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Regional Anesthesia Complications

Terms in this set (53)

What is the most frequent cause of systemic toxicity of a local anesthetic?
Accidental intravascular injection.

[Barash, Clin. Anes., 1997, p664]
Systemic toxicity of a locl anesthetic is due to an excess plasma concentration of the drug. What are four determinants of systemic absorption?
Systemic absorption of a local anesthetic is determined by:

(1) the total dose administered;

(2) the vascularity of the injection site;

(3) the presence of epinephrine or phenylephrine (vasoconstrictor) in the solution;

(4) the physicochemical properties of the drug (the greater the protein binding and the greater the lipid solubility, the slower the absorption).

[Stoelting, PPAP, 1991, p159; Barash, Clin. Anes., 2001, p460]
List ten symptoms of local anesthetic toxicity in order of appearance.
(1) Numbness of tongue (circumoral numbness),

(2) auditory distur- bance (tinnitus),

(3) skeletal muscle twitching,

(4) systemic hypoten- sion (lightheadedness),

(5) myocardial depression,

(6) seizures,

(7) unconsciousness,

(8) respiratory arrest (apnea),

(9) coma, and

(10) cardiovascular depression.

[Stoelting, PPAP, 4th ed., p191; Barash, Clin. Anes., 5th ed., 2006, p464
How can local anesthetic systemic toxicity (LAST) best be avoided?
The best practice for managing systemic local anesthetic intoxication starts with vigilance and prevention.

Elevated plasma levels of local anesthetics can occur by inadvertent intravascular injections or systemic absorption.

The risk for intravascular injections can be reduced by a using a local anesthetic test dose (about 3 mL), frequently aspirating the injectate for signs of blood return, and dividing the dose of the local anesthetics.

[Barash, Clin. Anes, 7th. 2013 p575; Nagelhout, NA, 5th. 2013 p135-136, 138b, 140b; Hadzic & NYSORA, Hadzic's Peripheral Blocks, 2nd. 2012 p120-121]
After an epidural injection of local anesthetic, your patient complains of lightheadedness, dizziness, and ringing in the ears. What immediate actions should you take?
Lightheadedness, dizziness, and tinnitus are initial symptoms of local anesthetic systemic toxicity (LAST).

Your immediate concern is airway management and circulatory support.

Maintain ventilation with 100% oxygen and secure the airway, if necessary. Hypoxia, hypercapnia and acidosis will exacerbate the toxicity.

Hypercapnia enhances cerebral blood flow and thus more rapid delivery of local anesthetic to the brain.

In addition, both hypercapnia and acidosis decrease plasma protein binding of local anesthetics, increasing the proportion of free drug available for diffusion in the brain.

[Barash, Clin. Anes, 7th. 2013 p575; Nagelhout, NA, 5th. 2013 p135-136, 138b; Miller, et al, Miller's Anesthesia, 8e. 2015 p1047]
- (Q6) You have just performed intercostal nerve blocks at 5 levels to provide analgesia for fractured ribs. The patient becomes hypotensive, bradycardic, and has a seizure. Describe seven (7) actions to manage the situation.
The patient with hypotension, bradycardia, and seizures following intercostal nerve blocks has local anesthetic systemic toxicity (LAST), most likely due to an intravascular injection of local aesthetics.

The following checklist for managing LAST is provided by the American Society of Regional Anesthesia and Pain Medicine.

(1) Get help.

(2) Airway management: ventilate with 100% oxygen.

(3) Seizure suppression, benzodiazepines are preferred.

(4) BLS/ACLS with medication adjustments.

(5) Infuse 20% lipid emulsion.

(6) Alert the nearest facility having cardiopulmonary bypass capability. Failure to respond to lipid emulsion and vasopressor therapy necessitates institution of cardiopulmonary bypass.

(7) Post LAST events at www.lipidrescue.org and report use of lipid to www.lipidregistry.org.

[Nagelhout, NA, 5th. 2013 p136-140; Barash, Clin. Anes, 7th. 2013 p575; Miller, et al, Miller's Anesthesia, 8e. 2015 p1048-1049; Hadzic & NYSORA, Hadzic's Peripheral Blocks, 2nd. 2012 p120-122
Describe the recommended lipid emulsion dosing for treatment of local anesthetic systemic toxicity (LAST).
The recommended lipid emulsion dosing for treatment of LAST is:

(1) intravenous bolus of 1.5 mL/kg (LBW) of 20% lipid emulsion, such as Intralipid 20%, over 1 minute.

(2) Continuous infusion at 0.25 mL/kg/ min for at least 10 minutes after cardiac function returns.

(3) If cardiovascular instability continues, repeat bolus once or twice and consider increasing the infusion to 0.5 mL/kg/min.

(4) Recommended upper limit is 10 mL/kg lipid emulsion over the first 30 minutes.

