SPINAL

ANESTHESIA

PRESENTED BY
DR DEBANARAYAN BISWAL
Spinal anesthesia involves the use of small amounts of local
anesthetic injected into the subarachnoid space to produce
a reversible loss of sensation and motor function. Spinal
anesthesia provides excellent operating conditions for
– Hernia (Inguinal or epigastric).
– Hemorrhoidectomy , fistula , fissure.
– cystoscopy
– Transurethral resection of the prostate and
transurethral resection of the bladder tumors.
– Abdominal and vaginal hysterectomies
– Caesarean sections.
– Lower limb surgery(orthopedic, plastic, vascular)
SITE-
 Adult- L3-L4 or L4-L5 ( or even L2-L3)
Infant- L4-L5
A line drawn b/w the highest Point of iliac crests
(Tuffier’s line) usually cross either body of L4 or
the L4-L5 interspace
POSITION-
Sitting
lateral
Prone(anorectal procedure, jack knife
position)
SPINAL NEEDLES
Standard spinal needle consist of
three parts: -Hub
-Cannula
-Removable stylet
Sizes available- 16 to 30 gauge.
Length of spinal needle- 90 to 110 mm
Dura cutting needle:
QUINCKE-BABCOCK
Dura seprating:
WHITACRE, SPORTTE
APPROACHES FOR SPINAL ANAESTHESIA
 TWO APPROACHES:-
1. Midline Approach
2. Para-median Approach.
 STRUCTURES PIERCED IN MIDLINE APPROACH
1.Skin
2.Subcutanious tissue
3.Supraspinous ligaments: Connecting the tips of spinous process
4.Interspinous ligaments: joins the spinous processes together
5.Ligamentum flavum: Running from lamina to lamina. Composed of
yellow
elastin fibers so called yellow ligament
6.Dura
7.Arachonid
 STRUCTURES PIERCED IN PARA MEDIAN APPROACH-
Same as midline excluding supraspinous & interspinous ligaments
Midline approach
 Under full asepsis and sterile gloves worn the painted area is draped and
the spine is palpated
 Select widest interspace preferably L3-L4.
 Raise a skin wheal with 2% lidocaine infiltration
 Insert spinal needle in the midline with bevel parallel to the

longitudinal axis of the spine.

 Advance needle and asses the feel of dura puncture.
Remove stylet to observe the free flow of CSF.
 Attach the syringe containing drug to be injected in
subarachnoid space, by stabilizing the spinal needle with non-
dominant hand holding hub of needle between the thumb and
fingers
 Inject the prepared solution at the rate of 0.2ml/sec.
Para median approach
 Identify the caudal edge of cephalad spinous process.
 Raise a skin wheal 1cm lateral and 1cm caudal to this
point
 Needle is inserted at an angle of 10 -15 degree to the
sagittal
plane in a cephalo-medial direction.
Taylor Technique
Taylor’s approach is a modification of the paramedian
approach for spinal anesthesia.
 It is carried out at L5 -S1 interspace, the largest
interlaminar space of the vertebral column.
A 12cm Spinal needle is inserted in a cephalo-medial
direction through a skin wheal raised 1 cm medial and 1
cm caudal to the lowermost prominence of the posterior
superior iliac spine.
Indications- Spinal fusion, Arthritic spine, Opisthotonus,
skin infection in lumbar region.
Spinal Anaesthesia Levels
MECHANISM OF ACTION
 Site of action-Target binding sites are the superficial and deep
portions of spinal nerve roots in subarachnoid and epidural
space and dorsal root ganglia.
 Speed of neural blockade depends on size, surface area, degree of
myelination of nerve fibers. S1 and L5 posterior roots are largest
and most resistant to blockade.
 Differential blockade-
Autonomic>sensory>motor
For e.g. the level of anesthesia to cold sensation most cephalad
and is one to two segments higher than the level of pinprick
anesthesia which in turn is one to two segments higher than the
level of touch anesthesia
 PHYSIOLOGICAL EFFECTS OF SPINAL
ANANESTHESIA
1.CARDIOVASCULAR SYSTEM
Combined α+β blocking effect on heart.
Venodilatation and fall in venous return lead to low cardiac output and
hypotension.
Cardiac output shows a biphasic response i.e. early transient increase
followed by eventual decrease. (Initial increase is due to greater decline in
SVR than the venous return) especially in old age with preexisting
hypertension.
In old age with cardiac disease SVR tend to fall by 25% whereas CO falls
by only 10-15%.
Block of cardio accelerator sympathetic fibers from T1-T4 leads to
subsequent bradycardia
 Heart rate may decrease during a high neuraxial block as a result of
blockade of the cardioaccelerator fibers arising from T1 to T4.
Extensive peripheral sympatholysis (T5-L2) also leads to
bradycardia and pooling in lower extremities.
Hypotension triggers compensatory baroreceptor response leading
to vasoconstriction and tachycardia above block level, reduction in
venous return/RA filling which decreases signal output of intrinsic
chronotropic receptors of RA leading to increase in parasympathetic
tone (vagal tone) and causes bradycardia.
The Bezold-Jarisch reflex may be a possible cause of profound
bradycardia and circulatory collapse after spinal anesthesia, especially in
the presence of hypovolemia, when a small end-systolic left ventricular
volume may trigger a mechanoreceptor-mediated bradycardia.
 2.GASTROINTESTINAL FUNCTIONS

