complications of neuraxial blockade developing countries regional anesthesia lecture series daniel...

COMPLICATIONS OF NEURAXIAL BLOCKADE

Developing Countries Regional Anesthesia Lecture Series

Daniel D. Moos CRNA, Ed.D. U.S.A. [email protected] Lecture 13

Soli Deo Gloria

mailto:[email protected]

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


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


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 > T6 Prolonged P-R interval

Urinary Retention

Urinary Retention

Due to blockade of S2-S4 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)


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


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


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


Septations within the epidural space may create a barrier to the spread of local anesthetic and some segments may lack anesthesia

L5, S1, S2 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


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

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 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 6th 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


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.


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


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


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


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


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


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


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 L1 in adults and L3 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 (L4, L5). 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 (L2, L3, L4). 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 (L2, L3). This will alter sensation on the anterolateral thigh.

Incorrect lithotomy position with knee extension and external hip rotation may injure the sciatic nerve (L4,L5,S1,S2,S3). 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 (L2,L3,L4). This may lead to weak or paralyzed thigh adduction.

Compression of lateral knee may lead to common peroneal nerve injury (L4, L5, S1, S2). This will result in foot drop and the inability to stand erect.

Obstetric Causes

Lithotomy positioning may result in injury to the saphenous nerve (L2, L3, L4). 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)


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


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


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


Rapid diagnosis is essential MRI/CT scan can diagnose this

complication Surgical decompression must occur in 8-

12 from the onset of symptoms to avoid permanent injury

Meningitis

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


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


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.


Incidence for spinal anesthetics 1:20,000-30,000

Incidence for epidural in OB was 1:25,000

Incidence for non OB epidural was 1:3,600

(this differs from US experience)


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


Analyzing Complications of Spinal and Epidural Anesthesia- Risk Factors

Spinal deformity Trauma while during the block Osteoporosis



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.


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


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% O2 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.

References Ankcorn C. & Casey WF. Spinal Anaesthesia- A Practical Guide. Update in Anaesthesia. Issue 3; Article 2. 1993. Baer ET. Post-dural puncture bacterial meningitis. Anesthesiology, 105:2, 2006. Brown DL. Spinal, Epidural, and Caudal Anesthesia. In Miller’s Anesthesia 6th edtion. Miller, RD ed. Pages 1653-1675. Elsevier, Philadelphia,

Penn. 2005. Burkard J, Lee Olson R., Vacchiano CA. Regional Anesthesia. In Nurse Anesthesia 3rd edition. Nagelhout, JJ & Zaglaniczny KL ed. Pages 977-1030. Casey WF. Spinal Anaesthesia- A Practical Guide. Update in Anaesthesia. Issue 12; Article 8. 2000. Dijkema LM, Haisma HJ. Case Report- Total Spinal Anaesthesia. Issue 14; Article 14. 2002. Dobson MB. Conduction Anaesthsia. In Anaesthesia at the District Hospital. Pages 86-102. World Health Organization. 2000.

Kleinman, W. & Mikhail, M. (2006). Spinal, epidural, & caudal blocks. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. New York: Lange Medical Books.

Nitti, J.T. & Nitti, G.J. (2006). Anesthetic complications. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. New York: Lange Medical Books.

Pollard, JB. Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesthesia & Analgesia, 92:252-6, 2001.

Sime, AC. Transient neurologic symptoms and spinal anesthesia. AANA Journal, April 2000.

Tsui, B.C.H & Finucane, B.T. (2008). Managing adverse outcomes during regional anesthesia. In D.E. Longnecker et al (eds) Anesthesiology. New

York: McGraw-Hill Medical. 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.

complications of neuraxial blockade developing countries regional anesthesia lecture series daniel...

Documents