This document provides information on regional anesthesia techniques including spinal and epidural anesthesia. It discusses indications, contraindications, mechanisms of action, physiological effects, positioning, anatomical approaches, factors affecting the block, doses of local anesthetics, and complications. Specifically, it focuses on the cardiovascular, respiratory, gastrointestinal, and renal effects of spinal anesthesia as well as complications such as hypotension, bradycardia, high or total spinal blocks.
5. Mechanism of action
Local anaesthetic acts on nerve roots and conduction block
occurs
LA binds to α subunit of VG Na+ channels and prevent
channel activation ,Na+ influx and depolarisation
6. PHYSIOLOGICAL EFFECTS
Direct effects:
Site of action:
1 Primary – nerve roots
2 Secondary– dorsal root ganglia , post. Horn & Ant. Horn
3 Limited & incomplete – ascending & descending tracts in
spinal cord .
In spinal: LA act directly on nerve roots
; fast onset and fast sympathetic block (need small LA volume
)
In Epidural: LA act on nerve roots covering with dural sleeves
; Slow onset and gradual sympathetic block (need large LA
volume )
7. EFFECT ON NERVE FIBERS
Smaller & non myelinated sensory fiber of nerve root are more
sensitive than motor fibers.
Large myelinated- less blockade
Autonomic fibers are blocked first followed by sensory &
motor fibers are last to be blocked.
Differential blockade: A>S>M ( 2 segment difference)
Posterior root: sensory, pain
Anterior root: Efferent Somatic
Autonomic
Point near site of anaesthetic agent deposition is the last to
recover.
8. SEQUENCE OF NERVE BLOCK
Autonomic block
Loss of temperature sensation
Loss of slow pain, then fast pain
Loss of tactile sensation
Motor paralysis
Loss of pressure sensation
Loss of proprioception and joint sensation
9. POSITIONING DURING SPINAL
Lateral decubitus position (fetal position)
Sitting position – max flexion
Prone position for hypo, isobaric drugs
(Buie’s Jack knife position)
Adv- position not changed (for anorectal sx)
Disadvantage- CSF free flow absent
10. ANATOMICAL APPROACH
(1) Midline : Most popular approach.
Needle should be inserted in midline
Spinous process little caudad from origin, So needle
directed slight cephalad
If bone contacted superficially- hitting lower spinous process
(redirect cephalad)
If bone contacted deep - hitting upper spinous process (redirect
caudad)
If in lateral – lamina is hitted –redirect needle
11. (2) Paramedian:
Selected for pts. Who cant
position (severe arthritis ,
kyphoscoliosis & prior lumbar spine
surgery.)
Needle inserted 2 cm lateral to
inferior aspect of superior spinous
process of desired level
Needle directed and advanced at
an angle of 10-25◦ to mid line.
If bone contacted superficially-
hitting medial part of lower lamina
(redirect upward & laterally)
If bone contacted deep - hitting
lateral part of lower lamina (redirect
upward & medially)
12. Midline Approach Paramedian approach
Skin Skin
Subcutaneous fat Subcutaneous fat
Supraspinous ligament Paraspinous muscle
Interspinous ligament
Ligamentum flavum Ligmentum flavum
Epidural space Epidural space
Dura mater Dura mater
Subdural space Subdural space
Arachnoid mater Arachnoid mater
Subarachnoid space Subarachnoid space
13. (3) Taylor approach:
Needle is directed 1 cm medial & 1 cm caudal to posterio
superior iliac spine.
Needle is directed upwards, medially & forward at an
angle of about 50° to reach L5 –S1 space.
Usefulness in spine fusion, kyphoscoliosis, skin infection
in lumbar region.
14. PROCEDURE
Preparation of patient
Premedication
Securing I V line
Preloading
Monitors
Aseptic precautions-
sterile gown, mask, scrub
Povidone iodine
Alcohol (spirit)
Meningitis-
Infective- oral/nasopharyngeal microorganism can go in
CSF
Chemical- if betadine not cleared
15. Spinal Needles
Needle gauge available 19G-30G.
but 22G-27G used these days.
Cutting tip- end injection, easy to insert in skin,
subcut. eg- quincke
Blunt tip/ pencil tip- side injection, easy to
identify dura, reduce the damage of dural fibres
and loss of CSF, promote healing of dura. eg-
whitacre, sprotte
(less PDPH, failed block)
Length- 9cm/3.5 inch long
- 12.7cm/5 inch long for obese
EYE: parallel to dura fibres, so fibres are
separated not teared.
