Soli Deo Gloria COMPLICATIONS OF NEURAXIAL BLOCKADE Developing

Soli Deo Gloria COMPLICATIONS OF NEURAXIAL BLOCKADE Developing Countries Regional Anesthesia Lecture Series Lecture 13 Daniel D. Moos CRNA, Ed. D. U. S. A. moosd@charter. net

Disclaimer 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.

Introduction Exaggerated physiological response Associated with needle placement Associated with catheter placement Associated with medication toxicity

Medical Liability- In General Administration of regional anesthesia constitutes 18% of all claims in the US 64% are temporary and non disabling 13% involve death 10% permanent nerve injury 8% brain damage 4% are “other”

Medical Liability- Neuraxial Blockade 76% of all claims were related to neuraxial blockade Epidural’s comprised 42% Spinal’s comprised 34% Caudal comprised 2% The population most affected is the obstetric population

Adverse or Exaggerated Physiological Response Include: High neural blockade Cardiac arrest Urinary retention

Adverse or Exaggerated Physiological Response This category is an extension of “normal” physiologic manifestations. The main point is vigilance and early treatment. Treat hypotension early and do not let it progress to cardiac arrest. Knowledge, preparation, and anticipation can help reduce adverse or exaggerated physiological responses

High Neural Blockade Can occur with either spinal or epidural techniques

High Neural Blockade Causes Excessive doses of local anesthetic are administered Failure to reduce dose in patients susceptible to excessive spread (i. e. the elderly, pregnant, obese, or short patients) Unusual sensitivity Unusual excessive spread

High Neural Blockade Constant monitoring of the patients vital signs and block level are imperative Use of alcohol wipes (to assess cold sensation) and/or pinprick test will help Incremental dosing is important with an epidural With hyperbaric techniques you can change the patients position to slow down the cephalad spread (i. e. reverse Trendelenberg)

High Neural Blockade-Prevention Careful consideration in dosing your block Anticipation of potential complications Plan of action if complications occur Continual monitoring of the patient as the block progresses

High Neural Blockade- Initial Symptoms Dyspnea Numbness and tingling of the upper extremities (i. e. fingers) Nausea generally precedes hypotension due to hypoperfusion of the chemoreceptor trigger zone Mild to moderate hypotension

High Neural Blockade- Initial Treatment Change position with hyperbaric technique Stop the administration of local anesthetics with an epidural technique Supplemental oxygen Open up the IV fluids Treat hypotension with ephedrine or phenylephrine Treat bradycardia

High Neural Blockade- Initial Treatment Choose your vasopressor carefully. If patient is hypotensive and bradycardic then ephedrine would be indicated Ephedrine will increase heart rate as well as constrict blood vessels Phenylephrine can result in reflex bradycardia as it constricts blood vessels If patient is hypotensive and tachycardic or normal in respect to heart rate then phenylephrine may be indicated

High Neural Blockade- Initial Treatment Refractory hypotension and/or hypotension should be treated rapidly with 5 -10 mcg of epinephrine

High Neural Blockade- Spread to Cervical Dermatomes Signs and Symptoms May Include: Severe hypotension Bradycardia Respiratory insufficiency including apnea Unconsciousness

High Neural Blockade- Cervical Dermatomes Treatment The A, B, C’s Airway and breathing- supplemental oxygen, maintain a patent airway, intubation, mechanical ventilation Circulation- aggressive intravenous fluid administration, ephedrine, phenylephrine, epinephrine Bradycardia should be treated with atropine Dopamine infusions may help

High Neural Blockade- Cervical Dermatomes Treatment Early and aggressive treatment may help avoid a cardiac arrest! Once patient has been stabilized and successfully treated the decision to proceed is based on individual circumstances Considerations include time spent hypotensive, indications of myocardial ischemia, etc. The respiratory compromise associated with high neural blockade are often transient

Cardiac Arrest Due to Neuraxial Blockade

Cardiac Arrest Due to Neuraxial Blockade Cardiac arrest can occur with either epidural or spinal anesthesia More common with spinal anesthesia and the incidence may be as high as 1: 1, 500 Usually preceded by bradycardia Can easily occur in the young and healthy

