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Spinal Anesthesia - Complete MD Anaesthesiology Viva Question Bank

Sourced from Miller's Anesthesia 10e, Morgan & Mikhail's Clinical Anesthesiology 7e, Barash Clinical Anesthesia 9e, and Goodman & Gilman's Pharmacological Basis of Therapeutics.

SECTION 1: ANATOMY

Q1. Describe the anatomy of the spinal canal relevant to spinal anesthesia.
The spinal canal contains the spinal cord, which typically ends at L1-L2 in adults (conus medullaris). The exact level varies - the cord may extend more caudally in children. The cord is covered by three meninges: pia mater (innermost, adheres to cord), arachnoid mater (middle), and dura mater (outermost). The subarachnoid space lies between the pia and arachnoid and contains CSF. The epidural (extradural) space lies outside the dura. Spinal anesthesia is performed in the lumbar region (L3-L4 or L4-L5) to avoid cord injury.
Q2. What is the significance of the conus medullaris in spinal anesthesia?
The conus ends at L1-L2 in adults. Performing spinal anesthesia below this level (L3-L4 or L4-L5) avoids direct cord injury. However, the cord can terminate as low as L3 in some individuals, and anesthesiologists using palpation frequently misidentify interspaces - studies show they insert needles at a higher level than intended. Permanent conus medullaris damage has been reported at the presumed L2-L3 interspace, hence L3-L4 or L4-L5 is preferred. (Miller's Anesthesia, p. 6113)
Q3. Name the ligaments traversed by a spinal needle from skin to subarachnoid space.
  1. Skin and subcutaneous tissue
  2. Supraspinous ligament
  3. Interspinous ligament
  4. Ligamentum flavum
  5. Epidural space
  6. Dura mater
  7. Subdural space (potential)
  8. Arachnoid mater
  9. Subarachnoid space (CSF obtained here)
Q4. What are the anatomical landmarks for performing spinal anesthesia?
  • The intercristal (Tuffier's) line connecting the iliac crests corresponds to the L4-L5 interspace or the L4 spinous process.
  • The L3-L4 interspace is just above this line.
  • Midline approach: needle inserted in the midline between adjacent spinous processes.
  • Paramedian (lateral) approach: needle inserted 1-1.5 cm lateral to midline at the lower edge of the superior spinous process, angled slightly medially and cephalad.
Q5. What is the volume and composition of CSF? How does it affect spinal anesthesia?
Total CSF volume: ~150 mL; lumbosacral CSF volume: ~75 mL. CSF is clear, colorless, with density 1.00059 g/mL at 37°C, pressure ~15 cm H2O, pH 7.32, contains minimal protein. CSF volume is inversely correlated with peak block height - smaller lumbosacral CSF volume leads to higher, more unpredictable blocks. CSF volume does not correlate well with anthropomorphic measurements except body weight. (Miller's Anesthesia, p. 6049)
Q6. Why is the L3-L4 or L4-L5 level preferred for spinal anesthesia?
Below the termination of the conus medullaris (L1-L2), only nerve roots of the cauda equina are present. These roots are bathed in CSF and are mobile, making cord injury less likely. There is also more CSF around the nerve roots, facilitating drug mixing.

SECTION 2: MECHANISM OF ACTION AND PHYSIOLOGY

Q7. What is the mechanism of action of local anesthetics in spinal anesthesia?
Local anesthetics block voltage-gated sodium channels on neuronal cell membranes in a use-dependent manner, preventing the generation and propagation of action potentials. They enter the channel predominantly in the open (activated) state and bind to a receptor site within the channel pore (amino acid residues in the D4 S6 transmembrane segment). This prevents Na+ influx, stabilizes the resting membrane potential, and blocks conduction. The ionized (quaternary) form is the active form inside the channel; the un-ionized lipid-soluble form traverses the cell membrane.
Q8. What is the order of nerve fiber susceptibility to local anesthetic block in spinal anesthesia?
Classically: smallest unmyelinated fibers are blocked first. Order of block:
  1. B fibers (preganglionic sympathetic) - blocked first at lowest concentration
  2. C fibers (pain, temperature, postganglionic sympathetic) - unmyelinated, slow pain
  3. A-delta fibers (fast pain, temperature, touch)
  4. A-gamma fibers (muscle spindle efferents)
  5. A-beta fibers (touch, pressure, proprioception)
  6. A-alpha fibers (motor, proprioception) - blocked last, highest concentration required
Clinical consequence: sympathetic block extends 2-3 segments above sensory block; sensory block extends 2-3 segments above motor block.
Q9. What are the physiological effects of spinal anesthesia on the cardiovascular system?
  • Hypotension: Sympathetic blockade causes vasodilation (decreased SVR). Blocked cardioaccelerator fibers (T1-T4) reduce heart rate and cardiac output. Hypotension is more pronounced with higher blocks.
  • Bradycardia: Blockade of T1-T4 cardioaccelerator fibers; also Bezold-Jarisch reflex (decreased venous return activates ventricular mechanoreceptors, causing reflex bradycardia).
  • Cardiac arrest: Can occur with total spinal, particularly when high sympathetic block combined with deep sedation or hypoxemia causes sudden arrest in otherwise healthy young patients. Epinephrine should be administered promptly. (Barash, p. 2865)
  • Decreased preload from venodilation contributes significantly to hypotension.
Q10. What are the effects of spinal anesthesia on the respiratory system?
  • Low and mid-thoracic blocks: minimal respiratory effect; patients may complain of "chest tightness" but spirometry is largely unchanged.
  • High thoracic blocks: intercostal muscle paralysis impairs forced expiration and cough.
  • Cervical blocks (C3-C5): diaphragmatic paralysis - patient can only whisper, requires immediate ventilatory support and intubation.
  • Phrenic nerve (C3-C5) is usually spared in high thoracic spinals.
  • The sensation of difficulty breathing is often more subjective (loss of chest wall proprioception) than objective in thoracic-level blocks.
Q11. What is the Bezold-Jarisch reflex? How is it relevant in spinal anesthesia?
The Bezold-Jarisch reflex is a cardioinhibitory reflex mediated by mechanoreceptors/chemoreceptors (C-fibers) in the inferoposterior wall of the left ventricle. When ventricular volume falls (e.g., due to venodilation from spinal anesthesia and the sitting or head-up position), these receptors are activated, sending afferent signals via the vagus nerve to the brainstem, resulting in reflex bradycardia, hypotension, and vasodilation. In spinal anesthesia, it contributes to sudden severe bradycardia or cardiac arrest, particularly in the setting of hypovolemia or the sitting position.
Q12. What is the effect of spinal anesthesia on the gastrointestinal system?
Sympathetic blockade (T5-L1) leaves parasympathetic activity unopposed, causing increased GI motility, contracted bowel (good for surgery), and sphincter relaxation. Nausea and vomiting during spinal anesthesia result from hypotension (leading to cerebral ischemia and stimulation of the vomiting center), unopposed vagal activity, and traction on viscera (T4 peritoneal innervation).
Q13. What is the effect of spinal anesthesia on the hepatic and renal systems?
  • Liver: Decreased hepatic blood flow proportional to the fall in mean arterial pressure. Hepatic metabolism of drugs is reduced.
  • Kidney: Decreased renal blood flow and GFR with hypotension. Urinary retention is a recognized complication due to sacral parasympathetic blockade (S2-S4), causing bladder detrusor relaxation and internal sphincter contraction. Duration of urinary retention correlates with the local anesthetic used.