- keep eye up in lateral position.
- keep eye on side in sitting.
16. FACTORS AFFECTING BLOCK
1)Patient related
Age
Height
Weight
Gender
Intra abdominal
pressure(pregnancy,ascities,obesity,abd tumor
Anatomy of vert column/spinal cord(kyphoscoliosis)
Position-T4 is apex of thoracolumbar curve
Supine- T4-T8 is most dependent area
T5,6,7 lowest point where LA settles
17. FACTORS AFFECTING BLOCK
2)Technique of injection
Site
Direction of injection
Direction of bevel
Use of barbotage
Rate of injection
BARBOTAGE : Technique of repeated stirring up to
inc.turbulance & mixing of anaesthetic sol. to increase
distribution in SA space. It can achieve a higher block then the
usual.
18. FACTORS AFFECTING BLOCK
3)Characteristics of drug
Density(baricity) [most important]
Temperature(inversely prop to baricity)
Amount- Directly proportional
Concentration Directly proportional
Volume- Directly propotional
Vasoconstrictors(prolonged duration)
4)Characteristics of CSF
Volume(dec CSF vol – high block =ELDERLY, INC IAP)
Pressure(high CSF pr –high
block=COUGHING,STRAINING)
19. Baricity of LA
Specific gravity of CSF- 1.003-1.008
Isobaric - same SG as CSF- remain at the level of injection
Hyperbaric- heavy than CSF (by adding dextrose)
spread towards gravity
Hypobaric- lighter than CSF (by adding water/fentanyl)
spread away from gravity
Temp inversely prop to baricity
so at 37 degree all plain solution are hypobaric.
20. Head down position
Hyperbaric -spread cephalad,Hypobaric- spread caudad
Head up position
Hyperbaric - spread caudad,Hypobaric- spread cephalad
Lateral position
Hyperbaric- dependant side,Hypobaric- non dependant side
Hyperbaric sol are used in spinal- predictable and reliable
Difficulty in maintaining pharmacological stability of
hyperbaric solution for clinical use
21. Baricity of LA
Specific Gravity of CSF 1.003-1.008
0.5%BUPIVACAINE (plain) 0.999
2%LIDOCAINE (plain) 1.00004
0.5%BUPIVACAINE (heavy) 1.025(8.25% dextrose)
5%LIDOCAINE (heavy) 1.03(7.5% dextrose)
0.5%LEVOBUPIVACAINE (plain) 1.004
0.5%/0.75%ROPIVACAINE (plain) 1.009
2%CHLORPROCAINE 1.002
22. DOSES OF BUPIVACAINE 0.5% H
(gold standard agent for spinal)
Wt. Dose
0-5kg 0.5-0.6 mg/kg
5-15kg 0.4 mg/kg
>15kg 0.3 mg/kg
23. Dosages and Actions of Commonly Used Spinal Anesthetic Agents
Doses (mg) Duration
Drug Preparatio
n
Perineum
, Lower
Limbs
Lower
Abdomen
Upper
Abdome
n
Plain Epinephrin
e
Lidocaine 5% in 7.5%
glucose
25-50 50-75 75-100 60-75 60-90
Bupivacai
ne
0.5% in
8.25%dextr
ose
4-10 12-14 12-18 90-120 100-150
levobupiv
acaine
0.5%,
0.75%
8-12 12-16 16-18 90-120
Ropivacai
ne
0.2-1%
Soln
8-12 12-16 16-18 90-120
Chlorproc
aine
2%,3% 30-60 mg <60 min
Epinephrine is not used now, as it causes vasoconstriction and neurological
ischemic injury
24. Paediatric spinal Adult spinal
Lumbar puncture site below L3,
Because spinal cord end @ L3
Below L1
Spinal cord end @ L1
Dural sac end at S3
So during caudal subarachnoid inj
can
End at S2
Spinal anaesthetic dose is high
(0.5 & 0.4 mg/kg) because,
i) CSF volume is more 4ml/kg
ii) 50% CSF in spinal subarach
space (more dilution)
Dose is low (0.3 mg/kg)
i) 2ml/kg
ii) 25% CSF in spinal space
Duration of block is SHORT(1hrs)
Because of high spinal blood flow
Prolong duration (2hrs)
Hypotension is less,
Preloading is not needed,
Because of imature
sympathetic system
Hypotension is common,
hence preloading is needed.