Cardiac Arrest Due to Neuraxial Blockade- Keys to Prevention Appropriate hydration (i. e. 1 liter to an average sized adult)- must be administered within approximately 15 minutes since the majority of crystalloid solution will leave the intravascular space Aggressively treat bradycardia, atropine, ephedrine, epinephrine Do not be fooled by the 26 year old marathon runner- patients with a slow heart rate and high vagal tone are at risk for cardiac arrest during spinal anesthesia Total sympathectomy with unopposed vagal stimulation Error on the conservative and treat the patient

Cardiac Arrest Due to Neuraxial Blockade- Risk Factors Baseline heart rate < 60 bpm ASA class I Use of Beta Blockers Sensory level > T 6 Prolonged P-R interval

Urinary Retention

Urinary Retention Due to blockade of S 2 -S 4 Leads to a decrease in bladder tone and inhibition of normal voiding reflex Neuraxial opioids may contribute to urinary retention More common in elderly men and those with a history of benign prostatic hypertrophy

Urinary Retention Urinary catheterizes should be provided for patients undergoing moderate to lengthy procedures Postoperative assessment is important to detect urinary retention Prolonged urinary retention may be a sign of serious neurological injury

Complications Associated with Needle Placement or Catheter Insertion Inadequate anesthesia or analgesia Inadvertent intravascular injection Total spinal Subdural injection Backache Postdural puncture headache Neurological injury Spinal or epidural hematoma Meningitis and arachnoiditis Epidural abscess Sheering off the tip of the epidural catheter

Inadequate Analgesia or Anesthesia Rate of block failure is low but can be frustrating Must always be prepared to convert to general anesthesia or supplement Rate of block failure decreases as experience increases

Inadequate Analgesia or Anesthesia- May be associated with: Outdated or improperly stored local anesthetics (tetracaine looses potency when stored for long periods in a warm environment)

Inadequate Analgesia or Anesthesia- May be associated with: Needle movement once free flowing CSF is noted- helpful to confirm aspiration before, during, and after injection Even with free flowing CSF it is possible that the spinal needle is not entirely in the subarachnoid space resulting in a partial subdural injection and partial spinal

Inadequate Analgesia or Anesthesia- May be associated with: Epidural anesthesia is more subjective since you have to rely on confirmation by loss of resistance or hanging drop technique Either technique can lead to false positives Spread of local anesthetic is less predictable

Inadequate Analgesia or Anesthesia- May be associated with anatomical factors with epidural Soft spinal ligament can occur in the very young and in obstetrics…this results in never achieving a good loss of resistance If you are off the midline slightly you may be in the paraspinous muscle and not in the spinal ligaments

Inadequate Analgesia or Anesthesia- May be associated with anatomical factors with epidural Block failure may occur if the epidural catheter migrates into the subdural space Injection of local anesthetics into this space may result in Horner’s syndrome, a high spinal, or an absence of any effect

Inadequate Analgesia or Anesthesia Local anesthetic toxicity can occur if the epidural catheter is placed into a vessel A high spinal can occur if the epidural catheter is placed in a subarachnoid space- stresses importance of the test dose

Inadequate Analgesia or Anesthesia Septations within the epidural space may create a barrier to the spread of local anesthetic and some segments may lack anesthesia L 5, S 1, S 2 are all large nerve roots and the large size may prevent penetration of local anesthetic- correct by making the area dependent and adding local anesthetic

Inadequate Analgesia or Anesthesia Visceral pain can occur even if the epidural is adequate. Visceral afferent fibers travel with the vagus nerve. May increase the level of epidural anesthesia to the thoracic levels with additional local anesthetic IV sedatives and opioids may help

Inadequate Analgesia or Anesthesia- Failed Epidural Not waiting long enough to let it work Catheter is inserted too far resulting in a “unilateral” block…pull back the catheter 1 -2 cm and add local anesthetic with the unaffected side down

Inadvertent Intravascular Injection Risk with spinal anesthesia is extremely low Risk generally lies with epidural or caudal anesthesia Toxicity will affect the central nervous system and cardiovascular system

Inadvertent Intravascular Injection Local anesthetics vary in their potential to cause toxicity Least to most toxic local anesthetics are as follows: Chloroprocaine< lidocaine < mepivacaine < levobupivacaine< ropivacaine < bupivacaine

Inadvertent Intravascular Injection- Symptoms Hypotension Arrhythmias Cardiovascular collapse Seizures Unconsciousness

