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EPIDURAL ANAESTHESIA
PRESENTOR : ARTHI (P.G)
MODERATOR :Dr.YASHA (Asst.Professor)
Epidural is a combination of sympathetic , sensory , or motor blockade
depending on the dose, concentration, or volume of local anesthetic
administered.
Lumbar epidural anesthesia in humans was first
described by Pagés in 1921
The loss-of-resistance technique by Dogliotti in
1930,
Lumbar epidural catheterization for surgery by
Curbelo in 1947.
The use of epidural morphine analgesia was first
reported by Behar in 1979.
The spinal cord is continuous with the brainstem
proximally and terminates distally in the conus
medullaris as the filum terminale (fibrous
extension) and the cauda equina (neural
extension).
This distal termination varies from L3 in infants
2. Arachnoid mater
3. Dura mater
• The cerebrospinal fluid (CSF) resides in the space
between the pia mater and the arachnoid mater
subarachnoid (or intrathecal) space.
• The pia mater is a highly vascular membrane that
closely invests the spinal cord and brain.
• Approximately 500 mL of CSF is formed daily by the
choroid plexuses of the cerebral ventricles, with 30
to 80 mL occupying the subarachnoid space
• The arachnoid mater is a delicate nonvascular
membrane that functions as the principal barrier to
drugs crossing into and out of the CSF
• Arachnoid act as the primary barrier ,spinal CSF
resides in the subarachnoid and not the subdural
space.
longitudinal ligaments,
2. Laterally - pedicles and
intervertebral foramina
3. Posteriorly- ligamentum
flavum.
• Contents - nerve roots and fat, areolar
tissue, lymphatics, and blood vessels
including the well-organized venous
plexus.
• Posterior to the epidural space is the
ligamentum flavum (yellow ligament),
which also extends from the foramen
magnum to the sacral hiatus. posterior to
the ligamentum flavum are the lamina and
spinous processes of vertebral bodies or
the interspinous ligaments.
• Thoracic spinous process - angulated steeply cauded
Lumbar spinous process - horizontal angulation.
• This is a clinically important for needle insertion in
thoracic versus lumbar levels.
• The sacral canal contains the terminal portion of the dural
sac ends at S2 (lower in children)
• Sacral canal contains a valveless internal venous plexus
,the volume of the caudal canal in adults(excluding the
foramina and dural sac)is about 10 to 27 mL. volume
accounts for variation in block height with caudal
anesthesia
size and structure.
These differences help to explain the
differences in neuraxial block quality when
equivalent techniques are used on similar
patients.
Anatomic relationship may affect neuraxial
blocks
• The dorsal (sensory) roots are often
blocked more easily ventral (motor)
roots,
• This is explained by organization of the
dorsal roots which creates a much larger
surface area on which the local
anesthetics act.
Mechanism of Action
• Local anaesthetic binding to nerve tissue disrupts nerve transmission,
resulting in neural blockade.
• For spinal and epidural anaesthesia the target binding sites are located
within the spinal cord (superficial and deep portions) and on the spinal
nerve roots in the subarachnoid and epidural spaces.
• The spinal nerve roots and dorsal root ganglia are the important sites of
action.
• Nerves in the subarachnoid space are highly and easily anaesthetised
even with a small dose of local anaesthetic, compared with the
extradural nerves, which are often ensheathed by dura mater (the
“dural sleeve”).
The speed of neural blockade depends on the size, surface area, and
degree of myelination of the nerve fibers exposed to the local anesthetic.
thus most resistant to blockade during epidural anesthesia.
Smaller nerves are more sensitive to local anesthetics because of their
relatively high membrane surface area to axon unit volume ratio.
Small preganglionic sympathetic fibers B fibers 1 to 3 μm minimally
myelinated are most sensitive to local anesthetic blockade.
Among the sensory nerves, the C fibers (0.3 to 1 μm, unmyelinated)
conduct cold temperature sensation are blocked more readily or earlier
than the A-delta fibers
A-delta fibers (1 to 4 μm, myelinated), which conduct pinprick sensation.
A-beta fibers (5 to 12 μm, myelinated), which conduct touch sensation,
are the last to be affected among the sensory fibers.
The larger A-alpha motor fibers (12 to 20 μm, myelinated) are more
resistant than any of the sensory fibers.