SECTION 3: DRUGS USED IN SPINAL ANESTHESIA

Q14. Classify the local anesthetics used in spinal anesthesia with doses.
DrugClassBaricityDoseOnsetDuration
BupivacaineAmideHyper/Iso7.5-15 mg5-8 min2-4 h
LevobupivacaineAmideIso10-15 mg5-8 min2-4 h
RopivacaineAmideIso15-22.5 mg5-10 min2-3 h
LidocaineAmideHyper50-100 mg3-5 min1-1.5 h
TetracaineEsterHyper5-20 mg3-5 min2-3 h
ChloroprocaineEsterIso30-60 mgFast30-60 min
PrilocaineAmideIso/Hyper40-60 mg3-5 min1.5-2.5 h
(Miller's Anesthesia, Table 41.4)
Q15. What is baricity? How does it affect the spread of spinal anesthesia?
Baricity is the ratio of the density of a local anesthetic solution to the density of CSF (density of CSF = 1.00059 g/mL at 37°C). Density = mass per unit volume (g/mL).
  • Hyperbaric (density > CSF): spreads to dependent (gravity-dependent) regions. Made by adding dextrose (e.g., 8% glucose). Most predictable spread.
  • Hypobaric (density < CSF): spreads to non-dependent regions. Made by adding sterile water.
  • Isobaric (density = CSF): not significantly influenced by gravity/position.
Clinical use: In lateral decubitus, hyperbaric solution produces preferential block on the dependent side; hypobaric solution blocks the non-dependent side. Hyperbaric solutions have less interpatient variability. (Miller's Anesthesia, pp. 6045-6046)
Q16. What are the factors affecting spread of spinal anesthetic (determinants of block height)?
Drug factors (most adjustable):
  • Baricity - most important
  • Dose - most important
  • Volume and concentration
  • Temperature of solution
  • Speed of injection (faster = slightly higher block)
  • Addition of vasoconstrictors
Patient factors:
  • CSF volume (inversely proportional to block height)
  • Age (elderly - higher block due to decreased CSF volume, increased neuronal sensitivity)
  • Height (at extremes only)
  • Weight/obesity (decreased CSF volume - higher blocks, especially hypobaric)
  • Pregnancy (higher blocks - decreased CSF density, reduced CSF volume, progesterone-mediated sensitivity, lordosis)
  • Sex (higher blocks in females - lower CSF density)
  • Spinal anatomy (kyphosis, scoliosis)
Procedural factors:
  • Patient position during and after injection
  • Level of injection
  • Needle bevel direction (bevel cephalad = slightly higher block)
  • Speed and direction of injection
(Miller's Anesthesia, pp. 6044-6052)
Q17. Why is bupivacaine the drug of choice for spinal anesthesia?
  • Long duration (2-4 hours), allowing completion of most surgical procedures
  • High protein binding (95%) and high lipid solubility - selective sensory blockade with less motor block at lower doses
  • Available as hyperbaric preparation (0.5% in 8% dextrose) - predictable spread
  • Isobaric preparation (0.5% in normal saline) also available
  • Safe cardiac and neurological profile at spinal doses
  • Well-established safety record
  • Unlike lidocaine, no association with transient neurological symptoms (TNS) at clinical doses
Q18. What are the advantages of levobupivacaine and ropivacaine over racemic bupivacaine for spinal anesthesia?
  • Levobupivacaine: The S(-) enantiomer of bupivacaine. Less cardiotoxic than racemic bupivacaine (R(+) isomer responsible for cardiotoxicity). Similar efficacy.
  • Ropivacaine: Structurally related to bupivacaine; same pKa (8.1), slow onset, long duration. Potency is 0.6 that of bupivacaine. When given in equivalent doses to bupivacaine, produces slightly less motor block and earlier motor recovery. Greater motor-sensory differentiation.
  • Practical caveat: both are only available as isobaric preparations; hyperbaric bupivacaine remains the most predictable.
(Miller's Anesthesia, p. 6058)
Q19. What is transient neurological syndrome (TNS)? Which drugs are implicated?
TNS (formerly transient radicular irritation, TRI) is:
  • Pain or dysesthesia in the buttocks and/or lower extremities after spinal anesthesia
  • Occurs within 24 hours of block resolution, resolves within 72 hours (usually)
  • No objective neurological deficit
  • Severity ranges from mild to severe
  • Most strongly associated with lidocaine (especially 5% hyperbaric), incidence up to 30-40%
  • Also reported with mepivacaine, procaine, and chloroprocaine
  • Risk factors: outpatient/ambulatory setting, lithotomy position, obesity, early mobilization, knee arthroscopy
  • Bupivacaine has minimal association with TNS
  • Management: NSAIDs; opioids may be needed
Q20. What are the intrathecal adjuvants used in spinal anesthesia? Describe their mechanisms and side effects.
Opioids:
  • Morphine (hydrophilic): Slow onset (30-60 min), long duration (up to 24 h). Dose: 100-300 mcg. Mechanism: dorsal horn mu-receptor activation. Side effects: delayed respiratory depression (most serious - up to 12-24 h), pruritus, nausea/vomiting, urinary retention. Intrathecal:IV potency ratio = 200-300:1.
  • Fentanyl (lipophilic): Rapid onset (10-15 min), short duration (3-4 h). Dose: 12.5-25 mcg. Less rostral spread due to high lipid solubility. Side effects: less delayed respiratory depression, pruritus, nausea. Potency ratio = 10-20:1.
  • Sufentanil: 5-7.5 mcg. Similar to fentanyl but more potent.
  • Diamorphine (UK only): Lipid-soluble prodrug, clearer from CSF faster than morphine.
Alpha-2 Agonists:
  • Clonidine: 15-45 mcg. Prolongs sensory and motor block by 2-3 h. Acts on alpha-2 receptors in dorsal horn (pre- and post-synaptic). Side effects: hypotension, bradycardia, sedation.
  • Dexmedetomidine: More selective alpha-2 agonist. Dose: 3-10 mcg.
Vasoconstrictors:
  • Epinephrine (adrenaline): 0.1-0.2 mg. Prolongs block by vasoconstriction (decreased vascular uptake) + direct alpha-2 agonism. May cause TNS with lidocaine.
  • Phenylephrine: Prolongs tetracaine block but increases TNS risk with lidocaine.
Neostigmine: Intrathecal 25-100 mcg. Inhibits acetylcholinesterase, increases ACh in CSF. Prolongs analgesia. Significant nausea and vomiting limit use.
(Miller's Anesthesia, pp. 6058-6063)

