Revised Regional Anesthesia Manual—upper extremity blocks



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Revised Regional Anesthesia Manual—upper extremity blocks



Introduction
Peripheral nerve blocks are gaining widespread popularity for perioperative pain management

because of their specific advantages over general anesthesia and central neuraxial anesthesia.



  1. Pain relief with PNB avoids side effects such as somnolence, nausea and vomiting, hemodynamic instability and voiding difficulty inherent to general and central neuraxial anesthesia.

  2. Patients who undergo surgery under PNB can bypass phase I recovery room and frequently be discharged expeditiously following ambulatory surgery.

  3. Patients with unstable cardiovascular disease can undergo surgery under PNB without significant hemodynamic changes.

  4. Patients who have abnormalities in hemostasis or infection which contraindicate use of central neuraxial block can be candidates for surgery under PNB.

  5. A substantial savings in operating room turnover time can occur if PNB is done outside the operating room. If the patient has a functioning block preoperatively there is no induction or emergence time. Patients with a PNB can frequently position themselves.

  6. When used as part of a combined general regional technique, PNB facilitates lighter planes of anesthesia, avoiding the use of opioids and allowing a quick emergence and recovery.

In order to carry out a regional block safely and effectively, the anesthesiologist must be proficient in the following:



Anatomy


Have knowledge of the neural elements to be blocked, their relationship to muscular, vascular and other anatomic structures and their ultimate motor and sensory innervation. Knowledge of the innervation will provide guidance to select the most suitable technique for a particular surgical procedure. The bony, vascular, muscular and fascial relationships will serve as landmarks to guide the needle to the appropriate site, thus improving the success of the block and minimizing side effects and complications.

Pharmacology


Knowledge of local anesthetic pharmacology will assist in the selection of the most appropriate local anesthetic drug and dosage. The anesthesiologist must also be familiar with the clinical pharmacokinetics i.e. pattern of onset of and recovery of the nerve block. This allows an assessment of the clinical efficacy of the block with respect to operative anesthesia and approximate duration of postoperative analgesia after a particular local anesthetic drug has been injected.

Complications and side effects


Knowledge of the possible complications and the errors in the technique will help in preventing the complication and also in managing them effectively in case they do occur. Knowledge of the possible side effect which could occur from blockade of the other neural elements in the vicinity such as phrenic nerve, recurrent laryngeal nerve and the sympathetic nerves will help in patient education as well as in assessing the contraindication to the technique.

Local anesthetics: Clinical pharmacology, drug selection and toxicity

To select an appropriate local anesthetic drug for a specific clinical situation, one should be familiar with the clinical pharmacology of the local anesthetic drugs and adjuvants.


Local anesthetics exert their effect either by inhibiting the excitatory process in the nerve endings or in the nerve fibers. The following sequence of events is generally accepted as the mechanism of action of local anesthetic agents:


  1. Binding of the local anesthetic moiety to the receptor sites in the nerve membrane.

  2. Reduction in sodium permeability

  3. Decrease in the rate of depolarization

  4. Failure to achieve threshold potential

  5. Lack of development of propagated action potential

  6. Conduction blockade

The pharmacological activity of local anesthetic agents is influenced by their chemical structure, lipid solubility, protein binding, pKa.


Chemical Structure

Based on their chemical structure local anesthetics can be grouped into:




  1. Aminoesters – Procaine, cocaine, tetracaine, choroprocaine. Aminoesters have an ester linkage between the benzene ring and the intermediate chain. These are hydrolyzed in the plasma by pseudocholinesterase. One of the primary metabolites of ester compounds is paraminobenzoic acid. Paba has known allergic potential.

  2. Aminoamides – Lidocaine, mepivacaine, bupivacaine, ropivacaine. Aminoamides have an amide link between the benzene ring and intermediate chain. These are degraded in the liver by microsomal enzymes. The amide drugs are not metabolized to paraaminobenzoic acid and rarely produce allergic reactions. Multidose vials of amide local anesthetic may contain methylparaben (MPF should always be used for regional anesthesia) which is a paraaminobenzoic acid derivative with allergic potential.



Lipid Solubility
Lipid solubility is the primary determinant of intrinsic anesthetic potency. Potency increases as a function of lipid solubility until a blood/lipid partition coefficient of 4 is reached. Further increases in lipid solubility do not cause a further increase in the local anesthetic potency. Based on the lipid solubility and potency, local anesthetic drugs can be divided into 3 groups:


  1. Low lipid solubility/potency: Lipid partition coefficient < 1. These drugs must be administered in high concentrations (2 to 3 %) to achieve effective neural blockade. Local anesthetic drugs in this category include procaine and chloroprocaine.




