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Lecture 11
U.S.A
moosd@charter.net
Disclaimer
Doses are only general recommendations. There are several factors that may result in either an inadequate or high epidural block. Every effort was made to ensure that material and information contained in this presentation are correct and up-to-date. The author can not accept liability/responsibility from errors that may occur from the use of this information. It is up to each clinician to ensure that they provide safe anesthetic care to their patients.
Epidural anesthesia produces a reversible loss of sensation and motor function much like a spinal with the exception that local anesthetic is placed within the epidural space. Larger doses of local anesthetic are required to produce anesthesia when compared to a spinal anesthetic. Doses must be monitored to avoid toxicity.
An epidural catheter allows the versatility to extend the duration of anesthesia beyond the original dose by the administration of additional local anesthetic. Epidural catheters may be left in place for postoperative analgesia.
Cesarean section Procedures of the uterus, perineum* Hernia repairs Genitourinary procedures Lower extremity orthopedic procedures Excellent choice for elderly or those who may not tolerate a general anesthetic
Epidural Anesthesia
Should NOT be used in patients who are hypovolemic or severely dehydrated. Patients should be pre-hydrated with .5 1 liter of crystalloid solutions (i.e. ringers lactate) immediately prior to the block.
Epidural Anesthesia
Higher failure rate for procedures of the perineum. Lower lumbar and sacral nerve roots are large and there is an increased amount of epidural fat which may affect local anesthetic penetration and blockade. This is known as sacral sparing.
Easy to perform (though it takes a bit more practice than spinal anesthesia) Reliable form of anesthesia Provides excellent operating conditions The ability to administer additional local anesthetics increasing duration The ability to use the epidural catheter for postoperative analgesia
Return of gastrointestinal function generally occurs faster than with general anesthesia Patent airway Fewer pulmonary complications compared to general anesthesia Decreased incidence of deep vein thrombosis and pulmonary emboli formation compared to general anesthesia
Risk of block failure. The rate of failure is slightly higher than with a spinal anesthetic. Always be prepared to induce general anesthesia if block failure occurs. Onset is slower than with spinal anesthesia. May not be a good technique if the surgeon is impatient or there is little time to properly perform the procedure.
Normal alteration in the patients blood pressure and potentially heart rate (generally slower onset with less alteration in blood pressure and heart rate than with a spinal anesthetic). It is essential to place the epidural block in the operating room/preoperative area with monitoring of an ECG, blood pressure, and pulse oximetry. Resuscitation medications/equipment should be available. Risk of complications as outlined in Introduction to Neuraxial Blockade chapter. There is an increase in the complication rate compared to spinal anesthesia.
Continuous epidural catheters should not be used on the ward if the patients vital signs are NOT closely monitored. Risk for infection, resulting in serious complications.
Patient refusal Infection at the site of injection Coagulopathy Severe hypovolemia Increased Intracranial pressure Severe Aortic Stenosis Severe Mitral Stenosis Ischemic Hypertrophic Sub-aortic Stenosis
Relative Contraindications
Sepsis Uncooperative patients Pre-existing neuro deficits/neurological deficits Demylenating lesions Stenotic valuvular heart lesions (mild to moderate Aortic Stenosis/Ischemic Hypertrophic Sub-aortic Stenosis) Severe spinal deformities
Controversial
Prior back surgery Inability to communicate with the patient Complicated surgeries that may involved prolonged periods of time to perform, major blood loss, maneuvers that may complicate respiration
Mechanism/Site of Action
Administered at a physiologic distance when compared to spinal anesthesia. The intended targets are the spinal nerves and associated nerve roots. Several barriers to the spread of local anesthetic to the intended site of action results in the requirement of larger volumes of local anesthetic when compared to spinal anesthesia.
Barriers
Dura mater between the epidural space and spinal nerve and nerve roots act as a modest barrier. The majority of the solutions is absorbed systemically through the venous rich epidural space. Epidural fatty tissue acts as a reservoir. The remainder reaches the spinal nerve and nerve roots.
Local anesthetic injected into the epidural space moves in a horizontal and longitudinal manner. Theoretically the longitudinal spread could reach the foramen magnum and sacral foramina if enough volume was injected.
Horizontally the local anesthetic spreads through the intervertebral foramina to the dural cuff. Local anesthetics spread through the dural cuff via the arachnoid villa and into the CSF. Blockade occurs at the mixed spinal nerves, dorsal root ganglia, and to a small extent the spinal cord.
