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Ice Street Drug

Methamphetamine abuse has been a problem for many years. The highly pure, smokable form of D-methamphetamine hydrochloride, called "ice" or "crystal,"(1) has rapidly become a significant health problem in certain regions of the world, including parts of the United States. Limited information is available concerning this form of the drug, which probably originated in Korea and the Philippines.(1) Smokable methamphetamine was introduced in the United States in the early 1980s,(2) when it became a popular drug of abuse in Hawaii, Southern California and the Pacific coast.(3) The powder form of the drug was first called "shabu" in Japan.(4)(5) "D" or "L" forms, laden with impurities, are also called "crank" or "speed."(3)

Street names may vary, depending on the particular area or culture. Other illegal drugs may be known as ice. For example, in central Florida, the term ice is also used to describe a combination of crack cocaine and methamphetamine.(1) Ice is reported to cost between $400 and $500 a gram, which in many places is nearly four times the price of crack.(1)(2) However, one report from Southern California states that the cost of ice is comparable to crack.(4) With the increasing use of smokable methamphetamine and the drug's potentially devastating medical consequences, family physicians should familiarize themselves with its properties.

Prevalence

Because of the relatively recent emergence of ice as a drug of abuse, complete figures on its use are not yet available. Between 1986 and 1988, the National Institute on Drug Abuse reported a 1.7-fold increase in emergency department evaluations for methamphetamine abuse.(6) National figures on drug abuse from 1988 reveal that 64 percent of high school seniors indicated they could easily obtain amphetamines.(7) The Drug Abuse Warning Network (DAWN) system, which includes selected hospitals in 21 metropolitan areas, reported 3,030 methamphetamine-related visits to emergency departments in 1988.(8)

Small samples of patients have been studied in areas where methamphetamine abuse is highest.(9) In 1989, methamphetamine was reported to be the most abused drug in San Diego County, California, accounting for 60 percent of illicit drug seizures by law enforcement officials and up to 40 percent of all referrals to substance abuse treatment centers.(10) Figures from San Diego County reveal 32 deaths related to methamphetamine use in 1987. This figure compares with 66 deaths related to cocaine use. Sixty-six percent of the deaths involved the use of other drugs, most commonly ethanol. Ten deaths involved both methamphetamine and cocaine.(9)

Historical Perspective

Amphetamines and methamphetamines have long been drugs of abuse. Amphetamine was first synthesized in 1887. The first commercially available preparation appeared in 1932, as benzathine nasal spray, for the treatment of asthma and rhinitis. The first amphetamine tablet appeared in 1937 and was used to treat narcolepsy. Its euphoric properties were soon noted, along with its appetite-suppressant and stimulating effects. In the late 1930s and 1940s, amphetamine abuse became widespread, even among foreign armies during World War II.

Attempts to control the use of methamphetamine were unsuccessful until the Controlled Substance Act of 1970 regulated its manufacture. Some states have enacted laws that have decreased the availability of precursor chemicals.(3)(11)

Medical indications for the use of amphetamine and its derivatives include attention deficit disorder with hyperactivity, narcolepsy and exogenous obesity. These drugs carry significant warnings concerning the risk of tolerance and dependence.

Routes of Administration

Methamphetamine is a white powder that is most commonly used intranasally. It can be ingested and, on rare occasions, it may be used intravenously.(3)(10) Ice is the free-based form of methamphetamine (as crack is the free-based form of cocaine). One explanation for the popularity of smokable methamphetamine is its rapid absorption from the lungs, resulting in immediate clinical effects similar to those of intravenous drugs.(3) Following intravenous or intranasal administration, users report that the "high" peaks in approximately 30 minutes and that the effects are of similar magnitude with either route.(12)

The average "hit" of ice is one-tenth of a gram, with effects lasting up to 15 hours.(1) However, since the bioavailability of smokable methamphetamine is 50 percent that of the intravenous form, more of the drug must be used to achieve a similar effect. Some of the drug remains trapped in the smoking apparatus, as well as in the respiratory tract mucosa.(12) The long half-life of methamphetamine and the long plateau effect suggest that markedly high plasma concentrations accumulate with repeated inhalation of the drug, even over long intervals.(13) Based on animal studies, it appears that the effects associated with ice may last 10 times as long as the effects of cocaine.(3)