Inadvertent Intravascular Injection- Prevention Test dose Careful aspiration prior to injection Incremental dosing Vigilant monitoring for early signs and symptoms of intravascular injection Early symptoms include increase heart rate (if epi used), tinnitus, funny taste or metallic taste, subjective changes in mental status

Inadvertent Intravascular Injection- Prevention With early symptoms stop administration and anticipate impending complications such as seizures and hypotension, etc. Re-evaluate placement of catheter and reinsert as needed

Local Anesthetic Toxicity Treatment Standard ACLS treatment Bretyllium may be more effective than other forms of antiarrhythmics

On the Horizon- Intralipids Several successful resuscitations of local anesthetic overdose as well as other lipophilic medication overdoses Local anesthetics are amphipathic (have an affinity for both lipid and water) This makes local anesthetics potentially toxic for several tissues including the heart, brain, and skeletal muscles

On the Horizon- Intralipids expand the lipid compartment and allow for local anesthetic binding (there are more involved and technical explanations but lets keep it simple)

Lipid Rescue Protocol (Experimental) 20% Intralipid 1. 5 mg/kg initial bolus 0. 25 mg/kg/min infusion for 30 -60 minutes Bolus may be repeated 1 -2 times for persistent asystole May increase infusion rate if blood pressure decreases See lipidrescue. com for more information

Subdural Injection Subdural space is a potential space that is found between the dura and arachnoid space It contains a small amount of serous fluid Subdural space extends from the epidural space to the intracranial space Local anesthetics can travel further in the subdural space than they can in the epidural space

Subdural Injection Small doses of local anesthetic can travel far in the subdural space Small doses of local anesthetic associated with a spinal may result in no local anesthetic blockade Larger doses of local anesthetics associated with epidural analgesia may result in Horner’s Syndrome

Subdural Injection Manifestations of Horner’s syndrome include miosis (constriction of the pupil); ptosis (drooping of the upper eyelid); and anhidrosis (diminished or absent sweating).

Horner’s Syndrome

Subdural Injection Larger doses of local anesthetics associated with epidural anesthesia may result in a total spinal. Prevention is slightly more difficult as aspiration will generally be negative With slow incremental dosing you may note a higher and faster progression of blockade than would be normally expected

Backache

Backache Up to 30% of patients undergoing general anesthesia will complain of back pain Large number of patients suffer from chronic back pain Not a contraindication Patient should be aware that spinal or epidural anesthesia may result in some discomfort

Backache Inflammatory reaction due to tissue trauma May result in back spasms Short lived, analgesics, ice May last a few weeks Back ache may be a sign of serious complications such as epidural/spinal hematoma, abscess Careful evaluation to determine if a common/benign complication or something more serious

Postdural Puncture Headache Caused by disrupting the integrity of the dura Can occur due to: spinal anesthesia, “wet” tap with epidural, epidural catheter migration, tip of the epidural needle “indenting” the dura enough to cause a leak.

Postdural Puncture Headache occurs due to leakage of CSF through the dura Decrease in intracranial pressure occurs due to the leak Upright position in the patient leads to traction on the dura, tentorium, and blood vessels resulting in pain. Traction on the 6 th cranial nerve can result in diplopia and tinnitus

Postdural Puncture Headache- Symptoms Headache associated with upright position (i. e. sitting or standing). Relief found with a supine position Headache may be bilateral, frontal, retroorbital and/or occipital with or without radiation to the neck Described as “throbbing” or constant May be associated with nausea and/or photophobia

Postdural Puncture Headache- Symptoms Onset is generally 12 -72 hours; rarely is the onset immediate If untreated it may last for weeks

Postdural Puncture Headache- Associations Increased incidence related to needle size, needle type and patient population The larger the needle the higher the incidence Cutting point needles have a higher incidence of post dural puncture headache than pencil points When using cutting point needles orientate the bevel “sideways” so it will be parallel with the fibers. This will act to “spread” the fibers as opposed to cutting them

Postdural Puncture Headache- Associations Recent literature may indicate that pencil points actually cause more trauma then cutting needles. This actually may reduce the incidence of headache secondary to a localized inflammatory response. Increased post dural puncture headache in younger patients, in female patients, and in pregnant patients

