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Year : 2008  |  Volume : 52  |  Issue : 2  |  Page : 132-139 Table of Contents     

Anaesthetic Implications of Substance Abuse in Adolescent

1 Hon. Consultant Anaesthesiologist, Apollo Gleneagles Hospital, Kolkata, India
2 Consultant Paediatrician, Apollo Gleneagles Hospital, Kolkata, India
3 Assistant Professor of Anaesthesiology, Medical College & Hospital, Kolkata, India
4 Consultant Anaesthesiologist, Apollo Gleneagles Hospital, Kolkata, India

Date of Acceptance22-Feb-2008
Date of Web Publication19-Mar-2010

Correspondence Address:
A Rudra
1, Shibnarayan Das Lane, Kolkata - 700006
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Source of Support: None, Conflict of Interest: None

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Despite ongoing preventive and rehabilative efforts at the local and international level, substance abuse by adolescents has crossed social, economic, and geographic borders and - throughout the world remains one of the major problems facing society today. The diverse clinical manifestation of drug abuse combined with physiologic changes may significantly have impact on the anaesthetic management. Moreover, it is always difficult to predict the exact anaesthetic implications in chemically dependent patients. Therefore, a complete understanding of the pathophysiology and anaesthetic implications of drug abuse in adolescent is essential to tailor a safe anaesthetic plan for these high-risk groups of patients.

Keywords: Substance abuse;Adolescent;Anaesthesia;Anaesthetic implication

How to cite this article:
Rudra A, Bhattacharya A, Chatterjee S, Sengupta S, Das T. Anaesthetic Implications of Substance Abuse in Adolescent. Indian J Anaesth 2008;52:132-9

How to cite this URL:
Rudra A, Bhattacharya A, Chatterjee S, Sengupta S, Das T. Anaesthetic Implications of Substance Abuse in Adolescent. Indian J Anaesth [serial online] 2008 [cited 2020 Dec 4];52:132-9. Available from: https://www.ijaweb.org/text.asp?2008/52/2/132/60611

   Introduction Top

Illicit drugs have been of increasing social and medical concern. Abuse of illicit drugs is unfortunately not limited to adults. Although the rates of use of various substances vary from year to year and decade to de­cade, children, adolescents, and young adults continue to use tobacco, alcohol, and other drugs at terrifying high rates. Alcohol continues to be the drug of choice for intoxication, marijuana and hallucinogen use is slightly less than in previous decades; stimulant use continues its popularity in the form of methylenedioxyme­thamphetamine (MDMA; "Ecstasy") and other "club drugs". Smoking rates may go down while smokeless tobacco use goes up; and inhalants continued to go abused, particularly by young adolescents [1] . A survey of school children in Great Britain showed that 15.8% of boys have been offered the drug Ecstacy and that 5.7% have taken it [2] . A survey among school children revealed that, frequently used drugs are marijuana (59%), am­phetamines (19%), cocaine (18%), and LSD (18%) [3] .

Substance abuse has crossed social, economical, and geographic borders, and it remains one of the major problems facing society today. Because, drug abuse may result in increased morbidity and mortality during intra­and postoperative period, therefore, a thorough under­standing of the consequences of drug abuse is essential for practicing anaesthesiologists.

Anaesthesia and postoperative analgesia in patients dependent on psychoactive substances poses special problems. Often these patients suffer from severe medi­cal and psychotic illness. In addition, drug-specific adap­tations such as tolerance, physical dependence, and with­drawal may diminish the effectiveness of anaesthetic and analgesic drugs. Therefore, problems resulting from sub­stance intoxication, or recent ingestion of or exposure to a substance may arise in evaluation of patients for ana­esthesia. When patients present for anaesthesia and sur­gery there is a mandate to detect manifest mental prob­lems, as well as covert substance use patterns that may impact response to anaesthetic agents and the surgical procedures [4] .

   Substance abuse Top

Substance abuse may be defined as self-adminis­tration of drug(s) that deviate(s) from accepted medical or social use which if sustained can lead to physical and psychological dependence [5] .

   Adolescence Top

Between 10 and 20 years of age, children undergo rapid changes in body size, shape, physiology, and psy­chologic and social functioning. Adolescence precedes across three distinct periods -early (10-13 years), middle (14-16 years), late (17-20 years) [6] .

