A small number of patients have reported confusion and visual hallucinations while taking Benzonatate with their other prescribed drugs. Benzonatate should not be used in patients with allergies to Novocaine or tetracaine, because those are included in the capsule. If you are pregnant, breastfeeding, or have surgery coming up, your healthcare provider may look into an alternate option to help control your cough. In addition to benzonatate, the most common prescription antitussives include:.
Over-the-counter cough suppressants are also available, including:. Benzonatate comes in liquid-filled capsules and can be taken up to three times per day. The capsules should always be swallowed whole and never crushed, chewed, or dissolved. If you do this, you will lose feeling in your mouth and throat, and it may cause you to choke or have a severe allergic reaction. According to the manufacturer, dosing should be as follows. Your healthcare provider will most likely start you at a dose of a milligram mg capsule up to three times per day as needed for a cough.
Your practitioner may increase your dose to a mg capsule up to three times per day as needed, for a total of mg per day. All listed dosages are according to the drug manufacturer.
Check your prescription and talk to your healthcare provider to make sure you are taking the right dose for you. Because benzonatate capsules contain Novocaine, they should never be cut open or chewed. Novocaine is the numbing agent you have probably had at the dentist. It can quickly numb your mouth, and this could put you at risk for choking or trouble breathing.
Benzonatate can be taken with food or on an empty stomach. If you miss a dose, skip the missed dose and wait until your next scheduled time. Never double up on dosages. The capsules should be kept in a cool, dry room, avoiding humid rooms like the bathroom. Benzonatate can be deadly in children under 10 years old, so it is critical that you keep the prescription bottle sealed and on a high shelf out of their reach.
Keep the bottle out of sight, as children may be curious about the liquid-filled capsules. The best way to dispose of extra medication once you no longer need it is with a prescription take-back program at your local pharmacy or health department.
Avoid placing unused capsules in the garbage or flushing them down the toilet. Most side effects of Benzonatate are mild and uncommon. This drug may make you drowsy or dizzy.
Dextromethorphan is a dissociative agent, similar to ketamine and phencyclidine. Dextromethorphan contains an alkylated amine adjacent to a cyclohexane ring; a structural moiety common to the dissociative agents.
Dextromethorphan reaches maximum serum concentrations in 2. Dextromethorphan is metabolized by cytochrome CYP2D6.
In humans, CYP2D6 is a genetically polymorphic enzyme responsible for metabolizing numerous substances. Dextromethorphan undergoes 3-demethylation to dextrorphan and, to a lesser extent, N-demethylation to 3-methoxymorphinan. Dextrorphan is the active metabolite that produces neurobehavioral effects, while dextromethorphan does not exhibit the same actions. Dextromethorphan is therefore a prodrug, and the metabolic conversion of dextromethorphan to dextrorphan is an important determinant of the abuse potential of dextromethorphan in an individual.
Experienced dextromethorphan users describe tachyphylaxis to the drug, but whether this effect is from alterations in cytochrome function or other effects is not known. Dissociative agents also demonstrate adrenergic effects including hypertension, tachycardia, and diaphoresis by inhibiting peripheral and central catecholamine uptake. Most involve some type of cough syrup containing the opiate agonist codeine and promethazine hydrochloride, an antihistamine with sedative properties.
The cough syrup is typically mixed with a soft drink and candy, with some variants including alcohol. Codeine, or 3-methylmorphine, is a natural isomer of methylated morphine. It is a phenanthrenic alkaloid with three fused benzene rings at its backbone. Although codeine can be extracted from natural sources, a semi-synthetic process via methylation of morphine is the primary source of codeine for pharmaceutical use.
Onset of action occurs 30—45 minutes after administration, when given orally. Renal excretion accounts for the major elimination pathway, and the plasma half-life is 3 hours. Metabolism of codeine follows three major pathways: conjugation to codeineglucuronide, N-demethylation to norcodeine, and O-demethylation to morphine Figure 1.
Codeine, similar to dextromethorphan, is a prodrug and inactive opioid agonist, requiring metabolic activation by O-demethylation to morphine by CYP2D6. This typically represents a minor metabolite pathway for codeine metabolism. N-demethylation into norcodeine by CYP3A4 and glucuronidation are more prevalent but produce inactive metabolites.
Rarely, ultra-rapid CYP2D6 metabolizers produce an unexpectedly large amount of morphine, with resulting life-threatening opioid toxicity. Promethazine hydrochloride is a phenothiazine derivative that acts primarily as a histamine H1 receptor antagonist, with moderate muscarinic dopamine D2 -receptor-blocking effects Figure 2.