Regression of blockade (“recovery”) follows in the reverse order: motor
Another manifestation of relative sensitivity to the effects of local
anaesthetics is observed differences in the peak block height according to
each sensory modality - differential sensory block.
For example: the level of anaesthesia to cold sensation (also an
approximate level of sympathetic blockade) is more cephalad and about
one to two spinal segments higher than the level of pinprick anaesthesia.
Drug penetration and uptake is directly proportionate to (For Spinal)
The drug mass
CSF drug concentration
Contact surface area
lipid content (high in spinal cord and myelinated
nerves)
local tissue vascular supply
Inversely related to nerve root size.
For epidural anaesthesia, drug uptake is more complex.
• Some of the injected local anaesthetic will move from the epidural space
through the meninges into the CSF to exert its neural blocking effect
• Some will be lost through vascular absorption into the capillary vessels and
into the systemic circulation and uptake into epidural fat.
DRUG DISTRIBUTION
Diffusion is the primary mechanism of local anesthetic
Distribution in the CSF from areas of high concentration (i.e., at the site of
injection) to other segments of the spinal cord with low drug concentration.
Rostral spread after the administration of a small local anesthetic dose is often
evident within 10 to 20 minutes- is related to the CSF circulation time.
Drug distribution in the epidural space is more complex, with possible
contributions from one, some, or all of the following mechanisms:
(1) crossing the dura mater into the subarachnoid space
(2) rostral and caudal (longitudinal) spread within the epidural space
(3) circumferential spread within the epidural space
(4) exit of the epidural space through the intervertebral foramina
(5) binding to epidural fat
DRUG ELIMINATION
The rate of elimination
1. Dependent on the distribution of local anaesthetic , greater
spread will expose the drug to a larger area for vascular
absorption and thus a shorter duration of action.
2. Lipid-soluble local anaesthetics (e.g., bupivacaine) bind to
epidural fat to form a depot that can slow vascular absorption.
PHYSIOLOGICAL CHANGES - CVS
sympathetic block Effects
HYPOTENSION :
•Vasodilation of resistance and capacitance vessels causes hypovolemia and
tachycardia and drop in blood pressure
•Decreases the stroke volume and heart rate that in turn decrease the cardiac output and
blood pressure
•The vasomotor tone is primarily determined by sympathetic fibers arising from T5 to Ll,
innervating arterial and venous smooth muscles
BRADYCARDIA :
• Sympathetic blockade from Tl to T4 cause decreased heart rate
•Decreased venous return results in decreased stimulation of volume receptors in the
right atrium. This produces bradycardia (Bainbridge reflex)
•Patients with low blood volume or reduced venous return such as pregnancy, ascites,
or vena cava obstruction are prone to exaggerated decreases in systemic blood
pressure.
Patients complaining of coronary artery disease or congestive heart failure may get
benefited reduces the neuro-endocrine stress response to surgery reducing the
cardiovascular effects
RESPIRATORY SYSTEM
High Thoracic Blocakade :
• High subarachnoid or thoracic epidural block produces: No change in
tidal volume (due to diaphragmatic compensation) a small decrease in
vital capacity.
• Ineffective cough and clearing of secretions, dyspnea, and inability to
take deep respiration (due to loss of the accessory muscles of
respiration -the abdominal and intercostal muscles).
• This effect is more obvious on patients with limited respiratory reserve
as those with chronic obstructive pulmonary disease as they depend on
accessory muscles of respiration.
• In the same time, postoperative thoracic epidural analgesia in those
patients is very beneficial because it prevents pain-induced splinting
and permits uninhibited coughing and deep breathing.
• Therefore, for surgical procedures above the umbilicus in these
patients with limited respiratory function, combined light general
anaesthesia with thoracic epidural analgesia is the best choice.
GASTROINTESTINAL
CHANGES
Blockade of the sympathetic supply of the gut (T5 to Ll) leads to
unopposed parasympathetic action (i.e.dominance of vagal tone) that
causes the following effects:
• An increase in the peristaltic activity of the gut with relaxed sphincters
causes early return of postoperative gut function.
• Handling of viscera in high abdominal surgery causes stimulation of the
unblocked vagus that results in nausea, vomiting, and retching. So, it
needs either light general anesthesia or para esophageal infiltration of
local anesthetic to block the afferent vagus nerve.
• Nausea, vomiting, and retching may occur in awake patients due to
established hypotension.
