10 questions · 100 marks · Model answers with cited sources, key points, exam tips & extra-marks content.
Post Dural Puncture Headache (PDPH) – Clinical features, preventive strategies, recent guidelines for management
PDPH is a positional headache occurring after intentional or accidental dural puncture, caused by CSF leak through the dural hole leading to intracranial hypotension and traction on pain-sensitive intracranial structures.
Spinal anaesthesia with 25G Quincke: 1–2%. Accidental dural puncture (ADP) with 16–18G Tuohy epidural needle: 50–80% develop PDPH.
- Onset: 12–48 hours after dural puncture (rarely immediate)
- Character: Bilateral, frontal-occipital, dull-throbbing
- Postural: Worse on sitting/standing, relieved within 15–30 min of lying flat — PATHOGNOMONIC
- Associated: Neck stiffness, photophobia, phonophobia, diplopia (CN VI palsy — most common cranial nerve affected), tinnitus
- Duration: Untreated — resolves in 7–10 days spontaneously (most cases)
IHS diagnostic criteria: Headache within 5 days of LP, bilateral, postural (worsens within 15 min of sitting/standing, improves within 30 min of lying), plus at least one of: neck stiffness, tinnitus, hypacusia, photophobia, nausea.
- Use pencil-point (atraumatic) needles: Whitacre, Sprotte — reduce PDPH vs cutting Quincke needles (NNT ~13 vs 25G Quincke)
- Smallest gauge possible: 25–27G reduces incidence vs 22G
- Bevel of Quincke parallel to dural fibres (longitudinal insertion) — reduces dural fibres cut
- Minimise epidural needle passes
- If ADP occurs: consider intrathecal catheter placement at same level (reduces PDPH incidence)
- No proven benefit of prophylactic epidural blood patch
- Cosyntropin (ACTH analogue): May reduce PDPH — limited evidence
- Caffeine perioperatively: Not proven prophylactic
- Bed rest: Temporary relief only — does NOT speed recovery
- Adequate hydration: IV/oral — prevents further CSF depletion
- Simple analgesics: Paracetamol, NSAIDs
- Caffeine 300–500 mg oral/IV: Cerebral vasoconstriction — reduces headache. Effect lasts 4–6 hours. Give with caution in breastfeeding.
- Theophylline: Similar mechanism to caffeine — second choice
Injection of 15–20 mL autologous blood into the epidural space at the level of ADP. Blood spreads cranially and caudally, seals the dural hole.
Wait 24–48 hours after ADP (spontaneous improvement possible; early patch may fail). ACOG/SOAP guidelines: offer at any time if symptoms severe.
90% relief after first patch; 96–98% after second. Gold standard treatment.
Fever, sepsis, coagulopathy, patient refusal
Strict asepsis, same or adjacent level, inject slowly, patient supine for 1–2 hours post-procedure
- Sphenopalatine ganglion block: Intranasal or lateral approach. Provides rapid temporary relief. Non-invasive.
- Greater occipital nerve block
- Sumatriptan: 5-HT agonist — limited evidence
- ACTH (cosyntropin) IV: May stimulate CSF production and aldosterone
SOAP (Society for Obstetric Anaesthesia and Perinatology) 2024 consensus: (1) Pencil-point needles recommended. (2) Intrathecal catheter after ADP preferred over re-siting. (3) EBP remains gold standard — offer within 24–48h if not improving. (4) Sphenopalatine ganglion block as non-invasive alternative.
- Postural nature (relief on lying) is pathognomonic of PDPH
- CN VI (abducens) palsy is most common cranial nerve complication
- Epidural blood patch: 15–20 mL, >90% success, wait 24–48h
- Whitacre/Sprotte needles reduce PDPH vs Quincke — always use pencil-point in obstetrics
- Saying bed rest treats PDPH — it only provides temporary symptomatic relief
- Forgetting that ADP with Tuohy needle (16G) causes PDPH in 50–80% — far higher incidence than spinal
- Not mentioning intrathecal catheter as a preventive option after ADP
SOAP 2024 guidelines are fresh — mentioning them with specific recommendations will earn extra examiner marks. Know: intrathecal catheter after ADP, and SPG block as new non-invasive option.
- Intrathecal catheter after ADP: Threading a catheter through the Tuohy needle after ADP and leaving it for 24h — reduces PDPH (meta-analysis: OR 0.46). Mechanism unclear — possibly seals hole with catheter, or CSF leak from catheter reduces pressure differential.
- Subdural haematoma: Rare but life-threatening complication of PDPH — intracranial hypotension → tearing of bridging veins. Suspect if postural headache becomes non-postural or altered consciousness develops.
- SPG (Sphenopalatine ganglion) block: Intranasal lidocaine-soaked pledget application to SPG. 80% short-term relief in trials (Cohen et al. 2017). Advantage: non-invasive, rapid, can be repeated.
- Fibrin glue patch: Alternative to blood patch in patients with coagulopathy or needle-track infections. Used off-label.
A) LAST (Local Anaesthetic Systemic Toxicity) B) Role of Xenon in Anaesthesia
LAST — Local Anaesthetic Systemic Toxicity
LAST is a potentially life-threatening complication from excessive plasma levels of local anaesthetic (LA) due to inadvertent intravascular injection, rapid absorption, or overdose.
~1 in 1000 regional blocks. Higher with bupivacaine > ropivacaine > lidocaine.
High plasma LA → blocks cardiac Na+ channels (↓ conduction, re-entry, VF) + CNS Na+ channels (initial stimulation → seizures → CNS depression) + cardiac K+ and Ca2+ channels (bupivacaine uniquely).
- Early (excitatory): Circumoral tingling, metallic taste, tinnitus, lightheadedness, restlessness, agitation
- Late (inhibitory): Seizures, coma, respiratory arrest
- Hypotension, conduction abnormalities (PR prolongation, wide QRS)
- Ventricular arrhythmias (VT, VF)
- Cardiovascular collapse — most severe with bupivacaine ('cardiac toxicity disproportionate to CNS toxicity')
With ultrasound guidance and test doses, CNS signs may be absent — patient may present directly with cardiovascular collapse.
- STOP LA injection immediately
- Call for help
- 100% O2, airway management, IV access
Benzodiazepines first (midazolam 2–5 mg IV). Propofol if unavailable — but avoid in cardiovascular compromise (causes hypotension).
