Local anaesthetics secrets Flashcards
(32 cards)
Which regional anesthetic blocks are associated with the greatest degree of systemic vascular absorption of local anesthetic?
Intercostal nerve block > caudal > epidural > brachial plexus > sciatic-femoral > subcutaneous.
Because the intercostal nerves are surrounded by a rich vascular supply, local anesthetics injected into this area are more rapidly absorbed, thus increasing the likelihood of achieving toxic levels.
Why are epinephrine and phenylephrine often added to local anesthetics? What cautions are advisable regarding the use of these drugs?
These drugs cause local tissue vasoconstriction, limiting uptake of the local anesthetic into the vasculature and thus prolonging its effects and reducing its toxic potential (see Question 14).
Epinephrine, usually in 1:200,000 concentration, is also a useful marker of inadvertent intravascular injection.
Epinephrine is contraindicated for digital blocks or other areas with poor collateral circulation.
Systemic absorption of epinephrine may also cause hypertension and cardiac dysrhythmias, and caution is advised in patients with ischemic heart disease, hypertension, preeclampsia, and other conditions in which such responses may be undesirable.
How does a patient become toxic from local anesthetics? What are the clinical manifestations of local anesthetic toxicity?
Systemic toxicity is caused by elevated plasma local anesthetic levels, most often a result of inadvertent intravascular injection and less frequently a result of systemic absorption of local anesthetic from the injection site.
Toxicity involves the cardiovascular and central nervous systems (CNS).
Because the CNS is generally more sensitive to the toxic effects of local anesthetics, it is usually affected first.
The manifestations are presented below in chronologic order:
n CNS toxicity
- c Light-headedness, tinnitus, perioral numbness, confusion
- c Muscle twitching, auditory and visual hallucinations
- c Tonic-clonic seizure, unconsciousness, respiratory arrest
n Cardiotoxicity
- c Less common, but can be fatal
- c Hypertension, tachycardia
- Decreased contractility and cardiac output, hypotension c
- Sinus bradycardia, ventricular dysrhythmias, circulatory arrest
Is the risk of cardiotoxicity the same with various local anesthetics?
There have been multiple case reports of cardiac arrest and electrical standstill after bupivacaine administration, many associated with difficult resuscitation.
The cardiotoxicity of more potent drugs such as bupivacaine and etidocaine differs from that of lidocaine in the following manner:
- The ratio of the dosage required for irreversible cardiovascular collapse and the dosage that produces CNS toxicity is much lower for bupivacaine and etidocaine than for lidocaine.
- Pregnancy, acidosis, and hypoxia increase the risk of cardiotoxicity with bupivacaine.
- Cardiac resuscitation is more difficult following bupivacaine-induced cardiovascular collapse. It may be related to the lipid solubility of bupivacaine, which results in slow dissociation of this drug from cardiac sodium channels (fast-in, slow-out).
- By contrast, recovery from less lipid-soluble lidocaine is rapid (fast-in, fast-out). In an effort to minimize the risk of cardiac toxicity in the event of an accidental intravascular injection, the use of bupivacaine in concentrations greater than 0.5% should be avoided, especially in obstetric epidural anesthesia.
- For postoperative analgesia bupivacaine concentrations of 0.25% generally provide excellent effect.
How will you prevent and treat systemic toxicity?
Most reactions can be prevented by careful selection of dose and concentration,
use of test dose with epinephrine,
incremental injection with frequent aspiration,
monitoring patient for signs of intravascular injection, and judicious use of benzodiazepine to raise the seizure threshold.
n Seizures can quickly lead to hypoxia and acidosis, and acidosis worsens the toxic effects.
A patent airway and adequate ventilation with 100% oxygen should be ensured.
n If seizures develop, small doses of intravenous diazepam (0.1 mg/kg) or thiopental (1 to 2 mg/kg) may terminate the seizure.
Short-acting muscle relaxants may be indicated for ongoing muscle activity or to facilitate intubation if necessary.
n Cardiovascular collapse with refractory ventricular fibrillation following local anesthetics, particularly bupivacaine, can be extremely difficult to resuscitate.
Treatment includes sustained cardiopulmonary resuscitation, repeated cardioversion, high doses of epinephrine, and use of bretylium to treat ventricular dysrhythmias.
