Anatomy, Indication, contraindication, complications of spinal, epidural and caudal anesthesia

1. Neuraxial anesthesia(Spinal,
Epidural & Caudal block)
Dr. Tenzin Yoezer
KGUMSB

2. Roleofneuraxial
anesthesia in
anesthetic
practice
 Studies have shown – reduces postop morbidity when used alone
or in combination with GA
 Less convincing studies – it is associated reduced periop
mortality
 Reduces the incidence of venous thrombosis, PE, cardiac
complication, bleeding and transfusion, vascular graft occlusion,
pneumonia, respiratory depression in the Upper abdominal and
thoracic surgery
 Allows earlier return of bowel function
 Propose mechanism: avoidance of large dose of anesthetics and
opioids, reduces hypercoagulable state, increases tissue blood
flow, improving oxygenation from decreased splinting, enhances
persistalsis, suppressing neuroendocrine stress hormone

3. Theelderlysick
patient
 SA needs little or no sedation – reduces postop
delirium and cognitive dysfunction

4. Anatomy

5. Spinal
cord

6. Dural sacextends :
adult –S2
child –S3

7. Blood supply of spinal cord
Supplied by 2 arteries:
a) Single spinal artery – arises from vertebral artery
Supplies anterior 2/3
b) Paired posterior spinal arteries – supplies posterior 1/3
Receives additional supply from intercostal artery from
thoracic and lumbar
0ne important radicular artery arising from aorta– artery of
Adamkiewz/ arteria radicularis magna
Typically unilateral and nearly arises from left side
Provides major supply to anterior spinal cord
Injury to this artery – anterior spinal artery syndrome

8. Mechanism of action
• Principal action is at nerve root
• Blockade of posterior nerve root – somatic and visceral sensation
• Anterior nerve root blockade – motor and autonomic outflow
Somatic blockade
• Interrupts afferent transmission and abolishes efferent impulses
• Smaller and myelinated fibers – easily blocked
• Differential blockade – size and character of fiber, conc. of L A
• Judged by temperature sensitivity 2 segment cephalic whereas
sensation block(pain ,light touch) is usually several more cephalic
than motor blockade

9. Autonomic
blockade
 Sympathetic outflow – thoracolumbar
 Exist from T1 – L2
 Small and myelinated B fiber
 Parasympathetic outflow – craniosacral
 Neuraxial doesn't’t block vagus nerve
 Physiological response to neuraxial blockade is result
of decreased sympathetic tone or unopposed
parasympathetic tone, or both.

10. Cardiovascular
manifestation
 Variable BP drop and decrease in HR
 Determined by level of block
 More cephalic – more extensive sympathetic block
 Vasomotor tone is primarily determined by sympathetic fibers
from T5- L1
 Blocking those fibers – vasodilation of venous capacitance vessels
and pooling of blood in lower extremities and viscera.
 Effect of arterial vasodilation may be minimized by compensatory
vasoconstriction above the block
 High spinal – blocks compensatory vasoconstriction and blocks
cardiac sympathetic accelerator fibers (T1 – T4)
 Unopposed vagal tone – sudden cardiac arrest

11. Mxof
hypotension
andbradycardia
 Left uterine displacement in preganant woman
 Head-down position – autotransfusion
 IVF bolus 5-10 mL/kg
 Phenyephrine – direct alpha adrenergic,
 Vasoconstriction, increase SVR, reflexively increase
bradycardia
 Ephedrine – direct and indirect beta adrenergic effect
 Increase heart contractility and HR,vasocontriction
 Epinephrine – 2-5 mcg bolus
 vasopressor

12. Pulmonary
manifestation
 Minimal physiological alteration – diaphragm is innervated by C3-
C5
 Even with high thoracic – Vt is unchanged.
 Small decrease in vital capacity – loss of abdominal muscles
 But have to outweigh the advantages in severe chronic lung disease
– reply on intercostal and abdominal muscles
 In high spinal – impairs intercostal and abdominal muscles
 - impairs effective cough and clearing of secretion
 Surgery above umbilical – instead of SA, thoracic epidural with
diluted LA and opioids may be helpful
 Epidural analgesia – improves pulmonary outcome by reducing
incidence of pneumonia and respiratory failure, improves
oxygenation, decreases duration of ventilatory support

13. GI
manifestation
 Neuraxial block-induced sympathectomy allows vagal
dominance
 Leads to active peristalsis
 Therefore improves operative condition during
intestinal surgery when used adjunct to GA
 Post op epidural analgesia – earlier return of GI
function
 ** reduced hepatic blood flow due to decrease MAP

14. Urinarytract
manifestation
 Little effect on kidney function – RBF is maintained
with autoregulation
 Urinary retention – blockade of both sympathetic and
parasympathetic outflow of lumbosacral
 Thus need urinary catheter/ minimal use of fluid

