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Like any other dislocation acute dislocations of the glenohumeral  or shoulder joint should be reduced as quickly and gently as possible. There are many advantages of early reduction of shoulder dislocation.

* Eliminates the stretch and compression of neurovascular structures
* Reduces amount of muscle spasm that must be overcome to effect reduction
* Prevents further insult to  humeral head  and glenoid labrum

If patient reports within short time, some dislocations can be reduced without medication especially in thinly built patients. Reduction is difficult without medications if patient is very muscular , dislocation is of a long standing duration, the dislocation is locked in soft tissue.

In such cases, it is wise to use general anaesthesia .

Narcotics and muscle relaxants can be used to aid in the reduction of shoulder dislocations if appropriate.  However there is a danger of  respiratory depression after pain is relieved after reduction of the dislocated shoulder. EIther one should opt for GA or appropriate resuscitation measures should be kept ready before hand.

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Sedation is the most commonly reported adverse effect of muscle relaxant medications. These drugs should be used with caution in patients driving motor vehicles or operating heavy machinery. More absolute contraindications do exist to the use of carisoprodol, cyclobenzaprine, and diazepam. Rare idiosyncratic reactions have also been reported to carisoprodol and its metabolites such as meprobamate. Benzodiazepines have potential for abuse and their use should be avoided. By initially prescribing muscle relaxants at bedtime, the physician might take advantage of their sedative effects and minimize daytime drowsiness.

These agents have been found to be effective when used either alone or in combination with an analgesic/anti-inflammatory agent within seven days of symptom onset. The prescribing physician should monitor patients receiving these medications and tailor dosages in an attempt to minimize the drowsiness and sedation often associated with their use. The use of benzodiazepines does not appear to offer any significant benefit to patients experiencing acute low back pain. Further research is needed before the role of baclofen and dantrolene sodium in the treatment of muscle spasm of local origin can be more clearly defined.

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DESCRIPTION

SOMA (carisoprodol) Tablets are available as 250 mg and 350 mg round, white tablets. Carisoprodol is a white, crystalline powder, having a mild, characteristic odor and a bitter taste. It is slightly soluble in water; freely soluble in alcohol, in chloroform, and in acetone; and its solubility is practically independent of pH. Carisoprodol is present as a racemic mixture. Chemically, carisoprodol is N-isopropyl-2-methyl-2-propyl-1,3-propanediol dicarbamate and the molecular formula is C12H24N2O4, with a molecular weight of 260.33.

Other ingredients in the SOMA drug product include alginic acid, magnesium stearate, potassium sorbate, starch, and tribasic calcium phosphate.

INDICATIONS AND USAGE

SOMA is indicated for the relief of discomfort associated with acute, painful musculoskeletal conditions in adults. SOMA should only be used for short periods (up to two or three weeks) because adequate evidence of effectiveness for more prolonged use has not been established and because acute, painful musculoskeletal conditions are generally of short duration [ see Dosage and Administration.

DOSAGE AND ADMINISTRATION

The recommended dose of SOMA is 250 mg to 350 mg three times a day and at bedtime. The recommended maximum duration of SOMA use is up to two or three weeks.

DOSAGE FORMS AND STRENGTHS

250mg Tablets: round, convex, white tablets, inscribed with SOMA 250
350mg Tablets: round, convex, white tablets, inscribed with SOMA 350

CONTRAINDICATIONS

SOMA is contraindicated in patients with a history of acute intermittent porphyria or a hypersensitivity reaction to a carbamate such as meprobamate.

WARNINGS AND PRECAUTIONS

1. Sedation

SOMA may have sedative properties (in the low back pain trials, 13% to 17% of patients who received SOMA experienced sedation compared to 6% of patients who received placebo) and may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks such as driving a motor vehicle or operating machinery.

Since the sedative effects of SOMA and other CNS depressants (e.g., alcohol, benzodiazepines, opioids, tricyclic antidepressants) may be additive, appropriate caution should be exercised with patients who take more than one of these CNS depressants simultaneously.