• A decrease in hepatic blood flow due to hypotension.
GENITO URINARY SYSTEM
• Blood flow is maintained in spite of hypotension due to renal auto
regulation.
• Block of lumbar and sacral roots as in subarachnoid and lumbar or
caudal epidural anaesthesia results in blocking of both sympathetic
and parasympathetic autonomic control of
urinary bladder function leading to urinary retention until the block
wears off.
NEURO ENDOCRINE
• Neuroendocrine response occurs after stress such as surgery and
postoperative pain leading to increased blood cortisol,
catecholamines, vasopressin, and renin-angiotensin-aldosterone
system.
• This leads to intra- and postoperative hyperglycemia, hypertension,
tachycardia, protein catabolism, hypercoagulable state, and
suppression of immune system.
• Neuraxial anaesthesia abolishes this response and its effects.
EPIDURAL TECHNIQUES
Preparation
• Epidural anaesthesia consent, monitoring, and
resuscitation equipment, intravenous access, and
choosing the patient and drugs appropriately
depending on comorbidities and the nature of surgery.
• Sterility is important than in spinal anaesthesia
because a catheter is often left in situ.
• The extent of the surgical field must be understood so
that the epidural may be inserted at the appropriate
level.
“Huber” tip designed to both reduce the risk of
accidental dural puncture and guide the catheter
cephalad.
• The needle shaft is marked in 1-cm intervals so
that depth of insertion can be identified.
• The catheter is made of a flexible, calibrated,
durable, radiopaque plastic with either a single
end hole or multiple side orifices near the tip.
Several investigators have found that multiple-
orifice catheters (reduced incidence of
inadequate analgesia).
• multiorifice catheters in pregnant women resulted
in a more frequent incidence of epidural vein
cannulation.
The method of identifying the epidural space -
• Loss-of- resistance technique to either air or
saline, rather than the hanging drop technique
• If a loss-of-resistance technique is used an
positions necessary for epidural
puncture . inadequate positioning
of the patient can complicate the
procedure.
Projection and Puncture
The level of needle insertion
depends on the location of surgery.
• Important surface landmarks
include the intercrestal line
(corresponding to the L4-L5
interspace),
• Inferior angle of the scapula
(corresponding to the T7
vertebral body),
• Root of the scapular spine (T3)
lumbar and low thoracic approaches.
1. After local anesthetic infiltration of the skin,
2. The nondominant hand can be rested on the
back of the patient, with the thumb and index
finger holding the needle hub or wing.
3. The angle of approach should be only slightly
cephalad in the lumbar and low-thoracic regions,
whereas in the mid- thoracic region, the
approach should be more cephalad because of
the significant downward angulation of the
spinous processes .
4. In a controlled fashion, the needle should be
advanced with the stylet in place through the
supraspinous ligament and into the interspinous
ligament, at which point the stylet can be
removed and the syringe attached if it is in the
correct location.
5. If the needle is merely inserted into the
supraspinous ligament and then loss-of-
detect a loss-of-resistance when identifying the epidural space.
2. Each involves intermittent (for air) or constant (for saline) gentle pressure
applied to the bulb of the syringe with the dominant thumb while the needle
is advanced with the nondominant hand.
3. A combination of air and saline may also be used.
4. Incorporating 2 mL of saline and a small (0.25 mL) air bubble. Usually the
ligamentum flavum is identified as a tougher structure with increased
resistance, and when the epidural space is subsequently entered, the
pressure applied to the syringe plunger allows the solution to flow without
resistance into the epidural space
5. There are reports that air is less reliable in identifying the epidural space,
results in a higher chance of incomplete block, and may also cause both
pneumocephalus (which can result in headaches) and venous air embolism
in rare cases.
6. If air is chosen, the amount of air injected after loss-of-resistance should
therefore be minimized.
7. Analysis shows fluid inserted through the epidural needle before catheter
• After the needle is placed into the ligamentum flavum, a drop of
solution such as saline is placed within the hub of the needle.
• When the needle is advanced into the epidural space, the solution
should be “sucked in.”
• The theory behind this maneuver has traditionally been attributed to
subatmospheric pressure in the epidural space.The subatmospheric
pressure has been related to expansion of the epidural space as the
needle pushes the dura away from the ligamentum flavum
lumbar midline approach is used:
• Depth from skin to the ligamentum flavum commonly reaches 4 cm,
with the depth in most (80%) patients being between 3.5 and 6 cm, it
can be longer or shorter in obese or very thin patients
• Ultrasonography may be useful to predict the depth before needle
insertion.