SECTION 4: TECHNIQUE

Q21. Describe the technique of spinal anesthesia step by step.
  1. Consent, IV access, monitoring (ECG, SpO2, NIBP), resuscitation equipment ready
  2. Positioning: Sitting (best CSF identification, good for saddle block, hyperbaric solutions settle caudally for perineal surgery) or lateral decubitus (for unilateral block, preferred for hyperbaric solution)
  3. Surface anatomy: Identify Tuffier's line (L4-L5 interspace)
  4. Sterile preparation: Chlorhexidine 0.5% in alcohol (let dry), sterile drape
  5. Local anesthesia: Infiltrate skin and interspinous ligament with 1% lidocaine
  6. Needle insertion: Midline approach - insert introducer (for pencil-point needles), then spinal needle with bevel/opening oriented cephalad in midline between spinous processes. Paramedian approach if midline difficult.
  7. Confirm subarachnoid placement: Free flow of clear CSF
  8. Inject drug: Attach syringe, aspirate to confirm CSF, inject slowly (0.2 mL/s), re-aspirate at end to confirm still intrathecal
  9. Position patient: According to baricity and desired block level
  10. Monitor block onset: Cold sensation, pinprick, modified Bromage scale for motor block
  11. Monitor cardiovascular response: Blood pressure and heart rate every 1-2 minutes for 10-15 minutes
Q22. Compare the midline and paramedian approaches to spinal anesthesia.
FeatureMidlineParamedian
Needle pathThrough supraspinous and interspinous ligamentsLateral to midline, bypasses supraspinous/interspinous ligaments
Preferred whenYoung, flexible patients; normal spinesElderly, calcified ligaments; kyphoscoliosis; previous spinal surgery; inability to flex
Reference pointSpinous processesLower edge of superior spinous process, 1-1.5 cm lateral
AnglePerpendicular or slightly cephaladMedially angled 10-15 degrees
AdvantageSimple, classicalBetter for calcified/difficult spines
Q23. What are the types of spinal needles? How does needle design affect PDPH incidence?
By tip design:
  • Cutting tip (Quincke-Babcock): Bevel cuts dural fibers - higher PDPH rate (up to 5-10%)
  • Pencil-point (non-cutting): Separates dural fibers rather than cutting
    • Whitacre (solid tapered tip with lateral opening)
    • Sprotte (longer lateral opening)
    • Gertie Marx
    • Lower PDPH rate (0.5-1%)
By gauge: Finer gauge = smaller dural puncture hole = less CSF leak = lower PDPH
  • 25G, 26G, 27G pencil-point: lowest PDPH risk (<1%)
  • 22G Quincke: PDPH risk ~3-5%
Bevel orientation: Orienting bevel parallel (longitudinal) to the axis of the spine separates rather than cuts dural fibers - lower PDPH incidence.
(Miller's Anesthesia, p. 6116)
Q24. How do you assess block height after spinal anesthesia?
  • Cold (temperature): Ethyl chloride spray or alcohol swab. C-fiber and A-delta testing. Highest (most cephalad) block level measured.
  • Pinprick: Blunt needle; A-delta fibers. Level 2-3 segments lower than cold.
  • Touch: A-beta fibers. Lowest block level measured.
  • Motor block: Modified Bromage Scale
    • 0 = no block (full flexion of knees and feet)
    • 1 = inability to raise extended leg; can move knee and feet
    • 2 = inability to raise leg and move knee; can move feet
    • 3 = complete motor block
Practically: the combination of sympathetic block + adequate sensory level (2-3 segments above planned surgical stimulus level) + inability to straight-leg raise confirms efficacy.
Q25. What dermatomal levels are required for common surgical procedures?
SurgeryRequired Sensory Level
Lower limb (foot, ankle)T12
Lower limb (knee, thigh)T10
TURP, cystoscopyT10
Hip surgeryT10
Lower abdominal surgeryT6
Cesarean sectionT4
Upper abdominal surgeryT4
Peritoneum (all viscera)T4
Bladder/uterus visceral innervationT10