2. Drug Dependence, Withdrawal, and Abuse

In the postmarketing experience with SOMA, cases of dependence, withdrawal, and abuse have been reported with prolonged use. Most cases of dependence, withdrawal, and abuse occurred in patients who have had a history of addiction or who used SOMA in combination with other drugs with abuse potential. Withdrawal symptoms have been reported following abrupt cessation after prolonged use. To reduce the chance of SOMA dependence, withdrawal, or abuse, SOMA should be used with caution in addiction-prone patients and in patients taking other CNS depressants including alcohol, and SOMA should not be used more than two to three weeks for the relief of acute musculoskeletal discomfort.

One of the metabolites of SOMA, meprobamate (a controlled substance), may cause dependence.

3. Seizures

There have been postmarketing reports of seizures in patients who received SOMA. Most of these cases have occurred in the setting of multiple drug overdoses (including drugs of abuse, illegal drugs, and alcohol).

ADVERSE REACTIONS

1. Clinical Studies Experience

Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect rates observed in practice.

The data described below are based on 1387 patients pooled from two double blind, randomized, multicenter, placebo controlled, one-week trials in adult patients with acute, mechanical, lower back pain. In these studies, patients were treated with 250 mg of SOMA, 350 mg of SOMA, or placebo three times a day and at bedtime for seven days. The mean age was about 41 years old with 54% females and 46% males and 74 % Caucasian, 16 % Black, 9% Asian, and 2% other.

There were no deaths and there were no serious adverse reactions in these two trials. In these two studies, 2.7%, 2%, and 5.4%, of patients treated with placebo, 250 mg of SOMA, and 350 mg of SOMA, respectively, discontinued due to adverse events; and 0.5%, 0.5%, and 1.8% of patients treated with placebo, 250 mg of SOMA, and 350 mg of SOMA, respectively, discontinued due to central nervous system adverse reactions.

2. Postmarketing Experience

The following events have been reported during postapproval use of SOMA. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.

Cardiovascular: Tachycardia, postural hypotension, and facial flushing.
Central Nervous System: Drowsiness, dizziness, vertigo, ataxia, tremor, agitation, irritability, headache, depressive reactions, syncope, insomnia, and seizures.
Gastrointestinal: Nausea, vomiting, and epigastric discomfort.
Hematologic: Leukopenia, pancytopenia

DRUG INTERACTIONS

1. CNS Depressants

The sedative effects of SOMA and other CNS depressants (e.g., alcohol, benzodiazepines, opioids, tricyclic antidepressants) may be additive. Therefore, caution should be exercised with patients who take more than one of these CNS depressants simultaneously. Concomitant use of SOMA and meprobamate, a metabolite of SOMA, is not recommended.

2. CYP2C19 Inhibitors and Inducers

Carisoprodol is metabolized in the liver by CYP2C19 to form meprobamate. Co-administration of CYP2C19 inhibitors, such as omeprazole or fluvoxamine, with SOMA could result in increased exposure of carisoprodol and decreased exposure of meprobamate. Co-administration of CYP2C19 inducers, such as rifampin or St. John’s Wort, with SOMA could result in decreased exposure of carisoprodol and increased exposure of meprobamate. Low dose aspirin also showed an induction effect on CYP2C19. The full pharmacological impact of these potential alterations of exposures in terms of either efficacy or safety of SOMA is unknown.

USE IN SPECIFIC POPULATIONS

1. Pregnancy

Pregnancy Category C. There are no data on the use of SOMA during human pregnancy. Animal studies indicate that carisoprodol crosses the placenta and results in adverse effects on fetal growth and postnatal survival. The primary metabolite of carisoprodol, meprobamate, is an approved anxiolytic. Retrospective, post-marketing studies do not show a consistent association between maternal use of meprobamate and an increased risk for particular congenital malformations.

Teratogenic effects: Animal studies have not adequately evaluated the teratogenic effects of carisoprodol. There was no increase in the incidence of congenital malformations noted in reproductive studies in rats, rabbits, and mice treated with meprobamate. Retrospective, post-marketing studies of meprobamate during human pregnancy were equivocal for demonstrating an increased risk of congenital malformations following first trimester exposure. Across studies that indicated an increased risk, the types of malformations were inconsistent.

