Anesthetic management of the illicit-substance-using patient
Marcelle Hernandeza, David J. Birnbachb and Andre A.J. Van Zundertc
Purpose of review
During the last few years, drug abuse has risen to the point
that almost 20 million Americans are current abusers of
illicit substances. These patients present to us as
anesthesiologists in a variety of circumstances: in obstetrics
for labor and emergencies, in trauma for emergency
surgeries or life-saving (resuscitative) situations and in
everyday elective surgeries. Therefore it is important for
anesthesiologists to know about the most common illicit
drugs being used, to know their side effects and clinical
presentation if abused or intoxicated, and to know what
anesthetic options would be beneficial or detrimental.
Recent findings
In this article we will review some of the most commonly
used illicit drugs, their effects on the organ systems and
some tips to take into consideration when providing
anesthesia for these patients. We will discuss marijuana,
cocaine, opioids, hallucinogens, solvents and the newer
so-called rave or club drugs. Newer treatment options for
opioid detoxification will also be discussed.
Summary
Illicit substance abuse is a major health concern in the
United States. Drug use, either acute or chronic, has
potentially grave consequences which include changes
affecting the pulmonary, cardiovascular, nervous, renal and
hepatic systems. Anesthesiologists come into contact with
these patients in emergency and everyday situations. Due to
the diverse clinical presentations that may arise from single
substance or polysubstance abuse, anesthetic
management should be tailored to each individual and
universal precautions should always be followed when
providing care.
Keywords
anesthesia, illicit substance abuse
Curr Opin Anaesthesiol 18:315324. 2005 Lippincott Williams & Wilkins.
a
Jackson Memorial Hospital, University of Miami School of Medicine, Miami, FL,
USA, bDepartment of Anesthesiology, Miller School of Medicine of the University of
Miami, Chief, Womens Anesthesia, Jackson Memorial Hospital, Miami, FL, USA
and cCatharina Hospital - Brabant Medical School, Department of Anesthesiology,
ICU and Pain Clinic, Eindhoven, The Netherlands
Correspondence to Professor A.A.J. van Zundert, MD, PhD, FRCA, Catharina
Hospital - Brabant Medical School, Department of Anesthesiology, ICU & Pain
Clinic, Michelangelolaan 2, NL-5623 EJ, Eindhoven, The Netherlands
Tel: +31 40 2399 111; e-mail: zundert@iae.nl
Current Opinion in Anaesthesiology 2005, 18:315324
Abbreviations
CNS central nervous system
GHB g -hydroxybutyrate
IUGR intrauterine growth restriction
LSD lysergic acid diethylamide
MDMA 3,4-methylenedioxmethamphetamine
PSP phencyclidine
THC D9-tetrahydrocannabinol
2005 Lippincott Williams & Wilkins
0952-7907
Introduction
Through the years, abuse of illicit substances has been
escalating despite efforts in health education, prevention
and different detoxification or rehabilitation treatment
approaches. This is illustrated by the fact that in 2003 an
estimated 19.5 million Americans (8.2% of the popula-
tion) of ages 12 and older were current users of illicit
drugs [1]. Even though as anesthesiologists we are gen-
erally not the primary care physicians of these patients,
we encounter these patients as we administer anesthesia
to them for emergency or trauma situations, obstetrics
and even for regular elective surgeries. The latest find-
ings from drug-abuse-related visits to the Emergency
Department reported by the Substance Abuse and Men-
tal Health Services Administration (SAMHSA) in the
year 2000 are collected in the Drug Abuse Warning
Network (DAWN), a national probability survey of 466
hospital Emergency Departments in 21 metropolitan
areas of the USA. These findings include that there were
601 776 drug-related Emergency Department episodes.
In decreasing order, the following drugs were mentioned
at the time of admission: alcohol in combination with
other drugs (204 524), cocaine (174 896), heroin/mor-
phine (97 287) and marijuana (96 446). On the other
hand, the National Survey on Drug Use and Health
(NSDUH) has estimated that marijuana is the most
commonly used illicit drug (6.2% of the population or
14.6 million people), followed by cocaine (1% or 2.3 mil-
lion people). An increase in the number of people aged 12
or older abusing nonmedical pain relievers increased from
29.6 million to 31.2 million between 2002 and 2003.
Males were almost twice as likely to be classified with
substance abuse or dependence when compared to
females (12.2 versus 6.2%). However, in young people
(ages 1217) similar rates of drug abuse or dependence
were reported in males and females (8.7 versus 9.1%).
Understanding the complexity of the problem of sub-
stance abuse is a challenge, since an interplay of
biological, genetic, psychological, social, cultural, envir-
onmental and spiritual factors are involved.