Postdural Puncture Headache Some advocate the prophylactic treatment if a wet tap occurs with an epidural needle. Methods include epidural blood patch, epidural dextan, or epidural saline. A wet tap with a 17 g. epidural needle will yield a 50% incidence of pdph A prophylactic epidural blood patch performed within 24 hours of a “wet” tap has a 71% failure rate. After 24 hours there is a failure rate of 4%

Postdural Puncture Headache Epidural blood patches are not without risk. Remember 50% of the patients with a “wet” tap will not get a post dural puncture headache. Conservative measure would be to wait and see if symptoms occur Prophylactic treatment will only result in unnecessary treatment in 50% of the patients

Postdural Puncture Headache- Conservative Treatment Symptoms can be debilitating Start with conservative measures Supine position- will reduce symptoms, no evidence that bed rest will reduce the duration of post dural puncture headache. Theoretically it should decrease the amount of CSF leak and allow replacement of lost CSF

Postdural Puncture Headache- Conservative Treatment Hydration- theoretically helps to encourage the production of CSF. A dehydrated patient may experience more severe symptoms and hydration is important. The one study looking at this did not find that hydration decreased the incidence of post dural puncture headache.

Postdural Puncture Headache- Conservative Treatment Caffeine- theoretically helps to decrease sx by vasoconstriction of the cerebral vessels. May decrease symptoms but does not necessarily decrease the number of patients that will require an epidural blood patch. IV caffeine can be administered in a dose of 500 mg Oral caffeine can be encouraged. A dose of 300 mg of oral caffeine has been shown to decrease the intensity of pdph

Caffeine Content of Common Beverages

Postdural Puncture Headache- Conservative Treatment Analgesics- will decrease the severity of symptoms and include acetaminophen and NSAIDS Stool softners and soft diet may help decrease Valsalva straining which may increase leakage of CSF

Postdural Puncture Headache- Conservative Treatment Conservative treatment is mainly symptomatic

Postdural Puncture Headache- Epidural Blood Patch Definitive treatment Successfully resolves 90% of all post dural puncture headache after the first treatment Generally offered 12 -24 hours after the initiation of conservative treatment Not without risk

Postdural Puncture Headache- EBP Precautions Check patients history for contraindications Check coagulation status Ensure no anticoagulants have been administered (i. e. DVT prophylaxis) Ensure that the patient is not bacteremic Jehovah’s Witness patients may refuse an epidural blood patch based on religious beliefs

Postdural Puncture Headache- Epidural Blood Patch Involves injection of 15 -20 ml of the patients own blood at the level of dural puncture May be administered one space below the dural puncture site Blood patch works by mass effect and stops the leakage of CSF or alternatively by coagulating and “plugging” the hole

Postdural Puncture Headache- Epidural Blood Patch Inform the patient of risks and benefits Same as with any neuraxial technique with the addition of the increased risk of meningitis or infection (the blood that is removed can be contaminated and placed at an area that has breached the blood brain barrier Inform the patient that it is only 90% effective and not 100% effective

Postdural Puncture Headache- Epidural Blood Patch Technique Assemble your supplies- mask, sterile gloves, epidural tray, additional betadine and alcohol, sterile needle for venipuncture and tourniquet. Prior to locating the epidural space identify a suitable vein to draw blood. Prep the area with betadine and consider draping the area with sterile towels

Postdural Puncture Headache- Epidural Blood Patch Technique Perform usual steps for locating the epidural space Once epidural space is identified then have your assistant aseptically withdraw 15 -20 ml of blood. Keep the blood sterile. Ensure no contamination of the blood has occurred

Postdural Puncture Headache- Epidural Blood Patch Technique Place 15 -20 ml of blood into the epidural space

Postdural Puncture Headache- Epidural Blood Patch Technique The patient should not experience pain but may note pressure The patient should remain supine for 1 -2 hours The patient should avoid lifting heavy items or straining for 48 hours (thus avoiding the dislodgement of the epidural blood patch

Neurological Injury Can be transient or permanent Prevention is done by avoiding trauma to the nerve roots or spinal cord Identification of appropriate landmarks is essential Always document pre-existing neurological deficits Ask the patient if they suffer from neuropathy, chronic or acute low back pain, motor deficits.