Pharmacologic Action

Since it is a form of amphetamine, ice is a strong central nervous system stimulant. The dopaminergic receptor neurons in the synaptic cleft are hyperstimulated by the displacement of dopamine from the nerve terminals. These hyperstimulated neurons stimulate central nervous system pathways and the sympathetic nervous system. The effect of D-methamphetamine on the central nervous system is greater than that of D-amphetamine, because of a higher penetration.(3) Animal models indicate that methamphetamine is twice as toxic as amphetamine.(1) Direct stimulation of the peripheral nervous system and organs may also occur.(3)

Clinical Effects

ACUTE EFFECTS

The clinical effects of ice are similar to those of other stimulants, such as cocaine. High doses may cause irreversible damage to the central nervous system. Short-term clinical effects include intensified emotions, increased alertness, altered self-esteem, euphoria and an alleged increase in sexuality.(3)

Hyperpyrexia is a serious complication of methamphetamine use, and temperatures above 40[degrees]C (104[degrees]F) are associated with a poor prognosis. The rise in temperature is caused by the vasoconstricting properties of the drug, stimulation of the hepatic metabolism of fat and glucose, and the agitation and muscle rigidity produced by overdose.(1)

An acute toxic psychosis can be induced in healthy persons, as well as in persons with underlying psychiatric illness. Referral to a psychiatric center is often required in patients who present to the emergency department with toxic effects.(3)

Patients often present with extreme hyperactivity, restlessness and irritability.(1) Data from Hawaii indicate that the most common presentation in chronic users is acute psychosis with auditory hallucinations and extreme paranoia. Destructive behavior is common. Unlike cocaine psychosis, psychosis from methamphetamine use lasts much longer than a few hours, and may even last as long as several days or weeks.(14) All amphetamines may induce an acute choreoathetoid disorder.(3) Some users may develop dyskinesias.(1)

CHRONIC EFFECTS

Persons who chronically use methamphetamine may exhibit symptoms indistinguishable from paranoid schizophrenia, with delusions, paranoia and aggressive behavior.(1)(15) Patients who have methamphetamine-induced organic mental disorders differ from patients who have other drug- or alcohol-induced disorders in that they experience more hallucinations (both auditory and visual), more paranoid ideation and more aggressiveness.

Amphetamine-induced psychosis has been shown to resolve within 10 days of cessation of drug use. It may, however, persist for up to six months in approximately 10 percent of patients. After resolution of psychosis, further use of the drug may induce another psychotic episode within a shorter period of time than was so initially.(15) One study investigating the personality traits of alcohol users and methamphetamine users showed more impulsiveness and less inhibition of aggression in the methamphetamine users.(16)

CARDIOVASCULAR EFFECTS

Cardiovascular manifestations of methamphetamine use include chest pain (usually without electrocardiographic changes), palpitations, dyspnea, hypertension, tachycardia, myocardial ischemia and atrial and ventricular arrhythmias.(1)(3) The mechanisms responsible for the cardiovascular effects of the smokable form are not well established. The effects of smokable crystal methamphetamine appear to be similar to the effects of intravenous amphetamine, which are better documented.(6)

It is postulated that the increase in circulating catecholamine levels produced by amphetamines may enhance coronary tone and aggregation of platelets, contributing to acute vascular occlusion. Animal studies suggest taht elevated catecholamine levels may also precipitate rupture of atherosclerotic plaques and induce focal myocarditis. Catecholamine-related cardiomyopathy is also associated with myofibrillar degeneration.(17)(18) Autopsy findings in one group of methamphetamine abusers revealed a disarray of myofibrils, similar to that seen in hypertrophic cardiomyopathy.(19) Moderate doses of methamphetamine may actually increase cardiac output and myocardial contractility. Excessive doses result in myocardial depression.