- CPR if cardiac arrest — prolonged resuscitation may be needed
- Amiodarone for arrhythmias (avoid lidocaine, phenytoin in LA toxicity)
- Avoid vasopressin, beta-blockers, calcium channel blockers
Intralipid 20%
Lipid sink — sequesters hydrophobic LA molecules away from cardiac tissues. Also direct cardiac metabolic support.
Bolus: 1.5 mL/kg IV over 1 min. Then infusion: 0.25 mL/kg/min. Repeat bolus x2 for persistent arrest. Max 10 mL/kg over 30 min.
ACLS should continue throughout. Have Intralipid available wherever regional anaesthesia is performed.
If refractory cardiac arrest — ECMO/CPB. Arrange early.
- Ultrasound guidance for all nerve blocks
- Aspirate before each injection
- Fractionated injection (3–5 mL aliquots with pauses)
- Test dose: Adrenaline 15 mcg (1:200,000) — tachycardia within 20–30 sec if intravascular
- Use minimum effective dose and volume
- Avoid bupivacaine 0.75% in obstetrics (FDA ban since 1983)
Xenon in Anaesthesia
- Noble gas — colourless, odourless, non-flammable
- MAC: 71% (requires hyperbaric conditions or combination for surgical anaesthesia alone)
- Blood:gas partition coefficient: 0.115 (lower than N2O — extremely rapid onset and offset)
- Molecular weight: 131 Da
Primarily NMDA receptor antagonist. Also inhibits AMPA, kainate receptors. TREK-1 two-pore domain K+ channel activation (↓ excitability).
- Rapid onset and offset (extremely low solubility)
- No cardiovascular depression — maintains HR, BP, CO
- Analgesic properties (NMDA antagonism)
- No metabolism — 100% excreted unchanged via lungs
- Neuroprotective (NMDA antagonism, ischaemic preconditioning)
- Minimal PONV
- No teratogenicity
- No malignant hyperthermia trigger
- Extremely expensive (rare — atmospheric concentration 0.087 ppm)
- Requires closed-circuit rebreathing system (cannot waste xenon)
- MAC 71% — cannot use as sole agent at 1 atm without supplementation
- Expands gas-filled spaces (like N2O but less soluble — less diffusion hypoxia)
- No muscle relaxation
- Special xenon delivery systems required
- Neonatal hypoxic-ischaemic encephalopathy (neuroprotection trials)
- Cardiac surgery (cardioprotection)
- Limited adult anaesthesia — Sequoia system (commercially available in Europe)
GWP = 0. No ozone depletion. Truly 'green' anaesthetic agent.
- LAST: CNS features first, then cardiac. Bupivacaine — cardiac disproportionate to CNS.
- Intralipid 20%: 1.5 mL/kg bolus → 0.25 mL/kg/min infusion. Max 10 mL/kg.
- Xenon: NMDA antagonist, MAC 71%, GWP=0, most expensive anaesthetic
- Test dose for LAST prevention: Adrenaline 15 mcg — tachycardia in 20–30s if intravascular
- Using propofol for seizures in LAST when patient is haemodynamically compromised
- Forgetting to call for Intralipid early — it should be the first specific treatment
- Saying xenon is commercially widely available in India — it is not, only used in research/Europe
AAGBI LAST guidelines (2023 update): Draw the LAST management algorithm — Stop LA, call help, 100% O2, treat seizures, treat arrest, give Intralipid. Examiners want to see the algorithm, not just prose.
- Lipid emulsion mechanism controversy: 'Lipid sink' is accepted. 'Lipid shuttle' theory: lipids transport LA to metabolic organs (liver, heart) for detoxification.
- Why bupivacaine is most cardiotoxic: 'Fast-in, slow-out' kinetics for cardiac Na+ channels (unlike lidocaine: 'fast-in, fast-out'). Bupivacaine dissociates slowly → cumulative block → VF. This is why levobupivacaine and ropivacaine (S-enantiomers) are less cardiotoxic.
- Xenon neuroprotection: TOOXI trial (2013) — xenon + hypothermia in neonatal HIE showed feasibility. CoolXenon2 trial ongoing. Mechanism: NMDA antagonism reduces excitotoxicity after HIE.
- LAST in liposuction (tumescent anaesthesia): Very large volumes of dilute lidocaine (35 mg/kg with adrenaline) — peak plasma levels at 8–12 hours post-procedure. Late LAST is a recognised risk.
COPD — Anaesthetic implications and perioperative management
COPD is a common, preventable, and treatable disease characterised by persistent respiratory symptoms and airflow limitation due to airway and alveolar abnormalities, usually caused by significant exposure to noxious particles or gases (GOLD guidelines 2024).
- Exercise tolerance (METs, 6-minute walk test, flight of stairs)
- Baseline SpO2 on room air
- Frequency of exacerbations (>2/year = severe)
- Current medications (bronchodilators, steroids, theophylline, O2 therapy)
- Smoking history (pack-years) — smoking cessation ≥8 weeks before elective surgery
- Spirometry: FEV1/FVC <0.7 confirms obstruction. FEV1% predicted: >80% mild, 50–80% moderate, 30–50% severe, <30% very severe.