Nausea and vomiting due to GI hyper-peristalsis due to

unopposed vagal activity, Contracted bowel and relaxed
sphincters due to sympathetic blockade.
Colonic blood supply and oxygen availability is
increased.
 3.RESPIRATORY SYSTEM
 High spinal may cause paralysis of intercostal muscles, diaphragm and
accessory respiratory muscles.
Cautiously given in patients with limited respiratory reserve
Tidal volume remains unchanged.
Vital capacity decreases minimally d/t loss of abdominal muscle contribution in
forced expiration
Apnea due to hypotension which causes medullary ischemia in high/total
spinal cases.
4. THERMOREGULATION
Vasodilatation causes heat loss which is compensated by vasoconstriction
and shivering above the level of block.

5.RENAL SYSTEM
 Bladder and urogenital dysfunction (mostly urinary retention)
Spinal anesthesia in pregnancy

 Decreased dose requirement due to

 Mechanical factor : compression of IVC causes
shunting of blood to the venous plexus in the vertebral
canal leading to decreased vertebral canal space and
CSF volume thus requiring less dose of drug.

 Hormonal factor – higher progesterone levels

FACTORS AFFECTING BLOCK HEIGHT
A) DRUG FACTORS
i)Baricity-
Density of solution in relation to density of CSF.
-Hyperbaric- Density heavier than CSF.
Achieved by adding dextrose to the drug solution.

Settles to dependent part of the subarachnoid space .

-Isobaric- Density equal to that of CSF

Achieved by adding normal saline to the drug solution.
Stays where you put it.

-Hypobaric- Density less than that of CSF

Achieved by adding sterile water to the drug solution.

“Floats” on CSF, that is, moves against the gravity .

ii)Dose, Volume and Concentration-
-Inextricably linked as Volume × Concentration = Dose
-But Dose is the most reliable determinant of local anesthetic
spread(and thus block height) for isobaric and hypobaric local
anesthetic solutions.
-Hyperbaric local anesthetic solutions are primarily influenced by
baricity.
-Increasing the volume of fixed concentration will lead to higher
blocks.
-Additive drugs other than opioids do not affect spread.
PATIENT FACTORS
CSF VOLUME- inversely proportional to the block height.

OLD AGE- A/W increased block height as CSF volume decreases, specific
gravity increases and nerve roots appear more sensitive to LA
SEX- CSF density is higher in males, thereby reducing baricity of drug
and limiting the cephalad spread
HEIGHT- within range of normal sized adult patients height does not
seem to affect the spread as the length of lower limb bones rather
than vertebral column contributes most to adult height.
PREGNANCY-lower dosages are required.