315
316 Anaesthesia and medical disease
As anesthesiologists we need to be aware of the use of
illicit drugs because of the long-term negative conse-
quences that it may have on health and how it impacts on
anesthetic care. Medical adverse effects range from
pulmonary and cardiovascular effects, to irreversible
brain damage; these could manifest or worsen while
under anesthesia, when these substances interact with
the anesthetics provided. Illicit drugs may encourage
reckless driving and thus increase the potential for
motor-vehicle accidents and suicide attempts, often
requiring anesthesia for emergency and trauma situa-
tions. In a study performed in Los Angeles County
and the University of Southern California, an overall
53% of patients with gunshot wounds, 32.9% of victims
of motor-vehicle accidents, 32.9% of patients with falls
and 28.6% of pedestrians tested positive for illicit drugs or
alcohol use. But in that study they made clear that the
prevalence of illicit drug use by trauma victims, although
high, is associated with several factors, including: the
mechanism of injury; age, gender and ethnicity of the
patient; and geographic location of the trauma center
[2]. In another study, the risk for motor-vehicle
accidents was increased for drivers using alcohol,
benzodiazepines, amphetamines, cocaine and opiates.
Exposure to cannabis alone did not affect driving per-
formance, while the combination of cannabis with alcohol
had serious effects on this activity [3]. However, due to
conflicting reports, the effects of substance abuse on
trauma victims are unknown [2].
Injected drugs and high-risk sexual behaviors are key risk
factors for the transmission of blood-borne diseases such
as HIV/AIDS and hepatitis C. Numerous reports have
also described the involvement of skeletal structures in
injection-drug users with infections. These patients are
usually young and the entry of pathogens into the body is
allowed after injecting narcotics by nonsterile tech-
niques, including licking the needle or skin before injec-
tion (needle lickers osteomyelitis) [4]. These infecting
organisms may produce local disease at the site of
injection or involvement of bone or joint by hematogen-
ous spread (e.g. septic arthritis). Since some of these
patients may have HIV, they may have concomitant
tuberculosis which, if disseminated, may produce extra-
pulmonary tuberculosis involving the vertebral bodies.
Of note, vertebral osteomyelitis is most commonly
caused by bacterial pathogens after hematogenous
spread. In 5360% of patients the most common site
of involvement is the lumbar spine and these patients will
present with chronic low back pain and permanent
neurologic signs (in about 15%) [4]. Infection from bone
can extend into the epidural or subdural space forming an
abscess, which may lead to spinal-cord compression and
neurological deficits. It is important to remember that
patients using illicit substances are frequently under-
medicated for pain since they may require higher and
more frequent doses of analgesics to achieve expected
effects, especially since most have cross-tolerance to
opioid analgesics [4].
Anesthetizing pregnant women who use illicit drugs is
particularly complex and difficult, especially when the
effects of drug abuse mimic disease such as preeclampsia.
Substance abuse during pregnancy has ranged from 0.4 to
27% depending on the population being studied [5]. In one
particular study, the prevalence of antepartum cocaine use
among parturients without prenatal care in a New York
City hospital was reported to be 68% [6]. Drug-abusing
patients (especially when pregnant), due to social stigmas
and fear of punitive actions, usually deny their drug habit
and receive no prenatal care. Drug users have more health
problems and more pregnancy complications but measur-
ing the impact of drug exposure on the fetus has proven to
be difficult and only animal studies provide information
regarding toxic or teratogenic effects of some of these
drugs. Pregnant women and women of child-bearing age
may place the fetus at risk for developmental disabilities,
low birth weight and prematurity [5].
In this article we will be discussing some of the most
frequently used illicit substances, their effects and impor-
tance for anesthesiologists. We will also discuss why it is
important to know a patients history of substance abuse
prior to administering anesthesia or analgesia, allowing us
to predict adverse drug interactions, predict tolerance to
some anesthetic agents and recognize drug-withdrawal
signs and symptoms.
Marijuana
One of the most popular recreational drugs of abuse
among millions of people is the hallucinogenic agent
marijuana, also referred to as pot, hash, grass, weed
and THC. It is obtained from the plant Cannabis sativa,
which contains chemicals also known as cannabinoids,
including its active ingredient D9-tetrahydrocannabinol
(THC) and the tobacco carcinogen benzopyrene [7].
Marijuana can be smoked as a cigarette (a joint), using
a water pipe or using a hollow cigar filled with marijuana
(a blunt); it can also be taken orally. Its users experience
an intense feeling of relaxation within minutes and a
pleasant euphoria that last several hours. Marijuana com-
bined with drugs like alcohol or diazepam increases the
sedative effect, while when combined with ampheta-
mines or cocaine increases the stimulatory effects [7].
Other effects of acute marijuana ingestion include
tachycardia, conjunctival congestion and anxiety [8].
Although acute toxicity or major anesthesia interactions
from this drug are rare, every system is affected by its use
and its clinical picture is unpredictable.
Cannabinoids have a high fat solubility which leads to
rapid accumulation in adipose tissue, from which it is
 Anesthetic in illicit-substance-using patients Hernandez et al. 317
then released to the brain. Its elimination half-life in
occasional users is approximately 56 h, while it is approxi-
mately 28 h in chronic users. Nonetheless, cannabinoids
can be sequestered in adipose tissue, extending its tissue
half-life to approximately a week [8]. Complete elim-
ination of a single dose may require up to 30 days, as
THC can remain in the body a long time after being
smoked [7,9]. Metabolism of cannabinoids occurs in the
liver, into more than 20 metabolites, most with psycho-
active properties [7].