Pulmonary edema has been reported in patients who use oral dextroamphetamine and methamphetamine.(6)(17) The smokable crystal methamphetamine has also been reported to produce acute pulmonary edema 24 to 36 hours following inhalation.(5) In addition, vasospasm resulting in acute myocardial infarction, cardiogenic shock and death has been reported.(6) Myocardial infarction has also occurred following intranasal administration of the drug.(18)

OTHER SYSTEMIC EFFECTS

Other systemic effects of methamphetamine are listed in Table 1.(1)(6)(11)(20) Ingestion of 1.5 mg of methamphetamine per kg has been associated with fatality; however, in long-term abusers, doses up to 15,000 mg per kg may be tolerated.(3)

TABLE 1 Systemic Effects of Methamphetamine

Cardiovascular                     Neurologic(1)(11)(20)
Chest pain                         Mydriasis
Palpitations                       Cerebral edema
Dyspnea                            Hemorrhage (subarachnoid,
Hypertension
                                     intraventricular,
                                     intracerebral)
Tachycardia                        Metabolic(11)
Myocardial ischemia                Hyperpyrexia
Arrhythmias (atrial, ventricular)  Elevated serum
                                     thyroxin level
Psychiatric                        Musculoskeletal(6)
Intensified emotions               Hyperactivity
Increased alertness                Rhabdomyolysis
Altered self-esteem                Gastrointestinal(1)(11)
Euphoria                           Anorexia
Increased sexuality                Weight loss
Irritability                       Malnutrition
Hallucinations (auditory, visual)  Nausea, vomiting
Paranoia                           Diarrhea
Aggressive behavior

OBSTETRIC CONSIDERATIONS

Transplacental exposure to methamphetamine is an increasing problem, as are neonatal complications from almost any maternal drug use. In some centers, up to 25 percent of neonates have detectable levels of illicit drugs in their urine. In Los Angeles County, the number of such infants has doubled every year since 1983.(10)

The consequences of prenatal exposure to methamphetamine are similar to those of prenatal exposure to cocaine. Effects include intrauterine growth retardation, preterm labor, fetal distress (bradycardia or meconium aspiration), placental hemorrhage, decreased head circumference and neonatal anemia. In the first year of life, infants who have been exposed to methamphetamine exhibit lethargy, decreased alertness and poor feeding habits. Although most such infants have minor neurologic abnormalities, their first-year development is generally normal. Some abnormalities suggesting frontal lobe dysfunction may manifest at school age. A child's subsequent course is not predictable based merely on neonatal assessment.(10)

Management of Acute Intoxication

In patients suspected of having methamphetamine toxicity, amphetamine and other drug use must be confirmed by urine toxicology. Underlying metabolic disorders and infectious processes should be excluded.

Gastric lavage and administration of activated charcoal are recommended if the drug has been ingested, but ipecac-induced emesis should be avoided because of the possibility of inducing seizures, arrhythmias or hypertensive hemorrhages.(1) The patient should be kept in a quiet room to minimize sensory stimulation, and haloperidol (Haldol) should be administered for control of agitation.

Patients should be well-hydrated and should receive appropriate volume replacement.(3) Cardiac monitoring for arrhythmias is essential.(11) Diastolic hypertension of greater than 110 mm Hg may be managed with intravenous nitroprusside.(1) Chlorpromazine (Thorazine) and intravenous propranolol (Inderal) have also been recommended to help lower blood pressure, as well as treat agitation. Diazepam (Valium) is the drug of choice for seizure management. Uncontrolled seizures may warrant use of phenytoin (Dilantin) or phenobarbital. If hyperthermia occurs, external cooling with sponging and cooling blankets is appropriate.(11)

Acidification of the urine with intravenous ammonium chloride or oral ascorbic acid is controversial.(1) Although this technique may hasten the elimination of amphetamine, it may not be clinically helpful. The process is contraindicated if myoglobinuria is present, since urine acidification may accelerate this condition. In these cases, urine alkalinization is recommended.(11)

After abrupt cessation of amphetamine use, withdrawal symptoms peak in two to three days.(11) Withdrawal consists of abdominal cramping and symptoms of gastroenteritis, but with increased appetite. Patients experience headaches, lethargy, dyspnea and severe depression, and often have suicidal tendencies.(1) In many cases, methamphetamine toxicity can be treated conservatively, with referral for long-term therapy following release from the emergency department. Only about 10 percent of patients require hospital admission. Long-term treatment requires drug rehabilitation and intensive inpatient counseling.

