Nerve+Stimulators+and+Residual+Neuromuscular+Blockade

=**Peripheral Nerve Stimulation**= toc

**Indications**

 * Given the variation in patient sensitivity to neuromuscular blcoking agents, the neuromuscular function of all patients receiving intermediate- or long-acting neuromuscular blocking agents should be monitored.
 * In addition, peripheral nerve stimulation is helpful in assessing paralysis during RSIs or during continuous infusions of short-acting agents.
 * Also, peripheral nerve stimulators can help locate nerves to be blocked by regional anesthesia

**Contraindications**

 * None - although some sites may be precluded by the surgical procedure

**Techniques and Complications**

 * A peripheral nerve stimulator delivers a current of variable frequency and amplitude to a pair of either ECG silver chloride pads or subcutaneous needles placed over a peripheral motor nerve. The evoked mechanical or electrical response of the innervated muscle is observed.
 * Ulnar nerve stimulation of the adductor pollicis muscle and facial nerve stimuli of the orbicularis oculi are most commonly monitored.


 * To deliver a supramaximal stimulation to the underlying nerve, peripheral nerve stimulators must be capable of generating at least a 50-mA current across a 1000-ohm load.This current is uncomfortable/painful for a conscious patient.
 * Complications of nerve stimulation are limited to skin irritation and abrasion at the site of the electrode attachment.

**Clinical Considerations**

 * The degree of neuromuscular blockade is monitored by applying various patterns of electrical stimulation.


 * All stimuli are 0.2ms in duration, of square-wave pattern, and of equal current intensity. A twitch is a single pulse that is delivered from every 1 to every 10 s (1-0.1 Hz). Increasing block results in decreased evoked response to stimulation.
 * **Train-of-four stimulation** - denotes 4 successive 0.2ms stimuli in 2 sec (2Hz). The twitches in a TOF pattern progressively fade as relaxation increases. The ratio of the responses to the first and fourth twitches is a sensitive indicator of nondepolarizing muscle paralysis. It is however more convenient to visually observe the sequential disappearance of the twitches. Disappearance of the fourth twitch represents a 75% block, the third twitch an 80% block, and the second twitch a 90% block. Clinical relaxation usually requires 75-95% neuromusular blockade.
 * **Tetany** - at 50Hz or 100 Hz is a sensitive test of neuromuscular function. Sustained contraction for 5 s indicates adequate - but not necessarily complete - reversal from neuromuscular blockade.
 * **Double-burst stimulation (DBS)** - consists of 3 short (0.2ms) high frequency bursts separated by 20-ms intervals (50Hz) followed 750ms later by either another 3 or 2 bursts. DBS is more sensitive than TOF for the clinical evaluation of fade.
 * **Posttetantic potentiation** - The ability of tetanic stimulation during a partial nondepolarizing block to increase the evoked response to a subsequent twitch. This phenomenon may relate to a transient increase in Ach mobilization following tetanic stimulation.
 * In contrast, a phase I depolarization block does not exhibit fade during tetanus or TOF, neither does it demonstrate posttetanic potentiation. If enough depolarizer is administered, however, the quality of the block changes to resemble a nondepolarizing block (phase II block).
 * [[image:http://bentollenaar.com/_MM_Book/Ch.9_files/image026.gif width="560" height="520" caption="ttp://bentollenaar.com/_MM_Book/Ch.9_files/image026.gif" link="http://bentollenaar.com/_MM_Book/Ch.9_files/image026.gif"]]
 * The diaphragm, rectus abdominus, laryngeal adductors, and orbicularis oculi muscles recover from neuromuscular blockade sooner than the adductor pollicis.
 * Other indicators of adequate recovery include sustained (>/= 5s) head lift, the ability to generate an inspiratory pressure of at least -25cm H2O, and a forceful hand grip.