- ABG: Hypercapnia (PaCO2 >45) = significant CO2 retention — hypoxic drive possible
- CXR: Hyperinflation, bullae, flattened diaphragm
- ECG: Right heart strain, P pulmonale, right axis deviation
- Echo: Cor pulmonale, pulmonary hypertension
- Smoking cessation — ideally >8 weeks (reduces secretions, improves mucociliary function)
- Bronchodilators: Continue LABAs, LAMAs, ICS perioperatively
- Treat active infection if present
- Physiotherapy: Incentive spirometry, breathing exercises
- Nutritional support if malnutrition (COPD associated with wasting)
- Steroids: Short course oral prednisolone 40 mg for 5 days if FEV1 <50% or recent exacerbation
- Regional > GA wherever possible (avoids airway manipulation, postoperative respiratory depression)
- If GA required: avoid triggers of bronchospasm
- Propofol: Bronchodilatory — preferred induction agent
- Avoid thiopentone (bronchospasm risk)
- Ketamine: Bronchodilatory — good alternative
- Thorough preoxygenation: FRC reduced → faster desaturation
- LMA preferred over ETT where possible (less airway stimulation)
- If ETT needed: deep anaesthesia or lidocaine 1.5 mg/kg IV before intubation to obtund reflexes
- Salbutamol nebuliser preoperatively
- Pressure-controlled ventilation preferred (gentler, maintains low Paw)
- Low RR (8–12/min), high tidal volume (8–10 mL/kg) to allow complete expiration
- Prolonged expiratory time: I:E ratio 1:3 or 1:4 (prevents dynamic hyperinflation)
- Allow permissive hypercapnia — do NOT hyperventilate COPD
- Avoid PEEP unless intrinsic PEEP (auto-PEEP) management required
- Target SpO2 88–92% (not 98–100%) to avoid hypercapnia and maintain hypoxic drive in some
SpO2 88–92% intraoperatively and postoperatively (BTS guidance) — unnecessary hyperoxia suppresses drive, worsens V/Q mismatch.
- High-dose opioids (respiratory depression)
- Atracurium (histamine release — bronchospasm)
- NSAIDs in aspirin-exacerbated respiratory disease (AERD)
- Extubate awake — adequate reversal confirmed by TOF ratio ≥0.9
- Sitting up position — improves FRC
- Bronchodilators via nebuliser
- Multimodal analgesia: Thoracic epidural (for thoracic/abdominal surgery), PCA with low opioids, NSAIDs if not contraindicated
- Physiotherapy and early mobilisation
- HDU/ICU if FEV1 <50% or preoperative hypercapnia
- NIV: If PaCO2 rising post-op — CPAP/BiPAP rather than re-intubation
- FEV1/FVC <0.7 = obstructive; FEV1 <30% predicted = very severe
- I:E ratio 1:3 to 1:4 — allow complete expiration, prevent auto-PEEP
- SpO2 target 88–92% NOT 98–100% in COPD
- Propofol and ketamine are bronchodilatory — prefer over thiopentone
- Targeting SpO2 100% in COPD — causes hypercapnia and worsened outcomes
- Using I:E ratio 1:2 (normal) in COPD — causes dynamic hyperinflation
- Forgetting to continue all COPD medications on the morning of surgery
GOLD 2024 classification is examiners' favourite — quote it with FEV1% predicted values. Always mention smoking cessation ≥8 weeks and its physiological benefits.
- Auto-PEEP (intrinsic PEEP, iPEEP) in COPD: Incomplete expiration leads to gas trapping and elevated end-expiratory alveolar pressure. Detected by expiratory hold manoeuvre on ventilator. Managed by: ↓ RR, ↑ expiratory time, extrinsic PEEP (75% of iPEEP level).
- Smoking cessation timing: 8 weeks reduces sputum and airway reactivity. 12–24 months needed to reduce pulmonary complications. Nicotine is eliminated in 48h — no need to wait. Carbon monoxide half-life 4–6h — 12–24h cessation already improves COHb and O2 delivery.
- Hypoxic vasoconstriction and O2 therapy: In type B COPD (chronic hypercapnia), hyperoxia causes Haldane effect (O2 displaces CO2 from Hb) and removes hypoxic drive — progressive hypercapnia. Titrated O2 is essential.
- Prehabilitation: 4–8 weeks of supervised exercise training in COPD before major surgery reduces post-op respiratory complications (evidence from Gillis 2019 systematic review).
Blood Loss – Definition of ABL, calculation of ABL, intraoperative estimation of blood loss
Allowable Blood Loss (ABL) is the maximum volume of blood that can be lost before a blood transfusion becomes necessary to maintain adequate oxygen-carrying capacity and tissue oxygenation. It defines the 'trigger' point for transfusion.
ABL = EBV × (H0 – Hmin) / H0
- EBV = Estimated Blood Volume
- H0 = Starting haematocrit
- Hmin = Minimum acceptable haematocrit (typically 0.21–0.24 in healthy adults; 0.28–0.30 in IHD, elderly, obstetric)
- Premature neonate: 95 mL/kg
- Full-term neonate: 85 mL/kg
- Infant: 80 mL/kg
- Child: 70–75 mL/kg
- Adult male: 70–75 mL/kg
- Adult female: 65–70 mL/kg
- Obese adult: 55–65 mL/kg (use lean body weight)
70 kg male, H0 = 0.42, Hmin = 0.21. EBV = 70 × 70 = 4900 mL. ABL = 4900 × (0.42–0.21)/0.42 = 4900 × 0.5 = 2450 mL.
Gravimetric (weighing)
Weigh surgical sponges, towels before and after use. Difference in weight ≈ volume of blood (1g ≈ 1mL). Most accurate method for sponge blood. Count number of soaked swabs: fully soaked 4×4 gauze ≈ 10 mL; laparotomy pad ≈ 100–150 mL.
Colorimetric spectrophotometry
Wash blood from drapes into known volume of fluid → measure haemoglobin concentration by spectrometry → back-calculate blood volume. Most accurate overall but time-consuming.
Suction canister measurement
Volume in suction canister minus volume of irrigation fluid used. Underestimates as blood on drapes, floor not counted.
Visual estimation
Clinician estimate. Consistently inaccurate — underestimates by 30–50%. Standard deviation large. Not recommended as sole method.
Haematocrit/Haemoglobin method
Serial intraoperative Hb/Hct. Fall in Hb from baseline reflects blood loss once equilibration occurs. Disadvantage: delayed — Hb equilibrates over hours.
Calculated blood loss formula
CBL = EBV × (H1–H2)/Haverage. Gives blood loss between two time points. Useful in controlled surgical stages.
- Hb <7 g/dL: Transfuse in most patients (TRICC trial threshold)
- Hb <8 g/dL: Transfuse in cardiac surgery, severe IHD, elderly
- Hb <10 g/dL: Only if active myocardial ischaemia or severe symptoms
Tachycardia, hypotension, ST changes on ECG, lactate >2 — signs of inadequate O2 delivery despite Hb >7 → transfuse
- ABL = EBV × (H0 – Hmin) / H0 — memorise formula and normal EBV values
- Gravimetric: most practical intraoperative method
- Visual estimation underestimates by 30–50% — never rely on this alone
- TRICC trial: Hb <7 g/dL restrictive strategy non-inferior to liberal (Hb <10)
- Using total body weight for EBV in obese patients — use lean body weight
- Forgetting to subtract irrigation volume from suction canister
- Using Hb as sole transfusion trigger — clinical signs and context equally important
Always work through a clinical example of ABL calculation in the exam — 70 kg male is the standard question. Show formula, plug in numbers, state answer in mL.