Neurological Injury Document concurrent conditions that may contribute to postoperative neuro deficits such as peripheral vascular disease, diabetes, intervertebral disk injury, spinal disorders. Perform subarachnoid anesthesia below L 1 in adults and L 3 in children Multiple attempts will increase the risk of trauma- avoid this by proper positioning, identification of landmarks, and take your time being deliberate when performing neuraxial techniques

Neurological Injury If difficulty is encountered do not be afraid to ask another provider to help If a paresthesia is encountered make sure it is transient and redirect the needle When inserting a catheter or injecting and the patient experiences pain stop. Direct injection into the spinal cord can lead to paraplegia

Neurological Injury Document the presence of paresthesia or pain during neuraxial blockade Alternatively if the neuraxial technique has been performed without any problems document this (i. e. no pain, no paresthesia, etc. )

If the patient experiences a neuro deficit after neuraxial blockade: Possible causes include surgical positioning Improper positioning in the post op period Direct trauma related to surgery Rule out hematoma or abscess OB patients at risk for neuro deficits related to c-sec and vaginal delivery

Obstetric Causes Incidence of neurological complications in OB range from 1: 2, 600 -6, 400 and often related to difficult deliveries. Prolapse of intervertebral disk and subsequent nerve root compression can occur.

Obstetric Causes Injury related to descending head or mid to high forcep use include lumbrosacral injury (L 4, L 5). Results in foot drop, weakness of hip adduction and quadriceps. Acute hip flexion and retractors during a cesarean section can result in injury to the femoral nerve (L 2, L 3, L 4). Results in quadricep paralysis, abscent patellar reflex, and altered sensation of anterior thigh and medial calf.

Obstetric Causes Incorrect lithotomy positioning and retractors during a cesarean section can injury the lateral femoral cutaneous nerve (L 2, L 3). This will alter sensation on the anterolateral thigh. Incorrect lithotomy position with knee extension and external hip rotation may injure the sciatic nerve (L 4, L 5, S 1, S 2, S 3). This will result in sciatic type pain (from gluteal area to foot) and the inability to flex the leg.

Obstetric Causes Lithotomy position with acute flexion of thigh may lead to injury to the obturator nerve (L 2, L 3, L 4). This may lead to weak or paralyzed thigh adduction. Compression of lateral knee may lead to common peroneal nerve injury (L 4, L 5, S 1, S 2). This will result in foot drop and the inability to stand erect.

Obstetric Causes Lithotomy positioning may result in injury to the saphenous nerve (L 2, L 3, L 4). Loss of sensation in the medial foot and anteromedial lower leg.

Document New Neurological Deficits Is the neuropathy in the distribution of neuraxial blockade? (usually transient) Is there sharp back pain? Leg pain? (severe symptoms may indicate epidural hematoma or Transient Neurological Symptoms) Is there progressive numbness, motor blockade, or sphincter dysfunction? (may be spinal or epidural hematoma)

Document New Neurological Deficits Trauma to conus medullaris generally results in sacral dysfunction and you will see: Paralysis of biceps femoral muscle Sensory loss of the posterior thigh, perineal area, or great toes Bowel and bladder dysfunction

Document New Neurological Deficits After evaluation of sx it is reasonable to have a neurological consult

Spinal/Epidural Hematoma 1: 150, 000 for epidurals 1: 220, 000 for spinals

Factors associated with Spinal/Epidural Hematoma Abnormal coagulation due to disease/meds Multiple attempts at neuraxial blockade Formation after the removal of the epidural catheter

Spinal/Epidural Hematoma Presence of blood in the subarachnoid or epidural space will result in the compression of neural tissue There is no way to apply pressure and stop the bleeding due to the anatomy. Compression results in ischemia and subsequent injury

Spinal/Epidural Hematoma Symptoms (generally rapid) Sharp back and leg pain Progression of numbness and motor weakness Sphincter dysfunction

Spinal/Epidural Hematoma Rapid diagnosis is essential MRI/CT scan diagnose this complication Surgical decompression must occur in 8 -12 from the onset of symptoms to avoid permanent injury

Meningitis is very rare Must always use strict sterile technique Always wear a mask and change it frequently even in OB

Meningitis Most common cause of bacterial meningitis is from contamination of the puncture site by aerosolized mouth particles Viridans streptococcus is the dominant organism and is found in the mouth Stresses the importance of masks!