Nonteratogenic effects: In animal studies, carisoprodol reduced fetal weights, postnatal weight gain, and postnatal survival at maternal doses equivalent to 1-1.5 times the human dose (based on a body surface area comparison). Rats exposed to meprobamate in-utero showed behavioral alterations that persisted into adulthood. For children exposed to meprobamate in-utero, one study found no adverse effects on mental or motor development or IQ scores. SOMA should be used during pregnancy only if the potential benefit justifies the risk to the fetus.

2. Labor and Delivery

There is no information about the effects of SOMA on the mother and the fetus during labor and delivery.

3. Nursing Mothers

Very limited data in humans show that SOMA is present in breast milk and may reach concentrations two to four times the maternal plasma concentrations. In one case report, a breast-fed infant received about 4-6% of the maternal daily dose through breast milk and experienced no adverse effects. However, milk production was inadequate and the baby was supplemented with formula. In lactation studies in mice, female pup survival and pup weight at weaning were decreased. This information suggests that maternal use of SOMA may lead to reduced or less effective infant feeding (due to sedation) and/or decreased milk production. Caution should be exercised when SOMA is administered to a nursing woman.

4. Pediatric Use

The efficacy, safety, and pharmacokinetics of SOMA in pediatric patients less than 16 years of age have not been established.

5. Geriatric Use

The efficacy, safety, and pharmacokinetics of SOMA in patients over 65 years old have not been established.

6. Renal Impairment

The safety and pharmacokinetics of SOMA in patients with renal impairment have not been evaluated. Since SOMA is excreted by the kidney, caution should be exercised if SOMA is administered to patients with impaired renal function. Carisoprodol is dialyzable by hemodialysis and peritoneal dialysis.

7. Hepatic Impairment

The safety and pharmacokinetics of SOMA in patients with hepatic impairment have not been evaluated. Since SOMA is metabolized in the liver, caution should be exercised if SOMA is administered to patients with impaired hepatic function.

8. Patients with Reduced CYP2C19 Activity

Patients with reduced CYP2C19 activity have higher exposure to carisoprodol. Therefore, caution should be exercised in administration of SOMA to these patients.

OVERDOSAGE

Overdosage of SOMA commonly produces CNS depression. Death, coma, respiratory depression, hypotension, seizures, delirium, hallucinations, dystonic reactions, nystagmus, blurred vision, mydriasis, euphoria, muscular incoordination, rigidity, and/or headache have been reported with SOMA overdosage. Many of the SOMA overdoses have occurred in the setting of multiple drug overdoses (including drugs of abuse, illegal drugs, and alcohol). The effects of an overdose of SOMA and other CNS depressants (e.g., alcohol, benzodiazepines, opioids, tricyclic antidepressants) can be additive even when one of the drugs has been taken in the recommended dosage. Fatal accidental and non-accidental overdoses of SOMA have been reported alone or in combination with CNS depressants.

Treatment of Overdosage: Basic life support measures should be instituted as dictated by the clinical presentation of the SOMA overdose. Induced emesis is not recommended due to the risk of CNS and respiratory depression, which may increase the risk of aspiration pneumonia. Gastric lavage should be considered soon after ingestion (within one hour). Circulatory support should be administered with volume infusion and vasopressor agents if needed. Seizures should be treated with intravenous benzodiazepines and the reoccurrence of seizures may be treated with phenobarbital. In cases of severe CNS depression, airway protective reflexes may be compromised and tracheal intubation should be considered for airway protection and respiratory support.

The following types of treatment have been used successfully with an overdose of meprobamate, a metabolite of SOMA: activated charcoal (oral or via nasogastric tube), forced diuresis, peritoneal dialysis, and hemodialysis (carisoprodol is also dialyzable). Careful monitoring of urinary output is necessary and overhydration should be avoided. Observe for possible relapse due to incomplete gastric emptying and delayed absorption. For more information on the management of an overdose of SOMA, contact a Poison Control Center.