   Alcohol Top

Alcohol use among adolescents has increased dur­ing the past decade and poses a threat to the normal functioning of the teenager as well as to the lives of those potentially jeopardized by drunken drivers. The initiation of alcohol use at an early age is associated with an increased risk for alcohol-related problems. Adoption stud­ies indicate that male children of alcoholic parents are more likely to become alcoholic even when raised by nonalcoholic adoptive parents [5],[7] .

Alcohol is rapidly absorbed in the stomach and is transported to the liver and metabolized and leading to a fatty liver followed by fibrosis, the hallmark of cirrhosis, even in those who are well nourished. Furthermore, chronic alcohol consumption may result in malnutrition, altered drug metabolism, coagulopathy, pancreatitis, and cardiomyopathy. Acute alcohol intoxication increases gastric fluid acidity and volume, with simultaneous de­crease in the ability to protect the airway. If heavy alco­hol ingestion is not associated with food intake, pro­nounced hypoglycaemia may occur.

   Anaesthetic implications Top

Physiologic dependence on alcohol is manifested as a withdrawal syndrome when the drug is abruptly discontinued. Acute withdrawal manifestations include generalized tremor, tachycardia, cardiac arrhythmias, hypertension, nausea, vomiting, and confusion with agi­tation and hallucinations [8] . The withdrawal symptoms may be suppressed by the administration of benzodiazepines, alpha 2 adrenergic agonists. Acute alcohol intoxication may pose a significant risk of pulmonary aspiration.

Regional anaesthesia can be safely administered to adolescent with a history or alcohol abuse. However, regional anaesthesia may be influenced by occasional patients who are treated with disulfiram and in whom polyneuropathy develops. Alcohol-containing solutions, as used for skin cleansing, probably should be avoided in disulfiram - treated patients. Furthermore, acute, unex­plained hypotension could reflect inadequate stores of norepinephrine due to disulfiram-induced inhibition of dopamine â-hydroxylase [9] . Therefore, intravascular fluid volume must be optimized before induction of regional anaesthesia to avoid adverse consequences of sympa­thetic blockade. This hypotension may respond to ephe­drine, but direct - acting sympathomimetics such as phe­nylephrine may produce more predictable responses in the presence of norepinephrine depletion. Neuropathy also should be considered as a medicolegal contraindi­cation to regional anaesthesia.

If general anaesthesia is necessary, associated hepatic dysfunction, hypoalbuminemia, and cardiac fail­ure may require appropriate dose adjustments of intra­venous induction drugs. Chronic use of alcohol is usu­ally associated with resistance to the actions of central nervous system (CNS) depressants. The use of exces­sive concentrations of potent inhaled anaesthetics can lead to cardiovascular depression. The risk of aspiration increase is due to increased gastric fluid volume and acidity, as well as impaired laryngeal reflexes.

   Tobacco Top

   Cigarettes Top

Human and animal studies confirmed that the ef­fect of nicotine, the primary active ingredient in tobacco produces as syndrome of dependence. Nicotine is ab­sorbed by multiple sites in the body, e.g., lungs, skin, gas­trointestinal tract, and buccal and nasal nucosa [6] .

The average smokers start at age 12 years, and most are regular smokers by age to 14 years. Most alarming is the compelling evidence of the addictive na­ture of cigarette smoking with greater than 90% of ado­lescent smokers becoming adult smokers [6] .

Cigarette smoking affects pulmonary function pri­marily. The irritant effect of smoke decreases ciliary motility, increases sputum production, and impairs gas exchange [10] . Smoking is associated with an increase in the rate of development of atherosclerosis. Smokers have an increased prevalence of peripheral vascular disease, coronary artery disease, and an increased risk of acute myocardial infarction.

   Anaesthetic implications Top

In smokers, 4 to 6 weeks of abstinence from to­bacco smoke is required to decrease postoperative res­piratory morbidity to the level of a nonsmoker [9] . How­ever, any period of abstinence is recommended, and as little as a few days can improve mucociliary function[10].In tobacco-abusing patients who undergo as little 48 hours of abstinence, levels of carboxyhaemoglobin may return toward those levels seen in non-smokers. Ciga­rette smoke may affect hepatic enzyme function and alter the metabolism of induction drugs used for general anaesthesia.

Regional anaesthesia seem suitable for tobacco­abusing adolescents. Intraoperative complications, such as bronchospasm, as well as postoperative respiratory dysfunction, can be avoided with the administration of neuraxial anaesthetic technique and avoidance of air­way manipulation.