• In lumbar region ligamentum flavum is 5 to 6 mm thick in the midline.
When a thoracic approach is chosen the needle control is of equal or
where the angulation of the spine and the narrow spaces
render the midline approach problematic.
• The needle should be inserted 1 to 2 cm lateral to the
inferior tip of the spinous process corresponding to the
vertebra above the desired interspace.
• The needle is then advanced horizontally until the
lamina is reached and then redirected medially and
cephalad to enter the epidural space.
• The Taylor approach is a modified paramedian
approach via the L5-S1 interspace, which may be
useful in trauma patients who cannot tolerate or are not
able to maintain a sitting position. The needle is
inserted 1 cm medial and 1 cm inferior to the posterior
superior iliac spine and is angled medially and
cephalad at a 45 to 55 degree angle.
• Before initiating an epidural local anesthetic infusion, a
test dose may be administered.
The epidural space is a collapsible, distensible reservoir through which drugs
spread and are removed by diffusion, vascular transport, and leakage.
Drug Factors
• The volume and total mass of injectate are the drug-related factors that
affect block height after the administration of local anesthetic in the epidural
space.
• Blockage per segment -1 to 2 mL
• Additives : bicarbonate, epinephrine, and opioids influence onset, quality,
and duration of analgesia and anesthesia, these do not affect spread.
Patient Factors
• Age - less volume, greater spread ,increased sensitivity is found in elderly
• Weight is not well correlated with block height in either lumbar or thoracic
epidural anesthesia..
• Less local anesthetic is required to produce spread of anesthesia in
pregnant patients (result of engorgement of epidural veins secondary to
increased abdominal pressure)
FACTOR AFFECTING LOCAL ANESTHESIA
DISTRIBUTION AND BLOCK HEIGHT
that affects epidural block height.
1. Upper cervical region spread -more caudal
2. Midthoracic region spread -equally cephalad and caudal
3. Low thoracic region spread -primarily cephalad
4. Lumbar epidural spread - more cephalad than caudal.
• studies suggest that the total number of segments blocked is less in
the lumbar region compared with thoracic levels for a given volume
of injectate.
• Patient position has been shown to affect spread of lumbar epidural
injections, with preferential spread and faster onset to the
dependent side in the lateral decubitus position.
• The sitting and supine positions do not affect epidural block height.
• The head-down tilt position does increase spread in obstetric
patients.
PHARMACOLOGY
Local anesthetics for epidural use may be classified into
• Short, intermediate and long acting drugs.
• A single bolus dose of local anesthetic in the epidural space can
provide surgical anesthesia ranging from 45 minutes up to 4 hours
depending on the type of local anesthetic administered and the use
of any additives
• Most commonly, an epidural catheter is left in situ so that local
anesthetic based anesthesia or regular analgesia can be extended
indefinitely
Complications• Complications related to adverse or
exaggerated physiological response
1. Pain on injection
2. High block (Hypotension &
Bradycardia)
3. Total spinal anaesthesia
4. Horner’s Syndrome
5. Anterior spinal artery syndrome
6. Urinary Retention
7. Vasovagal Shock
Complications related to needle or catheter placement
A. Trauma
Backache
Dural Puncture- PDPH
Neural Injury
Vascular injury(Spinal or Epidural hematoma)
B. Misplacement
Inaderent intravascular or intraosseus injection
Inadverent subdural or subarachnoid block
C. Inflammation
• Infection
• Arachnoiditis
• Meningites
• Epidural Abscess
Complications related to Drug Toxicity
• Systemic Local Anaesthetic Toxicity
• Transient Neurological symptoms
• Cauda Equina Syndrome
• Lignocaine neurotoxicity
TREATMENT
Circulatory support
1. Rapid volume loading 10-20ml/kg
2. Vasopressors : Mephentramine/phenylephrine incremental
doses
3. Inj.Atropine 0.6mg IV to treat bradycardia
4. If profound Hypotension IV epinephrine 5 -10 mcg
Respiratory Support
100% Oxygen
Assisted ventilation if hypoventilation occurs
Control of airway if unconsciousness occurs - Intubation &
mechanical ventilation
Contraindications
1. Unexplained neurological symptoms
2. Active neurological disease
Localised sepsis in lumbar area
3. Generalised sepsis
4. Coagulopathy
THANK YOU
Epidural (1)
Epidural (1)

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Epidural (1)

  • 1. EPIDURAL ANAESTHESIA PRESENTOR : ARTHI (P.G) MODERATOR :Dr.YASHA (Asst.Professor)