- Patient Blood Management (PBM): WHO-endorsed 3-pillar approach: (1) Optimise preoperative anaemia, (2) Minimise iatrogenic blood loss, (3) Harness physiological tolerance of anaemia. Reduces transfusion rates by 30–40% (Althoff 2019 meta-analysis).
- Intraoperative cell salvage (ICS): Collects shed blood, washes, centrifuges, returns packed RBCs to patient. Reduces allogeneic transfusion. Contraindicated: bowel contamination, malignancy (relative), infection.
- TACO vs TRALI: TACO (Transfusion-Associated Circulatory Overload) — cardiogenic pulmonary oedema post-transfusion. TRALI — non-cardiogenic, antibody-mediated. TACO now more common than TRALI as leading transfusion death.
- Near-infrared spectroscopy (NIRS): Non-invasive real-time tissue oxygenation monitoring. Cerebral oximetry (rSO2) may guide transfusion decisions in cardiac and vascular surgery.
A) Epidural Dural Puncture B) Jugular Venous Oximetry
Epidural Dural Puncture (Accidental/Intentional)
Inadvertent puncture of the dura during epidural needle placement, resulting in CSF flow through a Tuohy needle (16–18G hole). Incidence: 0.5–2% of epidural placements.
- CSF flow through Tuohy needle — copious, clear, warm, glucose-positive
- Loss of resistance suddenly becomes very easy
- Wet tap confirmed: temperature (warm vs saline), glucose dipstick positive in CSF
- Remove needle — do NOT proceed at same level (risk of subarachnoid injection if epidural dose given)
- Inform patient immediately (duty of candour)
- Options: (1) Place epidural at adjacent level, (2) Thread catheter intrathecally
Threading 20G catheter through the Tuohy needle into the subarachnoid space and using as an intrathecal catheter.
Reliable CSF block, can use for further doses, may reduce PDPH (catheter mechanically reduces CSF leak)
Accidental high spinal if epidural doses are given — MUST label catheter CLEARLY as intrathecal. Use subarachnoid doses only.
Remove after 24 hours.
Deliberate dural puncture as part of a technique (combined spinal-epidural, dural puncture epidural — DPE).
Dural Puncture Epidural (DPE): Dura punctured with spinal needle through epidural needle, NO intrathecal injection, then epidural catheter placed. Benefits: faster onset, better sacral coverage, fewer epidural catheter failures.
See Q1 Paper 2 (above) — EBP is definitive treatment.
Jugular Venous Oximetry (SjO2)
Continuous monitoring of oxygen saturation in blood draining from the brain via the jugular bulb, reflecting the balance between cerebral O2 delivery and consumption. Represents global cerebral oxygenation.
Retrograde catheterisation of the internal jugular vein to the jugular bulb (C1–C2 level). Confirmed by X-ray. Right IJ dominant (drains superior sagittal sinus).
SjO2: 55–75%
- SjO2 <50%: Cerebral ischaemia — O2 delivery inadequate for demand (↑ O2 extraction by brain). Causes: ↓ CPP, ↓ Hb, vasospasm, hyperventilation.
- SjO2 >75%: Cerebral luxury perfusion OR cerebral infarction (dead tissue not extracting O2 → SjO2 rises paradoxically). Also: AVM, high cardiac output.
- SjO2 50–55%: Borderline — monitor closely, optimise CPP and Hb
Arteriovenous O2 difference for the brain = SaO2 – SjO2 × Hb × 1.34. Normal 4–8 mL/dL. Elevated = ischaemia; low = luxury perfusion.
- Traumatic brain injury — guide ICP management and ventilation
- Carotid endarterectomy — detect intraoperative cerebral ischaemia
- Cardiac surgery with CPB — guide pump flow, temperature
- Guide hyperventilation therapy (avoid excessive ↓ PaCO2 → ↓ CBF → SjO2 <50%)
- Only global monitor — misses focal ischaemia
- Requires IJ cannulation — risk of carotid injury, infection
- Intermittent sampling vs continuous fibreoptic catheter
- Artefacts from catheter position changes
- Wet tap with Tuohy: thread intrathecal catheter — reduces PDPH and gives reliable block
- Label intrathecal catheter CLEARLY — wrong dose causes high spinal
- SjO2 <50% = cerebral ischaemia; >75% = luxury perfusion OR infarction
- DPE technique: dura punctured but NO intrathecal injection — faster epidural onset
- Removing needle and re-siting at same level after ADP — risk of subarachnoid injection
- Interpreting high SjO2 as always 'good' — may indicate infarction
- Forgetting to use subarachnoid doses (not epidural doses) through intrathecal catheter
DPE technique is a recent hot topic — mention it separately from CSE and standard epidural. SOAP 2024 recommends considering DPE for labour analgesia to reduce catheter failures.
- CEMACH report (UK): Highlighted ADP and subsequent high spinal block as preventable causes of maternal morbidity. Recommended: clear labelling, structured handover, intrathecal catheter policy.
- SjO2 vs NIRS (cerebral oximetry): NIRS (rSO2) is non-invasive, measures both arterial and venous O2, lacks IJ cannulation risk. Correlation with SjO2: moderate. NIRS may miss posterior circulation events. Both provide complementary information in high-risk neurosurgery.
- Cerebral microdialysis: Advanced neuromonitoring — monitors brain metabolites (glucose, lactate, pyruvate, glutamate). Lactate/pyruvate ratio >25 = metabolic crisis even with normal SjO2 and ICP.
- DPE vs CSE: CSE gives spinal block effect immediately. DPE: no intrathecal drug, relies on epidural drug diffusing through dural hole. Meta-analysis (Chau 2017): DPE gives faster sacral spread and fewer epidural failures vs standard epidural.