It is used in cough syrups for its antihistaminic, antiemetic, and sedative effects. Clinical effects are apparent within 20 minutes after oral, rectal, or intramuscular administration, and the effects last 4—6 hours.
Volume of distribution is found to be Promethazine undergoes extensive hepatic metabolism to a variety of metabolites. The sulfoxides of promethazine and N-demethylpro-methazine are the predominant metabolites and are excreted in the urine. Negligible amounts of unchanged drug are recovered in the urine.
The plasma half-life is approximately 7—14 hours. Pretreatment with selective, potent CYP2D6 inhibitors like quinidine can produce a duration-dependent inhibition of O-demethylation of codeine and a decrease in the positive subjective effects of codeine. The dose of ingested dextromethorphan determines the neurobehavioral outcome.
The second plateau is described as similar to a combination of concurrent ethanol and marijuana intoxication, although some users describe hallucinations as occurring at this stage. The second plateau may be achieved with between and mg, while the third plateau can be achieved with between and mg of the drug.
An ingested dose of —1, mg dextromethorphan may produce a full-blown dissociative state. The clinical presentation of dextromethorphan intoxication therefore depends on the ingested dose. Minimally intoxicated persons may develop tachycardia, hypertension, vomiting, mydriasis, diaphoresis, nystagmus, euphoria, loss of motor coordination, and giggling or laughing.
Experienced dextromethorphan users describe a rapidly developing and persistent tolerance to the drug. Toxicity in the setting of dextromethorphan abuse can arise from additional sources. OTC cough formulations frequently contain, in addition to dextromethorphan, other pharmaceutical agents such as chlorpheniramine, acetaminophen, or pseudoephedrine.
Consequently, individuals who have abused chlorpheniramine-containing dextromethorphan formulations may also exhibit anticholinergic signs and symptoms eg, tachycardia; warm, dry, flushed skin; dry mucosa; mydriasis; agitated delirium; urinary retention; and gastrointestinal dysmotility. Severe chlorpheniramine intoxication has also been associated with seizure activity, rhabdomyolysis, and hyperthermia. In contrast, overdose of acetaminophen, an antipyretic and analgesic that is a component of over cough and cold preparations, produces delayed hepatic injury and, potentially, death.
Lastly, because dextromethorphan is produced as the crystalline hydrobromide salt, bromism is a rare consequence that has been identified in heavy chronic abusers of dextromethorphan. Drug interactions exist between dextromethorphan and other substances, the best characterized of which is serotonin syndrome. This condition typically occurs from the interaction between dextromethorphan and selective serotonin reuptake inhibitors or monoamine oxidase inhibitors, but concurrent administration of antibiotics eg, linezolide , opiate analgesics eg, meperidine and tramadol , or drugs of abuse eg, Syrian rue could precipitate the condition.
It is difficult to determine what constitutes a standard toxic or lethal dose of codeine. However, the lethal oral dose of codeine in an average adult is reported to be in the range of —1, mg. It is also difficult to predict the total amount of codeine or promethazine consumed by addicts on a daily basis to produce euphoric effects.
Mattoo et al noted that the average level of use by addicts in northern India was clearly much beyond the therapeutic daily dose of 15—30 mL all 46 treatment-seeking patients consumed 60 mL or more per day, and in half of them the daily quantity ranged between and mL.
The triad of coma, pinpoint pupils, and respiratory depression is strongly suggestive of opiate poisoning. In severe overdosage, particularly by the intravenous route, apnea, circulatory collapse, cardiac arrest, and death may occur. Seizure activity may be related to hypoxia. Promethazine may add to the depressant effects of codeine. Signs and symptoms of overdosage with promethazine HCl range from mild depression of the central nervous system and cardiovascular system to profound hypotension, respiratory depression, unconsciousness, and sudden death.
The anti-cholinergic toxidrome with hyperthermia, flushing, tachycardia, altered mental status, agitated delirium, dry mucosa, mydriasis, urinary retention, and gastrointestinal dysmotility may be seen. Other reported reactions include hyper-reflexia, hypertonia, ataxia, athetosis, and extensor-plantar reflexes Babinski reflex.
Convulsions may rarely occur. Taken in overdose, benzonatate can rapidly cause seizures, cardiac arrhythmias and death. In one well-documented case report, a year-old girl who intentionally took 10 or more mg capsules developed seizures, cardiac arrest from which she was resuscitated, and then blindness, which persisted. FDA Drug Safety Communication: Death resulting from overdose after accidental ingestion of Tessalon benzonatate by children under 10 years of age.
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