Meningitis To a lesser extent skin bacteria can result in meningitis Care should be taken in securing the device with sterile materials Skin bacteria could track there way into the epidural space

Meningitis Presentation is very similar to a post dural puncture headache Exception is there is no postural component to the headache, there is generally a fever, and alteration in level of consciousness

Arachnoiditis Very rare More common in the past when supplies where reused Chemical arachnoiditis can occur with intrathecal injection of steroids Lumbar arachnoiditis is more commonly associated with surgical procedures or trauma

Epidural Abscess Rare Incidence 1: 6, 500 - 1: 500: 000 May develop independent of neuraxial techniques

Epidural Abscess-risk factors Back trauma IV drug abuse Neurological surgical procedures Those associated with neuraxial techniques are commonly due to indwelling epidural catheters Symptoms develop between 5 days and several weeks

Epidural Abscess-Stages of Development Stage 1: back and vertebral pain intensified by percussion. Any patient with back pain and a fever should alert the anesthesia provider to the possibility of an abscess Stage 2: progresses to nerve root and radicular pain

Epidural Abscess-Stages of Development Stage 3: motor, sensory and/or sphincter dysfunction Stage 4: paralysis and or paraplegia

Epidural Abscess-Prognosis Dependent upon when diagnosed, the earlier the better Epidural catheter should be removed immediately Tip sent for cultures (not always accurate) Epidural site should be examined for signs and symptoms of infection Blood cultures should be sent for evaluation Any drainage from the site should be sent for evaluation

Epidural Abscess-Prognosis/Treatment Neuro consult Most common agents include staph auerus and staphylococcus epidermis Antibiotic coverage MRI/CT Possible decompression lami

Epidural Abscess-Prevention Sterile technique (hat, mask, sterile gloves, hand washing, sterile field, proper prep of the skin etc. ) If there is any doubt to contamination, stop and start over If epidural cath becomes disconnected you must decide whether to aseptically reattach it or remove the catherter

Epidural Abscess-Prevention Reduce epidural catheter manipulation Maintain a closed system always Use bacterial filter that comes with the kit Remove the catheter after 96 hours and if needed then replace it with a new one at a new site

Shearing Off the Tip of the Epidural Catheter Never attempt to withdraw the epidural catheter through the epidural needle If you need to remove the catheter remove both the needle and catheter as one unit When dc an epidural catheter use steady pressure never jerk the catheter If difficulty is encountered change the patients positions (i. e. fetal position) to maximize the intervertebral space

Shearing Off the Tip of the Epidural Catheter If tip breaks off deep in the epidural space leave it and observe for complications If tip breaks off in the superficial tissue it should be surgically removed A remnant of epidural catheter superficially can lead to infection

Complications Associated With Medication Toxicity Systemic toxicity (covered earlier) Transient neurological symptoms Cauda equina syndrome

Transient Neurological Symptoms Described in 1993 Most common after spinal anesthesia/rare for it to occur with epidural anesthesia Symptoms include LBP with radiation to the legs Sx occur after anesthetic has regressed and normal sensation has occurred Sx occur from 1 -24 hours after normal sensation Almost any local anesthetic can cause TNS

Transient Neurological Symptoms- Associated Local Anesthetics Lidocaine Tetracaine Bupivacaine Mepivacaine Prilocaine Procaine Ropivacaine

Transient Neurological Symptoms- Associated Local Anesthetics Most common local anesthetic to cause TNS is lidocaine Most in the anesthesia community have abandoned lidocaine as a spinal anesthetic Leaves us with few good choices Procaine often too short lived Prilocaine has a high incidence of nausea and vomiting Mepivacaine has similar profile to lidocaine for both duration and incidence of TNS

Transient Neurological Symptoms Unknown mechanism of action Theorized that lidocaine is more neurotoxic to the unsheathed nerve

Transient Neurological Symptoms. Contributing Factors Lithotomy position – may be due to stretching of the lumbrosacral nerve roots and decreased perfusion Early ambulation after the spinal reason not elucidated Treatment is symptomatic and generally is short lived

Cauda Equina Syndrome Associated with spinal catheters and 5% lidocaine Differs from TNS in that it is permanent and associated with sphincter dysfunction, sensory and motor deficits, and paresis