   Smokeless tobacco Top

Smokeless tobacco, comes in the forms of snuff, quid (khaini), guraku and chewing tobacco. Smokeless tobacco contains more nicotine than smoking tobacco [11] .

In Central, Southern, and South -East Asia, the abuse of smokeless tobacco popularly involves the chew­ing of betal quid or "paan-supari" [12] . The mixture is held adjacent to the buccal mucosa and slowly chewed over a long period of time [13] . The abuse of smokeless tobacco can lead to oral submucosal fibrosis (OSMF). OSMF typically affects the buccal mucosa, lips, retromolar ar­eas, soft palate and occasionally the pharynx and oe­sophagus. Finally, results in progressive inability to open the mouth, pain, burning sensation and dysphagia [14],[15] .Chewing of tobacco result in lesions, primarily in the mandibular mucobuccal fold. With chronic use, these lesions may become malignant.

   Anaesthetic implications Top

Anaesthesiologist should have a high degree of suspicion and carefully examine the airway of patient who abuse betal quid or "paan-supari". Mallampati clas­sification and Cormack's grading should be incorporated with routine preoperative assessments to decide whether these patients would need awake fibreoptic guided intu­bation. It is worthwhile to categorize all these patients as having "anticipated difficult airways". Mahajan et al [16] have reported a case of "unanticipated difficult airway" in a patient with betal quid abuse, suggesting that indi­rect laryngoscopy be included in the routine preopera­tive assessment of these patients.

   Opioids Top

Opiate abuse by adolescents decreased consider­ably during the 1980s, but the magnitude and variety of its medical sequelae warrant continued attention. Although it has been one of the least frequently reported drugs of use since 1991, heroin produces euphoria and analgesia. Heroin is hydrolyzed to morphine, which undergoes he­patic conjugation with glucoronic acid before excretion, through kidney, usually within 24 hours of admission.

Addiction to opioids is possible, in less than 14 days if the drug is administered daily in ever increasing doses [4],[7] . Opoids are abused orally, subcutaneously, or intravenously for their euphoric and analgesic effects. Numerous medical complications such as cellulitis, su­perficial skin abscess, septic thrombophlebitis, hepatitis, autoimmune deficiency syndrome (AIDS), endocarditis, and malnutrition have been observed in opioid -addicted patients [5] .

Clinical manifestations of opioid overdose include slow respiratory rate (RR) with increased tidal volume (VT) however, the increase in VT may not always be present. The pupils are characteristically miotic. Acute opioid withdrawal syndrome is manifested by symptoms of increased sympathetic nervous system activity. Cen­tral nervous system manifestations range from dyspho­ria to various forms of bizarre behavior and unconscious­ness. The ability to protect airway may be compromised and the risk of aspiration greatly increased.

   Anaesthetic implications Top

Opioid addicts should have opioids maintained dur­ing the perioperative period. Preoperative medication may also include opioids [16] . Opioid agonist-antagonists are not recommended as these drugs could precipitate acute withdrawal reactions.

The symptoms of withdrawal from opioids may be treated with clonidine, or diphenhydramine [17] . Clonidine attenuates opioid withdrawal symptoms by replacing opioid-mediated inhibition with alpha-2 agonist-mediated inhibition of the central nervous system [18] .

Regional anaesthesia may be safely administered to opioid-addicted patients. However, increased tendency for hypotension should be anticipated following the in­duction of spinal or epidural anaesthesia. However, re­gional anaesthesia may be relatively contraindicated in AIDS patients with central nervous system HIV infec­tion and progressive demyelination.

General anaesthesia may be indicated in the pa­tient with haemodynamic instability, coagulopathy, or sepsis. Reduced intravascular fluid volume, malnutrition or liver disease may require appropriate dose adjustments of anaesthetic drugs. Chronic opioid use leads to cross­tolerance to central nervous system depressants that may manifest as decreased analgesic responses to inhaled anaesthetics such as nitrous oxide. Conversely, acute opioid administration decreases anaesthetic requirements (MAC). Opioid overdose may cause respiratory depres­sion and loss of the airway. There is a tendency for perioperative hypotension to occur, which may reflect in­adequate intravascular fluid volume secondary to chronic infections, fever, malnutrition, adrenocortical insufficiency, or inadequate opioid concentrations in the brain [19] .