  • 2. Epidural is a combination of sympathetic , sensory , or motor blockade depending on the dose, concentration, or volume of local anesthetic administered. Lumbar epidural anesthesia in humans was first described by Pagés in 1921 The loss-of-resistance technique by Dogliotti in 1930, Lumbar epidural catheterization for surgery by Curbelo in 1947. The use of epidural morphine analgesia was first reported by Behar in 1979. The spinal cord is continuous with the brainstem proximally and terminates distally in the conus medullaris as the filum terminale (fibrous extension) and the cauda equina (neural extension). This distal termination varies from L3 in infants
  • 3. 2. Arachnoid mater 3. Dura mater • The cerebrospinal fluid (CSF) resides in the space between the pia mater and the arachnoid mater subarachnoid (or intrathecal) space. • The pia mater is a highly vascular membrane that closely invests the spinal cord and brain. • Approximately 500 mL of CSF is formed daily by the choroid plexuses of the cerebral ventricles, with 30 to 80 mL occupying the subarachnoid space • The arachnoid mater is a delicate nonvascular membrane that functions as the principal barrier to drugs crossing into and out of the CSF • Arachnoid act as the primary barrier ,spinal CSF resides in the subarachnoid and not the subdural space.
  • 4. longitudinal ligaments, 2. Laterally - pedicles and intervertebral foramina 3. Posteriorly- ligamentum flavum. • Contents - nerve roots and fat, areolar tissue, lymphatics, and blood vessels including the well-organized venous plexus. • Posterior to the epidural space is the ligamentum flavum (yellow ligament), which also extends from the foramen magnum to the sacral hiatus. posterior to the ligamentum flavum are the lamina and spinous processes of vertebral bodies or the interspinous ligaments.
  • 5. • Thoracic spinous process - angulated steeply cauded Lumbar spinous process - horizontal angulation. • This is a clinically important for needle insertion in thoracic versus lumbar levels. • The sacral canal contains the terminal portion of the dural sac ends at S2 (lower in children) • Sacral canal contains a valveless internal venous plexus ,the volume of the caudal canal in adults(excluding the foramina and dural sac)is about 10 to 27 mL. volume accounts for variation in block height with caudal anesthesia
  • 6. size and structure. These differences help to explain the differences in neuraxial block quality when equivalent techniques are used on similar patients. Anatomic relationship may affect neuraxial blocks • The dorsal (sensory) roots are often blocked more easily ventral (motor) roots, • This is explained by organization of the dorsal roots which creates a much larger surface area on which the local anesthetics act.
  • 7. Mechanism of Action • Local anaesthetic binding to nerve tissue disrupts nerve transmission, resulting in neural blockade. • For spinal and epidural anaesthesia the target binding sites are located within the spinal cord (superficial and deep portions) and on the spinal nerve roots in the subarachnoid and epidural spaces. • The spinal nerve roots and dorsal root ganglia are the important sites of action. • Nerves in the subarachnoid space are highly and easily anaesthetised even with a small dose of local anaesthetic, compared with the extradural nerves, which are often ensheathed by dura mater (the “dural sleeve”). The speed of neural blockade depends on the size, surface area, and degree of myelination of the nerve fibers exposed to the local anesthetic.
  • 8. thus most resistant to blockade during epidural anesthesia. Smaller nerves are more sensitive to local anesthetics because of their relatively high membrane surface area to axon unit volume ratio. Small preganglionic sympathetic fibers B fibers 1 to 3 μm minimally myelinated are most sensitive to local anesthetic blockade. Among the sensory nerves, the C fibers (0.3 to 1 μm, unmyelinated) conduct cold temperature sensation are blocked more readily or earlier than the A-delta fibers A-delta fibers (1 to 4 μm, myelinated), which conduct pinprick sensation. A-beta fibers (5 to 12 μm, myelinated), which conduct touch sensation, are the last to be affected among the sensory fibers. The larger A-alpha motor fibers (12 to 20 μm, myelinated) are more resistant than any of the sensory fibers. Regression of blockade (“recovery”) follows in the reverse order: motor
  • 9. Another manifestation of relative sensitivity to the effects of local anaesthetics is observed differences in the peak block height according to each sensory modality - differential sensory block. For example: the level of anaesthesia to cold sensation (also an approximate level of sympathetic blockade) is more cephalad and about one to two spinal segments higher than the level of pinprick anaesthesia.