Smoking marijuana on a frequent basis can lead to the
development of cognitive impairment, shortened mem-
ory span, confusion, altered time perception and dulled
reflexes, making it difficult to maintain normal daily
activities at home or work. Some of the adverse reactions
mostly seen in smokers include anxiety, fear, depression,
delusions, violent behavior and hallucinations. This
makes the smoker enjoy the so-called high while being
unaware of the behavioral disabilities or how dysfunc-
tional he or she has become. Abstinence following expo-
sure to four or five cigarettes a day, even for a short period
of 3 days, has been associated with a withdrawal syn-
drome where there is increased latency to fall asleep,
negative mood and behavioral symptoms [10].
Anesthetic considerations
As previously mentioned, cannabis can affect numerous
body systems. On the autonomic nervous system, if low or
moderate doses are taken, an increase in sympathetic
activity occurs with a reduction of parasympathetic activ-
ity; this results in tachycardia and increased cardiac out-
put. If high doses are ingested, there is inhibition of the
sympathetic activity but not of the parasympathetic
activity, leading to possible hypotension and bradycardia
[8]. Life-threatening arrhythmias have not been
reported, but an increase in supraventricular or ventri-
cular ectopic activity can occur as well as reversible
ST-segment and T-wave abnormalities [8]. The com-
bination of marijuana with other sedative hypnotic drugs
may enhance depression of the central nervous system
(CNS). Cross-tolerance has been seen with cannabis
and alcohol, barbiturates, opioids, benzodiazepines and
phenothiazines.
Marijuanas effect on the cardiovascular system includes
increased myocardial depression and tachycardia. There-
fore it is not surprising that its use may potentiate the
effect of anesthetic drugs that affect blood pressure and
heart rate [8]. This can be seen when a patient is
receiving general anesthesia and the effects of marijuana
are added to the ones from potent inhalational agents
resulting in profound myocardial depression. Adverse
reactions such as this may interfere with a safe induction
of anesthesia. Because of the tachycardia which occurs in
patients with acute marijuana abuse, drugs increasing
heart rate (such as ketamine, pancuronium, atropine
and epinephrine) should be avoided.
As with tobacco, cannabis inhalation affects lung func-
tion as it is smoked unfiltered, exposing the user to
carcinogens and contaminants. Its association with
upper-airway irritability, in addition to impairment on
airway epithelial function and damage to bronchial tissue,
predisposes to chronic cough, bronchitis, emphysema
and bronchospasm [11,12]. There have been reports of
oropharyngitis, acute upper-airway edema and obstruc-
tion in cannabis-smoking patients who have undergone
general anesthesia. Some even recommend administer-
ing dexamethasone as prophylaxis to these patients if
undergoing general anesthesia [12].
In pregnant patients it seems that chronic use of mari-
juana may reduce uteroplacental perfusion and may thus
result in fetal intrauterine growth restriction (IUGR) [13].
Although it is not a proven teratogen, some research
suggests that cannabis is associated to low neonatal birth
weight, increased risk of complications during labor and
delayed cognitive development in infants [13,14].
Attempts to legalize this drug are controversial and
complex. Its promoters enhance its antiemetic, analgesic
and anticonvulsant properties in addition to its potential
to increase appetite. In addition it may improve glau-
coma. Others, however, discourage its therapeutic use
because of its potential for tolerance and abuse and its
psychoactive properties.
Cocaine
Cocaine abuse has become a serious health concern
throughout the world. In the USA almost 5 million people
use it regularly [15]. Cocaine is extracted from the leaves
of Erythroxylon coca, a plant indigenous to South America.
The drug was first introduced as a local anesthetic due to
its topical anesthetic properties, commercially available
in a hydrochloride form as powder, granules or crystals.
But the hydrochloride form can be converted back to its
alkalinized form by the addition of baking soda or ammo-
nia plus water followed by heating; the alkalinized form is
widely smoked and known as crack or free base. This
crack cocaine (also called rock) is highly addictive and
smoked in a base pipe, injected, snorted or ingested orally.
Its low molecular weight and high lipid solubility allow
easy diffusion across lipid membranes. Oral and snorted
cocaine, due to slower rates of absorption, yields lower
plasma levels. It has a biological half-life of 0.51.5 h as it is
metabolized by plasma and liver cholinesterases to water-
soluble metabolites that are excreted in the urine. Only
15% of the ingested drug is cleared unmetabolized in the
urine, allowing its detection only 36 h after its use. On the
other hand, two of cocaines metabolites (ecgonine methyl
ester and benzoylecgonine) account for 7590% of
318 Anaesthesia and medical disease
its metabolism and can be detected in urine for
1560 min after intake [16,17].