Cauda Equina Syndrome Generally appears in a peripheral nerve pattern and may be due to misdistribution of the hyperbaric lidocaine

Cauda Equina Syndrome Neurotoxicity of local anesthetics is as follows: Lidocaine=tetracaine > bupivacaine > ropivacaine Pain is similar to nerve root compression Has been reported after single shot spinals as well as rarely after epidural anesthesia

Analyzing Complications of Spinal and Epidural Anesthesia Sweden 1990 -1999 Reviewed 1, 260, 000 spinals and 400, 000 epidurals (half of which were for OB) Overall incidence of complications were 127 out of 1, 660, 000. Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockade in Sweden 1990 -1999. Anesthesiology. 2004; 101: 950 -959.

Analyzing Complications of Spinal and Epidural Anesthesia Incidence for spinal anesthetics 1: 20, 00030, 000 Incidence for epidural in OB was 1: 25, 000 Incidence for non OB epidural was 1: 3, 600 (this differs from US experience) Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockade in Sweden 1990 -1999. Anesthesiology. 2004; 101: 950 -959.

Analyzing Complications of Spinal and Epidural Anesthesia- Risk Factors LMWH administered within 10 hours before a spinal or epidural or removing a catheter 2 hours before treatment Disease that cause coagulation problems such as renal/liver, OB syndrome with hemolysis, elevated liver enzymes, low platelets Ankylosing Syndrome Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockade in Sweden 1990 -1999. Anesthesiology. 2004; 101: 950 -959.

Analyzing Complications of Spinal and Epidural Anesthesia- Risk Factors Spinal deformity Trauma while during the block Osteoporosis Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockade in Sweden 1990 -1999. Anesthesiology. 2004; 101: 950 -959.

Analyzing Complications of Spinal and Epidural Anesthesia Most complications seen with orthopedic surgery followed by general surgery and then urology Complications higher after epidural anesthesia when compared to spinal anesthesia Patients with cauda equina syndrome, traumatic cord injury, and paraplegia had a 100% of permanent injury. Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockade in Sweden 1990 -1999. Anesthesiology.

Analyzing Complications of Spinal and Epidural Anesthesia- The take home Complications occur 4 -5 times more frequently after spinal anesthesia when compared to epidural OB population had a lower incidence of complications compared to non ob female population Osteoporosis is now a risk factor Severe complications have a high rate of being permanent Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockade in Sweden 1990 -1999. Anesthesiology. 2004; 101: 950 -959.

Allergic Reactions Very low incidence with local anesthetics. Esters are more likely to cause reactions. They are metabolized into PABA (a known allergen). Methylparaben is a preservative used in some multi dose vials and is structurally similar to PABA. Should use preservative free local anesthetics.

Allergic Reactions Most reactions are related to vagal reactions, toxicity of local anesthetics, effects of epinephrine such as tachycardia, flushing, and tachypnea. Allergic reactions to anesthetics are rare. Propensity to cause allergic reactions are as follows muscle relaxants> thiopental > propofol > etomidate = ketamine = benzodiazepines > local anesthetics

Allergic Reactions Anaphylactic reactions involve in a number of mediators that result in an exaggerated response. Airway- angioedema of upper airway, bronchospasm, and edema of the lower airway. Signs and symptoms include bronchospasm, cough, dyspnea, pulmonary edema, laryngeal edema, and hypoxia. Vascular- increased permeability allows edema to occur resulting in hypovolemia and shock. Primary symptom will be hypotension and shock. Heart- hypoperfusion and hypoxemia results in arrhythmias and myocardial ischemia. Coronary vasoconstriction may occur. Tachycardia and arrhythmias are common. Other vital organs- resulting shock and lactic acidosis leads to additional ischemic trauma. The effect of mediators will manifest dermatologically as urticaria, facial edema, and pruritus.

Allergic Reactions Treatment includes the following: Stop the administration of the suspected medication Administer 100% O 2 and consider intubation if the patient is not already intubated. Epinephrine administered in doses of 0. 01 -0. 5 mg IV or IM Administer fluids rapidly to combat the hypovolemia and shock (1 -2 L of crystalloid) Diphenhydramine in a dose of 50 -75 mg IV Rantidine or cimetidine IV Hydrocortisone up to 200 mg IV or alternatively methylprednisolone in a dose of 1 -2 mg/kg IV.

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