15. Metabolicand
endocrine
 Surgical trauma and activation of somatic and visceral afferent
nerve – activation of systemic neuroendocrine stress response
 Releases adrenocorticotropic hormones, cortisol, epinephrine,
norepinephrine, vasopressin, RAS
 With neuraxial blockade:
 Partial suppression – major invasive abdominal/thoracic
surgery
 Total blockade – lower extremities surgery

16. Clinical
considerationto
SA&EA
ABSOLUTE CI
CONTROVERSIAL
 Lack of consent
 Infection at the site of injection
 Coagulopathy/bleeding diathesis
 Severe hypovolemia
 Increase ICP
RELATIVE CI
 Sepsis
 Uncooperative
 Preexisting neurology deficit
 Demyelinating lesion
 Stenotic valvular heart lesions
 LVO obstruction(hypertrophic obstructive cardiomyopathy)
 Severe spinal deformity
• Prior back surgery
• Complicated surgery
• Prolong operation
• Major blood loss
• Maneuvers that
compromise respiration

17. Neuraxial blockade in the setting of Anti-cogulant and antiplatelet
agent
American society if reginal and Pain medicine issue guideline
Incidence of epidural haematoma – 1:150,000

18. Oralantiplatelet
drugs
 Ticlopidine – 14 days
 Clopidogrel – 7days
 Prasugrel – 7-10 days
 Ticagrelor – 5 days
 Abiciximab – 48 hr
 Eptifibatide – 8 h
 Metabolite of clopidogrel and prasugrel inhits P2Y12
receptors – inhibits platelet aggregation

19. StandardUFH
 Mini-dose SC prophylaxis – not CI


21. Patient position
Sitting – “angry cat back”
Lateral decubitus –
fetal position
Buie’s(Jacknife) position

22. Factors
influencinglevel
ofspinalblock
MOST IMPORTANT FACTORS
 Baricty of anesthetic solution
 Position of the patient
 During injection
 Immediately after injection
 Drug dose: large dose more cephalic
 Site of injection
OTHER FACTORS
 Age
 CSF
 Curvature of the spine
 Drug volume
 Intra-abdominal pressure
 Needle direction: cephalic vs lateral/caudad
 Patient height
 pregnancy

23. Position of the spine
• With normal spine anatomy: apex of
thoracolumbar curvature is T4
• In supine position hyperbaic solution
produce block below T4
• “Glass spine effect”

24.  Specific gravity of CSF = 1.003 to 1.008 at 37oC
 Hyperbaracity = adding glucose
 Hypobaricity = adding steril water/fentanyl
 Lumbar CSF inversely correlates with dermatomes
spread
 Increase abdominal pressure – decrease CSF– greater
dermatomal spread
 Eg: epidural vein engorgement, pregnancy, ascites,
large abdominal tumor, obesity
 Age related low volume CSF
 Kyphoscolosis – low volume CSF

25. Spinal anesthetic agents

26. Epidural anesthesia

27. Epidural
anesthesia
 Performed at lumbar, thoracic, cervical, sacral(caudual
block)
 Content of epidural space:
 Nerve root - travel in the space laterally
 Fatty connective tissue
 Lymphatics
 Venous (Batsons) plexus
 Septa/connective tissue bands – reason for unilateral
block

28. Angulation of epidural needle
Note that acute angle (30 -50oC
is required for thoracic whereas only
slightly cephalid orientation is required
for cervical and lumbar

29. Epidural
activation
 Volume and conc. in epidural is larger- high chance of
toxicity if given intrathecally or intravascular if full
dose given
 To safegaurd – test dose / increamental dose
 Classic test dose: 3 mL of 1.5% lidocaine with 1:200,00
epiephrine(0.005 mg/mL)
 Intravacular injection: tachycardia, increasing size of T
wave

30. Caudad block

31.  Dosage – 0.5 -1 mg/kg of 0.125% to .25% bupi/ ropi with
or without epinephrin
 ***Armitage formula: 0.25% 0f bupi
 0.5 mL/kg for lumbosacral
 1 mL/kg for thoraco-lumbar
 1.25 mL/kg for mid thoraci
 Opiods, morphine can be included
 Anorectal surgery:
 15-20mL of 1.5% to 2% lidocaine with or without epi
 May add 50-100mcg Fentanyl
 **Avoid caudal block in Pionidal cyst- risk of infection

32. Factorsaffecting
levelof block
 Is not predictable as SA
 Generally in Aduly 1-2 mL of LA per segment block is
accepted
 Eg: to achieve T4 sensory level from L4/5 would
injection require 12-24 mL
 For segmental or analgesic block, less volume is
required