  • 10. Drug penetration and uptake is directly proportionate to (For Spinal) The drug mass CSF drug concentration Contact surface area lipid content (high in spinal cord and myelinated nerves) local tissue vascular supply Inversely related to nerve root size. For epidural anaesthesia, drug uptake is more complex. • Some of the injected local anaesthetic will move from the epidural space through the meninges into the CSF to exert its neural blocking effect • Some will be lost through vascular absorption into the capillary vessels and into the systemic circulation and uptake into epidural fat.
  • 11. DRUG DISTRIBUTION Diffusion is the primary mechanism of local anesthetic Distribution in the CSF from areas of high concentration (i.e., at the site of injection) to other segments of the spinal cord with low drug concentration. Rostral spread after the administration of a small local anesthetic dose is often evident within 10 to 20 minutes- is related to the CSF circulation time. Drug distribution in the epidural space is more complex, with possible contributions from one, some, or all of the following mechanisms: (1) crossing the dura mater into the subarachnoid space (2) rostral and caudal (longitudinal) spread within the epidural space (3) circumferential spread within the epidural space (4) exit of the epidural space through the intervertebral foramina (5) binding to epidural fat
  • 12. DRUG ELIMINATION The rate of elimination 1. Dependent on the distribution of local anaesthetic , greater spread will expose the drug to a larger area for vascular absorption and thus a shorter duration of action. 2. Lipid-soluble local anaesthetics (e.g., bupivacaine) bind to epidural fat to form a depot that can slow vascular absorption.
  • 13. PHYSIOLOGICAL CHANGES - CVS sympathetic block Effects HYPOTENSION : •Vasodilation of resistance and capacitance vessels causes hypovolemia and tachycardia and drop in blood pressure •Decreases the stroke volume and heart rate that in turn decrease the cardiac output and blood pressure •The vasomotor tone is primarily determined by sympathetic fibers arising from T5 to Ll, innervating arterial and venous smooth muscles BRADYCARDIA : • Sympathetic blockade from Tl to T4 cause decreased heart rate •Decreased venous return results in decreased stimulation of volume receptors in the right atrium. This produces bradycardia (Bainbridge reflex) •Patients with low blood volume or reduced venous return such as pregnancy, ascites, or vena cava obstruction are prone to exaggerated decreases in systemic blood pressure. Patients complaining of coronary artery disease or congestive heart failure may get benefited reduces the neuro-endocrine stress response to surgery reducing the cardiovascular effects
  • 14. RESPIRATORY SYSTEM High Thoracic Blocakade : • High subarachnoid or thoracic epidural block produces: No change in tidal volume (due to diaphragmatic compensation) a small decrease in vital capacity. • Ineffective cough and clearing of secretions, dyspnea, and inability to take deep respiration (due to loss of the accessory muscles of respiration -the abdominal and intercostal muscles). • This effect is more obvious on patients with limited respiratory reserve as those with chronic obstructive pulmonary disease as they depend on accessory muscles of respiration. • In the same time, postoperative thoracic epidural analgesia in those patients is very beneficial because it prevents pain-induced splinting and permits uninhibited coughing and deep breathing. • Therefore, for surgical procedures above the umbilicus in these patients with limited respiratory function, combined light general anaesthesia with thoracic epidural analgesia is the best choice.
  • 15. GASTROINTESTINAL CHANGES Blockade of the sympathetic supply of the gut (T5 to Ll) leads to unopposed parasympathetic action (i.e.dominance of vagal tone) that causes the following effects: • An increase in the peristaltic activity of the gut with relaxed sphincters causes early return of postoperative gut function. • Handling of viscera in high abdominal surgery causes stimulation of the unblocked vagus that results in nausea, vomiting, and retching. So, it needs either light general anesthesia or para esophageal infiltration of local anesthetic to block the afferent vagus nerve. • Nausea, vomiting, and retching may occur in awake patients due to established hypotension. • A decrease in hepatic blood flow due to hypotension.