Cocaine interferes with presynaptic uptake of sympatho-
mimetic neurotransmitters (e.g. norepinephrine, seroto-
nin and dopamine) [17]. A powerful euphoria (lasting
510 min if smoked and 1030 min if snorted) is pro-
duced as a result of free catecholamines stimulating the
sympathoadrenal axis and the prolongation of dopami-
nergic activity in the limbic system and adrenal cortex.
Blood flow to arteries in areas like the heart and brain may
be compromised as these vessels vasoconstrict or vasos-
pasm temporarily, severely compromising oxygenation
and supply; this may lead to irreversible brain damage,
stroke and myocardial infarction or depression [16]. At
higher doses, cocaine can depress ventricular function
and slow electrical conduction of the heart; pathologic
changes of contraction-band necrosis and ventricular
hypertrophy also contribute to the potentially lethal
sequelae of this drug [18]. Although quite rare, acute
aortic dissection can occur in these patients, perhaps a
consequence of abrupt, severe hypertension and catecho-
lamine release [19]. Other adverse effects, many of which
have implications to the anesthesiologist, include infec-
tion or perforation of the nasal septum, anxiety, rest-
lessness, irritability, confusion, papillary dilatation,
seizures, tachycardia, peripheral blood vessel constric-
tion, hypertension, angina or myocardial infarction,
ventricular arrhythmias and death [7]. Pulmonary com-
plications associated with cocaine range from simple
asthma to pulmonary hemorrhage [20]. Cocaine addiction
is the result of tolerance, both psychological and physio-
logical. Sudden discontinuation leads to craving for the
drug, mental depression and fatigue.
Anesthetic considerations
Serious complications are associated with both regional
and general anesthesia when administered to cocaine
abusers. Although it is controversial if a platelet count
is required for an otherwise healthy cocaine abuser,
cocaine-induced thrombocytopenia can occur. Many
theories for this have been proposed, including that
this is the result of platelet activation due to arterial vaso-
spasm or part of an autoimmune response [16]. When
regional anesthesia is provided, the hemodynamic con-
sequences of cocaine use should be taken into considera-
tion: hypertension may occur (a result of the peripheral
vasoconstriction); as well as hypotension, which may
lead to cardiac arrhythmias or myocardial dysfunction.
Ephedrine-resistant hypotension may be encountered;
however, it appears that low doses of phenylephrine,
titrated to effect, usually restore blood pressure.
Patients under regional anesthesia may also show com-
bative behavior and altered pain perception, perhaps
due to changes in m- and k-opioid receptor densities
and abnormal endorphin levels [16].
Cocaine-abusing patients under general anesthesia may
also exhibit hypertension and cardiac arrhythmias, with
their subsequent complications. As mentioned pre-
viously, the pathogenesis of cocaine-related myocardial
ischemia is due to increased myocardium oxygen
demand, the result of the vasoconstriction of the coronary
arteries and/or because of enhanced platelet aggregation,
leading to thrombus formation [21]. The latter is the
reason why sometimes these patients are placed in throm-
bolytic therapy during an acute infarction thought to be
related to cocaine use [16]. Severe hypertension may
also occur as a result of direct laryngoscopy in cocaine-
intoxicated patients undergoing general anesthesia. To
reduce this complication, it is recommended that blood
pressure be controlled with medications prior to induc-
tion. b-Blockers, such as propanolol, are contraindicated
in these patients because of the potential for unopposed
a-adrenergic stimulation [22]. Although some may con-
sider that the short elimination half-life of esmolol is
advantageous, its b-blockade may also enhance cocaine-
induced coronary vasoconstriction. Intravenous hydrala-
zine has also been used for the treatment of hypertension
in these patients because of its beneficial vasodilatation
and decrease in systemic vascular resistance. However, a
suboptimal aspect of this medication would be the occur-
rence of reflex tachycardia, in a patient already tachycar-
dic [23]. Labetalol has been another medication
recommended, but its use is also controversial. Its non-
selective b- and a-adrenergic blockade which acts fast
and restores blood pressure without changes in heart
rate, seems useful in cardiovascular changes resulting
from cocaine toxicity [16]. However, unopposed
a-stimulation may occur. Other drugs mentioned include
nitroglycerin, nitroprusside and calcium-channel block-
ers. Cocaine-related chest pain has been treated with
phentolamine (a-adrenergic blocker), nitroglycerin,
verapamil, benzodiazepines and aspirin.