Note: Intra-abdominal structures have more cephalad innervation than their overlying skin - the peritoneum is innervated at T4.
Q26. What is a saddle block? When is it used?
A saddle block is spinal anesthesia restricted to the perineal/sacral area (dermatomal distribution matching the "saddle" - perineum, buttocks, inner thighs, and genitalia). Achieved by:
  • Injecting a small dose of hyperbaric local anesthetic (e.g., hyperbaric bupivacaine 2.5-5 mg, or tetracaine 3-4 mg, or lidocaine 20-40 mg)
  • With the patient sitting upright for 3-5 minutes after injection (gravity keeps hyperbaric solution in the sacral region)
  • The patient is then placed in lithotomy with left uterine displacement
Uses: operative vaginal delivery, perineal surgery, hemorrhoidectomy, cystoscopy, anal fissure repair.
Q27. What is continuous spinal anesthesia (CSA)? What are its advantages and disadvantages?
CSA involves threading a catheter into the subarachnoid space (via a 17-19G Tuohy needle), allowing repeated or continuous dosing of local anesthetic.
Advantages:
  • Titrate block level precisely (small incremental doses)
  • Extend duration of block
  • Valuable in elderly and high-risk cardiac patients (slow titration minimizes hemodynamic changes)
  • Useful for long operations
Disadvantages:
  • Higher PDPH risk (large needle required)
  • Cauda equina syndrome risk if microcatheters used (pooling of hyperbaric lidocaine)
  • Infection risk
  • Limited availability of appropriate catheters (microcatheters withdrawn from US market)
Q28. What is unilateral spinal anesthesia? How is it achieved?
Blocking only one side of the body (the operative side). Technique:
  • Patient placed in lateral decubitus with operative side down
  • Small dose of hyperbaric local anesthetic injected slowly
  • Patient remains lateral for 15-20 minutes
  • Slow injection (0.1 mL/s), small volumes, hypobaric solutions (with patient on non-operative side up)
Benefits: Less hemodynamic instability, faster discharge, preserved mobility on contralateral side. Useful for unilateral lower limb surgery.

SECTION 5: CONTRAINDICATIONS

Q29. What are the absolute contraindications to spinal anesthesia?
  1. Patient refusal
  2. Local infection at the site of injection
  3. Septicemia/bacteremia
  4. Coagulopathy or therapeutic anticoagulation within time limits (see ASRA guidelines)
  5. Raised intracranial pressure (risk of cerebral herniation due to sudden CSF loss)
  6. Hypovolemic shock (unresuscitated)
  7. Allergy to local anesthetics
Q30. What are the relative contraindications to spinal anesthesia?
  1. Pre-existing neurological disease (e.g., multiple sclerosis, peripheral neuropathy) - block may exacerbate, difficult to attribute new deficits
  2. Aortic stenosis, severe fixed cardiac output states (hemodynamic compromise with sudden vasodilation)
  3. Dementia/uncooperative patient
  4. Fixed spinal deformity (technical difficulty)
  5. Previous spinal surgery
  6. Thrombocytopenia (platelet count <80,000 is generally a relative contraindication)
  7. Tattoo over injection site (theoretical risk of tattoo ink injection)
  8. Systemic sepsis without antibiotic coverage
  9. Hypertrophic obstructive cardiomyopathy
Q31. What are the ASRA guidelines for anticoagulants and neuraxial anesthesia?
Key intervals (ASRA 4th Edition, 2018):
DrugBefore blockAfter block
Unfractionated heparin (prophylactic SC)4-6 hours (check aPTT/anti-Xa)After 1 h
LMWH (prophylactic)12 hours12 hours
LMWH (therapeutic)24 hours24 hours
WarfarinINR ≤1.4-
AspirinNo restrictionNo restriction
Clopidogrel5-7 days-
Prasugrel7-10 days-
Ticagrelor5-7 days-
Dabigatran (Cr Cl >30)72 hours6 hours
Rivaroxaban72 hours6 hours
Apixaban48 hours6 hours
Fondaparinux (prophylactic)36-42 hours12 hours
(Miller's Anesthesia, Table 41.1)

