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Presenter - Dr Amit/Dr Abhay
Guide - Dr Vinod Sir
Moderator - Dr Surendra sir
ANESTHESIA
Anesthesia
Regional
Anesthesia
Local
anesthesia
Peripheral
nerve block
Neuraxial
block
Spinal Epidural CSE
General
Anesthesia
INDICATIONS
 Hernia repair
 Gynaecological operations
 Caesarean section.
 Urological surgery
 For sx on genitalia & perineal region.
 For lower limb surgery
CONTRAINDICATIONS
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
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 )
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.
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
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
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
(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)
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
(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.
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
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.
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
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.
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)
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.
 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
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
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
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
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
Sensory Block
 Level assessed by blunt pin prick, cold temp (spirit swab)
for dermatomal spread.
Motor Block
 Assessed by Modified bromage score
B-3
B-2
B-1
B-0
Physiological Effect of
Spinal Anaesthesia
Cardiovascular Effects
Arterial
vasodilation
SVR
BP
Sympathetic block (T1-L2)
Vasomotor tone block T5-L1
Vasodilation
Venous return
venodilation
Venous pooling
Cardiovascular Effects
 Marey’s law - BP  HR Decreased BP/CO
Decreased baroreceptor
discharge in carotid and aortic
bodies
Nucleus tractus solitarius in
Medulla
Vagal -
Increased HR
Symapathetic +
HR
CO
Vasoconstriction
Cardiovascular Effects
 Bainbridge reflex - venous return: HR
 Atrial reflex
Increased
cardiac
preload
(VR)
Atrial(RA)
stretch
receptor
stimulated
NTS
Decreased
vagal
discharge
Increased
HR
Decreased
preload
(VR)
Less
stretch of
atrial
receptors
NTS
Increased
vagal
discharge
Decreased
HR
Xt
h
Xt
h
Cardiovascular Effects
 Bezold Jarisch reflex- venous return: HR
Poor venous
return
Increased
contraction
on empty
ventricle
Vent.
Endocardial
receptors
(75%) RA
receptors
(25%)
Nucleus
Tractus
Solitarius of
medulla
X
Vagal +
Bradycardia
Cardiac arrest
in spinal
Resp centre (–)
Respiratory
arrest in
spinal
 Seen in hemorrhage,
hypovolemia, spinal anesthesia,
MI, contrast injection, exercise in
severe AS, Interscalene BP block,
vasovagal syncope, astronauts.
Respiratory Effects
Hypotension
Hypoperfusion
of MO
Resp centre - Resp arrest
Diaphragm (C3,4,5)- Aα- large, myelinated fibres
Not blocked even in high spinal
So resp arrest does not occur due to diaphragmatic paralysis
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
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
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
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
 Backache
 Dural puncture/leak
-Postdural puncture
headache
-Diplopia
-Tinnitus
 Neural injury
-Nerve root damage
-Spinal cord damage
-Cauda equina syndrome
 Bleeding
-Intraspinal/epidural
hematoma
• Misplacement
-No effect/inadequate
anesthesia
-Subdural block
-Inadvertent subarachnoid block
-Inadvertent intravascular
injection
• Inflammation
-Arachnoiditis
• Infection
-Meningitis
-Epidural abscess
Complications related to needle/catheter
placement
Hypotension & Bradycardia
 Cause: i) T5-L1 block Vasodilation
ii) T1-T4 block HR
 Volume preload 10-20ml/kg
 Bolus 5-10 ml/kg if hypotension occurs
 Mixed agent- ephedrine/ mephentermine
(direct/ indirect β adrenergic effect)
Vasoconstriction (inc- BP, HR and contractility)
 Adr 2-5ug bolus, dopamine
 Pure α agonist (phenylephrine): Inc SVR- reflex
bradycardia
 Atropine for bradycardia
Urinary Retention
• Block of S-2,3,4
SVR BP
Venous return Vagal
+
HR
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.
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
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
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
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.
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
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
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.
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.
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.
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
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
1:Mechanism/causes of failed block
2:
Management
options
3: Measures to
revive the
block
Algorithm:
safe approach
to failed spinal
anaesthesia.
THANK YOU

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Regional Anesthesia Techniques and Physiological Effects

  • 1. Presenter - Dr Amit/Dr Abhay Guide - Dr Vinod Sir Moderator - Dr Surendra sir
  • 3. INDICATIONS  Hernia repair  Gynaecological operations  Caesarean section.  Urological surgery  For sx on genitalia & perineal region.  For lower limb surgery
  • 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.
  • 26. Motor Block  Assessed by Modified bromage score B-3 B-2 B-1 B-0
  • 28. Cardiovascular Effects Arterial vasodilation SVR BP Sympathetic block (T1-L2) Vasomotor tone block T5-L1 Vasodilation Venous return venodilation Venous pooling
  • 29. Cardiovascular Effects  Marey’s law - BP  HR Decreased BP/CO Decreased baroreceptor discharge in carotid and aortic bodies Nucleus tractus solitarius in Medulla Vagal - Increased HR Symapathetic + HR CO Vasoconstriction
  • 30. Cardiovascular Effects  Bainbridge reflex - venous return: HR  Atrial reflex Increased cardiac preload (VR) Atrial(RA) stretch receptor stimulated NTS Decreased vagal discharge Increased HR Decreased preload (VR) Less stretch of atrial receptors NTS Increased vagal discharge Decreased HR Xt h Xt h
  • 31. Cardiovascular Effects  Bezold Jarisch reflex- venous return: HR Poor venous return Increased contraction on empty ventricle Vent. Endocardial receptors (75%) RA receptors (25%) Nucleus Tractus Solitarius of medulla X Vagal + Bradycardia Cardiac arrest in spinal Resp centre (–) Respiratory arrest in spinal  Seen in hemorrhage, hypovolemia, spinal anesthesia, MI, contrast injection, exercise in severe AS, Interscalene BP block, vasovagal syncope, astronauts.
  • 32. Respiratory Effects Hypotension Hypoperfusion of MO Resp centre - Resp arrest Diaphragm (C3,4,5)- Aα- large, myelinated fibres Not blocked even in high spinal So resp arrest does not occur due to diaphragmatic paralysis
  • 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
  • 37.  Backache  Dural puncture/leak -Postdural puncture headache -Diplopia -Tinnitus  Neural injury -Nerve root damage -Spinal cord damage -Cauda equina syndrome  Bleeding -Intraspinal/epidural hematoma • Misplacement -No effect/inadequate anesthesia -Subdural block -Inadvertent subarachnoid block -Inadvertent intravascular injection • Inflammation -Arachnoiditis • Infection -Meningitis -Epidural abscess Complications related to needle/catheter placement
  • 38. Hypotension & Bradycardia  Cause: i) T5-L1 block Vasodilation ii) T1-T4 block HR  Volume preload 10-20ml/kg  Bolus 5-10 ml/kg if hypotension occurs  Mixed agent- ephedrine/ mephentermine (direct/ indirect β adrenergic effect) Vasoconstriction (inc- BP, HR and contractility)  Adr 2-5ug bolus, dopamine  Pure α agonist (phenylephrine): Inc SVR- reflex bradycardia  Atropine for bradycardia Urinary Retention • Block of S-2,3,4 SVR BP Venous return Vagal + HR
  • 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
  • 53. Algorithm: safe approach to failed spinal anaesthesia.