The potent volatile anesthetics may also produce cardiac
arrhythmias and increase the systemic vascular resistance
in patients acutely intoxicated with cocaine. Halothane is
an example of a volatile agent best avoided, because of its
sensitizing effects on the myocardium to catecholamines
[22]. Ketamine should be used with caution or avoided
since it may stimulate the CNS and increase catechola-
mine levels, potentiating cardiac effects, or alternatively
it may cause myocardial depression in the absence of
catecholamines [24]. Etomidate administration should
also be used with caution because of possible myoclonus,
seizures and hyperreflexia. Induction with propofol and
thiopental has proven to be safe in cocaine-abusing
patients. It is controversial whether or not succinylcho-
line produces prolonged blockade because of depletion of
cholinesterase by cocaine metabolism or a competition
between cocaine and succinylcholine for plasma cho-
linesterases [25]. Dexmedetomidine a highly selective
 Anesthetic in illicit-substance-using patients Hernandez et al. 319
a2-adrenoreceptor agonist, recently introduced into
anesthesia practice for its sedative and analgesic proper-
ties, has demonstrated in rats that it delays the onset of
cocaine-induced seizure activity and consequently
increases the cumulative doses of cocaine necessary to
produce seizures [26]. In addition, this may be related to
dexmedetomidine-induced attenuation in the nucleus
accumbens dopamine concentrations in the brain.
Research still continues on how cocaine affects other
organ systems. Some authors emphasize that cardiovas-
cular consequences persist after cessation of long-term
cocaine use, and insist that asymptomatic patients may
have subclinical cardiovascular pathology that should be
assumed as an important cardiac risk factor [27]. Others
show that even without acute intoxication, severe cardi-
ovascular problems are still possible if there is chronic
cocaine abuse and recommend a cocaine-free interval of
at least 1 week before elective surgical procedures [28].
The powerful vasospasm caused by cocaine may also
contribute to the acute renal insufficiency sometimes
seen in these patients, although this could also be sec-
ondary to rhabdomyolisis [29]. Brazilian researchers have
warned about the various effects this drug has on the
respiratory system and stress those related to long-term
use. Some of these pulmonary complications include
infections (pulmonary tuberculosis, AIDS, Staphylococcus
aureus), aspiration pneumonia, lung abscess, septic embo-
lism, noncardiogenic pulmonary edema, barotraumas,
pneumonias, lung infiltrates, vasculitis, pulmonary infarc-
tion, pulmonary hypertension and alterations in gas
exchange [30].
The prevalence of cocaine abuse in young adults has
increased markedly and nearly 90% of cocaine-abusing
women are of child-bearing age [31]. Lack of prenatal
care, history of premature labor and cigarette smoking
are associated risk factors that may arouse suspicion of
cocaine use in pregnancy [31]. Careful and non-
judgmental history-taking, physical examination and
toxicology screening are necessary to confirm the diag-
nosis [32]. Pregnancy enhances the cardiovascular toxi-
city of cocaine and its complications worsen due to the
increased oxygen demand and limited or decreased sup-
ply, due to the increases in heart rate, blood pressure and
left-ventricular contractility [16]. As mentioned above,
due to its solubility there is rapid transplacental diffusion
and high fetal-blood and -tissue cocaine levels, which
may affect fetal blood vessels and uterine blood flow
[16]. Decreased uteroplacental blood flow may lead to
uteroplacental insufficiency, acidosis, hypoxia and fetal
distress [33]. Acute effects from cocaine intake in
parturients include fetal distress, placental abruption,
preterm delivery, fetal tachycardia, hypertension and
intrauterine fetal death [34]. There is also a 4-fold
increase in emergency abdominal delivery in these
parturients. Chronic cocaine abuse produces permanent
biochemical and functional changes in the fetus, affecting
brain structures (e.g. manifested as low IQ scores), and it
is still controversial if there is also an increased risk of
congenital anomalies [34].
In the future it is possible the administration of ondanse-
tron (0.2 mg/kg, subcutaneous), given during the acute
cocaine-withdrawal period, may attenuate intake the
following day, proving to be an effective cocaine-abuse
therapy [35] and help in the perioperative period. This
requires further research.
Opioids
The analgesic and/or euphoric effects of this class of
medication is what attracts people to start using them;
unfortunately, it leads rapidly to tolerance, physical
addiction, psychological dependence and narcotic absti-
nence syndrome [7]. Addiction to opioids occurs rapidly if
the drug is administered daily in increasing doses. These
drugs may be abused orally, subcutaneously or intraven-
ously. Codeine, oxycodeine, meperidine, pentazocine,
fentanyl, propoxyphene, methadone, morphine and her-
oin are all opioids that have been abused. Approximately
30% of adolescents who smoke heroin end up as adult
heroin addicts and the younger the addict and the greater
the number of years of addiction, the greater the risk for
relapse after discontinuation [7]. Heroin abuse may lead
to tetanus, botulism, multiple skin infections, hepatitis (B
and C), HIV/AIDS, pneumonia, endocarditis (by S.
aureus), osteomyelitis, fat necrosis, lipodystrophy, skin
atrophy, peptic ulcer disease, amenorrhea, false-positive
VDRL (venereal disease research laboratory) and many
other complications, all which can be encountered in a
patient requiring surgery [7]. Clinical manifestations of
opioid overdose include slow respiratory rate with an
occasional increase in tidal volume and miotic pupils
[31]. When symptoms of restlessness, insomnia, mydria-
sis, tachycardia, tachypnea and hypertension are mani-
fested, acute opioid withdrawal may be occurring [31].