A) Fetomaternal transfer of anaesthetic agents B) BURP manoeuvre
Fetomaternal Transfer of Anaesthetic Agents
Drug transfer across the placenta is governed by Fick's law of diffusion: Transfer rate = (concentration gradient × surface area × membrane permeability) / membrane thickness.
- Low molecular weight (<500 Da)
- High lipid solubility
- Low ionisation (un-ionised fraction crosses better)
- Low protein binding (only free drug crosses)
UV/MA ratio (umbilical vein:maternal arterial concentration). Ratio <0.5 means poor transfer (e.g., muscle relaxants). >0.7 means significant transfer (e.g., benzodiazepines).
Induction agents
- Propofol: Rapid transfer (lipophilic, low MW). UV/MA ~0.7. Neonatal sedation possible at high maternal doses.
- Thiopentone: Rapid transfer but quickly redistributed — 'ion trapping' keeps fetal levels low.
- Ketamine: Crosses readily. Used for induction in haemorrhage — but >1.5 mg/kg may cause neonatal depression.
Volatile agents
- All cross rapidly and completely. Low blood:gas solubility agents cross fastest. Cause neonatal CNS and respiratory depression at high concentrations.
Opioids
- Morphine: UV/MA ~0.9 — significant transfer, neonatal respiratory depression.
- Fentanyl: Lower UV/MA than morphine. Preferred opioid in obstetrics.
- Remifentanil: Rapidly metabolised by fetal plasma esterases — low effective fetal exposure despite UV/MA ~0.9.
Muscle relaxants
- Highly ionised, large molecules. Minimal transfer. UV/MA <0.12. No neonatal paralysis with routine doses.
Local anaesthetics
- Bupivacaine: 95% protein-bound — low transfer. UV/MA ~0.3.
- Lidocaine: Less protein-bound — more transfer. Fetal acidosis causes 'ion trapping' — fetal pH lower → lidocaine ionised in fetus → trapped.
- Ropivacaine: Intermediate — preferred for epidurals.
Benzodiazepines
- Diazepam: UV/MA >1.0 — high transfer. Neonatal hypotonia, hypothermia, respiratory depression ('floppy infant syndrome'). AVOID in obstetrics.
BURP Manoeuvre
BURP = Backward, Upward, Rightward Pressure applied to the thyroid cartilage externally to improve laryngoscopic view by moving the larynx into the line of sight.
BURP is an external laryngeal manipulation (ELM) applied by the assistant on the anaesthetist's instruction, whereas Sellick's manoeuvre (cricoid pressure) is applied to the CRICOID cartilage to prevent regurgitation. These are DIFFERENT manoeuvres on DIFFERENT cartilages.
- Identify thyroid cartilage
- Apply pressure Backward (posteriorly toward spine)
- Upward (cephalad toward head)
- Rightward (patient's right)
- Optimal amount of pressure determined by direct laryngoscopic view
Improves Cormack-Lehane grade in ~60% of difficult laryngoscopy cases. Converts grade 3 to grade 2 in many cases.
Optimal External Laryngeal Manipulation (OELM) — anaesthetist's own hand adjusts position during laryngoscopy for best view, then assistant holds the position. OELM > BURP for improving view.
Laryngoscope in left hand, right hand manipulates thyroid cartilage — find best position, then assistant maintains it. This is the recommended technique in DAS (Difficult Airway Society) guidelines.
- Muscle relaxants: minimal transfer (ionised, large MW) — safe for fetus
- Diazepam: UV/MA >1 — floppy infant syndrome. AVOID in obstetrics.
- BURP = thyroid cartilage; Sellick = cricoid cartilage — DIFFERENT structures
- Remifentanil: crosses placenta but rapidly metabolised by fetal esterases — safe
- Confusing BURP (thyroid cartilage) with Sellick (cricoid) — extremely common exam error
- Saying muscle relaxants cross the placenta significantly — they do NOT
- Forgetting ion trapping concept — fetal acidosis traps local anaesthetics and increases fetal drug levels
Ion trapping is high-yield: In fetal acidosis, fetal pH is lower → more ionised drug trapped in fetal compartment. This is why fetal distress increases LA toxicity to fetus. DNB loves this concept.
- Ion trapping quantification: Henderson-Hasselbalch: For weak base lidocaine (pKa 7.9), at pH 7.4 (maternal) vs pH 7.2 (acidotic fetus): fetal/maternal concentration ratio = 10^(pKa-pHf)/10^(pKa-pHm) = significant accumulation in acidotic fetus.
- Remifentanil labour analgesia: CONSORT trial — remifentanil PCA comparable to epidural for moderate pain in labour. Advantage: rapid metabolism limits neonatal effects. Risk: maternal apnoea — 1:1 midwife monitoring and SpO2 mandatory.
- Thiopentone induction 'sleep-awake-sleep' interval: Time from induction to delivery determines neonatal exposure. Classical teaching: deliver within 8 minutes of induction to minimize fetal drug effect.
- Sugammadex placental transfer: Rapidly reverses rocuronium. Placental transfer studies in animals suggest low UV/MA ratio. Case reports of sugammadex use in obstetric RSI as reversal agent for rocuronium — gaining favour.
Bedside Pulmonary Function Tests (PFTs)
Bedside PFTs are simple, non-invasive tests that can be performed at the bedside without spirometry equipment, providing useful information about respiratory function in preoperative assessment and ICU monitoring.
Breath-holding time (BHT)
Patient takes a normal breath and holds. Time measured.
- >25 seconds: Good cardiorespiratory reserve
- 15–25 seconds: Moderate impairment
- <15 seconds: Poor reserve — high anaesthetic risk
Effort-dependent, patient cooperation required. Not specific.
Stair climbing test
Patient asked to climb stairs. Number of flights and symptoms recorded.
- >3 flights without stopping: >10 METs — low risk
- 1–2 flights: 4–10 METs — moderate
- <1 flight: <4 METs — high risk
- Unable to climb at all + desaturation: Very high risk
Single most useful bedside functional test for thoracic surgery risk.
Single breath count (SBC)
Patient takes maximum breath, then counts aloud as fast as possible until complete exhalation.
- SBC >30: VC likely >2L — adequate reserve
- SBC <15: VC likely <1L — poor reserve
SBC approximately corresponds to VC: SBC × 67 mL ≈ VC in mL.
