use test dose
• Consequence of IV injection of epidural dose (15–20 mL of 0.5% bupivacaine):
  • CNS: perioral tingling, tinnitus, metallic taste → confusion → seizures
  • Cardiovascular: ventricular arrhythmias, bradycardia, cardiac arrest (bupivacaine "sodium channel lockout" — very difficult to resuscitate)
  • Treatment of LA systemic toxicity (LAST): Lipid Emulsion Rescue — Intralipid 20% bolus 1.5 mL/kg IV, then infusion 0.25 mL/kg/min

C. Hypotension

• Slower and more predictable than spinal hypotension (can titrate)
• More easily prevented by co-loading and phenylephrine infusion in obstetrics
• Treatment: same as for spinal (phenylephrine, ephedrine, IV fluids)

D. High or Total Spinal from Accidental Intrathecal Injection

• If full epidural dose is given intrathecally → total spinal
• Risk: rapid deterioration, apnoea, cardiovascular collapse
• Management: Airway control (RSI), vasopressors, supportive care

E. Inadequate / Patchy Block

• One-sided block: Catheter lateralised; connective tissue septa in epidural space
• Window (missed segment): Septa preventing complete spread
• Solutions: Withdraw catheter 1 cm, reposition patient, top-up with larger volume, add different drug, re-site

F. Spinal Haematoma

• Same risk factors and management as for spinal haematoma
• Slightly higher risk with epidural catheter (more traumatic; catheter may damage vessels on manipulation)
• Monitor: unexpected return of motor deficit after resolution of block → urgent MRI

G. Epidural Abscess

• Rare but catastrophic
• Presents: back pain, fever, leukocytosis, then neurological deficit (days to weeks after catheter removal)
• Risk factors: immunosuppression, diabetes, prolonged catheter use, poor asepsis
• Diagnosis: MRI
• Treatment: urgent surgical drainage + antibiotics; outcome depends entirely on speed of diagnosis

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MODULE 4 — COMPARISON TABLE: SPINAL vs. EPIDURAL AT A GLANCE

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MODULE 5 — COMBINED SPINAL-EPIDURAL (CSE)

• Spinal for immediate, dense onset
• Epidural catheter for prolonged use, titration, and rescue

1. Identify epidural space with Tuohy needle (LOR as usual)
2. Pass a long (120–130 mm) 25–27G pencil-point spinal needle through the Tuohy needle
3. Advance until a "click" confirms dural puncture — free CSF flow
4. Inject intrathecal dose (often reduced — 7.5–9 mg bupivacaine for CS + fentanyl 15–25 mcg)
5. Remove spinal needle
6. Thread epidural catheter as normal
7. Use epidural for top-up if spinal wears off or block is inadequate

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MODULE 6 — THE PROFESSOR'S CLINICAL SCENARIOS

1. Call for help
2. 100% O₂
3. Trendelenburg or leg elevation (increases venous return)
4. Atropine 0.3–0.6 mg IV (for bradycardia)
5. Ephedrine 6–12 mg IV (α + β) — raises both HR and BP
6. Epinephrine (adrenaline) 10–100 mcg IV if not responding — do not hesitate
7. IV fluid bolus 500 mL
8. Be prepared to intubate if consciousness deteriorates

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1. Stop all local anaesthetic immediately
2. Call for emergency help, obstetric team
3. 100% O₂ face mask, airway management ready
4. If seizures: midazolam 1–2 mg IV or propofol 0.5–1 mg/kg to terminate (brief)
5. Intralipid 20% — 1.5 mL/kg bolus IV (lipid sink — binds circulating bupivacaine)
6. Continue Intralipid infusion 0.25 mL/kg/min
7. If cardiac arrest: CPR + Intralipid + avoid vasopressin, calcium channel blockers, beta blockers (can worsen); use adrenaline in lower doses than standard (1–10 mcg/kg)
8. Prolonged resuscitation — ECMO if available if refractory

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1. Confirm diagnosis: Positional test — severe when upright, relieved within 30 minutes supine
2. Conservative first (24–48 h): Bed rest, oral/IV hydration, paracetamol, NSAIDs, caffeine (300 mg oral bd or IV)
3. If not resolving → Epidural Blood Patch (EBP):
   • Under strict aseptic conditions, re-perform epidural at same or adjacent level
   • Draw 15–20 mL of autologous blood from the patient's arm (IV cannula)
   • Inject slowly into epidural space — patient will feel back pressure and may feel leg paraesthesia when 10–15 mL in
   • Blood clot tamponades the dural hole; CSF pressure rises immediately
   • Success: 70% complete relief with first EBP; 90–95% after second EBP
4. Severe PDPH with focal neurology or other features → MRI to exclude subdural haematoma (extremely rare but can occur from bridging vein tear under low CSF pressure)

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SUMMARY: THE RESIDENT'S MENTAL FRAMEWORK

NEURAXIAL ANAESTHESIA — CORE FRAMEWORK

ANATOMY           TECHNIQUE          PHARMACOLOGY      COMPLICATIONS
─────────         ─────────          ────────────      ────────────
Know your layers  Spinal:            Local anaesthetic Hypotension
  Supraspinous    25G Whitacre       Bupivacaine 0.5%  Bradycardia
  Interspinous    Lateral/sitting    Hyperbaric        High/total spinal
  Lig. flavum     L3-4, L4-5        Ropivacaine       PDPH
  Epidural space  Clear CSF = good  Levobupivacaine   Spinal haematoma
  Dura                               Prilocaine        LA toxicity
  Subarachnoid    Epidural:                            TNS
                  18G Tuohy needle   Intrathecal add:  Epidural abscess
Tuffier's line    LOR with saline    Fentanyl 25 mcg
= L4-L5           Test dose ALWAYS   Morphine 0.1 mg
                  3cm catheter in    Clonidine 30 mcg
Cord ends L1-2   Fractionate doses
  Below = safe
                  ASRA timings       Order of block:
                  for anticoagulants Autonomic > Pain
                  are MANDATORY      > Motor (highest)
                  check before every Sympathetic
                  neuraxial block    +2-6 levels above
                                     sensory

1. Know your anatomy before you pick up the needle — feel it in your mind before you feel it with your hands
2. Test dose before every epidural bolus — no exceptions, ever
3. Haematoma after neuraxial = urgent MRI and neurosurgery call — do not wait to see if "the block is just wearing off slowly"

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