CLINCIAL PHARMACOLOGY

1. Mechanism of Action

The mechanism of action of carisoprodol in relieving discomfort associated with acute painful musculoskeletal conditions has not been clearly identified.

In animal studies, muscle relaxation induced by carisoprodol is associated with altered interneuronal activity in the spinal cord and in the descending reticular formation of the brain.

2. Pharmacodynamics

Carisoprodol is a centrally acting skeletal muscle relaxant that does not directly relax skeletal muscles.

A metabolite of carisoprodol, meprobamate, has anxiolytic and sedative properties. The degree to which these properties of meprobamate contribute to the safety and efficacy of SOMA is unknown.

3. Pharmacokinetics

The pharmacokinetics of carisoprodol and its metabolite meprobamate were studied in a crossover study of 24 healthy subjects (12 male and 12 female) who received single doses of 250 mg and 350 mg SOMA. The exposure of carisoprodol and meprobamate was dose proportional between the 250 mg and 350 mg doses. The Cmax of meprobamate was 2.5 ± 0.5 μg/mL (mean ± SD) after administration of a single 350 mg dose of SOMA, which is approximately 30% of the Cmax of meprobamate (approximately 8 μg/mL) after administration of a single 400 mg dose of meprobamate.

Absorption: Absolute bioavailability of carisoprodol has not been determined. The mean time to peak plasma concentrations (Tmax) of carisoprodol was approximately 1.5 to 2 hours. Co-administration of a high-fat meal with SOMA (350 mg tablet) had no effect on the pharmacokinetics of carisoprodol. Therefore, SOMA may be administered with or without food.

Metabolism: The major pathway of carisoprodol metabolism is via the liver by cytochrome enzyme CYP2C19 to form meprobamate. This enzyme exhibits genetic polymorphism (see Patients with Reduced CYP2C19 Activity below).

Elimination: Carisoprodol is eliminated by both renal and non-renal routes with a terminal elimination half-life of approximately 2 hours. The half-life of meprobamate is approximately 10 hours.

Gender: Exposure of carisoprodol is higher in female than in male subjects (approximately 30-50% on a weight adjusted basis). Overall exposure of meprobamate is comparable between female and male subjects.

Patients with Reduced CYP2C19 Activity: SOMA should be used with caution in patients with reduced CYP2C19 activity. Published studies indicate that patients who are poor CYP2C19 metabolizers have a 4-fold increase in exposure to carisoprodol, and concomitant 50% reduced exposure to meprobamate compared to normal CYP2C19 metabolizers. The prevalence of poor metabolizers in Caucasians and African Americans is approximately 3-5% and in Asians is approximately 15-20%.

NONCLINICAL TOXICOLOGY

1. Carcinogenesis, Mutagenesis, Impairment of Fertility

Long term studies in animals have not been performed to evaluate the carcinogenic potential of carisoprodol.

SOMA was not formally evaluated for genotoxicity. In published studies, carisoprodol was mutagenic in the in vitro mouse lymphoma cell assay in the absence of metabolizing enzymes, but was not mutagenic in the presence of metabolizing enzymes. Carisoprodol was clastogenic in the in vitro chromosomal aberration assay using Chinese hamster ovary cells with or without the presence of metabolizing enzymes. Other types of genotoxic tests resulted in negative findings. Carisoprodol was not mutagenic in the Ames reverse mutation assay using S. typhimurium strains with or without metabolizing enzymes, and was not clastogenic in an in vivo mouse micronucleus assay of circulating blood cells.

SOMA was not formally evaluated for effects on fertility. Published reproductive studies of carisoprodol in mice found no alteration in fertility although an alteration in reproductive cycles characterized by a greater time spent in estrus was observed at a carisoprodol dose of 1200 mg/kg/day. In a 13-week toxicology study that did not determine fertility, mouse testes weight and sperm motility were reduced at a dose of 1200 mg/kg/day. In both studies, the no effect level was 750 mg/kg/day, corresponding to approximately 2.6 times the human equivalent dosage of 350 mg four times a day, based on a body surface area comparison. The significance of these findings for human fertility is not known.

