Regional Anesthesia Flashcards
Benefits of block?
- Fast Pain relief
- Decreased risk of intraoperative bleeding, stroke, and MI
- Decreased intraoperative need for narcotics
* less N/V, less constipation, faster wake up and discharge
- Decreased intraoperative need for narcotics
- Minimal Risk compared to Traditional Pain Management
* no respiratory depression
- Minimal Risk compared to Traditional Pain Management
- May be able to avoid General Anesthesia for certain cases
* good for patient with bad heart, kidney, brain
- May be able to avoid General Anesthesia for certain cases
Risks and contraindications of blocks?
- In rare cases, nerve damage can cause persistent numbness, weakness, or pain.
- most cases resolve within 6 months and almost all by a year
- 0.05% risk of nerve damage
- typically position related and generally a strip of numbness that is gone in a couple of weeks
- if persistent weakness- dx- EMG- tests signal from the nerve, have to wait a couple of weeks before pt can get it
- always think of who you’re blocking. If pt relies on arm for professional reasons (ie football player), don’t block them. too risky
- Risk of systemic toxicity if the anesthetic is absorbed through the bloodstream into the body.
- if patient is maxed out on LA for block placement. DON’T GIVE IV LIDOCAINE ON INDUCTION
- Block depending risks such as hematoma, pneumothorax, phrenic n. paralysis, etc.
- Contraindications are decided on a case by case basis. Each person should be evaluated for their lung and heart function, prexisting motor or sensory loss, diabetic neuropathy, history of block failure or block related nerve injury in the past, body habitus, and coagulation status
- if you can compress the PNB site (IE ISB/SCB, you can hold pressure. But ICB, hard to hold pressure. Bad to block someone at increase r/f bleeding if you can’t hold pressure at PNB site.
Who is a block candidate?
- hose who have capacity and understand that they will have a numb arm
- Those who are are IN-capacitated but the risk of GA for urgent/ emergent cases is life threatening compared to the risk of a block
- while she would not block someone with only one finger left from diabetic neuropathy, she would block them if there was a high risk of the patient dying on the table during induction
- Patients with a history of Chronic Pain who are on high doses of opioids at home or who are on drugs such as suboxone that render administered opioids ineffective
Who is NOT a block candidate?
- Patient’s you do not trust to take care of themselves
- Patient’s who do not have reliable help or will not be able to get into their homes due to the block
- Patients who say NO
- never push someone to get a block. you can explain why the block is helpful but never coerce someone to do a block
- Infection over the site (local anesthetic rendered ineffective)
- Anti-coagulated and case requires a “deep” block
- ** granted based on local anesthetic chosen, if you feel someone would benefit from a block but it needs to wear off you can use a shorter acting local anesthetic
Allergy to LA? System toxicity?
True allergy to LA extremely rare
- Mostly due to preservatives, additives and metabolites
- Amides may contain methylparaben (amide’s have 2 i’s)- according to apex a preservative that can rarely cause allergic reaction
- Esters have PABA which is more susceptible to allergic reaction (esters = only one “i” in name)
- No cross-sensitivity between classes of LA
- Often Epinephrine side effects mistaken as allergy
Systemic toxicity: dose- and time-dependent
- Adverse reactions more likely with higher serum levels/faster onset
- Rate of systemic absorption proportional to vascularity of site of injection: IV > Tracheal > Intercostal > Caudal > Epidural > Brachial plexus > Sciatic > Subcutaneous
- Main targets of toxicity: CNS, heart
- Receive relatively large fractions of cardiac output
DOA for commonly used LA?
Ropivacaine – 12 hrs
Bupivacaine- 15 hrs *** with adjuncts, ropi and bupi can last 24 hours
Lidocaine- 2 hrs
Mepivacaine – 6 hrs **can be used for pts that need strong block for sx but the block also needs to wear off before they go home
Adjuncts can push the block time 2-12 hours
Clinical symptoms of LA toxicity?
Propagation of subcortical limbic excitation
- Clinical symptoms (with increasing doses):
- Circumoral numbness, dizziness, tinnitus, blurred vision
- Restlessness, agitation, nervousness, seizures
- CNS depression: slurred speech, drowsiness, unconsciousness
- May bypass earlier symptoms with arterial (esp. vertebral) injections and manifest as a seizure
Cardiotoxicity with LA?
LA-induced dysrhythmias: sodium channel blocking effect of LA
- Prolongation of impulse conduction may lead to malignant arrhythmias
- Lidocaine: less potent and toxic: “fast-in, fast-out”
- Bupivacaine: more potent and toxic: “fast-in, slow-out”
- R(+) enantiomer has greater affinity for Na+ channel binding and thus toxicity
Treatment:
- Supportive (correct any hypoxemia or acidosis)
- ACLS protocol (except should not use lidocaine); previously used Bretylium
- INTRALIPID (not propofol)
Intralipid treatment for LA toxicity?
- Equipment:
- 20% lipid emulsion
- Treatment regimen (NB: no standard method)
- 1.5 mL/kg as an initial bolus, followed by
- 0.25 mL/kg/min for 30-60 minutes
- Bolus could be repeated 1-2 times for persistent asystole
Max doses for common local anesthetics?