Intravenous intralipid has been used successfully in cases in which conventional resuscitation measures were unsuccessful. Suggested dose is initial bolus of 1.5 ml/kg of 20% intralipid solution, which can be repeated every 3 to 5 minutes up to a total maximum dose of 8 ml/kg.
What is the risk of neurotoxicity with local anesthetics?
The overall risk of permanent neurologic injury from regional anesthesia is extremely small.
However, in recent years the following two complications have been described after spinal and epidural anesthesia:
n Transient neurologic symptoms manifest in the form of moderate-to-severe pain in the lower back, buttocks, and posterior thighs. These symptoms appear within 24 hours of spinal anesthesia and generally resolve within 7 days. The delayed onsetmay reflect an inflammatory etiology for these symptoms. They are seen most commonly with lidocaine spinal anesthesia and are rare with bupivacaine. Patients having surgery in the lithotomy position appear to be at increased risk of neurologic symptoms following either spinal or epidural anesthesia.
n Cauda equina syndrome: A few cases of diffuse injury to the lumbosacral plexus were initially reported in patients receiving continuous spinal anesthesia with 5% lidocaine dosed via microcatheters. The mechanism of neural injury is thought to be that nonhomogeneous distribution of spinally injected local anesthetic may expose sacral nerve roots to a high concentration of local anesthetic with consequent toxicity.
Rare cases in the absence of microcatheters have also been described. Avoid injecting large amounts of local anesthetic in the subarachnoid space, especially if less than an anticipated response is obtained with the initial dose.
What are the advantages of spinal anesthesia over general anesthesia?
- n The metabolic stress response to surgery and anesthesia is reduced by subarachnoid block (SAB).
- n Particularly in elective hip surgery, there may be up to a 20% to 30% reduction in blood loss.
- n SAB decreases the incidence of venous thromboembolic complications by as much as 50%.
- n Pulmonary compromise appears to be less.
- n Endotracheal intubation is avoided.
- n Mental status can be followed.
- Where are the principal sites of effect of spinal local anesthetics?
The principal sites are the spinal nerve roots and spinal cord.
Interestingly nerve roots may have different anatomic configurations (rootlets vs. roots); and there may be variability in fascial compartmentalization of the roots, especially between the dorsal and ventral nerve roots, accounting in part for differences between motor and sensory blockade.
What factors determine the termination of effect?
- Resorption of the agent from the cerebrospinal fluid (CSF) into the systemic circulation limits duration.
- Addition of a vasoconstrictor that slows resorption prolongs duration of effect.
- Vasoconstrictor efficacy decreases with local anesthetics with intrinsic longer durations of effect.
Describe the factors involved in distribution (and extent) of conduction blockade.
- n Patient characteristics include height, position, intra-abdominal pressure, anatomic configuration of the spinal canal, and pregnancy.
- There is great interindividual variation in lumbosacral CSF volumes; magnetic resonance imaging has shown volumes ranging from 28 to 81 ml. Lumbar CSF volumes correlate well with the height and regression of the block. With the exception of an inverse relation with weight, no external physical measurement reliably estimates lumbar CSF volumes.
- CSF volumes are also reduced in pregnancy. n
- Needle direction and site when anesthetic is injected are important.
- n The total injected dose of local anesthetic is important, whereas the volume or concentration of injectant is unimportant.
- n The baricity of the local anesthetic solution is important. Baricity is defined by the ratio of the density of the local anesthetic solution to the density of CSF. A solution with a ratio >1 is hyperbaric and tends to sink with gravity within the CSF. An isobaric solution has a baricity of 1 and tends to remain in the immediate area of injection. A ratio
At what lumbar levels should a spinal anesthetic be administered? What structures are crossed when performing a spinal block?
The selected level should be below L1 in an adult and L3 in a child to avoid needle trauma to the spinal cord.
As an anatomic landmark, the L3-L4 interspace is located at the line intersecting the top of the iliac crests.
Either a midline or paramedian approach can be used.
The anatomic layers passed through include skin, subcutaneous structures, supraspinous ligament, interspinous ligament, ligamentum flavum, dura mater, and arachnoid membrane.
What are the most common complications of spinal anesthesia?
Common complications include hypotension, bradycardia, increased sensitivity to sedative medications, nausea and vomiting (possibly secondary to hypotension), postdural puncture headache (PDPH), and residual back pain and paresthesias (usually associated with the use of lidocaine.