CLINICAL STUDIES

The safety and efficacy of SOMA for the relief of acute, idiopathic mechanical low back pain was evaluated in two, 7-day, double blind, randomized, multicenter, placebo controlled, U.S. trials. Patients had to be 18 to 65 years old and had to have acute back pain (≤ 3 days of duration) to be included in the trials. Patients with chronic back pain; at increased risk for vertebral fracture (e.g., history of osteoporosis); with a history of spinal pathology (e.g., herniated nucleus pulposis, spondylolisthesis or spinal stenosis); with inflammatory back pain, or with evidence of a neurologic deficit were excluded from participation. Concomitant use of analgesics (e.g., acetaminophen, NSAIDs, tramadol, opioid agonists), other muscle relaxants, botulinum toxin, sedatives (e.g., barbiturates, benzodiazepines, promethazine hydrochloride), and anti-epileptic drugs was prohibited.

In Study 1, patients were randomized to one of three treatment groups (i.e., SOMA 250 mg, SOMA 350 mg, or placebo) and in Study 2 patients were randomized to two treatment groups (i.e., SOMA 250 mg or placebo). In both studies, patients received study medication three times a day and at bedtime for seven days.

The primary endpoints were the relief from starting backache and the global impression of change, as reported by patients, on Study Day 3. Both endpoints were scored on a 5-point rating scale from 0 (worst outcome) to 4 (best outcome) in both studies. The primary statistical comparison was between the SOMA 250 mg and placebo groups in both studies.

The proportion of patients who used concomitant acetaminophen, NSAIDs, tramadol, opioid agonists, other muscle relaxants, and benzodiazepines was similar in the treatment groups.

HOW SUPPLIED/STORAGE AND HANDLING

250mg Tablets: round, convex, white tablets, inscribed with SOMA 250; available in bottles of 100 (NDC 0037-2250-10).

350mg Tablets: round, convex, white tablets, inscribed with SOMA 350; available in bottles of 100 (NDC 0037-2001-01).

Storage:
Store at 25° C (77° F); excursions permitted between 15° and 30° C (59° and 86° F) (see USP Controlled Room Temperature).

PATIENT COUNSELING INFORMATION

Patients should be advised to contact their physician if they experience any adverse reactions to SOMA.

1. Sedation

Since SOMA may cause drowsiness and/or dizziness, patients should be advised to assess their individual response to SOMA before engaging in potentially hazardous activities such as driving a motor vehicle or operating machinery.

2. Avoidance of Alcohol and Other CNS Depressants

Patients should be advised to avoid alcoholic beverages while taking SOMA and to check with their doctor before taking other CNS depressants such as benzodiazepines, opioids, tricyclic antidepressants, sedating antihistamines, or other sedatives.

3. SOMA Should Only Be Used for Short-Term Treatment

Patients should be advised that treatment with SOMA should be limited to acute use (up to two or three weeks) for the relief of acute, musculoskeletal discomfort. If symptoms still persist, patients should contact their healthcare provider for further evaluation.

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The muscle relaxing properties of “muscle relaxants” arise not from direct activity at the muscular or neuromuscular junction level but rather from an inhibition of more central polysynaptic neuronal (nerve cells that end in synapses) events. These agents have also been shown in some studies to demonstrate superior analgesia to either acetaminophen or aspirin, and it remains uncertain if muscle spasm is a prerequisite to their effectiveness as analgesics.

Range of Motion
Muscle relaxants are often prescribed in the treatment of acute low back pain in an attempt to improve the initial limitations in range of motion from muscle spasm and to interrupt the pain-spasm-pain cycle. Limiting muscle spasm and improving range of motion will prepare the patient for therapeutic exercise.