-
Bupivicaine 2.5 mg/kg,
- with epi 3mg/kg
-
Ropivacaine 2.5-3 mg/kg
- with epi 3.5 mg/kg
-
Lidocaine 4mg/kg
- with epi 7 mg/kg
-
Mepivicaine 4mg/kg
- with epi 7 mg/kg
- Chloroprocaine 12mg/kg
Lidocaine (drug card)
CLASS=amide LA (& Class IB antiarrhythmic – its active metabolite monoethyglycinexylidide blocks Na+ channels in cardiomyocytes,decrease AP duration & refractory period)
- LA MOA- bind to H-gate of Na channel and physically obstruct the channel
- keeps Na channel in closed/inactivated state and prevents further transmission AP (unionized portion diffuses across membrane, ionized portion blocks channel)
Pharmacokinetics=
- pKa- 7.9; non-ionized- 24%, PB- 70% (PB 50% for antiarrhythmic); low potency & low lipid solubility
- Fast onset & moderate DOA (1-2hr); E1/2- 1.5hr (antiarrhythmic- 1-8 hrs)
- Intrinsic vasodilator activity; uptake into the lungs
- CYP450 liver metabolism that depends on HBF & excreted in urine
- 2 active metabolites- xylidide & monoethylglycinexylidide
SE= TNS, high incidence of cauda equina syndrome (specfiically high concentraiton lidocaine); BLUNT SNS TO DVL
LA toxicity
5-10 mcg/ml: circumoral numbness, lightheadedness, tinnitus, skeletal muscle twitching, visual disturbances, systemic hypotension, myocardial depression, & tachycardia, decreased SVR & cardiac output.
10-15 mcg/ml: seizures, unconsciousness
15-25 mcg/ml: apnea, coma
>25 mcg/ml: cardiovascular depression/collapse
CI= methemoglobinemia
LA hypersensitivity to amide LA, coagulopathies, infection, hypovolemia, refusal, inability to cooperate inexperience of provider
Antiarrhythmic hypersensitivity; WPW syndrome, HB, hepatic disease; CYP450 inhibitors such as Cimetidine & Propranolol decrease metabolism
Dose=
MAX: 4mg/kg & with epi 7mg/kg;
Spinal MAX- 30-100mg (1-2mL) (1.5-5%)
Epidural: 15-30 ml of 1-2%
PNB- volume depends on location- 1-2%
Intubation to blunt DVL & antiarrhythmic- 1-2 mg/kg (max antiarrhythmic: 3mg/kg)
Bupivicaine (drug card)
CLASS= amide LA
Pharmacokinetics=
- pKa- 8.1; non-ionized- 17%, PB- 95%; very potent & highly lipid soluble
- Moderate onset & long DOA (4-8hr); E1/2- 3.5hr
- CYP450 liver metabolism that depends on HBF
SE= differential blockade; TNS, “very low risk for neuro complications with spinal” (CB) ; highly CV toxic hypotension, myocardial depression, AV block, arrhythmias; local anesthestic toxicity (cirucmoral numbness, tinnitus, vision changes, dizziness, restlessness, muscle twitching in face/extremities–> seizures)–> CNS depression, apnea, hypotension).
CI= refusal, inability to cooperate, coagulopathies, hypovolemia, infection @ site; inexperience of clinician; extreme caution in poor CV function & HB
Dose=
- MAX- 2.5mg/kg
- Spinal MAX - spinal-15-20mg (0.5, 0.75%, 3-4 mL)
- Epidural- 15-30 ml of 0.125-0.5%
- PNB- amount depends on location- 0.25-0.5%
Where do each of the UE PNB work on the brachial plexus?
- Interscalene- Roots/trunks
- Supraclavicular- division
- easiest block to have in arsenal
- all the nerves are packaged in one location
- infraclavicular- cords
- axillary- branches
- fails the most because you have to get them individually
Targets for ISB?
- Start at clavicle, look at divisions (SCB) then follow it up until you see the “stoplight” of C5, C6, C7
- in theory the stoplight is C5-C7. There are sometimes anatomical variation in C5,C6 C7 and C5 will have to 2 branches. Never put needle between the 2 because you can cause nerve damage.
- only used for shoulder surgery. you don’t get coverage of C8 (ulnar nerve)
Link for VIDEO
- Brachial plexus sandwiched b/w anterior and middle scalene muscles
-
recognize the brachial plexus is lateral/superficial to Carotid artery and internal jugular vein
-
many vasculature in brachial plexus
- vertebral artery is very close to target- risk for intravascular injection
-
many vasculature in brachial plexus
- Pre-vertebral fascia has to be breached by needle to place LA in interscalene groove
Technique for ISB?
- Sterilize skin
- Some providers admin LA
- don’t place needle too deep. placement of small gauge needle can result in intraneural injection
- needle placed lateral to medial
- enters prevertebral fascia and transveres the middle scalene muscle
- if using nerve stim- elicit nerve response, then decrease to <0.3 mA to ensure motor stim is lost and decreases r/f intraneural injection.
- maintain injection pressure <15 psi
- typically uses 15- 25 mL to ensure fast, reliable onset of anesthesia