These symptoms may occur 46 h after the last opioid
intake, with a peak between 48 and 72 h. Dysphoria,
bizarre behavior and unconsciousness are some of the
CNS manifestations that can be seen; the risk of aspira-
tion may also be increased since the patient may lose his
or her ability to protect the airway. Pulmonary edema and
death may result from heroin overdose. Studies on rats
have shown that heroin can injure the myocardium by
changing its myocardial ultrastructure, thought to be a
result of myocardial apoptosis [36]. Craving for the drug
is associated with lacrimation, rhinorrhea, yawning and
piloerection [31].
In parturients, intravenous opioid abuse may affect the
fetus indirectly, as a result of maternal malnutrition or
infection, or directly, by transplacental opioid transfer
320 Anaesthesia and medical disease
and its direct effect on the fetus [31]. Consequences from
intrauterine drug exposure include fetal IUGR, fetal
distress and neonatal opioid withdrawal. Although metha-
done administration has its risks, its maintenance poses
fewer hazards to mother and fetus [31].
Anesthetic considerations
Various medications have been beneficial in helping
heroin addicts stay off this drug. Methadone is one of
these alternatives that serves as a substitute blocking the
narcotic effects, prevents withdrawal symptoms and
reduces the addicts craving for more drugs. It still
provides the classic euphoric state of heroin but allows
the user to re-enter society [7].
Opioid antagonists or agonistantagonists administered
via any route must be avoided in these addicts since they
can precipitate acute withdrawal syndrome. For example,
this occurs minutes after naloxone administration. These
symptoms can be treated with clonidine, which replaces
opioid-mediated inhibition with a2-agonist-mediated
inhibition of the CNS [37]. Diphenhydramine and dox-
epine have also been used. The withdrawal syndrome
may also be reversed by administration of an opioid or by
substituting methadone.
Regional anesthesia can be administered safely to these
patients. An increased tendency for hypotension, how-
ever, should be anticipated. It has been reported that
these patients have an increased incidence of spinal,
epidural and disc-space infection [38]. Since these
patients may have HIV as part of their medical history,
it is important to know that regional anesthesia is not
contraindicated [39]. HIV is a neurotropic virus, which
means that the CNS is infected early in the course of the
disease [40]. However, if any of the patients has AIDS
with CNS HIV infection, progressive demyelination and
neurologic deficits, regional anesthesia may be contra-
indicated [31].
Opioid addicts may have difficult peripheral and central
venous access. Sepsis, coagulopathy and hemodynamic
instability may increase the risk associated with general
anesthesia. These patients may have concomitant liver
disease, malnutrition and reduced intravascular fluid
volume which may require adjustments in anesthetic
drug doses. Acute administration of opioids decrease
minimal alveolar concentration or anesthetic require-
ments [31]. Chronic opioid abuse leads to cross-tolerance
of anesthetic drugs and other depressants, usually a result
of chronic receptor stimulation. Postoperatively, due to
decreased pain tolerance secondary to decreased produc-
tion of endogenous opioids, these patients may experi-
ence exaggerated pain. Perioperative management of the
opioid-dependent patient poses a challenge to anesthe-
siologists and pain specialists due to the conflict between
the patients rights and concerns for safety and abuse,
raising ethical issues [41].
While many opioid addicts want to undergo detoxifica-
tion, most go through unpleasant and sometimes fatal
detoxification processes. Often these prove to be unsuc-
cessful. Newer methods are being studied for detoxifica-
tion [42]. Ultrarapid detoxification allows the individual
to withdraw from the opioid without suffering from with-
drawal syndrome and, if done properly, with few adverse
events. This is done in a controlled setting, like an
intensive-care unit. The patient is not allowed to eat
the night before and given a clonidine patch of 0.2 mg
(12 h before the procedure). Aspiration prophylaxis,
ondansetron and an anticholinergic are administered
before the procedure. Once the patient is monitored,
clonidine is administered to lower the heart rate to 60
beats per minute and systolic blood pressure is kept be-
low 100 mmHg. Rapid sequence induction is performed
and anesthesia is maintained with propofol, methohexital
or inhalational agents. Patients are not maintained para-
lyzed after the induction dose of succinylcholine to
observe the signs of withdrawal (mentioned above).
Withdrawal is then precipitated by an antagonist (intra-
venous naloxone being one of the preferred choices).
After the procedure is finished and extubation is accom-
plished, the patient is monitored and maintained on
naltrexone (50 mg by mouth) for at least 6 months of
the detoxification process. There is continued debate
regarding new treatments like this, the use of naltrexone
implants and the use of gabapentin after rapid opioid
detoxification (ROD), and still more research has to be
done.
Hallucinogens and other so-called club drugs
The hallucinogen group of drugs includes lysergic acid
diethylamide (LSD), phencyclidine (PCP), psilocybin
and mescaline. All are ingested orally and cause auditory,
visual and tactile hallucinations with distortions of body
image, surroundings and reality, anxiety, panic attacks
and a fear of going crazy [31]. These drugs are not
associated with physical dependence or withdrawal
symptoms but do cause psychological dependence and
tolerance. They activate the sympathetic nervous system
by causing hypertension and tachycardia, increase body
temperature and dilate pupils. The effects of acute
ingestion develop over 12 h and last for approximately
12 h. Unrecognized injuries can occur while intoxicated
because of intrinsic analgesic properties (a2-agonist) [31].