Postoperatively, the opioid -abusing patient often seems to experience an exaggerated degree of pain. De­creased pain tolerance is secondary to decreased pro­duction of endogenous opioid peptides. Alternative meth­ods of postoperative pain relief in these patients include continuous regional analgesia with local anaesthetics, neuraxial opioids, and transcutaneous electrical nerve stimulation.

   Volatile substances (solvent abuse) Top

Young adolescents are attracted to these sub­stances because of their rapid action, easy availability, and low cost. "Huffing"i.e. directly inhaling, or inhaling deeply from a paper bag containing a chemical soaked cloth is the common method used by teens.

There are enormous variety of solvents and fuels that are used, including almost any household cleaning agent or propellant, paint thinner, glue and lighter fluid. Children and teenagers are more likely to abuse solvent than other CNS-depressant substances. Solvent produce euphoria and other effects similar to subanaesthetic con­centrations of volatile anaesthetics, as well as CNS de­pression similar to alcohol intoxication [20] . Physical de­pendence is rare but psychological dependence and tol­erance can develop [21] .

Glue sniffing can cause a unique distal and proxi­mal tubular acidosis [22] . Toluene, causes relaxation and pleasant hallucination for up to 2 hours. Toluene sniffing may lead to autonomic cardiac dysfunction, ventricular fibrillation, and myocardial infarction [23],[24] . Gasoline, con­tains a complex mixture of organic solvents. Euphoria is followed by violent excitement. Volatile nitrites, such as amyl nitrite, butyl nitrite, and related compounds mar­keted as room deodorizers, are used as euphoriants, en­hancers of musical appreciation, and aphrodisiacs among older adolescents and young adults. They may result in profound hypotension and cutaneous flushing followed by vasoconstriction and tachycardia; methemoglobinemia, and increased bronchial irritation. Chronic use of gaso­line may cause pulmonary hypertension, restrictive lung defects or reduced diffusion capacity, peripheral neur­opathy, acute rhabdomyosis, haematuria, and possibly cerebral and cerebellar atrophy. Increased airway re­sistance, pulmonary hypertension, acute respiratory dis­tress syndrome (ARDS) and liver toxicity have all been reported in patients with documented exposure to sol­vents [25] .

Diagnosis of inhalant abuse is particularly difficult, relying almost entirely on a through history and high in­dex of suspicion. No laboratory tests confirm solvent inhalation [26] . However, complete blood counts, coagula­tion studies, and hepatic and renal studies may identify the complications [27] .

   Anaesthetic implications Top

Optimal anaesthetic management of solvent-abus­ing adolescent requires a high level of suspicion and early diagnosis. Altered perception of sensory stimuli, loss of coordination, headache, nausea, vomiting, and respira­tory compromise may result from vapour sniffing. Care­ful physical examination, including determination of pos­sible sensory and motor deficits, is indicated before in­duction of anaesthesia.

Chronic inhalant abuse can cause cardio-vascular and respiratory depression and the interaction with halo­genated hydrocarbons may induce life-threatening dysrhythmias [5] .

   Hallucinogens Top

Adolescents for their hallucinogenic properties have used several naturally occurring and synthetic sub­stances. Psychedelic agents are ingested orally to in­duce hallucinations, illusions, and distorted thought pro­cess. The hallucinogenic substances lysergic acid diethy­lamine (LSD), phencyclidine (PCP) and 3, 4­methylenedioxymethamphetamie (MDMA; Ecstasy) are the most commonly reported hallucinogens in high school. Although there is a high incidence of psychological de­pendence, there appears to be no evidence of physical dependence or withdrawal symptoms when hallucino­gens are discontinued [5] .

Ingestion of these drugs activates the sympathetic nervous system as evidenced by increased body tem­perature, tachycardia, hypertension, and dilated pupils. Psychological characteristics of intoxication include anxi­ety, panic attacks, hallucinations, and fear of "going crazy". Chronic hallucinogen use is uncommon.

   Anaesthetic implications Top

The mechanisms of action of both PCP and LSD are quite complex and include agonist, partial agonist, and antagonist effects at various serotonin, dopaminer­gic, and adrenergic receptors [28] . Anaesthesia during acute exposure with excitatory drugs is dangerous and should be avoided until acute effects have disappeared. Exag­gerated response to sympathomimetic drugs should be anticipated in these patients (PCP is a structural ana­logue of ketamine). Hallucinogens may prolong the an­algesic and ventilatory depressants effects of opioids. Prolongation in the effects of suxamethonium is pos­sible due to inhibition of plasma cholinesterase activity by PCP and LSD [29] .