33. Factorsaffecting
levelof block
 1) Age – dose requirement decreases with age (probably
due to age related decrease in the size of compliance of
epidural space)
 2) Height – shorter require 1mL/segment, taller
2mL/segment
 3) Gravity
 4) Additive to LA –
 Opioids affects quality of block than duration
 Epinephrine 5mcg/mL prolongs duration by decreasing
vascular absorption and reduces peak systemic blood
volume

34. Epidural agents
• Following initial 1-2mL/segment, repeated dose
on fixed interval until desired dose is achieved
• Once some regression in sensory level has
occurred – 1/3 or ½ of initial activation dose is
reinjected at incremental dose
• Previously chlorprocaine with bisulfite was
associated with neurotoxicity, with EDTA severe
backache(?local hypocalcemia)
• Surgical anesthesia – 0.5% Bupivacaine
• 0.75% Bupi no longer used in obstetric – cardiac
arrest after accidental IV injection
• 0.0625% Bupi fro Labour analgesia
• Ropivacaine produces less motor block than at
Bupi at similar conc maintaining satisfactory
sensory block

35. LApH
adjustment
 LA solution is acidic for cheamically stable and
bacteriostatic
 Addition of epinephrine makes more acidic than palin
 Weak bases – primarily exist as ionic form
 Onset of action is slow with low pH
 Need incharged ion to cross lipid membrane
 Addition of NaHCO2 (1mEq/10mL) speeds onset
 With Bupivacaine above pH 6.8, NaHCO2 precipitates
and thus not added

36. Failedepidural
block
 1) False epidural space –
 Soft ligament
 Entry into paraspinous muscle
 Intrathecal
 Subdural
 Intravenous
 2) Unilateral block – withdraw 1-2 cm
 Reinject and turn pt to unblocked side
 3) Segmental sparing – due to septation
 Additional LA and turning to unblocked side
 4) Sacral sparing – large nerve root of L5, S1, S2 and delay
onset
 Elevate the bed and reinject the LA
 5) Visceral pain during traction despite good block –visceral
fibers that travel with vagus nerve isresponsible

37. Caudual block

38.  Commonly employed to peadiatric surgery with GA in
surgeries below diaphragm –mainly to avoid toxic
effect from GA
 In adult used in anorectal surgery
 Needle/catheter penetrates sacrococcygeal ligament
 Dural sac extends till S1 in adult and S3 in infants (
high chance of intrathecal injection)

39. Complicationof
neuraxialblock
 Large survey shows low incidence of serious
compliction
 ASA closed claim project data over 20yr(1980 – 1999):
 Regional anesthesia accounts for 18% liability
 Temporary/nondisabling -13%
 Permanent nerve injury – 10%
 Permanenant brain damage – 8%
 Other permanent injuries – 4%
 Majority of claim involved lumbar epidural (42%),
spinal anesthesia (34%).
 Occurs mostly in obstetric patients

40. A)Complication
associated with
excessresponses
toappropriately
placed drug
 1) High neural blockade
 can occur both in SA and EA
 Casues:
 Excessive dose
 Failure to reduce standard doses in selected pts ( elderly,
pregnant, obese, short stature)
 Unusual sensitivity/ speed of LA
 Clinical features:
 Dyspnea,numbness or weakness of UL, nausea,
hypotension
 Mx:
 Reassurance to pt
 O2
 Treatment of bradycardia and hypotension

41. 2)Highspinal
3)Totalspinal
 SA ascending into cervical levels cases severe
hypotension, bradycardia, and respiratory insufficiency
 Unconsciousness, apnea, and hypotension resulting
from high level of anesthesia are referred to as “HIGH
SPINAL”, or when it extends to cranial nerves –
”TOTAL SPINAL”
 Apnea is result of severe sustained hypotension and
medullary hypoperfusion
 Mx of high/total spinal:
 Supporting ventilation
 Supplementing oxygen
 Supporting circulation- fluids, vasopressors, fluid
 Intubation if necessary/ indicated

42. 4)Cardiacarrest
duringSA
 High incidence -1:1500
 Many cases were preceded by bradycardia.
 Many cases in young and healthy pts
 Prevention:
 Correction of hypovolemia
 Prompt treatment of hypovolemia and bradycardia

43. 5)Urinary
retention
 Blockade of S2-4 roots – decrease urinary bladder tone
and inhibits voiding reflex
 Other complications:
 6) Anterior spinal artery syndrome
 7) Horner syndrome

44. B)Complication
associated with
needle or
catheter insertion
 1) Inadequate anesthesia or analgesia
 Inversely proportional to experience
 Movement of needle during injection
 Incomplete entry of needle opening into the space
 Injection of LA solution into nerve root sleeve