WEIGHT- in obese CSF volume decreases causing increase cephalad

spread
PROCEDURE FACTORS
POSITION of patients during injection:-

i. In sitting position:-heavy solutions tends to fall, hypobaric solutions

tend to rise.
ii. In lateral position:- after patient turned supine, hyper baric solution
move cephalad or caudal depending upon the tilt of table.
CHOICE OF INTERSPINOUS SPACE- Higher interspace chosen when
higher blocks desired in isobaric solution but in hyperbaric solutions, the
level of injection does not appear to influence the spread.
RATE OF INJECTION- Slower rate of injection increases the spread(0.2
ml/sec), and this is also safer as forceful injection can cause the syringe to
disconnect from the needle.
NEEDLE TYPE AND ALIGNMENT- With hypobaric solutions,
cephalad alignment of the orifice of Whitacre, but not Sprotte, needles
produces greater spread. The orientation of the needle orifice does not
appear to affect the spread of hyperbaric solutions. When directing the
needle orifice to one side (and using hyperbaric anesthetic), a more
marked unilateral block is achieved again when using a Whitacre, rather
than a Quincke needle.
PHARMACOLOGY
 Local Anesthetics are used for spinal anesthesia.
 They are classified according to their duration of action, because the choice and
dose of local anesthetic depends on the duration of surgery.
A) SHORT AND INTERMEDIATE-ACTING LOCAL ANAESTHETICS
1. Procaine
2. Chloroprocaine- Preservative-free preparations of chloroprocaine administered in
small doses (30-60 mg) produce reliable, short-duration spinal anesthesia, with a
faster recovery time than procaine, lidocaine, and bupivacaine.
3. Articaine
4. Lidocaine
5. Prilocaine
6. Mepivacaine
B) LONG-ACTING LOCAL ANAESTHETICS
1. Tetracaine
2. Bupivacaine- It is appropriate for procedures lasting up to 2.5 to 3
hours. Bupivacaine is available as 0.25% and 0.5% clear isobaric solutions
and also as a hyperbaric 0.5% solution containing 80 mg/ mL glucose.
Dose-
<5kg—0.5mg/kg body wt
5-15kg—0.4mg/kg body wt
>15kg—0.3mg/kg body wt
3. Levobupivacaine- Levobupivacaine is the pure S (−) enantiomer of
racemic bupivacaine. Although it is used in similar doses to bupivacaine
and has a similar onset and duration, levobupivacaine potency appears to
be slightly less than bupivacaine. The main advantage of levobupivacaine
is that it is less cardiotoxic than bupivacaine.
4. Ropivacaine- The proposed advantages of spinal ropivacaine were less
cardiotoxicity and greater motor-sensory block differentiation, resulting
in less motor block.
C) SPINAL ADDITIVES
 Administered into the CSF in conjunction with a local anesthetic or
alone.
 Exert a direct analgesic effect on the spinal cord and nerve roots, or
prolong the duration of sensory and motor blockade.
 The coadministration of these agents often allows for a reduction in the
required dose of local anesthetic, with the advantage of motor block
sparing and faster recovery while still producing the same degree of
analgesia.
1. OPOIDS-
 The effects of opioids within the CSF are complex, because of a
combination of
a)direct spinal cord dorsal horn opioid receptor activation,
b)cerebral opioid receptor activation after CSF transport,
c)and peripheral and central systemic effects after vascular uptake.
 Highly lipid-soluble drugs such as fentanyl and sufentanil (onset time of 10 to
20 minutes and relatively short duration of 4 to 6 hours) have a more rapid
onset and shorter duration of action than more hydrophilic opioids such as
morphine (It has a slow onset but provides analgesia for up to 24 hours).
 As a result, hydrophilic opioids have a greater risk of late respiratory
depression, which is one of the rare but most serious consequences of
intrathecal opioid administration.
 In addition to respiratory depression, intrathecal opioids have other side effects
including nausea and vomiting, pruritus, and urinary retention.
2. VASOCONSTRICTORS
 Vasoconstrictors, such as epinephrine and phenylephrine, prolong the
duration of sensory and motor blockade when added to local anesthetics.
 The mechanism of action is reduced systemic local anesthetic uptake caused
by an α1-mediated vasoconstriction.
 Epinephrine may also enhance analgesia via a direct α2-mediated effect.
 The addition of phenylephrine has declined in popularity because of its
association with TNS.
3. α2-AGONISTS-
 Clonidine, dexmedetomidine, and epinephrine all act on
prejunctional and postjunctional α2 receptors in the dorsal horn of
the spinal cord.
 Activation of presynaptic receptors reduces neurotransmitter release,
whereas postjunctional receptor activation results in
hyperpolarization and reduction of pulse transmission.
4. OTHER DRUGS-
 Neostigmine
 Midazolam
 Ketamine
 Adenosine
 Tramadol, etc
SPECIAL SPINAL TECHNIQUES
 Continuous Spinal Anesthesia- Continuous spinal
anesthesia allows incremental dosing of local anesthetic and
therefore predictable titration of the block to an appropriate
level, with better hemodynamic stability than a single-shot
spinal.
 Unilateral Spinal Anesthesia and Selective Spinal
Anesthesia -The terms unilateral spinal anesthesia and
selective spinal anesthesia overlap slightly, but both refer to
small-dose techniques that capitalize on baricity and patient
positioning to hasten recovery.
ASSESSMENT OF BLOCK
 Once the spinal anesthetic has been administered, the onset,
extent, and quality of the sensory and motor blocks must be
assessed while heart rate and arterial blood pressure are also
being monitored for any resultant sympathetic blockade.
 There are many methods of assessing sensory block, but cold
sensation and pinprick representing C- and A-delta fibers,
respectively, are used more often.
 Motor block is assessed using Modified Bromage Scale:-
ORDER OF BLOCKADE OF NERVE FIBRES

 pre ganglionic B fibers

 Temperature fibers (C fibers).
 Pin prick fibers (A delta)
 Touch fibers( A beta )
 Deep pressure fibers
 Somatic motor fibers(A alpha)
 Vibratory sense and proprioception
Complication of Spinal
anesthesia
A)INTRAOPERATIVE B)POSTOPERATIVE