[Nagelhout, NA, 5th. 2013 p136-140; Barash, Clin. Anes, 7th. 2013 p575]
In question 6, you stated "BLS/ACLS with medication adjustments « C for managing local anesthetic toxicity (LAST). What are the specific adjustments? What drugs should be avoided?
During the management and treatment of local anesthetic systemic toxicity (LAST), the following adjustments should be made to standard BLS/ACLS protocols.

(1) Reduce individual epinephrine doses to less than l mcg/kg (epinephrine appears to reduce efficacy of Intralipid emulsion).

(2) Avoid vasopressin.

(3) Avoid calcium channel blockers.

(4) Avoid beta-adrenergic antagonists (beta-blockers).

(5) Avoid local aesthetics (!). Amiodarone is preferred for ventricular dysrhythmias.

(6) Propofol (for seizures) should not be used when there are signs or expectation of cardiovascular instability.

[Nagelhout, NA, 5th. 2013 p136-140]
Six mechanistic actions may contribute to lipid resuscitation during the management of local anesthetic systemic toxicity (LAST). List the six mechanisms of action of lipid emulsion rescue.
Six mechanistic actions may contribute to lipid resuscitation:

(1) capture of local anesthetic in the blood (lipid sink effect);

(2) increased fatty acid uptake by mitochondria (metabolic effect);

(3) interference with local anesthetic binding of sodium channels (membrane effect);

(4) activation of Akt cascade (a serine/threonine protein kinase important in cell survival, proliferation, and migration, also called protein kinase B; note: this is signal transduction) leading to inhibition of GSK-3 which is glycogen synthase kinase (cytoprotective effect);

(5) promotion of calcium entry via voltage-dependent calcium channels (ionotropic/inotropic effect); and

(6) accelerated shunting (pharmacokinetic effects).

[Nagelhout, NA, 5th. 2013 p136-140|
List nine (9) complications of spinal anesthesia.
Complications of spinal anesthesia include

(1) postural puncture head- ache,

(2) backache,

(3) high spinal,

(4) nausea,

(5) urinary retention,

(6) hearing loss,

(7) spinal hematoma,

(8) shivering, and

(9) neurologic injury (rare).

[Barash, Clin. Anes, 7th. 2013 p664; Miller, et al, Miller's Anesthesia, 8e. 2015 p1711-1715]
What is the most common complication of spinal anesthesia? What is the second most common complication of spinal of anesthesia?
Backache (incidence of 11% to 13%) is the most common complication of spinal anesthesia.

Postural puncture headache (incidence of 0.4% to 7.8%) is second most common complication of spinal anesthesia.

[Benumof and Saidman, Anes. and Periop. Compl., 1999, pp54, 56
What is the incidence of post-dural puncture headache with spinal anesthesia?
The incidence of post-dural puncture headache with spinal anesthesia is up to 25%.

[Barash, Clin. Anes, 7th. 2013 p926]
What causes a spinal headache?
Postural puncture headache is due to decreased cerebrospinal fluid pressure resulting from the leakage of cerebrospinal fluid through the opening in the dural sheath.

[Barash, Clin. Anes., 1997, pp663-664]
What eight (8) factors are related to a greater likelihood of a post-dural puncture headache following neuraxial anesthesia?
The likelihood of a post-dural puncture headache is related to:

(1) age younger > older;

(2) gender , females > males;

(3) BMI , low BMI > high BMI (increased intra-abdominal pressure is obese raises SF pressure);

(4) pregnancy , pregnant > non-pregnant;

(5) needle size, larger gauge > smaller gauge;

(6) needle bevel, less incidence when bevel is placed in long axis of the neuraxis (in other words, bevel parallel to dural fibers);

(7) dural thickness , thicker dura, less incidence; and,

(8) history of dural punctures , greater incidence with prior dural punctures.

[Miller, et al, Miller's Anesthe- sia, 8e. 2015 p1712t; Chestnut, OB Anes., 5th. 2014 p720-722; Suresh et al., Shnider and Levinson's OB Anes., 5. 2012 p428]
The frequency of post-dural puncture headache (PDPH) is related to needle size and needle style. Identify the frequency of PDPH for the following needles: Quincke 22g, Quincke 27g, Quincke 32g; Sprotte 22g, Pencan (Sprotte) 27g; Whitacre 20g, Whitacre 27g? What is the conclusion?
The frequency of post-dural puncture headache (PDPH) associated with various needles is: Quincke 22g, 36%Quincke 27g , 1.5% to 5.6% Quince 32g , 0.4%Sprotte 22g 12.2% Pencan (Sprotte) 27 g, 0.98% Whitacre 20g, 2% to 5% Whitacre 27g , 0% to 1.7%Tuohy 16g , 70%

The conclusion: smaller, non-cutting needles are associated with a a lower frequency of post-dural puncture headache as complication of neuraxial anesthesia.

[Suresh et al., Shnider and Levinson's OB Anes., 5. 2012 p428]
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