Because of sympatholysis
25. Sensory Block
Level assessed by blunt pin prick, cold temp (spirit swab)
for dermatomal spread.
33. Gastro – intestinal Effects
T5-L1 Sympathetic blockade, vagal parasymp to GIT
causes contracted gut with active peristalsis
Vagal stimulation causes increase in peristalsis and
intraluminal pressure.
That’s why stool is passed after spinal if enema is not
given
As BP decrease- Hepatic blood flow
34. Renal effects
Renal blood flow maintained by autoregulation (MAP 80-180)
Urinary tract- T10-L2 (symp), S2,3,4 (parasymp)
both blocked- so urinary retention
35. Stress response blunting
Neuraxial block inhibits stress response (symp - )
Stress response: Surgical trauma
Somatic and visceral afferent N fibres and local
inflammation
Secretion of pituitary H and sympathetic stimulation
Secondary effect on endocrine glands
Increase of- Adr, Noradr, cortisol, ACTH, vasopressin, renin,
angiotensin, aldosterone
36. Complications OF NEURAXIAL BLOCK
Adverse Or Exaggerated
Physiological Responses
• Hypotension:
nausea,vomiting
• Bradycardia
• High spinal block
• Total spinal anesthesia
• Cardiac arrest
• Subdural injection
• Anterior spinal artery
syndrome
• Horner syndrome
• Urinary retention
Drug Toxicity
• Systemic local anesthetic
toxicity
• Transient neurological
symptoms
• Cauda equina syndrome
39. High Spinal and Total Spinal
Anaesthesia
Due to exagerrated dermatomal spread of neural block with
spinal or epidural anaesthesia.
Due to excess dose – epidual dose injected in spinal, or
failure to reduce the dose (eg: in elderly,pregnant, obese,
short stature), unpredictable spread (kyphoscoliosis)
High spinal: spinal anaesthesia spreading to cervical level
Total spinal: when block extends to cranial nerves
S/S: Severe hypotension, bradycardia, resp.insuffciency,
apnea, unconsciouness.
Apnea: is due to sustained hypotension and medullary
hypoperfusion, rather then phrenic nerve
paralysis(C3,C4,C5) Bcoz large A-alpha fibres are difficult to
block.
Rx: Supportive to CVS and RESP.
Self regression of block occurs with time.
40. Cardiac arrest
Cause
High Spread: T1-4 Cardioacceleratory fibres block- Bradycardia
T1-L2 sympathetic block- Vasodilation
Decreased venous return stimulates bezold jerisch reflex and
reverse bainbridge, leads to intense vagal stimulation l/t cardiac
arrest and resp arrest. (high vagal tone, young adult, dec.preload)
Over sedation, unrecognised hypoventilation and hypoxia.
To prevent cardiac arrest:
i) correction of hypovolumia/preload
ii)Prompt Rx of hypotension and bradycardia
by early use of atropine,ephedrine,adrenaline(3-5mcg bolus)
Remember:
Bezold Jarisch reflex-
Venous return: HR
41. Anterior Spinal Artery Syndrome
Cause: decreased blood flow in ant.spinal artery d/t
prolonged severe hypotension together with indcreased
intraspinal pressure, this l/t
Loss of function of anterior 2/3rd of spinal cord (descending
corticospinal , ascending apinothalamic tract, & autonomic
fibres)
S/S: i) bilateral lower limb weakness/paralysis
ii) loss of bowel n bladder function
iii) loss of pain, temp sensation
iv) hypotension
v) with/without loss of sensation
42. Subdural Block
Subdural space is potential space between
dura and arachenoid , which continues in
cranium
Accidentally L.A is injected in this space.
S/S: i) disproportinate high sensory block,
involving cranial nerves
ii) slow onset of neural block( 15-30mins)
iii) failure of intended block
iv) relative lack of sympathetic block and
motor spared
v) progressive resp depression and
incordination rather then apnea.
Rx: Supportive, Recovery 1hr to several
hours
43. Horner’s Syndrome
Due to sympathetic block of eye n face (C8-T1, rarely upto
T4)
S/S: miosis, ptosis, enophthalamos, anhidrosis.
It’s a temporary effect
Recovers as block regress.
44. Intravascular injection
High dose of L.A effect CNS & CVS
S/S:
CNS: early – tinnitus, lingual sensation, perioral
numbness.