Less frequent but more ominous complications include nerve injury, cauda equina syndrome, meningitis, total spinal, and hematoma/abscess formation.
Particular issues associated with these complications are discussed subsequently.
What are the physiologic changes and risk factors found with subarachnoid block–associated hypotension?
Hypotension occurs as a result of a loss of sympathetically mediated peripheral vascular resistance.
Arterial and central venous pressure decrease with only mild decreases in heart rate, stroke volume, and cardiac output.
Hypovolemia, age greater than 40 years, sensory level greater than T5, baseline systolic blood pressure below 120 mm Hg, and performance of the block at or above L3-L4 increase the incidence of hypotension.
Hypotension (and possibly decreased cerebral blood flow) may be responsible for nausea and vomiting observed with SAB.
Patients should receive a bolus of crystalloid or colloid (250 to 1000 ml) before SAB. Because of the pattern of distribution, colloid is more effective, although more expensive. Volume expansion and intravenous sympathomimetics usually reverse hypotension should it occur.
Trendelenburg position may raise the level of blockade and should be used with caution and vigilance.
Volume loading should also be used cautiously in patients with limited cardiac reserve. In these patients, as the block recedes, vascular tone increases, raising the central blood volume, which may precipitate heart failure.
Strategies to create a unilateral block may also decrease the hypotension associated with SAB.
What are the etiology and risk factors for subarachnoid block–associated bradycardia? Bradycardia may
Bradycardia may occur secondary to unopposed vagal tone from a high sympathectomy, blockade of the cardioaccelerator fibers (T1-T4), and the Bezold-Jarisch reflex (slowing of the heart rate secondary to a decrease in venous return).
Patients with underlying increased vagal tone (children and adults with resting heart rates
Review the clinical features of total spinal anesthesia.
- Total spinal anesthesia results from local anesthetic depression of the cervical spinal cord and brainstem.
- Signs and symptoms include dysphonia, dyspnea, upper extremity weakness, loss of consciousness, pupillary dilation, hypotension, bradycardia, and cardiopulmonary arrest.
- Early recognition is the key to management.
- Treatment includes securing the airway, mechanical ventilation, volume infusion, and pressor support.
- The patient should receive sedation once ventilation is instituted and the hemodynamics stabilize.
- The effects of total spinal anesthesia usually resolve by the conclusion of the surgical procedure, and, unless otherwise contraindicated, the patient can be extubated.
What are the clinical features of a postdural puncture headache and the treatment?
A potentially severe headache may develop after dural puncture, presumably secondary to the rent in the dura and resultant CSF leak, which may cause traction on the meninges and cranial nerves.
The headache typically occurs soon after the puncture. It is characteristically intense, often localized to the occipital region and neck, and worse in the upright position. Diplopia or blurred vision may occur.
Newer pencil-point needles have reduced the incidence of PDPH to about 1%.
Women, younger patients, parturients, and obese patients tend to have a higher incidence of PDPH.
Hydration, analgesics, and caffeine mostly temporize the headache; epidural blood patching (administration of about 20 ml) has >75% success rate.
It is important to rule out severe hypertension or central nervous system maladies as a cause of the symptoms before assuming that the patient has a PDPH.
What is the risk of neurologic injury after spinal anesthesia?
Direct trauma to nerve fibers may occur from the spinal needle and may be heralded by a paresthesia, for which the spinal needle should be redirected.
Hematoma formation from epidural venous bleeding (from direct trauma or coagulopathy) or abscess formation is suggested by persistent neurologic deficits or severe back pain.
Early recognition and management are imperative to avoid permanent neurologic sequelae.
In patients who have received any medication with anticoagulant potential, it is important not to attribute persistent neurologic deficits to residual effects of local anesthesia.
Adhesive arachnoiditis has been reported and is presumably caused by injection of an irritant into the subarachnoid space.
What are contraindications to spinal anesthesia?
Absolute contraindications include local infection at the puncture site,
bacteremia, severe hypovolemia,
coagulopathy,
severe stenotic valvular disease,
infection at the site of the procedure,
and intracranial hypertension.
Relative contraindications include progressive degenerative (demyelinating) neurologic disease (e.g., multiple sclerosis), low back pain, and sepsis.
Where is the epidural space? Describe the relevant anatomy.