Headache
•Urinary retention
Hypotension •Postdural puncture
Bradycardia headache
Apnea •Backache
Nausea vomiting •Infection
Aphonia •Intracranial
complications
Cardiac arrest
High or total spinal block
Respiratory depression
Pruritis
Shivering
Neurological complications
HYPOTENSION Results from sympathetic nervous system block

Decreases venous return to heart and decrease cardiac output

Decreases systemic vascular resistance

Prevented by: Volume Pre loading with 10-20 mL/kg of intravenous fluid.
Predictors of hypotension-
low intravascular volume in case of hypovolemia due external loss by
trauma,
dehydration, internal loss
sensory block ≥ T5
age > 40 years
systolic BP < 120 mm Hg
combined spinal and general anesthesia
dural puncture between L2-3 and above
patient with h/o uncontrolled hypertension
underlying autonomic dysfunction
TREATMENT
 Oxygen inhalation
 Increase speed of I .V crystalloid/colloid infusions
 If associated with bradycardia, give atropine.
 Appropriate vasopressors.

SYMPATHOMIMETICS:
Phenylephrine: Increase in SVR, SBP, DBP. Causes reflex
bradycardia, coronary blood flow increased.

Ephedrine; Increase myocardial contractility

Mephenteramine
Post dural puncture headache
 Due to leak of CSF from dural defect leads to traction in supporting
structure especially in dura

 Postural in nature- increase in sitting and relieved in lying down position.

 Most PDPHs develop 24 to 72 hours after dural puncture.

 Occur in frontal or occipital region, pain and stiffness in neck may be
present.
 Headache may last days, weeks or even months but usually resolves
within 1- 2weeks.
 Average loss of CSF is 10ml/hr.
 Types
-Low CSF pressure PDPH occurs due to CSF leakage
-High CSF pressure due to meningeal irritation by chemicals or
microbes.
MECHANISM OF PDPH
Loss of
CSF
intracerebral CSF volume
decreases.
brain to sag toward the foramen
magnum
stretching the pain-sensitive
meningeal vascular covering.

Compensatory increase in cerebral blood

volume
vascular headache.
 TREATMENT
PROPHYLACTIC:-
 Smaller the needle gauge, lower the incidences of headache.
 Needle point having pencil point tip as in Whitacre type has lower incidences of
PDPH.
 Orienting needle bevel parallel with axis of spine.
 Maintain hydration and Early ambulation.
TREATMENT OF ESTABLISHED CASES OF PDPH
 Simple analgesics(NSAIDS)and Bed rest
 Frequent caffeine drinks.
 Injection of 10-20ml of autologous blood into
extradural space just above the site of dural puncture to
form a blood patch for sealing of puncture (Epidural
blood patch)
 Oxygen inhalation.
HIGH SPINAL ANAESTHESIA
Due to blockade of cervical nerve roots. As the level of sensory anesthesia ascends ,there
occurs hypotension, aphonia, altered sensorium, profound bradycardia and respiratory
insufficiency.
FACTORS RESPONSIBLE
Total dose injected.
Position of patient
Obesity
Short stature
TREATMENT
Support airway and circulation.
Supplemental oxygen along with assisted ventilation may be required.
Decrease in BP and HR should be treated by I.v fluids , vasopressors and/or atropine.
TOTAL SPINAL-
Cerebral hypoxia due to drug reaching the cranial sub arachnoid space leading to ischemia
of vital control centres and sometimes associated with cranial nerve palsies. It is rarely seen
with spinal anaesthesia but seen with accidental deposition of drug intrathecally during
epidural anaesthesia.
 CARDIAC ARREST
 If the block progresses (High Spinal) to the mid thoracic
region involving the heart.

 Usually due to hypoxaemia <85% without obvious

changes in respiration and cyanosis.

 Incidence is commoner in young healthy adults,

preceded by bradycardia.

 Treatment-CPR, conventional doses of atropine and

ephedrine is given, Full resuscitation dose of
epinephrine is given.
Saddle block
 It is the subarchnoid block given in sitting position
and patient remains seated for up to 5 mins since
most of the drug migrates downwards and only sacral
segments are blocked.
 Used in perianal surgeries like hemorrhoids, fistula in
ano and anal fissures
 Advantages-
i) Minimal hemodynamic fluctuations and high spinal
risk.
ii) Early ambulation