SECTION 6: COMPLICATIONS

Q32. Classify the complications of spinal anesthesia.
Cardiovascular:
  • Hypotension (most common)
  • Bradycardia
  • Cardiac arrest (rare)
Respiratory:
  • High/total spinal (respiratory arrest)
  • Hypoventilation with heavy sedation
Neurological:
  • Post-dural puncture headache (PDPH)
  • Transient neurological syndrome (TNS)
  • Cauda equina syndrome
  • Anterior spinal artery syndrome
  • Direct needle trauma to nerve roots/cord
  • Epidural/subdural hematoma
  • Meningitis (bacterial, chemical)
  • Arachnoiditis
Systemic:
  • Local anesthetic systemic toxicity (LAST) - if inadvertent IV injection
  • Allergic reaction
Other:
  • Urinary retention
  • Backache
  • Nausea and vomiting (from hypotension)
  • Failed block
Q33. What is post-dural puncture headache (PDPH)? Describe its pathophysiology, features, risk factors, and management.
Definition: Headache occurring after intentional (spinal anesthesia) or unintentional (epidural) dural puncture.
Pathophysiology (two theories):
  1. CSF leaks through dural hole - CSF volume and pressure fall - brain sags - traction on pain-sensitive meningeal and vascular structures (veins, sinuses, dura) - headache
  2. Compensatory intracranial vasodilation in response to decreased intracranial pressure
Clinical Features:
  • Frontal or occipital headache (most common)
  • Postural: worsens sitting/standing, relieved lying flat (pathognomonic)
  • Associated: nausea, vomiting, neck stiffness, tinnitus, diplopia (VI nerve palsy), hearing loss, dizziness
  • Onset: within 3 days in >90% cases; 66% within 48 hours
  • Resolution: spontaneous in 72% by 7 days; 87% by 6 months
  • Serious complications: cerebral venous thrombosis, subdural hematoma (aOR 19.0), bacterial meningitis (aOR 39.7)
Risk factors:
  • Young age (<40 years)
  • Female sex
  • Pregnancy
  • Larger needle gauge
  • Cutting needle tip
  • Multiple puncture attempts
  • Bevel perpendicular to dural fibers
  • History of prior PDPH
Protective factors:
  • Small gauge (25G, 26G)
  • Pencil-point needles
  • Bevel parallel to spinal axis
Management:
  • Conservative: Bed rest, oral/IV hydration, paracetamol, NSAIDs, caffeine (300-500 mg oral/IV), analgesics, abdominal binder
  • Caffeine: 300-500 mg orally or IV. Works by cerebral vasoconstriction. Temporary relief.
  • Epidural blood patch (EBP): Gold standard. 15-20 mL of autologous blood into epidural space at or below puncture site. Mechanism: tamponade effect, gelatinous clot seals dural hole, increases epidural/intrathecal pressure. Success rate: ~70-90% with first patch. Indicated when conservative treatment fails, for moderate-severe PDPH.
  • Epidural saline/dextran: Temporary relief, less effective than blood patch.
  • Cosyntropin (ACTH): May stimulate CSF production and endorphin release.
  • Surgical repair: Very rare, for persistent leaks.
(Miller's Anesthesia, pp. 6115-6116)
Q34. What is high/total spinal anesthesia? How do you recognize and manage it?
Definition: Block extending to cervical levels or above - T1-T4 or higher.
Causes:
  • Excessive dose
  • Inadvertent intrathecal injection during intended epidural
  • Hyperbaric solution in Trendelenburg
  • Unrecognized dural puncture with epidural catheter dose
  • Short stature, pregnancy, obesity
Clinical Features (in order of ascending block):
  • Nausea and anxiety
  • Hypotension (sympathetic block)
  • Dyspnea, chest tightness (thoracic motor block - patient can feel but cannot breathe well)
  • Handgrip weakness (cervical roots)
  • Whispering voice (phrenic nerve compromise - C3-C5)
  • Apnea (C3-C5 diaphragm block)
  • Loss of consciousness (brainstem involvement, hypoperfusion)
  • Cardiac arrest (sympathetic block + hypoxia)
Management:
  • Call for help immediately
  • Airway: Secure airway - intubate if block at C3-C5, patient whispers or cannot breathe
  • Circulation: Aggressive fluid resuscitation; vasopressors (phenylephrine, ephedrine, norepinephrine); epinephrine for cardiac arrest - give early and aggressively
  • Position: Supine. Do NOT use Trendelenburg (worsens hypotension, decreases cerebral perfusion). Avoid reverse Trendelenburg (decreases cerebral blood flow). Flex neck to limit further cephalad spread.
  • Support: Continue IPPV as needed; bradycardia - atropine/epinephrine; reassure the patient
  • Important: delayed epinephrine in subarachnoid-induced cardiac arrest leads to poor neurological outcomes (Barash, p. 2865)
Q35. What is cauda equina syndrome in the context of spinal anesthesia?
A rare but catastrophic complication characterized by:
  • Perineal anesthesia/saddle anesthesia
  • Bowel and bladder dysfunction (incontinence or retention)
  • Variable lower extremity motor and sensory deficits
  • Usually permanent
Causes:
  • Neurotoxicity of local anesthetics (concentrated lidocaine pooling around sacral roots)
  • Associated with microcatheters for continuous spinal (now removed from US market)
  • Repeated dosing through single-shot techniques when block inadequate
  • Direct neural trauma
Pathophysiology: High concentrations of local anesthetic (especially 5% hyperbaric lidocaine) in dependent sacral subarachnoid space cause focal neurotoxicity. Microcatheters poorly disperse injected drug. Prevention: use dilute solutions, limit total dose, ensure uniform spread.
Q36. What is anterior spinal artery syndrome?
Infarction of the anterior two-thirds of the spinal cord due to compromise of the anterior spinal artery (ASA) or its feeding vessels (artery of Adamkiewicz). Causes:
  • Profound hypotension during spinal anesthesia
  • Vasopressors causing extreme vasoconstriction
  • Epidural hematoma compression
  • Aortic surgery, atherosclerosis
Features: Bilateral motor paralysis and loss of pain/temperature below the level; preserved vibration and proprioception (posterior columns spared - "dissociated sensory loss").
Q37. What is meningitis after spinal anesthesia? How is it prevented?
Types:
  1. Bacterial meningitis: From skin flora (commonest: Streptococcus viridans from the operator's oropharynx via droplet contamination), external contamination, hematogenous seeding from bacteremia. Strict aseptic technique, face mask wearing mandatory.
  2. Aseptic (chemical) meningitis: From detergents, antiseptics, preservatives in local anesthetic preparations. Use preservative-free drugs.
Prevention:
  • Strict asepsis (sterile gloves, mask, sterile field)
  • No talking over the sterile field
  • Chlorhexidine antisepsis (let dry completely before puncture)
  • Use single-use, preservative-free local anesthetic preparations
Q38. What is spinal/epidural hematoma? How is it managed?
A collection of blood in the epidural or subdural/subarachnoid space compressing the spinal cord.
Risk factors: Anticoagulant use, coagulopathy, thrombocytopenia, difficult traumatic placement, vascular malformation.
Features: New or progressive back pain, lower extremity weakness and sensory loss after initial block regression - "return of deficit after recovery." Bladder/bowel dysfunction.
Diagnosis: Urgent MRI spine
Management: Neurosurgical emergency - decompressive laminectomy within 6-8 hours of symptom onset for best neurological outcome. Reversal of anticoagulation.