Overdose with these medications can cause respiratory
depression, seizures, coma (without respiratory depres-
sion) and death.
LSD is a chemical found in morning glory seeds and
ergot, a rye fungus. It is colorless, odorless and tasteless.
Its action is thought to involve an interaction with

serotonin neurotransporters. PCP, or angel dust, leads to
adrenergic potentiation by inhibiting catecholamine
reuptake in the neurons. It is found in liquid, tablet or
powder forms and is manufactured easily. Helpful med-
ications used to treat agitation produced by these drugs
include diazepam or haloperidol. PCP coma may present
with nystagmus, muscle rigidity and increased deep-
tendon reflexes [7].
Another drug that has the properties of both a hallucino-
gen and a stimulant is 3,4-methylenedioxmethampheta-
mine (MDMA), otherwise known as ecstasy. Other street
names for this drug are X, E, XTC, the love drug, clarity
and Adam, to name just a few. It was first synthesized and
used as an appetite suppressant but its euphoric and
energizing effects made it popular on college campuses
and dance parties [7]. It has also been used as a date-rape
pill. It is swallowed or inserted rectally, being absorbed
readily by the gastrointestinal tract [43]. Its effects
usually last 36 h but it can last as long as several days.
Some of its effects include memory dysfunction, cogni-
tive disabilities and behavioral problems, a result of the
damage done to serotonergic neurons in the CNS [7].
High doses of MDMA may induce malignant hyperther-
mia, cause breakdown of muscle tissue which may pro-
gress to kidney and heart failure [7,44]. Fulminant liver
damage and disseminated intravascular coagulopathy
have also been documented [45]. Several cases of seizures
have been attributed to the severe hyponatremia and
cerebral edema that results from profound sweating and
increased water consumption (water intoxication) [43].
Rohypnol or flunitrazepam is a CNS depressant from the
same family as diazepam and midazolam. It has anxio-
lytic, anticonvulsant and sedative/hypnotic properties. It
can be snorted or taken orally; if used on a regular basis, in
order to get a high, increasingly larger doses need to be
taken. It is also another of the date-rape drugs and is
administered as a pill or dissolved in liquids. Anterograde
amnesia occurs with blackouts of short-term memory loss
or suppression of events happening while under the
drugs influence. Effects are observed within 30 min of
ingestion, peak within 12 h and last as long as 810 h
[43].
g-Hydroxybutyrate (GHB), or liquid ecstasy, is another
popular club drug which acts as a CNS depressant,
leading to euphoria and the reduction of ones inhibitions
[7]. Its usefulness as an anesthetic declined after the
development of newer anesthetic agents and because of
its side effects (severe nausea and vomiting, seizures,
and lack of analgesic properties) [43]. It is a so-called
designer drug, easy to make at home, and is often abused
by being placed in party drinks to produce sedation
and amnesia. GHB addicts undergo a withdrawal
syndrome when stopping the drug [7]. Its effects are
Anesthetic in illicit-substance-using patients Hernandez et al. 321
noted within 1020 min, can last for up to 4 h. Because
it is cleared so rapidly from the body, is metabolized into
carbon dioxide and water, and has no residue of toxic
metabolites, it is very difficult to detect by drug testing
[7]. An overdose of GHB (which generally requires large
doses) can result in respiratory depression, coma and death.
Ketamine is a PCP derivative with sedative, anesthetic,
amnesic and analgesic properties. It can be given orally,
intravenously or intramuscularly; when used illicitly, its
common form is a white powder that can be snorted,
smoked or used intravenously, intramuscularly or orally
[43]. Its attraction to users comes from its out-of-body
experience and its dissociative effects. Delirium, amne-
sia, depression and long-term memory and cognitive
problems are some of its common effects. In high doses
respiratory arrest can occur, the sympathetic nervous
system is upregulated and increases in systemic and
pulmonary artery pressures can occur, along with
increases in cardiac output and heart rate that could result
in coronary ischemia in predisposed patients [7].
Fry is an altered form of marijuana that is smoked in
PCP-laced, formaldehyde-soaked marijuana cigarettes
[43]. The primary effect of smoking these cigarettes is
toxic psychosis. Other effects include hallucinations,
delusions, panic, paranoia and loss of consciousness. Side
effects are associated with embalming fluid, which
include disorganized thoughts, decreased attention span,
psychomotor agitation and upregulation of the sympa-
thetic nervous system. Exposure to the embalming fluid
formaldehyde can cause bronchitis, brain and lung
damage, inflammation, impaired coordination and sores
in the throat, nose and esophagus [43].