=**Residual Neuromuscular Blockade**=

**Depolarizing Muscle Relaxant**

 * **Succinylcholine -**The duration of action is prolonged by high doses or by abnormal metabolism. The later may be due to hypothermia (decreases rate of hydrolysis), low pseudocholinesterase levels (seen in pregnancy, liver disease, renal failure, various drugs), or a genetically aberrant enzyme (heterozygous atypical in 1/50 patients - prolongs block 20-30min, homozygous atypical in 1/3000 patients will have long block 4-8 hours).
 * **Dibucaine number -** The percentage of inhibition of pseudocholinesterase activity. Normal is 80%, Heterozygous atypical is 40-60%, and homozygous atypical is 20%
 * Prolonged paralysis from succinylcholine cause by abnormal pseudocholinesterase (atypical cholinesterase) should be treated with continued mechanical ventilation until muscle function returns to normal

**Nondepolarizing Muscle Relaxants -**

 * Various factors can affects duration
 * **Temperature -** Hypothermia prolongs blockade by decreasing metabolism (eg. mivacurium, atracurium, and cisatracurium), and delaying excretion (eg. pancuronium and vecuronium)
 * **Acid-Base Balance -** Respiratory acidosis potentiates the blockade of most and antagonizes its reversal.
 * **Electrolyte Abnormalities -** Hypokalemia and hypocalcemia augment a nondepolarizing block. Hypermagnesemia, as seen in treated preeclamptic patients, potentiates a nondepolarizing block by competing with Ca at the motor end-plate.
 * **Age -** Neonates have an increased sensitivity to nondepolarizing relaxants because of their immature neuromuscular junctions.
 * **Drug Interactions -**
 * **Drug** || **Effect of Depolarizing Blockade** || **Effect of Nondepolarizing Blockade** || **Comments** ||
 * **Antibiotics** || + || + || Streptomycin, aminoglycosides, kanamycin, neomycin, colistin, polymyxin, tetracycline, lincomycin, clindamycin ||
 * **Anticonvulsants** || ? || -- || Phenytoin, carbamazepine, primidone, sodium valproate ||
 * **Antiarrhythmics** || + || + || Quinidine, CCB ||
 * **Cholinesterase Inhibitors** || + || -- || Neostigmine, Pyridostigmine ||
 * **Dantrolene** || ? || + ||  ||
 * **Inhalational anesthetics** || + || + || Volatile anesthetics ||
 * **Ketamine** || ? || + ||  ||
 * **Local anesthetics** || + || + || High doses only ||
 * **Lithium carbonate** || + || ? || Prolongs onset and duration of succinylcholine ||
 * **Magnesium sulfate** || + || + || Doses to treat preclampsia and ecclampsia of pregnancy ||
 * **Concurrent Disease**
 * **Disease** || **Response to Depolarizers** || **Response to Nondepolarizers** ||
 * **ALS (Amyotrophic lateral sclerosis)** || Contracture || Hypersentivity ||
 * **Autoimmune disorders (SLE, polymyositis, dermatomyosistis)** || Hypersentivity || Hypersentivity ||
 * **Burn Injury** || Hyperkalemia || Resistance ||
 * **Cerebral Palsy** || Slight hypersensitivity || Resistance ||
 * **Familial periodic paralysis (hyperkalemic)** || Myotonia and hyperkalemia || ?Hypersensitivity ||
 * **Guillain-Barre syndrome** || Hyperkalemia || Hypersensitivty ||
 * **Hemiplegia** || Hyperkalemia || Resistance on affected side ||
 * **Muscular denervation (Peripheral n injury)** || Hyperkalemia and contracture || Normal response or resistance ||
 * **Muscular dystrophy (Duchenne type)** || Hyperkalemia and malignant hyperthermia || Hypersensitivity ||
 * **Myasthenia Gravis** || Resistance and proneness to phase II block || Hypersensitivity ||
 * **Myasthenia syndrome** || Hypersensitivity || Hypersensitivity ||
 * **Myotonia (dystrophica, congenita, paramyotonia)** || Generalized muscular contractions || Normal or hypersensivity ||
 * **Severe chronic infection (tetanus, botulism)** || Hyperkalemia || Resistance ||

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