  • 16. GENITO URINARY SYSTEM • Blood flow is maintained in spite of hypotension due to renal auto regulation. • Block of lumbar and sacral roots as in subarachnoid and lumbar or caudal epidural anaesthesia results in blocking of both sympathetic and parasympathetic autonomic control of urinary bladder function leading to urinary retention until the block wears off. NEURO ENDOCRINE • Neuroendocrine response occurs after stress such as surgery and postoperative pain leading to increased blood cortisol, catecholamines, vasopressin, and renin-angiotensin-aldosterone system. • This leads to intra- and postoperative hyperglycemia, hypertension, tachycardia, protein catabolism, hypercoagulable state, and suppression of immune system. • Neuraxial anaesthesia abolishes this response and its effects.
  • 17. EPIDURAL TECHNIQUES Preparation • Epidural anaesthesia consent, monitoring, and resuscitation equipment, intravenous access, and choosing the patient and drugs appropriately depending on comorbidities and the nature of surgery. • Sterility is important than in spinal anaesthesia because a catheter is often left in situ. • The extent of the surgical field must be understood so that the epidural may be inserted at the appropriate level.
  • 18. “Huber” tip designed to both reduce the risk of accidental dural puncture and guide the catheter cephalad. • The needle shaft is marked in 1-cm intervals so that depth of insertion can be identified. • The catheter is made of a flexible, calibrated, durable, radiopaque plastic with either a single end hole or multiple side orifices near the tip. Several investigators have found that multiple- orifice catheters (reduced incidence of inadequate analgesia). • multiorifice catheters in pregnant women resulted in a more frequent incidence of epidural vein cannulation. The method of identifying the epidural space - • Loss-of- resistance technique to either air or saline, rather than the hanging drop technique • If a loss-of-resistance technique is used an
  • 19. positions necessary for epidural puncture . inadequate positioning of the patient can complicate the procedure. Projection and Puncture The level of needle insertion depends on the location of surgery. • Important surface landmarks include the intercrestal line (corresponding to the L4-L5 interspace), • Inferior angle of the scapula (corresponding to the T7 vertebral body), • Root of the scapular spine (T3)
  • 20. lumbar and low thoracic approaches. 1. After local anesthetic infiltration of the skin, 2. The nondominant hand can be rested on the back of the patient, with the thumb and index finger holding the needle hub or wing. 3. The angle of approach should be only slightly cephalad in the lumbar and low-thoracic regions, whereas in the mid- thoracic region, the approach should be more cephalad because of the significant downward angulation of the spinous processes . 4. In a controlled fashion, the needle should be advanced with the stylet in place through the supraspinous ligament and into the interspinous ligament, at which point the stylet can be removed and the syringe attached if it is in the correct location. 5. If the needle is merely inserted into the supraspinous ligament and then loss-of-
  • 21. detect a loss-of-resistance when identifying the epidural space. 2. Each involves intermittent (for air) or constant (for saline) gentle pressure applied to the bulb of the syringe with the dominant thumb while the needle is advanced with the nondominant hand. 3. A combination of air and saline may also be used. 4. Incorporating 2 mL of saline and a small (0.25 mL) air bubble. Usually the ligamentum flavum is identified as a tougher structure with increased resistance, and when the epidural space is subsequently entered, the pressure applied to the syringe plunger allows the solution to flow without resistance into the epidural space 5. There are reports that air is less reliable in identifying the epidural space, results in a higher chance of incomplete block, and may also cause both pneumocephalus (which can result in headaches) and venous air embolism in rare cases. 6. If air is chosen, the amount of air injected after loss-of-resistance should therefore be minimized. 7. Analysis shows fluid inserted through the epidural needle before catheter
  • 22. • After the needle is placed into the ligamentum flavum, a drop of solution such as saline is placed within the hub of the needle. • When the needle is advanced into the epidural space, the solution should be “sucked in.” • The theory behind this maneuver has traditionally been attributed to subatmospheric pressure in the epidural space.The subatmospheric pressure has been related to expansion of the epidural space as the needle pushes the dura away from the ligamentum flavum lumbar midline approach is used: • Depth from skin to the ligamentum flavum commonly reaches 4 cm, with the depth in most (80%) patients being between 3.5 and 6 cm, it can be longer or shorter in obese or very thin patients • Ultrasonography may be useful to predict the depth before needle insertion. • In lumbar region ligamentum flavum is 5 to 6 mm thick in the midline. When a thoracic approach is chosen the needle control is of equal or
  • 23. where the angulation of the spine and the narrow spaces render the midline approach problematic. • The needle should be inserted 1 to 2 cm lateral to the inferior tip of the spinous process corresponding to the vertebra above the desired interspace. • The needle is then advanced horizontally until the lamina is reached and then redirected medially and cephalad to enter the epidural space. • The Taylor approach is a modified paramedian approach via the L5-S1 interspace, which may be useful in trauma patients who cannot tolerate or are not able to maintain a sitting position. The needle is inserted 1 cm medial and 1 cm inferior to the posterior superior iliac spine and is angled medially and cephalad at a 45 to 55 degree angle. • Before initiating an epidural local anesthetic infusion, a test dose may be administered.