Types of Muscle Relaxants
In an attempt to determine the mechanism of action of carisoprodol (Soma®) in the treatment of low back pain, a double blind study was carried out comparing its effectiveness to that of a sedative control, butabarbital (a sedative), and a placebo in the treatment of 48 laborers with acute lumbar pain. Carisoprodol was found to be significantly more effective in providing both subjective pain relief and objective improvements in range of motion when evaluated by finger to floor testing. The results of this study suggest that the effects of carisoprodol are not secondary to its sedative effects alone.

In 1989, Basmajian compared the effectiveness of cyclobenzaprine (Flexeril®) alone with diflunisal (Dolobid®), placebo, and a combination of cyclobenzaprine and diflunisal in the treatment of acute low back pain and spasm. During the ten-day study period, the combined treatment group demonstrated significantly superior improvements in global ratings on day four, but not on day two or seven. This study suggested some effectiveness of combined analgesic and muscle relaxant therapy when utilized early in the initial week of pain onset.

Borenstein compared the effects of combined cyclobenzaprine and naproxen (Naprosyn®) with naproxen alone and also found combination therapy to be superior in reducing tenderness, spasm, and range of motion in patients presenting with ten days or less of low back pain and spasm. Adverse effects, predominantly drowsiness, were noted in 12 of 20 in the combined group and only four of 20 treated with naproxen alone.

Cyclobenzaprine and carisoprodol were compared in the treatment of patients with acute thoracolumbar pain and spasm rated moderate to severe and of no longer than seven days duration. Both drugs were found to be effective, without significant differences between the treatment groups. Significant improvements were noted in physician rated mobility and in patients’ visual analogue scores on follow up days four and eight. While 60% of patients experienced adverse effects in the form of drowsiness or fatigue, these differences were not significantly different between groups, and only eight percent of patients from each group discontinued treatment.

Baratta found cyclobenzaprine, 10-mg t.i.d. (three times per day), superior to placebo in a randomized, double blind study of 120 patients with acute low back pain presenting within five days of symptom onset. Significant improvement was noted in range of motion, tenderness to palpation, and pain scores on follow up days two through nine. Sixty percent of treatment group patients reported drowsiness or dizziness compared with 25% of those in the placebo group.

In an earlier study, diazepam (Valium®) was found to offer no significant subjective or objective benefit, when compared to placebo, in patients treated for low back pain. Carisoprodol was found to be superior to diazepam in the treatment of patients with “at least moderately severe” low back pain and spasm of no longer than seven days duration. In this study, the overall incidence of adverse reactions was higher in the diazepam treated group but was not of statistical significance.

Origin of Muscle Spasm
Muscle spasm of local origin needs to be clinically differentiated from spasticity and sustained muscle contraction in the setting of the central nervous system (CNS) and upper motor neuron injury. Baclofen (Lioresal®) and dantrolene sodium (Dantrium®) are two agents whose use is indicated in the setting of spasticity of CNS etiology. Dantrolene sodium is of particular interest, as its mechanism of action is purely at the muscular level where it serves to inhibit the release of calcium form the sarcoplasmic reticulum.

Casale studied the effectiveness of dantrolene sodium, 25-mg daily, in the treatment of low back pain and found patients to demonstrate significant improvements in visual analogue scores, pain behavior, and electromyographic (EMG) evaluations of “antalgic reflex motor unit firing,” when compared with the placebo group. The findings of this study are interesting in that they demonstrate improvement secondary to a pure muscle relaxant, which does not possess other outside anti-nociceptive properties.

Baclofen is a derivative of gamma-aminobutryic acid (GABA) and is believed to inhibit mono and polysynaptic reflexes at the spinal level. Treatment with baclofen was compared to placebo in a double blind, randomized study of 200 patients with acute low back pain. Patients with initially severe discomfort were found to benefit from baclofen, 30- to 80-mg daily, on days four and ten of follow up. Forty-nine percent of treatment patients complained of sleepiness, 38% of nausea, and 17% discontinued treatment.