Late- seizures, uncosciousness.
CVS: Hypotension, arrythemia, decreased cardiac
contractlity
Seen more in Epidural and Caudal
Rx: i) Supportive
ii) Lipid emulsion
Precaution: Carefull aspiration before injection.
Close observation of early signs
45. PDPH and Cranial Nerves Palsy
Headache developing within 5days of dural puncture and resolving
spontaneously within 1 wk/48hrs after epi.blood patch
Mech: CSF leak from dural hole lead to intracranial hypotension, traction
on meninges, dura, tentorium, blood vessels, cranial nerves (coning may
occur )
S/S: Headache- bilateral, frontal/retro orbital/occipital
extending upto neck.
-It is throbbing/constant asso. with photophobia, nausea
-aggrevated by sitting n standing, relived by lying down
-onset 12-72hrs after procedure
Traction on cranial nerves lead to diplopia(CN 6th),tinnitus(CN 8th)
Predisposing factors: young age, female, pregnancy, large bore needle,
cutting tip needle.(so,use of 27G pencil tip needle)
Rx:Recumbent position, oral/I.V fluid, analgesic, caffeine, ACTH.
Epidural blood patch
46. Spinal & Epidural hematoma
Incidence- epidural(1:150000), spinal(1:220000)
Lead to hematomas mass effect, compressing neural
tissue and ischemic injury.
S/S: sharp back and leg pain with motor weakness and/or
bowel n bladder dysfunction
Suspect when, block recovery not occurs in 6hrs
Confirmed by MRI n CT
Rx: surgical decompression in 8-12hrs, to prevent
irreversiable neural damage.
Use proper coagulation guidelines to be followed.
47. Neurological Injury
Direct neurological injection into spinal cord causes
paraplegia
Damage to conus medullaris causes isolated sacral nerve
dysfunction, including paralysis of biceps femoris,
anaesthesia of post.thigh n saddle area, loss of bowel n
bladder function.
Cauda equina syndrome(CES): disrupt of motor and sensory
function of lower extremities and bladder.
Prevention: Intense pain during drug injection signals the
intraneural injection and to be avoided
Was seen when spinal catheters were used, hence its use is
stoppped now.
48. Transient Neurological
Symptoms
also referred to as transient radicular irritation
Characterized by dysesthesia, burning pain n aching in lower extremitis and
buttocks, occurring after the resolution of spinal anesthesia and resolving
spontaneously within several days(1-4wks).
It is most commonly associated with hyperbaric lidocaine (incidence up to
11.9%), but has also been reported with tetracaine (1.6%), bupivacaine
(1.3%), mepivacaine, prilocaine, procaine, and subarachnoid ropivacaine.
There are also case reports of TNS following epidural anesthesia.
The incidence of this syndrome is greatest among outpatients, undergoing
surgery in the lithotomy position, and least among inpatients undergoing
surgery in positions other than lithotomy.
The pathogenesis of TNS is believed to represent concentration-dependent
neurotoxicity of local anesthetics.
49. Meningitis/Arachnoiditis
Iatrogenic
0-0.04% incidence
d/t: -breach in aseptic
precautions
-needles,drugs,infective
-chemical meningitis
S/S:-fever/apyrexia
-headache, not relived by
recumbent, analgesics
-neck stiffness, +ve kerning
Onset: acute within 24hr of L.P
• Dx:-CSF exam- TLC,CSF Culture
-blood culture
-CT scan, MRI
-fundoscopy: rule out
papilledema
• Rx: Antibiotics
• Precautions:
-strict aseptic precaution
-wear mask
-cleansing prep to be dried, to
avoid chemical meningitis
-autoclaving,ETO of equipment
50. Repeat Spinal Anaesthesia
After failed spinal.
No block/minimal block (B-
0,1)
Sensory level < L-4/L-1
risk of exagerrated
sympathetic block, CVS
collapse, High spinal.
Risk of neurological damage
Use reduced dose, safe LA
Lido(H)+dibucaine(H)
reported to cause prolonged
neurological defecit.
Frequent Spinal.
• For repeated
surg.procedure(eg.trauma)
• ensure complete block
recovery from previous spinal
• to assess neurlogical damage,
hematoma,PDPH due to
prev.LP
• So keep safe gap of 24-48hr
• Consider other risk factors
Risk lies on anaesthesiologist,
as there is no clear guidelines