SECTION 7: SPECIAL CLINICAL SCENARIOS

Q39. Describe spinal anesthesia for cesarean section.
  • Preferred technique in elective and most urgent cesarean sections
  • Level required: T4 (nipple line) - ensures block of uterine and peritoneal innervation
  • Drug: Hyperbaric bupivacaine 0.5%, typically 10-12.5 mg + intrathecal fentanyl 12.5-25 mcg + intrathecal morphine 100-150 mcg (for postoperative analgesia)
  • Positioning: Left lateral tilt (15 degrees) after positioning supine to prevent aortocaval compression
  • Hypotension prophylaxis: Phenylephrine infusion is currently preferred over ephedrine for most patients (maintains uteroplacental blood flow better; ephedrine crosses placenta more, associated with fetal acidosis). Co-loading with 1-1.5 L crystalloid preferred over pre-loading.
  • Height of block: Monitored by cold sensation; bilateral T4 confirmed before surgery starts
  • Complications specific to obstetric setting: Aortocaval compression, failed block requiring GA with difficult airway, high spinal from spread in pregnant patients
Q40. What are the precautions when performing spinal anesthesia in an elderly patient?
  • Reduced dose required - decreased CSF volume, increased neuronal sensitivity, increased spread
  • Higher block levels with standard doses
  • More pronounced cardiovascular effects (hypotension) - reduced cardiac reserve, inability to compensate
  • Degenerative spinal changes may make identification and needle placement difficult - paramedian approach often preferred
  • Calcified ligaments - more resistance felt
  • Pre-existing neurological deficits must be documented before block
  • Monitor for urinary retention
Q41. What are the considerations for spinal anesthesia in a patient with severe aortic stenosis?
Spinal anesthesia is relatively contraindicated in severe AS due to:
  • Fixed cardiac output cannot compensate for sudden fall in SVR
  • Acute severe hypotension can cause coronary ischemia, VF, circulatory collapse
If necessary: very small, incremental doses of local anesthetic (e.g., continuous spinal technique); aggressive pretreatment with vasopressors; arterial line monitoring; avoid hypovolemia; phenylephrine preferred to maintain SVR.
Q42. What is the management of hypotension during spinal anesthesia?
Incidence: up to 20-33% for non-obstetric cases; up to 70-80% with cesarean section spinals without prophylaxis.
Prevention:
  • Co-loading with crystalloid or colloid (crystalloid is effective but requires larger volumes)
  • Prophylactic vasopressor infusion: phenylephrine (preferred in obstetrics), norepinephrine
  • Avoid excessive dose of local anesthetic, avoid Trendelenburg
Treatment:
  • Lay patient supine; elevate legs
  • IV fluid bolus (500-1000 mL crystalloid)
  • Vasopressors: Ephedrine 5-10 mg IV bolus (mixed alpha and beta agonist; crosses placenta) or Phenylephrine 50-100 mcg IV bolus (pure alpha agonist; first-line in obstetrics)
  • Severe/refractory: norepinephrine or epinephrine
  • Bradycardia <50 bpm: atropine 0.6 mg IV; if severe: epinephrine 0.01-0.1 mg IV