Sedation: Side Effect
Sedation is the most commonly reported adverse effect of muscle relaxant medications. These drugs should be used with caution in patients driving motor vehicles or operating heavy machinery. More absolute contraindications do exist to the use of carisoprodol, cyclobenzaprine, and diazepam. Rare idiosyncratic reactions have also been reported to carisoprodol and its metabolites such as meprobamate. Benzodiazepines have potential for abuse and their use should be avoided. By initially prescribing muscle relaxants at bedtime, the physician might take advantage of their sedative effects and minimize daytime drowsiness.

These agents have been found to be effective when used either alone or in combination with an analgesic/anti-inflammatory agent within seven days of symptom onset. The prescribing physician should monitor patients receiving these medications and tailor dosages in an attempt to minimize the drowsiness and sedation often associated with their use. The use of benzodiazepines does not appear to offer any significant benefit to patients experiencing acute low back pain. Further research is needed before the role of baclofen and dantrolene sodium in the treatment of muscle spasm of local origin can be more clearly defined.

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Non-depolarising muscle relaxants are commonly used during anaesthesia to provide relaxation for surgery, to allow mechanical ventilation and they are also regularly used in intensive care. This article describes the mechanisms by which the drugs work and also the differences between specific drugs.

Mechanism of action

Non-depolarising muscle relaxant drugs (NDMRD) compete with acetyl choline (ACh) molecules released at the neuromuscular junction to bind with the ACh receptors on the post synaptic membrane of the motor endplate. They therefore block the action of ACh and prevent depolarisation (or activation) of the muscle contraction process. Muscle groups differ in their sensitivity to muscle relaxants; ocular muscles responsible for opening and moving the eyes are the most sensitive followed by the muscles of the jaw, neck, limbs, intercostals and abdomen. The diaphragm is the least sensitive muscle, which is why patients undergoing surgery sometimes hiccup or breathe as an early sign that the relaxants are wearing off.

Non-depolarising muscle relaxant drugs also act on presynaptic receptors interfering with the entry of calcium which causes an inhibition in the release of ACh. Other drugs such as the aminoglycoside antibiotics (eg gentamicin) and volatile agents may also effect this mechanism and increase sensitivity to relaxants.

A variety of relaxant drugs are in use in different parts of the world. All produce profound muscle paralysis but have varying effects on the autonomic nervous system. None of the drugs cross the blood brain barrier as they are water soluble, polar molecules and therefore have no effect on the central nervous system. All non depolarising drugs should be used with care in patients suspected to be suffering with myasthenia gravis or myasthenic syndrome as patients with these conditions are extremely sensitive to their effects.

General considerations in the use of muscle relaxants

Muscle relaxants are principally used to provide good muscular relaxation for surgery. When they are used respiration must be controlled via an endotracheal tube. A few general guidelines for the use of relaxants are listed below:

1. Always be certain that you will able to ventilate the patient by face mask before paralysing them.

2. If a rapid onset of action is required then suxamethonium should be used as it acts more quickly than any of the non-depolarising drugs. If a short duration of paralysis is required suxamethonium is most suitable and may be given in repeated doses provided atropine is administered prior to the second dose of suxamethonium to avoid bradycardia.

3. Non-depolarising muscle relaxants take about one and a half to two minutes to act and you should allow time for relaxation to develop before attempting intubation.

4. The supplemental dose should be about 25% of the initial dose. Never attempt to reverse the relaxation until at least 15-20 minutes after the last dose of relaxant was given.

5. Never extubate a patient until you are certain that the paralysis has been reversed and they have adequate muscle strength to protect their airway and breathe. One way of testing this is to assess whether they are able to lift their head off the pillow for 5 seconds. Ensure that breathing is of adequate depth and frequency.

6. It takes some time before the larynx is able to protect the airway and so the patient is best placed in the lateral position for recovery.

7. If a nerve stimulator is available it can be used to monitor the degree of relaxation. However it is not essential and relaxants can be safely be used without a nerve stimulator by careful observation of clinical signs.

8. When muscle relxants are administered awareness is always a danger since a paralysed patient cannot move in response to pain. It is therefore essential to ensure that the depth of anaesthesia is adequate.

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