The epidural space lies just outside the dural sac containing the spinal cord and cerebrospinal fluid (CSF).
As the epidural needle enters the midline of the back over the bony spinous processes, it passes through:
n Skin n Subcutaneous fat n Supraspinous ligament n Interspinous ligament n Ligamentum flavum n Epidural space
Beyond the epidural space lie the spinal meninges and CSF.
The epidural space has its widest point (5 mm) at L2.
In addition to the traversing nerve roots, it contains fat, lymphatics, and an extensive venous plexus.
Superiorly the space extends to the foramen magnum, where dura is fused to the base of the skull.
Caudally it ends at the sacral hiatus.
The epidural space can be entered in the cervical, thoracic, lumbar, or sacral regions to provide anesthesia.
In pediatric patients the caudal epidural approach is commonly used (see Question 3).
Differentiate between a spinal and an epidural anesthetic.
When performing a spinal anesthetic, a small amount of local anesthetic drug is placed directly in the CSF, producing rapid, dense, predictable neural blockade.
An epidural anesthetic requires a tenfold increase in dose of local anesthetic to fill the epidural space and penetrate the nerve coverings, and onset is slower.
The anesthesia produced tends to be segmental (i.e., a band of anesthesia is produced, extending upward and downward from the injection site).
The degree of segmental spread depends largely on the volume of local anesthetic.
For example, a 5-ml volume may produce only a narrow band of anesthesia covering three to five dermatomes, whereas a 20-ml volume may produce anesthesia from the upper thoracic to sacral dermatomes.
Placement of an epidural anesthetic requires a larger needle, often includes a continuous catheter technique, and has a subtle end point for locating the space.
The epidural space is located by following the feel of the ligaments as they are passed through until there is loss of resistance, whereas the subarachnoid space is definitively identified by CSF flow from the needle.
How is caudal anesthesia related to epidural anesthesia? When is it used?
Caudal anesthesia is a form of epidural anesthesia in which the injection is made at the sacral hiatus (S5).
Because the dural sac normally ends at S2, accidental spinal injection is rare.
Although the caudal approach to the epidural space provides dense sacral and lower lumbar levels of block, its use is limited by major problems:
n Highly variable sacral anatomy in adults
n Risk of injection into a venous plexus
n Difficulty in maintaining sterility if a catheter is used Caudal anesthesia is primarily used in children (whose anatomy is predictable) to provide postoperative analgesia after herniorrhaphy or perineal procedures.
A catheter can be inserted for long-term use if desired.
What are the advantages of using epidural anesthesia vs. general anesthesia?
n Avoidance of airway manipulation; useful for asthmatics, known difficult airways, and patients with a full stomach
n Decreased stress response; less hypertension and tachycardia and cortisol release
n Less thrombogenesis and subsequent thromboembolism; a proven benefit in orthopedic hip surgery
n Improved bowel motility with less distention; sympathetic blockade provides relatively more parasympathetic tone
n The patient can be awake during the procedure; desirable for cesarean deliveries and certain arthroscopic procedures
n Less postoperative nausea and sedation
n Better postoperative pain control, especially for thoracic, upper abdominal, and orthopedic procedures
n Less pulmonary dysfunction, caused by both better pain control and absence of airway manipulation
n Faster turnover at the end of the case because there is no emergence time
What are the disadvantages of epidural compared with general anesthesia?
n Initiation is slower at the beginning of the case.
n It is less reliable, with higher failure rate.
n There are occasional contraindications, including coagulopathy, hemodynamic instability, spinal instrumentation, or patient refusal.
What are the advantages of epidural anesthesia over spinal anesthesia?
n Epidural anesthesia can produce a segmental block focused only on the area of surgery or pain (e.g., during labor or for thoracic procedures).
n The gradual onset of sympathetic block allows time to manage associated hypotension.
n Duration of anesthesia can be prolonged by redosing through an indwelling epidural catheter.
n There is more flexibility in the density of block; if less motor block is desired (for labor analgesia or postoperative pain management), a lower concentration of local anesthetic can be used.
n Theoretically with no hole in the dura there can be no spinal headache;
however, an inadvertent dural puncture occurs 0.5% to 4% of the time with the large-bore epidural needle, and about 50% of such patients require treatment for headache.
Because newer technology in spinal needles has decreased the incidence of headache requiring treatment to less than 1%, this advantage is probably no longer true.