SECTION 8: COMPARISON AND ADVANCED TOPICS

Q43. Compare spinal and epidural anesthesia.
FeatureSpinalEpidural
SpaceSubarachnoid (intrathecal)Epidural space
OnsetRapid (3-5 min)Slower (15-30 min)
Dose of LASmall (mg)Large (mL)
Quality of blockDense, reliableVariable, segmental possible
Spread controlLess (once injected)Better (incremental dosing via catheter)
DurationFixed by drug usedUnlimited with catheter
LAST riskVery lowHigher (large dose)
PDPH riskHigher (intentional dural puncture)Lower (unless ADP)
Blood pressure effectRapid, profoundMore gradual
Test doseNot neededMandatory
CSF markerYes (CSF in hub)No
CatheterRarely (CSA)Yes (continuous)
Q44. What is combined spinal-epidural (CSE) anesthesia? What are its advantages?
Technique: Spinal needle inserted through epidural (Tuohy) needle, intrathecal drug given, spinal needle removed, epidural catheter threaded.
Advantages:
  • Rapid onset from spinal component
  • Ability to extend/top up with epidural catheter (extending block duration, titrating for higher levels)
  • Reduces total spinal LA dose
  • Very popular for labor analgesia (low-dose spinal opioid + epidural catheter for ongoing labor)
  • Cesarean section: initial spinal; catheter available for top-up if surgery prolonged or conversion needed
Disadvantages:
  • More complex technique
  • Epidural catheter may not be reliable (not tested before spinal)
  • Higher risk of catheter migration or failure than standard epidural
Q45. What is the effect of pregnancy on spinal anesthesia?
Pregnant patients are more sensitive to local anesthetics and have:
  1. Reduced dose requirements (20-30% less) due to:
    • Decreased lumbosacral CSF volume (dilated epidural veins from IVC compression, displacing CSF)
    • Reduced CSF density (lower by ~0.001 g/mL)
    • Progesterone-mediated increase in neuronal sensitivity
    • Increased spread due to lumbar lordosis
    • Aortocaval compression increasing extradural vascular engorgement
  2. Risk of aortocaval compression in supine position
  3. Increased risk of high block
  4. Altered pharmacokinetics
Q46. How is block failure in spinal anesthesia defined and managed?
Complete failure: No block develops (approximately 0.5-2%). Due to:
  • LA not in subarachnoid space (subdural injection, needle tip outside subarachnoid space)
  • Drug error/empty syringe
  • Inadequate dose
Partial failure: Inadequate height or patchy block. Management:
  • Wait 15-20 minutes for full development
  • If truly failed: reposition patient, supplemental IV analgesia/sedation for minor deficiencies
  • Repeat spinal at different level with reduced dose (caution - total dose)
  • Convert to epidural or general anesthesia
  • Partial blocks: do not supplement with large epidural doses (risk of total spinal)
Q47. What is the "sitting" vs "lateral" position for spinal anesthesia? When is each used?
FeatureSittingLateral Decubitus
CSF identificationBest; CSF pressure highestAdequate
Hyperbaric spreadSaddle block (caudal)Dependent side preferentially
Hypobaric spreadCephalad spreadNon-dependent side
Cardiovascular stabilityLess stable (orthostatic)More stable
UseSaddle block, perineal surgeryUnilateral block, less cooperative patients
DifficultyRequires patient cooperation to flexEasier for anxious patients

SECTION 9: PHARMACOLOGY DEPTH

Q48. Compare hyperbaric and isobaric bupivacaine for spinal anesthesia.
Hyperbaric 0.5%Isobaric 0.5%
Preparation0.5% bupivacaine + 8% dextrose0.5% bupivacaine in normal saline
Density>CSF (hyperbaric)≈ CSF (isobaric)
SpreadGravity-dependent; predictablePosition-independent; less predictable
VariabilityLower interpatient variabilityHigher interpatient variability
Effect of positionSignificantMinimal
Block heightMore controllableLess controllable
DurationSimilarSimilar
Q49. What is the pharmacokinetic fate of intrathecally injected local anesthetics?
After intrathecal injection, local anesthetics:
  1. Distribute in CSF based on baricity, volume, dose, position
  2. Bind to neural tissue (nerve roots, spinal cord) - pharmacologically active component
  3. Absorbed into the epidural vasculature through arachnoid granulations and dural cuffs
  4. Undergo redistribution and systemic metabolism
  5. Amide LAs: hepatic metabolism (cytochrome P450)
  6. Ester LAs: plasma pseudocholinesterase hydrolysis
Block regression occurs as drug dissociates from Na+ channels and is removed by vasculature.
Q50. Why is cocaine no longer used in spinal anesthesia?
Cocaine was the first drug used for spinal anesthesia (Bier, 1898). It was replaced due to:
  • Significant toxicity: CNS stimulation, cardiovascular toxicity, addiction potential
  • Narrow therapeutic index
  • Cocaine inhibits reuptake of norepinephrine and dopamine - causing arrhythmias, hypertension, coronary spasm
  • Procaine replaced it, then lidocaine replaced procaine