  • 24. The epidural space is a collapsible, distensible reservoir through which drugs spread and are removed by diffusion, vascular transport, and leakage. Drug Factors • The volume and total mass of injectate are the drug-related factors that affect block height after the administration of local anesthetic in the epidural space. • Blockage per segment -1 to 2 mL • Additives : bicarbonate, epinephrine, and opioids influence onset, quality, and duration of analgesia and anesthesia, these do not affect spread. Patient Factors • Age - less volume, greater spread ,increased sensitivity is found in elderly • Weight is not well correlated with block height in either lumbar or thoracic epidural anesthesia.. • Less local anesthetic is required to produce spread of anesthesia in pregnant patients (result of engorgement of epidural veins secondary to increased abdominal pressure) FACTOR AFFECTING LOCAL ANESTHESIA DISTRIBUTION AND BLOCK HEIGHT
  • 25. that affects epidural block height. 1. Upper cervical region spread -more caudal 2. Midthoracic region spread -equally cephalad and caudal 3. Low thoracic region spread -primarily cephalad 4. Lumbar epidural spread - more cephalad than caudal. • studies suggest that the total number of segments blocked is less in the lumbar region compared with thoracic levels for a given volume of injectate. • Patient position has been shown to affect spread of lumbar epidural injections, with preferential spread and faster onset to the dependent side in the lateral decubitus position. • The sitting and supine positions do not affect epidural block height. • The head-down tilt position does increase spread in obstetric patients.
  • 26. PHARMACOLOGY Local anesthetics for epidural use may be classified into • Short, intermediate and long acting drugs. • A single bolus dose of local anesthetic in the epidural space can provide surgical anesthesia ranging from 45 minutes up to 4 hours depending on the type of local anesthetic administered and the use of any additives • Most commonly, an epidural catheter is left in situ so that local anesthetic based anesthesia or regular analgesia can be extended indefinitely
  • 27. Complications• Complications related to adverse or exaggerated physiological response 1. Pain on injection 2. High block (Hypotension & Bradycardia) 3. Total spinal anaesthesia 4. Horner’s Syndrome 5. Anterior spinal artery syndrome 6. Urinary Retention 7. Vasovagal Shock Complications related to needle or catheter placement A. Trauma Backache Dural Puncture- PDPH Neural Injury Vascular injury(Spinal or Epidural hematoma) B. Misplacement Inaderent intravascular or intraosseus injection Inadverent subdural or subarachnoid block C. Inflammation • Infection • Arachnoiditis • Meningites • Epidural Abscess Complications related to Drug Toxicity • Systemic Local Anaesthetic Toxicity • Transient Neurological symptoms • Cauda Equina Syndrome • Lignocaine neurotoxicity
  • 28. TREATMENT Circulatory support 1. Rapid volume loading 10-20ml/kg 2. Vasopressors : Mephentramine/phenylephrine incremental doses 3. Inj.Atropine 0.6mg IV to treat bradycardia 4. If profound Hypotension IV epinephrine 5 -10 mcg Respiratory Support 100% Oxygen Assisted ventilation if hypoventilation occurs Control of airway if unconsciousness occurs - Intubation & mechanical ventilation
  • 29. Contraindications 1. Unexplained neurological symptoms 2. Active neurological disease Localised sepsis in lumbar area 3. Generalised sepsis 4. Coagulopathy