General anaesthesia and surgery have been re­ported to precipitate panic responses in these patients. In the event that such responses occur, diazepam is likely to be useful [5] . Postoperative hallucinations in patients undergoing general anaesthesia have been reported as well [30] .

In regional anaesthesia, ephedrine should be used carefully (which has both direct and indirect actions) for the treatment of sympathectomy - induced hypotension.

   Cocaine Top

Cocaine use for non-medical purposes is a public health problem with important economic and social con­sequences. Cocaine is an alkaloid (benzoylmet hylecgonine) that is prepared from the leaves of Erythroxylon coca plant[31] . Cocaine can be abused via every possible route, including oral, nasal, intravenous, and rectal. The hydrochloride form can be chemically altered to the base form, which is then concentrated by extraction in ether or baking soda [31] . The residue from this method is a form of cocaine base commonly called "crack" (based on the cracking sounds it makes when heated) [31] . The metabolism of cocaine occurs primarily through plasma and hepatic cholinesterase, and patients with pseudocholinesterase deficiency are at increased risk for cocaine toxicity. Less than 5% of ingested co­caine is excreted unchanged in the urine [32] .

Cocaine produces prolonged adrenergic stimulation by blocking the presynaptic uptake of sympathomimetic neurotransmitters including norepinephrine, serotonin, and dopamine [33],[34] . The euphoric effects of cocaine "cocaine high" also result from prolongation of dopamine's activity in the limbic system and the cerebral cortex.

   Anaesthetic implications Top

Preoperative assessment presents a special chal­lenge, as self-reporting of drug abuse is notoriously unre­liable. The nasal mucosa should be carefully observed for ulceration signs. All extremities should be examined for sclerosis of peripheral veins and needle marks from intra­venous injections. Auscultation over the lungs is important to exclude cocaine-induced asthma and a careful cardio­vascular and neurologic examination is necessary [31] .

Preoperative laboratory tests include complete blood cell count, with a platelet count, to rule out throm­bocytopenia; ECG to identify signs of rhythm disturbance or myocardial ischaemia; chest radiography to rule out any pulmonary or cardiac involvement; and abdominal radiography to detect pseudo-obstruction [35] .

General or regional anaesthesia in the cocaine abuse adolescent may be associated with serious com­plications. Any event or drug likely to increase already enhanced sympathetic nervous system activity must be carefully considered before its selection to avoid myo­cardial ischaemia and cardiac dysrhythmias. However, beta-blockade also cause cocaine - induced coronary vasoconstriction. Esmolol may provide effective control of tachycardia and hypertension. The short elimination half-life of esmolol may offer some advantages if drug administration is deemed necessary. Of concern is that (1) ketamine should be used with extreme caution in these patients because it can markedly potentiate the cardiovascular toxicity of cocaine; (2) because both co­caine and suxamethonium undergo metabolism by plasma cholinesterase, the use of suxamethonium may result in prolonged paralysis; however, they may produce car­diac arrhythmias; (3) an increased anaesthetic require­ment for volatile anaesthetics may be present in the acutely intoxicated patient; and (4) the temperature rise and sympathomimetic effects associated with cocaine can mimic malignant hyperthermia (MH), and it may be difficult to differentiate between the two.

When regional anaesthesia is used, combative behavior; altered pain perception, cocaine - induced thrombocytopenia; and ephedrine - resistant hypotension may be encountered. Low doses of phenylephrine ti­trated to the effect usually restore blood pressure to nor­mal values. Pronounced abnormalities in endorphin lev­els and changes in both mu and kappa opioid receptor densities resulting from cocaine addiction which may result in perception of pain despite adequate spinal - epi­dural anaesthesia sensory levels [36] .

   Marijuana Top

Marijuana is the most commonly used illegal drug. The hemp plant Cannabis sativa, from which marijuana grows throughout the world, flourishes in most temper­ate and tropical regions [35] . Marijuana is commonly in­gested by smoking, which increase the bioavailability of the primary psychoactive constituent, tetrahydrocannab­inol (THC) [37],[38]. Inhalation of marijuana smoke produces euphoria, with signs of increased sympathetic nervous system activity and decreased parasympathetic nervous system activity. The most consistent cardiac change is an increased resting heart rate, although orthostatic hy­potension may occur. Chronic marijuana abuse leads to increased tar deposits in the individual's lungs, impaired pulmonary defense mechanisms, and decreased pulmo­nary function. As such an increased incidence of sinusi­tis and bronchitis is likely. Smoke from cannabis ciga­rettes is known to suppress both hormonal and cell-me­diated immune responses [39] . In predisposed persons, mari­juana may evoke seizures [5] .