Spread of Local Anesthetics- Local anesthetics gain access to CSF via arachnoid granules
Takes 6-8 times the dose of a spinal anesthetic to create a comparable block.
Larger mixed nerves are found in the epidural space when compared to the subarachnoid space. Local anesthetics must penetrate arachnoid and dura mater. Local anesthetics are lipid soluble and will be absorbed by tissue and epidural fat. Epidural veins absorb a significant amount of local anesthetic with blood concentrations peaking in 10-30 minutes after a bolus.
Local anesthetics absorbed in the epidural veins will be diluted in the blood. The pulmonary systems acts as a temporary buffer and protects other organs from the toxic effects of local anesthetics. Distribution occurs to the vessel rich organs, muscle, and fat.
Long acting amides will bind to alpha-1 globulins which have a high affinity to local anesthetics but become rapidly saturated. Amides are metabolized in the liver and excreted by the kidneys. Esters are metabolized by pseudocholinesterase so rapidly that there are rarely significant plasma levels.
Volume
Can be variable General rule: 1-2 ml of local anesthetic per dermatome i.e. epidural placed at L4-L5; you want a T4 block for a C-sec. You have 4 lumbar dermatomes and 8 thoracic dermatomes. 12 dermatomes X 1-2 ml = 12-24 ml Big range! Stresses importance of incremental dosing!
Volume
If you require only segmental anesthesia than the dose would be less. Volume of local anesthetic plays a critical role in block height. Dose of local anesthetics administered in thoracic area should be decreased by 30-50% due to decrease in compliance and volume.
Age
As age increases the amount of local anesthetic to achieve the same level of anesthesia decreases. A 20 year old vs 80 year old This is due to changes in size and compliance of the epidural space
Height
The shorter the patient the less local anesthetic required. A patient that is only 53 may require 1 ml per dermatome while someone who is 63 may require the full 2 ml per dermatome
Gravity
Position of patient does affect spread and height of local anesthetic BUT not to the point of spinal anesthesia. i.e. lateral decubitus position will concentrate more local anesthetic to the dependent side will a weaker block will occur in the non-dependent area. A sitting patient will have more local anesthetic delivered to the lower lumbar and sacral dermatomes
Gravity
L5-S2 sometimes will have patchy anesthesia due to sparing. By having the patient sitting or in a semifowlers position one can concentrate local anesthetic to this area. Trendelenberg or reverse trendelenberg may help spread local anesthetic cephalad or alternatively limit the spread.
Considerations in choosing
Understanding of local anesthetic potency & duration Surgical requirements and duration of surgery Postoperative analgesic requirements
Use only preservative free solutions Read the labels, ensure that it is preservative free or prepared for epidural/caudal anesthesia/analgesia
Short Acting: 2-chloroprocaine Intermediate Acting: lidocaine and mepivacaine Long Acting: bupivacaine, etidocaine, ropivacaine, levobupivacaine
Ester local anesthetic Initially associated with disconcerting neurotoxicity (adhesive arachnoiditis) when administered in the intrathecal space (inadvertently) Attributed to bisulfate concentrations
1985 bisulfate content decreased 1987 preservative free solution introduced 1996 bisulfate free solution available Since the change in formulation no more reports of neurotoxity. However the other preparations may be available so you need to read labels! Large volumes of local anesthetic injected inadvertently into the subarachnoid space may still cause neurotoxicity
Other problem, in the past, was patient complaints of back pain after large doses of > 25 ml of local anesthetic Formulations contained EDTA, thought that it leached calcium out of the muscle and resulted in hypocalcemia. The preservative free formulations do not appear to cause back pain after large doses have been used
Best suited for short procedures Good agent for the outpatient Available in concentrations of 2% (for procedures that do not require absolute muscle relaxation) and 3% which provides for dense muscle relaxation. 2-chloroprocaine will interfere with the action of epidurally administered opioids
Prototypical amide local anesthetic 1.5-2% concentrations used for surgical anesthesia Epinephrine will prolong the duration of action by 50% Addition of fentanyl will accelerate the onset of analgesia and create a more potent/complete block