Parturients abusing hallucinogenic drugs have a higher
risk of premature labor and delivery, fetal IUGR,
meconium-stained fluid and neonatal withdrawal syn-
drome. The hyperthermia induced by these drugs is
thought to increase maternal and fetal oxygen consump-
tion, leading to possible fetal heat-induced neurological
injury [46]. If MDMA is taken during pregnancy, the risk
for congenital effects is increased (cardiac anomalies,
cleft lip and palate, biliary atresia, fetal IUGR, intrauter-
ine fetal demise and cerebral hemorrhage) [7,47,48].
It is important to be aware that these illicit drugs are often
used in combination with other drugs and alcohol. This
may potentiate most of their side effects and intoxication
would be more harmful. There are no known antidotes
for intoxication with rave or club drugs and treatment
would be supportive if such a case arises.
Anesthetic considerations
During anesthesia and surgery, some issues can be
anticipated in these patients. The risk of autonomic
322 Anaesthesia and medical disease
dysregulation is high and wide swings in blood pressure
and tachycardia should be prevented since there is an
increased risk of cardiomyopathy, coronary and cerebral
vasospasm [43]. There have been reports of arterial
vasospasm leading to nonhemorrhagic cerebral vascular
accidents, myocardial ischemia and infarction [49,50].
Due to its sympathomimetic stimulation effects, extreme
caution should be taken when using vasopressors such
as ephedrine, even if regional anesthesia produces
sympathectomy-induced hypotension [31]. These patients
exhibit an exaggerated response to sympathomimetic
drugs and arrhythmias are likely. It is also thought that
hallucinogens may prolong the analgesic and ventilatory-
depressant effects of opioids. The overzealous consump-
tion of water by ecstasy users may not only bring us a
patient with water intoxication and cerebral edema, as
mentioned above, but also a patient with pulmonary
edema [51,52]. Fluids and electrolytes must be evaluated
closely while in the operating room [43]. It has also been
suggested that LSD and PCP may cause prolongation of
succinylcholine effects, a result of presumed inhibition of
plasma cholinesterase activity [44]; but most important in
patients with a history of MDMA-related hyperthermia is
the avoidance of volatile agents and succinylcholine.
Anesthetics metabolized through liver and eliminated
through the kidneys may have a prolonged effect that
may be due to fatty liver changes and acute renal failure
in MDMA abusers.
In parturients, these amphetamine-like medications may
pose a problem from their initial presentation to an
anesthesiologist. The combination of hypertension and
proteinuria with or without seizures from their acute
intake may be mistaken for preeclampsia or eclampsia.
Routine laboratory studies (liver- and kidney-function
tests) along with urine toxicology screening may help rule
out one or another of the diagnoses.
Solvents
Inhalants include a variety of substances, such as organic
solvents and volatile agents, that affect the CNS.
Toluene is the most commonly used solvent and a major
component of household paints, glue, rubber cement and
cleaning agents. These drugs can be sniffed or ingested
orally. The ease of obtaining these solvents and the
transient euphoria that toluene yields is what attracts a
great number or adolescents to abuse it. Inhalant-abuse
complications include cardiac arrhythmias, bronchial irri-
tation, acute respiratory distress syndrome, liver toxicity,
pulmonary hypertension, methemoglobinemia and death
from cerebral or pulmonary edema [7,31]. Chronic expo-
sure causes changes in the CNS such as cerebellar
degeneration and diffuse brain atrophy [53,54]. Lead
poisoning is linked to gasoline sniffing and renal and
hepatic toxicities are linked to trichloroethylene [7]. In
pregnancy, the use of these solvents has been associated
with an increased risk of preterm delivery, prenatal
mortality and fetal IUGR [55,56].
Anesthetic considerations
As mentioned previously, these patients are at an
increased risk of developing cardiac arrhythmias due to
autonomic cardiac dysfunction caused by the abuse of
these solvents. Myocardial infarction and labile blood
pressures might also be encountered. In acutely intoxi-
cated patients, general anesthesia is sometimes the best
option due to their respiratory compromise and increased
incidence of nausea and vomiting. Pulmonary complica-
tions may reflect increased airway resistance. When
regional anesthesia is considered, it is important to con-
sider the patients altered perception and combative
behavior. Distal and proximal acidosis could be of con-
cern in these patients.
Conclusion
Substance abuse remains one of the biggest societal
problems around the world despite education on preven-
tion and rehabilitation of illicit drugs. Anesthesiologists
should be aware of this problem and the most likely
effects and potential risks associated with the abuse of
illicit substances. Some of these patients may present at
preadmission testing, emergency situations (even critical
care) or in the obstetric suite for anesthesia or analgesia. It
is very important to enquire in a nonjudgmental way
about addiction and substance abuse, obtain toxicology
screens, and identify these patients in order to minimize
the adverse effects of anesthetic agents and other drugs
provided while in care. It is equally important to mini-
mize postoperative risks from inadequate analgesia. Due
to the diverse clinical presentations that may arise from
substance or polysubstance abuse, the anesthetic
management should be tailored to each individual and
universal precautions should always be followed when
providing care.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
 of special interest
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