   Anaesthetic implications Top

Anaesthesia during acute exposure with excitatory drugs is dangerous and should be avoided until the acute effects have disappeared. Severe tachycardia should be controlled preoperatively with labetalol or esmolol [35]. Marijuana may enhance the sedative-hypnotic effects of drugs that depress the CNS. Studies have shown cross­tolerance of marijuana with barbiturates, opioids, benzo­diazepines, and phenothiazines [40] .Additive effects of marijuana and potent inhaled anaesthetic can result in pronounced myocardial depres­sion in general anaesthesia [41] . Drugs that increase heart rate such as atropine, ketamine, pancuronium and ephe­drine should be avoided. Barbiturate and ketamine sleep times are prolonged in THC - treated animals, and opioid induced depression of ventilation may be potentiated [42] .

Possible intraoperative complications include bron­chospasm secondary to airway irritability by the mari­juana smoke, although marijuana is a bronchodilator. Adverse psychiatric and autonomic reactions to cannabis may interfere with postoperative recovery.

   Amphetamines Top

Stimulants, particularly amphetamines, are among the most frequently reported illicit drugs other than mari­juana. Methylamphetamine, commonly known as "ice", is accounted for more than 25% of its use as a stimu­lant. Methylamphetamine is particularly popular among adolescents and young adults because of its potency and ease of absorption. It can be used by snorting, smoking, ingesting by mouth, or absorption across mucous mem­brane such as vaginal mucosa. Amphetamines are abused individually or in conjunction with other CNS stimulants such as opioids or cocaine. Amphetamines stimulate the release of catecholamines from presynaptic vesicles, resulting in euphoria, increased cortical alertness, de­creased fatigue, and appetite suppression.

The symptoms of acute amphetamine intoxication include, hypertension, arrhythmias, tachycardia, dilated pupils, hyperreflexia, proteinuria, and confusion. Chronic abuse of amphetamines results in depletion of body stores of catecholamines, which may be manifested as anxiety, somnolence, or psychotic state. Agitation and delusional behaviours can be treated with haloperidol or droperidol. Phenothiazines are contraindicated and may cause a rapid drop in blood pressure or seizure activity. Other support­ive treatment consists of cooling blanket for hyperthermia and treatment of the hypertension and arrhythmias, which may respond to sedation with lorazepam or diazepam.

   Anaesthetic implications Top

Avoidance of halothane is recommended in gen­eral anaesthesia as, it may sensitize the myocardium to endogenous catecholamines. Acute intake of amphet­amine increases the minimum alveolar concentration of potent inhaled anaesthetics [43] . However, chronic intake decreases the dose for general anaesthetic [44] .

Sympathectomy caused by neuraxial blocks in re­gional anaesthesia may precipitate severe hypotension. The response to treatment of hypotension with vasopres­sors is unpredictable in amphetamine abusing adolescents.

   Conclusion Top

Environmental, social and perhaps genetic factors lead to behavioral disorders from abuse of psychotropic (mind altering) substances. Knowledge of a patient's substance abuse preoperatively may prevent adverse drug interactions, predict tolerance to anaesthetic agents, and facilitate the recognition of drug withdrawal.

Anaesthetic requirements for substance abusers vary depending on whether the drug exposure is acute or chronic. Elective procedures should be postponed for acutely intoxicated patients and those with signs of with­drawal. Regional anaesthetics should be considered when possible. For general anaesthesia, a technique primarily relying on a volatile inhalational agent may be prefer­able so that anaesthetic depth can be readily adjusted according to individual need.