Tidal volume and respiratory rate
Observe and count RR at rest.
RR 12–20/min. TV ~7 mL/kg.
RR >25/min at rest = significant respiratory compromise.
Peak Expiratory Flow Rate (PEFR)
Peak flow meter — patient blows maximum forced exhalation.
Variable by age/sex/height (>400 L/min typically adequate for males).
Reflects large airway function and expiratory effort. Reduced in asthma, COPD, weakness.
Match test
Patient blows out a lit match held 6 inches from the open mouth without pursing lips.
Inability to blow out match = poor ventilatory reserve.
Very crude, not validated formally.
6-Minute Walk Test (6MWT)
Distance walked in 6 minutes on a flat surface.
>400m considered adequate.
Best validated bedside functional test for predicting postoperative complications in thoracic and cardiac surgery. Correlates with VO2max. SpO2 drop >4% during 6MWT = significant.
- FEV1 <800 mL or <40% predicted: High risk for post-thoracic surgery respiratory failure
- ppo-FEV1 (predicted post-operative): <40% predicted = high risk for pneumonectomy
- VO2max <10 mL/kg/min: Very high surgical risk
- 6MWT best validated bedside test — >400m adequate; SpO2 drop >4% significant
- SBC >30 ≈ VC >2L — adequate for most surgeries
- Stair climbing: 3 flights = 10 METs = low risk
- BHT <15 sec = poor reserve; >25 sec = good reserve
- Saying spirometry is a 'bedside test' — formal spirometry is NOT bedside
- Confusing PEFR (large airway) with FEV1 (spirometry) — PEFR IS available bedside via peak flow meter
- Forgetting 6MWT SpO2 monitoring — the drop during exertion is as important as the distance
DNB examiners like to ask 'which bedside test best predicts surgical risk' — answer is 6MWT for thoracic surgery, stair climb test for general surgical risk assessment.
- ppo-FEV1 calculation (predicted post-operative): ppo-FEV1 = preoperative FEV1 × (1 – fraction of lung removed). For right upper lobectomy (3 segments of 19 total): ppo-FEV1 = preop FEV1 × (1 – 3/19). If <40%, high risk.
- Cardiopulmonary Exercise Testing (CPET): Gold standard for preoperative functional assessment. Measures VO2max and anaerobic threshold (AT). AT <11 mL/kg/min → high-risk surgery. Increasingly available at tertiary centres in India.
- Incentive spirometry as bedside monitor: Plastic device measuring sustained slow inspiratory flow. Target volume >70% predicted inspiratory capacity. Used postoperatively to prevent atelectasis — reduces pulmonary complications by 50% in upper abdominal surgery (RCT evidence).
- ARISCAT score: Calculates risk of postoperative pulmonary complications (PPC). Includes age, SpO2, respiratory infection in past month, anaemia, surgical incision site, duration, emergency surgery. Score >45 = high risk of PPC.
Neuromuscular Monitoring – A) Various techniques B) Application in laparotomy
Techniques of Neuromuscular Monitoring
Force transducer measures isometric contraction force of thumb. Gold standard but impractical — not portable, requires calibration.
Accelerometer measures thumb acceleration (T-probe/TOF-watch). Portable, commonly used. TOF ratio ≥0.9 confirms adequate recovery. Most widely used clinically.
Records muscle action potential (MAP). More sensitive than AMG. Less affected by position. Not widely available at bedside.
Single Twitch (ST)
Single supramaximal stimulus at 1 Hz. Shows only presence/absence of block. Cannot determine depth. Historically used.
Train of Four (TOF)
4 stimuli at 2 Hz over 2 seconds. T4/T1 ratio (TOF ratio). TOF ratio <0.9 indicates residual block. Most important clinical pattern. At complete block: all 4 twitches absent.
- 4 twitches present = <75% block
- 3 twitches = 75–80% block
- 2 twitches = 80–85% block
- 1 twitch = 90–95% block
- 0 twitches = >95% block
Double Burst Stimulation (DBS)
Two brief bursts of 50 Hz stimulus. Detects residual block more sensitively than TOF count by tactile assessment. DBS ratio <0.9 = residual block. Preferred for tactile assessment when quantitative monitoring unavailable.
Tetanic Stimulation (50 Hz, 5 sec)
Evaluates deep block. Post-tetanic potentiation (PTP) follows. Used with PTC.
Post-Tetanic Count (PTC)
Tetanic stimulus → single twitches at 1 Hz. Counts responses. PTC 1–5 = intense block. PTC >15 = TOF responses about to return. Used to guide reversal timing (neostigmine should not be given at PTC <10).
Ulnar nerve at wrist (thumb adductor pollicis) is standard. Alternatives: facial nerve (orbicularis oculi — represents respiratory muscles, wakes first), tibial nerve, common peroneal nerve.
TOF ratio ≥0.9 by acceleromyography (some advocate ≥1.0). Clinical signs unreliable — cannot detect TOF ratio <0.9 by 5-second head lift alone.
Application of Neuromuscular Monitoring in Laparotomy
Induction and intubation
If succinylcholine used: no monitoring needed. If rocuronium used: wait for TOF count 0 (or PTC 0 for RSI doses of 1.2 mg/kg) before laryngoscopy — ensures optimal intubating conditions.
Maintenance
For abdominal wall relaxation: TOF count 1–2 (deep block) required for adequate surgical field. Atracurium/rocuronium top-up guided by TOF count returning to 1–2. Monitor every 15 minutes.
Fascial closure
Deep block (TOF 0, PTC 1–5) for laparoscopic and difficult closures if surgeon requests. Avoid in open cases — peritoneal stretch provides closure. Monitor PTC during deep block.
Peritoneal closure
Surgeon may request TOF count 0–1 for tight abdomen. Communicate clearly with surgeon and monitor closely.
Wound closure and reversal
Do NOT give neostigmine at TOF 0 (no point — needs twitches to reverse). Neostigmine effective at TOF count ≥2. Sugammadex can reverse at any depth including PTC 1–2.
- Neostigmine: 0.04–0.07 mg/kg at TOF ≥2 (+ glycopyrrolate 0.2 mg per 1 mg neostigmine)
- Sugammadex: 2 mg/kg at TOF ratio ≥0.5 or TOF count ≥2; 4 mg/kg at PTC ≥1–2; 16 mg/kg immediate post-intubation
Extubation
TOF ratio ≥0.9 confirmed by quantitative monitoring before extubation. Clinical signs (5-second head lift, hand grip, tongue depressor test) unreliable for TOF <0.9.