Similar to lidocaine Amide local anesthetic used in similar concentrations Lasts about 15-30 minutes longer than lidocaine Epinephrine will prolong the duration of action by 50%
Long acting amide local anesthetic 0.5-0.75% concentrations used for surgical anesthesia 0.125-.25% used for epidural analgesia Epinephrine will prolong duration of action but not to the extent of lidocaine, mepivacaine, and 2-chloroprocaine
0.75% concentration should not be used in OB In 1983 the FDA came out with this recommendation There were several cardiac arrests due to inadvertent intravascular injection in OB patients Bupivacaine (as well as etidocaine) are more likely to impair the myocardium and conduction system with toxic doses than other local anesthetics
Bupivacaine has a high degree of protein binding and lipid solubility which accumulate in the cardiac conduction system and results in the advent of refractory reentrant arrhythmias
S isomer of bupivacaine Used in the same concentrations Clinically acts just like bupivacaine with the exception that it is less cardiac toxic
Long acting amide local anesthetic Mepivacaine analogue Used in concentrations of 0.5-1% for surgical anesthetic Used in concentrations of 0.1-0.3% for analgesia Ropivacaine is unique among local anesthetics since it exhibits a vasoconstrictive effect at clinically relevant doses
Similar to bupivacaine in onset, duration, and quality of anesthesia Key differences include: in doses for analgesia there is excellent sensory blockade with low motor blockade and it is less cardiotoxic than bupivacaine
Long acting amide local anesthetic Not used clinically very often due to the profound motor blockade it induces When used for surgical anesthesia it is used in a concentration of 1%
Epidural Additives
Epinephrine will increase the duration of action of all epidurally administered local anesthetics. There is a large variability among local anesthetics as to the degree of increase The greatest effect is found with lidocaine, mepivacaine, 2-chloroprocaine. Lesser effects found with bupivacaine, levobupivacaine, etidocaine Minimal effects have been found with ropivacaine
Epidural Additives
Epi vs phenylephrine Epi is more effective in reducing peak blood levels Phenylephrine does not appear to reduce the peak blood levels
Epidural Additives
Carbonation of local anesthetics has been touted to improve the quality of epidural blocks due to increased penetration of connective tissue and intraneural diffusion Studies are ambivalent Carbonation may not improve quality or onset; may lead to increased blood levels of local anesthetic; result in a higher incidence of hypotension when compared to non carbonated local anesthetics
Epidural Additives
Sodium bicarbonate can be added to lidocaine, mepivacaine, and 2-chloroprocaine Addition will increase the amount of free base which increases rate of diffusion and speeds onset Studies have found that when added to 1.5% lidocaine speeds onset of blockade and results in a more solid block
Epidural Additives
Generally 1 meq of bicarbonate is added to 10 ml of local anesthetic (i.e. lidocaine, mepivacaine, 2-chloroprocaine) The addition of bicarbonate to bupivacaine is not as popular. Usually 0.1 ml of bicarbonate is added to 10 ml of bupivacaine Bupivacaine precipitates occurs at a pH > 6.8
Epidural Additives
Mixing long acting and short acting local anesthetics may not have much advantage for epidural anesthesia Many choices for local anesthetics and additives
References
Brown, D.L. (2005). Spinal, epidural, and caudal anesthesia. In R.D. Miller Millers Anesthesia, 6th edition. Philadelphia: Elsevier Churchill Livingstone.
Burkard J, Lee Olson R., Vacchiano CA. Regional Anesthesia. In Nurse Anesthesia 3rd edition. Nagelhout, JJ & Zaglaniczny KL ed. Pages 977-1030.
Kleinman, W. & Mikhail, M. (2006). Spinal, epidural, & caudal blocks. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. New York: Lange Medical Books.
Niemi, G., Breivik, H. (2002). Epinephrine markedly improves thoracic epidural analgesia produced by smalldose infusion of ropivacaine, fentanyl, and epinephrine after major thoracic or abdominal surgery: a randomized, double-blind crossover study with and without epinephrine. Anesthesia and Analgesia, 94, 1598-1605.
Reese CA. Clinical Techniques of Regional Anesthesia: Spinal and Epidural Blocks. 3rd edition. AANA Publishing, 2007.
Visser L. Epidural Anaesthesia. Update in Anaesthesia. Issue 13, Article 11. 2001.
Warren, D.T. & Liu, S.S. (2008). Neuraxial Anesthesia. In D.E. Longnecker et al (eds) Anesthesiology. New York: McGraw-Hill Medical.