SECTION 10: HISTORICAL, APPLIED, AND EXAMINER FAVORITES

Q51. Who first described spinal anesthesia? Describe the history.
  • 1898: August Bier (German surgeon) first performed spinal anesthesia with cocaine on a patient and also performed it on himself (administered by his assistant Hildebrandt). Both experienced PDPH afterward.
  • 1900s: Harvey Cushing and others in the US adopted the technique.
  • Procaine replaced cocaine; lidocaine replaced procaine.
  • Bupivacaine became standard in 1960s.
  • Pencil-point needles developed to reduce PDPH.
Q52. What is the "test dose" for epidural anesthesia? Is it used in spinal anesthesia?
The test dose (typically 3 mL of 1.5% lidocaine with epinephrine 1:200,000) is used before epidural dosing to detect:
  • Intravascular injection: tachycardia (HR increase >20 bpm within 45 seconds from epinephrine)
  • Intrathecal injection: rapid dense motor and sensory block within 3-5 minutes (from lidocaine dose)
For spinal anesthesia, a formal test dose is NOT required (confirmation is CSF flow in the needle hub). The drug is injected directly into CSF.
Q53. How does a spinal anesthetic affect intraocular pressure?
Spinal anesthesia causes a modest decrease in intraocular pressure (IOP) due to:
  • Systemic hypotension decreasing aqueous humor production
  • Cardiovascular depression
  • This effect is transient
Q54. What are the cardiovascular effects of spinal anesthesia at T4 level?
At T4, all sympathetic preganglionic fibers are blocked:
  • Complete sympathectomy of the lower body (splanchnic, renal, lumbar vasculature)
  • Blockade of cardioaccelerator fibers (T1-T4) - loss of reflex tachycardia, bradycardia, decreased cardiac output
  • Profound vasodilation (arterioles and venules)
  • Reduced venous return (venodilation, venous pooling)
  • Hypotension (decreased preload + decreased SVR)
  • No compensatory tachycardia
Q55. What is the density and specific gravity of CSF? Why does this matter?
  • CSF density: 1.00059 g/mL at 37°C
  • CSF specific gravity: 1.002-1.009
Baricity = density of LA solution / density of CSF
  • Hyperbaric: density > 1.00059 (achieved by adding glucose)
  • Hypobaric: density < 1.00059 (achieved by adding sterile water)
  • Isobaric: density ≈ 1.00059
This determines gravitational spread within the subarachnoid space. CSF density varies by sex, hormonal status, and pregnancy - clinically this may modestly affect baricity but is not routinely measured.
Q56. What are the effects of intrathecal morphine and what monitoring is required?
Effects:
  • Excellent postoperative analgesia (up to 24 hours with 100-300 mcg)
  • Side effects: respiratory depression (early <2 h and late 6-24 h), pruritus (most common, 30-100%, histamine-independent, opioid receptor-mediated, responds to naloxone or low-dose naltrexone), nausea/vomiting, urinary retention
Monitoring:
  • Respiratory monitoring for at least 12-24 hours post-injection (due to risk of delayed respiratory depression)
  • SpO2 monitoring recommended
  • Reversal: naloxone 40-100 mcg IV (may need infusion); caution - reverses analgesia too
Q57. What is the difference between sympathetic, sensory, and motor block levels in spinal anesthesia?
  • Sympathetic block: extends 2-3 segments ABOVE the sensory block level
  • Sensory block: clinical level tested with cold/pinprick
  • Motor block: 2-3 segments BELOW the sensory block level
This has practical significance: even a T10 sensory level produces sympathetic blockade up to T7-T8, with corresponding hemodynamic effects. A patient with T4 sensory block has sympathetic block to T1-T2 and cervical levels.

SECTION 11: RAPID-FIRE / SHORT ANSWER VIVA QUESTIONS

Q58. What is the minimum platelet count generally accepted for spinal anesthesia?
  • ~80,000/mm³ (80 × 10⁹/L) - institutional policies vary; some accept lower in certain obstetric contexts if trend is stable.
Q59. What is the maximum baricity at which a solution is still considered isobaric?
  • Isobaric range: density within ±0.001 g/mL of CSF density (approximately 0.9990-1.0010 g/mL).
Q60. What position should a patient be placed in to prevent further cephalad spread of a high spinal block?
  • Flex the neck (not Trendelenburg - this worsens hypotension). Some also suggest a slight head-up tilt for hyperbaric solutions.
Q61. What is the maximum safe dose of intrathecal morphine?
  • Doses >300 mcg are associated with increasing side effects without additional analgesic benefit. Most recommend keeping doses at 100-200 mcg for obstetrics and 200-300 mcg for major surgery.
Q62. What is the incidence of PDPH with a 25G Whitacre needle?
  • Approximately 0-1% (compared to ~3-5% with 22G Quincke).
Q63. What glucose concentration is used to make hyperbaric bupivacaine?
  • 8% dextrose (glucose). Commercial hyperbaric bupivacaine 0.5% is prepared in 8% dextrose.
Q64. What is the usual volume of autologous blood used for epidural blood patch?
  • 15-20 mL. Injected slowly until headache relieves or back/buttock pressure felt.
Q65. What is the "cauda equina" and at what spinal level does the cord end?
  • The cauda equina is the collection of lumbar and sacral nerve roots below the conus medullaris, resembling a horse's tail. The conus ends at L1-L2 in adults (range L1-L3).
Q66. What is the safe time interval between stopping LMWH (therapeutic dose) and performing spinal anesthesia?
  • 24 hours.
Q67. Name three drugs that can be used intrathecally as adjuvants to prolong block duration.
  • Morphine, fentanyl, clonidine (also: epinephrine, neostigmine, dexmedetomidine).
Q68. What ECG change is classically associated with massive sympathetic block from high spinal?
  • Bradycardia; in severe cases - sinus arrest, AV block, asystole.
Q69. What is the name of the scale used to assess motor block in spinal anesthesia?
  • Modified Bromage Scale (0-3).
Q70. What is the most common complaint after spinal anesthesia that is not a true complication?
  • Backache (injection site soreness) - occurs in ~5-30% and is usually transient (resolves in days).

Sources: Miller's Anesthesia 10e (Chapter 41), Morgan & Mikhail's Clinical Anesthesiology 7e (Chapter 41), Barash Clinical Anesthesia 9e (Chapter 35), Goodman & Gilman's Pharmacological Basis of Therapeutics.
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