   References Top

1.Johnston LD, O'Malley PM, Bachman JG. Monitoring the future: National report on adolescent drug use. Washington DC : NIH Publication, Department of Health and Human Ser­vices; 2004.  Back to cited text no. 1      
2.Milroy CM. Ten years of "ecstasy". J R Soc Med 1999; 92:68-71.  Back to cited text no. 2      
3.Christophersen AS. Amphetamine designer drugs - an over­view and epidemiology. Toxicol Lett 2000; 112-113: 127-31.  Back to cited text no. 3      
4.Kaye AD, Hoover JM, Ertner RA, Sutker PB. Behavioral and psychiatric disorders. In:Anesthesia and uncommon diseases. Fleisher LA (editor), 5th edition , Saunders (Elsevier) 2006; pp. 469-91.  Back to cited text no. 4      
5.Stoelting RK, Dierdorf SF. Psychiatric diseases and substance abuse. In : Stoelting RK, Dierdorf SF (editors) : Anesthesia and co-existing disease (4th edition) . Churchill Livingstone : New York 2002; pp. 639-54.  Back to cited text no. 5      
6.Needlman RD. Growth and Development. In : Nelson text­book of pediatrics, 17th edition. Behrman RE, Kliegman RM, Jenson HB (editors). Saunders (Elsevier) : Philadelphia, Penn­sylvania 2004; pp. 27-63.  Back to cited text no. 6      
7.High School& Youth Trends. National Institute of Drug Abuse (NIDA). National Institute of Health - U.S. Department of Health and Human Services, 2006.  Back to cited text no. 7      
8.Beattie MC, Longabaugh R, Elliott G, Stout RL, Fava J, Noel NE. Effect of the social environment on alcohol involvement and subjective well-being prior to alcoholism treatment. J Stud Alcohol 1993; 54 : 283-96.  Back to cited text no. 8      
9.Diaz JH, Hill GE. Hypotension with anesthesia in disulfiram­treated patient. Anesthesiology 1979; 51: 355-8.  Back to cited text no. 9      
10.Rudra A, Das Sudipta. Postoperative pulmonary complica­tions (Review Article). Indian J Anaesth 2006; 50 : 89-95.  Back to cited text no. 10    Medknow Journal  
11.http://www.nlm.nih.gov/medlineplus/smokelesstobacco.html/ (accessed14th July 2007)  Back to cited text no. 11      
12.Shan B, Lewis MAO, Bedi R. Oral submucous fibrosis in an 11 year old Bangladeshi girl living in the United Kingdom. Br Dent J 2001; 191 : 130-2.  Back to cited text no. 12      
13.Merchant AT, Haider SM, Firkee FF. Increased severity of oral submucous fibrosis in young Pakistani men. Br J Oral Maxillo­facial Surg 1997; 35 : 284-7.  Back to cited text no. 13      
14.Epie N. The chewing of betal quid and oral submucosal fibrosis and anesthesia. Anesth Analg 2005; 100 : 1210-3.  Back to cited text no. 14      
15.Mahajan R, Jain K, Batra YK. Submucous fibrosis secondary to chewing of quids : another cause of unanticipated difficult intubation. Can J Anaesth 2002; 49 : 309-11.  Back to cited text no. 15      
16.Giuffrida JG, Bizzari DV, Saure AC, et al. Anesthetic manage­ment of drug abusers. Anesth Analg 1970; 49 : 273-82.  Back to cited text no. 16      
17.Gold MS, Pottash AL, Extein I, Kleber HD. Clonidine in acute opiate withdrawal. N Engl J Med 1980; 302 : 1421-2.  Back to cited text no. 17      
18.Gold MS, Pottash AL, Sweeney DR, Kleber HD. Opiate with­drawal using clonidine. A safe, effective, and rapid nonopiate treatment. JAMA 1980; 243 : 343-6.  Back to cited text no. 18      
19.Marck LC. Hypotension during anesthesia in narcotic addicts. NY State J Med 1966; 66 : 2685-97.  Back to cited text no. 19      
20.Jage J, Heid F. Substance use disorders and anaesthesia. In Recent advances in anaesthesia and intensive care : Cashman JN, Grounds RM (editors). Cambridge University Press, No. 23, 2005, pp. 195-216.  Back to cited text no. 20      
21.Wood PR, Soni N. Anaesthesia and substance abuse. Anaes­thesia 1989; 44 : 672-80.  Back to cited text no. 21      
22.Carlisle EJ, Donnelly SM, Vasuvattakul S, et al. Glue-sniffing and distal renal tubular acidosis : sticking to the facts. J Am Soc Nephrol 1991; 1 : 1019-27.  Back to cited text no. 22      