REFERENCES

(1.)Mack RB. The iceman cometh and killeth: smokable methamphetamine. N C Med J 1990; 51:276-8.

(2.)Su'a F. Street drugs: everyone's business. Hawaii Med J 1989; 48:452,454.

(3.)Derlet RW, Heischober B. Methamphetamine. Stimulant of the 1990s? West J Med 1990; 153:625-8.

(4.)Scheck A. New 'ice age' predicted. Methamphetamine use may surpass 'crack.' Fam Pract News 1990; 20:1.

(5.)Nestor TA, Tamamoto WI, Kam TH, Schultz T. Crystal methamphetamine-induced acute pulmonary edema: a case report. Hawaii Med J 1989; 48:457-8,460.

(6.)Hong R, Matsuyama E, Nur K. Cardiomyopathy associated with the smoking of crystal methamphetamine. JAMA 1991; 265:1152-4.

(7.)Drugs and crime facts, 1989. Rockville, Md.: U.S. Dept. of Justice, Office of Justice Programs, Bureau of Justice Statistics, 1990.

(8.)NIDA Capsule, CAP 35. Rockville, Md.: U.S. Dept. of Health and Human Services, Alcohol, Drug Abuse, and Mental Health Administration, 1990.

(9.)Bailey DN, Shaw RF. Cocaine- and methamphetamine-related deaths in San Diego County (1987): homicides and accidental overdoses. J Forensic Sci 1989; 34:407-22.

(10.)Dixon SD. Effects of transplacental exposure to cocaine and methamphetamine on the neonate. West J Med 1989; 150:436-42.

(11.)Kunkel DB. Amphetamines and amphetamine-like drugs. In: Tintinalli JE, Krome RL, Ruiz E, eds. Emergency medicine: a comprehensive study guide. 2d ed. New York: McGraw-Hill, 1988:713-4.

(12.)Perez-Reyes M, White R, McDonald S, Hill J, Jeffcoat R, Cook CE. Pharmacologic effects of methamphetamine vapor inhalation (smoking) in man. NIDA Res Monogr 1991; 105:575-7.

(13.)Cook CE, Jeffcoat AR, Perez-Reyes M, Sadler BM, Hill JM, White WR, et al. Plasma levels of methamphetamine after smoking of methamphetamine hydrochloride. NIDA Res Mongor 1991; 105:578-9.

(14.)Jackson JG. The hazards of smokable methamphetamine [Letter]. N Engl J Med 1989; 321:907.

(15.)Szuster RR. Methamphetamine in psychiatric emergencies. Hawaii Med J 1990; 49:389-91 [Published erratum appears in Hawaii Med J 1990; 49:451].

(16.)Mukasa H, Nakamura J, Yamada S, Inoue M, Nakazawa Y. Platelet monoamine oxidase activity and personality traits in alcoholics and methamphetamine dependents. Drug Alcohol Depend 1990; 26:251-4.

(17.)Jacobs LJ. Reversible dilated cardiomyopathy induced by methamphetamine. Clin Cardiol 1989; 12:725-7.

(18.)Furst SR, Fallon SP, Reznik GN, Shah PK. Myocardial infarction after inhalation of methamphetamine [Letter]. N Engl J Med 1990; 323:1147-8.

(19.)Matoba R, Shikata I, Fujitani N. Cardiac lesions in methamphetamine abusers. Acta Med Leg Soc 1986; 36:51-5.

(20.)Shibata S, Mori K, Sekine I, Suyama H. Subarachnoid and intracerebral hemorrhage associated with necrotizing angiitis due to methamphetamine abuse--an autopsy case. Neurol Med Chir 1991; 31:49-52.

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