45. 2)Intravascular
injection
 CNS – tinnitus, metallic test, circumoral
numbness,seizure, unconscious
 CVS – hypotension, arrhythmias, depressed contractility
 Common in epidural and caudual since SA uses small dose
 Prevention:
 Aspirating before injection
 Test dose
 Incremental dose
 Mx- ACLS
 20% Lipid emulsion (1.5 mL/kg bolus, 0.25 mL/kg/min or
15 mL/kg/h)
 Rank of LA potency is same rank in producing seizure and
cardiac toxicty
 Levobupivacaine, Ropivacaine, Bupivacaine, Tetracaine
>lidocaine, mepivacaine >chloroprocaine

46. 3)Totalspinal
anesthesia
 Accidental injection into intrathecal during epidural and
caudal
 4) Subdural injection
 Can happen during several attempts for EA
 Onset is 15- 30 minutes ( compared to rapid onset in
intrathecal) and is patchy block
 Can manifest as high spinal block
 5) Back ache
 Due to tissue trauma while inserting needle
 Bruising and local inflammatory response with or without
reflex muscle spasm
 Usually mild and self limiting
 May last for few weeks – subsides by PCM, NSAIDs
 Have to consider epidural haematoma or abscess
 *** majority of the population has chronic backache

47. 6)Neurologicalinjury
a)nerverootdamage
b)Spinalcordinjury
c)caudaequinal
syndrome
 More perplexing /distressing
 Must rule out epidural hematoma and abscess
 Nerve Root or Cord(if above L1 in adult and L3 in
children) may be injured
 Most resolve spontaneously but, some are permanent
 If sustained paresthesia during procedure – immediately
withdraw needle.
 Stop injection immediately if there is pain
 7) Dural puncture/leak
 PDPH
 Diplopia
 Tinnitus

48. 8)
Epidural/spinal
hematoma
 Needle or Cather trauma to epidural vein
 Incidence of Spinal hematoma – 1: 150,000
 For epidural hematoma – 1: 220,000
 Onset is sudden ( compared to epidural abscess)
 Red flag symptoms:
 Sharp back ache and leg pain with motor weakness or
sphincter dysfunction, or both
 If suspected: urgent CT/ MRI
 Neurological consultation
 Outcome – good neurological outcome in prompt
surgical decompression
 Prevention: avoid neuraxail with coagulopathy,
significant thrombocytopenia, platelet dysfunction,
those on fibrinolytic or thrombolytic therapy

49. 9)Meningitis
and
arachnoiditis
 Due to contamination of the equipment, solution or
organism tracked in from the skin
 Indwelling catheter may colonize with skin organism
 Strict aseptic technique- esp in obstetric where family
members want to see the procedure
 Family members should also wear mask and gown

50. 10) Epidural
abscess
 Spinal epidural abscess is rare but potentially
devastating complication
 Incidence varies from 1:6500 to 1:500,000 epidural
 Most commonly seen in epidural catheter
 There are 4 classic stages of EA:
 1st stage – back pain that is intensified by percussion
over the spine
 2nd stage – nerve root or radicular pain
 3rd stage – motor and sensory deficit or sphincter
dysfunction
 4th stage – paraplegia or paralysis

51. Prognosis correlates with degree if neurological dysfunction at the time of diagnosis
Clue – fever and back pain after epidural anesthesia
Once suspected, remove epidural catheter and tip send for culture
Injection site – examined for signs of infection: pus if present for culture
Blood culture
If highly suspicious start antibiotic that covers staphylococcus ( aureus and
epidermis)
MRI/CT spine to rule out
Urgent consultation with neurosurgical and infectious specialist
Surgery – in addition to pus drainage, laminectomy
Prevention:
Minimizing catheter manipulation and maintaining closed system
Using micropore(0.22um) bacterial filter
Removing after defined time( some clinician remove after 4 days)

52. 11)Shearingof
anepidural
catheter
 Risk of shearing and breaking of epidural catheter if
withdrawn through needle
 If catheter breaks off within space – observe the
patient
 If superficial – remove surgically

53. C) Complication
associatedwith
drugtoxicity
 1) LAST
 Excessive absorption of LA from epidural or caudal
 Rare if appropriate dose is administered
 2) Transient neurological symptoms(TNS)
 Also referred as transient radicular irradiation
 Characterized by back pain radiating to leg without sensory or motor
deficit, occurring after resolution of SA and resolving within few days
 Commonly associated with hyperbaric lidocaine (12%), tetracaine(2%),
Bupivacaine(1%), mepivacaine, prilocaine, procaine, subarachnoid
ropivacaine
 Pathogenesis – conc dependent neurotoxicity of LA
 Incidence is greatest among outpatient, particularly male pt
undergoing surgery in lithotomy position.
 Less incidence among other than lithotomy position
 3) Cauda equina syndrome

54. Thanks
Morgan and Makill