- TOF ratio ≥0.9 = adequate recovery; <0.9 = residual curarisation
- Laparotomy: TOF 1–2 for maintenance relaxation; TOF ≥2 before neostigmine
- Sugammadex reverses at any depth; neostigmine only effective at TOF ≥2
- DBS better than TOF for tactile residual block detection
- Giving neostigmine at TOF count 0 — completely ineffective, delays extubation
- Relying on clinical signs (head lift, grip) to confirm full recovery — unreliable below TOF 0.9
- Not monitoring during maintenance — only checking at reversal
Draw the TOF trace at different depths of block (4 twitches, 2 twitches, 0 twitches) and the post-tetanic count trace. This is a common DNB examiner request.
- Residual neuromuscular blockade (RNMB): TOF ratio 0.7–0.9 causes: impaired pharyngeal muscle function, silent aspiration, reduced hypoxic ventilatory response. Studies show 40–60% of patients extubated have TOF <0.9 without quantitative monitoring.
- Deep NMB for laparoscopy (DEEP-NMB trial): Deep neuromuscular block (TOF 0, PTC 1–5) during laparoscopy allows lower intraperitoneal pressure (8 vs 12 mmHg) → better surgical conditions, less postoperative pain. Sugammadex enables safe deep-block reversal.
- Acceleromyography vs mechanomyography: AMG can overestimate TOF ratio by 5–10% (requires preload on thumb). 'Normalised' AMG (control twitch set at 100%) more accurate. EMG does not require thumb preload — inherently more accurate.
- Laryngeal muscles vs adductor pollicis: Larynx (vocal cords, cricothyroid) is more resistant to NMB and recovers faster than adductor pollicis. TOF 0.9 at thumb confirms full laryngeal recovery — this is why AP is the monitoring site of choice.
Laparoscopy – Pathophysiology of pneumoperitoneum, complications in laparoscopic cholecystectomy
Laparoscopic surgery requires pneumoperitoneum (PP) — insufflation of CO2 into the peritoneal cavity at 12–15 mmHg pressure. This creates significant physiological changes that the anaesthetist must anticipate and manage.
- ↑ Intraabdominal pressure → compresses IVC → ↓ venous return → ↓ preload → ↓ CO (10–30%)
- ↑ SVR: peritoneal stretch + aortic compression → ↑ afterload → ↑ BP initially
- ↑ HR: CO2 absorption → ↑ PaCO2 → SNS activation → tachycardia
- Bradycardia: Vagal stimulation from peritoneal stretching (especially at insufflation onset)
- Head-down (Trendelenburg) partially offsets: ↑ venous return but worsens respiratory mechanics
- Head-up (reverse T): worsens venous return, ↓ CO further
- ↑ IAP splints diaphragm upward → ↓ FRC, ↓ compliance, ↑ peak airway pressure
- Atelectasis: basal collapse worsens V/Q mismatch → ↑ shunt → ↓ PaO2
- CO2 absorption → ↑ PaCO2 → need to ↑ MV by 15–25% to maintain normocapnia
- Risk of endobronchial intubation: cephalad diaphragm displacement pushes carina up
- ↑ ICP: ↑ IAP → ↑ venous pressure → ↑ ICP, also ↑ PaCO2 → cerebral vasodilation. Caution in TBI.
- ↑ IOP: ↑ ICP → ↑ intraocular pressure. Avoid in glaucoma, head-up if possible.
- ↑ IAP compresses renal parenchyma and renal vein → ↓ renal blood flow → ↓ UO
- ↑ renin-angiotensin-aldosterone: compensatory fluid retention
- Oliguria is common intraoperatively — not immediately treated unless hypotension
- CO2 embolism: Most feared. Massive embolism → 'mill-wheel' murmur, sudden ↓ etCO2 (↓ CO), cardiovascular collapse. Management: immediately desufflate, left lateral-head-down (Durant's manoeuvre), 100% O2, CPR if arrest, aspiration via CVC.
- Subcutaneous emphysema: CO2 tracking into subcut tissues → crepitus, ↑ etCO2 (↑ CO2 absorption surface). Usually self-limiting.
- Pneumothorax/pneumomediastinum: CO2 entering through pleural defect or via mediastinum.
- Capnoperitoneum → capnothorax: Especially right-sided (diaphragmatic defects or port injury)
Trocar injury to aorta, IVC, mesenteric vessels — catastrophic haemorrhage. Convert to open immediately.
- Bowel injury (usually not immediately apparent)
- Bile duct injury (most common serious complication of lap chole) — bile leak, obstructive jaundice
Referred phrenic nerve pain from CO2 irritating diaphragm. Treat: drain CO2 at end, head-up position post-op, NSAIDs.
Profound bradycardia/asystole at insufflation — vasovagal. Treat: stop insufflation, atropine, desufflate.
- Trendelenburg: Endobronchial migration (check ETT position), ↑ ICP, eye/nerve compression (brachial plexus)
- Reverse T: ↓ CO, air embolism risk increases
- General anaesthesia with IPPV — mandatory
- Increase MV by 15–25% to manage ↑ PaCO2
- Reduce IAP to 8–10 mmHg if haemodynamically compromised
- Head-down tilt to improve venous return during insufflation
- Lung-protective strategy: PEEP 5 cmH2O + RM after position change
- Decompress stomach with OGT/NGT — aids surgeon, reduces aspiration risk
- Warm and humidify gases — reduces hypothermia risk
- PP: ↑ SVR, ↓ CO, ↑ PAP, ↓ FRC, ↑ PaCO2 — all require active management
- CO2 embolism: sudden ↓ etCO2, mill-wheel murmur, cardiovascular collapse
- Left lateral head-down (Durant's manoeuvre) = treatment for CO2 embolism
- ↑ MV by 15–25% to compensate for CO2 absorption during PP
- Saying etCO2 suddenly increases in CO2 embolism — it initially rises then FALLS as CO drops
- Treating intraoperative oliguria aggressively with fluids in laparoscopy — oliguria from ↑ IAP is normal
- Forgetting shoulder tip pain is a postoperative complication — phrenic nerve irritation
CO2 embolism is a classic DNB question. Draw the capnography trace: initial brief rise then sudden fall with mill-wheel murmur and cardiovascular collapse. Treatment steps in order.