  1. Intermediate lipid solubility/potency: Lipid partition coefficient 1-3. These drugs may be in concentrations of 1 to 2%. Local anesthetic drugs in this category include lidocaine, mepivacaine, and prilocaine.




  1. High lipid solubility/potency: Lipid partition coefficient >4. These drugs are clinically effective at low concentrations <1%. Local anesthetic drugs in this category include tetracaine, bupivacaine, and ropivacaine.



Protein Binding
Addition of larger chemical radicals to the amine or aromatic end of a local anesthetic compound increases its binding to protein, which is a determinant of local anesthetic duration. Protein binding of commonly used local anesthetics is:
Bupivacaine-------------------------95%

Tetracaine---------------------------95%

Ropivacaine-------------------------94%

Mepivacaine------------------------74%

Lidocaine----------------------------65%

Procaine-------------------------------6%




PKa
Pka is the pH at which ionized and unionized fractions of a substance are present in an equal amount. The onset of local anesthetic effect will be determined by the total amount of unionized fraction of the local anesthetic agent because the unionized fraction primarily diffuses across the nerve membrane. The percentage of local anesthetic, which is present in the unionized form (cation or base) when injected into the tissue at (pH 7.4) is inversely proportional to the pKa of the agent. As the pH of the local anesthetic solution goes down, the unionized fraction will decrease when the pH increases the unionized fraction increases. There is a correlation between the onset of the block and the pKa of local anesthetic drug. The drugs with pKa of 7.6-7.8 ( lidocaine, mepivacaine, prilocaine) have a more rapid onset of action than do bupivacaine and tetracaine which have a pKa of 8.1 and 8.6 respectively. At the body pH (7.4), 35 % of lidocaine exists in unionized base form and only 5 % of bupivacaine exists in unionized base form.
Adjuvant Drugs
These drugs can reduce the onset time, prolong the duration, increase the density and reduce dosages of the commonly used local anesthetics.
Epinephrine- Prolongs duration by vasoconstriction and slowed absorption. Duration can be increased by 30-50%. Peak plasma concentrations can also be reduced by 50%. Can also be a marker for intravascular injection—tachycardia.
Clonidine- Prolongs duration of local anesthetics by synergistic alpha-2 effects. Lesser or no prolongation with Bupivacaine and Ropicacaine but can prolong Mepivacaine-Lidocaine by 40-400% with 100 micrograms. Larger doses are not additive and cause more side effects.


Upper Extremity Blocks
The plexus of nerves innervating the upper extremity is contained in a fascial sheath, which is surrounded by reliable anatomic landmarks. This allows an injection of local anesthetic to reliably block the sensory and motor innervation to the upper extremity with two exceptions—


  1. Areas of the upper extremity with cervical plexus innervation. The sensation of the skin overlying the shoulder is supplied by the nerve roots C3 and C4 of the cervical plexus. These nerve roots lie superior to the most cephalad aspect of the brachial plexus. Interscalene blocks done with large volume of local anesthetic (35-40ml) may block these nerve roots as well in the vast majority of cases. The surgical procedures where C3 and C4 blocks are beneficial usually involve the clavicle.

  2. Area of the upper extremity with intercosto-brachial (T2) innervation. The sensory innervation of the axilla and anterior shoulder is T2, which is also derived from outside the brachial plexus. A T2 block is required for shoulder surgery with anterior incisions (anterior stabilization for shoulder dislocation) and surgery involving the elbow and upper arm.



Innervation of the upper extremity
For convenience the branches of the brachial plexus which innervate the upper extremity can be divided into supraclavicular (branches from roots and trunks) and infraclavicular branches from the divisions, cords

and nerves.



All the supraclavicular branches are motor with the exception of the suprascapular nerve, which provides sensation to the shoulder joint. Suprascapular branches supply the scalene muscles, serratus anterior via the long thoracic nerve, muscles of the upper back and contribute to the phrenic nerve.


The infraclavicular branches comprise all of the sensory and motor innervations to the upper extremity and are important to the anesthesiologist both from the point of view of technique (distribution of parasthesia, motor response if nerve stimulator is being used to locate the plexus) and extent of the block and identification of missed nerves.



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