23.Murata K. Araki S, Yokoyama K, Yamashita K, Okajima F, Nakaaki K. Changes in autonomic function as determined by ECG R-R interval variability in sandal, shoe and leather work­ers exposed to n-hexane, xylene and toluene. Neurotoxicology 1994; 15 : 867-75.  Back to cited text no. 23      
24.Cunnigham SR, Dalzell GW, McGirr P, Kahn MM. Myocar­dial infarction and primary ventricular fubrillation after glue sniffing. Br. Med J 1987; 294 : 739-40.  Back to cited text no. 24      
25.Reyes de la Rocha S, Brown MA, Fortenberry JD. Pulmonary function abnormalities in intentional spray paint inhalation. Chest 1987; 92 : 100-4.  Back to cited text no. 25      
26.Brouette T, Anton R. Clinical review of inhalants. Am J Addict 2001; 10 : 79-94.  Back to cited text no. 26      
27.Anderson CE, Loomis GA. Recognition and prevention of in­halant abuse. Am Fam Physician 2003; 68: 869-74.  Back to cited text no. 27      
28.Abraham H, Aldridge A, Gogia P. The psychopharmacology of hallucinogens. Neuropsychopharma, 1996; 14: 285-98.  Back to cited text no. 28      
29.Beattie C, Mark L, Umbricht - Schneiter A. Evaluation of the patient with alcoholism and other drug dependencies. In: Rogers MC, Tinker JH, Covino BG, Longnecker DE (eds) : Principles and Practice of Anesthesiology, 1st ed. St. Louis : Mosby, 1993 ; pp. 537-59.  Back to cited text no. 29      
30.Morris G, Magee P. Anaesthesia and past use of LSD. Can J Anaesth 1995; 42 : 177.  Back to cited text no. 30      
31.Fleming JA, Byck R, Barash PG. Pharmacology and therapeu­tic applications of cocaine. Anesthesiology 1990; 75 : 518-31.  Back to cited text no. 31      
32.Inaba T, Stewart D J, Kalow W. Metabolism of cocaine in man. Clin Pharmacol Ther 1978 ; 23 : 547-52.  Back to cited text no. 32      
33.Gold MS, Washton AM, Dackis CA. Cocaine abuse neuro­chemistry, pharmacology, and treatment. NIDA Res Monogr 1985; 61 : 130-50.  Back to cited text no. 33      
34.Pitts DK, Marwah J. Autonomic actions of cocaine. Can J Physiol Pharmacol 1989; 67 : 1168-76.  Back to cited text no. 34      
35.Krane EJ, Davis PJ. Drug -abusing child and adolescent. In Motoyama EK, Davis PJ (eds.) : Smith's anesthesia for infants and children, 7th edition. Mosby (Elsevier), 2006; pp.262-5.  Back to cited text no. 35      
36.Kreek MJ. Cocaine, dopamine and the endogenous opioid sys­tem. J Addict Dis 1996; 15 : 73-96.  Back to cited text no. 36      
37.Hall W, Solowij N. Adverse effects of cannabis. Lancet 1998; 352 : 1611-6.  Back to cited text no. 37      
38.Musty R, Reggio P, Consroe P. A review of recent advances in cannabinoid research and the 1994 International Symposium on Cannabis and the Cannabinoids. Life Sci 1995; 56 : 1933-40.  Back to cited text no. 38      
39.Maykut MO. Health consequences of acute and chronic mari­juana use. Prog Neuropsychopharmacol Biol Psychiatry 1985; 9: 209-38.  Back to cited text no. 39      
40.Pertwee RG. Tolerance to and dependence on psychotropic cannabinoids. In : Pratt JA (ed) : The biological basis of drug tolerance and dependence. New York. Academic Press; 1991; pp. 232-63.  Back to cited text no. 40      
41.Stoelting RK, Martz RC, Gartner J, Brown DJ, Forney RB. Effects of delta 9-tetrahydrocannabinol on halothane MAC in dogs. Anesthesiology 1973; 38 : 521-4.  Back to cited text no. 41      
42.Johnstone RC, Lief PL, Kulp RA, et al. Combination of delta­9-tetrahydrocannabinol with oxymorphine or pentobarbital. Anesthesiology 1975; 42 : 674-9.  Back to cited text no. 42      
43.Michel R, Adams AP. Acute amphetamine abuse. Problems during general anesthesia for neurosurgery. Anaesthesia 1979; 34 : 1016-9.  Back to cited text no. 43      
44.Johnston RR. Way WL, Miller RD. Alteration of anesthetic requirement by amphetamine. Anesthesiology 1972; 36 : 357­-63.  Back to cited text no. 44      


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