- ERABS (Enhanced Recovery After Bariatric Surgery): Deep NMB (PTC 1–5) + low IAP (8 mmHg) for obese patients — reduces postoperative pain and respiratory complications. Sugammadex essential for reversal.
- Gasless laparoscopy: Mechanical abdominal wall lifting (Laparolift) — avoids CO2 insufflation. Used in cardiac/respiratory-compromised patients. Worse surgical view but safer haemodynamics.
- Needle aspiration for CO2 embolism: Some protocols recommend aspiration of CO2 via right heart catheter if CVC in situ — removes gas from PA. Rarely done in practice.
- Lung recruitment manoeuvres in laparoscopy: Sustained inflation at 40 cmH2O for 15-40 seconds before abdomen desufflated → reopens atelectatic alveoli → reduces postoperative hypoxaemia. Evidence from Heinzer et al. (2017).
Central Venous Pressure (CVP) – Waveform/diagram, indications, care and maintenance
CVP is the blood pressure in the superior vena cava (or right atrium), reflecting right ventricular end-diastolic pressure and right atrial filling pressure. Normal: 2–8 mmHg (or 5–12 cmH2O).
a wave
Atrial contraction
Absent in AF; giant cannon a waves in complete heart block (atrium contracting against closed TV)
c wave
Tricuspid valve closure and slight bulging into RA at start of systole
Small, often not visible clinically
x descent
Atrial relaxation + tricuspid valve moving downward during RV contraction
v wave
Venous filling of RA while TV is closed (during RV systole)
Giant v waves = tricuspid regurgitation (blood jets back into RA during RV systole)
y descent
TV opens → RA empties into RV
Prominent in constrictive pericarditis (Kussmaul's sign)
- AF: Loss of a wave (no coordinated atrial contraction)
- TR: Giant v waves
- Complete heart block: Cannon a waves (atrium contracts against closed TV)
- Cardiac tamponade: Elevated CVP, absent y descent, pulsus paradoxus
- Constrictive pericarditis: M/W shaped waveform, prominent x and y descents
- Volume status and filling pressure assessment in major surgery, cardiac surgery, sepsis
- CVP trend more useful than absolute value
- Assess RV function
- Administration of concentrated vasoactive drugs (noradrenaline, adrenaline, vasopressin)
- Total parenteral nutrition (TPN) — osmolality too high for peripheral veins
- Chemotherapy agents
- Long-term IV access when peripheral access exhausted
- Rapid volume infusion (large bore CVC)
- Pacing wire insertion
- Haemodialysis/CRRT (Vascath — typically subclavian or femoral IJ)
- PA catheter placement
- Blood sampling: Mixed venous saturation (ScvO2)
- Internal jugular (right preferred — straight path to RA, low pneumothorax risk)
- Subclavian (lower infection risk, uncomfortable during awake insertion)
- Femoral (high infection risk, avoid if possible for >48h, useful in emergencies)
- PICC (peripherally inserted CC) — not traditional CVC but serves similar purposes
- Full aseptic technique: cap, mask, sterile gown, sterile gloves, large sterile drape
- Ultrasound guidance — mandatory (NICE 2002, subsequently reaffirmed 2023)
- Confirm position: CXR post-insertion (tip at SVC-RA junction, 2cm above carina on CXR)
- Check for complications immediately: pneumothorax, haematoma, arterial puncture
- Daily assessment of need — remove ASAP when no longer required (↓ CLABSI risk)
- Sterile dressing: transparent semipermeable dressing changed every 7 days or when soiled
- Needleless connectors changed every 72 hours (or per institutional policy)
- Flush with 0.9% NaCl before and after drug administration
- Blood sampling: Discard first 5–10 mL, sample, flush
- Gluconate CHX (2%) skin antisepsis for catheter insertion and dressing changes
- CHX-impregnated dressings reduce CLABSI (Biopatch — NEJM evidence)
- Antibiotic-impregnated catheters if CLABSI rate remains high despite bundles
Central Line Insertion Bundle (CLIP bundle in UK; CLABSI bundle in India/USA): Hand hygiene + Full barrier precautions + CHX skin prep + Optimal insertion site + Daily review for removal. CUSP/On the CUSP Stop BSI programme reduced CLABSI by 66%.
- a wave = atrial contraction; v wave = venous filling with TV closed; y descent = TV opening
- Giant v waves = TR; absent a wave = AF; cannon a waves = CHB
- Ultrasound guidance for CVC — mandatory per NICE
- Daily assessment for need and removal — most important infection prevention strategy
- Confusing x descent (atrial relaxation) with y descent (TV opening)
- Placing femoral line without acknowledging high infection risk
- Using CVP absolute value to guide fluid therapy — trends and dynamic indices are superior
Draw the CVP waveform clearly with all 5 components (a, c, x, v, y) labelled with their physiological correlates. Then draw the AF trace (no a), TR trace (giant v), and CHB trace (cannon a). DNB examiners ALWAYS want the diagram.
- CVP vs fluid responsiveness: Static CVP has poor predictive value for fluid responsiveness (meta-analysis: Marik 2013). Dynamic indices (PPV — pulse pressure variation >13% = fluid responsive; SVV >10%) are superior in ventilated patients. CVP useful as upper limit safety marker (>15 mmHg → likely volume overloaded).
- Kussmaul's sign in constrictive pericarditis: CVP RISES on inspiration (paradoxical). Normally CVP falls on inspiration. Also seen in cardiac tamponade and RVMI.
- CLABSI rates in India: Average 3.4–5.1 per 1000 catheter-days (INICC data). Target <1 per 1000 with bundles. Staphylococcus epidermidis, Enterococcus, Gram-negative bacilli most common organisms.
- ScvO2 monitoring via CVC: Normal ScvO2 ≥70%. ScvO2 <65% = inadequate O2 delivery relative to demand (early sepsis, cardiac failure). Rivers EGDT trial used ScvO2 ≥70% as resuscitation endpoint (controversial but monitoring remains useful).